Adult  Psychiatry  II    

Paper  B   Syllabic  content  7.1x  
 
© SPMM Course

We claim copyright for our own text material, productions and adaptations. We claim no
rights to Images/Figures with CC-BY-SA license if they are used in this material.
©  SPMM  Course   1  
 1. Anxiety Disorders - Overview
15%   of   adults   in   the   UK   at   any   time   have   broadly   defined   neurosis   according   to   National   Psychiatric  
Morbidity   Survey   (NPMS,   1995).   In   this   study,   the   UK   prevalence   of   anxiety   disorder   was   higher   than  
depression   (consistent   with   ECA   and   NCS   studies   from   the   USA).   Phobic   disorder   the   most   common   in  
ECA  &  NCS  but  in  NPMS  –    the  most  common  anxiety  disorder  was  mixed  anxiety-­‐‑depression  followed  
by  GAD.  25%  of  all  GP  consultations  are  for  anxiety  related  symptoms.  

Considering  the  mean  age  of  onset  for  various  anxiety  disorders,  the  following  pattern  is  noted;  GAD  –  30  
years,  Panic  disorder  –  22  to  25  years,  OCD  –  20  years,  social  phobia  –  15  years,  specific  phobia  –  varies  
with   individual   categories   –   blood   injury   injection   or   environmental   types   start   around   age   5   to   9   years  
while  situational  phobia  starts  around  20  years  of  age.    

It   is   noted   that   with   each   generation,  

anxiety   disorders   are   diagnosed   at   a  
younger  age  than  the  previous  cohort.  

The   estimated   lifetime   prevalence   of  

blood-­‐‑injection-­‐‑injury   phobia   is  
around  3.5%.  The  median  age  of  onset  is  
around  5  to  6  years.  Subjects  with  blood-­‐‑
injection-­‐‑injury   phobia   have   higher  
lifetime   histories   of   fainting   and  
seizures.   Prevalence   was   lower   in   the  
elderly  and  higher  in  females  and  persons  with  less  education.    

Sex  distribution  of  anxiety  disorders  is  an  important  topic  often  tested  in  the  exams.  As  a  general  rule,  all  
anxiety  disorders  are  common  in  women  than  men.  Notable  exceptions  are  OCD,  which  is  more  in  boys  
than   girls,   but   equally   common   in   adult   men   and   women.   Also,   men   outnumber   women   in   attending  
health  care  centres  for  social  phobia.    

Summary  of  NICE  guidance:  treatment  for  generalized  anxiety  disorder,  panic  disorder  and  OCD  

Ø A  ‘stepped  care’  approach  to  help  in  choosing  the  most  effective  intervention  
Ø A  comprehensive  assessment  that  considers  the  degree  of  distress  and  functional  impairment;  
the  effect  of  any  co-­‐‑morbid  mental  illness,  substance  misuse  or  medical  condition;  and  past  
response  to  treatment  
Ø Treat  the  primary  disorder  first  
Ø Psychological  therapy  is  more  effective  than  pharmacological  therapy  and  should  be  used  as  
first  line  where  possible.    
Ø Pharmacological  therapy  is  also  effective.    Most  evidence  supports  the  use  of  SSRIs  
Ø Consider  combination  therapy  for  complex  anxiety  disorders  that  are  refractory  to  treatment  

©  SPMM  Course   2  
 2. Obsessive Compulsive Disorder:
Epidemiology:  The  point  prevalence  of  OCD  is  as  high  as  1-­‐‑3%  of  adults  and  1-­‐‑2%  of  children  and  
adolescents  (community  samples).  The  lifetime  prevalence  of  OCD  is  fairly  constant  –  around  2-­‐‑3%.  It  is  
the  fourth  most  commonly  prevalent  psychiatric  disorder  in  epidemiological  studies  (after  phobias,  
alcohol  use,  and  depression).  The  gender  ratio  of  OCD  in  clinical  samples  is  roughly  equal,  but  females  
predominate  in  community  populations  (~1.5:1),  this  may  be  because  men  have  more  severe  
psychopathology.    Males  with  OCD  showed  an  earlier  onset  and  a  trend  toward  more  tics  and  poorer  
outcome  than  females.  (Heyman  et  al.,  2006)  

Presentation:  Recent  factor  analytic  studies  of  obsessions  and  compulsions  in  OCD  tend  to  show  a  four-­‐‑
factor  model  (Castle  &  Phillips,  2006):    

• Aggressive,  sexual,  and  religious  obsessions,  and  checking  compulsions;    

• Symmetry  and  ordering  obsessions  and  compulsions;  (often  chronic  and  treatment  resistant)  
• Contamination  obsessions  and  cleaning  compulsions;    
• Hoarding  obsessions  and  compulsions  (may  be  neurobiologically  distinct  and  often  treatment  
resistant)  
Aetiology:  The  aetiology  of  OCD  is  unknown.  Hypermetabolism  of  basal  ganglia  structures  (caudate)  has  
been  reported  in  several  neuroimaging  studies.  D2  antagonists  such  as  clozapine  and  other  antipsychotics  
can  cause  secondary  OCD-­‐‑like  symptoms  in  some  patients.  Children  with  autoimmune  reactions  (e.g.  
PANDAS  -­‐‑see  below)  have  a  higher  prevalence  of  OCD.    OCD  also  overlaps  with  a  spectrum  of  other  
disorders.  OCD  spectrum  disorders  can  be  classified  as:    

• 1.  Those  associated  with  somatic  preoccupation  e.g.body  dysmorphic  disorder,  hypochondriasis  or  
anorexia  nervosa.  
• 2.  Those  associated  with  neurological  disorders  (repetitive  behaviours)  e.g.  Tourette  syndrome,  
Sydenham'ʹs  chorea  and  autistic  spectrum.  
• 3.  Those  associated  with  impulse  control  disorders  or  with  rousing  or  pleasurable  repetitive  
behaviours  e.g.  paraphilias,  kleptomania,  trichotillomania,  and  pathological  gambling.  (Castle  &  
Phillips,  2006)  
• Anankastic  personality  can  also  be  considered  a  part  of  OCD  spectrum.    

PANDAS:  Paediatric  autoimmune  neuropsychiatric  disorders  associated  with  streptococcal  infection—

PANDAS  is  thought  to  be  secondary  to  streptococcal  infection  and  mediated  by  autoantibodies  binding  to  
basal  ganglia.  This  produces  tics,  fluctuating  obsessive-­‐‑compulsive  symptoms  and  anxiety.    

National  Institute  of  Mental  Health  Clinical  Diagnostic  Criteria  for  PANDAS  
1.  The  presence  of  OCD  or  a  tic  disorder.  
2.  Onset  between  3  years  of  age  and  the  beginning  of  puberty.  
3.  Abrupt  onset  of  symptoms  or  a  course  characterized  by  dramatic  exacerbations  of  symptoms.  
4.  The  onset  or  the  exacerbations  of  symptoms  is  temporally  related  to  infection  with  GABHS.  
5.  Abnormal  results  of  the  neurologic  examination  (hyperactivity,  choreiform  movements,  and/or  tics)  during  an  
 
exacerbation.  

©  SPMM  Course   3  
Note  that  the  neuropsychiatric  symptoms  need  not  have  onset  during  the  streptococcal  (group  A  
beta-­‐‑hemolytic)  infection;  exacerbation  correlated  temporally  is  also  acceptable  for  a  diagnosis.  

AntiDNAseB  or  Antistreptolysin  O  titres  are  likely  to  be  elevated  in  most  with  recent  
streptococcal  infection.  A  fraction  of  these  may  have  autoantibodies  to  neurons  in  basal  ganglia  
called  anti  basal  ganglia  antibodies.    

Treatment  of  OCD  (according  to  NICE  guidelines)  

 
mild  to  moderate step  1  self-­‐‑help step  2:  CBT  with  ERP step  3:  SSRIs+/-­‐‑  CBT

assess  severity Responders:  continue  

SSRI  for  1-­‐‑2  years  +/-­‐‑    
booster  CBT
severe step  1:  SSRIs+/-­‐‑  CBT
 
Non-­‐‑responders:  
switch  to  different  
  SRI  or  clomipramine

Exposure  and  response  prevention  is  a  key  element  of  CBT  for  of  OCD.  Patients  are  trained  to  confront  
(directly  or  in  imagination)  anxiety-­‐‑provoking  situations  while  abstaining  from  compulsive  behaviours  in  
response.    Periodic  exposure  and  response  prevention  “booster”  sessions  can  reduce  the  risk  of  relapse  
and  provide  more  durable  remission  than  using  pharmacotherapy  alone.  

OCD  shows  a  selective  response  to  serotonergic  medications  such  as  clomipramine  and  SSRIs.  Around  60  
to  70%  of  patients  experience  some  degree  of  improvement  after  SSRI  treatment  (typically  at    a  higher  
dose,  given  for  a  longer  duration  than  for  depression).  NNT  for  SSRIs  (vs.  placebo)  varies  between  6  and  
12.  Antipsychotic  augmentation  is  indicated  if  no  response  is  seen  after  a  three-­‐‑month  trial  of  a  maximal  
dose  of  SSRI.  This  is  especially  useful  when  tics  are  also  seen.  

©  SPMM  Course   4  
 3. Post-Traumatic Stress Disorder:
Diagnostic  criteria  for  PTSD  have  been  altered  in  DSM-­‐‑5.  PTSD  (as  well  as  Acute  Stress  Disorder)  have  
been  moved  from  anxiety  disorders  into  a  new  class  of  "ʺtrauma  and  stressor-­‐‑related  disorders."ʺ    A  history  
of  exposure  to  a  traumatic  event  that  meets  specific  stipulations  and  symptoms  from  each  of  four  
symptom  clusters:  intrusion,  avoidance,  negative  alterations  in  cognitions  and  mood  (including  self-­‐‑blame  
or  blaming  others  persistently),  and  alterations  in  arousal  and  reactivity  (including  reckless  and  
destructive  behaviour).  A  clinical  subtype  "ʺwith  dissociative  symptoms"ʺ  has  also  been  added.    

