Neurosis

Neurosis: Understanding
Common Mental Illness
Published online by Cambridge University Press

‘Psychiatry cannot advance without a good classification. We have failed to
achieve this, most particularly with common mental disorders. This important
book by Peter Tyrer shows a way forward, giving special attention to mixed
anxiety and depressive disorders, the most important diagnosis of all. It should
be mandatory reading for all psychiatrists.’
David Goldberg, Professor Emeritus, Institute of Psychiatry,
King's College London, UK
‘DSM-5 & ICD-11 are splitter systems that artificially divide the diagnostic pie
into tiny slices. The resulting artificial and misleading “comorbidity” often leads
to fragmented and excessive treatments. Tyrer beautifully demonstrates the
clinical realities that patients are necessarily more complicated than diagnostic
systems and that flexible formulation is more important than rigid adherence to
criteria sets. This is an extremely valuable book for all mental health profes-
sionals at all levels of training and experience.’
Allen Frances, MD, Professor and Chair Emeritus, Department of Psychiatry,
Duke University, Durham, NC, USA, and Chair, DSM-IV Task Force
‘This highly readable book has long been needed. It is an essential reference for
improving clinical thinking, whether you are a physician or a psychologist. It
helps building unitary perspectives that may shed light on phenomena that
would otherwise remain scattered in the patient’s story. What is shared by
syndromes such as anxiety, panic, phobic disturbances and irritability may be
as important as the differences between them and conditions that are apparently
comorbid could be part of the same general neurotic syndrome.’
Giovanni A. Fava, MD, Clinical Professor of Psychiatry, University at Buffalo,
State University of New York, Buffalo, NY, USA

Neurosis
Understanding Common Mental Illness
Peter Tyrer
Emeritus Professor of Community Psychiatry Imperial College of Science, Technology and Medicine, London, and Consultant
in Transformation Psychiatry, Lincolnshire Partnership NHS Foundation Trust

University Printing House, Cambridge CB2 8BS, United Kingdom
One Liberty Plaza, 20th Floor, New York, NY 10006, USA
477 Williamstown Road, Port Melbourne, VIC 3207, Australia
314–321, 3rd Floor, Plot 3, Splendor Forum, Jasola District Centre,
New Delhi – 110025, India
103 Penang Road, #05–06/07, Visioncrest Commercial, Singapore 238467
Cambridge University Press is part of the University of Cambridge.

It furthers the University’s mission by disseminating knowledge in the pursuit of
education, learning, and research at the highest international levels of excellence.
www.cambridge.org
Information on this title: www.cambridge.org/9781911623656
DOI: 10.1017/9781911623823
© Royal College of Psychiatrists 2022
This publication is in copyright. Subject to statutory exception
and to the provisions of relevant collective licensing agreements,
no reproduction of any part may take place without the written
permission of Cambridge University Press.
First published 2022
Printed in the United Kingdom by TJ Books Limited, Padstow Cornwall
A catalogue record for this publication is available from the British Library.
Library of Congress Cataloging-in-Publication Data
Names: Tyrer, Peter J. author.
Title: Neurosis : understanding common mental illness / Peter Tyrer.
Description: Cambridge, United Kingdom ; New York, NY : Cambridge University Press, [2022] | Includes
bibliographical references and index.
Identifiers: LCCN 2022004173 (print) | LCCN 2022004174 (ebook) | ISBN 9781911623656 (paperback) |
ISBN 9781911623823 (ebook)
Subjects: MESH: Syndrome | Neurotic Disorders | Comorbidity | Depressive Disorder | Anxiety Disorders |
Personality Disorders | Longitudinal Studies
Classification: LCC RC346 (print) | LCC RC346 (ebook) | NLM WM 170 | DDC 616.8–dc23/eng/20220412
LC record available at https://lccn.loc.gov/2022004173
LC ebook record available at https://lccn.loc.gov/2022004174
ISBN 978-1-911-62365-6 Paperback
Cambridge University Press has no responsibility for the persistence or accuracy of
URLs for external or third-party internet websites referred to in this publication
and does not guarantee that any content on such websites is, or will remain,
accurate or appropriate.
Every effort has been made in preparing this book to provide accurate and up-to-date information that is in
accord with accepted standards and practice at the time of publication. Although case histories are drawn
from actual cases, every effort has been made to disguise the identities of the individuals involved.
Nevertheless, the authors, editors, and publishers can make no warranties that the information contained
herein is totally free from error, not least because clinical standards are constantly changing through
research and regulation. The authors, editors, and publishers therefore disclaim all liability for direct or
consequential damages resulting from the use of material contained in this book. Readers are strongly
advised to pay careful attention to information provided by the manufacturer of any drugs or equipment
that they plan to use.

Dedicated to the memory of Philip Snaith (1933–2003), Senior Lecturer in Psychiatry,
University of Leeds, who taught not wisely but too well

Contents
List of Figures viii
List of Tables ix
Foreword by Robert Kendell xi
Acknowledgements xii
Introduction 1 6 The General Neurotic Syndrome at 12

Years 52
1 The General Neurotic Syndrome 8
7 The Last Phase: The General Neurotic
2 DSM-III and the Generation of New
Syndrome after 30 Years 68
Diagnoses 21
8 Is the Notion of the General Neurotic
3 The Hypotheses of the Nottingham
Syndrome Useful? 82
Study of Neurotic Disorder 28
4 Interpretation of the Results of the
1988 Lancet Randomised Trial 37
5 The Medium-Term Outcome of the Appendix 101
General Neurotic Syndrome 44 References 134
Index 141
vii

Figures
1.1 The initial formulation of the general neurotic syndrome and its components, includ-
ing its variation over time in response to stresses 11
1.2 The confusing relationship between duration of symptoms and diagnosis in DSM-III
and ICD-10 14
4.1 Results of the Nottingham Study of Neurotic Disorder trial separated by randomised
group for each of the main outcomes 37
4.2 Results of the Nottingham Study of Neurotic Disorder randomised trial separated by
initial DSM diagnosis 38
5.1 Mean changes in total psychopathology scores (CPRS) for patients with the general
neurotic syndrome (GNS+) (n = 66) and those without (GNS–) (n = 115). The GNS
positive cases represent scores of ≥ 6 on the GNS scale 45
6.1 Effect of personality status on global symptomatology (measured by the
Comprehensive Psychopathological Rating Scale (CPRS) at baseline and 12 years) 63
7.1 Flow chart of missing individuals for outcome assessments by follow-up time
point 71
8.1 The neurotic spectrum of common mental disorders 86
viii

Tables
1.1 The General Neurotic Syndrome Scale (GNSS) 13
1.2 The association of depression and anxiety with the symptoms of common mental
illness 15
2.1 Differentiation of patients in my personal practice between 1975 and 1981 22
3.1 Randomised trial and treatment numbers 33
4.1 Baseline data in all treatment groups in randomised trial 39
4.2 Adjustment of diagnosis after accounting for cothymia 39
4.3 Personality status of patients with GNS at baseline 40
5.1 Summary of regression analysis on outcome in first two years of Nottingham Study 44
5.2 Global outcome in 182 patients after five years 46
5.3 Service outcomes separated by general neurotic syndrome (GNS) status five years after
randomization 48
5.4 Service outcomes separated by baseline personality disorder 49
5.5 Service outcomes separated by DSM-III diagnosis after adjustment for cothymia 50
6.1 Measures included in the 12-year follow-up of the Nottingham Study 52
6.2 Comparison between initial and cold-call responders for selected initial variables 55
6.3 Univariate predictors of 12-year costs ($) 58
6.4 Neurotic Disorder Outcome Scale [NDOS] 60
6.5 Relationship between baseline characteristics and outcome as measured by the
Neurotic Disorder Outcome Scale (NDOS) over 12 years in 193 patients 61
6.6 Final model showing the elements contributing most to clinical outcome at 12
years 63
6.7 Relationship between other baseline variables and outcome in terms of social function
(SFQ) at 12 years 64
6.8 Final model of variables predicting social functioning score at 12 years in 177
patients 67
7.1 The 24 components of the Personality Assessment Schedule (PAS) and the Personality
Assessment Schedule-Strengths Version (PAS-SV) 69
7.2 Factor analysis of the Personality Assessment Schedule-Strengths Version
(PAS-SV) 70
7.3 Distribution of deaths in the Nottingham Study by personality status 72
7.4 Formal psychiatric diagnosis (DSM) at long-term follow-up points 73
7.5 Total psychopathology scores (CPRS) at long-term follow-up points 74
7.6 Clinical outcome by GNS status at long-term follow-up points and mean CPRS
scores 74
7.7 Social function – measured by the Social Functioning Questionnaire (SFQ) and the
Neurotic Disorder Outcome Scale (NDOS) at long-term follow-up points 75
7.8 Differences in treatment and service contacts between patients with or without the
general neurotic syndrome 76
7.9 Personality strengths by baseline characteristics of patients 77
7.10 Personality strength by characteristics of patients at 30-year follow-up 79
8.1 Details of patients rated as recovered at 30-year assessment 87
ix

Foreword
Books that are primarily concerned with the implications of classifications of psychiatric
disorders have always been less common than new classifications themselves.1 This is
unfortunate, because all classifications, including those which aspire to being ‘atheoretical’,
embody many fundamental assumptions about the nature of their subject matter. They also
have a major influence on how their users conceptualise the phenomena in question.
Indeed, this may well be why new typologies appear so frequently, for those who are
persuaded to adopt them will also, wittingly or unwittingly, adopt most of their authors’
underlying assumptions. Treatises devoted to the classification of neuroses are particularly
uncommon. It is generally assumed that the classification of psychotic disorders or of
depressive illnesses is more important, and also that these topics can be more profitably
discussed because more relevant empirical evidence is available. This book is therefore as
unusual as it is welcome.
Dr Tyrer describes what will be for the next decade or so the two most influential and
widely used classifications of neurotic disorders – the forthcoming (10th) revision of the
International Classification of Diseases (ICD-10) and the American Psychiatric Association’s
classifications, DSM-III and DSM-III-R.2 He focuses on the differences between them and
the novel concepts, like panic disorder, which are common to both. He also discusses the
implications of these differences and the relevant empirical evidence – the clinical trials and
family studies and follow-up studies – that helps to establish the validity of the diagnostic
concepts concerned. He therefore not only describes the phenomena of neurotic illness and
contemporary classifications of these phenomena; he also raises important practical and
theoretical questions that might otherwise have remained unasked.
Dr Tyrer writes as a practising clinician, observing as he does so, with only the faintest hint
of menace, that as ‘the fate of any classification depends on the reaction of its main users, it is
clinicians who hold the key to success’ (Tyrer, 1989, p. xi). This stance is one of this book’s
greatest strengths, for it is apparent in every chapter that the text has been written by someone
who combines a comprehensive knowledge of the literature with extensive personal experi-
ence of the symptomatology, treatment, and prognosis of neurotic disorders. Dr Tyrer has, of
course, prejudices of his own. He remains convinced that ‘neurosis’ is still a valuable concept,
that different clinical presentations are less discrete and stable than the architects of DSM-III
have assumed, that new concepts should not be adopted until they have been validated by
long-term follow-up studies, and that patients with a fluctuating mélange of depressive,
anxious, and obsessional symptoms are so common that the term ‘general neurotic syndrome’
must be retained to describe them. Several experienced psychiatrists already share these views;
others will be converted to them by reading this important monograph.
R. E. Kendell
Department of Psychiatry, Edinburgh University
1
This was the foreword to the precursor of this book published in 1989. It is highly relevant today.
Robert Kendell died in December, 2002.
2
The current text uses ICD-11, throughout.
xi
https://doi.org/10.1017/9781911623823.001 Published online by Cambridge University Press

Acknowledgements
This book has benefited greatly from frank comments received from colleagues. These have
reduced some of my egotistical opinions and helped to create a more balanced text.
Unadulterated criticism from friends is always a great leveller. In alphabetical order,
I thank Gavin Andrews for our harmonious interaction about the general neurotic syn-
drome; Dr Barbara Barrett and Professor Sarah Byford for economic advice; Professor
German Berrios and his wife, Doris, for helping me to understand Cullen’s work on
neurosis; Professor Patricia Casey for helping to define the position of adjustment disorders
in common mental illness; Professor Kate Davidson for getting my CBT language in order;
the late Sir Richard Doll for his advice about follow-up; Professor Chris Dowrick and
Dr Jayati Das-Munshi for discussions about mixed anxiety and depression; Professor Sir
David Goldberg for his stimulating and sometimes provocative comments about the
classification of common mental disorders; the late Robert Kendell, his daughter, Kate,
and his widow, Ann, for their help in understanding the purpose of diagnosis; Alan Kerr for
helping me to understand the work of the 1972 Newcastle group in their publications on
affective disorders; Michael King and the members of the MENCOG MRC Collaborative
Research Group for their assistance in the 12-year follow-up, Phil Levy for help with
illustrations; Professor Glyn Lewis for pointing out the real reasons for reluctance to
diagnose anxiety and depression together, and for creating the Lewis Prediction; ‘Lizzie’,
one of the patients in the study for her story; Professor Richard Mindham for giving me
context to the Nottingham psychiatric services in the 1970s; Professor Roger Mulder for
saying it like it is; NHS Digital and Sylvia Teale for their help in following up patients in the
longer term; Northampton Research Ethics Committee for their understanding about cold-
calling; Jessica Papworth of Cambridge University Press for guiding the book to publication;
Professor Gene Paykel for constant encouragement; Dr George Stein for giving historical
substance to personality disorder; the Library Services at the Royal College of Psychiatrists
for helping with background material, especially the works of Adolf Meyer; and my wife,
Helen, for being the most effective follow-up interview specialist on the planet.
But my greatest indebtedness is to the people who carried out the initial assessments in
the study so conscientiously (Paul Barczak, Judith Brothwell, Claire Darling, Brian
Ferguson, Susan Gregory, David Kingdon, Siobhan Murphy, and Nick Seivewright) and
the statisticians who have helped in the analyses at all stages. Dr Tony Johnson, formerly of
the MRC Biostatistics Unit in Cambridge, carried out almost all the analyses of the data
from the randomised trial in 1988 to the 12-year follow-up, and who also assisted at 30
years. Professor Min Yang has been tireless in assessing and analysing the data over the
whole period of follow-up and without her help this book would not have been completed.
My brother, Stephen, and my son, Jonathan, were also very helpful in the early stages of the
study. The full data of the study, including the anonymised data base, have been placed in
the University of Nottingham Manuscripts and Special Collections, MS 1048.
xii

Introduction
Neurosis is passé, neurosis belongs to history, neurosis is dead. So why am I writing this
book? The reason is that we need to be aware of, even if we do not embrace, information
that suggests the way we now look at common mental illness is not necessarily the most
accurate or productive way of understanding, and more importantly, treating it. I also
introduce this book with the foreword to its predecessor (Tyrer, 1989), written by the late
Robert Kendell, and this also explains why I am publishing at this time. Robert, whom I will
refer to as Bob from now on, was a stickler for accuracy and rarely wrote anything down that
he could not defend with facts. His foreword was written 32 years ago but is just as apposite
today – he actually could have written it today with the same wording, and this in itself
reflects the poverty of attention that this subject has received since 1989. His statement ‘new
concepts should not be adopted until they have been validated by long-term follow-up
studies, and the patients with a fluctuating mélange of depressive, anxious and obsessional
symptoms are so common that the term “general neurotic syndrome” must be retained to
describe them’, is the keynote to this book. The central part of this book presents the results
of a long-term follow-up study of the general neurotic syndrome, and even allowing for my
prejudices (as Bob K rightly points out) it is difficult to ignore the findings that support it.
Is it appropriate to go back to the old concept of neurosis? Of course not. That is not
what I am arguing, but the old concepts still offer us a level of understanding that should at
least make us pause before we gallop off into the extremes of neuroscience or abandon
classification altogether in favour of holistic understanding.
The arguments presented here are based on current evidence, much of it relatively new
in connection with a 30-year study, and although the gaps sometimes have to be filled by
opinion, I hope this will be regarded as informed and consistent, and where there are cogent
alternatives, I hope they will all be acknowledged. The current notions of common mental
disorders are all open to both support and criticism, but most would agree that they have not
yet greatly advanced the lot of those who suffer from them.
Let us go back to some lines from three centuries ago. ‘Have you no consideration for my
poor nerves?’ ‘You mistake me, my dear. I have a high respect for your nerves. They are my
old friends. I have heard you mention them with consideration these twenty years at least.’
Many people will recognise these lines immediately1. A Mr Bennet uttered them,
deciding to respond to his neurotic wife with detached amusement rather than conflict.
But therein lies his quandary. He makes no attempt to reform his wife, to alleviate her
continuing ‘nerves’ and what are now frequently named ‘medically unexplained symptoms’,
1
Of course, they come from Jane Austen’s Pride and Prejudice, so well known that no reference is
needed.
1

2 Neurosis
and when they become too much to bear, he retires to his sanctuary, The Library. He
assumes, and the world will assume, that his wife, Mrs Bennet (she appears to lack a first
name as in the Bennet household only the children have Christian names), will continue her
merry dance with neurotic symptoms until she is released by death.
Do we look on Mrs Bennet in a completely different way now? I do not think we do. We
still, at least in conversations in off-hand moments to people we feel we can trust, refer to
people as ‘nervous’ or ‘neurotic’, and even though the Mrs Bennets, when seen by health
professionals, often come away with a Greco-Latin epithet followed by disorder, the
outcome is often not very different from that of the original Mrs Bennet. We have improved
in mental health literacy so that she is no longer a figure of fun (Jane Austen could have been
a little more generous here but it would have spoiled the novel), but are those who have
followed her much improved in life satisfaction or personal satisfaction? It would be hard to
say ‘yes’.
But when you look at textbooks of psychiatry you might think very differently. Each of
the disorders formerly described as neurotic are demarcated, walled off, and details given of
their epidemiology, their origins, their clinical manifestations, their preferred treatment,
and their outcomes. Even better, a case history can be added that encapsulates all that is
pertinent to the condition. ‘So here we have a classical case of social anxiety’, or ‘a beautiful
example of panic disorder progressing to agoraphobia’, or ‘a paradigm of all the features of
generalised anxiety disorder’, but in practice the newly qualified doctor finds it very hard to
identify them. Maurice Pappworth, a scourge of the medical establishment in the middle
years of the last century, was a very effective teacher of medicine, and he reminded his
students that their most important tasks were to observe, examine, and record what they
found, rather than be a slave to texts on the subject (Pappworth, 1971). He stressed that
‘classical examples’ of diseases became classical because they were good for textbooks but in
practice are very rare, and most diseases present in more complicated ways.
It is the same with the conditions that have followed the loss of neurosis. They look good,
smell good, and seem convincing, but in practice tend to merge together, and the textbook
chapters betray this when they add a section on comorbidity at the end, a subject that we will
come to later on many occasions in the rest of this book. But because these new conditions
have been given special status, especially since the introduction of the DSM-III in 1980, they
are respectable diagnoses, and are almost always examined separately in research studies.
This means that there are now very few studies in which two or more common mental
illnesses are examined together as though they might represent a unity.
But to understand what has happened with neurosis in the last 300 years we need to re-
enact its beginnings and its demise.
The Birth of Neurosis

The four humours of Hippocrates, black bile, yellow bile, phlegm and blood, dominated
medical understanding for 3,000 years, and medical advances only came with better
knowledge of anatomy, physiology, and technology right at the end of this period.
Psychiatry had very little part to play in this: as we are reminded repeatedly by all who
criticise the profession, mental illness very rarely leaves evidence of its presence on the
structure of the body.
The period at the end of the eighteenth century is referred to as the Scottish
Enlightenment, when, following the example of the philosopher David Hume, every aspect

Introduction 3
of knowledge was questioned and re-examined, and so it was not surprising that mental
illness came under the focus of enlightenment too and was followed by others. ‘Neurosis’
became the new word for common mental illness. It was first formulated as ‘nervous
diseases’ by Robert Whytt (1765) to ‘describe the common features of the disorders which
are the subject of the following observations . . . under the name of flatulent, spasmodic,
hypochondriac or hysteric’. Whytt was an experimenter too and attempted to find patho-
logical differences in his patients. This, not surprisingly, led him up the blind alley of
reductionism. His investigations suggesting the nerves of women were more motile than
those of men and so predisposed them to neurosis, fell flat.
His successor as Professor of the Practice of Medicine at Edinburgh University, William
Cullen, was not primarily a researcher but a synthesiser. He organised the writings of Whytt
more coherently and described neuroses as a unitary group of nervous disorders (Cullen,
1777) with a much wider focus than the concept subsequently possessed, but included
depression, anxiety, hysteria, and hypochondriasis. This was new. Although hypochondria-
sis and hysteria were described in earlier texts from Theophrastus onwards, they were only
brought together by Cullen. Piñero also gives particular credit to Thomas Willis and
Thomas Sydenham in their writings a century earlier in clarifying earlier definitions
(Piñero, 1983, pp. 2–4) of hypochondriasis and hysteria in advance of Cullen. When two
or more disorders represent two aspects of the same disorder the word ‘consanguinity’ is
more appropriate than co-occurrence or comorbidity (Tyrer, 1996) and the diligent Scottish
investigators were the first to join this range of disorders together as a consanguineous
condition.
In a curious paradox, just as Robert Spitzer destroyed the concept of neurosis in the
DSM-III by harnessing groups of experts and creating consensuses to split neurosis,
William Cullen did the same in harnessing all the terms for nervousness and linking
them. Both men planned in the same way. Cullen thought of the neuroses in the same
way as the stellar classifier of the day, Carl Linnaeus, as genera and species. The four genera
were the comas (species: apoplexy and paralysis – including hysterical paralysis); adynamiae
(species: dyspepsia, hypochondriasis, and chlorosis – a nervous disease of blood-forming
organs [cf. anaemia]); spasmi (species: tetanus, trismus, epilepsy, palpitations, colic, hys-
teria); and vesaniae (species: melancholia, mania, somnolence). Cullen’s followers expanded
and modified this list in subsequent decades, and although the neuroses are included here,
the full classification looks very much like an early edition of DSM-III, but with each
condition spared the epithet of the ubiquitous noun ‘disorder’.
Because the Scottish Enlightenment led the way in European science the works of Whytt
and Cullen became widely known across the continent and were quickly translated into
other languages. In retrospect they probably had more traction and popularity in Europe as
a whole than in England, where the Enlightenment was not looked on with universal
approval.
The Recognition of Personality Status in Neurosis

Adolf Meyer (1866–1950) is now almost totally forgotten as a psychiatric innovator. This is
curious as he was the pre-eminent figure in American psychiatry in the first half of the
twentieth century. This is partly because he was one of the few people who could bridge the
gap between the Kraepelinian search for meaningful diagnoses similar to those in medicine,
and the psychoanalytical school, who generally abhorred diagnosis as an unwelcome

4 Neurosis
interloper interfering in the real enquiry, the search for psychiatric meaning. One of the
reasons he is not remembered is that his writings are almost indecipherable. Meyer was born
in Swiss Germany and although he mastered English well when it came to lecturing, he
seemed to view the written page as a place where there was competition to write the longest
and most impenetrable sentences.
This is a pity, as he had some important observations to make. He could be regarded as
the originator of ‘whole person medicine’. He is best known for the emphasis he makes on
getting to know patients properly before deciding how to help them. This may seem an
unnecessary aphorism now but it certainly wasn’t in 1902 when he wrote, ‘we need a crusade
against empty utterances of opinion when facts are available, against the use of diagnostic
terms which have no definite meaning’ (Meyer 1902, p. 101). Bob Kendell, in his masterly
book, The Role of Diagnosis in Psychiatry, noted that most psychiatrists, whether in training
or very experienced, reach their final diagnosis within a few minutes of an interview
(Kendell, 1975a). You could regard this as an efficient diagnostic system but if the wrong
decision is made prematurely the outcome can be disastrous.
Meyer would have been heavily critical of diagnostic guidelines (especially easily
learned operational criteria) that dominate current assessment because he rightly felt
that attaching a diagnosis could deflect interest about other important elements that were
not included in that diagnosis. At worst, the person becomes a diagnosis and loses
individuality.
But the real reason I am giving attention to Adolf Meyer is that he gave more attention to
personality status than all his predecessors and most of those who followed him. He felt very
strongly that without the assessment of personality the mental state examination was
incomplete. Many people consider that he went too far in emphasising the uniqueness of
the individual and their personality, but he made sure that everyone knew his views. He
argued that psychiatric disorders were reactions of the person to events – you could call this
the beginning of life-events research – and as each person had limited ways of reacting, these
‘reaction types’ could be used to delineate psychiatric disorders. These ideas were adopted
more strongly in the United Kingdom than in the Americas, and one of the most popular
mental health textbooks of all time, Henderson and Gillespie’s Textbook of Psychiatry, first
published in 1927 and extending to a tenth edition by 1969, used Meyer’s concepts
throughout.
It is sad that Meyer did not develop his ideas further with respect to personality.
Nonetheless, he felt the subject was extremely important and insisted on teaching it
himself when his colleagues proved to be inadequate in getting the message across to
students. His textbook pronouncements became lost in the verbal thicket but in his
teaching he was very persuasive and convincing, and even this comes through when he
writes about personality.
In my training of medical students, I have each student work out a fairly systematic
personality study of the worker himself or herself and a more summary sketch of a few
outstanding contrasting classmates or known persons. (Meyer, 1902, p. 247)
For this reason each student is asked to make a study of a specific person, preferably
of himself, together with comparisons with three classmates showing particularly out-
standing contrasts and differences. Our study deals with the concrete objective and not
really introspective performances, the methods of their presentation and formulation,
and the testing and using of the data and problems of adjustment of a personality.
(p. 259)

Introduction 5
He gave them tests, asking to what extent satisfaction was determined by performance and
mood, capacity, opportunity and ambition, and the need to be appreciated by others. He
maintained that every medical practitioner should assess the ‘person and attending person-
ality’ whenever they assessed a patient.
Where Meyer went off the rails was in setting up a system of classification emphasising
that everything that impacted on the ‘oneness’ of the person was a reaction to the genetic,
developmental, and environmental factors that made that person unique. He called these
reactions the ‘ergasias’, and this word was translated by others into ‘reaction types’ in
place of psychiatric diagnoses. So, his followers, eventually more outside the United States
than within it, used this phrase repeatedly between 1925 and 1960. This included the 10th
edition of Henderson and Gillespie’s frequently edited textbook (Henderson and
Batchelor, 1969), the most interesting parts of which are the case histories, which are
not only described in great detail but are clearly authentic, not airbrushed into matched
diagnoses like the ones Pappworth so disparaged. It is interesting how Henderson estab-
lished the accuracy of his case accounts. Morrison (2016) describes how he established
routine ‘staff meetings’ at Gartnavel Hospital in Glasgow in which a psychiatrist asked
questions of a patient and a stenographer in the room recorded word-for-word the
conversation that passed between the two parties. Henderson was following his mentor,
Adolf Meyer, identifying the person clearly before making any judgement about
diagnosis.
Why didn’t Meyer go further and attempt to tease out the personality component of his
diagnostic system? Nobody knows, but by concentrating on the ‘ergasias’, a term nobody
ever used in practice, he lost the support of those who might otherwise have taken his views
forward more systematically.
Neurosis and Neuroticism

What is surprising is that so few people have made any sort of diagnostic connection
between neurosis and neuroticism. The terms have just melded together without their
implications being considered. It is this relationship that led me to suggest the existence
of the general neurotic syndrome in the 1980s and led to the book published late in the
decade (Tyrer, 1989).
The central argument was a simple one. If so many common mental illnesses are linked
to neuroticism in the form of a personality variable, might it not be that the mental disorders
from which they suffer are also linked to neuroticism to the extent that they form a common
group of disorders. Time after time in the 1980s, when I was writing to general practitioners
about my assessment of patients in the clinic, I had to write sentences such as ‘according to
current classification this patient has an episode of depression but this only explains a tiny
part of the clinical picture. I would regard the patient as having a mixed neurotic disorder
with both anxiety and depressive symptoms with a degree of social phobia that could easily
progress to agoraphobia.’
I will illustrate this, as I will repeatedly throughout this book, by describing a patient who
has long-term generalised anxiety, other mood disturbance, and hypochondriasis. Yes, here
she is again. She is Mrs Bennet from Pride and Prejudice, and as she is fictitious, she cannot
take offence, and, indeed, so much will her assets impress you over the course of her
evaluation, that at the end she may be proud of her diagnosis. Yes, as you might expect,
I am going to argue that she exemplifies the general neurotic syndrome.

6 Neurosis
It may seem odd that Jane Austen, despite her excellent powers of observation and
understanding, describes Mrs Bennet’s symptoms as though they were entirely made up,
or factitious in current parlance (whoever thought up this word with only one letter
different from ‘fictitious’ deserves to be arraigned for language offences). So Jane describes
Mrs Bennet as ‘a woman of mean understanding, little information and uncertain temper’,
following it up by the crushing statement ‘when she was discontented she fancied herself
nervous’. But as every psychiatrist and general practitioner knows, Mrs Bennet is not
faking her symptoms. Mr Bennet knows this too. She doesn’t fancy herself nervous; she
has always been nervous. When she accuses her husband of having no respect for her
nerves, he again crushes her with his comments about her nerves being his old friends.
And while Austen implies artifice in the words ‘when she was discontented she fancied
herself nervous’, she is really telling us, very clearly, that Mrs Bennet has both depressive
and anxious symptoms.
But, to maintain the comedy, Jane Austen will not let Mrs Bennet off the hook of
ridicule. So when Elizabeth rejects the odious advances of Mr Collins, Mrs Bennet is
beside herself, and clearly beside everybody else too, in her protestations of suffering:
‘Not that I have much pleasure indeed in talking to anybody. People who suffer as I do from
nervous complaints can have no great inclination for talking. Nobody can tell what I suffer! –
But it is always so. Those who do not complain are never pitied.’
Of course, she complains over and over again about her symptoms and suffering, so we
snigger into our hands at the thought that she suffers in silence. Nobody is spared the
expression of her distress;
‘Don’t keep coughing so, Kitty, for Heaven’s sake! Have a little compassion on my nerves. You
tear them to pieces.’
‘Nobody is on my side, nobody takes part with me, I am cruelly used, nobody feels for my
poor nerves.’
What is also clear is that the physical symptoms she experiences are those of pathological
anxiety; they could in no way be factitious:
‘I am frightened out of my wits; and have such tremblings, such flutterings, all over me, such
spasms in my side, and pains in my head, and such beatings at heart, that I can get no rest by
night nor by day.’
In case you get the idea that I am over-preoccupied with Mrs Bennet, I need to state the
reasons why I am dwelling on her to such an extent. It is because she is now so well known
that she has become a real person, a celebrity, but is being remembered for the wrong
reasons, as a target of mirth and derision, who is manipulating her symptoms to get
attention for herself and has no concern for anybody else.
But this is the opposite of the truth. Mrs Bennet is the only clear-headed member of
the Bennet household and she illustrates the evolutionary benefit of the general
neurotic syndrome, developed in more detail in the last chapter of this book. At the
family home in Longbourn, her husband has opted out of all responsibility; her eldest
daughter, Jane, is besotted and cannot think straight; Elizabeth, on whom we now all
dote, is pursuing an idealistic path in life with no consideration of nineteenth century
realpolitik; and the three other daughters are just capricious and silly. Only Mrs Bennet

Introduction 7
has the understanding, the drive, and the foresight to ensure that the estate stays in the
family.
I hope your interest has been stimulated. But now we need to formulate the general
neurotic syndrome in more detail, knowing that Mrs Bennet will be looking over my
shoulder to make sure I do not err.

Chapter
The General Neurotic Syndrome
1
As this book is primarily about the general neurotic syndrome (GNS), I need to be convincing
in creating the groundwork to persuade the reader to continue to read. Some may feel this
syndrome is a fictitious creation and so I will have to work even harder to persuade these
sceptics; all I would ask at this point is for people to have an open mind. The general neurotic
syndrome is not (yet) a familiar term, even though it should be. As it has been a subject I have
had in my head for over 45 years – I hope not as an obsession but as a guiding light – I need to
put my thinking about it into context.
1.1 Initial ideas

In the 1970s, when I was working in Southampton as a senior lecturer, my view of the general
neurotic syndrome was very simple: ‘If a person has both anxiety and depressive symptoms and
some personality disturbance, the diagnosis of the general neurotic syndrome is the best way of
defining the problem.’ At this stage I was not certain how to define anxiety or depression or the
exact nature of the personality disturbance. In defining it in this way I was also aware from my
clinical practice that people with this syndrome tended to have poor outcomes.
This was a fairly limited definition, or rather an initial hypothesis that needed testing,
and at the time I was not thinking of other disorders within the neurotic spectrum. Many
people had theories about these and were prolix in expressing them. Alfred Adler, the well-
known psychoanalyst, described most mental disorders as related to the desire to exercise
power and overcome inferiority. He dwelt on this subject in writing about the ‘neurotic
constitution’, an escape from the failure to become powerful. The neurotic symptoms each
had a significant personal meaning for the patient; they became fictionalised and detached
from reality (Adler, 1921). This led to the idea of a unified neurotic syndrome (‘Die
Einheitsneurose’) but was not developed further and never really embraced in classification.
At this time, the view of ‘neurosis’ as an entity in clinical practice was an inchoate one in my
mind. At its simplest level, it was manifest as a split between disorders in which common
understandable symptoms are excessive but grounded in reality (neurosis) and those where
bizarre inexplicable symptoms and behaviour are divorced from reality (psychoses). My view at
this time conformed to this general idea but with the addendum that core neurosis was linked to
personality.
But this was thrown into debate by what is now commonly called the Newcastle Group,
a research mix of academics and clinicians together with a statistician, Roger Garside, who
claimed that the common disorders of anxiety and depression could be separated using
appropriate statistical methodology, and that clinicians should be able to make a primary
diagnosis of anxiety or depression, with no need for both (Gurney et al., 1972; Roth et al.,

The General Neurotic Syndrome 9
1972). The authors were unequivocal in their conclusions: ‘the first component extracted
from a principal components analysis of the data was bipolar, with anxiety symptoms at one
pole and depressive symptoms at the other; maladaptive personality traits were mainly
associated with anxiety symptoms. This finding confirms that within an affective material
there are two distinct syndromes corresponding to anxiety and depression’ (Roth et al.,
1972, p. 158). And again, ‘using discriminant function analysis the bimodality of the
patients’ scores (i.e., clear separation between groups) indicated that there were two distinct
groups, which, moreover, corresponded closely to the clinical differentiation into anxiety
state and depressive illness, thereby confirming the hypothesis’ (Gurney et al., 1972, p. 165).
But did these findings tell us that anxiety and depression were separate disorders? No.
Anxiety and depression were identifiable as distinct entities but were they distinguishable in
practice and did this have clinical meaning? Was the evidence of separation just a statistical
method to separate symptoms but not patients? There has been debate about this ever since,
increasingly unsupportive of this notion over the years. Perhaps the most economical
summary was Dobson’s, who made a full review of the literature and ended with a delphic
summary. ‘The distinction’ between anxiety and depression ‘may be more conceptually
satisfying than empirically demonstrated’ (Dobson, 1985).
But there is no doubt the Newcastle Group had stirred the neurosis pot from its position of
quiet somnolence. Discussions about the anxiety/depression distinction and its value in
selecting treatment (Kerr et al., 1972; Schapira et al., 1972) became very common in clinical
practice. I recall arguments at ward rounds in Knowle Hospital near Fareham in Hampshire;
vigorous discussions where junior colleagues were castigated for not committing themselves to
a single diagnosis in a patient who had both symptoms of anxiety and depression. Sometimes
the argument that as personality disturbance had been described in the presentation of the
case this showed the diagnosis must be an anxiety one, ‘as Professor Roth has said so’.
My own view of the work of the Newcastle Group, given nearly 50 years of reflection, is
that it was rather like shining a light into a dark corner for the first time. You are not quite
sure what you are seeing but you carefully sketch what you can and report back. But you
know you are missing a lot. It was a pity that the Newcastle Group’s study only included
inpatients (most patients with primary anxiety disorders rarely go into hospital) and did not
test their hypotheses with another equivalent group of patients. They were also using
statistical approaches that were relatively new to psychiatry but not fully understood, and
in retrospect should not have been relied on to justify their arguments.
And what was the real purpose of the study? The exercise seemed almost like comparing two
kinds of eating apples such as Worcester Pearmain and Cox’s Orange Pippin. Visual examin-
ation reveals consistent differences between the two types of apple but when you take the
broader picture the two apples are virtually identical. They come from a similar looking tree,
belong to the same botanical species, and have very similar textures and flavours. Of course, it is
possible to separate one from the other using the highly discriminant analysis of observation
and so the two types of apple can be separated into different baskets and sold at different prices,
but the fact remains they are eating apples with many more similarities than differences.
During this period I had also been involved in comparing the effectiveness of day
hospitals and outpatient clinics for the treatment of anxious, phobic, and depressed patients
(Tyrer & Remington, 1979; Tyrer et al., 1987). Our findings in these studies showed
consistency of phobic symptoms but great inconsistency of anxiety and depressive ones
over a two-year period. This reinforced the notion that the universal separation of anxiety
and depression was not a useful clinical practice.

10 Neurosis
It is reasonable to ask why this subject seemed so important to me at that time, as some
might find the whole issue esoteric. I had been trained in medicine and had completed
higher training in the subject and had always felt that diagnosis was a very important
medical task – one that could only be taken on by a doctor at that time. If the most common
conditions in mental health could not be properly diagnosed, what hope was there for
psychiatry? (This, of course, was at a time when diagnosis was considered a critical part of
psychiatric practice; the doubts that are being expressed today hardly existed at that time.)
I do not want to give the impression I was moving towards a catastrophe in my thinking but
the subject had to be addressed if I was to feel confident as a practitioner.
1.2 Later Stage (1980s)

A more coherent formulation of my view of the general neurotic syndrome was made in the
early 1980s, but it was created as part of a concept not too different from ‘Die
Einheitsneurose’. In 1985, I wrote a paper on the subject in the Lancet. The Lancet always
prides itself on being at the beginning of a medical story and also being there at the end, but
not caring about what is in between, so they were very generous in publishing this paper
before anyone else had mentioned the general neurotic syndrome, which to many others
must have sounded bizarre. In this paper I wrote:
It is more appropriate to regard many of these conditions (i.e., neuroses) as manifestations of
one disorder, which may be termed the ‘general neurotic syndrome’. To qualify for this
diagnosis patients should show at least three of the following features:
(a) two or more of the following symptomatic diagnoses are present together, either now
or at times in the past: agoraphobia and social phobias, panic disorder, non-psychotic
depression, anxiety, and hypochondriasis (including somatoform disorders);
(b) at least one episode of illness has developed in the absence of major stress;
(c) There are abnormal personality features of a passive dependent or an anankastic type;
(d) There is a history of a similar syndrome in first-degree relatives. (Tyrer, 1985)
I also added: ‘these symptoms can be placed in a “handicap hierarchy” depending on the degree of
social impairment for the symptoms produced’. This was accompanied by a figure of concentric
circles showing the different disorders with the outer ones showing the greater handicap
(Figure 1). (Because ‘handicap’ is now felt to be pejorative it could be replaced with disability).
Thus, generalised anxiety, which is associated with the least degree of social impairment, occupies
less space than the other syndromes, and agoraphobia, social phobia and hypochondriasis
occupies a larger space. But I was careful to emphasise that this was not a diagnostic hierarchy;
it was merely to illustrate that there was more social impairment in the outer rings.
My justification of each of these four elements follows, and here I am updating and
adding to my arguments, but not changing them in any fundamental way.
1 Simultaneous and Past Presentation of Two or More Symptoms of Six Conditions

I chose these six: agoraphobia, social phobia, panic disorder, non-psychotic depression,
anxiety, and hypochondriasis (including somatoform disorders), as they are the most prevalent
conditions in the neurotic group. At the time of writing in 1985 there was already much
evidence that there was overlap between all these disorders. This was explained in different
ways:
(a) there is a hierarchy of symptomatology (Boyd et al., 1984, Coryell et al., 1988);

(b) they are a common group of disorders (Aronson, 1987);

(c) although the symptoms appear to overlap they are genuinely separate and successful
intervention demonstrates their distinctiveness (e.g., pharmacological dissection,
Klein, 1964, 1981).
2 The Triggering Effect of Stress

The requirement that at least ‘one episode of illness has developed in the absence of
major stress’ was included to illustrate the importance of life events in creating mood
disorders (Figure 1.1), as well as the relevance of what became known as adjustment
disorders. But I specified the absence of major stress to exclude post-traumatic stress
disorder, a completely separate condition, but left the option open for minor stresses at
home, at work, and in relationships, to create a stepwise increment in symptoms.
So, when Mrs Bennet says to her daughter, ‘Don’t keep coughing so, Kitty, for Heaven’s
sake! Have a little compassion on my nerves. You tear them to pieces’, she is illustrating the
consequences of minor stress in creating symptoms, stresses which for the average person
would go unnoticed. Here again personality is involved. Some years ago (Tyrer, 2007),
I suggested the term ‘personality diathesis’ was a better one than personality disorder as the
possession of such a vulnerability was a lifelong one that lowered the threshold to stress.
I still think this is a better term than ‘disorder’ but as disorder is applied universally to all
mental health conditions, we have to accept the common parlance (but see Chapter 8 for its
implications).
3 There Are Abnormal Personality Features of a Passive Dependent or an Anankastic

Type
I have to admit this was a partial guess at the time, but in retrospect it is justified. The
reason for the choice of these two personality features emanated from a study of neurotic
patients who also had a personality disorder (Tyrer, Casey & Gall, 1983). We found that
anankastic and passive-dependent personality traits were most often found in those with
neurotic disorder.
Life event score

a and so
hobi cia
ap l
or Panic
ph
Ag
ob
sthymia
Dy
ia
a and so
hobi cia
Anxiety ap l
or Panic
ph
Ag
ob
sthymia sthymia
Dy Dy
ia
Hy s Anxiety Anxiety Anxiety Anxiety

poch o n dri a si
Figure 1.1 The initial formulation of the general neurotic syndrome and its components, including its variation
over time in response to stresses
(From Tyrer, 1985, with kind permission of the publishers of the Lancet)

12 Neurosis
The simultaneous presence of a clinical syndrome (cothymia) and personality disorder

might best be described as a Galenic syndrome. Galen, in his 192 AD commentary, De
Temperamentis, described how the four (personality) humours, melancholic, sanguine,
choleric, and phlegmatic, were associated with specific diseases. His four humours domin-
ated medicine for the next 1,500 years, accompanied by the dictum that too much of one
humour led to disease. The sanguine person could accumulate too much blood and so
needed leeches to reduce it, the phlegmatic person with lung disease created too much
phlegm, and the choleric patient needed a purgative to remove an excess of bile.
Although Galen clearly had no good knowledge of the nature of bodily diseases, his
linking of personality to them was novel and needs to be resurrected in modern psychiatry.
A Galenic syndrome can therefore be defined as ‘a combination of personality disorder and
clinical symptom complex so frequently associated that the two conditions should be
considered as a single disorder’.
4 History of a Similar Syndrome in First-Degree Relatives

This is a clear reference to the genetic elements of neurotic disorder, a subject that has
attracted much attention. There is unequivocal evidence that there is a genetic contribu-
tion to all the disorders within the neurotic spectrum. There is much less agreement about
the role of the family environment in causation. In the words of a recent meta-analytical
review: ‘Panic disorder, generalized anxiety disorder, phobias, and obsessive-compulsive
disorder all have significant familial aggregation. For panic disorder, generalized anxiety
disorder, and probably phobias, genes largely explain this familial aggregation; the role of
family environment in generalized anxiety disorder is uncertain’ (Hettema et al., 2001,
p. 1568).
In the case of generalised anxiety, the hypothesis that an anxious mother can create an
anxious child is a very persuasive one. Behavioural psychologists call this ‘modelling’; the
child observes the mother (sometimes the father) showing anxious avoidance and imitates
it, is also often then taught to show anxious avoidance, and, hey presto, you have an anxious
child who grows up to be an anxious adult. But the data do not give strong evidence in
favour of this. One of the most influential researchers in the area, Roy Plomin, asked this
question in 1987: ‘why are children in the same family so different from one another?’
(Plomin & Daniels, 1987). Twenty-four years later he admitted he did not have an answer.
He summarises his dilemma clearly:
It was reasonable to assume that the key influences on children’s development are those
that are shared by children growing up in the same family: their parents’ personality and
family experiences, the quality of their parents’ marital relationship, their parents’ educa-
tional background and socioeconomic status, the neighbourhood in which they are raised
and their parents’ attitude to school or to discipline. Yet to the extent that these influences
are shared environmentally, they cannot account for individual differences in children’s
development because the salient environmental influences are non-shared [my italics]. The
message is not that family experiences are unimportant but rather that the relevant experi-
ences are specific to each child in the family, not general to all children in the family. (Plomin,
2011)
This is a subject highly relevant to the treatment called nidotherapy (Tyrer, 2009) that
became a subject of particular interest in the Nottingham Study, and this will appear again
in this book.

