4 - Lec 4 Schizophrenia
4 - Lec 4 Schizophrenia
4 - Lec 4 Schizophrenia
Key Features That Define the Psychotic Disorders (SEE DSM-5TR for details page 101)
• Delusions
• Hallucinations
• Disorganized Thinking (Speech)
• Grossly Disorganized or Abnormal Motor Behavior (Including Catatonia)
• Negative Symptoms
DELUSIONS (see DSM 101 and for further details consult the book on comer’s chapter on
schizophrenia) ..example of few delusions
• Persecutory delusions ( eg. Being followed or tracked by punjab university)
• Referential delusions (eg. believe that certain news bulletins have a direct reference
to them, that music played on the radio is played for them, or that car licence plates
have a relevant meaning. Another example a person who touches his hair may be
thought by the patient to be signalling that he, the patient, is turning into a woman.)
• Grandiose delusions (A patient believe that I have supernatural power and have
been sent to save the world)
• erotomanic delusions ( eg. A patient believe that actor fawad khan is in love with her
and want to marry her)
• somatic delusions (for example--people with somatic delusions often believe they've
been infected by parasites that have taken over their internal organs, or by tiny
insects that have burrowed under their skin to lay their eggs
• Nihilistic delusions
• Delusion thought withdrawal
• Delusion of thought insertion
• delusions of control
HALLUCINATIONS
Hallucinations are perceptions that are experienced without any external stimulus to the
corresponding sense organ. They differ from illusions because they are experienced as
originating in the outside world or from within the person's body, rather than as imagined.
Hallucinations cannot be terminated by willpower alone.
Hallucinations are typically associated with significant psychiatric disorders, and specific
types of hallucinations are characteristic of different disorders. However, it is worth noting
that hallucinations can also occur in otherwise healthy individuals. In addition, it is common
to experience hallucinations when falling asleep (known as hypnagogic hallucinations) or
upon waking up (known as hypnopompic hallucinations).
These two types of hallucinations may be either visual or auditory, with the latter
sometimes manifesting as the experience of hearing one's own name being called. Such
hallucinations are common in narcolepsy (Narcolepsy is a chronic neurological disorder that
involves a decreased ability to regulate sleep–wake cycles). Furthermore, it is not
uncommon for recently bereaved individuals to experience hallucinations of the deceased
person.
Hallucinations can occur after sensory deprivation, in people with blindness or deafness of
peripheral origin, occasionally in neurological disorders that affect the visual pathways, in
epilepsy, and in Charles Bonnet syndrome.
TYPES OF HALLUCINATION
Hallucinations can be classified based on their complexity and sensory modality. The term
"elementary hallucination" refers to simple experiences such as bangs, whistles, and flashes
of light. On the other hand, "complex hallucination" refers to more complicated experiences
like hearing voices or music, or seeing faces and scenes.
Auditory hallucinations can take the form of noises, music, or voices. These voices can be
heard clearly or indistinctly and may speak words, phrases or sentences. They may also
directly address the patient (second-person hallucinations) or refer to the patient as 'he' or
'she' (third-person hallucinations). In some cases, patients report that the voices seem to
anticipate their thoughts a few moments before they occur. In other cases, the voices seem
to speak the patient's thoughts as they are thinking them, a phenomenon known as
Gedankenlautwerden. or to repeat them immediately after he has thought them (écho de la
pensée).
Visual hallucinations may also be elementary or complex. The content may appear normal
or abnormal in size; hallucinations of dwarf figures are sometimes called lilliputian.
Occasionally, patients describe the experience of visual hallucinations located outside the
field of vision, usually behind the head (extracampine hallucinations).
Many people with schizophrenia eventually enter a residual phase in which they return to a
prodromal-like level of functioning. They may retain some negative symptoms, such as
blunted emotion, but have a lessening of the striking symptoms of the active phase.