Epidemiology:  The  incidence  varies  across  the  world.    Point  prevalence  is  1%.  The  National  Comorbidity  
Survey  Replication  (NCS-­‐‑R)  found  the  lifetime  prevalence  of  PTSD  among  adult  Americans  to  be  6.8%.    
The  lifetime  prevalence  among  men  was  3.6%,  and  among  women  was  9.7%.    It  is  unclear  whether  the  
gender  difference  is  due  to  higher  exposure  to  trauma  or  greater  vulnerability  to  develop  PTSD.    

Males   are   more   likely   than   females   to   be   exposed   to   traumatic   events   (60%   males   vs.   50%   females).   But  
females  develop  PTSD  two  times  more  frequently  (12%  vs.  6%  in  NCS)  even  after  controlling  the  type  of  
trauma.  It  is  unclear  if  this  is  due  to  higher  exposure  to  trauma  or  greater  vulnerability  to  develop  PTSD.    

Up  to  30%  of  people  exposed  to  trauma  may  develop  PTSD.  The  most  frequently  experienced  trauma  is  
witnessing  someone  being  badly  injured  or  killed,  followed  by  exposure  to  fire,  flood  or  natural  disaster,  
being   involved   in   a   life-­‐‑threatening   accident   and   combat   exposure.   Molestation   is   more   common   in  
females   than   males.   Mugging   is   more   common   in   males   than   females.   But   in   both   instances   women  
develop  more  PTSD.  The  only  trauma  where  men  develop  more  PTSD  is  rape.    

PTSD   is   more   common   in   younger   than   older   individuals;   more   common   in   those   with   higher   anxiety  
response   to   the   initial   event   and   in   those   who   perceive   external   locus   of   control   (as   opposed   to   internal  
locus).  

NICE  encourages  primary  care  diagnosis  and  screening,  as  PTSD  is  probably  underdiagnosed.  

Aetiology:  Resilience  to  trauma  is  a  dynamic  factor;  individuals  who  may  not  develop  PTSD  after  
one  trauma  may  develop  after  another.
Factors  associated  with  post-­‐‑traumatic  stress  disorder  (from  Bisson,  2007)  include  pre-­‐‑traumatic  factors  
such  as  previous  psychiatric  disorder,  females  gender,  personality  (external  locus  of  control  greater  than  
internal  locus  of  control),  lower  socioeconomic  and  educational  status,    ethnic  minority  status  and  
personality  disorders  (cluster  B);  peritraumatic  factors  include  the  higher  severity  of  trauma,  perceived  
threat  to  life  and  peritraumatic  dissociation.  Post-­‐‑traumatic  factors  include  perceived  lack  of  social  
support,  subsequent  life  stress  or  physical  illness  (especially  chronic  pain).  Protective  factors  include  high  
IQ,  higher  social  class,    and  getting  an  opportunity  to  grieve  for  the  loss  (e.g.  viewing  the  dead  body  of  
friend/relative  after  trauma).  

Hippocampus  and  amygdala  show  neuroimaging  abnormalities.  Hypocortisolaemia  is  reported  in  PTSD.  
Strong  avoidance  features  may  predict  chronicity  in  PTSD.  

©  SPMM  Course   5  
Prevention  of  PTSD:  

What  are  the  effects  of  interventions  to  prevent  post-­‐‑traumatic  stress  disorder  (Bisson,  Clinical  evidence  
2004)?  

Likely  to  be  beneficial   Multiple-­‐‑session  CBT  to  prevent  PTSD  in  people  with  acute  
stress  disorder  (reduced  PTSD  compared  with  supportive  
counselling)    

Unknown  effectiveness   Multiple-­‐‑session  CBT  to  prevent  PTSD  in  all  people  exposed  to  
a  traumatic  event    
Propranolol  to  prevent  PTSD    
Single-­‐‑session  group  debriefing  to  prevent  PTSD    
Temazepam  to  prevent  PTSD    

Unlikely  to  be  beneficial   Single-­‐‑session  individual  debriefing  to  prevent  PTSD    
Supportive  counselling  to  prevent  PTSD  
(Prescriber  2005;  15(8):40-­‐‑48,  Ballanger  et  al.,  J  Clin  Psychiatry  2000;  61  (Suppl  5):60-­‐‑66)  

Treatment  of  PTSD:    

NICE  suggests  the  following:  

Initial  Management  in  Primary  Care  

• Watchful  waiting  where  symptoms  are  mild  and  have  been  present  for  less  than  4  weeks  after  the  
trauma  
• The  prescription  of  a  non-­‐‑benzodiazepine  sleeping  tablet  after  four  consecutive  nights’  sleep  
disturbance  is  recommended  

Further  Specialist  Management:  

• Psychological  treatment  should  be  done  in  a  regular  and  continuous  (usually  at  least  once  a  week)  
manner  and  should  be  delivered  by  the  same  person  
• Non-­‐‑trauma-­‐‑focused  interventions  such  as  relaxation  or  non-­‐‑directive  therapy  should  not  be  used  
routinely  since  these  do  not  address  traumatic  memories    
• Interventions  used  when  symptoms  are  present  within  3  months  of  a  trauma  
o trauma-­‐‑focused  cognitive  behavioural  therapy  which  includes  a  combination  of  exposure  
therapy,  cognitive  therapy  and  stress  management    
o Should  be  offered  to  those  with  severe  post-­‐‑traumatic  symptoms  or  with  severe  PTSD  in  
the  first  month  after  the  traumatic  event  and  people  who  present  with  PTSD  within  3  
months  of  the  event  
o Normally  provided  on  an  individual  outpatient  basis;  around  8–12  sessions  are  usually  
offered  (five  sessions  if  the  treatment  starts  within  1  month  of  the  event)  

©  SPMM  Course   6  
 o The  prescription  of  a  nonbenzodiazepine  medication  after  four  consecutive  nights  of  sleep  
disturbance  is  recommended.  For  short-­‐‑term  use  -­‐‑  hypnotic  medication;  For  longer-­‐‑term  
use  –  an  early  introduction  of  a  suitable  antidepressant  should  be  done  to  avoid  
dependence.  
• Interventions  used  when  symptoms  are  present  for  more  than  3  months  after  a  trauma  
o trauma-­‐‑focused  CBT  or  eye  movement  desensitisation  and  reprocessing  (EMDR)  
o Up  to  12  sessions  can  be  offered.  In  case  of  treatment  failure  or  limited  improvement  with  a  
specific  trauma-­‐‑focused  psychological  treatment,  consider  an  alternative  form  of  trauma-­‐‑
focused  psychological  treatment;  if  no  improvement  considers  pharmacological  treatment.  
o Paroxetine,  mirtazapine  for  general  use;  amitriptyline  or  phenelzine  for  specialist  use.  

Drug   Evidence  &  practice  in  the  UK  

Paroxetine   Good  RCT  evidence.  NICE  second  line.  Licensed  for  PTSD    

Sertraline   RCT  evidence;  but  NICE  appraisal  did  not  show  significance.  Licensed  for  females  
not  males  with  PTSD  in  the  UK.  

Fluoxetine   1  RCT  but  not  significant  

Imipramine  &   Poor  quality  of  evidence;  but  a  statistically  significant  result  for  Amitriptyline;  not  
Amitriptyline   so  for  imipramine.  
Phenelzine   Poor  quality  of  evidence;  but  statistically  significant  result  

Mirtazapine     One  small  strongly  positive  RCT.  NICE  second  line.  

Venlafaxine   One  large  RCT  no  benefit  

Olanzapine   Monotherapy  RCT  negative;  augmentation  of  SSRIs  positive  

Risperidone   Tested  only  as  adjunct  –  no  effect  

Considerable  research  has  been  conducted  in  particular  approaches  to  the  psychotherapy  of  PTSD.    The  
evidence  indicates  that  modalities  tested  in  Randomised  Controlled  Trials  are  far  from  100%  applicable  
and  effective.    The  RCT  model  itself  is  inadequate  for  evaluating  treatments  of  conditions  with  complex  
presentations  and  multiple  comorbidities.    Psychotherapy  studies  often  exclude  patients  with  comorbidity  
and  complexity  (Corrigan  &  Hull,  2015)  

In  a  meta-­‐‑analysis  by  Bisson  et  al.  (2007)  no  evidence  of  a  difference  in  efficacy  between  TFCBT  and  EMDR  
was  noted,  but  there  was  some  evidence  that  TFCBT  and  EMDR  were  superior  to  stress  management  and  
other  therapies,  and  that  stress  management  was  superior  to  other  therapies.  In  a  Cochrane  review  it  was  
shown  that  psychological  debriefing  after  trauma  is  either  equivalent  to,  or  worse  than,  control  or  
educational  interventions  in  preventing  or  reducing  the  severity  of  PTSD,  depression,  anxiety  and  general  

©  SPMM  Course   7  
psychological  morbidity  after  trauma.  There  is  some  suggestion  that  it  may  increase  the  risk  of  PTSD  and  
depression.  

Trauma-­‐‑focused   CBT:   May   includes   exposure   therapy   wherein   repeated   confrontation   of   traumatic  
memories   and   repeated   exposure   to   avoided   situations   take   place   together   with   relaxation   and   anxiety  
reduction.   In   trauma-­‐‑focused   cognitive   component   modification   of   misinterpretations   that   lead   to  
overestimation  of  current  threat  and  modification  of  other  beliefs  related  to  the  traumatic  experience  and  
the  individual'ʹs  behaviour  during  the  trauma  (for  example,  guilt  and  shame)  are  attempted  via  cognitive  
restructuring   process.   Trauma-­‐‑focused   psychological   treatment   should   usually   be   given   for   eight   to   12  
sessions  

Eye  movement  desensitisation  and  reprocessing:  This  was  serendipitously  discovered  by  a  psychologist  
(Shapiro)  when  she  first  applied  it  to  herself.  It  is  based  on  the  theory  that  bilateral  stimulation,  in  the  form  
of   eye   movements,   allows   the   processing   of   traumatic   memories.   While   the   patient   focuses   on   specific  
images,   negative   sensations   and   associated   cognitions,   bilateral   stimulation   is   applied   to   desensitize   the  
individual  to  these  memories  and  more  positive  sensations  and  cognitions  are  introduced.  