1.3 Progress in Understanding the General Neurotic Syndrome

since 1985
In a book I wrote in 1989, I formalised the definition of the general neurotic syndrome in the
following words:
The general neurotic syndrome is characterised by the simultaneous presence of various
anxiety and depressive symptoms occurring in the absence of major psychological or
physical trauma in individuals who have inhibited or dependent personalities. The diagnosis
is made through a three-stage process:
(1) Identification of the co-occurrence of anxiety and depressive symptoms in the absence
of severe depressive illness or another significant psychiatric disorder;
(2) Examination of environmental evidence of the symptoms and measurements of their severity;
(3) Determination of the premorbid personality of the subject.
(Tyrer, 1989, p. 154)
I also created the General Neurotic Syndrome Scale (Table 1.1)

This scale has deficiencies – not least that it was not formally tested – but the central
elements are ones that I still think after a gap of 23 years are relevant to the diagnosis. I also
Table 1.1 The General Neurotic Syndrome Scale (GNSS)
Positive characteristics Score Negative characteristics Score
Simultaneous presence of +2 Persistent phobic and −2

syndromal anxiety and depressive obsessional symptoms
disorders (cothymia)
Variation in the primacy of +3 Symptoms of anxiety and −3
depressive and anxiety symptoms depression only occur in
at different times response to immediate life
events
If symptoms of panic, obsessive +1
compulsive disorder, and
hypochondriasis are present they
do not last longer than three
months
Premorbid anxious or dependent +3
personality disorder
Premorbid anankastic (obsessive- +1 Premorbid impulsive, −3
compulsive) personality disorder borderline or antisocial
personality disorder
At least one parent has mixed +2
anxiety depressive syndrome
(cothymia)
TOTAL SCORE (no general neurotic syndrome) 0–3
TOTAL SCORE (likely general neurotic syndrome) 4–5
TOTAL SCORE (definite general neurotic syndrome) ≥6

14 Neurosis
excluded phobic and obsessional symptoms by giving them a minus score, and some (that
now includes me) would regard a negative score as inappropriate as these conditions, as
suggested in my 1985 paper, could be regarded as extensions of the syndrome. On the other
hand, the better definition and consistency of phobic and obsessional symptoms can make
these conditions more amenable to diagnosis. The score needed to attribute the diagnosis of
the general neurotic syndrome has not changed but now I feel more strongly that the higher
score of 6 is the best threshold and that a GNS score of 4 only makes the diagnosis suspect.
(In the rest of the book both versions of the GNS will often appear; this is of value in showing
the linear transition of what is clearly a dimensional scale.
One important advantage of the general neurotic syndrome as a diagnosis is that it does
not depend on time lines. The formal classifications of the neurotic group of disorders at
that time had conditions varying from a few hours (acute stress reaction) to several years
(dysthymic disorder) (Figure 1.2), which really made it impossible to make clear decisions
when assessing a patient for the first time. All the requirements for making the diagnosis of
the general neurotic syndrome are immediately clear in the scale; the examination of present
symptoms and their precipitants (if any) are all that is needed.
One of the great sources of resistance that has prevented acceptance of the general
neurotic syndrome is the antipathy to joining anxiety and depression together as
a single diagnosis. It is difficult to know why the resistance has been so strong. David
Goldberg set the scene many years ago when he and colleagues produced the first
standardised interview schedule for common mental disorders (Goldberg et al., 1970).
In the second part of the schedule, the nine most common symptoms of mental illness
are listed: I have placed them in Table 1.2 in terms of the most prominent mood
associated with each.
I am sure everybody looking at this table will agree the overlap between anxiety and
depression is massive and cannot be ignored in any sensible classification.
The schedule described by Goldberg et al. (1970), 12 years later changed its name to the
Clinical Interview Schedule (Lewis, 1992). The major symptoms were the same as in 1970 but
Acute stress
SEVERE
reaction
Post-traumatic Agoraphobia and panic disorder

stress disorder Severe depressive episode (including recurrent)
and depressive symptoms
Severity of mixed anxiety
Mixed anxiety and depressive disorder

(ICD-10 only)
Adjustment
disorder
Dysthymic
Mild depressive episode
disorder
MILD
0 50 100 150
Time (days)
Figure 1.2 The confusing relationship between duration of symptoms and diagnosis in DSM-III and ICD-10

Table 1.2 The association of depression and anxiety with the symptoms of
common mental illness
Nature of symptom Associated mood
Somatic symptoms anxiety and depression

Fatigue anxiety and depression
Sleep disturbance anxiety and depression
Irritability anxiety and depression
Lack of concentration anxiety and depression
Depression depression
Anxiety and worry anxiety
Phobias anxiety
Obsessions and compulsions anxiety and depression
had two more added – worry about physical health (which might now be called hypochondria-
sis or health anxiety) and depressive ideas – and all of these were rated reliably. The first
addition was understandable and a clear omission from the first schedule. The section on
depression was split into frequency and severity of depression (depression per se) and related
symptoms of depression such as hopelessness and guilt (depressive ideas) (Lewis, personal
communication, 2021). With so many mixed symptoms, it was therefore not at all surprising
that mixed anxiety and depression became an important feature in the responses. Still, only the
revised Clinical Interview Schedule (CIS-R) reported this finding; no other scales addressed it.
Its importance to public health was highlighted by Das-Munshi et al. (2008) who found,
through analysis of data from the National Psychiatric Morbidity surveys, the one-month
prevalence of Mixed Anxiety and Depressive Disorder (MADD, a very unfortunate acronym)
was 8.8 per cent and accounted for 20 per cent of all days off work in the population.
The authors made a strong case for including mixed anxiety and depression in epi-
demiological surveys as this condition was also associated strongly with health-related
quality of life. They concluded, ‘our findings strongly support the inclusion of
a dimensional perspective, without which the population burden of psychological morbidity
is markedly underestimated’ (Das-Munshi et al., 2008, p. 176).
But we also need to be clear that the mixed anxiety and depression label in the Das-Munshi
et al. paper was not a diagnosis. It was a sub-syndromal condition that was immediately
disqualified once a patient had symptoms of sufficient severity of either anxiety or depression
to qualify for one of these disorders. So here we had a ‘non-diagnosis’ of sufficient severity to
create major problems in living that was wiped out once one of the thresholds of formal
diagnosis was reached, when a single anxiety or depressive diagnosis took over.
The paper by Das-Munshi et al. (2008) has been well cited (over 100 times) but its subject
matter remains isolated in research. It is difficult to understand why there has been so much
resistance to defining a mixed anxiety depressive syndrome despite all the evidence of the
last 50 years. The question has to be asked: ‘If a very common combination of symptoms
creates so much pathology in the population at a sub-syndromal level, why is it not
recognised at a syndromal one?’

16 Neurosis
Looking at the way it is dealt with in the psychiatric literature reminds me of the
reluctance people now have about referring to the British Isles. There is a tremendous
degree of affinity between England, Scotland, Wales, and Ireland but for reasons that
are primarily political we do not use ‘British Isles’ very often. It is felt to be a colonial
expression, a hangover from the time of Irish oppression. The people from the island
of Ireland are even denoted separately in ethnic population studies; ‘the Irish’ are
a separate group. It is the same with anxiety and depression. We keep them separate
because it seems politically correct to do so; depression is a mood disorder; anxiety is
a conurbation of like states all associated with high levels of arousal (Craske & Stein,
2016) and so differs from typical depression. So many like to keep them apart, and
when those annoying epidemiologists keep reminding us that they are joined together,
we just wish they would go away.
In a separate study, Lewis (1991) compared the level of agreement between anxiety and
depressive symptoms using a well-known scale (Hospital Anxiety and Depression Scale:
HADS) and the Clinical Judgement Scales of the CIS-R. The correlations between anxiety
and depression scores in the HADS were 0.59 but only 0.29 in the Clinical Judgment Scales.
It could be argued that the psychiatrists were better assessors of anxiety and depression than
the patients but in a separate study (described in the same paper) Lewis also found that when
psychiatrists (all Maudsley trainees) rated their own anxiety and depression they showed
a similar poor correlation. It was therefore reasonable to conclude that psychiatrists were
showing bias in finding a degree of separation between anxiety and depression that simply
wasn’t there.
Lewis therefore concluded from these findings that ‘the use of neuroses as, in part,
a unitary concept, may be useful and is certainly a legitimate way of describing the current
empirical data’ (1991, p. 272). Jay Das-Munshi (personal communication) has also sug-
gested that the tendency in insurance-based national systems (e.g., USA, Germany) to bill
individually for anxiety and depressive disorders also exaggerates the separation. You could
say, if you so wished, that these studies constituted one up for the general neurotic
syndrome early in the history of this concept.
1.4 Gavin Andrews and the General Neurotic Syndrome

The general neurotic syndrome suddenly achieved a measure of respectability, if a limited
one, by a publication by Gavin Andrews and colleagues in 1990. In this paper, they
generously acknowledged and referenced my 1985 publication but Gavin admitted to me
(in 2012, when I visited his amazing home close to Botany Bay) that he did not mention that
the essential three words in the title were in my 1985 paper. This really did not matter but it
was generous of him to confess.
His data came from a study of 15,000 twins involved in the Australian National
Health and Medical Research Council Twin Registry, who were also interested in
participating in medical research. (It is a pity there was not a UK equivalent as my
brother and I would have been keen to be involved). In Andrew’s study of 892 twins,
and a separate clinic sample of another 165 twins attending for treatment of panic and
agoraphobia, there was no evidence of diagnostic stability over time, or to use the
words of the authors, no suggestion of ‘patterns of co-occurrence of diagnoses being
associated with particular syndromes’ (Andrews et al., 1990, p. 6). Of more seeming
relevance was the background presence of personality vulnerability, so the author had

captured the essential parts of the 1985 paper. He took the personality factor one stage
further in a later paper:
In all three domains of information, a general vulnerability factor, associated with personality
trait measures of high trait anxiety and poor coping, emerges as a principal cause of these
symptoms or disorders, and accounts for the majority of the variation in the comorbidity of
symptoms or disorders. This vulnerability factor is shown to be under substantial genetic
control. (Andrews, 1996)
He also offered prospects for treatment.
As these vulnerability factors can be measured, treatment programmes for anxiety and depres-
sive disorders should ensure that they are reduced if relapse is to be inhibited. Prevention
programmes, aimed at people with high levels of this personality vulnerability which increases
their risk of developing anxiety and depressive disorders, would appear to be practical.
So we, on opposite sides of the globe, had come to the same conclusion. All that
remained was for others to follow this up. It was noted in further studies (e.g., Duggan
et al., 1996) as a research finding but never appreciated at the clinical level until just recently.
Now, after realising that treating resistant depression and anxiety with more and more of
the same, it looks at last as though the penny is beginning to drop and the focus will change
to examining the personality component (Berk et al., 2018).
1.5 Developments and Changes in Classification since 2010

In the last 15 years, the notion of independent specific psychiatric disorders has received
quite a beating. The debates about endogenous and neurotic depression (Kiloh et al., 1972)
have all disappeared, and there is increasing knowledge and acceptance of the dimensional
nature of psychiatric disturbance. We also have studies that show poor reliability of anxiety
and depressive diagnoses as currently described (Andrews et al., 2010) and a host of
pharmacological studies that show the terms antidepressants and anxiolytics are inappro-
priate and ‘drugs for depression’ and ‘drugs for anxiety’ are now preferred (Haddad & Nutt,
2020). So why is there such a reluctance to talk about mixed anxiety and depression?
I suggest two reasons. The first is that there has been a gradual separation of anxiety and
depression research groups in the last 30 years. The anxiety research groups never study
depression and vice versa so there is an innate tendency for each to ignore the other.
The second reason is related to treatment. Officially, diagnosis should be made independ-
ently of treatment. In the case of anxiety and depression there has been a growing trend for
all practitioners to believe that anxiety disorders should be treated by behavioural means
and depressive ones by pharmacological ones. So psychiatrists who treat mixed anxiety and
depression make the diagnosis a depressive one when they prescribe drugs and an anxiety
one when they prescribe cognitive and behavioural methods of treatment. There has also
been the influence of training that could be called the Lewis Prediction after his 1991 paper –
expressed as ‘when symptoms of anxiety and depression are both present the psychiatrist is
trained to separate them even when they are of equal importance’.
In this mess of contradiction, the admission that we are mistaken in separating these
conditions is almost an admission of failure. The fear that most people might diagnose mixed
anxiety and depression and use their discretion as to what treatments they offer is too much to
bear. It implies that we know much less about mood disturbance that we think we do.

18 Neurosis
At the risk of getting too tied up in minutiae these points are worth expanding in the
context of the latest classifications.
1.6 Identification of the Co-occurrence of Anxiety

and Depressive Symptoms
There has continued to be dispute over the relationship between these symptoms ever since,
with only a very slight shift towards the acknowledgement of mixed symptoms as a useful
concept. The International Classification of Diseases ICD-10 and ICD-11 (world classifica-
tions) have allowed mixed anxiety and depressive disorder to be used as a diagnosis but at
a very low level when other anxiety and depressive disorders have been excluded. This is the
wording in ICD-11:
Mixed depressive and anxiety disorder is characterised by symptoms of both anxiety and
depression more days than not for a period of two weeks or more. Depressive symptoms
include depressed mood or markedly diminished interest or pleasure in activities. There are
multiple anxiety symptoms, which may include feeling nervous, anxious, or on edge, not
being able to control worrying thoughts, fear that something awful will happen, having
trouble relaxing, muscle tension, or sympathetic autonomic symptoms. Neither set of symp-
toms, considered separately, is sufficiently severe, numerous, or persistent to justify a diagnosis
of another depressive disorder or an anxiety or fear-related disorder (my italics). The symptoms
result in significant distress or significant impairment in personal, family, social, educational,
occupational or other important areas of functioning. There is no history of manic or mixed
episodes, which would indicate the presence of a bipolar disorder. (World Health
Organisation, 2018)
The clinician has many other diagnostic options that are considered more acceptable.
Dysthymic disorder, a chronic depressive condition, is described clearly in ICD-11 (and
essentially the same in DSM-5):
Dysthymic disorder is characterised by a persistent depressive mood (i.e., lasting 2 years or

more), for most of the day, for more days than not. In children and adolescents depressed
mood can manifest as pervasive irritability. The depressed mood is accompanied by
additional symptoms such as markedly diminished interest or pleasure in activities,
reduced concentration and attention or indecisiveness, low self-worth or excessive or
inappropriate guilt, hopelessness about the future, disturbed sleep or increased sleep,
diminished or increased appetite, or low energy or fatigue. During the first 2 years of the
disorder, there has never been a 2-week period during which the number and duration of
symptoms were sufficient to meet the diagnostic requirements for a Depressive Episode.
There is no history of Manic, Mixed, or Hypomanic Episodes. (World Health Organisation,
2018)
What is most odd about this description is that anxiety symptoms are not mentioned at all –
yet another example of the Lewis Prediction that airbrushes every diagnostic conjunction of
anxiety and depression away.
If there is a gap in the presence of depressive episodes but there are still many of them,
the diagnosis becomes ‘recurrent depressive disorder’ in ICD-11:
Recurrent depressive disorder is characterised by a history or at least two depressive
episodes separated by at least several months without significant mood disturbance.

A depressive episode is characterised by a period of almost daily depressed mood or

diminished interest in activities lasting at least two weeks accompanied by other symptoms
such as difficulty concentrating, feelings of worthlessness or excessive or inappropriate guilt,
hopelessness, recurrent thoughts of death or suicide, changes in appetite or sleep, psycho-
motor agitation or retardation, and reduced energy or fatigue. There have never been any
prior manic, hypomanic, or mixed episodes, which would indicate the presence of a Bipolar
disorder. (World Health Organisation, 2018)
But again there is no mention of anxiety in any form in recurrent depressive disorder,
so it will not surprise anyone to read that the descriptions of anxiety disorders do not
include even a smidgeon of depressive symptomatology. Generalised anxiety disorder is
‘characterised by marked symptoms of anxiety that persist for at least several months, for
more days than not’, but are ‘not a manifestation of another health condition’ (presumably
including depression), and panic disorder is described by more serious symptoms of
anxiety, ‘palpitations or increased heart rate, sweating, trembling, shortness of breath,
chest pain, dizziness or lightheaded-ness, chills, hot flushes, and fear of imminent death’,
but again excludes any other health conditions. Similarly, social anxiety disorder is
‘characterised by marked and excessive fear or anxiety that consistently occurs in one or
more social situations such as social interactions’, again with no mention of any depressive
components.
1.7 Categories and Dimensions

In trying to set the criteria for the diagnosis of the general neurotic syndrome, I need to
emphasise that I am not pretending that this is a very clear category. Almost all psychiatric
disorders are best seen as a spectrum from totally absent to strongly present – a continuum
with points of diagnosis along the way. The points we choose are ones that are useful to
clinicians, not ones that are clear and unambiguous. Bob Kendell emphasised this point
many times during his career. Diagnoses are not set in stone, especially in psychiatry; they
are merely functional abbreviations that help communication and decision-making
(Kendell, 1975a; Kendell & Jablensky, 2003). The diagnosis of the general neurotic syn-
drome has no status or usefulness unless it helps practitioners to treat their patients. The last
chapter of this book explains how this is possible.
It is useful to take an example from medicine to illustrate this, not least as medical
diagnoses are often held up as real conditions, as opposed to the fanciful ones of
psychiatrists. In the late 1950s, there was a vigorous debate about the status of hyperten-
sion in medicine. On the one hand there was Robert Platt, a scion of clinical excellence,
who argued that severe hypertension was a genetically determined disease that was
completely separate from other conditions in which there was high blood pressure. On
the opposite side was George Pickering, an epidemiologist as well as a clinician, who
argued that hypertension was a continuously distributed physiological trait, with some
people having blood pressure at the upper end of the scale and others further down, but
with no clear distinction between the two. It was therefore inappropriate to refer to two
groups of people as having either ‘normal blood pressure’ or hypertension. At the time,
there was gladiatorial combat in the Lancet between the two antagonists (Platt, 1959;
Oldham et al., 1960; Pickering, 1960), all carried out with the utmost politeness, and most
commentators, including the editorial staff of the journal (Lancet, 1959), supported the
Platt argument.

20 Neurosis
We now know that Pickering was right and Platt was wrong. There is no genetic basis to
hypertension and no clear dividing line between the different hypertension diagnoses, but
clinicians, understandably, still find it useful to use higher blood pressures as markers of
severity. Even these have come under criticism as it is only night-time recorded (preferably
during sleep) hypertension that predicts future cardiovascular events (ABC-H Investigators,
2014).
The hypothesis stated here is that the general neurotic syndrome is similar to hyperten-
sion. It represents the extreme of a range and whether it is regarded as clinically useful or
a recondite reminder of the past depends on how useful it is in practice. Of course, as all
psychiatrists know to their cost, when talking with medical colleagues, we do not have an
independent measure of the syndrome like blood pressure to decide what level is pathological,
but we do have other assessments that are reliable and sound.

Chapter
DSM-III and the Generation
2 of New Diagnoses
At the time of the instigation of the Nottingham Study of Neurotic Disorder, the revolution
instigated by DSM-III was in full swing. ‘Neurotic disorders’ still received some attention
but usually as a precursor to newer (superior) descriptions. Philip Snaith (1991) was still
able to entitle the second edition of his book, Clinical Neurosis, and explained why in his first
chapter.
The retention of the term neurosis in the title of this book does not imply affiliation to any
particular theory or view of the nature of the disorders. On the contrary, it is my purpose to
attempt to unite disparate views which have surrounded the concept and to consider how
all have contributed to present knowledge although doctrinaire theory has had a retarding
effect on progress. (Snaith, 1991, p.1)
He then continued with separate chapters on anxiety, depressive, professional, somato-

form, and dissociative conditions, and eating disorders, ending with a chapter on deperson-
alisation, irritability, and fatigue. His intention was to bring the subject into the framework
of the then-developing ICD-10 classification of mental disorders.
2.1 More Personal Experience

In the late 1970s, when I was working in Southampton as a senior lecturer with clinical
responsibility for a catchment area to the west of the city, most of the new patients I saw
had, in the words of the time, ‘neurotic disorders’. The catchment area was relatively
affluent and there were many more patients with severe mental illness in hospital then
there are today. What struck me most about the patients I was seeing was the common-
ality between them. I remember time after time writing to general practitioners after
a first assessment that the patient had ‘a mixed neurotic disorder in which anxious,
depressed and phobic symptoms were all present at different times’. Other patients,
usually ones presenting for the first time, had symptoms that were much purer in nature.
In these instances, I was able to write more confidently that there was a depressive,
anxiety, or phobic syndrome with little overlap. With this experience I found the general
rubric of the word ‘neurotic’ to be helpful.
At this time, I was also carrying out clinical research into personality disorder using
a new instrument, the Personality Assessment Schedule. (This will be mentioned in more
detail later in the book; it plays an important part.) In testing out this schedule, it became
increasingly apparent that the group of patients that I classified as neurotic also had
significant personality disturbance. So there appeared to be a clear distinction between
these groups, summarised in Table 2.1.
21

22 Neurosis
Table 2.1 Differentiation of patients in my personal practice between 1975 and 1981
Neurotic group Non-neurotic group
Had previous episodes from adolescence Usually presented for the first time. Previous
onwards episodes rare
Presented with mixed symptoms (depression, Had clear-cut symptoms of either depression
anxiety, phobias, hypochondriasis, panic) or anxiety, or less commonly, panic and
phobias
Had personality disturbance mainly in terms Demonstrated no personality disturbance
of dependence, obsessionality, and
anxiousness
Did not respond well to most treatments Responded well to both drug and
psychological treatments
Were difficult to discharge as rarely was there Discharged when well, did not re-attend
resolution of symptoms. Often re-referred
when discharged
It was while I was working in Southampton that we organised a randomised controlled

trial of the treatment of neurotic disorder (anxiety, depressive, and phobic symptoms) by
comparing the clinical outcome and social functioning in patients randomised to day hospital
and outpatient care. Day hospitals were promoted strongly for the care of neurotic disabilities
as it was felt that the psychologically orientated approach and consequent milieu therapy
would be of particular value in day hospital settings. But the results of the study (89 patients)
showed no differences between the two approaches (Tyrer & Remington, 1979).
But in looking at the results of the studies, the same findings that I observed in clinical
practice were being shown again. Half the patients did well and improved irrespective of
setting and the other half continued with symptoms, and this seemed to be related to
personality status (although in this study these were not measured). What was abundantly
clear was that the inclusion of all anxiety, depressive, and similar symptoms into a general
category of neurotic disorder was far from satisfactory.
Before the DSM was published in 1980, there were several indications of what it might
contain. David Goldberg, then professor of psychiatry in Manchester, visited Southampton
to give a lecture and described the splitting of diagnoses of neurotic disorder that was likely
to come after Robert Spitzer had finished his gargantuan task of reforming all psychiatric
diagnoses. David, in his inimitable style, pointed out the ludicrous timelines of each
diagnosis. We had the separation of panic disorder, which could be diagnosed within
a week if you had several panic attacks, from that of dysthymic disorder, which required
symptoms of depression to have been present for most of the last two years. In between we
had a diagnosis of major depressive episode which required two weeks of suffering before it
could be diagnosed, and generalised anxiety disorder, when symptoms had to be present for
the last month (also see Figure 1.2). The time limits for phobic disorders did not appear to be
so important. David Goldberg presented these proposals in graphical form and in multi-
dimensional space; this made them sound even more fantastical than they probably were.
But it did not make sense; I did not want to have a clock behind me making the diagnosis
(even though it still happens in DSM-5 and ICD-11).

DSM-III and the Generation of New Diagnoses 23
All this work had been generated in the United States and had been triggered by the
research of Donald Klein who claimed to have demonstrated ‘pharmacological dissection’
in showing that imipramine was apparently selective in reducing panic attacks but had no
effect on generalised anxiety (Klein, 1964). (He told an impressive story at international
meetings: ‘The nurses came up to me. “The patients aren’t coming to the nursing station any
more.” I said, “why not?” “They’ve all lost their panic attacks; is it something you’ve given
them?”’). Yes, of course, imipramine had worked its miracle.
Now we realise that response to antidepressants does not a diagnosis make. The drug
words ‘anxiolytic’ and ‘antidepressant’ are becoming part of history and have been aban-
doned in the latest authoritative book on the subject (Haddad & Nutt, 2020). But in the
1970s we were still in the white heat of the psychopharmacological revolution and these new
developments were applauded with gusto.
So here was I at this point, as a relatively junior psychiatrist, trying to make sense of
a profession in which diagnosis was felt to be an important badge of knowledge.
Psychiatrists were esteemed as the decision makers in the mental professional system.
Their knowledge of nosology, the science of classification, gave them status and, more
importantly, led to (allegedly) correct treatment being given and followed by the rest of the
clinical team. Yet here we had earnest discussions at journal clubs in the academic unit at
that time disputing diagnosis, especially over the separation of anxiety and depression, not
least as, noted in the previous chapter, Sir Martin Roth and his colleagues in Newcastle had
published a series of papers claiming a breakthrough in understanding of affective disorders
(Gurney et al., 1972; Kerr et al., 1972).
What also bothered me was the relative uselessness of these particular labels when seeing
patients in the clinic and writing to fellow doctors with my findings. I also had similar
puzzlement when patients were referred to my clinic by psychiatrists and general practi-
tioners and finding that the diagnosis was of very little value unless the writer had disclosed
something about the background and circumstances of the patient, with even the occasional
mention of a personality profile.
I would not claim to be in any way special in these doubts. Many other psychiatrists,
when placed in the same position, have decided that diagnosis in this area of medicine was
pretty pointless and abandoned it all together. Dr Ronald Sandison, the original UK
enthusiast for psychedelic interventions, was one of these. He was a psychotherapist in
Southampton at that time and could not understand my concerns: ‘If I don’t understand
a diagnosis, or feel it is so vague it can apply to anybody how can I treat people successfully?’
I asked him. ‘That is immaterial’, he replied loftily. ‘We are in the growth and development
business, not the treatment one.’
Of course, that was not going to satisfy me, and these discussions set in mind a great deal
of further questions. If this amorphous construction called neurosis, which seemed to be the
most common condition in psychiatry, could be harnessed into some sort of order, would
we then be able to be more confident about prescribing for, and managing, patients and
would we be able to predict their futures?
2.2 Clap of Thunder: The Introduction of DSM-III

Then the skies were opened and down came DSM-III. Would this be the answer to my
doubts and questions? It is useful to get DSM-III into context. For younger psychiatrists, it
may seem odd that an upgrade of a slightly curious system of classification developed in the

24 Neurosis
United States that was quite independent of the official ICD (International Classification of
Diseases) published by the World Health Organisation, had such an impact when it was
published (American Psychiatric Association, 1980).
The reason was psychiatric classification was in a total mess before DSM-III. This was
highlighted by what has become known as the Rosenhan experiment. David Rosenhan was
a professor of both law and psychology and was particularly concerned about the ethics of
involuntary detention. After listening to a lecture by Ronnie Laing, he became interested in
testing the ability of psychiatrists to detect severe mental illness even when it was simulated.
He conceived the study in two parts.
The first part involved the use of healthy associates or ‘pseudopatients’. Rosenhan was
one of nine people who took part in this experiment. The others were three psychologists,
a psychology graduate student in his 20s, a pediatrician, a psychiatrist, a painter, and
a housewife. Three pseudopatients were women, five were men. All of them employed
pseudonyms. To make the experiment generalisable, 12 hospitals on the East and West
coasts of the United States were chosen: 11 state hospitals and one university one. (It would
have been interesting to see if the findings would have differed in any way in hospitals in the
central states of the USA).
All the pseudopatients were trained in the same way. They were not specifically asked to
imitate the common symptoms of severe mental disorder, only to hint at them. These were
Rosenhan’s (published) words:
After calling the hospital for an appointment, the pseudopatient arrived at the admissions
office complaining that he had been hearing voices. Asked what the voices said, he (or she)
replied that they were often unclear, but as far as he could tell they said “empty,” “hollow,”
and “thud.” The voices were unfamiliar and were of the same sex as the pseudopatient. The
choice of these symptoms was occasioned by their apparent similarity to existential symp-
toms. Such symptoms are alleged to arise from painful concerns about the perceived
meaninglessness of one’s life. It is as if the hallucinating person were saying, “My life is
empty and hollow.” The choice of these symptoms was also determined by the absence of
a single report of existential psychoses in the literature. (Rosenhan 1973, p. 252)
In other words, they should have led to some doubt in the psychiatrist’s mind that these
were in any way typical of psychosis, because clearly, they were not.
Nevertheless, all the ‘pseudopatients’ were admitted to the hospital for investigation.
Each of them was asked to behave normally if they were admitted. They were surprised at
the ready acceptance of their curious symptoms. In fact,
none of the pseudopatients really believed that they would be admitted so easily. Indeed,
their shared fear was that they would be immediately exposed as frauds and greatly
embarrassed. Moreover, many of them had never visited a psychiatric ward; even those
who had, nevertheless had some genuine fears about what might happen to them. Their
nervousness, then, was quite appropriate to the novelty of the hospital setting, and it abated
rapidly. (Rosenhan 1973, p. 253)
So we had a curious situation where patients with fictitious symptoms were admitted
readily and then behaved quite normally. But they were not encouraged to leave.
The pseudopatient, very much as a true psychiatric patient, entered a hospital with no
foreknowledge of when he would be discharged. Each was told that he would have to get

out by his own devices, essentially by convincing the staff that he was sane. The psychological
stresses associated with hospitalisation were considerable, and all but one of the pseudo-
patients desired to be discharged almost immediately after being admitted. They were,
therefore, motivated not only to behave sanely, but to be paragons of cooperation. That
their behavior was in no way disruptive is confirmed by nursing reports, which have been
obtained on most of the patients. These reports uniformly indicate that the patients were
“friendly,” “cooperative,” and “exhibited no abnormal indications.” (Rosenhan 1973, p. 253)
As a condition of their release, all the patients were forced to admit to having a mental
illness and had to agree to take antipsychotic medication. The average time that the patients
spent in the hospital was 19 days. All but one were diagnosed with schizophrenia ‘in
remission’ before their release. What alarmed Rosenhan was that the label of schizophrenia
was affixed to each pseudopatient on very limited assessment, if indeed it can be called an
assessment at all. As he put it in his paper ‘the evidence is strong that, once labeled
schizophrenic, the pseudopatient was stuck with that label. If the pseudopatient was to be
discharged, he must naturally be ‘in remission’; but he was not sane, nor, in the institution’s
view, had he ever been sane.’
The second part of his study involved a hospital administration challenging Rosenhan to
send pseudopatients to its facility, whose staff asserted that they would be able to detect the
pseudopatients. Rosenhan agreed, and in the following weeks, 41 out of 193 new patients
were identified as potential pseudopatients, with 19 of these considered suspicious by at
least one psychiatrist and one other staff member. Rosenhan sent no pseudopatients to the
hospital.
Rosenhan titled his paper ‘on being sane in insane places’. It is not a great scientific paper
and has been criticised heavily for its many errors and misperceptions (Lilienfeld et al.,
2009), but it is described here in detail because I think it did have a big impact on the
development of DSM-III. If Rosenhan had carried out his study in the United Kingdom the
results may have been very different. The diagnosis of schizophrenia was made much more
conservatively there than in the United States, and an important set of data from the UK/US
Diagnostic Study a few years earlier (Kendell et al., 1971) had already established the
excessive use of the diagnosis of schizophrenia in the Unites States for a wide range of
conditions which others just found odd or unusual.
So the stage was prepared for major diagnostic reform and Robert (Bob) Spitzer was
there to fill the role of leader. He took over as Chair of the DSM-III task force after
frustration in taking part in the anaemic DSM-II classification, introduced in 1968 and
still largely dominated by psychodynamic thinking (Spitzer and Wilson, 1968). The DSM-II
group was handicapped by many psychiatrists wanting to make their own personal diagno-
ses based on their clinical judgement, so contained clauses such as ‘in the case of diagnostic
categories about which there is current controversy concerning the disorder’s nature or
cause, the Committee has attempted to select terms which it thought would least bind the
judgment of the user’. Expressed somewhat differently; ‘we have made things as vague as
possible so you can easily fit your own pet ideas into the diagnosis’.
Burnished by these experiences, Spitzer took a different approach with DSM-III. First of
all, he realised it was important for everyone to have their say, so they did, but he did not
necessarily take notice of what they said. Then he organised the meetings in such a way that
at the end, before people could leave, Bob got them to agree to a statement of what they had
decided.

26 Neurosis
Alex Spiegel describes this process beautifully:
Members of the various committees would regularly meet and attempt to come up with
more specific and comprehensive descriptions of mental disorders. David Shaffer, a British
psychiatrist who worked on the DSM-III and the DSM-III-R, told me that the sessions were
often chaotic. ‘There would be these meetings of the so-called experts or advisers, and
people would be standing and sitting and moving around,’ he said. ‘People would talk on
top of each other. But Bob would be too busy typing notes to chair the meeting in an orderly
way.’ One participant said that the haphazardness of the meetings he attended could be
‘disquieting’. He went on, ‘Suddenly, these things would happen and there didn’t seem to be
much basis for it except that someone just decided all of a sudden to run with it. (Spiegel,
2005)
Allen Frances, who was also a member of the DSM-III Task Force, describes this
similarly in his flowing obituary of Bob Spitzer, except that he exposed the design behind
the chaos:
When Bob began work on DSM III in the mid-1970s, precious little scientific evidence was
available to guide how the different disorders should be defined. So Bob created working
groups on the various disorders and invited the experts to numerous meetings that all
followed the same pattern. He would let us rant and rave in the mornings, blowing off steam
promoting competing concepts. Bob would type at blazing speed and was like a magician
who seemed to pull DSM III out of a hat—or rather, his computer.
A giant deli lunch would eventually arrive that made everyone drowsy and less argumen-
tative. Bob would then present a beautifully-worded criteria set that captured the best of the
morning’s suggestions and pacified most disagreements. Thus, DSM III was born. (Frances,
2016, p. 110)
Spitzer kept everyone in the loop afterwards and ensured that agreement to these
decisions was maintained until publication. Nevertheless, this was not achieved without
a struggle between the Titans of psychoanalytic and conventional psychiatrists. Otto
Kernberg led the charge: ‘It is a straitjacket and a powerful weapon in the hands of people
whose ideas are very clear, very publicly known, and the guns are pointed at us.’ (Kernberg,
quoted in Bayer & Spitzer, 1985, p.190). But an uneasy harmony was achieved, partly by
making personality disorder a separate axis of classification (Axis II) which allowed psy-
choanalysts much more freedom.
For the DSM-III task force, and most of American psychiatry, neurosis was an aetio-
logical rather than a descriptive concept. It assumed, as DSM-II noted, an underlying
process of intrapsychic conflict resulting in symptom formation that served uncon-
sciously to control anxiety. However, there was no empirical basis for assuming the
universal presence of such conflict in those disorders that had traditionally been
termed neurotic. There was, for example, no justification for asserting that intrapsychic
conflict was always present in what had been denominated ‘neurotic depression.’
Furthermore, since intrapsychic conflict was present in both those with and those
without psychiatric disorders, it could not possibly serve as the basis for discrete
class formation, the very purpose of a diagnostic manual. Finally, the task force held
that the term neurosis had lost even its earlier specificity as contemporary psychoana-
lytic theory had shifted its focus of interest from the ‘symptom neuroses’ to the
‘character neuroses (personality disorders)’(Bayer & Spitzer, 1985).

2.3 Hypotheses in the Nottingham Study

The concern I had in 1982, when the ideas behind the Nottingham Study were generated,
was that if, as seemed likely, the splitting of many different strands of old neurosis was going
to proceed apace, there would be little interest in a different view, namely that the unitary
lumping of neurosis still had merit, particularly if it was subsequently found to have
a common pathology. I was also singularly unimpressed by the argument that different
specific treatments could be selected for each of these new entities. I also needed to have
personality assessment at the core of the study if the relationship between neurotic person-
ality and neurotic symptomatology was to be teased out.
2.4 Summary
The theoretical arguments for the acceptance of the general neurotic syndrome have been
presented in this chapter, with various lines of independent evidence in support. It is
probably one of many Galenic diagnoses that will become increasingly recognised in
coming years. But these lofty words alone are not sufficient. Evidence is needed to test out
the hypotheses put forward, especially the importance of cothymia and the nature of the
personality links. The remaining chapters of this book attempt to provide this evidence in
a detailed assessment of the Nottingham Study of Neurotic Disorder.