Each of these phases may last for days or for years. A fuller recovery from schizophrenia is
more likely in people who functioned quite well before the disorder (had good premorbid
functioning); whose initial disorder is triggered by stress, comes on abruptly, or develops
during middle age; and who receive early treatment, preferably during the prodromal phase
(Remberk et al., 2014). Relapses are apparently more likely during times of life stress.
POSITIVE SYMPTOMS
NEGATIVE SYMPTOMS
ETIOLOGICAL FACTORS
Biological Explanations
The biological explanations of schizophrenia point to genetic, biochemical, brain
structure and circuitry, and viral causes. The genetic view is supported by studies of
relatives, twins, adoptees, and genes.
ARE RELATIVES VULNERABLE? Family pedigree studies have found repeatedly that
schizophrenia and schizophrenia-like brain abnormalities are more common among
relatives of people with the disorder. And the more closely related the relatives are
to the person with schizophrenia, the more likely they are to develop the disorder.
Genetic factors---(twin studies, genetic link)---Research has revealed that if one
identical twin develops schizophrenia, there is a 48% chance that the other twin will
also develop the disorder. However, if the twins are fraternal, the risk drops to
around 17%.
Biochemical abnormalities---- (dopamine hypothesis)--The leading biochemical
explanation holds that dopamine may be overactive in the brains of people with
schizophrenia.
Studies have also identified a brain circuit whose dysfunction may lead to
schizophrenia. The circuit includes structures such as the prefrontal cortex,
hippocampus, amygdala, thalamus, striatum, and substantia nigra.
Abnormal brain structure-- brain circuit that may be contributing to schizophrenia. The
structures that comprise this schizophrenia-related circuit include the prefrontal
cortex, hippocampus, amygdala, thalamus, striatum, and substantia nigra, among
other brain regions. You may notice, once again, that several of the structures in this
circuit are also members of brain circuits that contribute to other disorders, but in
cases of schizophrenia the structures function and interconnect in problematic ways
that are, collectively, unique to this disorder.
The dysfunction of this schizophrenia-related circuit cannot be characterized in broad
terms as, for example, a generally “hyperactive” or generally “underactive” circuit.
But numerous studies suggest that the circuit does indeed operate abnormally in
persons with schizophrenia. Brain scans have shown repeatedly that the circuits of
schizophrenic and nonschizophrenic individuals differ significantly whether study
participants are at rest, performing cognitive tasks, or experiencing hallucinations
(Han et al., 2018; Wang et al., 2017).
Studies have found, for example, that under certain circumstances, particular
structures in the circuit may be hyperactive (for example, the substantia nigra) or
underactive (for example, the prefrontal cortex) among people with schizophrenia
(Schoonover et al., 2017; Yoon et al., 2014, 2013). In addition, and perhaps most
important, research indicates that the interconnectivity (flow of communication)
between particular structures in the circuit is typically excessive or diminished for
people with schizophrenia. Studies have found, for example, that interconnectivity is
abnormally low between their substantia nigra and prefrontal cortex and between
their striatum and thalamus, while it is abnormally high between their substantia
nigra and striatum, their thalamus and prefrontal cortex, and their hippocampus and
prefrontal cortex (Martino et al., 2018; Wang et al., 2017; Amad et al., 2014; Yoon et
al., 2014, 2013).
Just to complicate things a bit more, recent research suggests that the schizophrenia-
related circuit may actually be two distinct subcircuits whose various structures
sometimes overlap. Dysfunction by one of the subcircuits (which includes the
substantia nigra and striatum) might be more responsible for cases of schizophrenia
that are characterized by positive symptoms such as hallucinations and delusions. In
contrast, dysfunction by the other subcircuit (which includes the hippocampus and
amygdala) might be responsible for cases of schizophrenia that are dominated by
negative symptoms like flat affect and poverty of speech (Mitra et al., 2016; Shaffer
et al., 2015).