Outcome:  More  than  a  third  of  people  reported  having  the  disorder  six  years  after  they  first  developed  it.  
50%  chance  of  remission  at  two  years.  

Acute  stress  disorder  is  a  diagnostically  different  entity  from  PTSD.  To  diagnose  acute  stress  reaction,  
there  must  be  an  immediate  and  clear  temporal  connection  between  the  impact  of  an  exceptional  stressor  
and  the  onset  of  symptoms.  The  symptoms  usually  appear  within  minutes  of  the  impact  of  the  stressful  
stimulus  or  event  and  disappear  within  2-­‐‑3  days  (often  within  hours).  Partial  or  complete  amnesia  for  the  
episode  may  be  present.  In  addition,  the  symptoms:    
(a)  Show  a  mixed  and  usually  changing  picture;  in  addition  to  the  initial  state  of  "ʺdaze"ʺ,  depression,  
anxiety,  anger,  despair,  overactivity,  and  withdrawal  may  all  be  seen,  but  no  one  type  of  symptom  
predominates  for  long;    
(b)  Resolve  rapidly  (within  a  few  hours  at  the  most)  in  those  cases  where  removal  from  the  stressful  
environment  is  possible;  in  cases  where  the  stress  continues  or  cannot  by  its  nature  be  reversed,  the  
symptoms  usually  begin  to  diminish  after  24-­‐‑48  hours  and  are  usually  minimal  after  about  3  days.    
This  diagnosis  should  not  be  used  to  cover  sudden  exacerbations  of  symptoms  in  individuals  already  
showing  symptoms  that  fulfill  the  criteria  for  any  other  psychiatric  disorder,  except  for  those  in  F60  
(personality  disorders).  However,  a  history  of  previous  psychiatric  disorder  does  not  invalidate  the  use  of  
this  diagnosis.    

©  SPMM  Course   8  
 4. Generalised Anxiety Disorder:
The  feature  of  avoidance  seen  in  other  anxiety  disorders  is  not  needed  for  a  diagnosis  of  GAD;  it  is  often  
punctuated  by  depressive  episodes  and  co-­‐‑existent  with  a  number  of  comorbid  diseases.  

Epidemiology:  the  lifetime  prevalence  of  DSM-­‐‑IV  GAD  is  estimated  to  be  about  5%;  point  prevalence  is  
about  2%  to  3%  (Weisberg,  2009)  

Aetiology:  Twin  studies  suggest  MZ  concordance  41%  vs.  DZ  4%,  though  the  rates  vary  in  different  
samples  (e.g.  Andrews  et  al.  study  -­‐‑  21.5%  concordance  in  MZ  twins,  compared  with  a  13.5%  in  DZ).    Risk  
factors  include  exposure  to  civilian  trauma,  bullying  or  peer  victimisation.  a  higher  number  of  life  events,  
being  a  first-­‐‑degree  relative  of  a  GAD  patient  and  female  gender.  

Hamilton  anxiety  scale  is  a  14-­‐‑item  instrument  that  emphasizes  somatic  symptoms.  Treatment  response  is  
generally  defined  as  a  50%  reduction  in  baseline  score.  Clinical  recovery  is  often  defined  as  a  score  of  less  
than  7  on  the  Hamilton  anxiety  scale.  
Treatment:  

Acute  treatment   SSRIs:  escitalopram,  paroxetine,  sertraline.    

TCAs:  imipramine.    
Benzos:  alprazolam  and  diazepam  (not  suited  for  long-­‐‑term  
therapy).    
Venlafaxine,  duloxetine  &  Buspirone    
CBT    
Long-­‐‑term  efficacy/relapse   Paroxetine,  escitalopram,  CBT,  venlafaxine,  pregabalin.  
prevention  
Adjuncts  for  non-­‐‑response   Antipsychotics  olanzapine/risperidone  low  doses.  
Adapted  from  Tyrer,  P  &  Baldwin,  D  (2006).  Generalised  anxiety  disorder.  368,  9553:  2156-­‐‑2166  

NICE  recommends  that  an  SSRI  should  be  used  as  a  first  line.    SNRIs  and  pregabalin  are  alternative  
choices.    Among  psychological  treatments,  both  CBT  and  anxiety  management  therapy  are  useful  though  
CBT  may  be  better  in  efficacy.    CBT  includes  education,  relaxation  training,  and  exposure  and  cognitive  
restructuring.  

Guidelines  including  NICE  suggest  that  there  is  insufficient  evidence  to  recommend  combined  
psychological  and  pharmacological  treatment  initially,  although  this  can  be  considered  if  initial  treatment  
fails.  

Outcome:  At  12-­‐‑year  follow-­‐‑up  of  adults  at  an  anxiety  clinic,  42%  of  patients  had  recovered  from  
generalised  anxiety  disorder,  but  the  disorder  was  a  marker  for  poor  outcome  in  those  patients  who  had  
another  anxiety  disorder.  

©  SPMM  Course   9  
Herbal  Treatment  of  Anxiety:  The  kava  shrub  (Piper  methysticum)  has  been  studied  in  anxiety  disorders  
and  appears  to  be  effective  in  some  trials.  Gingko  and  valerian  are  not  effective;  common  lavender,  saffron,  
German  chamomile  and  lemon  balm  appear  promising  (Ernst  13  (4):  312.  APT  (2007).  

o The  effects  of  kava  are  due  to  the  kavapyrones,  which  in  animal  models  act  as  muscle  relaxants  and  
anticonvulsants,  protect  against  strychnine  poisoning,  and  reduce  limbic  system  excitability.    
o They   may   cause   inhibition   of   voltage-­‐‑dependent   sodium   channels,   increase   GABAA   receptor  
densities,  block  norepinephrine  reuptake,  and  suppress  the  release  of  glutamate.  
o Several  double-­‐‑blind,  placebo-­‐‑controlled  trials  have  shown  kava  to  be  more  effective  than  placebo  
in   reducing   HAM-­‐‑A   scale   scores,   and   this   effect   is   detectable   even   within   1   week   of   therapy.  
Werneke  et  al.  in  found  that  kava  (Piper  methysticum)  was  the  most  researched  remedy  for  anxiety  
and  that  there  was  good  evidence  for  its  anxiolytic  effect.  A  Cochrane  review  reported  of  11  RCTs  
showed  that  kava  is  the  only  herbal  remedy  that  has  been  proven  to  be  effective  in  reducing  anxiety.  
But   kava   cannot   be   recommended   for   clinical   use   because   of   an   association   with   hepatotoxicity,  
which  has  led  to  its  withdrawal  from  the  UK  market.  
o Kava   is   associated   with   allergic,   sometimes   fatal   hepatotoxicity   and   so   not   recommended   for  
general  use.  (Beaubrun  &  Gray,  2000)  
o Cochrane  reviews  of  valerian  and  passiflora  showed  no  efficacy  in  anxiety  compared  to  diazepam.  
o Kava   can   interact   with   levodopa   and   alprazolam,   causing   extrapyramidal   symptoms   or   lethargy.  
Valerian   can   interact   with   loperamide   and   fluoxetine,   causing   delirium.   Evening   primrose   oil   can  
interact  with  phenothiazides,  causing  epileptic  seizures.  

5. Social Phobia:
Point  prevalence  is  2.8%.  Two  types  are  recognised  (Schneier,  2003):  A  generalised  subtype  where  fear  
occurs  in  most  social  situations.  This  leads  to  higher  impairment  and  patients  are  more  likely  to  seek  
treatment,  than  the  second  subtype.    A  situational  or  non  generalised  subtype  presents  as  fear  of  public  
speaking  or  performance  anxiety.      

Treatments:    The  best-­‐‑established  treatments  are  CBT  &  SSRIs.    Benzodiazepines  should  not  be  used.  

• Paroxetine,  sertraline,  fluoxetine  and  fluvoxamine,  escitalopram,  venlafaxine  have  been  evaluated  
in  RCTs  with  a  favourable  outcome.  Normal  antidepressant  doses  can  be  used  but  may  need  a  
longer  12-­‐‑week  trial  to  establish  outcome.  Drug  treatment  should  continue  for  at  least  6-­‐‑12  months  
after  the  response.      
• Phenelzine  is  the  second  line  treatment.    Moclobemide  is  also  effective.      
• Short-­‐‑term  use  of  benzodiazepines  including  clonazepam  and  novel  anticonvulsant  gabapentin  
has  been  evaluated  with  some  evidence.    
• SSRI  +  clonazepam  combination,  gabapentin  or  pregabalin  can  be  tried  as  third-­‐‑line  agents.  
•    Blockers  are  not  significantly  different  from  placebo  in  generalised  subtype,  but  they  can  be  used  
on/off  in  performance  anxiety  subtype.  
Ø Self-­‐‑help  principles  should  be  encouraged.  
 
©  SPMM  Course   10  
 6. Panic Disorder:
Panic  can  exist  in  different  forms.  Major  classificatory  systems  recognise  panic  disorder,  agoraphobia  and  
comorbid  panic  disorder  with  agoraphobia.  DSM  puts  panic  disorder  as  primary  dysfunction  while  ICD  
focuses   on   agoraphobia.   To   diagnose   panic   disorder,   there   must   be   frequent   panic   attacks   within   a  
specified  time  interval.  