Chapter
The Hypotheses
3 of the Nottingham Study

of Neurotic Disorder
The reasons for the generation of the Nottingham Study of Neurotic Disorder were at their
core a series of important questions:
(1) Is personality an important component of what has been called ‘neurosis’?
(2) Is it clinically useful to regard mixed anxiety and depression (which from henceforth in
this book is called cothymia) as a syndromal rather than a sub-syndromal condition?
(3) Is there evidence that the anxiety and depressive symptoms in neurosis differ in their
response to different treatments?
(4) Do patients with neurosis and personality difficulties get better over time or do their
problems persist?
These questions would answer the issue of whether there was value in maintaining the
neurotic concept, formulated as described earlier as the general neurotic syndrome.
To answer the first of these questions, it was necessary to record personality status
reliably; to answer the second, cothymia needed to be diagnosed as a clinical syndrome; to
answer the third, it was necessary to carry out a randomised controlled trial of treatments;
and to answer the fourth, a long period of follow-up was needed.
3.1 Reliable Assessment of Personality Disorder

In 1982 there were no world-wide accepted measures of personality disorder. Many assess-
ment interviews had been created, including Bernreuter’s Personality Inventory
(Bernreuter, 1931), the Rorschach Inkblot Test (Rorschach, 1921), the Minnesota
Multiphasic Personality Inventory (Hathaway & McKinley, 1940), the Thematic
Apperception Test (Murray, 1943), and the 16PF Personality Questionairre (Cattell &
Stice, 1957). But none of these was focused on personality disorder and there were many
doubts about their value in a personality-disordered population.
In any case, DSM-III had just been published and it was clear that this revolution in
diagnosis would lead to new measures, especially for personality disorder. I wrote to Bob
Spitzer at the New York Psychiatric Institute and he was interested and attentive, admitting
that he was in the process of developing an instrument for recording personality disorder
and asking for advice. It was subsequently published and, in its later version with Michael
First as the first author, became the most widely used instrument in the 1990s (First et al.,
1995).
But we were keen on getting the Nottingham Study started and there was also concern
that any instrument linked to the DSM classification would be likely to change over time.
We needed a measure that was reliable, comprehensive, and unchanging for the duration of
a follow-up study. I had developed a measure a few years earlier called the Personality
28

The Hypotheses of the Nottingham Study 29
Assessment Schedule (PAS) which seemed to satisfy these requirements (Tyrer &
Alexander, 1979; Tyrer et al., 1979). This instrument is not particularly well known, partly
because it has not been made available commercially or through an academic institution,
but also because in the course of its development I realised that training in its use was very
important before it could be scored properly. I therefore wanted tight control of training
before the instrument could be more widely used. (This is not a very sensible way of
popularising a scale as the wider the use the better, but I have stuck to it over the years,
and those who want to use it have to be determined.)
The Nottingham Study was envisaged in 1981 and initiated in 1982, but did not begin
recruiting patients until later in 1983. This was not a study carried out in a high-powered
academic centre with many resources, and the hypotheses could have been considered as
reactionary rather than progressive, so getting the resources and people to support it was
not easy. At the time, I was working as a consultant psychiatrist in Nottingham and had
recently transferred my extra-hospital activities to general practice. This was professionally
the most satisfying time of my career in respect of patient care (Tyrer, 2013) and I need
a section to explain why and also describe the advantages that the clinics held for the
Nottingham Study.
There were two big advantages of the PAS. It was not tied to any other system of
recording personality so could not be changed or suddenly made redundant by
a successor, and the conclusion of the analysis of the data suggested that personality
could be placed on a single spectrum, as the results ‘supported the concept of personality
disorders as being at the extreme of a multidimensional continuum’ (Tyrer & Alexander,
1979, p. 166). Thus, the PAS was equipped to record personality disturbance in terms of
severity as well as type, and this was to be of particular value for the future of the
Nottingham Study.
3.2 The Importance of Recording Cothymia

As cothymia is defined as the simultaneous presence of anxiety and depressive symptoms, it
was necessary to include patients in the study who had both anxiety and depressive
diagnoses. Good diagnosis could readily be achieved by using the most reliable diagnostic
system at the time, DSM-III, and formally scoring anxiety and depression using the
Structured Clinical Interview for DSM-III that had just been introduced (Spitzer &
Williams, 1983).
But the DSM-III did not make any allowance for comorbidity, so mixed anxiety and
depression in any form was not permitted. Instead, a hierarchy was created in which panic
disorder trumped dysthymic disorder and both panic and dysthymic disorder trumped
generalised anxiety disorder. Of course, this was anathema to the thinking of the
Nottingham Study and as we had recorded both anxiety and depressive disorders at baseline
assessment, we were able to include cothymia as an additional diagnosis.
3.3 Testing Whether Anxiety and Depressive Symptoms Differ

in Their Response to Treatment
This hypothesis could only be tested adequately in a randomised controlled trial. Such trials
are not easy to set up and need large numbers to yield definitive results. As we were trying to
test efficacy in both anxiety and depression separately and together (cothymia) we needed to

30 Neurosis
test three groups. As specific efficacy had been claimed for antidepressants in the treatment of
panic disorder it was necessary to have patients with panic disorder included in the study also.
Psychological treatments were also to be included if the trial was to be a comprehensive one.
3.4 Long-Term Outcome

Long-term outcome studies in mental health are difficult. It is very different with physical
health disorders, when patients often feel privileged to be involved in doctors’ concern for
their care. It is even better when you have doctors themselves involved in the research, as
they tend to be even more assiduous in agreeing and providing data for follow-up studies.
In October 1951, Richard Doll and Austin Bradford Hill sent a questionnaire on
smoking habits to all registered British doctors. In the previous year, they had just demon-
strated the association between smoking and carcinoma of the bronchus and wanted to
know more about the effects of smoking long-term. They sent out 59,600 questionnaires:
41,024 replies were received and 40,701 (34,494 males and 6,207 females) provided enough
data to be included in the follow-up (Doll & Bradford Hill, 1954). You would never get
figures like this in a psychiatric follow-up study. Short follow-up was followed by further
questionnaires about changes in smoking habits up to 2001. The study has yielded a mass of
information, not the least of which is that even if smokers reduce or stop their cigarette
consumption late in life, it still makes them less likely to get bronchial carcinoma than if they
persist (Doll et al., 1994).
I met with Richard Doll in 1982 when he was visiting Nottingham; he was a friend of my
father and had stayed with us in the past. I talked to him about the Nottingham Study and
three pieces of advice he gave were followed in the study. Firstly, he emphasised the need to
have simple measures of outcome. ‘Its easy for me, because most of my studies involve death
as an outcome, and that is unequivocal. But you can’t do this in psychiatry. But you can
choose a simple outcome that everyone can recognise. Are people after treatment ill or no
longer ill? Choose a simple measure of illness.’
Secondly, he emphasised the need for a placebo control in the randomised trial, and,
thirdly, he pointed out the advantages of long-term follow-up. ‘If a treatment only gets
people better for a few weeks and they get worse afterwards there is not much point in
choosing it. And if you don’t know the natural history of a condition you will be tripped up
time and time again in making premature conclusions.’
3.5 How to Recruit Patients to the Study?

Most patients with common mental disorders are treated entirely in primary care. If
a hospital or outpatient population is chosen, it may not be representative. This is one of
the criticisms that could be directed against the Newcastle Group studies of anxiety and
depression; they were carried out with inpatients. I wanted to avoid studying a population
that could be criticised as being at the severe end of the spectrum of mood disorders.
Fortunately, a suitable population was available in Nottingham and a service was
available to treat them. Nottingham, unlike many other areas in the country in the
nineteenth century, was not allowed to place its mental hospital somewhere in the back of
beyond. The ‘out of sight, out of mind’ mentality was there but could not be followed
through on as the city was compelled to build its hospital services within the city boundaries,
so had to choose local, not distant. In the end it was decided the new hospital would be built
on the top of a hill at the northern limit of the town at a place called Mapperley (ever since

called Mapperley Top). It was not an ideal site, ‘long and narrow, bordered by a main road to
the east and a deep valley to the west’ (Mindham, 2020). It might have been a nightmare
to create but fortunately it had a highly competent architect in the form of George Hine to
design it. The ‘long corridor’ hospital subsequently had a celebrated 114-year history,
helped greatly near its end by the pioneering community work of Duncan MacMillan,
a dour but far-seeing Scot, who was one of the first twentieth-century psychiatrists to
recognise that autonomy is good for patients and seclusion from the world is not.
But because the hospital was local, it attracted considerable stigma. When patients were
admitted they were often taken there in one of a fleet of cream-coloured vans linked to the
hospital. This was noted immediately by Nottingham mothers; children’s bad behaviour
was often controlled with a threat to arrange ‘a visit from the yellow van’ (Tyrer, 2008a). So
the hospital, despite its mainly good reputation among the profession, became a place to
avoid, and this unfortunately extended to its fellow hospital, St Ann’s, built in 1934, and its
outpatient clinics close by. People generally did not like going there for appointments and
the setting was glum.
However, it was very different in the 1980s in general practice. Spanking new premises
were being opened up every year. They were closer to people’s homes and very pleasant to
visit. Several consultants and I set up, with agreement and great enthusiasm from GPs,
psychiatric clinics in general practice settings. These were both refreshing and efficient. I got
to know the GPs well and we had frequent conversations about patients at crucial times in
their care – so much better than a stilted letter (Darling & Tyrer, 1990). From the point of
view of the Nottingham Study, these clinics were ideal as patients were referred there earlier
in the course of their problems and so I was in a better position to assess the general
problems of neurosis before too many other labels had been applied.
This form of care was possible in the 1980s as resources were adequate and there was still
considerable enthusiasm for developing new forms of community care. At this time, I was
holding 19 clinics a month across Nottingham and the yellow bags (the ones provided by the
hospital and containing the notes for each clinic – no extra technology then) clearly replaced
the yellow vans. The service was effective and efficient and before long most of my colleagues
had joined in. We subsequently had strong evidence that this enterprise reduced the
demand for inpatient beds (Tyrer, Turner & Johnson, 1989; Williams & Balestrieri, 1989),
even though they created some extra referrals (Jackson et al., 1993; Tyrer, Ferguson &
Wadsworth, 1990). During one special period in 1987, admittedly only for two days, I had
no patients in hospital; everyone was an outpatient. But these were the days when the
community cycle was in top gear and running downhill. It has been an uphill struggle ever
since and though for a short time the Department of Health was interested in moving
forward with general practice clinics across the country, it was only in Scotland where this
was considered seriously as an alternative provision. Despite this, in other countries, the
idea of these clinics in primary care or in separate non-psychiatric settings is still being
developed (Carr & Donovan, 1992; Grenyer et al., 2018; Anjara et al., 2019). The key is to
have senior people in these settings who have extensive knowledge of the patient (Darling &
Tyrer, 1990); just placing a single mental health practitioner in the clinic is not sufficient
(Emmanuel et al., 2002).
Seeing patients in general practice clinics was ideal for the Nottingham Study, as
referrals often took place much earlier than in normal outpatient practice. From the
beginning of the planning of the study it was decided only to include patients who were

32 Neurosis
not taking any treatment at the time of assessment. This reduced the pool of potential
participants but made the cohort a more homogeneous one.
3.6 Generating the Randomised Controlled Trial

and Follow-Up
The trial plan that I developed was a complex one and needs justification. I was aiming to
examine the general concept of neurosis with a particular emphasis on anxiety and
depression. Even if my hypothesis was correct and combined anxiety and depression
was found to be a very different condition from the individual diagnoses of these condi-
tions, if there was an obvious diagnostic difference in response to treatment (as Klein,
1964, 1981, and others would argue), then this would justify the existing diagnostic
system. This made it necessary to include antidepressant and antianxiety treatments,
preferably drug and psychological, and because the design of the study was unusual
there had to be a placebo arm in the randomised treatments. (Having support from
Richard Doll here was very valuable when dealing with the local ethics committee,
which initially refused to contemplate a placebo component until I emphasised that
Richard deemed it essential.)
The selection of diagnoses was also important. The most difficult was the choice of the
right diagnosis of depression. The umbrella diagnosis of ‘major depressive episode’ was felt
to be too vague and would overlap with more serious depressive disorders, so instead the
diagnosis of dysthymic disorder was chosen, and as its alternative title was given as
‘depressive neurosis’ in DSM-III (American Psychiatric Association, 1980, p. 220), it was
felt to be a more appropriate diagnosis to include.
As noted in all classifications of depression, there was no mention of anxiety symptoms
in the DSM-III description (American Psychiatric Association, 1980, p. 221) but all practi-
tioners recognised that anxiety was a component to the diagnosis. This was subsequently
summarised very neatly by Gene Paykel:
In the last 20 years dysthymia has proved a useful concept, delineating a form of mood
disorder which can produce many problems and have an adverse impact on the life of the
sufferer, and it has generated much research. There is a high rate of comorbidity,
particularly of anxiety disorders and substance abuse. The majority of dysthymics ultim-
ately also develop an episode of major depression, and such episodes, so-called double
depression, have a worse prognosis than pure major depression, both in respect of
remission and of recurrence. There appears therefore to be continuity between dysthymia
and major depression. The DSM-IV definition rules out an episode of major depression in
the first 2 years, but the ICD-10 definition does not. In practice the differentiation of
dysthymia from milder chronic major depression or from the residual symptoms with
partial remission which frequently occur after major depression, is difficult and may be
artificial. (Paykel, 2008)
There was also the problem of the sample size. Three diagnoses and five treatments were
eventually chosen, but when calculations were made and it was decided to only recruit 210
patients, an obvious criticism was made that this might lead to a Type II error (i.e., a true
difference that was not identified as the sample size was too small). In the end, we decided to
have a constrained randomised sample in which a computer-generated algorithm allocated
the 210 patients in the following fashion (Table 3.1).

Table 3.1 Randomised trial and treatment numbers
Treatment Number
Diazepam 28
Dothiepin 28
Placebo 28
Cognitive and behaviour therapy 84
Self-help 42
TOTAL 210
It will immediately be noticed that the numbers in the drug groups are small. This
was because the intention at the beginning of the trial was to continue it as a follow-up
study after 10 weeks. The self-help and psychological treatments were clearly known to
the investigators but double-blind methodology meant that the drug groups could not
be identified. After 10 weeks, if people felt they had responded to their allocated
treatment, they were encouraged to continue it ‘in the same mode’. This translated
into the 84 allocated to drug therapy continuing drug treatment in the form of
dothiepin (without breaking the blind of the original allocation), 84 continuing with
CBT or similar psychological treatments, and 42 continuing with self-help. (Dothiepin
was chosen as at that time it was the most commonly prescribed antidepressant in the
UK; Boots Pure Drug Company also provided the placebo and diazepam capsules of
identical appearance.)
3.7 Duration of Treatment

At the time when we carried out the Nottingham Study, it was commonplace to have the end-
point of a trial when the last treatment was given. We anticipated later concerns about adverse
effects, partly because of evidence we had found that withdrawal symptoms with diazepam
could be identified when withdrawing after only six weeks of treatment (Murphy, Owen &
Tyrer, 1984). So we set the duration of treatment of all types to be six weeks only, and then to
gradually withdraw medication (and CBT) so that at 10 weeks all patients were on no therapy.
3.8 Inclusion and Exclusion Criteria

There is always a battle, when deciding on whom to recruit to a trial, between those who
would like a completely representative population with as few exclusions as possible, and
those who would prefer a tightly selected homogeneous group who represent the best
population to test your hypotheses. We decided to err in favour of the former in the
Nottingham Study.
We only had the following exclusion criteria:
(i) existing diagnosis of major depressive episode after the Structured Clinical Interview
for DSM-III (SCID) assessment,
(ii) patient taking psychotropic drugs at time of assessment,
(iii) past history of schizophrenia or manic-depressive psychosis.

34 Neurosis
3.9 Assessments in the Randomised Trial

Because the Nottingham Study required assessments of both anxiety and depression, as
well as a detailed interview about personality status, it was decided at the outset that all
assessments should be carried out by face-to-face interviews. This sounds straightforward
but it is not, and nowadays digital technology is increasingly being used in place of direct
contact. This is a pity, as the clinical interview, even a research clinical interview, yields so
much more than a set of ratings on a scoresheet. Particularly in a follow-up study, frequent
contact with the same investigator often leads to an easy informal relationship that
promotes excellent understanding. Indeed, at later assessments, when we asked each
patient what had helped them most over the course of treatment, several identified our
researchers as top of their list, even though no treatment of any sort had been provided by
them.
At baseline in the randomised trial, six assessments were made. The procedure in each
case was a two-stage process. The first stage involved screening the patient for eligibility at
assessment at the general practice clinic by a consultant (me) or a senior registrar. If the
patient was regarded as eligible and was willing to take part in the trial, the Structured
Interview for DSM-III was given and assessments made for all depressive and anxiety
diagnoses. If the patient satisfied the requirements for the diagnosis of panic, dysthymic or
generalised anxiety disorder, or any combination of these, the next sealed envelope was
opened and one of five treatments disclosed, the three drug treatments (A, B or C),
cognitive behaviour therapy (CBT), or self-help. The second interview, carried out within
a day or so of the first, involved a visit from a previously trained research assistant (all
junior psychiatrists), who administered the Personality Assessment Schedule and five
other scales:
1 The Comprehensive Psychopathological Rating Scale (CPRS) (Åsberg et al., 1978).
(Although I like to avoid acronyms, because this scale has a long title I will
abbreviate this to CPRS in most of the references that follow). This is a 65-item
observer-rated scale that includes both the assessment of symptoms (40 items) and
observed behaviour (25 items) with each item scored on a four-point scale. It has the
advantage of being truly comprehensive, being able to assess present psychiatric state,
the severity of a full range of symptoms, and the change in symptoms over time. It
was said to take about 50 minutes to administer but when being used frequently this
time could be shortened greatly. It also has a summary four-point rating (CPRS-
Global). Greater severity is shown by higher scores.
Although most of the scales selected for the Nottingham Study have been continued to
be used to the present day, the CPRS is the only one that has fallen out of favour.
2 Montgomery and Åsberg Depression Rating Scale (MADRS)
If the CPRS is the also-ran in the rating scale stakes, the MADRS is the Olympic
champion (Montgomery and Åsberg, 1979). It was derived directly from the CPRS, but
the poor chap at the back of the field never gets much credit. The MADRS scale has been cited
nearly 10,000 times in the scientific literature and is the most highly cited paper ever
published in the British Journal of Psychiatry. It records 10 items from the CPRS and has
expanded the scoring to make change easier to detect so there is a maximum score of 6 for
each item. Later studies suggest scores of 7 to 19 indicate mild depression, 20–34 moderate
depression and >34 severe depression (Herrmann et al., 1998).

3 The Brief Anxiety Scale (BAS)

This scale was developed by me and tested out with other colleagues in studies carried
out in the early 1980s (Tyrer, Owen & Cicchetti, 1984). It is the anxiety equivalent of the
MADRS as it also contains 10 items from the CPRS and scores them in a similar fashion with
a maximum score of 6 for each item. Two of the items (inner tension and reduced sleep) are
the same as in the MADRS, and yet again this illustrates the overlap between anxiety and
depression described in earlier chapters. The scale correlates well with self-ratings of anxiety
(and depression), as does the MADRS (Evenden et al., 1996), but the agreement is not quite
strong enough to regard a self-rated measure as redundant (0.76–0.83).
4 Hospital Anxiety and Depression Scale (HADS)
This scale was only introduced in 1983 (Zigmond & Snaith, 1983) but has been cited over
25,000 times in the scientific literature. It is a simple 14-point scale that has 7 anxiety and 7
depression items.
Assessing depression and anxiety with two rating scales for each might be thought
unnecessary but here the Lewis Prediction also applied. Any tendency of the assessing
psychiatrists to overstate anxiety when present with depression would be counteracted by
the self-rating HADS scales.
5 Personality Assessment Schedule (PAS)
The Personality Assessment Schedule is listed as the Appendix of this book. It is a 24-
item scale that has not been used widely. This is partly my fault. As noted earlier in this
chapter, when testing the schedule we noted that reliable assessment of personality with the
scale was highly dependent on training. Those very new to personality assessment tended to
overscore on some items and minimise others. There was also the problem of the nature of
the informant (for example, if this was the recently estranged spouse of a person the
assessment of the other might contain elements of bias). In general, we found women to
be better than men in making assessments (Brothwell, Casey & Tyrer, 1992).
Because of these concerns, the PAS was only released for formal studies after negotiation
and only a handful of studies outside our group have used it, with perhaps the most interesting
being the study by Manuel Cuesta and colleagues (2002) that suggested that the schizoid
(detached) dimension in the PAS in patients with first-episode psychosis was associated with
the development of negative symptoms in schizophrenia. The PAS studies have included
comparisons with other instruments and these in general have supported its structure and
likely accuracy, especially with regard to its slightly shorter version, the Quick Personality
Assessment Questionnaire (Hill et al., 2000; Germans, Guus & Hodiamont, 2011, 2012).
The other advantage of the PAS was that it did not change over time. If other instru-
ments had been used, they would have had to be updated with DSM-III-R and DSM-IV
replacements. Because the PAS recorded severity of personality disorder as one of its regular
components, it was also very much in tune with the new ICD-11 classification of personality
disorder (Tyrer et al., 2019), and a separate validation study was carried out to allow the
baseline PAS scores to be converted into ICD-11 severity categories (Tyrer et al., 2014). This
has allowed ICD-11 categories to be incorporated into the results.
3.10 Setting Up the Financial Aspects of the Trial

One of the main problems in carrying out research that is not a natural development from
pre-existing studies is that funding is difficult to obtain. This was particularly difficult in my

36 Neurosis
position at the time as I was an NHS consultant, not with an academic title, although I had
general encouragement to carry out research. What follows in this section might be useful
advice for others placed in the same position.
First, you need some independent advice that what you are planning is not completely
inappropriate or simply not feasible. If you persist at this point you will only achieve the
epithet of being stupidly pig-headed and stubborn and the work will go nowhere. (Some
people said that to me anyway, but because I had good opposing voices I could continue).
I spoke to several colleagues, principally Gene Paykel, at that time Professor of Psychiatry at
the University of Cambridge, and he was supportive. Bob Kendell in Edinburgh was similar
in his encouragement. ‘Why not go ahead’, Gene said, ‘but you will find it a struggle to get
the money.’ I decided not to go for the major grant funders on the grounds that they would
turn the application down in view of my status at the time, and as the world was then so
attuned to the splitting of so many diagnoses one that was unashamedly linked to ‘the
lumpers’ would get short shrift.
So, a range of different options were considered for funding, the details of which are
summarised at the end of this book. But it was not only the funding that mattered. Far more
important were the people who supported the project from the beginning, many of them
junior doctors in training posts, who carried out extra work in learning the assessment
procedures, training on the Personality Assessment Schedule, visiting patients at home
repeatedly over the period of follow-up, and generally providing encouragement when
problems arose.
Accumulating the necessary funds for a large trial is analogous to moving to a new house
and finding out that a piece of wasteland at the back of the house is masquerading as your
garden. You go outside, plant a spade in the rock-hard ground, get stung by nettles, pricked
by thistles, and coiled in bindweed and feel like giving up. But if you plan, a little at a time,
things begin to change. Better still, once you have made some progress, others notice, give
suggestions and maybe even some help, and before long the waste area looks a little like
a proper garden. At this tipping point everyone realises that the garden is a real creation,
offers plants and more suggestions, and finally you have something of beauty to see when
you look out of your bedroom window.
Once we had sufficient funds to start the trial, and received a positive ethical opinion, we
were able to start. The first patient was recruited to the study in October 1983. We did not
have an ‘end day’ for recruitment as we needed to continue until all 210 patients were
randomised, and this was not until August 1987.

Chapter
Interpretation of the Results
4 of the 1988 Lancet Randomised

Trial
The results of the 10-week randomised trial were published in the Lancet in July 1988
(Tyrer, Seivewright, Murphy et al., 1988). The main findings at this point did not
include any analysis of the general neurotic syndrome as this was not a term that
would have been understood by the average reader and would have just led to
confusion. The results were presented in a standard manner, focusing on the effects
of the five treatments (Figure 4.1) and of the outcome of the three diagnostic groups
(Figure 4.2).
The summary of the trial’s findings was expressed thus:
There were no important differences in treatment response between the diagnostic groups,
but diazepam was less effective than dothiepin, cognitive and behavioural therapy, or self-
help, these treatments being of similar efficacy. Significantly more patients in the placebo
group took additional psychotropic drugs in the 10 week period, and those allocated to
dothiepin and cognitive behaviour therapy took the least. (Tyrer, Seivewright, Murphy et al.,
1988, p. 235)
25 2
20 1.5
CPRS CPRS
Total 15 Global 1
Score Score
10 0.5
0 2 4 6 8 10 0 2 4 6 8 10
Weeks since start of trial Weeks since start of trial
CBT diazepam dothiepin placebo self-help
Figure 4.1 Results of the Nottingham Study of Neurotic Disorder Trial separated by randomised group for
each of the main outcomes (adapted from Tyrer, Seivewright, Murphy et al., 1988a with kind permission of the
Lancet)
NB. Significant differences in diazepam-treated patients in CPRS total scores (F = 2.91; df 4,196; P = 0.023), CPRS
global score (F = 2.7; df 4,177; P = 0.03) and MADRS scores (F = 2.47; df 4,196; P = 0.046)
Patients allocated to placebo were more likely to take additional treatments (31%) in the trial than the other groups,
diazepam (15%), dothiepin (7%), CBT (9%), and self-help (18%) (odds ratio 3.4, 95% CI 1.2–9.8) (Χ2 = 7.1; df 1, P < 0.01)
37

12
11
25
10
20 9
HADS 8
Brief
Depression
Anxiety 7
15 Score
Scale
Score 6
10 5
4
0 2 4 6 8 10 0 2 4 6 8 10
25
16
15
20
14
15 13
MADRS HADS 12
Score Anxiety
10 Score 11
10
7 9
8
0 2 4 6 8 10 0 2 4 6 8 10
CBT diazepam dothiepin placebo self-help
Figure 4.1 (cont.)
16
15
25
14
20 13
HADS
12
Brief Anxiety
Anxiety 15 Scale 11
Scale
10
10 9
0 2 4 6 8 10 0 2 4 6 8 10
Panic Dysthymia Generalised Anxiety Disorder
Figure 4.2 Results of the Nottingham Study of Neurotic Disorder randomised trial separated by initial DSM diagnosis
(adapted from Tyrer, Seivewright, Murphy et al., 1988 with kind permission of the Lancet)
NB. Mean CPRS scores were lower in patients with GAD (14.1, 95% confidence interval 12.4–16.0) than in dysthymic
disorder (18.1, 95% CI 16.1–20.3) and panic disorder (17.4, 95% CI 15.5–19.3) (F = 4.6; df = 2,198; P = 0.012)

Interpretation of the 1988 Lancet Randomised Trial 39
4.1 Baseline Data in Randomised Trial

Table 4.1 Baseline data in all treatment groups in randomised trial
No. of Diazepam Dothiepin Placebo CBT Self-help Total

patients 28 28 28 84 42 210
Gender M 8: F 20 M 9: F 19 M 6: F 22 M 34: F 50 M 8: F 34 M 65: F 145

Age (median) 33 36 32 36 35 35
Social class 2 5 6 13 2 28
1–2
Social class 3 9 4 7 17 8 45
Social class 4 11 12 6 32 16 77
Social class 5 6 7 9 22 16 60
Main DSM
diagnosis
Dysthymia 10 11 8 23 13 65
GAD 11 10 10 28 12 71
Panic disorder 7 7 10 33 17 74
Mean CPRS 20 19 24 21 20 21
score
Mean MADRS 18 22 19 19 16 18
score
Mean BAS 20 18 22 20 19 19
score
Mean HADS-A 15 15 15 14 13 14
score
Mean HADS-D 8 14 9 11 9 10
score
4.2 Differences in Diagnosis

Table 4.2 Adjustment of diagnosis after accounting for cothymia
Initial Dysthymic Generalised Panic Cothymia

disorder anxiety disorder
disorder (GAD)
Main diagnosis at 65 71 74 –
randomisation (n)
Revised diagnosis after 9 70 60 71
adjustment for
comorbidity (n)
Change −56 −1* −14 +71
* One patient with GAD had a virtually equal depression diagnosis so counted as cothymia.

40 Neurosis
4.3 Distribution of GNS Positive Cases by DSM-III Personality

Status
Table 4.3 Personality status of patients with GNS at baseline
DSM-III PD % of total % of those Significance of GNS vs non-

diagnosis assessed (n=181) with GNS GNS numbers (χ2)
Histrionic 12.7 15.2 ns

Paranoid 12.2 12.1 ns
Dependent 10.5 22.2 P < 0.001
Avoidant 10.5 19.7 P < 0.01
Antisocial 9.4 4.5 ns
Borderline 9.4 6.1 ns
Obsessive- 8.8 16.7 P < 0.02
compulsive
Passive- 6.6 6.1 ns
aggressive
Narcissistic 6.1 4.5 ns
Schizotypal 4.4 4.5 ns
Note: each patient can have more than one personality disorder.
Personality status was recorded with the Personality Assessment Schedule (PAS) at
baseline. This was completed by assessors who were unaware of GNS status or initial
diagnosis. The PAS also includes an algorithm to convert the personality status, if all
information is available, into the DSM-III personality disorder diagnoses. The results
were not unexpected. Those with DSM-III diagnoses of dependent, avoidant, and obses-
sive-compulsive disorders were more likely to have the general neurotic syndrome
(Table 4.3).
4.4 Clinical Outcomes

The graphical presentation of the results best explains the differences between the
three DSM diagnoses and the outcomes of each of the five treatments. The only
significant result was that patients on diazepam had poorer outcomes than all other
groups. We are sure that this is because we included the period of withdrawal as well
as that of active treatment so that any symptomatic benefits were partly erased during
withdrawal.
But it is important to stress that the numbers in the study were still relatively small
and so only big differences were likely to be significant. We also were hiding the main
reasons for the differences in outcome between the diagnoses. What is clear from the
scores on the two anxiety measures, the Brief Anxiety Scale and the Hospital Anxiety
and Depression Scale – Anxiety Section (4.2), is that panic disorder has more severe

symptoms than generalised anxiety disorder. A score of between 16 and 17 on the

Brief Anxiety Scale indicates pathological anxiety (Tyrer et al., 1984) and one of 8 or
more is commonly accepted as the threshold for pathological anxiety (Stern, 2014),
and the mean scores in the Nottingham Study were well above these thresholds. Still,
the patients with panic disorder had scores nearly 50 per cent higher than those with
generalised anxiety disorder. Those with dysthymic disorder, allegedly a depressive
disorder but one we have already noted to consist mainly of cothymia, had baseline
levels similar to those with generalised anxiety but improved less well over the 10-
week period than the other two groups (Figure 4.1), so explaining their overall higher
ratings.
4.5 Differences in Treatments

As the summary of the paper and Figure 4.1 indicate, no differences were found
between the treatments in the randomised trial apart from an inferior result with
diazepam. So why did diazepam do so badly compared with the other treatments?
The answer is simple, although it has taken many years for most people to under-
stand why. Diazepam, ever since it came to be regarded as an addictive drug even in
therapeutic dosage, has been recommended to be taken for four weeks and then
gradually reduced. That is what we did in the Nottingham Study, unlike most
other studies in which improvement is measured while patients are taking the
drug. But we now know that withdrawal symptoms can occur after stopping benzo-
diazepines after only a few weeks (Murphy et al., 1984), and that is precisely what
happened in the Nottingham Study. There was improvement on the anxiety measures
and total CPRS score at first but when the drugs were gradually withdrawn this
improvement disappeared and patients’ scores returned to very similar levels to those
at baseline.
4.6 Reaction to Publication

There was a generally positive reaction to the Lancet publication, but some predictable
criticism from Donald Klein in New York. He had four major complaints: (1) the
numbers in the study, particularly the ones taking drug treatments, were too low so
a Type II error was very likely; (2) the drug doses of dothiepin and diazepam were
trivial; (3) he objected to the statements that ‘panic disorder was a quantitatively more
severe form of generalised anxiety disorder rather than a specific entity’ and that
dothiepin was a ‘typical antidepressant’; and (4) he concluded that ‘the study produced
an expensive Type II error with no useful therapeutic or nosological implications’
(Klein, 1988).
We responded by pointing out that, as the dosage regime was a flexible one starting with
a low dose, the dosage at six weeks was the better one to record; there was evidence of
gradual improvement over the six-week period; dothiepin was indeed a tricyclic antidepres-
sant (the most commonly used in the UK at the time); and there was absolutely no
suggestion of specific treatment/diagnosis differences over time with any of the measures
recorded. If there was a Type II error, there should have been at least an inkling of
a difference shown in some of the depression and anxiety scores; there was none (Tyrer,
Seivewright, Ferguson et al., 1988).

42 Neurosis
But Klein was right in pointing out that the numbers of patients with panic
disorder treated with antidepressants were not large enough to reach firm conclusions.
Other experts also suggested that dothiepin was not a typical tricyclic antidepressant,
but this was a footling comment; dothiepin is directly related to amitriptyline.
Others commented, sometimes with glee, that the trial showed that all treatments for
anxiety and depression were useless as placebo was just as good. But placebo was not just as
good – its outcome path was similar to diazepam for the CPRS global score and anxiety
scores (Figure 4.1) and those in this group took significantly more additional treatments
than the others (Tyrer, Seivewright, Murphy et al., 1988).
But the important result, hidden from the publication in the Lancet, was that the general
neurotic syndrome, showing strong overlap with dysthymic disorder, had a worse outcome
than other diagnoses. In other words, cothymia, the diagnosis that everyone chooses to
ignore, was much more resistant to short-term treatment. Dysthymic disorder, despite
having no mention of anxiety in its definition, was riddled with anxiety. Almost all the
patients at baseline with this condition had generalised anxiety as well, but our other
hypotheses were concerned with more acceptable diagnostic conditions and so in our
published work we felt it best to stay with the conventional labels. But throughout we still
recorded the progress of those with the GNS.
The study also showed that personality disorder had little impact on the outcome
measures. Those with more severe personality disorders had higher symptom scores on all
measures both at baseline and 10 weeks but the improvement was similar in all groups
(Tyrer, Seivewright, Ferguson et al., 1990). This is, in itself, an important finding, as
subsequent studies have often challenged the now fully accepted view that personality
disorder has no influence on the outcome of depression. The doubters and the believers
have been reconciled in a definitive paper by Newton-Howes et al., (2014). The key issue is
the length of follow-up.
Although the randomised trial finished after 10 weeks, if the patients had made
progress and wished to continue in the same mode of treatment they were prescribed
antidepressants in the three drug groups, encouraged to stay with psychological treat-
ments in the CBT group, and with self-help and other similar supports in the self-help
group. This was not in any way forced, but as the greatest improvement in the whole 30
years was found in the first 10 weeks, it was not surprising that many followed the
suggested procedure.
4.7 Placebo Response

Much of the reaction to the Lancet publication was related to the placebo response. The
nature of the positive elements of the placebo response had not been fully appreciated in
1988, and the hard-nosed reaction was that the trial must be valueless if other treatments
were not shown to be superior. But the setting of the trial was very much in keeping with
practice at that time. A treatment was prescribed, progress assessed after a few weeks, and if
improvement was achieved the treatment was withdrawn. With this design, placebo effects
may be more marked.
We now know that much of the improvement in mental symptomatology can be
explained by the placebo response. The 30 per cent improvement in symptoms shown
in most groups in the trial illustrates a common law of mental health – taking part in
a randomised trial is good for you, no matter to what treatment you are allocated.

4.8 Conclusions about the General Neurotic Syndrome after

the 10-Week Trial
The general neurotic syndrome in the Lancet was the disguised elephant in the room. He
was there, if you were clever enough to look for him, but he had already set down a marker if
you noticed him or not. Mixed anxiety-depression (cothymia) was a highly important
diagnosis that would not be going away in a hurry.

Chapter
The Medium-Term Outcome
5 of the General Neurotic Syndrome
The main hypothesis of the Nottingham Study was that the general neurotic syndrome
would have a more complex and likely poorer outcome in the long-term, so follow-up data
were critical in evaluating this. Assessments were made of the main outcome measures at 16,
32, 52 (one year) and 104 weeks (two years) after randomisation. At five years, assessment
was only made through examination of the patients’ GP and hospital notes.
5.1 Outcome in the Shorter Term

The results of the clinical outcomes are shown in Table 5.1 and Figure 5.1. Whereas those
without the GNS improved by over 50 per cent in the year after randomisation, those with
the definite syndrome improved by only 25 per cent in the same period, and similar
differences were shown at five years. The regression analysis showed the significant differ-
ence evident as early as 10 weeks in those with the GNS was not found with other variables,
including personality status (Table 5.1) (Tyrer, Seivewright, Ferguson et al., 1990).
Although the treatments in the study were similar after 10 weeks (apart from diazepam),
a subsequent analysis of the CBT therapists in the trial showed that the patients treated by
the therapists who were judged to be highly competent by the main supervisor (David
Kingdon), had significantly better outcomes at two years than the others (Kingdon et al.,
1996). At two years, the patients who had improved most were those treated by these
competent therapists.
Table 5.1 Summary of regression analysis on outcome in first two years of Nottingham Study
Variable 10 weeks 16 weeks 32 weeks 52 weeks 2 years
N 180 180 178 179 173

Initial CPRS score 0.30 (P < 0.01) 0.36 (P < 0.001) 0.21 (P < 0.04) 0.23 (P < 0.03) 0.38 (P < 0.005)
General neurotic 0.18 (P < 0.02) 0.27 (P < 0.0005) 0.20 (P < 0.004) 0.16 (P < 0.03) 0.17 (P < 0.02)
syndrome (Y/N)
Personality disorder 0.05 (NS) 0.04 (NS) 0.07 (NS) 0.00 (NS) 0.14 (P = 0.05)
(Y/N)
Initial observed 0.09 (NS) −0.02 (NS) 0.21 (NS) 0.26 (P < 0.025) 0.01 (NS)
anxiety (BAS)
The full analysis can be found in Table 7 of Tyrer et al. (1992).
44

The Medium-Term Outcome of the GNS 45
40
30
Mean
CPRS 20
score
10
0 10 16 32 52 104
Time (weeks)
GNS – GNS +
Figure 5.1 Mean changes in total psychopathology scores (CPRS) for patients with the general neurotic syndrome
(GNS+) (n = 66) and those without (GNS–) (n = 115). The GNS positive cases represent scores of ≥ 6 on the GNS scale
5.2 Five-Year Outcome

The 5-year assessment was made, after ethical approval, by examination of medical records
by the same investigator who carried out the 12-year assessments, my wife, Helen. (I should
here stress that Helen is a stickler for accurate recording and independent working, and
made absolutely sure that she knew nothing about the baseline status of the patient when she
made her assessments.)
Exactly five years after original referral, she contacted the relevant mental health units
and general practice surgeries and, if permission was given, visited to record the details of all
treatments received. After all data had been collected on each patient, she made a judgement
of overall outcome using a standardised scale (Global Outcome Scale), as will be discussed.
The same data were recorded at 5 years and again at 12 years, including the numbers of
contacts with all health professionals for psychiatric disorder over the period, the contacts
with the general practitioner for non-psychiatric conditions (as best as could be done from
the content of the notes), the number and length of psychiatric admissions and day-hospital
attendance, all psychotropic drugs treatment received and the total time the patient was not
taking psychotropic drugs during the 5 years (after completing the original trial). Private
medical consultations were not recorded but in the Nottingham area these constituted
a small proportion of total contacts.
To ensure that the Global Outcome Scale was being consistently and reliably
assessed, 10 sets of records were evaluated independently by PT. All were scored
similarly.
The results were very similar to other studies of this group of common disorder – about
one third do very well, another third improve a little, and the final third remain unwell. This
was first reported in an early study by Hans Eysenck (1952).
It was appreciated that examination of records alone was not a substitute for direct
contact with the patient, and that the outcomes recorded were primarily those of
service receipt. Nevertheless, the results of the later assessments, when both global

46 Neurosis
Table 5.2 Global outcome in 182 patients after five years
Outcome category Description of outcome Number (%)
1. Very good No psychiatric contact with 50 (27)

either general practice or psychiatric
services since initial period of care (up
to nine months)
2. Good Some contact for psychiatric 57 (31)
problems in general practice or
psychiatric clinics but at least half time
well
3. Fair Frequent contact with services for 38 (21)
psychiatric problems for more than half
of time of follow-up, but intensity of
care not great (e.g., short period of daycare,
many outpatient contacts but no
inpatient care)
4. Poor Little or no time in follow-up 28 (15)
period well. Intermittent contact as
outpatient or day-patient
5. Very poor Continuously ill with frequent 9 (5)
contact with all parts of psychiatric
services or death from deliberate self-harm
outcome and clinical ratings were recorded, showed a surprising level of agreement
between them. We also examined the data at two years and again the service outcome
at that time correlated well with the clinical outcome recorded by rating scales (Tyrer
et al., 1993).
5.3 Analysis of Data

In this part of the study, we were especially looking at the success of the baseline data
in predicting the outcome at five years. The method chosen by our excellent statisti-
cian, Tony Johnson of the MRC Biostatistics Unit in Cambridge, was polychotomous
stepwise logistic regression. This allows the creation of different models to examine
data that are not binary ones, so many ordered outcomes can also be included. Thus
we were able to examine all the baseline variables; age, sex, marital status (married,
single, separated or divorced or widowed), social class, randomised treatment group
(drug, psychological treatment, and self-help), original DSM-III diagnosis (dysthymic,
generalised anxiety, and panic disorder), duration of symptoms, categorisation of
original episode as new or recurrence, precipitating factors into four groups (none,
loss, conflict, and addition events), personality disorder classified by type and severity
using the PAS classification, and the presence or absence of the general neurotic
syndrome (GNS).