• PSYCHOLOGICAL VIEW
PSYCHODYNAMIC VIEW—SCHIZOPHRENOGENIC MOTHERS
The majority of people with schizophrenia do not appear to have mothers who fit the
schizophrenogenic description. Thus most of today’s psychodynamic theorists have rejected
Fromm-Reichmann’s view. Indeed, they typically assign a role to biological predispositions in
their psychodynamic explanations of schizophrenia. For example, self theorists, those
psychodynamic theorists who believe that the most basic human motive is to strengthen the
wholeness of the self , suggest that biological deficiencies cause people with schizophrenia
to develop a fragmented, rather than integrated, self (Lysaker & Hermans, 2007).
COGNITIVE-BEHAVIORAL EXPLANATIONS
Cognitive-behavioral theorists have offered two explanations of how and why people
develop schizophrenia. One focuses largely on the behaviors of people with schizophrenia
and applies the principles of operant conditioning. The other focuses on the unusual
thoughts of such individuals and stresses the possible role of misinterpretations.
OPERANT CONDITIONING As you have read, operant conditioning is the process by which
people learn to perform behaviors for which they have been rewarded frequently. The
operant explanation of schizophrenia begins with the general observation that most people
in life become quite proficient at reading and responding to social cues—that is, other
people’s smiles, frowns, and comments. People who respond to such cues in a socially
acceptable way are better able to satisfy their own emotional needs and reach their goals.
Some people, however, are not reinforced for their attention to social cues, either because
of unusual circumstances or because important figures in their lives are socially inadequate.
As a result, they stop attending to such cues and focus instead on irrelevant cues—the
brightness of light in a room, a bird flying above, or the sound of a word rather than its
meaning. As they attend to irrelevant cues more and more, their responses become
increasingly bizarre (Pinkham, 2014). Because the bizarre responses are rewarded with
attention or other types of reinforcement, they are likely to be repeated again and again.
Today the operant view is usually considered at best a partial explanation for schizophrenia.
Although it may help explain why a given person displays more psychotic behavior in some
situations than in others, it is too limited, in the opinion of many, to account for
schizophrenia’s origins and its many symptoms.
When first confronted by voices or other troubling sensations, these people turn to friends
and relatives. Naturally, the friends and relatives deny the reality of the sensations, and
eventually the sufferers conclude that the others are trying to hide the truth. They begin to
reject all feedback, and some develop beliefs (delusions) that they are being persecuted. In
short, according to this theory, people with schizophrenia take a “rational path to madness”
(Zimbardo, 1976). This process of drawing incorrect and bizarre conclusions (delusions) may
be helped along by a cognitive bias that many people with schizophrenia have—a tendency
to jump to conclusions (Sarin & Wallin, 2014).
SOCIOCULTURAL THEORISTS
Sociocultural theorists, recognizing that people with mental disorders are subject to a wide
range of social and cultural forces, believe that multicultural factors, social labeling, and
family dysfunction all contribute to schizophrenia. Research has yet to clarify what the
precise causal relationships might be.
Multicultural Factors Rates of schizophrenia appear to differ between racial and ethnic
groups, particularly between African Americans and non-Hispanic white Americans
(Coleman et al., 2016; Schwartz & Blankenship; 2014; Folsom et al., 2006). As many as 2.1
percent of African Americans receive a diagnosis of schizophrenia, compared with 1.4
percent of non-Hispanic white Americans. Research also suggests that African Americans
with schizophrenia are overrepresented in state hospitals (Durbin el al., 2014; Barnes,
2004).
It is not clear why African Americans are more likely than non-Hispanic white Americans to
receive this diagnosis. One possibility is that African Americans are more prone to develop
schizophrenia. Another is that clinicians from majority groups are unintentionally biased in
their diagnoses of African Americans or misread cultural differences as symptoms of
schizophrenia.