Epidemiology:  It  is  increasingly  being  realised  that  panic  attacks  can  occur  without  fully  satisfying  panic  
disorder   criteria.   Patients   with   such   panic   attacks   have   a   significant   impairment,   help   seeking   and  
medication   requirement.   Point   prevalence   of   panic   disorder   is   0.9%.   The   NCS-­‐‑R   collected   data   on   four  
composite   groups:   Isolated   panic   attacks   (PA   only),   Panic   attacks   with   AG   (PA-­‐‑AG),  Panic  disorder  (PD  
only),  PD  with  AG  (PD-­‐‑AG).  Lifetime  prevalence  of  PA  only  was  28%  while  4.7%  had  lifetime  PD.  Only  
1.1%   had   PD-­‐‑AG   while   0.8%   had   lifetime   PA-­‐‑AG.   Cued   panic   attacks   are   common   in   PD   and   AG  
compared   to   isolated   PA   where   non-­‐‑cued   out   of   blue   panic   is   seen.   The   mean   age   of   onset   of   any   panic  
attack  –  irrespective  of  diagnosis  –  is  around  22  years.    All-­‐‑cause  mortality  is  increased  by  1.9  times  (SMR)  
in  those  with  panic  disorder.  

The   ICD-­‐‑10   classifies   panic   disorder   as   recurrent,   unpredictable   panic   attacks,   with   sudden   onset   of  
palpitations,   chest   pain,   choking   sensations,   dizziness,   and   feelings   of   unreality,   often   with  
associated  fear  of  dying,  losing  control,  or  going  mad,  but  without  the  requirement  for  the  symptoms  
to  have  persisted  for  1  month  or  longer.  

Aetiology:  An  estimated  heritability  of  30%-­‐‑40%  is  noted.  According  to  cognitive  theory  patients  with  
panic  disorder  have  a  heightened  sensitivity  to  internal  bodily  sensations.  A  fear  network  involving  the  
amygdala,  orbitofrontal  cortex  and  hypothalamus  has  been  implicated  in  some  neuroimaging  studies.  

Treatment:  NICE  guideline  summary  

• CBT  psychotherapy  -­‐‑  seven  to  14  hours  of  cognitive  behaviour  therapy—usually  weekly  sessions  of  
one  to  two  hours,  completed  within  four  months  is  recommended.  
• Self-­‐‑help  by  bibliotherapy  and  self-­‐‑help  groups  and  support  groups  are  useful  in  primary  care.  
• SSRIs  are  useful  first-­‐‑line  drug  treatments.  
• If  no  improvement  is  seen  after  a  12-­‐‑week  course  of  SSRIs,  imipramine  or  clomipramine  should  be  
considered.    
• Benzodiazepines  are  associated  with  a  worse  outcome  in  the  long  term  and  should  not  be  
prescribed.  
 
BAP  recommendations  for  panic  disorder:  
For  acute  management  according  to  patient  choice:  
• pharmacological:  all  SSRIs,  some  TCAs  (clomipramine,  imipramine),  some  benzodiazepines  
(alprazolam,  clonazepam,  diazepam,  lorazepam),  venlafaxine,  reboxetine  have  evidence  base  or  
psychological:  cognitive-­‐‑behaviour  therapy.  
• Both  pharmacological  and  psychological  approaches  have  broadly  similar  efficacy  in  acute  
treatment.  
©  SPMM  Course   11  
 • Consider  an  SSRI  for  first-­‐‑line  pharmacological  treatment.  
• Consider  increasing  the  dose  if  there  is  an  insufficient  response,  but  there  is  only  limited  evidence  
for  a  dose-­‐‑response  relationship  with  SSRIs.  
• Treatment  periods  of  up  to  12  weeks  are  needed  to  assess  efficacy.  
Longer-­‐‑term  treatment  
• Consider  cognitive  therapy  with  exposure  as  this  may  reduce  relapse  rates  better  than  drug  
treatment.  
• Continue  drug  treatment  for  a  further  six  months  in  patients  who  are  responding  at  12  weeks:  first  
line  drug  choice  is  an  SSRI;  imipramine  is  a  second-­‐‑line  choice  
• Routinely  combining  drug  and  psychological  approaches  is  not  recommended.  
When  initial  treatments  fail  
• Consider  switching  at  12  weeks  
• Consider  combining  evidence-­‐‑based  treatments  only  when  there  are  no  contraindications  Consider  
adding  paroxetine  or  buspirone  to  psychological  treatments  after  partial  response    
• Consider  adding  paroxetine,  whilst  continuing  with  CBT,  after  initial  non-­‐‑response.  
 

7. Other related disorders

 

A. Hypochondriasis
Classed  in  ICD-­‐‑10  as  a  preoccupation  with  the  fear  of  having  a  serious  disease  based  on  the  
misrepresentation  of  bodily  symptoms.    DSM-­‐‑V  has  removed  hypochondriasis  as  a  disorder  as  the  
name  was  perceived  as  pejorative  and  most  patients  with  a  former  diagnosis  of  hypochondriasis  
would  now  be  diagnosed  as  having  Somatic  Symptom  Disorder  or  Illness  Anxiety  Disorder  (see  
below).
Prevalence  and  Risk  Factors  
Most  information  comes  from  studies  conducted  in  primary  care.    Prevalence  has  been  reported  
between  0.8  and  4.5%.    There  is  no  conclusive  data  about  specific  risk  factors,  but  there  are  
associations  with  anxiety,  depressive  and  other  somatoform  disorders.  
Treatment  
CBT  has  been  shown  to  be  efficacious,  and  group  cognitive-­‐‑behavioural  therapy  may  also  be  useful.    
SSRIs  may  also  be  efficacious.  
 

B. Body Dysmorphic Disorder:

A  patient  with  body  dysmorphic  disorder  (BDD)  (dysmorphophobia)  is  convinced  that  part  of  their  body  
has  a  defect  or  is  flawed  in  some  way.  To  the  observer,  the  appearance  is  normal  or  of  a  minor  
abnormality.    The  patient  engages  in  repetitive  behaviours  or  mental  acts  in  response  to  preoccupations  
with  perceived  defects  or  flaws.    BDD  has  both  psychotic  and  non-­‐‑psychotic  variants,  classified  in  DSM-­‐‑
V  as  BDD  with  delusional  or  without  delusional  component,  suggesting  they  can  be  considered  as  part  of  
the  same  disorder,  characterized  by  a  spectrum  of  insight.  
©  SPMM  Course   12  
Aetiology:  Factors  that  may  predispose  persons  to  BDD  include:  
• low  self-­‐‑esteem  
• critical  parents  and  significant  others  
• early  childhood  trauma  
• unconscious  displacement  of  emotional  conflict  
Epidemiology:  Patients  with  BDD  also  had  an  earlier  onset  of  major  depression  and  higher  lifetime  rates  
of  major  depression  (26%),  social  phobia  (16%),  obsessive-­‐‑compulsive  disorder  (6%),  and  psychotic  
disorder  diagnoses  as  well  as  higher  rates  of  substance  use  disorders  in  first-­‐‑degree  relatives.    Studies  
have  reported  rates  of  BDD  of  7%  and  15%  of  patients  seeking  cosmetic  surgery  and  a  rate  of  12%  in  
patients  seeking  dermatologic  treatment.  

Treatment:  High-­‐‑dose  SSRIs  used  for  a  longer  duration  than  the  usual  antidepressant  trial  period  can  be  
effective.  Fluoxetine  has  RCT  evidence  in  this  regard.  Antipsychotics  have  also  been  studied  with  variable  
success.  Pimozide  has  anecdotal  support  though  the  risk  of  QT  prolongation  precludes  wider  use.  CBT  
has  been  shown  to  be  effective  in  a  number  of  case  series;  combination  with  fluoxetine  may  treat  resistant  
cases.  

Outcome:  The  prognosis  of  psychotic  variant  is  generally  poor  with  waxing  and  waning  course.  But  there  
is  often  a  relatively  preserved  psychosocial  functioning  in  many  patients,  in  line  with  the  outcomes  seen  in  
persistent  delusional  disorders.  

C. Medically Unexplained Symptoms and Somatisation Disorder:

Somatisation   Disorder:   Community   surveys   in   the   United   States   and   Western   Europe   have   found  
prevalence  rates  of  less  than  1  per  cent.  Primary  care  surveys  using  structured  interviews  have  found  only  
a   slightly   higher   prevalence—typically   1   to   2%.   An   analysis   of   follow-­‐‑up   data   from   the   World   Health  
Organization  multicentre  primary  care  survey,  however,  indicates  that  recall  during  structured  interviews  
may  significantly  underestimate  the  lifetime  prevalence  of  somatization  disorder  and  unexplained  somatic  
symptoms.   The   prevalence   of   somatization   disorder   and   of   less   severe   somatization   syndromes   is  
typically  twice  as  high  in  women  as  men.  The  survey  also  noted  that  approximately  20  percent  of  primary  
care   patients   suffered   from   persistent   pain   (one   or   more   pain   symptoms   present   for   most   of   the   last   6  
months).  Pain  syndromes  are  approximately  twice  as  prevalent  in  women  as  in  men.  

A   high   proportion   of   patients   with   MUS   have   undiagnosed   and,   therefore,   untreated   mental   disorder.    
Rohricht   and   Elanjithara   (2009)   reported   that   42%   of   those   with   MUS   had   a   primary   diagnosis   of  
somatoform  disorder,  36%  had  a  depressive  disorder  and  depressive  symptoms  medicated  by  the  effect  of  
somatic  symptoms.  

Presentation:  The  reliability  of  medically  unexplained  symptoms  is  limited;  they  are  a  feature  of  Somatic  
Symptom  Disorders  (DSM-­‐‑V);  Somatic  Symptom  Disorders  can  also  accompany  diagnosed  medical  
disorders.    The  emphasis  on  a  diagnosis  of  Somatic  Symptom  Disorder  is  on  the  maladaptive  thoughts,  
feelings,  and  behaviours  associated  with  the  somatic  symptoms.  