5.4 Results
The results of the regression analysis showed two major findings; (i) older age and the
identification of a recurrent disorder at baseline led to an odds ratio of 4.20 for a poor
outcome, and (ii) the combination of a personality disorder and the GNS had a similar odds
ratio of 3.28 for a poor outcome. An interesting subsidiary finding was that higher scores on
the main clinical outcome at 10 weeks, the Comprehensive Psychopathological Rating Scale
(CPRS) also predicted a poor outcome (odds ratio 2.88) (Seivewright et al., 1998).
It is worth reflecting on these findings. They show that a good global outcome was
achieved in those who had a new episode of anxiety or depression, who were young, and
who improved greatly in the original randomised controlled trial (when they may have
received a placebo). This is exactly what you would expect in the sometimes misunderstood
diagnosis, adjustment disorder, defined as ‘a condition that arises in response to a stressful
event or situation’, and ‘which resolves spontaneously when the stressor is removed or when
a new level of adaptation is reached’ (Casey, 2018, p. 2).
But all the patients in the Nottingham Study had a formal DSM-III diagnosis of panic
or dysthymic or generalised anxiety disorder, which are above adjustment disorder in
a hierarchical system of classification. The conclusion must be that at least a proportion
of the patients seen would have been best classified as adjustment disorders rather than
the more serious conditions. As one might have expected, those with the general neurotic
syndrome were more likely to have had recurrent episodes and so fit in with the other
data.
5.5 Contacts with services in first five years in GNS patients

and those with personality disorder
The service contacts of patients with scores of four or more on the GNS scale are shown in
Table 5.3, and those separated by initial ICD-11 personality disorder in Table 5.4. Those
with possible or definite syndrome had significantly more GP and outpatient appointments
than those without the syndrome and also had longer periods of day care and more contacts
with community nurses. The only significant difference in the other group was a higher level
of contact with social workers in those with personality disorders, although the trends were
generally similar in both GNS and personality disordered patients.
5.6 Diagnosis at Baseline and Service Outcomes

Cothymia was also examined in the five-year data and, as this was postulated to be central to
the GNS, the service data for this group were needed (Table 5.5).
The results gave some support to the expectation that cothymia would lead to more
service contacts but they were not striking (Table 5.5). Appointments for non-psychiatric
illness in primary care and non-psychiatric admissions were more frequent in cothymic and
dysthymic patients. There were also more psychiatric admissions and contact with social
workers.
5.7 Summary of Findings at Five Years

We concluded at the time we published most of these findings that the pithy description of
Surtees and Barkley (1994) that the outcome in these disorders was ‘future imperfect’ was an

Table 5.3 Service outcomes separated by general neurotic syndrome (GNS) status five years after randomisation
Follow-up time point GNS <4 GNS 4–5 GNS ≥6 Pa difference P (linearity)
Service contacts
0–5 years
N: Mean ± SD N: Mean ± SD N: Mean ± SD
No. of GP/OP appts for psych illness 94: 14.0 ± 15.6 30: 18.9 ± 18.0 65: 18.3 ± 16.6 0.031 0.011
No. of GP/OP appts for non-psych 94: 22.6 ± 18.2 30: 21.9 ± 20.5 65: 26.7 ± 17.8 0.165 0.111
illness
Length of day care (weeks) 94: 1.34 ± 5.8 30: 5.17 ± 15.0 65: 5.1 ± 12.4 0.009 0.002
Weeks of non-psych hospitalization 94: 0.54 ± 0.96 30: 0.63 ± 1.0 65: 0.71 ± 1.3 0.585 0.302
Weeks of psych hospitalization 94: 0.29 ± 1.4 30: 0.27 ± 1.0 65: 0.17 ± 0.82 0.818 0.541
No. of admission 94: 0.65 ± 1.1 30: 0.90 ± 1.4 65: 0.92 ± 1.3 0.326 0.155
Months free from psychotropic 99: 47.0 ± 18.9 31: 46.5 ± 19.5 70: 39.8 ± 21.3 0.194 0.083
medication
N (%) N (%) N(%)
Contact self-help groups
No 89 (94.7) 27 (90.0) 62 (95.4) 0.579 0.915

Yes 5 (5.3) 3 (10.0) 3 (4.6)
Contact social workers
No 84 (89.4) 25 (83.3) 52 (80.0) 0.225 0.099
Yes 10 (10.6) 5 (16.7) 13 (20.0)
Contact community
psychiatric nurses
No 43 (45.7) 7 (23.3) 17 (26.2) 0.014 0.008
Yes 51 (54.3) 23 (76.7) 48 (73.8)
Contact psychologists
No 89 (94.7) 29 (96.7) 61 (93.8) 1.000 0.848
Yes 5 (5.3) 1 (3.3) 4 (6.2)
a
Exact test
Table 5.4 Service outcomes separated by baseline personality disorder
No PD PD Pa
0–5 years
N: Mean ± SD N: Mean ± SD
No. of GP/OP appts for psych illness 118: 14.7 ± 13.6 66: 19.5 ± 20.4 0.173
No. of GP/OP appts for non-psych illness 118: 24.4 ± 19.5 66: 20.0 ± 16.5 0.991
Length of day care (weeks) 118: 3.36 ± 10.7 66: 3.30 ± 10.2 0.383
Weeks of non-psych hospitalization 118: 0.39 ± 1.1 66: 0.53 ± 1.1 0.778
Weeks of psych hospitalization 118: 0.62 ± 1.1 66: 0.58 ± 0.9 0.651
No. of admission 118: 0.75 ± 1.2 66: 0.82 ± 1.2 0.699
Months free from psychotropic medication 126: 44.8 ± 20.2 69: 42.6 ± 20.2 0.785
N (%) N (%)
No 109 (92.4) 64 (97.0) 0.176
Yes 9 (7.6) 2 (3.0)
No 109 (91.5) 50 (75.8) 0.007
Yes 10 (8.5) 16 (24.2)
Contact community
psychiatric nurses
No 40 (33.9) 25 (37.9) 0.631
Yes 78 (66.1) 41 (62.1)
Contact psychologists
No 115 (97.5) 60 (90.9) 0.072
Yes 3 (2.5) 6 (9.1)
a
Exact test
accurate one. Forty per cent were still adversely affected through persistent or recurring
symptoms. The evidence that older patients presenting with neurotic symptoms had a worse
outcome was also consistent with data from Surtees and Barkley’s study.
The finding that personality status, linked to the general neurotic syndrome, was an
important clinical indicator of longer term outcome was consistent with other evidence
(Duggan, Lee & Murray, 1990; Quinton, Gulliver & Rutter, 1995).
The evidence that the general neurotic syndrome linked to a personality disorder
diagnosis was a better predictor than personality disorder alone suggests the identification
of dependent and obsessional features of personality abnormality (the anxious-fearful
cluster C in the DSM classification) and the presence of cothymia and family history of
a similar disorder all contribute to poor prognosis.
It was interesting to note that many of the other possible predictors of outcome were
negative. The negative predictors are at least as informative as the positive ones. In
particular, the initial diagnostic group contributed little of importance to the prediction

Table 5.5 Service outcomes separated by DSM-III diagnosis after adjustment for cothymia
Dys GAD Panic Cothymia Pa

(difference)
0–5 years
N: Mean ± SD N: Mean ± SD N: Mean ± SD N: Mean ± SD
No. of GP/OP appts for psych illness 8: 11.4 ± 12.4 68: 15.4 ± 17.4 57: 17.8 ± 15.8 61: 15.6 ± 16.1 0.214
No. of GP/OP appts for non-psych illness 8: 16.4 ± 11.7 68: 24.2 ± 19.5 57: 20.9 ± 17.9 61: 27.9 ± 19.0 0.108
Length of day care (weeks) 8: 0 ± 0 68: 2.44 ± 7.7 57: 4.25 ± 11.5 61: 3.39 ± 12.0 0.460
Weeks of non-psych hospitalization 8: 0.38 ± 0.5 68: 0.84 ± 1.3 57: 0.35 ± 1.0 61: 0.70 ± 1.1 0.048
Weeks of psych hospitalization 8: 0.25 ± 0.7 68: 0.34 ± 1.6 57: 0.12 ± 0.7 61: 0.23 ± 0.9 0.783
No. of psychiatric admissions 8: 0.63 ± 1.1 68: 0.87 ± 1.3 57: 0.44 ± 0.7 61: 1.03 ± 1.4 0.054
Months free of psychotropic 8: 51.1 ± 19.5 69: 43.8 ± 21.1 59: 43.3 ± 19.0 68: 45.1 ± 20.7 0.832
medication
N (%) N (%) N (%) N (%)
No 8 (100.0) 65 (95.6) 52 (91.2) 58 (95.1) 0.744
Yes 0 (0.0) 3 (4.4) 5 (8.8) 3 (4.9)

No 5 (62.5) 59 (86.8) 53 (93.0) 48 (78.7) 0.037
Yes 3 (37.5) 9 (13.2) 4 (7.0) 13 (21.3)
Contact community
psychiatric nurses
No 4 (50.0) 27 (39.7) 16 (28.1) 21 (34.4) 0.436
Yes 4 (50.0) 41 (60.3) 41 (71.9) 40 (65.6)
Contact with psychologists
No 7 (87.5) 63 (92.6) 56 (98.2) 58 (95.1) 0.286
Yes 1 (12.5) 5 (7.4) 1 (1.8) 3 (4.9)
a
Exact test
of outcome, with only a little added by cothymia. Only 40 of the patients had no precipitat-
ing events but this did not lead to a better outcome as might have been expected. The
duration of symptoms was also not predictive as might have been expected.
After only five years, it was too early to predict the course of the general neurotic
syndrome but these early data suggested that people with this core neurotic condition:
(i) were high users of primary care services,
(ii) were high users of psychiatric care,
(iii) could be identified better by their core symptoms and personality than by duration and
initial manifestation,
(iv) had a fluctuating course.
The evidence that the general neurotic syndrome conferred a better prediction of service
outcome than personality disorder diagnosis alone was not entirely unexpected. The elements
of personality dysfunction in the GNS – dependence, anxiousness, and obsessionality – are
ones that have subsequently been shown to be related to treatment seeking (Tyrer, Mitchard
et al., 2003), whereas the others are associated with treatment resistance or indifference.
Overall, the results at five years allowed the following tentative comments to be made on
the basis of global outcome and service contacts:
(1) DSM-III diagnosis does not predict outcome.
(2) Personality disorder does predict outcome but the strength of this is reinforced by
including the general neurotic syndrome.
(3) Initial improvement in symptoms is associated with a good outcome and suggests a re-
diagnosis of adjustment disorder.
(4) Those with the general neurotic syndrome are the highest users of general practice and
secondary psychiatric care services.

Chapter
The General Neurotic Syndrome
6 at 12 Years
The patients in the Nottingham Study after 12 years had not been assessed in person since
the two-year outcome. In planning the assessments at 12 years, additional information was
felt to be needed to reinforce the collection of previous data (Table 6.1).
Table 6.1 Measures included in the 12-year follow-up of the Nottingham Study
Data collected at 2 years Data collected at 12 Reasons for 12-year data

years inclusion
Personality Personality To check on stability of personality

assessment (PAS) assessment (PAS) disorder*
Comprehensive Main rating outcome Main rating outcome measure
Psychopathological Rating measure
Scale (CPRS)
Montgomery and Åsberg Important secondary Important secondary outcome
Depression Rating Scale outcome
(MADRS)
Brief Scale for Anxiety (BAS) Important secondary Important secondary outcome
outcome
Hospital Anxiety and Important secondary Important secondary outcome
Depression Scale (HADS-A outcome
and HADS-D)
DSM-III diagnosis Not specifically Simple dichotomous outcome
recorded (Richard Doll choice)
GP contacts Important service Important service outcome
outcome
Out-patient psychiatric Important service Important service outcome
contacts outcome
Non-psychiatric GP contacts Important service Important service outcome
outcome
Hospital admissions Important service Important service outcome
outcome
Suicide attempts and deaths Key clinical outcome Key clinical outcome
52

The GNS at 12 Years 53
Table 6.1 (cont.)
Data collected at 2 years Data collected at 12 Reasons for 12-year data

years inclusion
Psychological services Important service Important service outcome
outcome
Social function Not recorded New: Recognition that social
function is a key measure in
neurotic disorder
Global outcome scale Recorded at 5 years Also recorded at 12 years
(important service
outcome)
Neurotic disorder outcome Not recorded New: A clinical outcome measure
scale (NDOS)
Costs of care Not recorded New: Important for public health
*Personality change over the 30 years is not reported here but the results showed personality disorder as
a diagnosis was very unstable over time (Yang, Tyrer, Johnson & Tyrer, (2022).
The three additional measures recorded at 12 years were social function, the Neurotic
Disorder Outcome Scale, and a full analysis of costs (Table 6.1). Social function was the most
significant of these. We included it as at the time there was accumulating evidence that many
of the negative consequences of mental illness are tied up with poor social function (Casey
et al., 1985; Casey & Tyrer, 1986; Fredman et al., 1988). There are many good measures of
social function but most of these are quite long. In the end we chose the Social Functioning
Questionnaire (SFQ)(Tyrer et al., 2005).
This could be considered a lazy choice as I was the main author. It may have been, but
after considerable discussion over a previous schedule that I had developed with Marina
Remington in Southampton (Remington & Tyrer, 1979) (also discussed in some detail with
Steve Platt, an international expert on the subject), it was felt to be an appropriate measure
as it covered all the essential elements of social function. It was also very short and, as the 12-
year follow-up was a long interview, particularly because much of the time was taken up
with personality assessment, brevity was a boon. Since the late 1990s, the Work and Social
Adjustment Scale (Mundt et al., 2002) has become the most widely used short instrument
and this only has five items. Nevertheless, detailed study of the Social Functioning
Questionnaire (SFQ) suggests that it, and a shorter form of only five questions, is a very
good initial screen for personality disorder (Tyrer, Yang et al., 2021). In itself this is very
interesting as it appears that, despite social functioning being influenced by many factors,
personality appears to be the major one.
6.1 Cold-Calling
This section of the chapter could be regarded as an aside. It is only concerned with the
acquisition of data in follow-up studies, but it is of interest to any investigators involved in
any follow-up work. It is now commonplace to ask for written consent when carrying out

54 Neurosis
research studies. This cannot be done in advance even though it would be desirable in
follow-up studies. If a patient agrees to have an interview two years after signing a consent
form when the time comes for the interview no consent form will be valid and a new one
has to be obtained. So, although in the Nottingham Study patients were usually informed
about the date of the next assessment and agreed or did not agree to be seen again, it
challenged the memory much more when the interval between the face-to-face interviews
was 10 years after the last one. The other problem frequently found in long-term follow-up
studies is a change of patient’s address. The standard way of approaching a patient is to
send a letter to the last known address (it may have changed greatly in 10 years, let alone
since the 1990s). This gives the opportunity for the patient to agree to a follow-up
interview or refuse if preferred.
There are several problems with this from the researcher’s point of view. The patient
may not receive the letter because they have moved address, they may receive it and have no
idea what it is all about and toss it in the bin, or they put it aside and do not reply (even
though a stamped addressed envelope was added to the letter). None of these actions
constitutes refusal to be seen. Although a second letter was sent if there was no reply to
the first, exactly the same responses may be shown.
This is where the vexed issue of cold-calling comes in. What should happen if there is no
response of any sort to the standard approaches? This is the procedure we used eventually –
exact wording – after discussion with the Nottingham Ethics Committee:
(a) Standard letter written to last known address inviting a follow-up appointment. If the
patient chose refusal of contact in their response no further action was taken;
(b) If the patient replied positively within four weeks a follow-up appointment was made;
(c) If no reply or patient thought to have moved the Family Health Service Authority
(FHSA) was contacted to determine any change of address;
(d) If no reply, and original address thought to be correct, a second copy of the standard
letter was sent with a hand-written letter explaining the project again;
(e) Similar approaches made to new addresses of patient if thought to have moved;
(f) If no response made the patient was either telephoned or called upon without prior
appointment to see if patient still living at address and to introduce project. If the
patient agreed the follow-up interview took place at this time, and if the patient
refused, no further action was taken.
Phase (f) of this procedure is cold-calling, and was only used when no other contact had
been established with the patient and all letters (which included stamped addressed enve-
lopes on every occasion) had failed to be returned. (Tyrer, Seivewright, Ferguson et al., 2003,
p. 239).
If we had relied on standard guidance in the 12-year follow-up, the study could well have
foundered at that point. In Table 6.2, the results of cold-calling are shown. Of all the patients
seen, 45.6 per cent were cold-called; our results would have been severely compromised if we
had only had a follow-up rate of 54.4 per cent, the completion rate that would have been
achieved without cold-calling. Those who needed cold-calling were very similar to those
who were seen using normal procedures. Only social class (classes 1 and 2 were responsive
to letters) showed any differences (Table 6.2).
Since the 12-year follow-up, the views about cold-calling have become more liberal. The
success of a public health research project, that all would normally support, can be
compromised by restrictions imposed by well-meaning barriers protecting the absolute

Table 6.2 Comparison between initial and cold-call responders for selected initial variables
Baseline variables Initial Cold call Summary Statistic and P-value**

responders responders statistics (95%CL)*
(n = 100) (n = 84) (%)
Gender: Male 29 30 (36) 1.0 χ2 = 0.9, P = 0.33

Female 71 54 (64) 1.36 (0.73, 2.53)
Personality disorder
Present 35 29 (35) 1.0 χ2 = 0.0, P = 0.97
Absent 62 52 (62) 0.99 (0.53, 1.87)
NK 3 3 (4)
Social class
1 6 1 (1)
} 1.0
2 13 5 (6)
3 20 20 (24) 0.32 (0.10, 0.96) Ns
4 34 33 (39) 0.33 (0.11, 0.92) (except for social class 1&2 vs rest)
5 27 25 (30) 0.34 (0.11, 0.99) X2 = 4.5 (after Yates correction), P<0.035

Marital status
Married 42 32 (38) 1.0 χ2 = 1.3, P = 0.52
Separated/divorced/widowed 29 21 (25) 1.05 (0.51, 2.18)
Single 29 31 (37) 0.71 (0.36, 1.42)
Initial treatment
Drug 45 28 (33) 1.0 χ2 = 3.8, P = 0.15
CBT 34 40 (48) 0.53 (0.27, 1.02)
Self–help 21 16 (19) 0.82 (0.36, 1.83)
Table 6.2 (cont.)
Baseline variables Initial Cold call Summary Statistic and P-value**

responders responders statistics (95%CL)*
(n = 100) (n = 84) (%)
Initial diagnosis
GAD 36 27 (32) 1.0 χ2 = 2.0, P = 0.37
Dysthymia 25 29 (35) 0.65 (0.31, 1.35)
Panic 39 28 (33) 1.04 (0.52, 2.11)
Age at entry
<20 5 4 (5)
20–29 28 26 (31)
30–39 30 29 (35)

40–49 25 15 (18)
50–59 8 7 (8)
60+ 4 3 (4) 1.26 (−2.11, 4.63) t180 = 0.74, P = 0.46
Mean 35.9 34.6
*Odds ratios or differences between means, reference categories indicated with OR = 1.0.
**chi-squared for binary and categorical variables, chi-squared for trend for original variables; t-test or Mann-Whitney test for continuous variables
Reproduced from Tyrer, Seivewright, Ferguson et al., (2003) with the permission of BMJ Publishing Group.
right of patients to refuse. All well and good, but if the initial consent form contained words
such as ‘this study involves long-term follow-up for the following reasons (these are then
specified). The success of the study will depend on your agreement to be seen in the future.
This will always be done at a time to suit you. Please let me know, at least in principle, if you
are prepared to support this arrangement.’ This would at least set the markers in advance.
And of course, circumstances can change. One of the patients seen at 30 years told me on the
doorstep: ‘I am sorry. I am dying of cancer and do not feel I can properly answer your
questions; I do not think they would help you very much.’ We commiserated by his door and
reflected on the awfulness of fate and the lottery of life, and then I went on my way. He died
five weeks later. Of course, he was right to refuse and his data would not have been helpful,
but at least we had some human contact.
The current attitude to cold-calling may be reflected in a quotation from a recent review
of the subject:
although the restriction of cold calling aims to promote patient privacy, given the
complexity and collaborative nature of medicine, the individual provider may not have
sufficient information or resources to facilitate recruitment decisions. We call for
institutions to abandon strict cold call policies, and adopt recruitment strategies that
balance patient choice, privacy, and research success. (McHugh, Swamy & Hernandez,
2018, p. 390)
I think the key word here is ‘balance’.
6.2 Costs
These are discussed here at the only time in this book, as it was only at 12 years that we had
a comprehensive assessment of the costs of the study carried out by Gerhard Knerer as part
of a Medical Research Council Collaborative Group investigating complex interventions.
We have always lived in times of rationing when it comes to health services. There are
always more demands on resources than we can possibly fill. But we should always remem-
ber that providing these resources is like filling a watering can with a small leak in the
bottom; some resources are wasted and will never be recovered.
In examining the justification for the use of the general neurotic syndrome, the total cost
over the 12 year period was the preferred statistic.
The results of the cost analyses show some important findings, some of which are
counter-intuitive, and in interpreting these it must be remembered that costs tend to scatter
over a wide range and only large differences are found to be significant.
The findings that showed important differences in costs can be summarised as (i) those
with dysthymia (original diagnosis) or cothymia (adjusted diagnosis) incur greater costs
than others, (ii) patients presenting with a recurrent disorder also create greater costs than
those presenting for the first time, and (iii) those with the general neurotic syndrome incur
costs more than 50 per cent greater than those without the syndrome.
Perhaps, equally importantly, the severity of symptoms (as measured by scores on each
of the scales) does not have an impact on costs, or personality disorder and disturbance.
This, although showing the linear tendency for costs to increase with each increment of
severity, also does not account for much of the cost differences. In this respect, the clinical
outcomes, which are related strongly to initial symptom severity (see Table 6.5), differ from
the cost findings.

58 Neurosis
The results in Table 6.3 show univariate analyses but because many of the variables
cross-correlate it is necessary to carry out multivariate analyses also. These are not
shown here but the results of the multivariate model showed that three factors – the
general neurotic syndrome, initial diagnosis (and cothymia), and the presence of
Table 6.3 Univariate predictors of 12-year costs ($) *The GNS threshold score was set at 4 in this analysis
Variable n Total cost ($) Standard Significance

per patient deviation of differences
(SD)
Randomised treatment
Drug therapy 84 11,517 12,112
CBT 84 12,669 20,529 0.854 (ns)
Self-help 42 11,308 8,736
Gender
Male 65 11,013 12,480 0.565 (ns)
Female 145 12,350 16,732
Age on entry
<30 years 70 10,452 13,459
30–44 years 91 12,104 18,542 0.103 (ns)
45 years or older 49 13,742 11,729
Social class
1&2 28 8,196 7,412
3 45 14,295 24,418 0.439 (ns)
4 77 10,999 9,976
5 60 13,115 15,561
Marital status
Married or cohabiting 83 11,888 18,596
Divorced, separated, 56 12,823 13,038 0.860 (ns)
widowed
Single 71 11,293 13,406
Diagnosis on entry
Dysthymia 65 15,747 23,110
Generalised anxiety disorder 71 11,446 11,473 P = 0.037
Panic disorder 74 9,059 8,594
Type of episode
New 142 9,368 9,250 P<0.001
Recurrent 68 17,298 22,988
General neurotic syndrome*
Absent 106 9,260 9,987 P = 0.011
Present 104 14,663 19,298

Table 6.3 (cont.)
Variable n Total cost ($) Standard Significance

per patient deviation of differences
(SD)
CPRS score on entry

0–16 52 9,895 10,301
17–21 59 10,875 13,275 P = 0.56
22–28 50 14,408 23,239
29 49 12,857 12,614
MADRS score on entry
0–15 61 9,919 9,730
16–19 49 14,758 24,492 P = 0.61
20–25 49 11,835 13,389
26 51 11,734 11,527
BAS score on entry
0–15 55 12,192 12,871
16–19 55 10,746 14,232 P = 0.62
20–25 53 11,612 11,019
26 47 13,395 22,831
HADS-D on entry
0–8 75 10,207 6,136
9–12 64 15,172 14,101 P = 0.365
13–15 46 10,018 4,435
16–22 25 12,368 11,171
HADS-A on entry
0–8 25 10,488 8,248
9–12 43 10,630 11,297 P = 0.354
13–15 66 11,661 11,922
16–22 76 13,389 21,492
Personality status on entry
No personality dysfunction 88 10,537 12,492
Personality difficulty 52 11,758 11,573 P = 0.20
Simple personality disorder 50 13,829 23,479
Complex personality 20 13,824 9,982
disorder
Adjusted diagnosis
Dysthymia 7 12,300 8,200
GAD 68 11,077 10,453 P = 0.03
Panic disorder 64 9,260 9,668
Cothymia 71 15,135 22,524
Reproduced from Knerer et al., (2005) with permission from John Wiley & Sons.

60 Neurosis
a recurrent disorder – were the three elements contributing most to costs at 12 years
(Knerer et al., 2005). Similarly, patients with general neurotic syndrome were more
likely to use specialist mental health services than patients without the syndrome.
6.3 Main Outcome Findings at 12 Years

At 12 years, an interim point in the follow-up study, we wished to examine the progress of
each patient in the 10-year interval since their last face-to-face contact. As the primary
outcome for this occasion, we chose the Neurotic Disorder Outcome Scale (NDOS)
(Table 6.4), as this was deliberately created to cover all mental pathology over this time
period.
The main results in Table 6.5 showed little difference in the demographic variables and
treatment groups – but with higher scores (i.e., worse outcomes) for patients with cothymia
(P = 0.011); for those who scored high on global psychopathology, anxiety, and depression
scales at baseline; and in those with personality disturbance (P < 0.001) – with increasing
NDOS scores with higher levels of severity (Figure 6.1).
Personality disorder contributed most to the final model of the outcome analysis created
by Tony Johnson at the MRC Biostatistics Unit in Cambridge (Table 6.6). It was of interest
that in this analysis the differences in scores on the observer-rated depression scale
(MADRS) did not quite reach significance whereas the HADS-D was the strongest
predictor.
Table 6.4 Neurotic Disorder Outcome Scale [NDOS]
1 More than one year with any of the following disorders: GAD, DYS, MDE, Ag, PAG,
Ob, SOP
2 Developed alcohol dependence syndrome (DSM or ICD criteria)
3 Developed organic brain disorder (ICD F04-06) or DSM amnestic disorder (294) but
excluding dementia
4 Follow-up SFQ score of 10 or greater
5 Subsequent disorder within the schizophrenia group (including delusional
disorder) (F20-29-ICD-10 and 293, 295, 297, and 298 in DSM-IV)
6 More than 70% of follow-up with diagnosis equivalent to or more serious than
original neurotic diagnosis (i.e., GAD, DYS, PAG, Ag, Ob, MDE, MEL, SOP)
7 Subsequent MDE or agoraphobia (any type) of more than two years’ duration
8 More than four episodes of MDE (including MEL) during follow-up
9 Unnatural death (including accidental death, open verdict, and suicide)
10 Admitted to psychiatric hospital during follow-up
TOTAL
Total score of 0–10 based on score of 1 for each of the 10 items
Key: GAD = generalised anxiety disorder, DYS = dysthymic disorder, MDE = major depressive episode,
Ag = agoraphobia, PAG = agoraphobia with panic, Ob = obsessive-compulsive disorder, SOP = social phobia,
MEL = melancholia

Table 6.5 Relationship between baseline characteristics and outcome as measured by the Neurotic Disorder Outcome Scale (NDOS) over 12 years in 193 patients
Mean NDOS score (SD) with 95% F value Significance (P)

CI for comparisons in brackets
Initial randomised treatment
Drug therapy (n = 77) 1.3 (1.6) 0.2 0.62 (ns)
CBT (n = 77) 2.1 (1.7) (−0.62 to 0.37) 0.8 0.38 (ns)
Self-help (n = 39) 1.9 (1.9) (−0.88 to 0.33)
Marital status
Married/cohabiting n = 80 1.9 (1.7) 2.8 P = 0.095
Single n = 60 2.4 (1.9) (−0.07 to 0.97)
Separated/divorced/widowed n = 53 2.2 (1.6) 0.02 (−0.53 to 0.56)
Revised diagnosis
Dysthymia n = 5 (1.9) 6.5 P = 0.011
GAD n = 64 1.8 (1. 5)
Panic disorder n = 57 1.8 (1. 7)
Mixed anxiety-depression (cothymia) n = 67 2.6 (1.8) 0.65 (0.15 to 1.16)

Total psychopathology (CPRS)
Score 0–16 n = 45 1.9(1.8) 0.057 (0.028 to 0.086) 14.9 P<0.001
17–21 n = 54 1.5 (1.4)
22–28 n = 49 2.5 (1.6)
≥29 n = 45 2.7 (1.9)
Observer-rated anxiety (BAS)
Score 0–15 n = 48 1.9 (1.7) 0.045 (0.011 to 0.079) 6.8 P = 0.011
16–19 n = 50 1.5 (1.5)
20–25 n = 51 2.5 (1.8)
≥ 26+ n = 44 2.7 (1.8)
Table 6.5 (cont.)
Observer-rated depression (MADRS)

Score 0–15 n = 55 1.8 (1.7) 0.028 (0.002 to 0.058) 3.4 P = 0.07
16–19 n = 43 2.1 (1.8)
20–25 n = 47 2.3 (1.6)
≥ 26 n = 48 2.4 (1.8)
Self-rated anxiety (HADS-A)
Score 0–8 n = 21 1.8 (1.8) 0.069 (0.001 to 0.14) 1.8 (1.7) 4.0 P = 0.049
9–12 n = 36 2.2 (1 .7)
13–15 n = 61 2.4 (1.8)
16–22 n = 75
Self-rated depression (HADS-D)
Score 0–8 n = 68 1.5 (1.4) 0.13 (0.07–0.18) 23.1 P < 0.001

9–12 n = 57 2.1 (1.7)
13–15 n = 44 2.6 (1.8)
16–22 n = 24 3.1 (1.8)
Personality status
No pers dys n = 84 1.7 (1.4) 0.50 (0.28 – 0.72) 19.8 P < 0.001
Pers diff n = 39 2.1 (2.0)
Mild p dis n = 50 2.3 (1.7)
Md/sev p dis n = 20 3.7 (1.4)
Table 6.6 Final model showing the elements contributing most to clinical outcome at 12
years
Variable Regression coefficient Cumulative

(95%CL) percentage
of variation
explained
Intercept 0.36 (−0.26, 0.97)

HADS depression 0.11 (0.06, 0.17) 10.8
Personality status 0.42 (0.20, 0.63) 16.9
Single marital 0.52 (0.05, 1.00) 18.9
status
This table shows the final model including the three baseline variables; excluding single marital
status, which produces only minor changes in the other two regression coefficients (and their
95% confidence limits). The model suggests that, on average, a change of one category in
NDOS score results from a change of 9 units on the HADS depression score, and a change of 2.5
‘units’ in personality status.
30
25
Mean CPRS score
20
Initial
15
12 years
10
0
level 0 level 1 level 2 level 3
Figure 6.1 Effect of personality status on global symptomatology (measured by the Comprehensive
Psychopathological Rating Scale (CPRS) at baseline and 12 years)
Personality severity code: level 0 = no personality disorder; level 1 = personality difficulty; level 2 = simple personality
disorder; level 3 = diffuse or complex personality disorder
6.4 Social Function

6.4.1 Analysis of Data
There were two main aims in the analyses of social function. The first was to examine if there
was any relationship between the initial personality ratings and social function at 12 years.
The second was to determine the associations of the other 18 clinical and demographic
variables with social function.

64 Neurosis
6.5 Findings – First Aim

Of the total number of patients, 187 (84 per cent) completed the Social Functioning
Questionnaire (SFQ) at 12 years. The mean SFQ score in those seen was 8.0, with
significantly lower mean scores for those with no personality disorder at baseline
using both the original categorical model (no personality disorder (n = 113) (mean
SFQ 6.8, SD 4.9), compared with those with cluster A (n = 11) (mean SFQ 11.6, SD
4.0), cluster B (n = 29)(mean SFQ 9.0, SD 5.8), and cluster C (n = 24) personality
disorders (mean SFQ 10.4, SD 6.1, (F = 5.9, df 3,173; P < 0.001).
6.6 Findings – Second Aim

At 12 years, the most common ICD-10 personality disorders were avoidant (n = 24),
paranoid (n = 17), dependent (n = 9), and antisocial (n = 8). The results of the first
stage of the univariate regression analysis are shown in Table 6.7. Those with little or
no personality disturbance, of higher social class, those with single diagnoses rather
than cothymia, those ever married, and those with lower levels of anxiety and
depression at baseline, all had better social function at 12 years than others. The 18
variables (Table 6.7) were then included in a multiple linear regression analysis
predicting SFQ scores at 12 years.
The results at 12 years (Table 6.8) generally support the hypothesis that personality
disorder and the general neurotic syndrome are associated with long-term social
dysfunction. This is not a trivial finding. Some look on diagnosis, particularly of
Table 6.7 Relationship between other baseline variables and outcome in terms of social function (SFQ) at 12
years
Baseline N SF Regression F (P ) %
variable score coefficient (95% CL)
[mean
(SD)]
Gender
Male 56 8.8 (4.6)
Female 121 7.6 (5.7) −1.27 (−2.96, 0.43) 2.1 (0.14) 1.2
Age group (years)
<30 59 8.9 (6.0) −0.53 (−1.21, 0.16) 2.3 (0.13) 1.3
30–44 81 7.7 (5.1)
45+ 37 7.1 (4.9)
Social class
1, 2 24 6.3 (4.5) 1.18 (0.39, 1.96) 8.7 (0.007) 4.7
3 38 6.6 (4.5)
4 67 8.2 (5.6)
5 48 9.5 (5.7)

Table 6.7 (cont.)
[mean
(SD)]
Marital status
Single 56 9.9 (5.5)
Married/ 73 6.8 (5.2) 2.91 (1.26, 4.57) 11.9 (<0.001) 6.4
cohabiting
Separated/ 48 7.4 (4.9) −0.80 (−2.58, 0.99) 0.8 (0.38) 0.4
divorced/
widowed
Initial randomised treatment
Drug therapy 71 8.0 (5.2)
CBT 71 8.0 (5.5) 0.15 (−1.47,1.77) 0.0 (0.90) <0.1
Self-help 35 7.7 (5.8) −0.37 (−2.37, 1.62) 0.1 (0.72) <0.1
Initial diagnosis
GAD 60 7.5 (5.1) −0.74 (−2.41, 0.94)
Dysthymia 51 9.8 (5.0) 0.8 (0.39) 0.4
Panic 66 7.0 (5.6) −1.57 (−3.20, 0.06) 3.6 (0.058) 2.0
disorder
Original episode
New 119 7.4 (5.4) 1.55 (−0.12, 3.23) 3.3 (0.069) 1.9
Recurrence 58 9.0 (5.2)
Total psychopathology (CPRS)
0–16 41 7.6 (5.8) 0.18 (0.08, 0.28) 13.1 (<0.001) 7.0
17–21 49 5.6 (4.4)
22–28 45 8.3 (5.2)
29+ 42 10.6
(5.0)
Observer rated depression (MADRS)
0–15 50 6.8 (5.1) 0.15 (0.05, 0.25) 9.2 (0.002) 5.0
16–19 40 6.6 (5.3)
20–25 43 8.4 (5.3)
26+ 44 10.0
(5.4)
Observer rated anxiety (BAS)
0–15 43 7.6 (5.2) 0.11 (0.0+, 0.22) 3.9 (0.049) 2.2
16–19 47 6.4 (4.7)
20–25 46 8.6 (5.9)
26+ 41 9.3 (5.4)

66 Neurosis
Table 6.7 (cont.)
[mean
(SD)]
Initial comorbidity
Dysthymia 4 13.3 2.79 (1.16, 4.42) 11.3 (<0.001) 6.1
(2.9)
GAD 60 7.5 (5.1)
Panic 53 6.0 (4.7)
disorder
Mixed 60 9.8 (5.6)
(cothymia)
General Neurotic Syndrome
Absent 84 6.9 (5.2)
Present 93 8.9 (5.4) 2.02 (0.45, 3.58) 6.4 (0.012) 3.5
Self-rated anxiety (HADS-A)
0–8 18 7.7 (5.6) 0.23 (0.0+, 0.46) 4.0 (0.046) 2.2
9–12 33 6.4 (4.2)
13–15 56 7.3 (4.9)
16–22 70 9.3 (6.0)
Self-rated depression (HADS-D)
0–8 64 5.9 (4.5) 0.48 (0.30, 0.65) 28.7 (<0.001) 14.1
9–12 53 7.4 (5.1)
13–15 39 10.0
(5.4)
16–22 21 11.8
(5.3)
From Seivewright, Tyrer & Johnson, 2004 (with kind permission of John Wiley & Sons).
The table shows the number of subjects in each category n; regression coefficient (95% confidence interval)
from a simple (univariate) linear regression; the associated F-statistic on 1 and 175 df, and its P-value; and the
percentage of variation (%) in Social Function scale score explained by the baseline covariate. The regression
coefficient for age is per decade). Personality coding follows Tyrer and Johnson (1996) with 0 = no
personality disorder, 1 = personality difficulty, 2 = simple personality disorder, 3 = diffuse (complex)
personality disorder.
common mental disorders, as an unnecessary exercise as the essential point of

presentation is to communicate distress. But if distress, as recorded in the form of
social function, is higher in some populations than others then it is useful to diagnose
these separately. The findings also show that although personality functioning may
change, its baseline impact on long-term social function does not, and, together with
the severity of self-rated depression and marital status, it was a key predictor of social
function at 12 years.

Table 6.8 Final model of variables predicting social functioning score at 12 years in 177 patients
Regression coefficient Cumulative percentage of variation

Variable (95% CI) explained
Intercept 0.83 (−1.09,2.74)

HADS 2.90 (1.44, 4.34) 14.1
depression
Single marital 0.81 (0.12, 1.49) 21.1
status
Personality 1.24 (0.58, 1.91) 27.7
status
Social class 0.41 (0.25, 0.58) 29.9
From Seivewright et al., 2004 (with kind permission of John Wiley & Sons).
6.7 Interpretation of Results

Not all the results at 12 years are presented in this chapter and the concentration on social
function and the NDOS scale has limitations, the main one being that it is not an established
scale and therefore is not likely to be used by others. But it was ideal for examining the
outcome of the general neurotic syndrome. The syndrome, if it develops further from its
combined anxiety and depressive components, will extend into other (neurotic) diagnostic
categories such as more severe depression, agoraphobia, social anxiety, and addictive
disorders (see Chapter 1). There are even some who argue that the prolonged stress of
such syndromes can lead to early dementia (evidence not strong so not cited here) and so
organic states are also included in the scale.
The NDOS and economic evidence support the conclusions of the earlier results in the
Nottingham Study and add some more layers to the argument that the general neurotic
syndrome is an important condition. In summary, the 12-year findings show the GNS and
its linked component of personality disorder are associated with:
(i) higher service costs,
(ii) a worse outcome than other diagnoses, and
(iii) poorer social function than other conditions.
The data from the initial trial onwards all point towards the general neurotic syndrome
having all the status of a good diagnosis.