Yet another explanation for the difference between African Americans and non-Hispanic
white Americans may lie in the economic sphere. On average, African Americans are more
likely to be poor; when economic differences are controlled for, the prevalence rates of
schizophrenia become closer for the two racial groups. Consistent with the economic
explanation is the finding that Hispanic Americans, who also tend to be economically
disadvantaged, appear to be more likely to be diagnosed with schizophrenia than non-
Hispanic white Americans, although their diagnostic rate is not as high as that of African
Americans (Coleman et al., 2016; Blow et al., 2004).
Social Labeling Many sociocultural theorists believe that the features of schizophrenia are
influenced by the diagnosis itself. In their opinion, society assigns the label “schizophrenic”
to people who fail to conform to certain norms of behavior. Once the label is assigned,
justified or not, it becomes a self-fulfilling prophecy that promotes the development of
many schizophrenic symptoms.
Family Dysfunction Many studies suggest that schizophrenia, like a number of other mental
disorders, is often linked to family stress. Parents of people with schizophrenia often (1)
display more conflict, (2) have more difficulty communicating with one another, and (3) are
more critical of and overinvolved with their children than other parents.
Family theorists have long recognized that some families are high in expressed emotion—
that is, members frequently express criticism, disapproval, and hostility toward each other
and intrude on one another’s privacy. People who are trying to recover from schizophrenia
are almost four times more likely to relapse if they live with such a family than if they live
with one low in expressed emotion.
According to theorists, the path to schizophrenia starts with a genetically inherited tendency
towards the disorder. This tendency is expressed by the dysfunctional brain circuit discussed
earlier (Nivard et al., 2018; Walker et al., 2016). The theorists argue that if an individual
experiences significant life stressors, difficult family interactions or other negative
environmental factors during their development, this genetic tendency may eventually lead
to schizophrenia.
1. Schizophrenia typically begins to unfold long before the actual onset of the disorder
in young adulthood. People with this disorder often show cognitive, perception, and
attention problems during earlier stages of their lives (Jansen et al., 2018; Fischer &
Buchanan, 2017). Researchers in developmental psychopathology have found that
such people also tend to be more socially withdrawn, disagreeable, and disobedient,
and have more motor difficulties, throughout their early development (Walker et al.,
2016; Dickson et al., 2012). Some of these early problems seem to result mainly from
the individual’s inherited predisposition. However, as per research, they may also
result from repeated experiences of childhood stress, family dysfunction, and/or
difficult social interactions (Kraan et al., 2018; Walker et al., 2016).
2. One of the key ways that a dysfunctional brain circuit may adversely affect the
functioning of people who later develop schizophrenia is by impacting the operation
of the hypothalamic-pituitary-adrenal (HPA) stress pathway, as explained on page
156. When we experience stress, the hypothalamus activates this brain-body
pathway, leading to the secretion of cortisol and other stress hormones and a
heightened state of arousal. Researchers in developmental psychopathology have
discovered that dysfunction by the schizophrenia-related brain circuit leads to
repeated overreactions by the HPA pathway in response to stress (Walker et al.,
2016, 2010, 2008). Such chronic overreactions leave individuals highly sensitive and
unsettled by stressors throughout their development, making them more likely to
develop schizophrenia when faced with stress (Pruessner et al., 2017).
TREATMENT:
Antipsychotic drugs
• Institutional care (token economy)
• Psychotherapy
• For more than half of the twentieth century, the main treatment for schizophrenia
and other severe mental disorders was institutionalization and custodial care.
Because patients failed to respond to traditional therapies, they were usually placed
in overcrowded public institutions (state hospitals in the United States), typically in
back wards where the primary goal was to maintain and restrain them. Between
1845 and 1955 the number of state hospitals and mental patients rose steadily,
while the quality of care declined.
• In the 1950s, two in-hospital approaches were developed, milieu therapy and token
economy programs. They often brought improvement and particularly helped
patients to care for themselves and feel better about themselves.
Reference
• American Psychiatric Association. (2022). Diagnostic and statistical manual of mental
disorders (5th ed., text rev.). https://doi.org/10.1176/appi.books.9780890425787
• Comer book on abnormal psychology