©  SPMM  Course   13  
Treatment:  A  review  of  studies  carried  out  in  primary,  secondary,  and  tertiary  care  settings  by  
Sumathipala  et  al  2007  showed  three  types  of  interventions  to  be  supported  by  evidence  for  medically  
unexplained  symptoms,  namely:  antidepressant  medication,  cognitive  behavioural  therapy  (CBT),  and  
other  nonspecific  interventions.    

• There  is  more  level  I  evidence  for  CBT  compared  to  other  approaches.    
• CBT  is  efficacious  for  the  broader  category  of  medically  unexplained  symptoms  by  reducing  
physical  symptoms,  psychological  distress,  and  disability.    
• No  studies  have  compared  pharmacological  and  psychological  treatments.    
• Most  trials  assessed  only  short-­‐‑term  outcomes.    
New   and   locally   derived   collaborative   care   models   of   active   engagement   in   primary   care   settings   are  
recommended.     Patients   with   somatoform   disorder   may   benefit   from   Body-­‐‑Oriented   Psychological  
Therapy,  mentalization-­‐‑based  CBT,  and  brief  psychodynamic  interpersonal  therapy.  
 

D. Dissociative Disorders:
Dissociative  disorders  refer  to  a  set  of  conditions  that  involve  disruptions  or  breakdowns  of  memory,  
identity,  or  perception.    ICD-­‐‑10  classifies  Conversion  Disorder  as  a  dissociative  disorder.    DSM-­‐‑V  lists:  
Dissociative  Identity  Disorder  (the  distinct  alternation  of  two  or  more  distinct  personality  states  with  
impaired  recall  among  personality  states;  and  Dissociative  Amnesia  (the  temporary  loss  of  recall  memory,  
specifically  episodic  memory,  due  to  a  traumatic  or  stressful  event.    Classed  under  this  is  Dissociative  
Fugue  (reversible  amnesia  for  personal  identity,  usually  involving  unplanned  travel  or  wandering,  
sometimes  accompanied  by  the  establishment  of  a  new  identity).    Included  in  the  Dissociative  Disorders  is  
Depersonalisation/derealisation  disorder.  
Prevalence:   Some   surveys   estimate   that   10%   of   the   adult   population   has   dissociative   disorder  
(according   to   DSM-­‐‑III   definition).     It   appears   to   be   as   common   as   anxiety,   mood   and   substance  
misuse   disorders.   It   may   be   that   more   women   present   with   the   severest   symptoms,   but   several  
studies  have  found  no  gender  differences  in  the  prevalence  of  Dissociative  Disorders.  

Aetiology:  Patients  with  Dissociative  Disorders  report  high  frequencies  of  childhood  psychological  
trauma,  in  particular  childhood  sexual  abuse  (57-­‐‑90%),  emotional  abuse  (57%),  physical  abuse  (62-­‐‑82%)  
and  neglect  (62%).  

Treatment:  The  aim  is  to  integrate  feelings,  perceptions,  thoughts  and  memories.    The  international  
Society  for  the  Study  of  Trauma  and  Dissociation  recommend  individual  psychotherapy  (especially  
structured  therapy  such  as  Acceptance  and  Commitment  Therapy  and  DBT)  and  skills  training,  
although  studies  in  this  field  are  in  their  infancy.  

©  SPMM  Course   14  
 8. Eating Disorders:
3  major  types  are  recognised  by  ICD-­‐‑10:  Anorexia  nervosa,  bulimia  nervosa  and  EDNOS  –  atypical  ED  or  
ED  not  otherwise  specified.  Binge  eating  disorder  is  the  increasingly  recognised  fourth  type,  but  falling  
under  EDNOS  currently.  But  the  stability  of  individual  ED  diagnoses  is  poor;  patients  migrate  from  one  to  
other  very  often.    Notably  at  least  1/4th  to  1/3rd  of  those  with  bulimia  have  a  past  history  of  anorexia  though  
migration  from  bulimia  to  anorexia  is  somewhat  rare.  

In  the  diagnostic  criteria  for  Anorexia  Nervosa  (AN)  the  value  of  the  amenorrhoea  criterion  is  
questionable  as  most  female  patients  who  have  BMI  around  17.5  and  body  image  disturbance  are  
amenorrhoeic;  those  who  have  intact  periods  have  same  clinical  features  and  outcome  as  those  who  satisfy  
all  3  criteria.    In  DSM-­‐‑5,  the  requirement  for  amenorrhoea  has  been  eliminated.  

In  bulimia  binge  eating  episodes  are  characteristically  seen  (may  also  occur  in  anorexia).    DSM-­‐‑V  specifies  
a  once-­‐‑weekly  frequency  for  binge  eating  and  inappropriate  compensatory  behavior  as  a  diagnostic  
criterion.  The  amount  of  food  intake  during  binges  varies  from  1000  kCals  to  2000  kCals.    Most  patients  
with  bulimia  have  an  immense  feeling  of  loss  of  control  and  so  seek  and  engage  in  treatment  better  than  
anorexia  patients.    

Epidemiology  of  bulimia  and  anorexia:  

Anorexia   Bulimia  
Onset  mostly  in  adolescents     Mostly  young  adults;  little  later  
onset  
Excess  in  higher  social  class   Even  class  distribution  
0.5-­‐‑1%  prevalence  in  teenage   1-­‐‑2%  prevalence  in  16-­‐‑35  age  
girls   group  
19/100  000  females  per  year   29/100  000  females  per  year  
      (adapted  from  Fairburn  &  Harrison,  2003)  

65%  patients  with  anorexia  have  depression;  34%  have  social  phobia  while  26%  have  OCD.  

Aetiology:  Shared  familial  liability  is  noted  among  the  three  EDs.  EDs  are  also  associated  with  certain  
personality  traits.  Substance  use  is  increased  in  families  of  bulimic  probands;  obsessional  and  perfectionist  
traits  are  increased  in  families  of  anorexic  probands.  

  Monozygotes   Dizygotes  
Anorexia  nervosa   55%   5%  
Bulimia  nervosa   35%   30%  
   

A  significant  heritability  exists  for  anorexia  nervosa  but  not  for  bulimia  nervosa.    

©  SPMM  Course   15  
Risk  factors:  (adapted  from  Fairburn  &  Harrison,  2003)  
§ Female  sex,  adolescence  and  early  adulthood  
§ Western  cultural  adaptation  
§ Family  history  of  ED,  depression,  substance  misuse,  especially  alcoholism  (for  bulimia  nervosa),  
obesity  (for  bulimia  nervosa)  
§ Adverse  parenting  (especially  low  contact,  high  expectations,  parental  discord),  childhood  sexual  
abuse,  critical  comments  about  eating,  shape,  or  weight  from  family  and  others    
§ Occupational  and  recreational  pressure  to  be  slim  
§ Low  self-­‐‑esteem,  perfectionism  (anorexia  nervosa  more  than  bulimia  nervosa)  
§ Past  history  of  being  obese  (bulimia  nervosa)  
§ Early  menarche  (bulimia  nervosa)  
 
Binge  eating  disorder  (BED)  is  characterized  by  recurrent  episodes  of  binge  eating  in  the  absence  of  
extreme  weight-­‐‑control  behaviour.  There  is  often  a  background  of  a  general  tendency  to  overeat.  An  
association  with  obesity  is  seen;  5–10%  of  those  seeking  treatment  for  obesity  have  BED.  Patients  typically  
present  in  their  40s,  with  more  males  compared  to  other  EDs,  but  only  25%  of  all  binge-­‐‑eating  population  
are  males.  A  high  degree  of  spontaneous  remission  is  seen;  stress  associated  overeating  is  a  common  
phenomenon  in  those  with  BED.  Self-­‐‑help,  behavioural  weight  loss  programmes  and  CBT/IPT  can  help.  
Physical  symptoms  of  EDs:  
• Increased  sensitivity  to  cold  
• Gastrointestinal  symptoms—e.g.,  constipation,  fullness  after  eating,  bloatedness  
• Dizziness  and  syncope  
• Amenorrhoea  (in  females  not  taking  an  oral  contraceptive),  low  sexual  appetite,  infertility  
• Poor  sleep  with  early  morning  wakening  
 
Physical  signs  of  EDs:  
• Emaciation;  stunted  growth  and  failure  of  breast  development  (if  prepubertal  onset)  
• Dry  skin;  fine  downy  hair  (lanugo)  on  the  back,  forearms,  and  side  of  the  face;  in  patients  with  
hypercarotenaemia,  orange  discolouration  of  the  skin    
• Russel’s  sign  –  calluses  in  knuckles  due  to  repeated  vomit  induction  
• Swelling  of  parotid  and  submandibular  glands  (especially  in  bulimic  patients)  
• Erosion  of  inner  surface  of  front  teeth  (perimylolysis)  in  those  who  vomit  frequently  
• Cold  hands  and  feet;  hypothermia  
• Bradycardia  (heart  rate  around  40  is  common);  orthostatic  hypotension;  cardiac  arrhythmias  
(especially  in  underweight  patients  and  those  with  electrolyte  abnormalities).  Systolic  BP  may  
drop  up  to  70  in  the  extremely  starved.  
• Dependent  oedema  (complicating  assessment  of  bodyweight)  
• Weak  proximal  muscles  (elicited  as  difficulty  rising  from  a  squatting  position)  
 
 

©  SPMM  Course   16  
Abnormalities  on  physical  investigation:  

•  Endocrine  

• Low  concentrations  of  luteinizing  hormone,  follicle  stimulating  hormone,  and  oestradiol  
• Low  T3,  T4  in  low  normal  range,  normal  concentrations  of  thyroid  stimulating  hormone  (low  T3  
syndrome)  
• Mild  increase  in  plasma  cortisol  
• Raised  growth  hormone  concentration  
• Severe  hypoglycaemia  (rare)  
• Low  leptin  (but  possibly  higher  than  would  be  expected  for  bodyweight)  
•  Cardiovascular  