Chapter
The Last Phase
7 The General Neurotic Syndrome

after 30 Years
It is never too late to do a long-term follow-up study. Through long-term follow-up,

a full knowledge of tardive dyskinesia, a condition once thought to be permanent, has
illustrated that this is far from the case (e.g., Cavallaro et al., 1993). However, there is
bound to be a loss of people to contact when you study follow-up at 30 years. The
common word for this is attrition – ‘the gradual reduction in the number of people
who are involved in a study that is achieved by not replacing those who leave’. I have
always found this word to be a somewhat euphemistic one; the usual cause of attrition
is death. In the case of cancer studies, death (mortality) is the primary outcome in
most cases. With the general neurotic syndrome, early death is clearly an important
outcome, but mental health at follow-up is more so. Following the advice of Sir
Richard Doll (see Chapter 3), we decided at this point to choose the dichotomous
outcome of the absence or presence of one of the main DSM diagnoses. The very
minor diagnoses such as simple phobia and adjustment disorders were not included
here. This choice can always be criticised as it is seen to be made at a single point in
time. But this is not exactly true. Most other diagnoses within the neurotic spectrum
have a long duration; they may come and go but they do not disappear entirely. Our
expectation was therefore that if there was no DSM diagnosis present at 30 years then
the patient could be regarded as mentally well.
There were other problems to overcome at 30 years. The Data Protection
Act has made it impossible to carry out studies in the NHS without approval
from NHS Digital, the organisation that holds all the relevant data, but it will
only release the data after you have overcome more hurdles than exist in the Grand
National. This is not a complaint, but it does lead to a tremendous amount of delay.
We also recognised that cold-calling would be essential at 30 years if patients do
not respond to the initial letters sent to their putative addresses. Fortunately, with
the assistance of colleagues at the Northampton Research Ethics Committee,
we were able to have cold calling approved using the same approach as we did at
12 years.
7.1 Procedure Used in 30-Year Follow-Up

Exactly the same procedure was used at 30 years as at 12 years, but with an additional
measure of personality, that of personality strengths (rarely recorded in personality
disorder research). The measure was a new one that examined each of the 24 variables
in the Personality Assessment Schedule from a different angle.
68

The Last Phase: The GNS after 30 Years 69
So, for example, the opposite of worthlessness in the Personality Assessment

Schedule-Strengths Version (PAS-SV) is self-confidence. Here are two questions
from the schedule:
Sometimes belief in your own worth can be of help in overcoming problems in life. Do you
have this belief in your worth?
Some people have such self-confidence that they achieve success in life. Has self-
confidence helped you in any way?
There are several limitations to the PAS-SV. It was created in 1983 at the time of
the start of the Nottingham Study but was never properly tested. It includes several
words that do not yet exist – ‘placatorianess’ is the ability to be placatory but there is
Table 7.1 The 24 components of the Personality Assessment Schedule

(PAS) and the Personality Assessment Schedule-Strengths Version (PAS-SV)
PAS PAS-SV
Pessimism Prudence
Worthlessness Self-confidence
Optimism Certainty
Lability Stability
Anxiousness Stress steadiness
Suspiciousness Openness
Introspection Decisiveness
Shyness Social competence
Aloofness Gregariousness
Sensitivity Ruthlessness
Vulnerability Toughness
Irritability Equanimity
Impulsivity Carefulness
Aggression Placatorianess
Callousness Empathicness
Irresponsibility High responsibility
Childishness Maturity
Resourcelessness Positive drive (resourcefulness)
Dependence Independence
Submissiveness Dominance
Conscientiousness Opportunism
Rigidity Adaptability
Eccentricity Conformity
Hypochondriasis Positive healthiness

70 Neurosis
no equivalent in the English language. The PAS-SV had still not been tested by the
time of follow-up but my wife, Helen, felt it must be included at the 30-year point as it
was a relevant measure – she was right. The PAS-SV also includes one of the important
components of the so-called Big Five, the key five traits underlying personality (Costa
and McCrae, 1992). ‘Openness to experience’ is one of the Big Five but does not appear
in any grouping of personality disorder traits. Why not? Because it is a personality
strength, not a handicap.
It is also quite possible for the same individual to score high on both the PAS and
the PAS-SV, usually at different times, even though they appear to be contradictory.
One of the early patients in the Nottingham Study had a very poor relationship with her
husband and found him ‘utterly boring’. She told me she had tried to kill him by
putting rat poison in his evening meal but he recognised the taste was odd and refused
to eat it. She was annoyed by her failure here and in her discussion with me she
justified her actions along the lines of ‘his life was pretty useless and there was not
much point in him staying alive’. Later on in the study he became ill (for reasons quite
unconnected with his wife’s behaviour) and eventually died. During the time of his last
illness, she was very assiduous in looking after him, being aware of and responding to
all his needs, and seemed to have forgotten entirely about the rat poison episode. So she
could score highly on being both callous and empathic.
The PAS-SV was administered to all the patients seen at 30 years. The results were
subjected to factor analysis, the standard method of determining how these 24
variables group together. Five clear factors emerged (Table 7.2)(Yang, Tyrer, and
Tyrer, 2022). The impact of the PAS-SV ratings is discussed in Section 7.7; it needs
more context.
Table 7.2 Factor analysis of the Personality Assessment Schedule-Strengths Version (PAS-SV)
Factor Variance Key items PAS-SV traits Collective

explained name
%
1 17.0 12, 14, 15, equanimity, placatorianess, Forceful/

16, 17 empathicness, high positive reliable
responsibility, maturity
2 31.5 1, 2, 3, 4, 5, prudence, self-confidence, Tough
18, 19 certainty, stability, stress mindedness
steadiness, positive drive,
independence
3 44.5 6, 8, 9, 21, 22 openness, social Sociability and
competence, gregariousness, personal
opportunism, adaptability independence
4 56.7 7, 11, 13, decisiveness, toughness, Cautiousness
23, 24 carefulness, conformity,
positive healthiness
5 65.9 10, 20 ruthlessness, dominance Focused
discernment

7.2 Results of 30-Year Assessments

Fewer patients were assessed at 30 years. The complete data from baseline onwards are
shown in Figure 7.1.
7.3 Deaths
There were 71 deaths recorded during the 30 years; 36 (34.3% of those with the
general neurotic syndrome) and 35 (34.0% of those without the syndrome). This was
a negligible difference (χ2 = 0.009; df 1, P = 0.92). So, despite all the accumulating
negative data from other parts of the study, there was no evidence of earlier mortality
in this condition.
Personality status showed a trend in favour of earlier death in more severely
personality disordered patients when these were studied by severity status alone, but
those with no personality dysfunction at baseline died earlier (Table 7.3). Analysis of
cause of death showed no particular associations; and when a multivariate linear
regression model was used to estimate effects of the severity of personality disorder
on the lifespan of patients with adjustment for clinical diagnosis at baseline, gender,
and age of patients at the point of randomisation to the study, the findings showed
that earlier death was more associated with initial clinical diagnosis than personality
(Table 7.3) (Tyrer, Tyrer, and Yang, 2021).
Follow-up time Clinical Personality

outcomes status ICD
t=0
N = 210: 200 assessed,
N = 210: 210 assessed
10 missed
t = 1yr
N = 210: 177 assessed, N = 210: 177 assessed,
1 died, 32 missed 1 died, 32 missed
t = 2yrs
44 missed 44 missed, no deaths
t = 12yrs
t = 30yrs
Figure 7.1 Flow chart of missing individuals for outcome assessments by follow-up time point

72 Neurosis
Table 7.3 Distribution of deaths in the Nottingham Study by personality status
PD diagnosis Patients at Death 30 years

baseline later (%)
No personality dysfunction (level 0) 87 38 (43.7)

Personality difficulty (level 1) 40 11 (27.5)
Mild personality disorder (level 2) 50 14 (28.0)
Moderate (level 3) & severe personality 23 8 (34.8)
disorder (level 4)
Missing data at baseline 10
All 210 71 (35.5)
χ = 4.853, df = 3, P = 0.18
2
7.4 Clinical Outcomes

7.4.1 DSM Status at 30 Years
The results of the primary outcome (DSM status) are shown in Table 7.4. These are
important in the context of the general neurotic syndrome as they help to refine my
original hypothesis in Chapter 1: ‘If a person has both anxiety and depressive symptoms
and some personality disturbance the diagnosis of the general neurotic syndrome is the
best way of defining the problem.’ The change is a small one but excludes panic from the
diagnostic framework of the syndrome, provided it is not associated with depressive
symptoms. The data in the original trial suggested panic was just a more severe form of
generalised anxiety (see Figure 4.1) but the data from 12 years onwards show differences
that are far from trivial and suggest that panic disorder has the best outcome of the
anxious depressive group of disorders (provided it is not combined with depressive
symptoms).
7.5 Psychopathology and Influence of the General Neurotic

Syndrome over 12 and 30 Years
The results by diagnosis were consistent with previous findings. Patients with panic had
total psychopathology scores 30% lower than those with cothymia, and those with moder-
ate/severe personality disorder had scores nearly twice as high as those with no personality
disorder (Table 7.5).
The outcome by GNS status is shown in Tables 7.6 and 7.7, and here it is useful to show
the data at both 12 and 30 years. The findings show little change over the 18-year period
between assessments, with only the HADS-D depression self-rating deviating from its mean
ratings at 12 years to show some improvement by 30 years, but the overall differences over
both time periods showed increasing pathology for all measures.
Social function in patients with baseline positive GNS findings was more than 50% worse
than in those without the syndrome (Table 7.7). The NDOS ratings were very similar.

Table 7.4 Formal psychiatric diagnosis (DSM) at long-term follow-up points
Condition at Joint and adjusted

baseline 12th year 30th year estimateb
N DSM+, % Pa N DSM+, % Pa AOR (95% CI) P
GNS status 0.024 0.170

GNS < 6 121 55.4 60 45.0 (Ref) 0.0074
GNS ≥ 6 65 72.3 28 60.7 2.25 (1.24–4.08)
DSM-III 0.609 0.027
GAD 63 57.1 26 57.7 (Ref)
Panic 55 60.0 32 31.3 0.76 (0.40–1.47) 0.422
Cothymia 64 65.6 30 63.3 1.41 (0.74–2.72) 0.299

ICD-11 status 0.027 0.061
No PD 76 56.6 34 34.3 (Ref)
PD difficulty 39 48.7 16 56.3 0.90 (0.45–1.84) 0.784
Mild PD 45 75.6 24 58.3 2.22 (1.10–4.47) 0.026
Moderate & 21 76.2 12 75.0 2.88 (1.10–7.56) 0.031
severe PD
a
Based on Chi-square test.
AOR = Odds ratio of joint outcome for both 12 and 30 years adjusted for age and sex.
74 Neurosis
Table 7.5 Total psychopathology scores (CPRS) at long-term follow-up points
Condition at Joint and

baseline adjusted
12th year 30th year estimateb
a
N Adjusted N Adjusteda Mean difference
Mean (95% CI) Mean (95% CI) (SE): P
Diagnoses
GAD 62 14.63 (11.48–17.78) 26 16.41 (11.49–21.34) (Ref)
Panic 54 13.49 (10.28–16.70) 32 15.48 (10.89–20.07) −1.04 (1.88): 0.578
Cothymia 62 18.77 (15.46–22.08) 29 20.81 (15.97–25.65) 4.20 (1.81): 0.021
Overall P 0.016 0.199 0.011
ICD-11 status
No PD 75 12.40 (9.41–15.39) 35 13.37 (9.02–17.72) (Ref)
PD difficulty 39 13.22 (9.54–16.90) 16 19.31 (13.16–25.46) 1.09 (1.98): 0.571
Mild PD 43 19.23 (15.80–22.66) 24 18.19 (13.14–23.24) 6.59 (1.89): 0.00048
Moderate & 21 17.48 (12.79–22.17) 12 23.55 (16.55–30.55) 5.60 (2.45): 0.022
severe PD
Overall P 0.0024 0.054 0.0018
a
Adjusted for age and sex, and conditional on measures of other time points. b Joint outcome of 12 and 30 years,
adjusted for age and sex and conditional on measures of other time points. Note differences at 30 years need to
be greater than at 12 years to achieve significance.
Table 7.6 Clinical outcome by GNS status at long-term follow-up points and mean CPRS scores
Outcome Joint and adjusted

12th year 30th estimateb
CPRS N Adjusteda N Adjusteda Mean difference

GNS < 6 119 13.35 (10.96–15.74) 59 14.65 (11.23–18.05) (Ref)

GNS ≥ 6 64 19.56 (16.44–22.68) 28 23.14 (18.40–27.88) 6.44 (1.52): 0.000022
P 0.00010 0.0019
HADS-A
GNS < 6 119 7.89 (6.73–9.05) 59 8.11 (6.53–9.69) (Ref)
GNS ≥ 6 63 11.49 (9.97–13.01) 28 10.37 (8.19–12.55) 3.37 (0.70): 0.0000
P 0.0000 0.071
HADS-D
GNS < 6 119 6.27 (5.03–7.51) 59 6.46 (4.91–8.01) (Ref)
GNS ≥ 6 63 8.53 (6.92–10.14) 28 7.83 (5.71–9.95) 2.11 (0.73): 0.0039
P 0.0060 0.249
BAS
GNS < 6 119 9.59 (7.70–11.48) 59 10.13 (7.56–12.70) (Ref)
GNS ≥ 6 64 14.55 (12.09–17.01) 28 14.98 (11.43–18.53) 5.00 (1.15): 0.000014
P 0.000058 0.017

Table 7.6 (cont.)

12th year 30th estimateb
CPRS N Adjusteda N Adjusteda Mean difference

MADRS
GNS < 6 119 11.24 (8.85–13.63) 59 10.72 (7.43–14.01) (Ref)
GNS ≥ 6 64 16.34 (13.21–19.47) 28 16.70 (12.11–21.29) 5.27 (1.42): 0.00020
P 0.0024 0.025
a
Adjusted for age and sex, and conditional on measures of other time points. b Joint outcome of 12 and 30 years,
adjusted for age and sex, and conditional on measures of other time points.
Table 7.7 Social function – measured by the Social Functioning Questionnaire (SFQ) and the Neurotic Disorder
Outcome Scale (NDOS) at long-term follow-up points

variable 12th year unadjusted 30th year unadjusted estimatea
N: Mean (SD) P N: Mean (SD) P Mean difference P

(95% CI)
SFQ 0.006 0.005

GNS < 6 119: 7.01 (5.23) 59: 6.80 (5.31) (Ref)
GNS≥ 6 64: 9.27 (5.38) 28: 10.32 (5.49) 3.04 (1.56–4.52) 0.000
NDOS 0.075 0.045
GNS < 6 119: 1.97 (1.78) 60: 1.42 (2.09) (Ref)
GNS ≥ 6 65: 2.45 (1.71) 28: 2.50 (2.40) 0.64 (0.12–1.16) 0.016
SFQ 0.077 0.033
GAD 63: 7.49 (5.09) 26: 8.15 (6.18) (Ref)
Panic 54: 5.91 (4.70) 32: 5.88 (5.76) −1.84 (−3.55–−0.13) 0.034
Cothymia 62: 9.53 (5.72) 29: 9.93 (5.26) 2.11 (0.44–3.78) 0.014
NDOS 0.056 0.145
GAD 63: 1.89 (1.55) 26: 1.58 (2.14) (Ref)
Panic 54: 1.87 (1.72) 32: 1.22 (2.18) −0.64 (−0.66–0.53) 0.824
Cothymia 63: 2.52 (1.83) 30: 2.30 (2.18) 0.71 (0.13–1.29) 0.016
SFQ 0.000 0.028
No PD 75: 6.27 (4.42) 35: 6.29 (4.59) (Ref)
PD difficulty 39: 7.82 (5.58) 15: 8.87 (6.28) 1.54 (−0.30–3.38) 0.102
Mild PD 43: 9.56 (5.70) 24: 8.17 (5.78) 2.66 (0.90–4.42) 0.031
Moderate & 21: 10.86 (5.51) 12: 11.67 (5.40) 4.51 (2.26–6.75) 0.000
severe PD
NDOS 0.006 0.079
No PD 75: 1.75 (1.46) 35: 1.31 (2.04) (Ref)
PD difficulty 39: 2.03 (2.01) 16: 1.69 (2.27) 0.24 (−0.41–0.88) 0.476
Mild PD 44: 2.61 (1.79) 24: 1.79 (2.19) 0.76 (0.14–1.37) 0.016
Moderate & 21: 3.00 (1.82) 12: 3.25 (2.49) 1.25 (0.45–2.05) 0.0065
severe PD
a
Estimation by bivariate linear models and adjusted for age and sex.

76 Neurosis
7.6 Treatments Received by GNS Status

In Table 7.8 the main treatments received by the patients separated by their GNS status
are summarised over the follow-up periods at 12 and 30 years. The most striking
findings are that in those who were GNS positive at baseline; there were (1) a greater
number of GP contacts, (2) longer duration of day care, and (3) greater psychotropic
drug consumption.
7.7 Influence of Personality Strengths

The results of the personality strengths analysis are of great interest but because they
constitute a new type of assessment there are no data by which they can be compared.
Female patients had somewhat greater strength scores than males, especially on cau-
tiousness; cothymic patients had lower scores on all measures (P = 0.02), but, interest-
ingly, GNS positive patients only had significantly lower scores on emotional toughness.
Personality disorder, not unexpectedly, was associated with lower strength scores in an
incremental association with severity. The CPRS scores at baseline showed indications
Table 7.8 Differences in treatment and service contacts between patients with or without the general neurotic
syndrome
0–12 years GNS (0–4) GNS (5–6) GNS (≥6) Sig Linear
level trend
N: Mean ± SD N: Mean ± SD N: Mean ± SD
No. of GP/OP appts 89: 27.9 ± 26.0 29: 26.8 ± 26.3 61: 38.3 ± 32.3 0.050 0.024
for psych illness
No. of GP/OP appts 90: 60.6 ± 42.9 29: 58.6 ± 38.3 61: 68.8 ± 42.5 0.392 0.211
for non-psych illness
Length of day care 90: 2.00 ± 6.6 29: 4.28 ± 14.7 61: 8.13 ± 15.0 0.004 0.002
(weeks)
Weeks of non-psych 90: 1.29 ± 2.1 29: 1.41 ± 1.9 61: 1.41 ± 2.0 0.608 0.385
hospitalisation
Weeks of psych 90: 0.67 ± 2.1 29: 0.17 ± 0.9 61: 1.36 ± 5.4 0.359 0.729
hospitalisation
No. of admission 90: 1.83 ± 2.8 29: 1.55 ± 2.4 61: 2.08 ± 2.7 0.638 0.405
Months with no 96: 113.4 ± 39.7 31: 112.6 ± 42.6 66: 91.7 ± 50.9 0.012 0.004
psychotropic
medication
0–30 years
Months with no 41: 293.1 ± 109.1 18: 265.4 ± 104.8 27:209.5 ± 141.2 0.008 0.004
psychotropic
medication
AOR = adjusted odds ratio.
For scale measures, ANOVA was performed based on logarithm transformed scale and so was the linearity test.
For the categorical measures, Fisher’s exact test was used to provide the p-values for both difference and linearity.

Table 7.9 Personality strengths by baseline characteristics of patients
PASP traits
Characteristics Forcefulness Emotional Cautiousness Independence Discernment Total
toughness
Sex: N
Female: 63 17.8 ± 7.2 19.6 ± 9.5 14.8 ± 7.2 13.3 ± 6.8 4.5 ± 3.1 70.0 ± 29.5
Male: 26 15.2 ± 6.8 17.7 ± 8.8 11.7 ± 6.5 13.0 ± 6.5 3.8 ± 3.1 61.4 ± 26.9
P-value 0.121 0.386 0.061 0.851 0.321 0.202
DSM Diag.
Dys: 1 8 ± n/a 11.0 ± n/a 7.0 ± n/a 12.0 ± n/a 2.0 ± n/a 40.0 ± n/a
GAD: 26 18.1 ± 7.5 20.6 ± 9.1 13.7 ± 8.3 14.5 ± 7.2 3.8 ± 3.3 70.7 ± 31.6
Panic: 32 19.6 ± 5.7 20.8 ± 10.1 16.8 ± 6.5 14.6 ± 6.5 5.1 ± 3.1 76.9 ± 26.9
Cothymia: 30 13.8 ± 7.1 16.0 ± 8.1 11.3 ± 5.7 10.7 ± 5.9 3.9 ± 2.9 55.7 ± 24.8
P-value 0.004 0.121 0.016 0.086 0.289 0.020
GNS score
< 4: 42 17.4 ± 7.3 20.9 ± 9.1 14.1 ± 7.2 14.1 ± 6.7 4.0 ± 3.2 71.0 ± 28.8
4–5: 18 19.3 ± 7.1 20.6 ± 10.0 14.6 ± 7.3 13.6 ± 7.5 5.3 ± 2.9 73.5 ± 29.8
≥ 6: 28 15.1 ± 7.0 15.4 ± 8.5 12.1 ± 6.8 11.7 ± 6.2 4.0 ± 3.1 58.4 ± 27.8
P-value 0.147 0.039 0.330 0.323 0.296 0.127

PD status
None: 35 20.2 ± 6.2 21.4 ± 8.6 16.2 ± 6.9 15.3 ± 6.2 4.9 ± 3.0 80.0 ± 26.5
Difficulty: 16 16.8 ± 7.6 16.6 ± 10.2 11.2 ± 8.2 11.2 ± 7.1 4.1 ± 2.5 59.9 ± 32.3
Simple: 24 15.4 ± 6.9 19.4 ± 8.6 14.5 ± 6.1 13.4 ± 6.4 4.0 ± 3.3 66.8 ± 25.7
Moderate/severe: 12 11.5 ± 6.6 14.6 ± 10.4 8.6 ± 5.1 9.1 ± 6.4 3.0 ± 3.8 46.8 ± 27.3
P-value 0.001 0.109 0.004 0.022 0.282 0.007
CPRS score
< 15: 15 17.4 ± 6.8 20.5 ± 8.9 14.2 ± 7.1 14.2 ± 6.2 2.8 ± 2.7 69.0 ± 26.7
15–25: 45 17.8 ± 7.4 20.5 ± 9.6 15.2 ± 7.8 13.8 ± 7.0 5.1 ± 3.0 72.4 ± 30.9
≥ 26: 27 15.6 ± 7.3 15.8 ± 8.6 11.1 ± 5.4 11.4 ± 6.5 3.7 ± 3.1 57.6 ± 25.6
P-value 0.460 0.093 0.060 0.278 0.023 0.109
PASP = positive personality traits from the Comprehensive Personality Assessment Scale (CPAS)
78 Neurosis
of lower strength scores with higher baseline pathology but the association was not
strong.
Comparison of the data at 30 years showed very important differences. Suicide attempts
were associated with few personality strengths, both for total scores and for each of the five
main traits (Table 7.10). Those attending day centres also had low scores (but the numbers
were small), and both social dysfunction (SFQ) and total psychopathology (CPRS) were much
more marked in those with fewer personality strengths. Those with strong elements of
forcefulness were more likely to be arrested and to be in custody (Table 7.10).
7.8 Synthesis of Findings

The study of a single syndrome, though unusual, over 30 years might be expected to yield a set
of complex results and difficulties in interpretation. This may well be true at some levels, but at
the level for justification of the general neurotic syndrome it is much easier. It is possible to
state with some confidence that the syndrome is clinically useful and, dare I say it, valid, in the
sense that it deserves to be studied further, rather than valid in the absolute sense.
The evidence from the 30 years of the Nottingham Study suggests the general neurotic
syndrome differs from single depressive, anxious, and panic disorders in important (or at
least non-trivial) ways:
(1) It is associated with greater symptomatology.
(2) It responds to treatment less well.
(3) It is associated with greater social dysfunction.
(4) It is associated with persistently worse clinical outcomes.
(5) It leads to greater service costs.
(6) It is associated with fewer personality strengths.
I will now examine each of these from the standpoint of a sceptical critic (as much as
I am able to dissociate in that direction).
1 Greater Symptomatology
This is an easy win for the sceptic. The general neurotic syndrome comprises symptoms of
both anxiety and depression and so is bound to have greater symptomatology than single
symptom disorders. I will allow the sceptic to win this one.
2 Poor Response to Treatment

The general neurotic syndrome does not respond to conventional psychiatric treatment.
This applies at every time point from 10 weeks onwards: the patients with the general
neurotic syndrome fared less well than other patients. The late James Birley, another
former president of the Royal College of Psychiatrists, used to quote among the many
human rights that ‘everyone should have the right to take part in a well-controlled
randomised controlled trial’. Not only was he right but there is much good evidence
that taking part in a good randomised trial in psychiatry is very good for your health,
no matter what treatment you receive. This is even true when the treatments tested are
no better than a placebo (Sanatinia et al., 2019). But even in the 10 weeks of the
randomised trial, those with the general neurotic syndrome had worse outcomes than
other groups, and these poorer outcomes were maintained over the whole 30-year
period.

Table 7.10 Personality strength by characteristics of patients at 30-year follow-up

toughness
Suicide attempts: N
None: 63 18.3 ± 6.8 20.9 ± 9.1 15.1 ± 7.1 14.7 ± 6.4 4.8 ± 3.2 73.8 ± 27.8
1–2 times: 12 13.9 ± 7.4 12.3 ± 5.3 11.1 ± 5.0 8.5 ± 5.1 3.0 ± 2.1 48.8 ± 19.1
3 times and more: 6 8.7 ± 3.8 10.3 ± 7.2 5.2 ± 3.4 5.8 ± 3.5 1.2 ± 1.5 31.2 ± 11.6
P-value 0.001 0.000 0.001 0.000 0.006 0.000
Social work contacts: N
None: 79 17.7 ± 7.0 19.6 ± 9.3 14.3 ± 7.3 13.7 ± 6.6 4.3 ± 3.2 69.7 ± 28.7
1–5 times: 3 11.0 ± 3.5 11.3 ± 7.6 8.7 ± 5.9 8.0 ± 5.0 3.3 ± 1.5 42.3 ± 12.7
6 times and more: 7 12.9 ± 8.6 15.4 ± 8.9 11.7 ± 5.6 10.0 ± 7.3 3.6 ± 3.0 53.6 ± 28.9
P-value 0.076 0.180 0.289 0.141 0.701 0.112
Day centre care: N
None: 85 17.5 ± 7.0 19.5 ± 9.2 14.2 ± 7.1 13.7 ± 6.4 4.4 ± 3.1 69.4 ± 28.2
Yes: 4 7.3 ± 3.5 10.0 ± 6.1 7.0 ± 3.7 2.8 ± 1.7 1.5 ± 1.7 28.5 ± 6.8

P-value 0.004 0.046 0.047 0.001 0.067 0.005
Arrested: N
None: 80 17.6 ± 7.2 19.4 ± 9.5 14.3 ± 7.1 13.7 ± 6.7 4.5 ± 3.1 69.4 ± 29.1
Yes: 9 12.3 ± 5.0 16.1 ± 7.2 10.0 ± 6.3 9.7 ± 5.9 2.7 ± 2.3 50.8 ± 21.3
P-value 0.036 0.323 0.084 0.090 0.101 0.066
In custody: N
None: 84 17.5 ± 7.1 19.5 ± 9.3 14.3 ± 7.2 13.5 ± 6.7 4.4 ± 3.1 69.2 ± 28.8
Yes: 5 10.0 ± 3.9 11.8 ± 6.2 7.4 ± 1.8 8.8 ± 4.0 2.0 ± 1.9 40.0 ± 10.1
P-value 0.022 0.074 0.035 0.127 0.091 0.027
Table 7.10 (cont.)

toughness
SFQ score: N
< 4: 33 21.8 ± 5.7 25.8 ± 8.4 19.0 ± 5.8 18.2 ± 5.4 5.4 ± 3.3 90.2 ± 23.4
5–14: 42 15.2 ± 6.5 16.4 ± 6.8 11.8 ± 6.2 11.2 ± 5.5 4.0 ± 2.7 58.7 ± 22.2
≥ 15: 13 11.7 ± 5.8 11.2 ± 7.8 8.3 ± 5.4 7.8 ± 5.5 2.5 ± 2.8 41.5 ± 21.2
P-value 0.000 0.000 0.000 0.000 0.012 0.000
CPRS score
< 15: 43 20.5 ± 6.7 25.0 ± 7.7 17.9 ± 5.7 17.3 ± 5.7 5.5 ± 3.1 86.2 ± 23.4

15–25: 21 15.5 ± 5.8 15.8 ± 7.0 11.7 ± 6.5 11.3 ± 5.1 3.0 ± 2.6 57.4 ± 22.0
≥ 26: 24 12.6 ± 6.0 11.6 ± 6.5 9.0 ± 6.2 7.9 ± 4.9 3.3 ± 2.7 44.4 ± 20.2
P-value 0.000 0.000 0.000 0.000 0.001 0.000
But the patients with the general neurotic syndrome were not neglected by services. They
received more GP and outpatient contacts and more day care than other patients, and also
many more psychotropic drugs (Table 7.8) (Tyrer et al., 2022). These treatments included
more than 20 different psychotropic drugs, intensive psychological treatments ranging from
analytical therapy, transactional analysis, cognitive behaviour therapy, and couple and
group therapy (but none of the newer treatments for personality disorder), as well as
more admissions to hospital. So they consulted more often, received more treatments,
had more specialised secondary care, but apparently did not benefit. But the message is
not all gloom. The conclusion should be ‘a poor response to standard evidence-based
treatments’, but elsewhere there is a more positive message.
3 Associated with Greater Social Dysfunction (see Table 7.7)
4 Associated with Persistently Worse Clinical Outcomes (see Table 7.6)
5 Leads to Greater Service Costs (see Table 6.3)
6 Associated with Fewer Personality Strengths (see Table 7.9)

Chapter
Is the Notion of the General
8 Neurotic Syndrome Useful?
In this last chapter, I want to write about the clinical implications of the general neurotic
syndrome as a central part of neurosis. Clearly, I am biased, but I will try to give opposite
arguments a fair airing too.
My starting point is a sentence from the ace nosologist, Bob Kendell; ‘All our diagnostic
terms are simply concepts, and the only fundamental question we can ask about them is
whether they are useful concepts, and useful to whom?’ (Kendell, 1991). This is the best
riposte to those who decry the notion of diagnosis altogether. What it comes down to is
utility. If the general neurotic syndrome is just a pimple on the side of common mental
disorder that has no value except as an esoteric talking point, it is useless. I suggest a debate
with six questions.
8.1 Does the General Neurotic Syndrome Add

to the Understanding of Common Mental Illness?
To those who regard diagnosis in psychiatry as a pointless self-serving example of medical
dominance, the notion of the general neurotic syndrome will just lead to eye-rolling and
shaking of heads. I can see the sharing of annoyance on social media – yet another example
of medical expansionism; creating a label in order to mask distress and normal human
emotion.
A more common view in more informed circles is that the general neurotic syndrome,
like almost all diagnoses in psychiatry, is just at the extreme end of the spectrum of common
mental disorder and does not need separate demarcation. This comes back to the notion of
usefulness. If the decisions made about the management of the general neurotic syndrome
do not apply to other common mental disorders, then the diagnosis might be regarded as
useful. The reasons why I think it is useful are expressed more fully here, and it also needs to
be pointed out that the syndrome is not at an extreme of the spectrum of neurosis; it covers
quite a large proportion.
It could also be said that comorbidity is all that is necessary to explain the syndrome. The
reason why I think this is a mistake is that the term ‘comorbidity’, when properly used,
describes the simultaneous presence of two separate disorders in the same person
(Feinstein, 1970). The combination of anxiety, depression, and personality disturbance is
not comorbidity; it is best expressed as consanguinity, manifestations of the same condition
(Tyrer, 1996). But because personality is usually ignored in making the diagnosis, the
general neurotic syndrome comes under the grouping described in Chapter 2, the Galenic
syndromes, those conditions in which personality and clinical symptoms and behaviour are
so closely intertwined that they have to be considered together. Now that the second axis of
82

Is the Notion of the GNS Useful? 83
classification has been abandoned in the DSM classification, there has to be greater
acknowledgement of the importance of personality in the description of these disorders.
My view here is not an isolated one. If we want to have a better understanding of mood
and anxiety disorders, we have to take account of personality. This is particularly obvious
when looking at the long-term outcomes of disorders. In Quinton et al.’s analysis of the 20-
year follow-up of psychiatric disorder there was a strong plea for the recognition of
personality as a key element of prediction: ‘the results provide strong evidence for the
value of a categorical diagnosis of personality disorder based on pervasive abnormalities in
social functioning, and for a broad vision of such disorders into ‘dramatic’ and ‘dependent/
avoidant’ types. Personality disorder proved to be a particularly strong predictor of the
recurrence of depression’ (Quinton et al., 1995, p. 321).
Michael Berk and an influential group of Australian and New Zealand colleagues have
become very frustrated with the neglect of personality.
We further argue for the benefit of adopting or incorporating a formulation-based
approach that incorporates personality style and/or disorder. The use of personality
and developmentally informed clinical formulations adds qualitative depth to clinical
understanding. This is normative in some countries and settings, but not internation-
ally. A formulation that includes personality would facilitate treatment involving psy-
chotherapy, aimed at equipping people with personality dysfunction with more
personalized adaptive regulation and coping skills to lead more fulfilling lives. (Berk
et al., 2018)
The argument that the general neurotic syndrome is not an odd outlier in the
diagnostic system but a main component of common mental illness is a powerful
one. People with brief episodes of mood disturbance, best identified as adjustment
disorders (Chapter 5), attend once or twice only and create few demands on the
services. Those with cothymia and the general neurotic syndrome consult repeatedly
and, as noted in Chapter 6, are responsible for most of the £7,450 per patient
incurred over the first 12 years of the Nottingham Study (Knerer et al., 2005).
So here we are addressing a very important public health issue. In the words of Bernard
Lahey (2009), who is using the synonym of ‘neuroticism’ to describe the general neurotic
syndrome, we have a call to action:
Although not widely appreciated, there is growing evidence that neuroticism is
a psychological trait of profound public health significance. Neuroticism is a robust
correlate and predictor of many different mental and physical disorders, comorbidity
among them, and the frequency of mental and general health service use. Indeed,
neuroticism apparently is a predictor of the quality and longevity of our lives.
Achieving a full understanding of the nature and origins of neuroticism, and the
mechanisms through which neuroticism is linked to mental and physical disorders,
should be a top priority for research. Knowing why neuroticism predicts such a wide
variety of seemingly diverse outcomes should lead to improved understanding of
commonalities among those outcomes and improved strategies for preventing them.
(p. 241)
We can safely conclude that the general neurotic syndrome, or any other name that
might be chosen for the condition, does indeed add to understanding and cannot be ignored
by health services.

84 Neurosis
8.2 Can the General Neurotic Syndrome Be Assessed Readily

in Clinical Practice?
The answer to this question is clearly positive, but it is important to answer it in both
primary and secondary care. The two elements of the diagnosis are the presence of cothymia
and detection of personality problems mainly, but not entirely, within the domains of
negative affectivity and anankastia (we have to get used to these terms). Because the Lewis
Prediction almost certainly still applies (i.e., psychiatrists are persuaded by their training to
avoid diagnosing anxiety and depression together), it would be best for therapists to provide
a self-rating questionnaire such as the Hospital Anxiety and Depression Scale (HADS) to
patients seen in their practice.
A large clinical trial carried out over 20 years ago tested whether a clinical guideline
combined with education helped general practitioners to diagnose and treat depression
more accurately (Thompson et al., 2000). It was ineffective on both counts; a four-hour
training session in the active arm of the trial did not improve recognition of depression or
the outcome of treatment. The yardstick of accuracy was determined by the score on the
HADS – a score of 8 or more on the HADS-D was the index of depression. This was a useful
trial to show the limitations of educational programmes in primary care, but what surprised
me was the nature of the trial. The fact that the HADS score was kept blind to the
participants helped to show that the intervention was unhelpful, but it would have been
a much better test to let half of the GP’s know the HADS score and the other half be kept
blind. Screening for anxiety and depression with the HADS scale is now commonplace in
secondary care, most frequently in cancer patients, where it is effective (Mitchell, Meader &
Symonds, 2010). If the HADS scale was handed out to patients on their first attendance it
could be a useful assessment of cothymia, and a score of 8 or more on the depression scale
and 9 or more on the anxiety section, would help to aid the diagnosis. If, within a few
minutes of interview, the GP is presented with numerical evidence of both anxiety and
depression, the task of detection is almost done. But much more can be done to point out the
clinical importance of anxiety combined with depression in primary care. In the ICD-11
classification, there is work being carried out on 28 possible disorders in the primary care
version (ICD-11-PHC) (Gask et al., 2018, p. 77) but agreement on these has not yet been
reached. One of these diagnoses is ‘anxious depression’, long argued by David Goldberg
(2013) to be an essential element of this classification, and this probably will be included –
half a generation after Das-Munshi et al. (2008) pointed out its importance – so it is long
overdue.
Eisenberg (1992) wrote a paper 30 years ago that still has relevance today about the
ability of general practitioners to identify mental illness and psychosocial problems:
Goldberg and Gater (1991) have illustrated just how skewed that population sample is. They
estimated that one in four of the patients attending a British general practice had one of the
common mental disorders: ‘becoming anxious, distressed or depressed.’ General practi-
tioners recognize only about 40 percent of that group; that is, they identify 1 in 10 of their
patients as having psychosocial problems. Of that number, only 20 percent – that is, 2 out of
100 patients – are treated by mental health workers. Yet it is on that unrepresentative
subgroup that the official classification scheme has been based. Barrett et al. (1988) exam-
ined patients seen in general office practice and found that many of them simply did not fit
into the specialists’ nomenclature. For one thing, mixed states of depression and anxiety are
common. Barrett et al. believe that a purpose-built nosology is needed so that general

medical patients can be sorted out in a fashion useful for making treatment decisions.
(Eisenberg, 1992)
I would like to think that matters improved in the subsequent 30 years but as the amount
of time that a GP gives to each consultation has steadily reduced – it is now around six
minutes – I am not convinced.
It should also be asked, is the diagnosis of general neurotic syndrome of any value to
a general practitioner? It is not really a difficult condition to identify but is it really
relevant to management. The average GP will know his or her GNS patients only too well;
they consult frequently, take up more time than the average consultation, and do not
seem to be satisfied with the interventions on offer. When given an opportunity, they will
talk at length about every minor symptom and often dominate a clinical interview –
reminding me of the Ken Dodd joke: ‘l never speak to my mother-in-law; I don’t like to
interrupt her.’
Bob Kendell has something else to say on this subject:
Many of the conditions which psychiatrists have come to regard as illness, and hence as
requiring treatment, do not qualify, or rather there is little evidence at present that they
do. The attempt to relieve suffering is medicine’s oldest and noblest tradition, and the
author is not suggesting that psychiatrists should stop trying to help husbands and
wives to live together in harmony, or aimless adolescents to find their feet. But if one is
to venture into such areas let it be in full recognition of the fact that in doing so one
may be straying outside one’s proper boundary, and that in the end it may turn out that
other people can deal with such problems as well as or better than the psychiatrist can,
and that in these areas their training and their concepts are more appropriate than his.
(Kendell, 1975b)
Here I would defend the case that the general neurotic syndrome is a valid area for
diagnosis in both primary and secondary care as it such a prominent part of clinical
presentation and so cannot be ignored or passed over to somebody else. Later in this chapter
the other people who may be able to help more effectively than the GP in dealing with the
syndrome are brought on board, but the first stage is to identify the group that needs such
additional help.
8.3 Is the Concept of the General Neurotic Syndrome Useful

to Patients?
Nobody likes to be called ‘neurotic’, so the word is normally spoken in the absence of the
person to whom it is being applied. Would the ‘general neurotic syndrome’ be equally
unpopular? It might well be, but there is no obvious alternative. What is useful for
patients is the introduction of the personality dimension along the lines of: ‘It’s fairly
obvious that you have anxiety/depression/fears or other symptoms, but I think there is
something else there as well. I suspect you have personality difficulties that are getting in
the way of your recovery. Have I got this wrong?’ (Tyrer, 2021). The doctor then
introduces the notion of personality problems nagging away in the background and
provoking relapse. The results of the Nottingham Study show that the general neurotic
syndrome does not go away; in one form or another it stays with you indefinitely. But the
important aspect of the syndrome is that it should not handicap a person in the future to
the same extent as in the past.

86 Neurosis
8.4 How Should the General Neurotic Syndrome Be Introduced

into Diagnostic and Clinical Practice?
The general neurotic syndrome could be regarded as a synonym for neurosis, but this is not
strictly accurate. It is better to think of neurosis as a neurotic spectrum in which the general
neurotic syndrome is positioned towards the end of the scale (Figure 8.1).
This condition is seen most often in primary care and it is there that it should be first
diagnosed. But GPs are not over-keen on diagnosis in psychiatry, and it is not difficult to see
why. As Linda Gask and her colleagues put it:
Patients in primary care settings are much less likely to present with clearly identifiable
diagnostic syndromes. People present with a wide variety of symptoms, concerns, worries,
and problems. These are not only undifferentiated as originally described by Balint (1964),
but also, crucially, at least at first presentation, unrehearsed by prior discussion with doctors
versed in the addenda and language of diagnosis. (Gask et al., 2018, p. 73)
One of the critical words in this passage is ‘unrehearsed’. This may not be quite as true today
as Dr Google is only too ready to spread diagnoses around like confetti, but it is generally
true that in primary care the need for a specific diagnosis is much less important than in
secondary care.
But how then can the general neurotic syndrome be identified? It is quite easy. It should
be suspected if any of the following apply:
(i) fat-folder patients
(ii) frequent attenders
(iii) failure to respond to standard treatments
(iv) a loquacious mixture of complaints covering many areas of life.
So, within a few minutes of arrival in the surgery the doctor should be able to identify
those who may have the general neurotic syndrome. It is fair to add that this is not very
different from the way psychiatrists look at diagnosis. Bob found that psychiatrists, both
young and old, experienced and inexperienced, made their diagnostic decisions within five
minutes of a clinical assessment (Kendell, 1975a). General practitioners probably take only
four minutes on a good day.
Spectrum of common mental disorders

6
4
Severity level
0
stress adjustment anxiety depression general neurotic
disorder disorder syndrome
Figure 8.1 The neurotic spectrum of common mental disorders

8.5 How Should the General Neurotic Syndrome Be Treated?

One of the gloomiest views that has been expressed about the Nottingham Study results is
along the lines of ‘since the results of your study show no benefit from any form of treatment
it should only be relegated to the side-lines of care’. Even if that were true, it would not be
a reason for disregarding the diagnosis. Randomised trials and large-cohort studies are
useful in showing how groups behave but do not identify every outcome. I have misquoted
Tennyson in the past in suggesting he might have written a critique about randomised trials:
‘so careful of the group they seem, so careless of the single case’ (Tyrer, 2008b).
Although the patients with the general neurotic syndrome in the Nottingham Study as
a group fared uniformly poorly, a significant number did improve and, at 30 years, 21 of the 46
GNS+ patients were rated as recovered in formal ratings, and all of these had no clinical or
social function scores within the range of pathology and had been well for at least two years.
These recovered patients were more than offset by the other 25 patients getting worse or staying
the same but it is of value to look at why and when the 21 patients recovered during the trial.
This is summarised in Table 8.1. Minor changes have been made to avoid identification
of the patients concerned.
Table 8.1 Details of patients rated as recovered at 30-year assessment
Gender Age at Initial Main factors identified as responsible for

entry randomised recovery
(decade) treatment
M 40–49 CBT Had mild symptoms at 12 years; had cerebro-

vascular accident leading to early retirement
from civil service in 1991. Much better mental
health from retirement onwards.
F 30–39 CBT Mental health completely changed when she
remarried in 2007. Much happier, spends most
of her time with grandchildren who rely on her
help greatly.
F 30–39 Diazepam Very handicapped by anxiety until 2002, which
extended to agoraphobia and social anxiety.
Better when she moved to village outside
Nottingham where she felt less pressured, and
also helped greatly by CBT from psychologist.
M 50–59 CBT A very nervous man with no self-confidence,
who after his wife died moved to a village
outside Nottingham and was helped greatly in
a community retirement scheme that improved
his social skills.
F 30–39 Self-help Two big positive events – happily married in
2001 and moved to West Country in 2006. Keen
on self-help and also helping others. Since
retirement in 2015 has been involved in much
voluntary work.