• ECG  abnormalities  (especially  in  those  with  electrolyte  disturbance):  conduction  defects,  especially  
prolongation  of  the  Q-­‐‑T  interval,  of  major  concern  
• Ipecac  (emetic  substance)  contains  emetine  an  alkaloid  that  can  cause  myopathy  and  fatal  
cardiomyopathy  which  may  be  reversible  in  early  stages.  
•  Gastrointestinal  

• Delayed  gastric  emptying  

• Decreased  colonic  motility  (secondary  to  chronic  laxative  misuse)  
• Acute  gastric  dilatation  (rare,  secondary  to  binge  eating  or  excessive  re-­‐‑feeding)  
•  Haematological  

• Moderate  normocytic  normochromic  anaemia  

• Mild  leucopenia  with  relative  lymphocytosis  
• Thrombocytopenia  
•  Other  metabolic  abnormalities  

• Hypercholesterolaemia  
• Raised  serum  carotene  
• Hypophosphataemia  (exaggerated  during  refeeding)  
• Dehydration  
• Electrolyte  disturbance  (varied  in  form;  present  in  those  who  vomit  frequently  or  misuse  large  
quantities  of  laxatives  or  diuretics):  vomiting  results  in  metabolic  alkalosis  and  hypokalaemia;  
laxative  misuse  results  in  metabolic  acidosis,  hyponatraemia,  hypokalaemia  
•  Other  abnormalities  

• Osteopenia  and  osteoporosis  (with  heightened  fracture  risk)  

• Enlarged  cerebral  ventricles  and  external  cerebrospinal  fluid  spaces  (pseudoatrophy)  
 

©  SPMM  Course   17  
Effects  on  pregnancy:    

• Decreased  fertility  –  but  regained  near  normally  on  complete  recovery.  

• May  have  more  abortions    
• Higher  rates  of  hyperemesis  gravidarum,  anaemia,  impaired  weight  gain    
• Compromised  intrauterine  foetal  growth    
• Premature  delivery  is  more  likely    
• Rates  of  caesarean  delivery  are  high  
• Post-­‐‑natal  complications  and  post-­‐‑partum  depression  are  higher    
• Associated  with  low  birth  weight,  microcephaly,  low  APGAR  scores.  
• In  actively  anorexic  mother,  the  neonate  may  have  hypoglycaemia  
 

Evidence-­‐‑based  management  of  eating  disorders:  

Evidence     Anorexia  nervosa     Bulimia  nervosa    

     
Antidepressants  (acute  treatment)   Modest   Considerable  
Antidepressants  (relapse   Modest   Modest  
prevention)  
Cognitive  analytic  therapy  (CAT)   Modest   None  
Cognitive  behaviour  therapy     Modest   Strong  
“Dialectical  behaviour  therapy”-­‐‑ None   Modest  
based  treatment  
Family-­‐‑based  therapy  for   Moderate   None  
adolescents  
Interpersonal  psychotherapy  (IPT)   None   Moderate  
(adapted  from  Fairburn  &  Harrison,  2003)  

Managing  bulimia:  

Ø Most  effective  treatment:  Cognitive  behaviour  therapy.    

Ø Typically  involves  about  20  individual  treatment  sessions  over  5  months;    
Ø 33-­‐‑50%  make  a  complete  and  lasting  recovery.    
Ø Antidepressant  drugs  have  an  antibulimic  effect.    
Ø Produce  a  rapid  decline  in  the  frequency  of  binge  eating  and  purging,  and  an  improvement  in  
mood.  
Ø Not  as  effective  as  CBT  but.    
Ø The  effect  is  often  not  sustained.    
 

Managing  anorexia:    

Major  therapeutic  goals:  

©  SPMM  Course   18  
 1. engagement  
2. weight  restoration  
3. psychological  therapy  –  cognitive  restructuring  
4. if  needed  use  of  compulsion  
Outpatient  therapy  for  anorexia  has  best  chance  if  

a. Illness  is  present  for  less  than  6  months  

b. No  bingeing  or  vomiting  
c. Have  parents  who  cooperate  and  are  willing  to  participate  in  family  therapy  
Summary  of  NICE  guidelines  
Anorexia:  
§ Drugs  should  not  be  used  as  sole  or  primary  treatment  for  anorexia  nervosa  
§ For  anorexia  nervosa,  consider  cognitive  analytic  or  cognitive  behavioural  therapies,  
interpersonal  psychotherapy,  focal  dynamic  therapy,  or  family  interventions  focused  on  
eating  disorders.  
§ Family  interventions  that  directly  address  the  eating  disorder  are  especially  useful  for  
children  and  adolescents  with  anorexia  nervosa  
§ Dietary  counselling  should  not  be  provided  as  sole  treatment  for  anorexia  nervosa  
 
Bulimia:  
§ Evidence-­‐‑based  self-­‐‑help  programme  is  first  line  for  bulimia;  as  an  additional  option  or  
alternative  choice  antidepressants  can  be  used  in  bulimia.  
§ Antidepressant  drugs  can  reduce  frequency  of  binge  eating  and  purging,  but  long-­‐‑term  
effects  are  unknown;    
§ Any  beneficial  effects  of  antidepressants  will  be  rapidly  apparent  
§ SSRIs  (specifically  fluoxetine)  are  drugs  of  first  choice  for  bulimia  nervosa  Effective  dose  
of  fluoxetine  is  higher  than  for  depression  (60  mg  daily)  
§ Specifically  adapted  cognitive  behavioural  therapy  should  be  offered  to  adults  with  
bulimia  nervosa,  16–20  sessions  over  4–5  months  
§ Interpersonal  psychotherapy  should  be  considered  as  alternative  to  cognitive  behavioural  
therapy,  but  patients  should  be  informed  it  takes  8–12  months  to  achieve  similar  results  
Binge  eating  disorder  has  similar  lines  of  management  guidelines  to  bulimia.  

http://apt.rcpsych.org/content/18/1/34  

©  SPMM  Course   19  
 9. Personality Disorders:
Epidemiology:    Personality  disorders,  as  a  group,  are  among  the  most  frequent  disorders  treated  by  
psychiatrists  (Zimmerman  et  al.,  2005).  Epidemiological  studies  suggest  that  between  5%  and  13%  of  the  
population  has  at  least  one  personality  disorder.  

In  general,  the  prevalence  of  personality  disorders  among  psychiatric  outpatients  and  inpatients  is  high,  
with  many  studies  reporting  a  prevalence  of  greater  than  50%  of  samples.  Borderline  PD  is  generally  the  
most  prevalent  in  psychiatric  settings.    Personality  disorders  are  particularly  prevalent  among  inpatients  
with   drug,   alcohol,   and   eating   disorders.     In   these   populations,   prevalence   figures   for   personality  
disorder  have  been  reported  to  be  in  excess  of  70%.      

Dissocial  personality  is  the  most  prevalent  category  of  personality  disorder  in  prison  settings.    A  survey  
of  a  randomly  selected  sample  of  one  in  six  prisoners  in  England  and  Wales,  found  that  the  prevalence  of  
any   personality   disorder   was   78%   for   male   remand,   64%   for   male   sentenced   and   50%   for   female  
prisoners   .     Antisocial   personality   disorder   had   the   highest   prevalence   of   any   category   of   personality  
disorder,  with  63%  of  male  remand  prisoners,  49%  of  sentenced  prisoners  and  31%  of  female  prisoners.  In  
Great  Britain,  the  prevalence  of  antisocial  PD  in  general  population  is  estimated  at  0.6%  (See  Coid  et  al  –  
Tables   below),   with   the   rate   in   men   (1%)   five   times   that   in   women   (0.2%).   Surveys   conducted   in   other  
countries   report   prevalence   rates   for   ASPD   ranging   from   0.2%   to   4.1%.   Higher   prevalence   rates   for  
personality   disorders   appear   to   be   found   in   urban   populations,   and   this   may   account   for   some   of   the  
range  in  reported  prevalence.  

Personality   Median  prevalence  rate   Weighted  prevalence    per   Prevalence  in  a  

disorder   per  1000  in  community   1000  in  community  sample   psychiatric  outpatient  
(from  Oxford  Textbook   (from  Coid  2006  BJPsych  –   sample  per  1000  
of  Psychiatry,  2000)   Great  Britain  data)     (Zimmerman  et  al.  2005)  
Paranoid   6   7   42  
Schizoid   4   8   14  
Schizotypal   6   0.6   6  
Antisocial   19   6   36  
Borderline   16   7   93  
Histrionic   20   12   10  
Narcissistic   2   8   23  
Anankastic   17   19   87  
Avoidant   7   8   147  
Dependent   7   1   14  
Passive   17   -­‐‑   No  data  
aggressive    
    Cluster  A  =  1.6%   Cluster  A  =  6%  
Cluster  B  =  1.2%   Cluster  B  =  13%  
Cluster  C  =  2.6%   Cluster  C  =  22%  
Any  PD  =  4.4%   Any  PD  =  46%  
 

©  SPMM  Course   20  
Borderline  personality  disorder  is  seen  in  nearly  2%  of  general  population,  10%  outpatients,  15-­‐‑20%  
inpatients  and  30-­‐‑60%  of  all  personality  disorders  in  some  clinical  samples.  The  estimated  female:  male  
ratio  is  3:1.  It  is  5  times  more  common  in  first-­‐‑degree  relatives  of  borderline  patients.  

Diagnostic  stability:    

§ For  a  long  time  it  was  thought  that  once  diagnosed  with  personality  disorder  the  diagnosis  remains  
forever,  and  no  change  takes  place.  This  pessimism  is  now  shifting  largely  due  to  long-­‐‑term  follow-­‐‑up  
studies  in  borderline  personality.  
§ Longitudinal  course  of  Borderline  Personality:  2  important  studies  to  date  are  the  McLean  study  and  
CLPDS  study.  In  McLean  Study  of  Adult  Development,  the  prevalence  of  five  core  borderline  
symptoms  was  found  to  decline  with  particular  rapidity:  quasi-­‐‑psychotic  thought,  self-­‐‑mutilation,  
help-­‐‑seeking  suicide  efforts,  treatment  regressions,  and  countertransference  problems.  In  contrast,  
feelings  of  depression,  anger,  and  loneliness/emptiness  were  the  most  stable  symptoms.  The  10  year  
follow-­‐‑up  of  McLean  sample  further  clarified  this.  Chronic  dysphoria,  intense  anger,  nondelusional  
paranoia,  general  impulsivity  (disordered  eating,  spending  sprees,  or  reckless  driving)  remained  
relatively  common  even  after  10  years  of  prospective  follow-­‐‑up  while  other  features  largely  abated.  
In  the  Collaborative  Longitudinal  Personality  Disorders  Study,  abandonment  fears  and  physically  self-­‐‑
destructive  acts  were  found  to  be  the  least  stable  (rapidly  remitting).    
§ Results  of  epidemiological  studies  suggest  a  J-­‐‑shaped  relation  between  personality  and  age,  with  an  
initial  decrease  followed  by  an  increase  in  some  personality  disorders  in  older  people.  
§ Seivewright  &  Tyrer  reported  a  12-­‐‑year  follow-­‐‑up  where  178  out  of  202  patients  were  reassessed  for  
the  personality  status.  The  personality  traits  of  patients  with  the  cluster  B  [flamboyant  group  -­‐‑  
antisocial,  histrionic]  became  significantly  less  pronounced  over  12  years,  but  those  in  the  cluster  A  
(odd,  eccentric  group  -­‐‑  schizoid,  schizotypal,  paranoid),  and  the  cluster  C  (anxious,  fearful  group  -­‐‑  
obsessional,  avoidant)  became  more  pronounced.    
§ Evidence  from  the  McLean  Study  of  Adult  Development  suggests  that  40%  of  patients  with  borderline  
personality  disorder  remit  after  2  years,  with  88%  no  longer  meeting  criteria  after  10  years  (Silk,  KR  
Am  J  Psychiatry  165:413-­‐‑415,  April  2008).  
 

Diagnostic  features  in  a  nutshell:  

Cluster  A  (odd,  eccentric)  

             Paranoid  personality  disorder:    
§ Suspicious  of  other  people  and  their  motives.    
§ hold  longstanding  grudges  against  people,    
§ believe  others  are  not  trustworthy,  
§ emotionally  detached  
§  Feel  other  people  are  deceiving,  threatening,  or  making  plans  against  them.  
 
Schizoid  personality  disorder:  
§ Have  difficulties  in  expressing  emotions,  particularly  around  warmth  or  tenderness.    
§ Prefer  loneliness  
©  SPMM  Course   21  
 § aloof  or  remote,    
§ have  difficulty  in  developing  or  maintaining  social  relationships  
§ remain  unaware  of  social  trends  
§ unresponsive  to  praise  or  criticism  
 
Schizotypal  personality  disorder  (in  ICD10  –  classified  as  a  type  of  schizophrenia)  
§ appear  odd  or  eccentric;    
§ may  have  illusions,  magical  thinking    
§ obsessions  without  resistance  
§ may  be  members  of  quasi-­‐‑cultural  groups    
§ Thought  disorders  and  paranoia.    
§ may  believe  in  ESP,  clairvoyance,  etc  
§ may  have  transient  psychotic  features  
 

Cluster  B  (dramatic,  erratic)  

Antisocial  personality  disorder:  
§ Lack  of  regard  for  the  rights  and  feelings  of  other  people.    
§ Lack  of  remorse  for  actions  that  may  hurt  others.    
§ ignore  social  norms  about  acceptable  behaviour,    
§ May  disregard  rules  and  break  the  law.  
§ Make  relations  easily  but  break  them  equally  easily  
§ A  small  proportion  may  be  psychopathic  
 
Borderline  personality  disorder:  
§ poor  self-­‐‑image,    
§ unstable  personal  relationships,    
§ Impulsive  behaviour  in  areas  such  as  personal  safety  and  substance  misuse.    
§ may  self-­‐‑harm,  feel  suicidal  and  act  on  these  feelings,    
§ experience  the  instability  of  mood,    
§ Have  episodes  of  micro-­‐‑psychosis.    
§ feelings  of  chronic  emptiness    
§ fears  of  abandonment  –  rejection  sensitivity  hence  form  intense  but  short  lasting  relations  
 
Histrionic  personality  disorder:  
§ Extreme  or  over-­‐‑dramatic  behaviour.      
§ may  form  relationships  quickly,  but  be  demanding    
§ Attention-­‐‑seeking.    
§ may  appear  to  others  as  being  self-­‐‑centred,    
§ having  shallow  emotions,    
§ Being  inappropriately  sexually  provocative.  
 
Narcissistic  personality  disorder:    
§ An  exaggerated  sense  of  own  importance.    
§ frequently  self-­‐‑centred    
§ Intolerant  of  other  people.    
§ grandiose  plans  and  ideas    
§ Cravings  for  attention  and  admiration.    
 
 

©  SPMM  Course   22  
Cluster  C  (anxious,  inhibited)  
Avoidant  personality  disorder    
§ fears  being  judged  negatively  by  other  people  
§ Feelings  of  discomfort  in  a  group  or  social  settings.    
§ may  come  across  as  being  socially  withdrawn    
§ Have  low  self-­‐‑esteem.    
§ May  crave  affection  but  fears  of  rejection  overwhelming.  
 
Dependent  personality  disorder    
§ assumes  a  position  of  passivity,    
§ Allowing  others  to  assume  responsibility  for  most  areas  of  their  daily  life.    
§ lack  self-­‐‑confidence,    
§ feel  unable  to  function  independently  of  another  person,    
§ Feels  own  needs  are  of  secondary  importance.    
 
Obsessive-­‐‑compulsive  personality  disorder  (1  -­‐‑2%  prevalence)  
§ Difficulties  in  expressing  warm  or  tender  emotions  to  others.    
§ frequently  perfectionists  
§ often  lack  clarity  in  seeing  other  perspectives  or  ways  of  doing  things,    
§ Rigid  attention  to  detail  may  prevent  them  from  completing  tasks.  
§ Some  may  be  hoarders,  scrupulous  with  money  
§ May  not  be  able  to  delegate  tasks;  workaholics.  
 
 

Though  presence  of  transient  stress-­‐‑induced  paranoid  ideations  in  borderline  PD  (DSM)  qualifies  for  
‘quasi-­‐‑psychotic’  label,  the  term  ‘quasi  psychotic  episode’  is  in  fact  used  only  for  schizotypal  disorder  in  
the  contemporary  classificatory  systems.  The  ICD10  schizotypal  disorder  is  characterised  by  ‘occasional  
transient  quasipsychotic  episodes  with  intense  illusions,  hallucinations  and  delusion-­‐‑like  ideas  usually  
occurring  without  external  provocation’.  

Evidence  for  pharmacological  management:  (Adapted  from  Tyrer  &  Bateman,  2004)  

§ Amitriptyline    -­‐‑  no  effect  on  borderline  disorder  even  if  depressed;  haloperidol  compares  better.  
§ Flupentixol  –  some  efficacy  on  self-­‐‑harm  behaviour.  
§ Antipsychotics  -­‐‑  low  dosage  these  drugs  might  be  effective  in  the  treatment  of  both  schizotypal  
and  borderline  personality  disorders    
§ SSRIs  –  reduce  aggressive,  impulsive  and  angry  behaviour  in  those  with  borderline  and  aggressive  
personality  disorders.  
§ Anticonvulsants  and  lithium  –  some  effect  against  affective  dysregulation  in  borderline  disorder  
and  aggressive  outbursts  in  cluster  B.  
Note  that  according  to  NICE  Guidelines,  pharmacological  treatment  is  not  recommended  for  the  features  
of  Personality  Disorder,  but  it  is  for  co-­‐‑morbid  illness  (such  as  depression  or  OCD).  

 
©  SPMM  Course   23  
Type  of  symptom   Preferred  drug  
treatment  
Cognitive/perceptual   Antipsychotics  
       Suspiciousness,  paranoid  ideation,  ideas  of  reference,  magical  thinking,  stress-­‐‑
induced  hallucinations  

Affective  dysregulation   SSRIs  

       Lability  of  mood,  ‘rejection  sensitivity’,  mood  crashes,  temper  outbursts,  chronic  
emptiness,  and  dysphoria.  

Impulsive-­‐‑behavioural  dyscontrol   Mood  stabilisers,  

       Sensation-­‐‑seeking,  risky  or  reckless  behaviour,  low  frustration  tolerance,   SSRIs  
impulsive  aggression,  impulsive  binges,  recurrent  suicidal  behaviour.  

Psychological  therapies  are  considered  with  psychotherapy  section.  

Differentiating  bipolar  and  borderline  disorder:  

Bipolar  Disorder   Borderline  Personality  Disorder  

Onset  in  teens  or  early  20s     No  defined  onset  

Observable,  spontaneous  mood  changes,  last  for   Often  not  observable;  changes  are  precipitated  by  internal  or  
days  to  weeks   external  events,  last  for  hours  
Dysphoric,  anxious  and  elated  mood  shifts   Dysphoric,  anxious  and  angry  but  elated  mood  is  rare  

Episodic  impulsivity  and  risk-­‐‑taking     Chronic  impulsivity  and  risk-­‐‑taking  

Episodic  suicide  attempts  related  to  depressive   Recurrent  suicidal  gestures    
episodes    

Self-­‐‑mutilation  rare     Self-­‐‑mutilation  common  

Endorse  ‘depressed  mood’  as  descriptor     Endorse  ‘emptiness’  as  descriptor  

Family  history  of  bipolar  I  or  II  or  recurrent   Family  history  negative  for  bipolar  I,  II  and  recurrent  
depression     depression  
Adapted  from  Yatham  L,    et  al.  Bipolar  Disord  2005:  7  (Suppl.  3):  5–69.  