88 Neurosis
Table 8.1 (cont.)

(decade) treatment
F 20–29 CBT After divorce from aggressive husband in 2001
has been better, especially so after moving to
village 20 miles from Nottingham and living
alone. ‘Happier now than I have ever been.’
M 30–39 Diazepam Remained on benzodiazepines for many years
to combat anxiety symptoms. Moved to
Northwest England in 1989. Developed multiple
sclerosis (MS) later and had to give up work. Has
been better mentally and more accepting of his
disability since getting MS.
F 20–29 Self-help Much better after divorce from husband ten
years ago. He was aggressive and blackmailed
her by preventing contact with her children.
Some help from counselling with psychologist
but felt that self-help was the best way forward.
M 40–49 CBT See full description of patient 86.
F 20–29 Self-help Much happier since marriage 27 years ago and
moving to a new post and home outside
Nottingham. On no drug treatment, relies on
her own efforts.
M 30–39 CBT Found working for a major utility very stressful
and retired early twelve years ago. Moved to
town 15 miles from Nottingham. Worked again
but made redundant in 2013. Mental health
dramatically improved at that time, loves spare
time now and looking after grandchildren.
F 20–29 Self-help Much better since her divorce in 1989. At that
time made visits to GP and out-patient clinics
but ‘then I noticed I was always much worse
after going there so decided to do it all myself’.
F 30–39 CBT Much better and moved to West Country 10
years ago. New life, new contacts and able to
maintain these after husband died. Loves
travelling.
M 30–39 CBT Very much better after stopping work – very
physically demanding job – advice to stop
drinking and smoking very helpful indeed. After
stopping work also learnt to drive, ‘one of the
best things I ever did’.

Table 8.1 (cont.)

(decade) treatment
F 20–30 CBT Much better after leaving Nottingham in 1993
and getting new post in hospital in Birmingham.
Very much better. Hardly ever consults doctor. ‘I
know myself better and now know what to do.’
F 30–40 Placebo Moved round country in teaching jobs but
retired in 2011. Found teaching repetitive and
not fully satisfying but after retirement moved
to Yorkshire and passed a Master’s degree
which made her very proud. Brief period on
sertraline when depressed but now stopped.
M 20–29 CBT Much better after moving to Manchester and
taking up post in public service. Did well and
with pay-out on leaving has set up
a construction firm which is very successful.
F 40–49 CBT Continuously unwell until she separated from
her husband and met a new partner –
‘completely changed my life’.
F 20–29 Self-help Better after moving to village 18 miles from
Nottingham, but also had persistent phobia of
death. Worse after brother and sister died within
5 months of each other 8 years ago but after
crisis at this point steadily improved. ‘I am
coming to terms with the fact that not
everybody is the same, that you have to accept
things and deal with problems yourself.’
F 20–29 Dothiepin Moved away to village 8 miles from Nottingham
in 1998. Left job in hospital 8 years ago and
toured the world for a year. Much better after
leaving job and set up beauty clinic from home.
Gets nervous at times, but has self-help routines,
including mind gym, that keeps symptoms
at bay.
M 40–49 CBT Developed severe attack of meningitis in 1999
which left him with mild memory impairment.
But from then on he says he is ‘looking after my
mental health myself’. Having a severe physical
illness has put this in perspective.
NB. The comments in quote marks come from the patients’ own comments in filling a section in the interview
asking what had helped them most in the study.

90 Neurosis
The case of patient number 86 in the trial needs a separate description as it describes the
biggest change in outcome in any patient in the study. He was recruited to the randomised
trial (with panic disorder as well as the general neurotic syndrome). His personality status at
entry was at the most severe of all the patients in the study. He was chronically anxious and
depressed, was taking large doses of benzodiazepines and antidepressants with very little
effect, and was infused with anger about the way he had been treated by his parents, who had
always favoured his younger brother, and this anger extended to all members of the family.
He continued to be unwell up to the 12-year follow-up point and it looked as though he
would have a very poor outcome at 30 years.
He then experienced what could be described as an epiphany moment. At a time when he
was feeling more depressed than he had ever done, he took it on himself to walk into a Catholic
church in Nottingham. He sat down in one of the pews and a priest came to see him. Our patient
professed to no religious faith but found the presence of the priest comforting, and when he left,
he was given a rosary. He left the church and made the decision to change his life around. He was
going to forget all the past troubles at home and forge a new life for himself. He also resolved to
stop all his medication and start afresh with no pharmacological help.
It was a great struggle to get off all his medication, taking nearly two years, but he
succeeded. He joined an allotment group, made new friends there who knew nothing about
his past, and became highly competent at gardening. At 30 years he could not properly
explain what had happened; only that seeing the priest had given him the realisation that he
could have a different life. When he was assessed at 30 years, he had symptom scores all
below the threshold of pathology and good social function.
Of course, I would love to know exactly what it was that effected the change. In trying to
figure this out I think the words of Francis Thompson, himself a lost soul who spent several
years homeless on the streets of London, are apposite: When you are at your absolute rock
bottom you can sometimes see the way ahead with much greater clarity than ever
before, especially if there is a religious connotation.
This is one of the verses from ‘In No Strange Land’:
But (when so sad thou canst not sadder)
Cry;—and upon thy so sore loss
Shall shine the traffic of Jacob’s ladder
Pitched betwixt Heaven and Charing Cross.
Yea, in the night, my Soul, my daughter,
Cry,—clinging to Heaven by the hems;
And lo, Christ walking on the water,
Not of Gennesareth, but Thames!
Examination of this group of recovered patients throws a new light on the general
neurotic syndrome that needs more exposure. Although the group is a heterogeneous one, it
is possible to find several common features:
(1) in most cases the improvement followed a very major life event,
(2) a move away from the city of Nottingham was a common feature,
(3) the change induced by the major event was so profound that a complete re-
examination of the person’s life was initiated,
(4) psychological means of resolving problems were more commonly employed than
pharmacological ones.

I should add that our analysis of these issues is still not finalised and will appear in other
publications shortly.
These findings point towards a possible way of managing those who present with the
general neurotic syndrome. The other findings of the study suggest that this intervention
should start early rather than late, as although the patients presented to general practice
clinics much earlier than would be expected in an outpatients clinic, nearly a third
(32 per cent) had a recurrent disorder on entry to the original trial, and these incurred
more costs and a poorer outcome than those who presented with a new episode.
8.6 How Should the General Neurotic Syndrome Be Treated?

Let us start here by returning to the case of Mrs Bennet, who is about to see her physician
again. This is the conversation they are now having. Mrs Bennet, as you might expect, is
mildly agitated in expectation.
‘Mrs Bennet, I have now made a full assessment of your nerves and have come to the
following conclusions . . .’
(She interrupts) ‘I do hope you can give me good news, doctor, because otherwise I may
become quite distraught.’
‘As you said earlier Mrs Bennet, you have suffered from your nerves for as long as you
can remember. This is an affliction that is likely to continue for quite a long time.’
‘Don’t say that, doctor. If you cannot offer me hope I am undone. That I cannot tolerate.
I can feel another wave coming on. I must lie down.’
‘Please let me finish, Mrs Bennet. When I said this is likely to continue for quite a long time
this does not mean it has to continue in the same way indefinitely. What you need to do is to
organise your life more carefully so that the ups and downs of your nerves can be made tolerable.’
‘But how can I do that doctor? Mr Bennet, and my five daughters, lead me up and down
with their fancy notions and I cannot keep up with them.’
‘You have to adapt Mrs Bennet. You have lived with your five daughters and Mr Bennet
for many years and know them, as you said yourself, like the back of your still-elegant hand,
if I may so venture a compliment at this difficult time. If you do understand them so
perfectly, you should be able to anticipate what they are going to say or do.’
‘You flatter me, doctor, but I can see through you. You add compliments to assuage bad
news. But when I say I understand them I just mean that I understand they are governed by
caprice and impulse. Lydia just needs to see a sergeant from the regiment and she is after
him like a moth to a flame. How can I anticipate that?’
‘Simply, you need a way of stopping your nerves making an unwanted entrance. You are an
intelligent woman and to allow your nerves to dictate is an unnecessary abrogation; they are not
worth it. I suggest another experiment. Please write down at the beginning of each day in the next
two weeks all the things that are likely to happen on that day and what you can do to avoid your
nerves being agitated. There is no need for you to be bullied by your nerves; now is the time to
start bullying them in their turn. I am sure if you went through this exercise, you would find an
answer. For example, you have told me already that Mr Bennet retires to the library whenever
trouble is around. Might it not be possible, Mrs Bennet, for you to retire to the library at these
times, just before he plans his escape, and let Mr Bennet deal with any problems that may arise.’
‘I am beginning to get an idea what you were talking about, doctor. I think the right word
is control. If I can control my circumstances, I can control my nerves.’

92 Neurosis
‘I really think you have it, Mrs Bennet. Up until now you have allowed events in your life
to control you; now is the time for you to control them.’
‘I don’t know how to thank you, doctor. I must go and tell my daughters immediately.’
‘I would advise against, Mrs Bennet. You are too ready to confide in others. It leaves you
exposed. I think this conversation should remain confidential until I see you again in three
months’ time. You can tell me then if your nerves have been securely locked away until you
permit them an airing.’
This is not an idle sojourn into Pride and Prejudice; there is a serious message behind it.
The 30-year study of the general neurotic syndrome has established that its symptoms and
behaviour will not be changed easily, if at all; that aggressive personal attempts to overcome
it are unlikely; and that the best advice in management is to work out a way of adapting to
the symptoms and accepting their persistence.
To give you a more apt illustration of ways in which the general neurotic syndrome both
progresses and might be treated, I am introducing Lizzie. Lizzie is a remarkably apt
equivalent of Elizabeth Bennet in Pride and Prejudice, first met on 7th May 1987 when
she was 21 and about to enter the Nottingham Study of Neurotic Disorder. She was
attending for her first appointment at one of my general practice psychiatric clinics in
Nottingham. I do not pretend that I made a full assessment at that time. I was carrying out
19 clinics a month so was very busy, but as I have written elsewhere, it was professionally still
the most satisfying part of my career (Tyrer, 2013).
Lizzie has symptoms of both anxiety and depression and a lot of life problems, but the anxiety
symptoms predominate, and these are marked at interview. But at this first interview she
describes the feelings that hundreds of people are disclosing to doctors and other therapists in
clinics every day. These could be lumped together, as I have done in this book, as typical
cothymia, but they are not typical; they are unique. Behind these symptoms there is so much
more that is normally unsaid and unheard. Now, 34 years later, I have finally opened my ears and
eyes and asked for her account in connection with this book and she has responded with
eloquence and enthusiasm. I hope her words show this to be far removed from a confession
forced on her by my request. In her words, ‘it has opened up the lidded boxes of my brain’ and she
is happy for all to read her account. It is the story of just one of the participants in the Nottingham
Study; each of whom could tell much more than was ever disclosed at any interview.
8.7 Lizzie’s story

‘It is not too difficult to pinpoint when my anxiety crept into my life. Leading up to becoming five
years of age, I lived in a much loving extended family, being adored by grandparents, other
relatives and, of course, my parents. I may have already picked up on my mother’s distress even
before then, as she had three children within three and a half years and although she was the most
incredible mother, it became clear to those close to her that she was struggling with the demands
of home and her own mental health.
Things then changed very quickly for me at such a young age, when unknowing to me,
my parents, in an act of kindness, offered board and lodgings to a man who had relocated to
the village to take up employment at the local garage. As we were brought up in a very social
home, initially I did not feel any fear towards the lodger and in fact I was often told by him
‘what a beautiful and clever child’ I was.
Obviously, now I realise that he was grooming me, and also my sister who is only
thirteen months older than me, but my confident younger brother was too much of

a risk to keep silent. Even at the age of three years he had a real sense of self, and he
knew nothing about what was happening to his siblings. The insight that I later gained
was how vulnerable children can be pinpointed by others to be groomed. By then I also
had a baby brother, who would later become the reason why I kept quiet about my
sexual abuse as I was told that he would be abused too if I told anyone else about the
sexual abuse. Despite hiding in my parents’ wardrobe each night before I was told that
I had to get into my own bed, there was still no understanding in their minds why I was
acting that way. I still have dreams about my parents’ wardrobe in which I am hiding
Jewish children from Nazis or am telling children to be quiet and hide under the
blankets when the family home has been invaded. Once put back into bed, I would
surround myself with my cuddly toys as a means of protection, an innocent thought at
such an innocent age. I still have those same childhood toys; I cannot part with them as
we had a bond which later I realised was a dark secret. The abuse continued to both my
sister and me and sometimes it would take place together. By this time, I feared the
physical abuse too, with threats of being held against the gas fire if I told anyone. In my
mind I think that my abuser was getting worried that he would be found out, but I felt
that I had no one to tell. A sense of deep anxiety had already been manifest. I carry this
with me today, my dreams are the nightmares of helplessness and of no one listening to
me, the frustration of telling the little ones that I was trying to protect not to make
a noise or to stay hidden under the covers.
I was already a quiet and sensitive child, but now was I full of fear, inner emotional, and
outer physical pain from the sexual abuse inflicted upon me. With no ability of being able to
escape from this, I disassociated with drawing, often with messages; if only someone could
have paid more attention to the detail within my artwork. There was always a house, with
the sun shining above it, but each house never had a front door, I guess that it was my
showing there was no escape. Following visits to my doctor for unexplained rectum injuries
and the school noticing that my behaviour had become even more withdrawn, the police
were alerted and at last we felt able to speak our truth, even though we did not understand
what had been happening to us. But I still dreaded going to bed at night or being left alone
with this man.
My police questioned my abuser about a theft at the local garage where he worked.
I think that at this point I felt able to tell my parents what had been happening as we had to
go for a medical examination, but after that time it was never mentioned again, nor did
I ever receive professional counselling or an explanation from my parents. The shame
intensified and my childhood would be blighted by the preceding year of child sexual abuse;
little did I realise then that it would still affect me now. I have PTSD, agoraphobia,
depression, chronic anxiety, and a continuing sense of never accepting my achievements
in life, still remaining forgotten, misunderstood, and unable to speak about exploitation
when it occurs in my adult life.
I have never been a relationship with a man who made me feel that he would protect me.
I have no libido and am content to be a single woman; I will not be controlled by a man
again. My father was also a controlling man, and I have seen recurring patterns of control in
my previous relationships. As an adult, I now need to be independent, self-reliant, and safe.
Due to the many fractures I have suffered, leading to lifelong mobility problems, I have not
been able to continue with a career that would have got me out of the poverty trap, given me
self-worth, and enabled me to mix with like-minded people. But I still want to be
independent.

94 Neurosis
From the moment of my original sexual assaults, I have felt the shame, added to my
abuser saying, it was all my fault. The shame was accentuated as I did not have the courage to
confide in my parents or be reassured that I had never asked for this to happen. Our family
home became dark with secrets, added to by the distress of my parents. We all had to contain
this; after all, how had this happened in such a loving and well-functioning family? I could
not find the words to write down my emotions, but I could make up poems in my head. My
dolls were my friends, they would understand because if I told any of my friends it would be
betrayal and more shame and judgement. I still have every toy from my childhood, as each
has such significance.
I then learnt to sew, making outfits for my dolls and new soft toys to become part of our
protection. I watched my mother sew and then I picked up the basics. My creative world was
now full of colour, full of new beginnings as I had produced something that I could relate to,
and give to someone else (this being new outfits for my dolls). Throughout junior school, we
were told about road safety and how a policeman would be coming to school each year to
talk to us. Every day, I had this feeling of dread, could this be the day that I am pointed out to
the school as that bad girl who had done bad things! This is a burden that no young child
should have to carry. I did not realise that I was the victim of the most horrific abuse,
because it was not spoken about again at home, as my parents thought that it was better to
sweep it under the carpet and once again contain it.
As I reached adolescence, the words of my abuser were still being repeated in my mind,
that because I was a pretty child he could not help himself. I did not wear makeup, once my
breasts had started to develop, I strapped them down, I did not tell my parents that I had
started my periods. My anxiety and fear that I would get noticed by older men made me miss
out on the adventures of teenage years. I excelled at school, but we did not have the career
advisors at school that I believe might have led me to a rewarding career in the arts!
Yet I would be allowed to change my bedroom and redecorate, and I would make my
own soft furnishings. Our home was always filled with our school friends and my mother
would make us all beautiful meals in which all of us would help.
When my mother died, I was just seventeen years of age. It was as though the world had
stopped again. We had just been on two wonderful family holidays, and I was beginning to
feel that I could now feel safe to go to discos and become a teenager. Everything at my home
changed again, its darkness and distress filled every part of our home. There we were, four
traumatised teenagers with a father who did not know how to cope. My sister had a place at
a university in London and my youngest brother was about to go to secondary school. My
role in becoming a mother to everyone became more intense, as I was working full time and
my father had teaching commitments in the evenings as well.
My mother was loved but vulnerable. She had the ability to make everyone feel that they
were special and important. So, I naturally took the children who were bullied at school
home for tea; that was my way of trying to save them. I also knew that my mother could not
cope with running the house, so I would do the housework before my father came home so
that he would not shout at us or see that my mother was not functioning. I took on my
mother’s emotional pain; we often heard her crying, she suffered from agoraphobia, and
self-harmed which she always said were accidents. I just wanted my father to be calm and my
mother to be happy. In many ways she was like a child; we had to fetch our own school
uniforms, wash our own clothes, and organise ourselves to function at school without the
other children knowing how difficult it was for us. Again, we were sweeping it all under the
carpet.

I worried about my mother, and noticed that I was unable to sleep. I paced around, as if
I laid down in bed everything would be so much worse in my thoughts, with an overwhelm-
ing feeling of despair and grief. This had happened when I studied for my exams, but also,
I realised as a consequence of my previous abuse, I did not really sleep when I went to bed.
I lay there pretending to be asleep, praying that the bedroom door would not open so that
my sister and I would not be taken out of our bunk beds. I had the same recurring dream for
many years, a nightmare of being rolled down a hill in a wooden barrel and if your number
was called you had to go down the hill once again, even if you had the fear that your barrel
would break. I feared that I would become like my mother, who, due to her own mental
illness, never realised what an impact her behaviour had on our childhood. This included
arguments with my father, whom she felt was still a ‘mummy’s boy’, holidays ruined by my
mother crying each morning in bed, seeing her biting her fingers down to the bone when
stressed, showing the distress felt throughout the home of an unhappy marriage accompan-
ied by her own feelings of failure.
Hope came when I started a job with Laura Ashley. I was surrounded by colours
each day – fabrics, wallpaper, beautiful clothes. My career took off at an early age and
by eighteen I was put forward for management posts, helping to train staff and open
new branches throughout the country. My training notes were used in the company
staff manuals. Each day at work gave me an escape. I could immerse myself in
creativity and, more importantly, become financially independent. But pressure grew
at work and I felt guilty about being away from my father and two younger brothers.
But my career escalated very quickly, perhaps too quickly, and I felt that I may have
been promoted too soon.
I had the ability to do the job and was very successful in my management role. But the
long hours, lack of support at work, combined with uncertainly about where my next
management role would be in the UK, added to my anxiety. The pressure began to affect
me. I started to experience agoraphobia and dissociation again. I felt I had too many
responsibilities too young, and I regretted not being able to socialise with friends of my
own age.
After several years, I started suffering more severe symptoms of depression and anxiety.
I felt dissociated and unable to cope, I become paranoid that I was failing and developed the
‘imposter syndrome’ that I had from primary school, feeling that whenever I did well, I was
not being the real person inside. This was when I suffered my first nervous breakdown. I still
dream about my time at Laura Ashley, at least once a fortnight, but these dreams are
distressing as I never get paid or acknowledged in them, no matter how much I try to be
back as part of the team on the shop floor in Nottingham. I know now that I should have
stayed there for much longer and not taken up a management post only a year after my
mother’s passing. It was a very strict work environment and very regimented. I have spoken
to others who worked alongside me and each said the same.
Further education provided me with a sense of fulfilment. I passed each exam with
distinction and went on to take exams at the highest level offered on each course. Money
was very tight, but I supported myself through bar jobs. At this time, I went into rented
accommodation in the form of bedsits. I felt however that I was living the student years that
I never had. It didn’t include drinking alcohol or one-night stands, more that I was helping
myself to achieve better work prospects and prove to my family that I wasn’t such a failure!
My empowerment is creativity, the ability to make items from fabric, yarn, a paint brush,
cookery, and floristry, just to name of few of skills that I have learnt mainly with the help of

96 Neurosis
YouTube as many creative courses are no longer available due to lack of funding. These
classes gave me structure, a reason to get up and meet like-minded people, and make many
long-term friends. I found that many other people who attended the classes were not
working because of anxiety and depression. We all shared how anxious we were when
going to the courses initially, but then we found creative expression, a feeling of self-worth,
simply just belonging and feeling understood.
But my life has taken many unexpected and tragic turns and prevented normal employ-
ment. I was away enjoying a family holiday in the UK when I fell some distance and broke
my left ankle and heel bone. I was told at the age of thirty-three years that I probably would
not walk with ease again, but my strong coping mechanisms made me believe otherwise.
Despite being put into non-weight-bearing plaster for much of the next fourteen years,
I never lost sight of gaining back my independence and my determination not to have to
depend on anyone else. Unfortunately, the bone density was reduced in my right kneecap,
right wrist and my right foot and ankle, and it needed many operations before I was able to
walk again.
It was decided that I should go back to stay with my father for several weeks following
each stay in hospital. Spending time back at our family home was of much comfort but
also full of traumatic memories. I coped by sewing using my left hand. I listened to talking
books and took my mind off an uncertain future by making my brain remember all the
happy times from my childhood, being surrounded by my siblings, cousins coming to stay
and the thoughts of love and understanding for my beloved mother. It was a healing time
for me and my father; we spoke in depth about how both of our lives had challenges but
being part of a supportive and loving family always got us through. Having long-lasting
mobility issues combined with chronic anxiety has reinforced the difficulties of living off
very little income and the battles to be rehoused in social housing suiting my needs. The
housing shortage means that you have long waiting lists and little option of which area you
will be rehoused.
I still have a constant fear of being exploited as throughout my life I have been seen as
a soft touch, and so have been taken advantage of by people who appear to be your good
friends and neighbours. I have always lived alone and, due to my medical issues, I tend to
feel very isolated which in turn makes me feel very vulnerable. For some reason, I still trust
the word of others; my life experiences have not made me cynical. I still want to protect
those who struggle too, almost as if they were the lost child that I once was, internally
begging for support.
I had my crafts to fill my days whilst recuperating, getting joy and fulfilment in
completing items that I gave to others. Although my right wrist still has not got full
movement and flexibility, I learnt how to sew and crochet. I got out an old paint set and
produced paintings of my friend’s pets. I had not painted since I was at school and yet the
gift was still there. I amazed people around me with my talents, some of which had lain
dormant, but I was pleased I still had artistic flair. My work has inspired others to heal
themselves through creativity, gain self-confidence through producing items, joining
groups to meet new friends. My sense of pride came back as I was reinforced and could
no longer ignore the reactions of other people who saw my work. I found that my
obsessionality and need for perfection lessened as there are no rules to follow if you have
your own ways of expressing yourself.
I remember that I told my psychiatrist once, that I just wanted to be ‘ordinary’, to be able
to do a 9–5 life like others around me who went to work but did very little outside of that,

and I got a reply that has always stayed with me, ‘you will never be ordinary, Lizzie, as you
were born to be extraordinary!’
Lizzie finishes her account with the comment: ‘I wish all can understand the creativity
that has helped me to find peace, fulfilment, and purpose.’
There are many insights into neurosis that come from this frank account, part harrow-
ing, part sympathy-provoking, and part fortifying. Some might even think that this is the
best way to formulate the subject; a book of 210 life accounts like Lizzie’s might offer more
than the selective groupings of what are no more than collective episodes of events and
outcomes. But there are elements of Lizzie’s story that help to understand the findings of the
Nottingham Study and also reinforce them.
8.7.1 Sexual Abuse

Lizzie may or may not have been of an anxious disposition when she was very young but
there is absolutely no doubt that the sexual abuse added to it immensely. Although we did
not formally assess sexual abuse as part of the Nottingham Study, the main assessor in the
latter stages, my wife, Helen, worked in a genitourinary medicine department, where abuse
is always asked about as a matter of course. A history of physical or sexual abuse was present
in approximately a quarter of all cases in our study.
Lizzie, sadly, describes a very typical account of the consequences of child sexual abuse.
Becoming withdrawn and getting anxious; not being able to disclose; taking refuge in toys,
painting and writing, are all common response to this uttermost violation of intimacy. What
might have been done to help Lizzie at this point and would it have prevented all her future
symptoms? This is impossible to answer, but we have clues that awareness is moving in the
right direction, and if she had a sympathetic counsellor who could assist in showing that no
blame whatsoever could be attached to her, that there was no reason for shame, and that her
self-worth could be preserved, how might have her life have changed for the better. If the
right combination of disclosure, support, enrichment, and prevention could be imple-
mented everywhere, it would have a major effect on the long-term outcome of so much of
mental illness. It is worth noting in the Nottingham Study that those who presented with
recurrent symptomatology generally had a worse outcome than those who presented with
new symptoms, so it could be argued that any intervention for those with early trauma who
presented in adult life was already too late.
8.7.2 Family Dynamics

One of the elements scored in the scale for the diagnosis of the general neurotic syndrome is
the presence of a similar condition in a first-degree relative. This is an acknowledgement to
both the genetic contribution to the disorder (Hettema et al., 2001) and the behavioural
effects of modelling described in Section 1.2 point 4. Children are very sensitive to parental
behaviour – this is shown very well in Lizzie’s account – and may imitate facets of this in
their own development.
8.7.3 Employment
Despite this early adversity, including the death of her mother, Lizzie was able to gain useful
employment. Then she made the decision to give her job up at Laura Ashley in favour of
further education. This almost certainly was a mistake. She had shop-floor and management

98 Neurosis
skills and was successful, and if she had received the right level of support and advice at this
point everything might have turned out very differently. As it was, her financial future from
then onwards became very insecure. This was aggravated intensely by the injuries she had
received it to her foot, which under normal circumstances would have been expected to lead
to full recovery. This was not achieved and I suspect her care and surgical interventions
could have been improved.
8.7.4 Psychological Treatment

Lizzie also received several sessions of private psychotherapy as well as psychotherapy
support from a highly regarded consultant psychotherapist. But the psychotherapist felt at
the point he saw Lizzie she was too disorganised to ‘use more productively more intensive
explorative work or other forms of challenging psychotherapy’. We cannot presume the
exact nature of these sessions, carried out at a critical time in Lizzie’s life, but it could be
argued that this was an opportunity missed.
8.7.5 Suicidal Behaviour

‘Is there any point to which you would wish to draw my attention?’
‘To the curious incident of the dog in the night-time.’
‘The dog did nothing in the night-time.’
‘That was the curious incident,’ remarked Sherlock Holmes.
This is the famous passage from Silver Blaze, the short story by Arthur Conan Doyle,
1892. The curious incident that should attract our attention in Lizzie’s life is the complete
absence of both suicidal thinking (found in our repeated assessments over 30 years) and
suicidal behaviour in her story. This might be thought to be unusual, not least as such
behaviour is described as a very frequent consequence, some claim a uniform one, of sexual
abuse and its ‘borderline’ sequelae. But because no element of suicidality was shown, despite
massive mental suffering, it deserves analysis. We have several clues in Lizzie’s story. She
never lost hope, she maintained optimism in adversity, and, perhaps most importantly, her
creative juices were always active. What her creativity and optimism illustrate were her
personality strengths. When these are lacking, suicidal behaviour is more common (see
Table 7.10) but because Lizzie had elements of all five of the personality strengths identified
in Chapter 7 – forcefulness, emotional toughness, cautiousness, independence, and discern-
ment – she never became completely overwhelmed by the disasters that surrounded her.
In this respect, we can see common elements in Lizzie and Jane Austen’s Mrs
Bennet. Both showed determination and strength in their core beliefs; both stood up
to a great deal of strain, especially within the family; both had a long-term strategy that
was never lost; and, in both cases, their persistence to follow their dreams was not idle
fantasy, but a constant awareness that others could be brought on board and, in time,
support them.
So here we find some positive aspects of the term ‘neurosis’. The people who show these
features in their personal and medical interactions are not weaklings who creep about under
the strong legs of others. They, often as a consequence of adversity, have inner toughness
that may need to be harnessed in therapy.
Because we have generally ignored the nature of Galenic syndromes like the general
neurotic syndrome, we are almost starting from scratch in determining a way forward. But

we have clues. If the findings of the Nottingham Study are confirmed in other populations, it
will be necessary for NICE (National Institute of Health and Care Excellence) and other
bodies to provide guidance for the management of cothymia and associated personality
disturbance.
I end this book by prematurely giving some advice to NICE in this task, in which I will
return to the new definition of neurosis in its rightful place as a Galenic syndrome. In so
doing, I will use the clumsy but cleverly ambiguous text common to NICE documents that is
always necessary when there are elements of uncertainty:
(1) People with neurosis should never be excluded from services or dismissed as
untreatable.
(2) It is necessary to provide autonomy and choice, working in partnership with those who
have neurosis, taking account of their own preferences in treatment, and allowing them
to make their own decisions about managing their condition, which may be a long-
term one.
(3) Develop an optimistic and trusting relationship with those with neurosis, exploring all
their personality strengths in addition to helping with immediate symptoms.
(4) Always bear in mind when providing services for neurosis that many people will have
experienced deprivation, rejection, abuse, and trauma in the past, and while their
experiences are sometimes the butt of jocular amusement, casual dismissal, or passive
acceptance, these people have been subject to considerable suffering and should always
be respected.
(5) Community mental health services should carry out a full review of all patients with
neurosis at least annually, examining what progress has been made and what new
interventions might be needed and implemented.
(6) Long-term psychotropic medication should be reviewed carefully as there is little
evidence that it provides continuing benefit, but nonetheless accept that a minority of
patients may give cogent reasons for its value.
(7) Attention should always be paid to changes in life style and environmental adjustments
as many people with neurosis may experience positive change when placed in different
settings or altering their life priorities. This discussion should always be carried out in
a collaborative fashion with any decisions to change being supported and embraced
fully by the person concerned, not forced externally by a therapist.
I could add more here but it might be indulging too much in speculation. Still, I like to
think that if Mrs Bennet was presented with this advice today, not only she but the Lizzies of
this world, would all be pleased. They might all choose to go off in entirely different
directions if the treatment known as Adaptive and Acceptance Therapy (AAT) (Tyrer,
2021, pp. 97–99) was developed in a personal way. Adaptive and Acceptance Therapy is an
extension of nidotherapy, a collaborative treatment in which the patient makes the major
decisions with the help of the therapist and which has at its theme, ‘find content in the
environment’. (The aim is to find the best possible adaptation of the personality to the
setting). Once this has been achieved, or even if it has failed and the best environment has
not been found, the process of acceptance takes place and the person is asked to look at the
advantages of what at first appears to be an unattractive position.
So in Lizzie’s and in Mrs Bennet’s case we are not offering anything approaching a cure
or even a major resolution of their symptoms. Lizzie is now settled with a clear path ahead
but will continue to need some support. As for Mrs Bennet, one hopes that with two of her

100 Neurosis
daughters settled in matrimony with two husbands ‘in possession of a small fortune’ she
might be more satisfied with the results of her endeavours. But of course, she will not be
until the future of Longbourn is assured, and she still has three rather silly daughters yet to
develop skills to enter early nineteenth-century society. By improving the balance in the
household between Mr Bennet and herself, she could make some progress, and in time could
develop a space for herself to carry out what she would like to do, indulging in herself rather
than perpetually worrying about what others are doing or not doing.
She need not be a candle blowing in the wind, instead, an established matriarch with
others admiring her ability to act as a marriage broker, even though such a title may be
partly undeserved. She is a resourceful woman and I have no doubt she could persuade one
of her daughters and a husband to come to live in Longbourn and deflect the odious Mr
Collins from his intention to purchase the property. She could retire to separate quarters
and appear from time to time to deliver her nuggets of advice to those who are still prepared
to hear. And I am sure she would make an excellent grandmother as she is so good at telling
stories. She might even create one about her own life, showing that for some the possession
of neurosis can be a proud exemplar of success.

Appendix
Personality Assessment Schedule
(Tyrer & Alexander, 1979)
(Bona fide researchers can use this instrument without the need for formal permission, but
are advised to test it out for agreement first in order to understand its scope and scoring
range.)
Personality Assessment Schedule (PAS) – Original version (Tyrer & Alexander, 1979)
This schedule is designed to formalise the assessment of personality disorder and may be used
with any subject irrespective of psychiatric status. The way in which the schedule is used will
depend on the current mental state of the patient and an assessment of this is a necessary
precursor to the personality ratings. It is recommended that the screening schedule of the
Present State Examination or SCID (Structured Clinical interview for DSM-III) be used for
the mental state examination, but, if this is not possible, sufficient information should be
obtained from the history and examination to make a diagnostic formulation of any psychi-
atric problems, which should be recorded on the assessment form. If this is not carried out,
there is a danger that the personality ratings will be contaminated by the mental state.
There are 24 personality variables to be assessed in the schedule. Each of these can be
rated by interview with the subject or interview with an informant.
An interview with an informant is desirable in all cases. The interview with the subject is
not necessary if he or she is unable to give coherent answers to questions because of gross
abnormalities in mental state; the interview with the informant indicates that there has been
a marked qualitative change in the subject’s personality so that replies to questions about
past personality are unlikely to be correct; or the subject displays severe memory disturb-
ance, whether of organic or psychological origin, and is unable to recall aspects of his or her
premorbid state. If an interview with an informant is not possible, additional independent
information about personality may be obtained from other sources (e.g., general practi-
tioner, social worker, probation officer), if this information is considered valid. If several
informants are available, the final score can be a composite of those in which the most
reliable informant carried the greatest weight.
Use of the Schedule

(1) The initial questions for each personality variable are obligatory. The questions
preceded by an asterisk are amplifying questions which may be asked in response to the
subject’s initial reply. The questions in brackets are direct closed questions which may
be asked if replies to other questions have been evasive, contradictory, or vague.
Although the questions are confined to a specific personality variable, there is
sometimes overlap with other variables. It may therefore be necessary to re-rate the
variable later in the interview.
101

102 Appendix
(2) Ratings of severity: The ratings are made on a nine-point scale for all variables. The
number is recorded in the appropriate box at the side of each item or an accompanying
sheet. The scale is specifically designed to record abnormal personality traits and most
normal variation will occur between scores 0 and 3. The greater the severity of the trait,
the greater will be the rating. In addition to the specific points mentioned for each scale,
the following general principles should be used to determine the score for a particular
trait. (The word trait is synonymous with personality variable in this account, although
it is less often used for severe personality disturbance).
0 Trait absent. Presence of the trait is undetected both in respect of feelings and of
behaviour.
1 Subject recognises the presence of the trait but it is shown chiefly in terms of
feelings rather than behaviour. When the trait does affect behaviour, it is not
a habitual response so much as a tendency to indulge more in that type of
behaviour when several choices are open. Knowledge of how the subject spends
spare time may help with this rating, as it is in spare-time activities that the
element of choice is most obviously shown. (An informant is unlikely to make
a distinction between 0 and 1 ratings.)
2 Personality trait is definitely present and affects behaviour, but only to a limited
extent. It is not associated with problems in occupational, social, and interpersonal
life. The changes in behaviour produced by the trait are such that those close to the
subject will notice them but most friends and acquaintances would not.
3 The personality trait markedly affects feelings and behaviour. The presence of the
trait may be noticed by others who are not closely related to the subject and may
occasionally give rise to the problems in occupational, social, and interpersonal
life. However, these problems will seldom be persistent and those around the
subject can normally accommodate to them without much difficulty.
4 The personality trait is marked and is apparent to the subject and to most people
who have frequent contact with the subject. The trait produces some difficulties in
occupational, social, and interpersonal adjustment and this tends to be of a mild
but persistent nature.
5 The personality trait is marked to both the subject and most people who come into
contact with the subject. It has a marked influence on behaviour and leads to
problems in occupational, social, and interpersonal relationships. This rating
differs from 4 in that the problems lead to more serious difficulties in adjustment
in society and marked underachievement (e.g., inability to settle in one job, refusal
to meet people, episodic aggression).
6 Personality trait has a major influence on behaviour and tends to affect all aspects
of life. The problems in occupational, social, and interpersonal relationships are
such that major breakdown occurs (e.g., divorce, social isolation, prolonged
unemployment), as a direct result of the personality abnormality.
7 The personality trait is so marked that it is noticed by almost all who come in
contact with the subject, even those who only see the subject once. Independent life
in the community is impossible because of the severity in occupational, social, and
interpersonal relationships so some form of supervision or continuous support is
necessary.

Appendix 103
8 The personality trait dominates behaviour completely (therefore it cannot be given

to more than one rating in the schedule). The disturbance produced by the trait is
so marked that prolonged periods of institutional care (e.g., hospital, prison,
nursing home) take up a large part of the subject’s life history in the absence of any
formal illness.
Note: most normal variation is accounted for between the ratings of 0 and 3. Only a small
number of individuals rate higher scores than 3. The key issues in deciding whether a score
of more than 3 is justified are as follows:
(a) The production of problems in daily living because of the severity of the trait.
(b) The suffering and underachievement that the trait produces.
(c) The inability of those around the subject to deal with these problems without asking for
additional (often professional) help.
An informant’s information is primarily of value for ratings of 3 and upwards. A reliable
subject is best fitted to rate lower ratings as these have little or no persistent effect on
behaviour.
In all instances of abnormal personality traits, try and get the subject or informant to
provide examples of the problems produced by the trait.
Assess the reliability of the subjects’ and informants’ replies at the end of the interview
and score on the nine-point scale. Wherever the informants’ and subjects’ ratings for an
item differ by three or more points, ask further questions and, where possible, obtain
independent information about the trait in question.
Additional Notes on PAS

Procedure for Scoring
It will be noticed on the final scoring sheet there is a space for ‘the final score’. If the reliability
of the informant’s ratings is considered to be greater than or equal to the subject’s ratings, the
final score will normally consist of the informant’s ratings alone. If, however, the difference
between informant’s and subject’s ratings for a personality attribute is greater than two
points, it is advisable to ask further questions to establish the reasons for the discrepancy,
possibly with both informant and subject present together. On an individual item it may also
be considered that the subject’s ratings are more reliable than those of the informant even
though the rest of the ratings may be more accurately determined by the informant. In such
instances the scoring may more closely approximate to the subject’s ratings for that item.
If the subject’s ratings are to be considered more reliable than those of the informant
(which is particularly likely if the informant is not a close relative and has only known the
subject for a limited period), the subject’s ratings will take greater precedence in the final
scoring. However, any informant rating that is greater than 3 must be carefully followed up
by further questioning if it significantly disagrees with that of the subject. This is because
any abnormal behaviour as a consequence of the personality attribute is likely to be more
accurately detected by the informant than by the subject.
If the informant is not available, the subject’s ratings alone can be used although this is
much less satisfactory than having the informant’s ratings also. If the subject’s ratings are to
be used, as much independent information as possible about premorbid personality is
needed to corroborate the subject’s ratings. This may be possible from past medical or
social records but recording of major life events (see Useful Facts, p. 143) may be useful.

104 Appendix
This is administered before the PAS, preferably with other independent information as well,
and any relevant positive findings introduced at the appropriate point in the PAS when this
is administered subsequently. The subject will then have to explain the reasons for the
apparently abnormal behaviour and, if the abnormality is judged to be related to
a personality attribute, it will be scored appropriately. The additional schedule therefore
serves in some way as a lie schedule.
When scoring each rating, use the notes below each personality trait for guidance only.
The scoring should follow the principles outlined in the Use of Schedule section pages 133
and 134 for all traits.
Comparison of Scores in Different Subgroups of Patients
The individual scores for personality attributes can be compared separately by the usual
statistical methods.
Useful Facts
Sometimes both subjects and informants have a distorted impression of previous personal-
ity and make it sound more favourable than it really was. The rater therefore needs as much
information as possible about the patient’s past experience so that this can be introduced
into the questioning at relevant points in the interview. Here follows a list of some of the
important events that are frequently affected by personality characteristics. The rater should
have information about these events, preferably obtained independently, before the inter-
view. If this is not possible, questions should be put to both subject and informant during
the interview. It would be wrong to assume that any of these events are necessarily
associated with personality abnormality but they are useful anchor points around which
questions about personality can be asked. If there are serious discrepancies between
independent evidence of these events and the subject’s or informant’s responses, the rater
should resolve these before making a final score for that personality item. As in other parts
of the schedule, independently derived information is given greater weight when making
this decision.
(1) Marital relationship. If unmarried, has the subject ever cohabited? If married or
divorced, how many times have the couple separated for any reason during marriage?
(2) Child care. Have there been any problems with the children of the patient? Have any
children been involved with the police or official agencies and have they ever been in
care?
(3) Has the subject ever been in debt. What were the circumstances?
(4) Employment. How many jobs has the subject had since leaving school? What were the
circumstances of leaving these jobs? Was the subject ever sacked from a job or did they
leave because of problems with colleagues?
(5) Legal. Has the subject ever been convicted of an offence? If so, what was the offence and
outcome?
(6) Alcohol. Does the subject drink, take illegal drugs, or gamble? If so, have any problems
arisen as a consequence of these activities?
(7) Housing. How many addresses has the subject had in the last 10 years? What were the
reasons for moving? Has the subject ever been homeless?
(8) Adolescent problems. Did the subject have any problems when attending school after
the age of 11? If so, what was the outcome?

Appendix 105
Interview Procedure
It is helpful to have a checklist of ratings of severity for each personality trait and the
aforementioned eight-point Useful Facts section when interviewing the patient or inform-
ant. These are appended and may be detached for ease of reference when interviewing. The
list of facts may be completed after the interview if necessary.
Subject
I am going to ask you some questions about the type of person you are normally.
*I am trying to find out what you were like before your present problems began.
In answering these questions, I would therefore like you to think about your personality as it
has been throughout your life. I am going to ask you some more questions about this but
first of all how would you describe your personality in a few words? (Note main features and
record on sheet at end of schedule).
Informant
I am going to ask you some questions about the type of person S is normally.
*I am trying to find out what S was like before his/her present problems began.
In answering these questions, I would therefore like you to think about S’s personality as it
has been throughout his/her life. I am going to ask you some more questions about this but
first of all how would you describe S’s personality in a few words? (Note main features and
record on sheet at end of schedule).
1 Pessimism
Subject
Do you get depressed easily or are you reasonably cheerful?
Are you pessimistic or optimistic about the future or do you just take it as it comes?
(1)
*Have you always felt depressed and low spirited, or has this only happened recently?
*Do other people notice it? (Give examples)
(Has this affected you at work, at home and with friends? In what way?)
(Have you ever thought seriously about suicide?)
Further questions may be needed to separate episodes of depressive illness from persistent
depressive attitudes and behaviour.
Informant
Does S get depressed easily or is he/she reasonably cheerful?

106 Appendix
Is he/she pessimistic or optimistic about the future or does he/she just take
it as it comes?
(2)
*Has S always felt depressed and low spirited or has this only happened recently?
*Does S appear gloomy to other people?
(Has this affected him/her at work, at home and with friends? In what way?)
(Do people avoid S because he/she is so miserable?)
Subject/Informant
Note Ratings 1–3 A pessimistic outlook on life with no effect on behaviour.
Ratings 4–6 Depressive behaviour including social withdrawal and morbid depression
to the extent that others notice and are affected by the behaviour.
Ratings 7–8 Persistent pessimism and depressive behaviour with almost complete
withdrawal and isolation.
Ratings of 5 and above are only justified when depressive feelings and behaviour,
associated with hopelessness about the future, are present or have been present in the
absence of formal psychiatric illness. Do not include recurrent depressive illness in this
category unless the personality between episodes is also abnormal or there is evidence that
S has been clinically depressed all his/her life. Short periods of pessimism or depressed
feelings of less than two weeks should be regarded as evidence of lability of mood rather than
evidence of abnormal pessimism. If in doubt, delay rating until lability trait scored.
2 Worthlessness
Subject
How do you think of yourself in relation to other people? Do you feel better, worse, or about the
same?
(3)
*Do you feel inferior to others? In what way? For how long?
*How does it affect you?
(Have you always felt like this or only just recently?)
*Do you think your like would have been different if you did not feel inferior to others? In
what way?
(Do you feel useless or worthless most of the time?)
(Have you ever thought you deserved more out of life?)
(How would you feel if you were promoted at work?)

Appendix 107
Informant
How does S think of himself/herself in relation to other people?

Does he/she feel better, worse, or about the same?
(4)
*Does he/she feel inferior to others?

*Do others notice this?
(Has he/she always felt like this or only just recently?)
*Does he/she think his/her life would have been different if he/she did not feel inferior to
others? In what way?
(Does S feel useless or worthless most of the time?)
Subject/Informant
Note Ratings 1–3 Mild feelings of inferiority, fully compensated and not
obviously apparent to others.
Ratings 4–6 Strong feelings of inferiority, affecting behaviour. Subject will not do
things he/she is capable of because of abnormally low self-esteem. At
least some impairment at work and social adjustment.
Ratings 7–8 Strong feelings of inferiority amounting to worthlessness. Because of
those feelings subject requires continuous reassurance and support.
Not able to work regularly or make any useful relationship.
Do not confuse worthlessness with depression although the two often coexist.
3 Optimism
Subject
I asked earlier whether you were normally a cheerful person. (Refer to answer)
(5)
*Are you more or less cheerful than most other people?

Have you always felt very cheerful no matter what has been happening in your life?
*Sometimes cheerfulness and overconfidence can lead to difficulties in life, such as over-
spending or making plans to do something which cannot succeed. Is this true of you?
*Would you describe yourself as too optimistic? (Examples of problems associated with
optimism.)

108 Appendix
*Have you any special abilities that make you feel optimistic and successful?
(Have you ever been in debt or got into trouble in any way because of overconfidence?)
Exclude problems associated with irresponsibility or childishness.
Informant
I asked earlier whether S was normally a cheerful person. Do you think of S as cheerful?
Would others describe him/her as cheerful? Has S always felt very cheerful no matter what
has been happening in his/her life?
(6)
*Sometimes even cheerfulness can lead to difficulties in life, such as overspending or making
plans to do something which cannot succeed.
*Would you describe S as too optimistic? (Examples of problems associated with optimism.)
*Does S think of himself/herself as a special person who is bound to succeed?
(Has S ever been in debt or got into trouble in any way because of overconfidence?)
Subject/Informant
Note Ratings 1–3 Subject is more cheerful than most others and is capable of
communicating his/her cheerfulness to them.
Ratings 4–6 Over-cheerfulness leads to unrealistic ambitions and aspirations,
including overspending, overconfidence and impaired judgement, so
subject may be sacked from work or be in serious debt. Subject
remains optimistic and self-important in spite of these problems.
Ratings 7–8 Breakdown in relationships, inability to maintain stability in any aspect
of social, occupational, or interpersonal life because of abnormal
cheerfulness, over-optimism and self-importance.
To merit a high rating, the optimism has to be more or less continuous and not part of
the manic phase of manic-depressive illness. Short periods of abnormal optimism of less
than two weeks should be regarded as evidence of lability of mood rather than evidence of
abnormal optimism. If in doubt, delay rating till lability trait is scored.
4 Lability
Subject
Do your spirits} change from day to day or week to week, or do they/does it remain
more or less the same?
Does your mood}
(7)

Appendix 109
*Are these changes connected with what is going on in your life or are they separate?
*How long do they last?
*Do they lead to problems?
(Can you predict your changes in mood?)
(How often do you laugh or cry?)
Informant
Does S’s mood change from day to day or week to week, or does it remain more or less the
same?
(8)
*Are these changes connected with what is going on in his/her life or are they independent?
*How long do they last?
*Do other people notice these changes? Do they lead to problems?
(Is S unpredictable because of these sudden changes in mood?)
(How often does he/she laugh and cry?)
(Do you ever feel that he/she can turn these feelings on when he/she wants?)
Subject/Informant
Note Ratings 1–3 A tendency towards mild exaggeration of mood swings in response to life
changes.
Ratings 4–6 Marked lability, noticeable to others and leading to problems because of
strength of mood swings. Most mood changes responsive to life events but
may be independent. Unpredictability of subject’s behaviour because of mood
change also a source of difficulties.
Ratings 7–8 Breakdown in social, occupational, and personal relationship because of
abnormal swings in mood. In these instances, it would be more likely that the
changes are independent of life events so that they cannot be manipulated in
any way. What is known as ‘cyclothymia’ will be included here if the swings in
mood occur at least as frequently as once every two weeks. If they occur less
frequently than this, but still produce important personality problems, then the
relevant rating should be included under the pessimism and optimism scales.
5 Anxiousness
Subject
Are you normally an anxious or a calm person?
When things go wrong in your life (e.g., illness in family, accident) do you get more nervous,
the same, or less nervous than most people?
(9)

110 Appendix
*Do you ever worry about things that most people would not be concerned about?
(Give examples)
*Do you show your nervousness to other people or do you cover it up?
*Have you always been an anxious person?
(Do you worry about something or someone most of the time?)
(Has your anxiety ever led to problems?) (Specify)
Informant
Is S normally an anxious or calm person?
When things go wrong in his/her life (e.g., illness in family, accident) does he/she get more
nervous, the same, or less nervous than most people?
(10)
*Does S ever worry about things that most people would not be concerned about?
(Give examples)
*Do other people notice that S is an anxious person or does he/she keep it to himself/herself?
*How has this worrying affected S?
(Does S worry about something or someone most of the time?)
Subject/Informant
Note Ratings 1–3 Mild anxiety-proneness which is normally suppressed so that
others are not aware of it.
Ratings 4–6 Anxiety noticeable to others, leading to changes in behaviour.
Ratings 7–8 Frequent or continuous free-floating anxiety of such severity
that breakdown in social adjustment occurs.
Life-long phobic anxiety may contribute to this rating but the severity of the rating
would depend on the same categories mentioned in the outline to scoring (i.e., it is the
extent to which it interferes with personal and social adjustment that determines the rating).
6 Suspiciousness
Subject
How well, in general, do you get on with other people?
Do you normally trust them or are you suspicious of them, at least at first?
How long does it take for you to get to know people before you will trust them?
(11)

Appendix 111
*Do you tend to worry about what is going on behind your back?
*Do you ever think that other people might be against you or criticise you unfairly?
(Have you many friends?)
(Are you worried in case someone might find out what you have been saying to me?)
Informant
How well, in general, does S get on with other people?
Does S normally trust them or is he/she suspicious of them, at least at first?
How long does it take for him/her to get to know people before he/she will trust
them?
(12)
* Would you say that S is a suspicious person?

* Does he/she have many friends? (If no) Is this because he/she will not trust anybody?
*Is S a jealous person?
Subject/Informant
Note Ratings 1–3 Mild feelings of suspiciousness, not noticed by others. Subject tends
to have relatively few friends but is capable of close relationships and
will trust those he/she knows well.
Ratings 4–6 Problems in social adjustment because of abnormal suspiciousness.
Takes a very long time to get to know people and only trusts a very
small number of people. Feels that others criticise him/her without
adequate cause.
Ratings 7–8 Breakdown in relationships and social adjustment because of
abnormal suspiciousness. At extreme ratings, the patient is
completely isolated because he/she feels all are against him/her.
7 Introspection
Subject
Do you think a great deal about how you feel and what you do or do you think about them very
little?
Do you prefer being on your own to being with other people?
(13)
*Are you a person who spends a lot of time thinking? (If yes) What about?
*Are you an introvert?
*Are you like this all the time or only when there is a problem on your mind?

112 Appendix
Informant
Does S think a great deal about how he/she feels and what he/she does or does he/she think
about them very little?
Does S prefer being alone to being with other people?
(14)
*Is S an introvert?
*Is S completely bound up in himself/herself? How often?
*Does S appear to live in a world of his/her own?
*How does this affect his/her relationship with other people?
*Do other people notice that S is like this?
Subject/Informant
Note Ratings 1–3 Mild introspection and introversion, not noticeable to others.
Ratings 4–6 Problems in adjustment because of excessive rumination and
introspection, often with a tendency to indulge in fantasy. These feelings
may lead to problems by indecision, impaired judgement, and poor
relationships.
Ratings 7–8 Completely bound up in self to the exclusion of other matters, indulges in
much fantasy. Self-neglect frequent.
8 Shyness
Subject
Are you normally a shy person or are you confident with other people?
Do you get to know people quickly or do you take a long time before feeling at ease with them?
Do you lack self-confidence?
(15)
*Do you ever go out of your way to avoid people because of shyness?
*Do you have difficulty in making friends because you are shy?
*Would you like to feel more at ease with people? Has shyness caused problems for you?
(Do you feel uncomfortable even in the presence of friends?)
(Are you feeling shy or uncomfortable now?)
Informant
Does S get to know people quickly or does he/she take a long time before feeling at ease with
them?
Is S normally a shy person or does he/she have no difficulty getting on with people?

Appendix 113
Is S a self-confident person?
(16)
*Does he/she ever go out of his/her way to avoid people because of shyness?
*Does S have difficulty in making friends because S is shy?
*Do other people notice that S is shy?
*Has shyness caused problems for S?
(Does S feel uncomfortable even in the presence of friends?)
Subject/Informant
Note Ratings 1–3 Mild shyness, but this is compensated and others do not notice it.
Ratings 4–6 Excessive shyness and lack of self-confidence leading to avoidance of
people and personal discomfort when with people.
Ratings 7–8 Subject unable to work adequately or make relationships because of
symptoms. In severe cases may be completely isolated.
It is important to exclude natural aloofness and detachment from shyness – the former
group are not distressed in the company of other people; shyness is always associated with
some feelings of anxiety.
9 Aloofness
Subject
Are you a person who likes to stay apart from other people or do you like to have close
relationships?
Have you any really close relationships? (If no, does this bother you?) (17)
Do you need people in any way or can you do without them?

(Would you mind living entirely on your own without any contact with other people?)
(Do others ever say you are stand-offish or aloof?)
Informant
Is S an isolated/aloof person who likes to stay apart from other people or does he/she like to
have close relationships?
Has he/she any really close relationships?
(18)
*Does S ever appear stand-offish or detached to other people?

*Is S happier when he/she is on his/her own?

114 Appendix
(Do other people tend to stay apart from S?)

(Has this tendency to be aloof led to any problems in S’s life?)
Subject/Informant
Note Ratings 1–3 Mild detachment leading to a reluctance to be involved in close
relationships. Not noticeable to others, and adequate relationships
made with close friends and relatives.
Ratings 4–6 Abnormal aloofness noticeable to others and leading to problems in
social adjustment, mainly in interpersonal relationships.
Ratings 7–8 Excessive detachment and lack of interest in other people. No close
relationships. Indifference to other people’s feelings and opinions.
Lack of interest in other people is unrelated to shyness or psychiatric symptomatology
such as social fears. Subject does not feel distressed with other people and merely has no
interest in them.
10 Sensitivity
Subject
Are you a {touchy/sensitive} person or does it take a lot to upset you?
How do you react to criticism? (Give examples)
(19)
*Do people ever say you are too touchy?

*How long does it take for you to get over criticism?
(Have any of my questions upset or disturbed you in any way?)
(Do you tend to take things personally?)
Informant
Is S a {touchy/sensitive} person or does it take a lot to upset him/her?

How does S react to criticism? (Give examples)
(20)
*Have people got to be careful what they say to S in order not to upset him/her?
*Do people ever say S is too touchy?
*Does he/she take a long time to get over criticism?
(Has this sensitivity led to problems in S’s relationships with others?)

Appendix 115
Subject/Informant
Note Ratings 1–3 Mild sensitivity. May be upset easily but does not show it except to close
friends and relatives.
Ratings 4–6 Excessive personal sensitivity with a tendency to self-reference (e.g., feels
people are being critical when they are not). This leads to problems in
social adjustment (e.g., frequent changes of job, broken relationships).
Ratings 7–8 Excessive sensitivity leads to breakdown in social performance. Extreme
tendency to self-reference.
Sensitivity to the feelings of others is not an abnormal phenomenon and should not be
included in this rating. This rating is concerned with personal sensitivity and touchiness. If
in doubt about this rating, delay till ratings of vulnerability and irritability are made. Also
differentiate between sensitivity and suspiciousness. Although the two may overlap, sensi-
tivity leads to emotional distress whereas suspiciousness is usually independent and may
frequently be prominent in insensitive people.
11 Vulnerability
Subject
Do you find that when things go wrong in your life it disturbs you a great deal or do you
remain on an even keel?
Does it take you a short time or a long time to get back to normal after some mishap (e.g.,
illness in family, accident, loss of job)?
(21)
(How do you think you would cope with a crisis such as death in the family, car accident or
loss of your job?)
Informant
Does S find that when things go wrong in his/her life it disturbs him/her a great deal or does
he/she remain on an even keel?
Does it take S a short time or a long time to get back to normal after some mishap (e.g.,
illness in the family, accident, loss of job)?
(22)
*Does S need to be protected from unpleasant things because others know he/she will take
them very badly? (If yes) Could you give an example?
*Are other people aware that S is vulnerable? How do they show it?
(Do you protect S from unpleasant events?)

116 Appendix
Subject/Informant
Note Ratings 1–3 Reacts more than most to adversity but does not show these feelings
to others.
Ratings 4–6 Abnormally vulnerable, reacts excessively to adversity, so leading to
social maladjustment for a prolonged period. Eventually, however,
more normal functioning is resumed until the next adverse episode.
Ratings 7–8 Subject vulnerable to even the minor stresses of life to which he/she
reacts as though they were major problems. Breakdown in social
adjustment because of this.
It is important to separate vulnerability from sensitivity and resourcelessness. Although
all three may be present in one individual, the characteristics are separate. The sensitive
person is touchy and reacts easily to implied criticism, the vulnerable person reacts to major
life events by feelings of distress which may take a long time to resolve and are not
commonly associated with compensatory action, and the resourceless person reacts to
adversity by not coping and just giving up. When assessing vulnerability, do not include
sensitivity and resourcelessness.
12 Irritability
Subject
Are you an irritable or a placid person?
Are you impatient at times? Under what kind of circumstances?
How do you show it?
(23)
*Do you keep it to yourself or do other people notice that you are impatient and
irritable?
*Does this lead to problems in your relationships with other people?
(When was the last time you were really irritable?)
(How did you show this?)
Informant
Is S an irritable or a placid person?
Is he/she impatient at times? Under what kind of circumstances?
How does he/she show it? (24)
*Does he/she keep it to himself/herself or do other people notice that S is impatient and
irritable?
*Does this lead to problems in S’s relationships with other people? (Specify)

Appendix 117
Subject/Informant
Note Ratings 1–3 Mild irritability, kept under control.
Ratings 4–6 Abnormally irritable. Leading to social adjustment problems (e.g.,
poor relationships with others).
Ratings 7–8 Severe irritability, making it very difficult for subject to make adequate
relationships with others. Inability of the subject to cope in any
environment which involves sudden changes because of severe
irritability.
In making this rating, impulsiveness and aggression should be excluded. An impulsive

act is followed by regret. Irritability is largely shown in verbal responses and does not
include physical violence, which should be scored under aggression. ‘Passive-aggressive’
features may be included here if the irritability leads to procrastination, obstruction, and
delay in completing tasks.
13 Impulsiveness
Subject
Do you always think carefully before you do something or do you act on impulse?
(25)
*Have you ever done things on impulse and regretted them afterwards? (Give examples)
*Have to ever been in trouble because you are impulsive? (Give examples)
*When you have been impulsive has it ever harmed other people?
If the ‘Useful Facts’ section (p. 143) suggests impulsivity is a problem (e.g., criminal
offences), mention them here if subject answers negatively.
Informant
Does S think carefully before he/she does something or does he/she act on impulse?
(26)
*Does he/she ever do things on impulse and regret it afterwards?

*Has S ever been in trouble because he/she is impulsive? (Give examples)
*Has his/her impulsiveness ever harmed other people?
(Has S had problems with drugs or drink because he/she is impulsive?)

118 Appendix
Subject/Informant
Note Ratings 1–3 Mild impulsiveness, not noticeable to others, causing no problems in
social adjustment.
Ratings 4–6 Impulsiveness associated with regret which has led to problems of
social adjustment (e.g., loss of job).
Ratings 7–8 Frequent impulsiveness leading to criminal behaviour and/or
breakdown in social functioning throughout adult life.
As impulsiveness may sometimes be associated with aggression, this rating may be
delayed until aggression is assessed.
14 Aggression
Subject
Do you lose your temper easily or does it take a lot to make you angry?
When you get angry how do you show it?
(27)
*Have you ever lost control completely?

*Are you normally like this or only on certain occasions (e.g., after heavy drinking)?
(Do you ever react by physical violence?)
(Have you ever been in trouble with the law?)
Informant
Does S get angry easily or is he/she generally placid?
When S does get angry how does he/she show it?
(28)
* Has he/she ever lost control completely?

* Is he/she normally like this or only on certain occasions (e.g., after heavy drinking)?
* How do other people react to S’s violence? What problems does it cause?
(Does he/she ever react by physical violence or does he/she keep it to himself/herself?)
(Has S ever been in trouble with police/law?)

Appendix 119
Subject/Informant
Note Ratings 1–3 Anger and aggression felt frequently but kept to himself/herself.
Ratings 4–6 Aggression abnormal and leads to social difficulties (e.g., trouble with
police), and violence at home. Do not rate criminal offences here
unless they are a direct consequence of aggressiveness.
Ratings 7–8 Breakdown of social adjustment with long history of antisocial
behaviour, usually with criminal record.
15 Callousness
Subject
Are you easily affected by other people’s feelings or can you ignore them?
(29)
* Do you care much about other people? (Do you care at all?)
(Do you find it difficult to sympathise with and understand other people’s feelings?)
(Have you ever enjoyed hurting other people?)
Informant
Is S easily affected by other people’s feelings or can S ignore them?
(30)
*Does S care much about other people?

Does S find it difficult to sympathise with and understand other people’s feelings?
*Does he/she ever appear to get pleasure from hurting people in any way?
*How does this affect his/her relationships with other people?
(Has he/she ever hurt people (physically or mentally) deliberately?)
(Give examples)
(Is S callous or sadistic?)
Subject/Informant
Note Ratings 1–3 Mild insensitivity and indifference to others feelings.
Ratings 4–6 Cold and indifferent to the extent that S is only capable of a few
relationships, and these are rarely close.
Ratings 7–8 Marked callousness with or without sadistic behaviour, leading to
breakdown in social functioning and frequent criminal involvement.

120 Appendix
16 Irresponsibility
Subject
Do you ever do things without caring about the consequences or are you always careful in
what you do?
Would you describe yourself as a responsible or an irresponsible person?
(31)
Do you ever get into serious difficulties because of irresponsibility (e.g., into debt, criminal
acts, sexual difficulties)? How has irresponsibility affected your life? (Give examples). Bring
up any information derived from the section ‘Useful facts’ if negative answers given but past
history suggests irresponsibility.
Informant
Does S ever do things without caring about the consequences or is S always careful in what
he/she does?
Would you describe S as a responsible or an irresponsible person?
(32)
*Does he/she ever get into serious difficulties because of irresponsibility (e.g., into debt,
criminal acts, sexual difficulties)?
*How does this affect his/her relationships with others? How has irresponsibility affected
his/her life? Has it caused serious problems?
Subject/Informant
Note Ratings 1–3 Mildly irresponsible, feelings kept under control, not noticed by
others or, if manifest, not causing real problems.
Ratings 4–6 Highly irresponsible, takes risks repeatedly, problems in social
adjustment (e.g., in debt, frequent accidents, unwanted
pregnancies). Do not rate criminal offences automatically unless
they stem from irresponsibility.
Ratings 7–8 Irresponsibility so great that S needs to be constantly supervised and
cannot live independently because of this.
17 Childishness
Subject
Do you ever act in a childish way or would you regard yourself as fairly mature?
Do you ever manipulate people to get your own way?
(33)

Appendix 121
*Do you like being the centre of attention?

*Have you ever acted selfishly, only thinking of yourself?
(Has this led to problems?)
Informant
Does S ever act in childish ways or would you regard him/her as fairly mature?
Does he/she ever manipulate people to get his/her own way?
Has this ever led to problems?
(34)
*Is S a selfish person who only cares about himself/herself?

*Does he/she appear to be younger than his/her years?
*Does he/she like being the centre of attention?
(How does this affect his/her relationships with others?)
(Has he/she any mature relationships?)
(Do other people tend to treat S as a child?)
Subject/Informant
Note Ratings 1–3 Self-centred attitudes with occasional childish behaviour but this is
seldom noticeable to others.
Ratings 4–6 Immature behaviour and marked selfishness leading to social
adjustment problems.
Ratings 7–8 Severe childishness, cannot live independently because of this. All
relationships involve others supervising or caring for S.
18 Resourcelessness
Subject
When you are faced with a challenge do you usually respond to it well or do you give in to it?
When there are problems in your life do you usually tackle them alone?
Are you somebody who can normally solve your own problems?
(35)
*How have you coped with major problems in the past? (Get examples)
(When was the last time you coped with a serious problem on your own?)
Informant
When S is faced with a challenge does he/she usually respond to it well or does he/she give in
to it?

122 Appendix
When there are problems in S’s life does he/she usually tackle them alone or does he/
she need help from others?
(36)
*Does S constantly need support to cope with life’s problems?

*How does this affect his/her relationships with others?
*How has S coped with major problems in the past?
Subject/Informant
Note Ratings 1–3 Copes with problems with some difficulty but does not involve others
to an unnecessary extent.
Ratings 4–6 Others involved in coping with S’s problems, impairing social
functioning. Frequent problems in work.
Ratings 7–8 Unable to cope with life’s practical difficulties without continuous
support. Not able to live independently because of this.
19 Dependence
Subject
Do you rely on other people a great deal or are you an independent person?
(37)
*Do you find it difficult to make up your mind without involving others?
*How would you like to live and/or work alone?
(Who do you depend on most?) (In what way?)
(Would you like to be less dependent?)
(Has your dependence led to problems in your relationships?)
Informant
Does S rely on other people a great deal or is he/she usually independent?

(38)
*Does he/she find it difficult to make up his/her mind without involving others?
*Do you think S could cope with living and/or working alone? What would happen?
(Do you think S is too dependent? On whom?)
(Does this lead to problems?) (Give examples)
(Has he/she always been like this?)

Appendix 123
Subject/Informant
Note Ratings 1–3 Some dependence in excessive need for advice and reassurance from
close relatives or friends but behaviour seldom abnormal.
Ratings 4–6 Excessive reliance on others, leading to social adjustment problems.
Ratings 7–8 Completely dependent on individual group or institution. Unable to
work or function independently at any level.
20 Submissiveness
Subject
Do you give in easily to others or do you stand up for yourself?
(39)
*Do you go along with decisions made by others even if you feel it is the wrong
decision?
*Do you prefer to avoid arguments?
*Do people ever take advantage of you? (Give examples)
(Are you easily dominated?)
(Do you wish you could stand up for yourself better?)
Informant
Does S give in easily to others or does he/she stand up for himself/herself?
(40)
*Does S go along with decisions made by others even if he/she feels they are the wrong
decisions?
*How does this affect relationships with others?
*Do people ever take advantage of S because they know he/she will not retaliate?
(Is S easily dominated?)
(Is he/she afraid to say what he/she really thinks?)
Subject/Informant
Note Ratings 1–3 Mild submissiveness and compliance, but stands firm on major issues.
Ratings 4–6 Very submissive, unwilling to express own views, is dominated in
most relationships.
Ratings 7–8 Gives in to everybody, no independent function, exploited by others.
Breakdown in social functioning.

124 Appendix
21 Conscientiousness
Subject
Are you normally a fussy or a carefree person?
Do you plan everything down to the last detail or do you seldom plan anything in
life?
(41)
*Do people ever say you are too fussy or conscientious, or even a perfectionist?
*Do you wish you were less conscientious?
*Are you a person with high standards?
*Does conscientiousness ever lead to problems in your life? (Specify)
(Did you worry that you might be late today?)
(If I had been late, would it have upset your routine?)
(Do you think you work harder than the average person?)
Informant
Is S normally a fussy or a carefree person?
Does he/she plan everything down to the last detail or does he/she seldom plan anything in
life?
(42)
*Do people ever say S is too fussy or conscientious, or even a perfectionist?

*How does this affect his/her relationships with others?
*Is he/she a person with high standards?
Subject/Informant
Note Ratings 1–3 Over-fussy and conscientious, preoccupied with routine and
excessively meticulous, but no social adjustment problems.
Ratings 4–6 Abnormal conscientiousness, plans excessively far ahead, adjustment
problems because of need for meticulous planning.
Ratings 7–8 Excessive conscientiousness accompanied by doubt. Unable to
achieve anything as the smallest of tasks becomes a major enterprise.
Unable to work or use leisure time, leads to interpersonal breakdown.
In severe cases subject will usually have many obsessional symptoms.
In making a rating do not include obsessional symptoms (i.e., symptoms which the
subject recognises to be silly and consciously tries to overcome), unless these are part of the
underlying personality of the subject. Also recognise that conscientiousness is thought to be
a favourable personality trait and may be exaggerated by S or informant.

Appendix 125
22 Rigidity
Subject
Do you find difficulty in adjusting to new situations or are you an adaptable person?
Do you get upset if your plans are changed for any reason or are you flexible?
(43)
*Can you adjust to others who act or feel differently from you (e.g., at work, with family)?
(Do you always have to have your own way?)
Informant
Does S find difficulty in adjusting to new situations or is he/she an adaptable person?
Does he/she get upset if his/her plans are changed for any reason or are they flexible?
(44)
*Can he/she adjust to others who act or feel differently from him/her (e.g., at work, with
family)?
*Is he/she a person of fixed ideas?
*Do other people get upset with S because he/she is inflexible?
(Give examples of problems caused by inflexibility.)
Subject/Informant
Note Ratings 1–3 Rigidity present but attempted compensation by subject leads to no
social adjustment problems.
Ratings 4–6 Rigidity extreme, refuses to change, often dominating others. Marked
problems in social adjustment because of rigidity, although if subject
is driving and energetic, he/she may appear successful initially.
Ratings 7–8 Inflexibility so severe that life is completely ritualistic and impairment
of adjustment so marked that independent life is impossible.
23 Eccentricity
Subject
Do you think you are very different from other people? In what way?
(45)
*Have you any unusual habits or interests? What are they?

*Have you any unusual beliefs in things like telepathy and mind control?

126 Appendix
(Have these beliefs caused problems in your life?)

(Direct questions may be asked about any eccentric features noted at interview.)
Informant
Do others ever regard S as eccentric in any way? In what way?
(46)
*Has he/she any unusual habits or interests? What are they?

*Does he/she tend to conform with other people or is he/she unaware of them?
*Does he/she deliberately set out to shock people by being unconventional?
*Has he/she any unusual beliefs about telepathy and mind control?
(Do you find his/her thoughts and speech difficult to follow?)
(Can you give examples and problems they have caused?)
Subject/Informant
Note Ratings 1–3 Mild eccentricity, often deliberately stressed because it does not
conform, but no social adjustment problems.
Ratings 4–6 Marked eccentricity. S unable or unwilling to conform, recognised as
odd by others, marked social impairment. Has odd thinking, speech,
and beliefs that cause problems in adjustment.
Ratings 7–8 Behaviour and attitudes so bizarre that life in society impossible
without supervision.
A low rating should be given if the subject acts in an eccentric way to attract attention.
The true eccentric is oblivious to others’ reactions. Any unusual beliefs or perceptions may
only be rated if they are independent of mental illness such as schizophrenia.
24 Hypochondriasis
Subject
Do you worry a great deal about your health or do you seldom give it a thought?
(47)
*When you have been ill, have you worried that it might be more severe than it turned out
to be?
*Are you more concerned about your health than most other people?
(How often do you visit the doctor? What for?)
(Have you ever been really well?)

Appendix 127
Informant
Does S worry a great deal about his/her health or does he/she seldom give it a
thought?
(48)
*When he/she has been ill, has he/she worried it might be more severe than it turned out
to be?
*Is S more concerned about his/her health than most other people?
*Do you or other people think of S as a hypochondriac?
Subject/Informant
Note Ratings 1–3 Mild hypochondriasis. Over-concerned about minor illness and health
(e.g., takes vitamins or health foods regularly).
Ratings 4–6 Hypochondriasis marked. S frequently considers himself/herself to be
ill even when physically healthy. Social adjustment problems;
hypochondriasis affects behaviour and relationships.
Ratings 7–8 Hypochondriasis dominates S’s life. Considers himself/herself to be ill
despite contrary evidence. Unable to live independently because
fears about health dominate behaviour.
Many people with a history of mental illness are naturally concerned about its likely
recurrence and its effects on other people. Do not rate such concern as abnormal unless it is
excessive.
Reliability of subject
On the basis of your interview, do you consider the subject to have been a reliable witness?
Note Rating 0 Highly reliable witness. Evidence from behaviour and demeanour at
interview and any previous knowledge of witness all consistent.
Ratings 1–3 Probably a reliable witness but independent information lacking.
Ratings 4–6 Possibly an unreliable witness from demeanour at interview but no
independent evidence of this.
Ratings 7–8 Unreliable witness. Report inconsistent with previous knowledge of
witness and evidence of incorrect report from demeanour at interview.
(49)

128 Appendix
Reliability of informant
On the basis of your interview, do you consider the informant to have been a reliable witness?
Note Rating 0 Highly reliable witness. Evidence from behaviour and demeanour at
interview and any previous knowledge of witness all consistent.
Ratings 1–3 Probably a reliable witness but independent information lacking.
Ratings 4–6 Possibly an unreliable witness from demeanour at interview but no
independent evidence of this.
Ratings 7–8 Unreliable witness. Report inconsistent with previous knowledge of
witness and evidence of incorrect report from demeanour at interview.
(50)
Combining Subject and Informant Information

The following procedure is used when both subject and informant versions are available and
the assessor wishes to combine them:
(i) If both informant and subject receive the same ratings the combined score is the same;
(ii) If the informant scores differ from the subject scores on one or more ratings decide the
‘most accurate’ score based on (a) item being tested (e.g., aggression towards others
more likely to be rated better by informant, wish to be solitary more likely to be rated
better by subject), (b) level of severity: scores of 4 or higher more likely to be rated
accurately by the informant, low scores of 2 or less more likely to be rated accurately by
subject (since expression of trait not always shown in general behaviour);
(iii) If more than one informant has completed scores, combine informant ratings in
a similar way but ensure that more credence is given to assessments that (a) include
knowledge of subject in premorbid (i.e., before mental state diagnosis) state, (b) are
dispassionate and independent of personal animosity towards the subject, (c) are based
on contact with the subject in a range of situations, not just one (e.g., workplace).
Personality Assessment Schedule – Scoresheet
Name: Date: Rater:

Write rating 0-8 in appropriate box
Variable No. Box no. Sub. Box no. Inf. Final score
Pessimism 1 1 2
Worthlessness 2 3 4
Optimism 3 5 6

Appendix 129
(cont.)
Name: Date: Rater:

Write rating 0-8 in appropriate box
Variable No. Box no. Sub. Box no. Inf. Final score
Lability 4 7 8
Anxiousness 5 9 10
Suspiciousness 6 11 12
Introspection 7 13 14
Shyness 8 15 16
Aloofness 9 17 18
Sensitivity 10 19 20
Vulnerability 11 21 22
Irritability 12 23 24
Impulsiveness 13 25 26
Aggression 14 27 28
Callousness 15 29 30
Irresponsibility 16 31 32
Childishness 17 33 34
Resourcelessness 18 35 36
Dependence 19 37 38
Submissiveness 20 39 40
Conscientiousness 21 41 42
Rigidity 22 43 44
Eccentricity 23 45 46
Hypochondriasis 24 47 48
Reliability of information 49 50
COMMENTS (Problems in scoring to be noted here) . . .. . .. . .. . .. . .. . .. . .. . .. . .. . .

. . .. . .. . .. . .. . .. . ... . .. . .
Revised Scoring of Personality Disorder Using PAS (with ICD-10 and DSM-IV Updates)
The schedule is scored in the usual way and a final score decided for each personality
variable before embarking on classification.
Stage 1
Examine all 24 scores. If none is greater than 2, code as ‘normal personality’ and do not
proceed further.

130 Appendix
Stage 2
Compute scores for individual personality groupings as follows:
(1) Sociopathic – add together the scores for variables 12, 13, 14, 15, and 16, divide total by
5 and subtract from this the sum of scores for variables 2, 21, and 23 divided by 30.
(2) Passive-dependent – add together the scores for variables 5, 11, 17, 18, and 19, divide
total by 5 and subtract from this the sum of scores for variables 15, 22, and 23 divided
by 30.
(3) Anankastic – add together the scores for variables 7, 10, 21, 22, and 24, divide total by 5
and subtract from this the sum of scores for variables 13, 15, and 16 divided by 30.
(4) Schizoid – add together the scores for variables 6, 7, 8, 9, and 23, divide total by 5 and
subtract from this the sum of scores for variables 4, 12, 14, divided by 30.
(5) Explosive – add together the scores for variables 12, 13, 14, and 16, divide total by 4 and
subtract from this the sum of scores for variables 2, 8, 20, and 21, divided by 40.
(6) Sensitive-aggressive – add together the scores for variables 6, 10, 12, and 14, divide total
by 4 and subtract from this the sum of scores for variables 3, 23, and 24, divided by 30.
(7) Histrionic – add together the scores for variables 4, 11, 17, and 19, divide total by 4 and
subtract from this the sum of scores for variables 9, 15, 22, and 23 divided by 40.
(8) Asthenic – add together the scores for variables 5, 10, 18, and 20, divide total by 4 and
subtract from this the sum of scores for variables 3, 14, and 15 divided by 30.
(9) Anxious – add together the scores for variables 5, 8, 20, and 21, divide total by 4 and
(10) Paranoid – add together the scores for variables 5, 6, 10, and 11, divide total by 4 and
(11) Hypochondriacal – add together the scores for variables 5, 19, 21, and 24, divide total by
4 and subtract from this the sum of scores for variables 3, 16, 20, and 23 divided by 40.
(12) Dysthymic – add together the scores for variables 2, 8, 9, and 21, divide total by 4 and
subtract from this the sum of scores for variables 3 and 14 divided by 20.
(13) Avoidant – add together the scores for variables 5, 7, 8, and 11, divide total by 4 and
subtract from this the sum of scores for variables 10, 12, 14, and 23 divided by 40.
Rating of Severity of Personality Disturbance

The ‘adjusted’ score for each of the 13 personality types is used. For the first four
types (sociopathic, passive-dependent, anankastic, and schizoid), a score of 2.5 or
more indicates simple (mild) personality disorder, and a score of 2–2.49 indicates
personality difficulty. For the remaining nine personality types (explosive, sensitive-
aggressive, histrionic, asthenic, anxious, paranoid, hypochondriacal, dysthymic, and
avoidant), a score of 2.75 or more indicates personality disorder, and 2.25–2.74
indicates personality difficulties. When a score in one cluster (sociopathic, passive-
dependent, anankastic, or schizoid) only is 3.75 or greater, the personality disturbance
is also classed as personality disorder. When a score of 2.75 or greater is found in
more than one cluster, the personality disturbance is classified as complex (moderate)
personality disorder unless there is a mean difference of 1.0 or greater between the
highest score in one cluster and the highest score in any of the remaining ones. (This
reflects the overlap between traits, when very high scores can affect several clusters.)

Appendix 131
Severe Personality Disorder

This is decided by a two-stage process. A score of 4.0 or more for one of the flamboyant
cluster personalities (sociopathic, sensitive-aggressive) together with a score of 3.0 in one of
the other personality disorders (except histrionic) suggests severe personality disorder. In
the second stage, the assessor has to decide the following:
(i) Does the personality disorder create significant distress and dysfunction not only to
immediate friends, family, or household members but also to wider society (defined as
all other people apart from friends, household, and family members)?
(ii) Is the extent of such distress great enough to affect at least 50 other individuals apart
from family members and close friends as a direct consequence of the personality
disorder (e.g., people alter the times of arriving and leaving their houses in order to
avoid encountering the individual)?
(iii) Is there clear evidence that threat is created by the pattern of personality
characteristics in that fear of mental or physical harm is an intrinsic part of the distress
or discomfiture created by the personality abnormality (e.g., fear of unprovoked
violence)?
If the answers to all these questions are positive, the individual can be described as
having severe personality disorder.
In obtaining this information, it is important to use more than one source, as individuals
with these disorders are unlikely to admit all these negative characteristics readily or
spontaneously. It is also important for the assessor to make their own judgement as to
whether the fears and concerns of the individuals concerned are justified and not based on
stigma or prejudice.
Combining Diagnoses
In some studies, it may be necessary to combine the diagnoses to obtain numbers large
enough for analysis. This can be done by reducing the numbers of personality types to four –
antisocial, dependent, inhibited, and withdrawn.
These are combined according to the following scheme.
Sociopathic
Explosive Antisocial group
Sensitive-aggressive
Passive-dependent
Histrionic
Asthenic Dependent group
Anankastic
Anxious
Hypochondriacal Inhibited group
Dysthymic
Schizoid
Paranoid Withdrawn group
Avoidant

132 Appendix
Key Traits
For some studies, research workers prefer to use a dimensional assessment of personality
rather than a categorical one. This has the advantage that all subjects being tested with the
schedule will have a key trait score for each of the main personality groups and this may be
useful in studies that are looking at personality traits and characteristics rather than specific
personality disorder. The key traits score for each of the four major personality types is
calculated as follows:
(1) Sociopathic – add scores for variables 12, 13, 14, 15, and 16, and divide total by 5.
(2) Passive-dependent – add scores for variables 5, 11, 17, 18, and 19, and divide total by 5.
(3) Anankastic – add scores for variables 7, 10, 21, 22, and 24, and divide total by 5.
(4) Schizoid – add scores for variables 6, 7, 8, 9. and 23, and divide total by 5.
The nine subcategories of personality disorder can also have their key traits scores
calculated in a similar way. However, it should be noted that many of these overlap as
they are subcategories of the main ones and therefore their key traits scores will be
similar. Explosive (impulsive) and sensitive-aggressive personalities are subtypes of the
sociopathic group; histrionic and asthenic personalities are subtypes of the passive-
dependent group; anxious, hypochondriacal, and dysthymic personalities are subtypes
of the anankastic group; and paranoid and avoidant personalities are subtypes of the
schizoid group.
(4) Explosive (impulsive) – add together the scores for variables 12, 13, 14, and 16, and
divide total by 4.
(5) Sensitive aggressive – add together the scores for variables 6, 10, 12, and 14 and divide
total by 4.
(6) Histrionic – add together the scores for variables 4, 11, 17, and 19, and divide total
by 4.
(7) Asthenic – add together the scores for variables 5, 10, 18, and 20, and divide total by 4.
(8) Anxious – add together the scores for variables 5, 8, 20, and 21, and divide total by 4.
(9) Paranoid – add together the scores for variables 5, 6, 10, and 11, and divide total by 4.
(10) Hypochondriacal – add together the scores for variables 5, 19, 21, and 24, and divide
total by 4.
(11) Dysthymic – add together the scores for variables 2, 8, 9, and 21, and divide total by 4.
(12) Avoidant – add together the scores for variables 5, 7, 8, and 11, and divide total by 4.
Personality Assessment Schedule: DSM-IV Version

Although the PAS was developed before DSM-III was introduced and includes some items
that are not present in DSM personality disorders (e.g., hypochondriasis), there is still
a considerable degree of overlap between the personalities derived from the PAS and those
in DSM-IV. The scoring system below is suitable for reaching a DSM-IV diagnosis with the
PAS. This is a simple procedure that can be done by hand as well as using a short computer
program.
Add the ratings for each of the four variables and divide by four to get the mean score.
A mean score of 2.75 or greater indicates a DSM personality disorder. Simultaneous
presence of several personality disorders is permitted in DSM-IV, but the personality type
with the highest score could be regarded as the most serious.