Richardson  &  Tracy  (2015)  highlight  six  core  illness-­‐‑differentiating  themes  influencing  patient  
perspectives  on  these  two  conditions:  

¬ Public  information:  for  bipolar  there  is  greater  public  awareness,  positive  celebrity  exposure,  more  
public  information  and  support  groups  
¬ Delivery  of  diagnosis:  this  is  perceived  to  be  taken  more  seriously  and  be  given  more  time  by  staff  
than  BPD  
¬ Illness  causes:  perceived  to  be  more  genetic,  and  to  do  with  brain  ‘wiring’  or  ‘chemical’  problem  in  
bipolar  than  in  BPD  
©  SPMM  Course   24  
¬ Illness  management:  more  medication-­‐‑orientated  in  bipolar  disorder,  better-­‐‑established  protocols  in  
comparison  with  BPD  
¬ Stigma  and  blame:  greater  stigma  for  BPD,  with  accompanying  feeling  of  staff  hopelessness  and  self-­‐‑
blame  
¬ Relationships  with  others:  a  diagnosis  of  bipolar  is  accompanied  with  greater  support  from  family  
and  friends;  its  infrequent  nature  makes  it  less  troublesome  and  easier  to  conceal,  whereas  BPD  is  
associated  with  insidious  destruction  and  sabotage  of  relationships,  felt  to  be  ever-­‐‑present  and  cannot  
be  concealed  from  relationships  

10. Psychosexual disorders

Sexual  dysfunctions  are  coded  in  F50  group  in  ICD10.  They  can  be  classified  as  (according  to  the  terms  
used  in  DSM)  
§ Sexual  desire  disorders  (sexual  aversion,  hypoactive  sexual  desire)  
§ Sexual  arousal  disorder  (female  sexual  arousal  disorder,  male  erectile  disorder)  
§ Orgasmic  disorders  (female  and  male  orgasmic  disorder,  premature  ejaculation)  
§ Sexual  pain  disorder  (Dyspareunia,  vaginismus)  
§ Others  (including  those  due  to  general  medical  or  substance  use  disorders)  
Hypoactive  sexual  desire  is  the  most  common  female  sexual  dysfunction.  It  is  the  most  difficult  to  treat  
too.  Testosterone  has  been  tried  as  a  treatment  in  both  males  and  females  but  with  modest  effects,  largely  
due  to  side  effects.  
 
DSM-­‐‑5  specified  paraphilic  disorders  (from  Yakeley  &  Wood,  2014)  
• Voyeurism  (spying  on  others’  sexual/  private  activities)  
• Exhibitionism  (deliberately  exposing  one’s  genitals)  
• Frotteurism  (deliberately  rubbing  against  a  non-­‐‑consenting  individual)  
• Sexual  masochism  (choosing  to  undergo  humiliation,  bondage  or  suffering  to  achieve  sexual  
arousal)  
• Sexual  sadism  (choosing  to  inflict  humiliation,  bondage  or  suffering  on  one’s  partner  to  achieve  
sexual  arousal)  
• Paedophilia  (sexual  focus  on  children)  
• Fetishism  (use  of  objects  or  focussing  on  non-­‐‑genital  body  parts  to  achieve  arousal)  
• Transvestic  disorder  (engaging  in  sexually  arousing  cross-­‐‑dressing)  
‘Other  specified  paraphilic  disorder’:  includes  zoophilia  (animals),  scatalogia  (obscene  phone  calls),  
necrophilia  (corpses),  coprophilia  (faeces),  klismaphilia  (enemas),  urophilia  (urine)  
 

©  SPMM  Course   25  
 DISCLAIMER: This material is developed from various revision notes assembled while preparing
for MRCPsych exams. The content is periodically updated with excerpts from various published
sources including peer-reviewed journals, websites, patient information leaflets and books.
These sources are cited and acknowledged wherever possible; due to the structure of this
material, acknowledgements have not been possible for every passage/fact that is common
knowledge in psychiatry. We do not check the accuracy of drug-related information using
external sources; no part of these notes should be used as prescribing information  

©  SPMM  Course   26  
 Notes  prepared  using  excerpts  from  
! Baldwin  et  al  (2005)  Evidence  based  guidelines  for  management  of  anxiety  disorders.  J  of  Psychopharmacology.  19;  567-­‐‑
596.  
! Beaubrun,  G  &  Gray,  GE  (2000)  A  review  of  herbal  medicines  for  psychiatric  disorders.  Psychiatric  Services  51:1130–
1134,  2000  
! Bisson  JI.  Post-­‐‑traumatic  stress  disorder.  BMJ  2007;334:789-­‐‑93  
! Bisson,  J  et  al.  Psychological  treatments  for  chronic  post-­‐‑traumatic  stress  disorder:  Systematic  review  and  meta-­‐‑analysis  
The  British  Journal  of  Psychiatry  2007;  190:  97-­‐‑104  
! Castle,  DJ  &  Phillips,  KA.  Obsessive  compulsive  spectrum  of  disorders:  A  defensible  construct?  Aust  N  Z  J  Psychiatry.  
2006;  40(2):  114–120.    
! Diagnostic  and  Statistical  Manual  of  Mental  Disorders  (Fifth  text  revision  ed.).  American  Psychiatric  Association,  
Washington  DC  2014  
! Fairburn  &  Harrison  (2003)  Eating  disorders.  The  Lancet.  361,  9355;  407-­‐‑416.  
! Gale,  C  &  Davidson,  O.  Generalised  anxiety  disorder.  BMJ    2007;334:579-­‐‑581    
!  Gunderson,  JG.  “Borderline  Personality  Disorder:  Ontogeny  of  a  Diagnosis,”  Am  J  Psychiatry  166,  no.  5  (May  1,  
2009):  530-­‐‑539.      
! Gunstad  J,  Phillips  KA.  Axis  I  comorbidity  in  body  dysmorphic  disorder.  Compr  Psychiatry.  2003;44:270-­‐‑6.  
! Heyman,  I  et  al.  Obsessive  compulsive  disorder.  BMJ  2006;333(7565):424  
! http://www.medscape.com/viewarticle/431268_4  
! Human  Reproduction  Update  2006  12(3):193-­‐‑207  
! Jones,  W.  R.,  Schelhase,  M.,  &  Morgan,  J.  F.  (2012).  Eating  disorders:  clinical  features  and  the  role  of  the  general  
psychiatrist.  Advances  in  psychiatric  treatment,  18(1),  34-­‐‑43.  http://apt.rcpsych.org/content/18/1/34  
! Magarinos  et  al,  Epidemiology  and  Treatment  of  Hypochondriasis,  CNS  Drugs,  2002;  16(1):  9-­‐‑22  
! Morris,  P  &  Lloyd,  C  (2004)  Vocational  rehabilitation  in  psychiatry:  a  re-­‐‑evaluation    Australian  and  New  Zealand  
Journal  of  Psychiatry  38  (7)  ,  490–494  
! NICE  (www.nice.org.uk/page.aspx?o=CG026quickrefguide)—Quick  reference  guide  to  NICE  guidelines  for  post-­‐‑
traumatic  stress  disorder  
! Phillips  KA,  Dufresne  RG,  Jr,  Wilkel  CS,  Vittorio  CC.  Rate  of  body  dysmorphic  disorder  in  dermatology  patients.  J  Am  
Acad  Dermatol.  2000;42:436-­‐‑41  
! Phillips  KA,  Gunderson  CG,  Mallya  G,  McElroy  SL,  Carter  W.  A  comparison  study  of  body  dysmorphic  disorder  and  
obsessive-­‐‑compulsive  disorder.  J  Clin  Psychiatry.  1998;59:568-­‐‑75.  
! Ross  CA,  Epidemiology  of  multiple  personality  disorder  and  dissociation.  Psychiatr  Clin  North  Am  1991,  Sept;  14(3):  
503-­‐‑17  
! Schneier,  FR.  Social  anxiety  disorder.  BMJ    2003;327:515-­‐‑516    
! Seivewright,  H  &  Tyrer,  P.    Change  in  personality  status  in  neurotic  disorders.  The  Lancet  2002.  359,  9325;2253-­‐‑2254.  
! Soomro,  GM  et  al.  Selective  serotonin  re-­‐‑uptake  inhibitors  (SSRIs)  versus  placebo  for  obsessive  compulsive  disorder  
(OCD).Cochrane  Database  Syst  Rev.  2008  23;(1):  CD001765.  
! Sumathipala,  A.  Psychosomatic  Medicine  69:889-­‐‑900  (2007)      
! Taylor,  CB.  Panic  disorder.  BMJ    2006;332:951-­‐‑955  
! Tyrer,  P.  &  Bateman,  A.  W.  (2004)  Drug  treatments  for  personality  disorder.  Advances  in  Psychiatric  Treatment,  10,  
389–398.  
! Vedat  S,  Epidemiology  of  Dissociative  Disorders:  An  Overview,  Epidem  Research  Int  2011  
! Weisberg,  R.  B.  (2009).  Overview  of  generalized  anxiety  disorder:  epidemiology,  presentation,  and  course.  Journal  of  
clinical  psychiatry.  
! Wilson,  GT  &  Shafran,  R  (2005).  Eating  disorders  guidelines  from  the  NICE.  The  Lancet.  365,  9453;79-­‐‑81.    
! Yakeley,  J.,  &  Wood,  H.  (2014).  Paraphilias  and  paraphilic  disorders:  diagnosis,  assessment  and  management.  Advances  
in  Psychiatric  Treatment,  20(3),  202-­‐‑213.  
! Zimmerman,  M  et  al  (2005)  The  Prevalence  of  DSM-­‐‑IV  Personality  Disorders  in  Psychiatric  Outpatients.  Am  J  
Psychiatry  162:1911-­‐‑1918  

©  SPMM  Course   27