Appendix 133
DSM-IV Personality type

coding
301.00 Paranoid suspiciousness + sensitivity + vulnerability + irritability

(6+10+11+12)
301.2 Schizoid introspection + aloofness + eccentricity + pessimism
(7+9+23+1)
301.22 Schizotypal shyness + eccentricity + suspiciousness + aloofness
(8+23+6+9)
301.5 Histrionic lability + dependence + childishness + irresponsibility
(4+19+17+16)
301.7 Antisocial callousness + aggression + impulsiveness +
irresponsibility
(15+14+13+16)
301.8 Borderline lability + impulsiveness + aggression + worthlessness
(4+13+14+2)
301.82 Avoidant vulnerability + shyness + anxiousness + submissiveness
(11+8+5+20)
301.6 Dependent dependence + submissiveness + resourcelessness +
sensitivity
(19+20+18+10)
301.4 Obsessive- conscientiousness + rigidity + introspection +
compulsive anxiousness
(21+22+7+5)
301.81 Narcissistic childishness + vulnerability + optimism + irritability
(17+11+3+12)
ICD-10
ICD-10 personality disorders show a close relationship with the PAS sub-classification. The
following diagnoses can be regarded as equivalent:
Sociopathic (PAS) and Dissocial (ICD-10)

Passive-dependent (PAS) and Dependent (ICD-10)
Explosive (PAS) and Impulsive (ICD-10)
Sensitive-aggressive (PAS) and Dissocial (ICD-10)
Histrionic (PAS) and Histrionic (ICD-10)
Asthenic (PAS) and Dependent (ICD-10)
Avoidant (PAS) and Anxious (ICD-10)
Schizoid (PAS) and Schizoid (ICD-10)
Paranoid (PAS) and Paranoid (ICD-10)
Anankastic (PAS) and Anankastic (ICD-10)
Other diagnoses in the PAS can be categorised under ‘Personality Disorder – other’ in
ICD-10.

References
ABC-H Investigators, Roush, G. C., Barrett, J. E., Barrett, J. A., Oxman, T. E. &
Fagard, R. H. et al. (2014). Prognostic impact Gerber, P. D. (1988). The prevalence of
from clinic, daytime, and night-time systolic psychiatric disorders in a primary care practice.
blood pressure in nine cohorts of 13,844 Archives of General Psychiatry, 45, 1100–6.
patients with hypertension. Journal of Bayer, R. & Spitzer, R. L. (1985). Neurosis,
Hypertension, 32, 2332–40. psychodynamics, and DSM-III: a history of
Adler, A. (1921). The Neurotic Constitution: the controversy. Archives of General
Outlines of a Comparative Individualistic Psychiatry 1985, 42, 187–96.
Psychology (translated from the German). Berk, M., Boyce, P., Hamilton, A. et al. (2018).
London: Routledge. Personality: distraction or driver in the
American Psychiatric Association (1980). diagnosis of depression. Personality and
Diagnostic and Statistical Manual of Mental Mental Health, 12, 126–30.
Disorders, Third Edition (DSM-III). Bernreuter, R. G. (1931). The Personality
Washington, DC: American Psychiatric Inventory. Palo Alto, CA: Consulting
Association. Psychologists Press.
Andrews, G. (1996). Comorbidity and the Bond, M. & Perry, J. C. (2006). Psychotropic
general neurotic syndrome. British Journal of medication use, personality disorder and
Psychiatry, 168 (Supplement 30), 76–84. improvement in long-term dynamic
Andrews, G., Stewart, G., Morris-Yates, A., psychotherapy. Journal of Nervous and
Holt, P. & Henderson, S. (1990). Evidence for Mental Disease, 194, 21–6.
a general neurotic syndrome. British Journal Boyd, J. H., Burke, J. D., Jr, Gruenberg, E. et al.
of Psychiatry, 157, 6–12. (1984). Exclusion criteria of DSM-III: a study
Andrews, G., Hobbs, M. J., Borkovec, T. D. et al. of co-occurrence of hierarchy-free
(2010). Generalised worry disorder: a review syndromes. Archives of General Psychiatry,
of DSM-IV generalised anxiety disorder and 41, 983–9.
options for DSM-V. Depression and Anxiety, Brothwell, J., Casey, P. R. & Tyrer, P. (1992).
27, 134–47. Who gives the most reliable account of
Anjara, S. G., Bonetto, C., Ganguli, P. et al. a psychiatric patient’s personality? Irish
(2019). Can general practitioners manage Journal of Psychological Medicine, 9, 90–3.
mental disorders in primary care? A partially Carr, V. J. & Donovan, P. (1992). Psychiatry in
randomised, pragmatic, cluster trial. PLoS general practice: a pilot scheme using the
One, 14, e0224724. liaison-attachment model. Medical Journal of
Aronson, T. A. (1987). Is panic disorder Australia, 156, 379–82.
a distinct diagnostic entity? A critical review Casey, P. (2018). Adjustment Disorders: From
of the borders of a syndrome. Journal of Controversy to Clinical Practice. Oxford:
Nervous and Mental Diseases, 175, 584–94. Oxford University Press.
Åsberg, M., Montgomery, S. A., Perris, C., Casey, P. R. & Tyrer, P. J. (1986). Personality,
Schalling, D. & Sedvall, G. (1978). functioning and symptomatology. Journal of
A comprehensive psychopathological rating Psychiatric Research, 20, 363–74.
scale. Acta Psychiatrica Scandinavica
(Supplement), 271, 5–27. Casey, P. R., Tyrer, P. J. & Platt, S. (1985). The
relationship between social functioning and
Balint, M. (1964). The Doctor, His Patient and psychiatric symptomatology in primary care.
the Illness. London: Pitman. Social Psychiatry, 20, 5–9.
134

References 135
Cattell, R. B. & Stice, G. E. (1957). The Sixteen smoking: 40 years’ observation on male
Personality Factors Questionnaire. British doctors. British Medical Journal, 309,
Champaign, IL: Institute for Personality and 901–11.
Ability Testing.
Duggan, C. F., Lee, A. S. & Murray, R. M. (1990).
Cavallaro, R., Regazzetti, M. G., Mundo, E., Does personality predict long-term outcome
Brancato, V. & Smeraldi, E. (1993). Tardive in depression? British Journal of Psychiatry,
dyskinesia outcomes: clinical and 157, 19–24.
pharmacologic correlates of remission and
persistence. Neuropsychopharmacology, 8, Duggan, C., Sham, P., Lee, A. & Minne, C.
233–9. (1996). Neuroticism: a vulnerability marker
for depression evidence from a family study.
Conan Doyle, A. (1892). The Adventure of Silver Journal of Affective Disorders, 35, 139–43.
Blaze. London: Strand Magazine.
Eisenberg, L. (1992). Treating depression
Coryell, W., Endicott, J., Andreasen, N. C. et al. and anxiety in primary care: closing
(1988). Depression and panic attacks: the the gap between knowledge and practice.
significance of overlap as reflected in New England Journal of Medicine, 326,
follow-up and family study data. American 1080–4.
Journal of Psychiatry, 145, 293–300.
Emmanuel, J. S., McGee, A., Ukoumunne, O. C.
Costa, P. T. & McCrae, R. R. (1992). Revised & Tyrer, P. (2002). A randomised controlled
NEO Personality Inventory (NEO-PI-R) and trial of enhanced key-worker liaison
NEO Five-Factor Inventory (NEO-FFI) psychiatry in general practice. Social
Manual. Odessa, FL: Psychological Psychiatry and Psychiatric Epidemiology, 37,
Assessment Resources. 261–6.
Craske, M. G. & Stein, M. B. (2016). Anxiety.
Evenden, M., Svanborg, P., Gustavsson, P. &
Lancet, 388, 3048–59.
Åsberg, M. (1996). Determinants of
Cuesta, M. J., Gil, P., Artamendi, M., self-rating and expert rating concordance in
Serrano, J. F. & Peralta, V. (2002). Premorbid psychiatric out-patients, using the affective
personality and psychopathological subscales of the CPRS. Acta Psychiatrica
dimensions in first-episode psychosis. Scandinavica, 94, 386–96.
Schizophrenia Research, 58, 273–80.
Eysenck, H. J. (1952). The effects of
Cullen, W. (1777). First Lines of The Practice of psychotherapy: an evaluation. Journal of
Physic. Edinburgh: Creech. Consulting and Clinical Psychology, 16,
Darling, C. & Tyrer, P. (1990). Brief encounters 319–24.
in general practice: an audit of liaison in Feinstein, A. R. (1970). The pre-therapeutic
general practice psychiatric clinics. classification of co-morbidity in chronic
Psychiatric Bulletin, 14, 592–4. disease. Journal of Chronic Diseases, 23,
Das Munshi, J., Goldberg, D., Bebbington, P. E. 455–68.
et al. (2008). Public health significance of
First, M. B., Spitzer, R. L., Gibbon, M. et al.
mixed anxiety and depression: beyond
(1995). The Structured Clinical Interview
current classification. British Journal of
for DSM-III-R Personality Disorders
Psychiatry, 192, 171–7.
(SCID-II): II. Multi-site test-retest
Dobson, K. S. (1985). The relationship between reliability study. Journal of Personality
anxiety and depression. Clinical Psychology Disorders, 9, 92–104.
Review, 5, 307–24.
Frances, A. (2016). Robert Spitzer: the most
Doll, R. & Hill, A. B. (1954). The mortality of influential psychiatrist of his time. The Lancet
doctors in relation to their smoking habits: Psychiatry, 3, 110–11.
a preliminary report. British Medical Journal,
Fredman, L., Weissman, M. M., Leaf, P. J. &
228, 1451–5.
Bruce, M. L. (1988). Social functioning in
Doll, R., Peto, R., Wheatley, K., Gray, R. & community residents with depression and
Sutherland, I. (1994). Mortality in relation to other psychiatric disorders: results of the

136 References
New Haven Epidemiological Catchment Haddad, P. M. & Nutt, D. J. (eds.). (2020).

Area study. Journal of Affective Disorders, Seminars in Clinical Psychopharmacology, 3rd
15, 103–112. ed. Oxford: Oxford University Press.
Galen (192 AD). Mixtures: De Temperamentis. Hathaway, S. R. & McKinley, J. C. (1940).
Ed. and tr. by P. N. Singer, P. J. van der Eijk & A multiphasic personality schedule
P. Tassinari, 2019. Cambridge: Cambridge (Minnesota): I. Construction of the schedule.
University Press. Journal of Psychology, 10, 249–54.
Gask, L., Dowrick, C., Klinkman, M. & Henderson, D. K. & Batchelor, I. R. C. (1969).
Gureje, O. (2018). Diagnosis and classification Henderson and Gillespie’s Textbook of
of mental illness: a view from primary care. In Psychiatry, 10th ed. Oxford: Oxford
Gask, L., Kendrick, T., Peveler, R. & Chew- University Press.
Graham, C. A. (eds.), Primary Care Mental Herrmann, N., Black, S. E., Lawrence, J.,
Health, 2nd ed., pp. 70–85. Cambridge: Szekely, C. & Szalai, J. P. (1998). The
Cambridge University Press. Sunnybrook Stroke Study: a prospective
Germans, S., Guus L. V. H. & Hodiamont, P.P.G. study of depressive symptoms and functional
(2011). Quick Personality Assessment outcome. Stroke, 29, 618–24.
Schedule (PAS-Q): validation of a brief Hettema, J. M., Neale, M. C. & Kendler, K. S.
screening test for personality disorders in (2001). A review and meta-analysis of the
a population of psychiatric outpatients. genetic epidemiology of anxiety disorders.
Australian and New Zealand Journal of American Journal of Psychiatry, 158, 1568–78.
Hill, J., Fudge, H., Harrington, R., Pickles, A. &
Germans, S., Guus L. V. H. & Rutter, M. (2000). Complementary
Hodiamont, P. P. G. (2012). Results of the approaches to the assessment of personality
search for personality disorder screening disorder. British Journal of Psychiatry, 176,
tools: clinical implications. Journal of Clinical 434–9.
Jackson, G., Gater, R., Goldberg, D.,
Goldberg, D. (2013). The central importance of Tantam, D., Loftus, L. & Taylor. H.
anxiety in common mental disorders. (1993). A new community mental health
Australian and New Zealand Journal of team based in primary care: a description
Psychiatry, 47, 983–5. of the service and its effect on service use
Goldberg, D. & Gater, R. (1991). Estimates of in the first year. British Journal of
need: a document prepared for the South Psychiatry, 162, 375–84.
Manchester District Health Authority. Kendell, R. (1975a). The Role of Diagnosis in
BJPsych Bulletin, 15, 593–5. Psychiatry. London: Blackwell.
Goldberg, D. P., Cooper, B., Eastwood, M. R., Kendell, R. (1975b). The concept of disease and
Kedward, H. B. & Shepherd, M. (1970). its implications for psychiatry. British Journal
A standardized psychiatric interview for use of Psychiatry, 127, 305–15.
in community surveys. British Journal of
Preventive and Social Medicine, 24, 18–23. Kendell, R. E. (1991). The major functional
psychoses: are they independent entities or part
Grenyer, B. F. S., Lewis, K. L., Fanaian, M. & of a continuum? In Kerr, A. & McClelland, H.
Kotze, B. (2018). Treatment of personality Concepts of Mental Illness: A Continuing
disorder using a whole of service stepped care Debate, pp. 1–16. London: Gaskell.
approach: a cluster randomized controlled
trial. PLoS ONE 13, e0206472. Kendell, R. E. & Jablensky, A. (2003).
Distinguishing between the validity and
Gurney, C., Roth, M., Garside, R., Kerr, T. & utility of psychiatric diagnoses. American
Schapira, K. (1972). Studies in the Journal of Psychiatry, 160, 4–12.
classification of affective disorders: the
relationship between anxiety states and Kendell, R. E., Cooper, J. E., Gourlay, A. J.,
depressive illnesses. II. British Journal of Copeland, J. R. M., Sharpe, L. & Gurland, B. J.
Psychiatry, 121, 162–6. (1971). Diagnostic criteria of American and

References 137
British psychiatrists. Archives of General McHugh, K., Swamy, G. K. &

Psychiatry, 25, 123–30. Hernandez, A. F. (2018). Engaging
Kerr, T. A., Roth, M., Schapira, K. & Gurney, C. patients throughout the health system:
(1972). The assessment and prediction of a landscape analysis of cold-call policies
outcome in affective disorders. British and recommendations for future policy
Journal of Psychiatry, 121, 167–74. change. Journal of Clinical and
Translational Science, 6, 384–92.
Kiloh, L. G., Andrews, G., Neilson, M. &
Bianchi, G. (1972). The relationship of the Meyer, A. (1902). Collected Papers, 2, 90–104.
syndromes called endogenous and neurotic Baltimore, MD: Johns Hopkins Press.
depression. British Journal of Psychiatry, 121, Mindham, R. H. S. (2020). Mapperley Hospital,
183–96. Nottingham and George Hine: a creative
Kingdon, D., Tyrer, P., Seivewright, N., relationship. British Journal of Psychiatry,
Ferguson, B. & Murphy, S. (1996). The 216, 174.
Nottingham Study of Neurotic Disorder: Mitchell, A. J., Meader, N. & Symonds, P. (2010).
influence of cognitive therapists on outcome. Diagnostic validity of the Hospital Anxiety
British Journal of Psychiatry, 169, 93–7. and Depression Scale (HADS) in cancer and
Klein, D. F. (1964). Delineation of two palliative settings: a meta-analysis. Journal of
drug-responsive anxiety syndromes. Affective Disorders, 126, 335–48.
Psychopharmacologia, 5, 397–408. Montgomery, S. A. & Åsberg, M. (1979). A new
Klein, D. F. (1981). Anxiety depression scale designed to be sensitive to
Reconceptualized. In Klein, D. F. & change. British Journal of Psychiatry, 134,
Rabkin, J. G. (eds.), Anxiety: New Research 382–9.
and Changing Concepts, pp. 235–62. Morrison, H. (2016). Constructing patient
New York: Raven Press. stories: ‘dynamic’ case notes and clinical
Klein, D. F. (1988). Nottingham Study of encounters at Glasgow’s Gartnavel Mental
Neurotic Disorder. Lancet, 332, 1015. Hospital, 1921–32. Medical History, 60,
67–86.
Knerer, G., Byford, S., Johnson, T.,
Seivewright, H. & Tyrer, P. (2005). The Mundt, J. C., Marks, I. M., Shear, M. K. &
Nottingham Study of Neurotic Disorder: Greist, J. H. (2002). The Work and Social
predictors of 12 years costs. Acta Psychiatrica Adjustment Scale: a simple measure of
Scandinavica, 112, 224–32. impairment in functioning. British Journal of
Psychiatry, 180, 461–4
Lahey, B. B. (2009). Public health significance of
neuroticism. American Psychologist, 64, Murphy, S. M., Owen, R. T. & Tyrer, P. J. (1984).
241–56. Withdrawal symptoms after six weeks
treatment with diazepam. Lancet, 324, 1389.
Lancet (editorial) (1959). The nature of essential
hypertension. Lancet, 274, 895–6. Murray, H. A. (1943). Manual for the Thematic
Appreciation Test. Cambridge, MA: Harvard
Lewis, G. (1991). Observer bias and the University Press.
assessment of anxiety and depression. Social
Psychiatry and Psychiatric Epidemiology, 26, Newton-Howes, G., Tyrer, P., Johnson, T. et al.
265–72. (2014). Influence of personality on the
outcome of treatment in depression:
Lewis, G. (1992). Measuring psychiatric disorder systematic review and meta-analysis. Journal
in the community: a standardized assessment of Personality Disorders, 28, 577–93.
for use by lay interviewers. Psychological
Medicine, 22, 465–86. Oldham, P. D., Pickering, G., Fraser
Roberts, J. A. & Sowry, G. S. C. (1960). The
Lilienfeld, S. O., Lynn, S. J., Ruscio, J. & nature of essential hypertension. Lancet, 275,
Beyerstein, B. L. (2009). 50 Great Myths of 1085–93.
Popular Psychology: Shattering Widespread
Misconceptions about Human Behavior. Pappworth, M. (1971). A Primer of Medicine.
Chichester: Wiley-Blackwell. London: Butterworth.

138 References
Paykel, E. S. (2008). Basic concepts of Seivewright, H., Tyrer, P. & Johnson, T. (1998).
depression. Dialogues in Clinical Prediction of outcome in neurotic disorder: a
Neuroscience, 10, 279–89. five-year prospective study. Psychological
Pickering, G. (1960). The nature of essential Medicine, 28, 1149–57.
hypertension. Lancet, 275, 170. Seivewright, H., Tyrer, P. & Johnson, T. (2004).
Piñero, J. M. L. (1983). Historical Origins of the Persistent social dysfunction in anxious and
Concept of Neurosis. Cambridge: Cambridge depressed patients with personality disorder.
University Press. Acta Psychiatrica Scandinavica, 109, 104–9.
Snaith, P. (1991). Clinical Neurosis. Oxford:
Platt, R. (1959). The nature of essential
Oxford University Press.
hypertension. Lancet, 274, 1092.
Spiegel, A. (2005). The dictionary of disorder:
Plomin, R. (2011). Commentary: Why are
how one man revolutionized psychiatry.
children in the same family so different?
New Yorker, January 3.
Non-shared environment three decades later.
International Journal of Epidemiology, 40, Spitzer, R. L. & Williams, J. B. (1983). Structured
582–92. Clinical Interview for DSM-III (1983 version).
New York: New York State Psychiatric
Plomin, R. & Daniels, D. (1987). Why are
Institute.
children in the same family so different from
each other? Behavioural and Brain Sciences, Spitzer, R. L. & Wilson, P. T. (1968). American
10, 1–16. Psychiatric Association, Diagnostic and
Statistical Manual of Mental Disorders: 2.
Quinton, D., Gulliver, L. & Rutter, M. (1995).
Washington, DC: American Psychiatric
A 15–20 year follow-up of adult psychiatric
Association.
patients: psychiatric disorder and social
functioning. British Journal of Psychiatry, Stern, A. F. (2014). The Hospital Anxiety and
167, 315–23. Depression Scale. Occupational Medicine, 64,
393–4.
Remington, M. & Tyrer, P. (1979). The Social
Functioning Schedule: a brief Surtees, P. G. & Barkley, C. (1994). Future
semi-structured interview. Social Psychiatry, imperfect: the long-term outcome of
14, 151–7 depressive disorder. British Journal of
Rorschach, H. (1921). Psychodiagnostik. Bern:
Hans Huber. Thompson, C., Kinmonth, A. L., Stevens, L. et al.
(2000). Effects of a clinical-practice guideline
Rosenhan, D. L. (1973). On being sane in insane
and practice-based education on detection
places. Science, 179, 250–8.
and outcome of depression in primary care:
Roth, M., Gurney, C., Garside, R. F. & Hampshire Depression Project randomised
Kerr, T. A (1972). Studies in the controlled trial. Lancet, 355, 185–91.
classification of affective disorders: the Thompson, F. (1887). In No Strange Land, from
relationship between anxiety states and The works of Francis Thompson. Leopold
depressive illnesses. British Journal of Classic Library, 2015
Tyrer, P. (1985). Neurosis divisible? Lancet, 325,
Sanatinia, R., Afzal, S., MacLaren, T. et al. 685–88.
(2019). Improved mental health among
LABILE study participants: a qualitative Tyrer, P. (1989). Classification of Neurosis.
exploration. Personality and Mental Health, Chichester: John Wiley.
13, 75–83. Tyrer, P. (1991). Neuroses and personality
Schapira, K., Roth, M., Kerr, T. A. & Gurney, C. disorders. In Kerr. A. & McClelland, H. (eds.),
(1972). The prognosis of affective disorders: Concepts of Mental Disorder, pp. 112–28.
the differentiation of anxiety states from London: Gaskell.
depressive illnesses. British Journal of Tyrer, P. (1996). Comorbidity or consanguinity.
Psychiatry, 121, 175–81. British Journal of Psychiatry, 168, 669–71.

References 139
Tyrer, P. (2007). Personality diatheses: Tyrer, P., Turner, R. & Johnson, A. L. (1989).
a superior explanation than disorder. Integrated hospital and community
Psychological Medicine, 37, 1521–5. psychiatric services and use of inpatient beds.
Tyrer, P. (2008a). The whys and wares of the British Medical Journal, 299, 298–300.
yellow vans. From the Editor’s Desk. British Tyrer, P., Tyrer, H. & Yang, M. (2021).
Journal of Psychiatry, 193, 350. Premature mortality of people with
Tyrer, P. (2008b). So careless of the single trial. personality disorder in the Nottingham
Evidence-Based Mental Health, 11, 65–6. Study of Neurotic Disorder. Personality and
Mental Health, 15, 32–39.
Tyrer, P. (2009). Nidotherapy: Harmonising the
Environment with the Patient. London: Tyrer, P., Tyrer, H. & Yang, M. (2022). Treatments
RCPsych Publications. received in the Nottingham Study of Neurotic
Disorder over 30 years: comparison of groups
Tyrer, P. (2013). The swings and roundabouts of by personality status. Personality and Mental
community mental health: the UK Health, January. https://doi.org/10.1002/pmh
fairground. In Thornicroft, G., Ruggeri, M. & .1535.
Goldberg, D. (eds.), Improving Mental Health
Care: The Global Challenge, pp. 25–40. Tyrer, P., Alexander, J., Remington, M. &
Chichester: Wiley-Blackwell. Riley, P. (1987). Relationship between
neurotic symptoms and neurotic diagnosis:
Tyrer, P. (2021). Overcoming personality a longitudinal study. Journal of Affective
disorder: it’s in your hands. Lincoln: Disorders, 13, 13–21.
Impspired.
Tyrer, P., Mitchard, S., Methuen, C. &
Tyrer, P. & Alexander, J. (1979). Classification of Ranger, M. (2003). Treatment-rejecting and
personality disorder. British Journal of treatment-seeking personality disorders:
Psychiatry, 135, 163–7. Type R and Type S. Journal of Personality
Tyrer, P. & Casey, P. (1993). Social Function in Disorders, 17, 265–70.
Psychiatry: The Hidden Axis of Classification Tyrer, P., Mulder, R., Kim, Y-R. &
Exposed. Petersfield: Wrightson Biomedical Crawford, M. J. (2019). The development of
Publishing. the ICD-11 classification of personality
Tyrer, P. & Johnson, T. (1996). Establishing the disorders: an amalgam of science,
severity of personality disorder. American pragmatism and politics. Annual Review of
Journal of Psychiatry, 153, 1593–7. Clinical Psychology, 15, 481–502.
Tyrer, P. & Remington, M. (1979). Controlled Tyrer, P., Seivewright, H., Ferguson, B. &
comparison of day hospital and outpatient Johnson, T. (2003). ‘Cold calling’ in
treatment for neurotic disorders. Lancet, 313, psychiatric follow-up studies: is it justified?
1014–16. Journal of Medical Ethics, 29, 238–42.
Tyrer, P., Casey, P. & Gall, J. (1983). The Tyrer, P., Seivewright, N., Ferguson, B. &
relationship between neurosis and Tyrer, J. (1992). The general neurotic
personality disorder. British Journal of syndrome: a coaxial diagnosis of anxiety,
Psychiatry, 142, 404–408. depression and personality disorder. Acta
Psychiatrica Scandinavica, 85, 201–6.
Tyrer, P., Ferguson, B. & Wadsworth, J. (1990).
Liaison psychiatry in general practice: the Tyrer, P., Yang, M., Tyrer, H. & Crawford, M.
comprehensive collaborative model. Acta (2021). Is social function a good proxy
Psychiatrica Scandinavica, 81, 359–63. measure of personality disorder? Personality
and Mental Health, 15, 261–72.
Tyrer, P., Owen, R. T. & Cicchetti, D. V.
(1984). The brief scale for anxiety: Tyrer, P., Alexander, M. S., Cicchetti, D.,
a subdivision of the Comprehensive Cohen, M. S. & Remington, M. (1979).
Psychopathological Rating Scale. Journal of Reliability of a schedule for rating personality
Neurology, Neurosurgery and Psychiatry, disorders. British Journal of Psychiatry, 135,
47, 970–5. 168–74.

140 References
Tyrer, P., Nur, U., Crawford, M., Karlsen, S., Whytt, R. (1765). Observations on the Nature,
McLean, C., Rao, B., & Johnson, T. (2005). Causes and Cure of Those Disorders Which
The Social Functioning Questionnaire: Have Commonly Been Called, Nervous
a rapid and robust measure of perceived Hypochondriac or Hysteric. Edinburgh:
functioning. International Journal of Social J. Balfour.
Psychiatry, 51, 265–75. Williams, P. & Balestrieri, M. (1989). Psychiatric
Tyrer, P., Seivewright, N., Ferguson, B., clinics in general practice: do they reduce
Murphy, S. & Johnson, A. L. (1993). The admissions? British Journal of Psychiatry, 154,
Nottingham study of neurotic disorder: 67–71.
impact of personality status on response to World Health Organisation (2018). ICD-11,
drug treatment, cognitive therapy and the 11th Revision of the International
self-help over two years. British Journal of Classification of Diseases [Online].
Psychiatry, 162, 219–26. Geneva: World Health Organisation.
Tyrer, P., Seivewright, N., Ferguson, B. et al. https://icd.who.int/ [accessed
(1988). Nottingham Study of Neurotic 21 January 2021].
Disorder. Lancet, 332, 1015. Yang, M., Tyrer, P. & Tyrer, H. (2022). The
Tyrer, P., Seivewright, N., Murphy, S. et al. recording of personality strengths: an
(1988). The Nottingham Study of Neurotic analysis of the impact of positive personality
Disorder: comparison of drug and features on the long-term outcome of
psychological treatments. Lancet, 332, common mental disorders. Personality and
235–40. Mental Health (in press).
Tyrer, P., Seivewright, N, Ferguson, B. et al. Yang, M., Tyrer, H., Johnson, T. &
(1990). The Nottingham Study of Neurotic Tyrer, P. (2022). Personality change
Disorder: relationship between personality in the Nottingham Study of Neurotic
status and symptoms. Psychological Medicine, Disorder: 30 year cohort study. Australian
20, 423–31. and New Zealand Journal of Psychiatry,
Tyrer, P., Crawford, M., Sanatinia, R. et al. (2014). 56, 260–9.
Preliminary studies of the ICD-11 classification Zigmond, A. S. & Snaith, R. P. (1983). The
of personality disorder in practice. Personality Hospital Anxiety and Depression Scale. Acta
and Mental Health, 8, 254–63. Psychiatrica Scandinavica, 57, 361–70.

Index
Adaptive and Acceptance Gavin Andrews and, 16–17 relative similar syndrome
Therapy (ACT), 99 Hospital Anxiety and history, 12
aggression in PAS, 118 Depression scale, 16 two or more symptoms (of
aloofness in PAS, 113–14 Newcaste Group hypothesis six conditions), 10–11
Andrews, Gavin, 16–17 on, 8–9 general neurotic syndrome
anxiety recurrent depressive outcomes
Clinical Interview Schedule, disorder, 18–19 by baseline personality
14–15 depressive neurosis disorder, 49
diagnosis separation from diagnosis, 32 personality strengths by
depression, 9–10 Diagnostic and Statistical baseline characteristics, 77
Gavin Andrews and, 16–17 Manual of Mental short term, 44
Hospital Anxiety and Disorders (DSM) general neurotic syndrome
Depression scale, 16 general neurotic syndrome, outcomes, 5-year
ICD-11, 19 5- and 30-year, 47, 72 data recording, 45–6
Newcastle Group hypothesis and GNSS DSM-III diagnosis at
on, 8–9 classification, 25–6 baseline and service
anxiousness in PAS, 109–10 Nottingham Study of outcomes, 47
Neurotic Disorder result global outcome, 46
Brief Anxiety Scale (BAS), 35 interpretation, 38, 40 regression analysis, 46–9
PAS and, 132–3 service, 48
callousness in PAS, 119 Rosenhan experiment summary, 47–51
childishness in PAS, 120–1 influence on, 24–5 general neurotic syndrome
Clinical Interview Schedule dysthymic disorder, 18 outcomes, 12-year
definition, 14–15 clinical outcomes, 72
as sub-syndromal eccentricity in PAS, 125–6 Comprehensive
condition, 15 epiphany moment, 90 Psychopathological Rating
cold-calling ergasias, 5 Scale (CPRS), 72, 74
30-year follow-up, 68 cost analysis, 57–63
issues, 53–7 Galenic syndrome, 12, 82 differences in treatment and
comorbidity, 82 general neurotic syndrome. See service contacts, 76
Comprehensive also cothymia; neurotic measures included, 52
Psychopathological Rating syndrome; Nottingham result interpretation, 67
Scale (CPRS) Study of Neurotic social function, 63–6, 75
12- and 30-year follow-up, Disorder general neurotic syndrome
72 clinical diagnosis stages, 13 outcomes, 30-year results
Nottingham Study of definition, 13 attrition, 68
Neurotic Disorder, 34 General Neurotic Syndrome clinical outcomes, 72
conscientiousness in PAS, 124 Scale (GNSS), 13 Comprehensive
cothymia, 29. See also general initial definition Psychopathological Rating
neurotic syndrome formulation, 10 Scale (CPRS), 72, 74
professional treatment Data Protection Act, 68
Data Protection Act, 68 tips, 98–9 deaths, 71
dependence in PAS, 122 resistance to, 14–16, 17–18 DSM status, 72
depression general neurotic syndrome findings synthesis, 78–81
Clinical Interview Schedule, features personality strengths by
14–15 anankastic and passive- baseline characteristics,
diagnosis separation from dependent personality 78
anxiety, 9–10 traits, 11–12 procedures, 68–71
dysthymic disorder, 18 major stress, 11 social function, 75
141

142 Index
general neurotic syndrome hypochondriasis, 3 procedure, 34

outcomes utility hypochondriasis in PAS, 126–8 randomised control trial
epiphany moment, 90 hysteria, 3 plan, 32
general practitioner (GP) reasons for, 28
clinical assessment impulsiveness in PAS, 117–18 startup, 29
feasibility, 84–5, 86 International Classification of testing treatment efficacy,
patient usefulness, 85–6 Disease (ICD) 29–30
recovered patient anxiety, 19 treatment duration, 33
features, 90 general neurotic syndrome Nottingham Study of Neurotic
treatment, 87–91 and, 18–19 Disorder, assessment
understanding of common PAS and, 133 Brief Anxiety Scale (BAS),
mental illness and, 82–3 introspection in PAS, 111–12 35
general neurotic syndrome irresponsibility in PAS, 120 Comprehensive
patient stories irritability in PAS, 116–17 Psychopathological Rating
child sexual abuse, 97 Scale (CPRS), 34
inner toughness, 98 lability in PAS, 108–9 financial aspects, 35–6
Lizzie, 92–7 Lewis prediction, 17, 84 Hospital Anxiety and
Mrs Bennet, 91–2 Depression Scale, 35
psychotherapy, 98 Meyer, Adolf, 3–5 Montgomery and Åsberg
suicidal behaviours, 98 Montgomery and Åsberg Depression Rating Scale
symptoms present in family Depression Rating Scale (MADRS), 34
member, 97 (MADRS), 34 Personality Assessment
value of employment, 97–8 Schedule (PAS), 35
General Neurotic Syndrome neurosis Nottingham Study of Neurotic
Scale (GNSS) demise of term usage, 3 Disorder, clinical
Clinical Interview Schedule, history of, 2–3 outcomes. See also general
14–15 neuroticism and, 5–7 neurotic syndrome
definition, 13 personality status in, 3–5 clinical, 40–1
definition update, 13–14 neurotic disorders placebo response
Gavin Andrews and, 16–17 classification reaction, 42
not time line dependent, 14 controlled study, 21–2 publication reaction,
General Neurotic Syndrome David Goldberg on, 22 41–2
Scale (GNSS) classification diagnosis difficulty, 23 treatment differences, 41
DSM-III task force, 25–6 history of, 21 Nottingham Study of Neurotic
evolving nature of diagnosis, neurotic syndrome. See also Disorder, results
19–20 general neurotic interpretation
ICD-11, 18–19 syndrome diagnosis adjustment, 39
Rosenhan experiment Newcastle Group hypothesis positive cases by DSM-
influence on DSM- on, 8–9 III, 40–1
III, 24–5 with separate anxiety/ randomised trial baseline
general practitioner (GP) depression data, 39
clinical assessment diagnoses, 9–10 separated by initial DSM
feasibility, 84–5, 86 traditional definition, 8 diagnosis, 38
genetics and general neurotic unified, 8 separated by random
syndrome, 12, 97 neuroticism, 5–7, 83 outcome group, 37
Goldberg, David, 22 Newcastle Group, 8–9 summary of findings, 37
Nottingham Study of Neurotic
Hospital Anxiety and Disorder. See also general optimism in PAS, 107–8
Depression Scale neurotic syndrome
clinical trial, 84 cothymia recording, 29 panic disorder, 19
general neurotic syndrome diagnoses selection, 32 personality and mood/anxiety
outcomes utility, 84 exclusion criteria, 33 disorders, 83
and Nottingham Study of long-term outcome, 30 Personality Assessment
Neurotic Disorder patient recruitment, 30–2 Schedule (PAS)
assessment, 35 Personality Assessment advantages of, 29
hypertension, 19–20 Schedule (PAS), 28–9 background, 35

Index 143
events affected by irresponsibility, 120 pseudopatient (Rosenhan

personality irritability, 116–17 experiment), 24–5
characteristics, 104 lability, 108–9
explanation for, 101–3 optimism, 107–8 recurrent depressive disorder,
original version, 101 pessimism, 105–6 18–19
patient subgroup score resourcelessness, 121–2 resourcelessness in PAS, 121–2
comparison, 104 rigidity, 125 rigidity in PAS, 125
reasons for, 28–9 sensitivity, 114–15 Rosenhan, David, 24–5
scoring procedure, 103–4 shyness, 112–13 Rosenhan experiment, 24–5
Personality Assessment submissiveness, 123
Schedule (PAS) evaluation suspiciousness, 110–11 sensitivity in PAS, 114–15
combining subject and vulnerability, 115–16 severe personality disorder in
informant worthlessness, 106–7 PAS, 131
information, 128 Personality Assessment sexual abuse, 97
score computation, 129–30 Schedule (PAS) personality shyness in PAS, 112–13
Personality Assessment disturbance rating social anxiety disorder, 19
Schedule (PAS) interview combining diagnoses, 131–2 Spitzer, Robert, 24–5
procedure DSM-IV version, 132–3 stress and general neurotic
aggression, 118 ICD-10, 133 syndrome, 11
aloofness, 113–14 key traits, 132 submissiveness in PAS, 123
anxiousness, 109–10 severe personality suspiciousness in PAS, 110–11
callousness, 119 disorder, 131
childishness, 120–1 personality disorder unified neurotic syndrome, 8
conscientiousness, 124 assessment
dependence, 122 reliability, 28–9 vulnerability in PAS, 115–16
eccentricity, 125–6 personality status, 3–5
hypochondriasis, 126–8 pessimism in PAS, 105–6 whole person medicine, 4
impulsiveness, 117–18 Pickering, George, 19–20 Whytt, Robert, 3
introspection, 111–12 Platt, Robert, 19–20 worthlessness in PAS, 106–7


Neurosis

Uploaded by

Copyright:

Available Formats

Neurosis

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Neurosis

Uploaded by

Copyright:

Available Formats

Neurosis: Understanding

Common Mental Illness

Published online by Cambridge University Press

Published online by Cambridge University Press

Published online by Cambridge University Press

Cambridge University Press is part of the University of Cambridge.

Published online by Cambridge University Press

Published online by Cambridge University Press

Introduction 1 6 The General Neurotic Syndrome at 12

Published online by Cambridge University Press

Published online by Cambridge University Press

Published online by Cambridge University Press

https://doi.org/10.1017/9781911623823.001 Published online by Cambridge University Press

Published online by Cambridge University Press

https://doi.org/10.1017/9781911623823.002 Published online by Cambridge University Press

The Birth of Neurosis

https://doi.org/10.1017/9781911623823.002 Published online by Cambridge University Press

The Recognition of Personality Status in Neurosis

https://doi.org/10.1017/9781911623823.002 Published online by Cambridge University Press

https://doi.org/10.1017/9781911623823.002 Published online by Cambridge University Press

Neurosis and Neuroticism

https://doi.org/10.1017/9781911623823.002 Published online by Cambridge University Press

https://doi.org/10.1017/9781911623823.002 Published online by Cambridge University Press

https://doi.org/10.1017/9781911623823.002 Published online by Cambridge University Press

1.1 Initial ideas

https://doi.org/10.1017/9781911623823.003 Published online by Cambridge University Press

https://doi.org/10.1017/9781911623823.003 Published online by Cambridge University Press

1.2 Later Stage (1980s)

1 Simultaneous and Past Presentation of Two or More Symptoms of Six Conditions

https://doi.org/10.1017/9781911623823.003 Published online by Cambridge University Press

(b) they are a common group of disorders (Aronson, 1987);

2 The Triggering Eﬀect of Stress

3 There Are Abnormal Personality Features of a Passive Dependent or an Anankastic

Life event score

Hy s Anxiety Anxiety Anxiety Anxiety

https://doi.org/10.1017/9781911623823.003 Published online by Cambridge University Press

The simultaneous presence of a clinical syndrome (cothymia) and personality disorder

4 History of a Similar Syndrome in First-Degree Relatives

https://doi.org/10.1017/9781911623823.003 Published online by Cambridge University Press

1.3 Progress in Understanding the General Neurotic Syndrome

I also created the General Neurotic Syndrome Scale (Table 1.1)

Table 1.1 The General Neurotic Syndrome Scale (GNSS)

Positive characteristics Score Negative characteristics Score

Simultaneous presence of +2 Persistent phobic and −2

https://doi.org/10.1017/9781911623823.003 Published online by Cambridge University Press

Post-traumatic Agoraphobia and panic disorder

Mixed anxiety and depressive disorder

https://doi.org/10.1017/9781911623823.003 Published online by Cambridge University Press

Nature of symptom Associated mood

Somatic symptoms anxiety and depression

https://doi.org/10.1017/9781911623823.003 Published online by Cambridge University Press

1.4 Gavin Andrews and the General Neurotic Syndrome

https://doi.org/10.1017/9781911623823.003 Published online by Cambridge University Press

He also oﬀered prospects for treatment.

1.5 Developments and Changes in Classiﬁcation since 2010

https://doi.org/10.1017/9781911623823.003 Published online by Cambridge University Press

1.6 Identiﬁcation of the Co-occurrence of Anxiety

Dysthymic disorder is characterised by a persistent depressive mood (i.e., lasting 2 years or

https://doi.org/10.1017/9781911623823.003 Published online by Cambridge University Press

A depressive episode is characterised by a period of almost daily depressed mood or