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Clinical Psychotic ◊ This term has been used to characterize many unusual behaviours
Behaviour ◊ In its strictest sense it usually involves delusions and/or hallucinations
Description,
◊ Schizophrenia is one of the disorders that involve psychotic behaviour
Symptoms, ◊ Mental health workers typically distinguish between positive and negative symptoms of schizophrenia
and Subtypes ◊ A third dimension, disorganized symptoms, also appears to be an important aspect of the disorder
◊ A diagnosis of schizophrenia requires that two/more positive, negative, and/or disorganized symptoms be present for at
least 1 month, with at least one of these symptoms including delusions, hallucinations, or disorganized speech
◊ DSM-5 also includes a dimensional assessment that rates the severity of the individual’s symptoms
Positive Active Delusions
Symptoms Manifestations Gross misrepresentations of reality is called a disorder of thought content, or
a delusion
Types
Grandeur (a mistaken belief that the person is famous or powerful)
Persecution (others are “out to get them”)
Capgras syndrome (in which the person believes someone he/she
knows has been replaced by a double)
Cotard’s syndrome (in which the person believes he is dead)
Motivational view
Would look at these beliefs as attempts to deal with and relieve
anxiety and stress
Deficit view
Sees these beliefs as resulting from brain dysfunction that creates
these disordered cognitions or perceptions
Hallucinations
Sensory experiences in absence of environmental stimuli or input
Can involve all senses
Most common
Auditory (hearing things that aren’t there)
Own vs. voice (people who experience hallucinations appear to have
intrusive thoughts, but they believe they are coming from somewhere or
someone else
They then worry about having these thoughts and engage in meta-worry – or
worrying about worrying
Researchers used a brain-imaging technique while men were experiencing
hallucinations and while they were not
They found that the part of the brain most active during hallucinations was
Broca’s area
This is surprising because Broca’s area is known to be involved in speech
production, rather than language comprehension
These observations support the metacognition theory
People who are hallucinating are not hearing voices of others but are
listening to their own thoughts or their own voices and cannot
recognize the difference
One possible explanation for this problem is referred to as poor
“emotional prosody comprehension”
Prosody is that aspect of our spoken language that communicates
meaning and emotion through our pitch, amplitude, pauses, etc.
Obvious signs
Distortions of normal behaviour
Exaggerations or excesses
50-70% experience hallucinations, delusions, or both
Historic Three Divisions They were dropped from the diagnostic criteria for DSM-5
Subtypes Historically The dimensional assessment of severity is now used instead of the three schizophrenia
Identified Paranoid ֒ Delusions of grandeur or persecution
Disorganized ֒ Or hebephrenic; silly and immature emotionality
Catatonic ֒ Alternate immobility and excited agitation
Other Schizo- ♦ Schizophrenic symptoms
phreniform ♦ Few months only
Psychotic
Disorder ♦ Associated with good premorbid functioning
Twin Studies If they are raised together, identical twins share 100% of their genes and 100% of their environment,
whereas fraternal twins share only about 50% of their genes and 100% of their environment
If the environment is solely responsible for schizophrenia, we would expect little difference between
identical and fraternal twins with regard to this disorder
If only genetic factors are relevant, both identical twins would always have schizophrenia (be
concordant) and the fraternal twins would both have it 50% of the time
Research from twin studies indicate that the truth is somewhere in the middle
Adoption The largest adoption study was conducted in Finland (Tienari, 1991)
Studies From a sample of almost 20 000 women with schizophrenia, the researchers found 190 children who
had been given up for adoption
The data from this study support the idea that schizophrenia represents a spectrum of related disorders,
all, which overlap genetically
If an adopted child had a biological mother with schizophrenia, that child had about 5% chance of
having the disorder (compared to only 1% in the general population)
However, if the biological mother had schizophrenia or one of the related psychotic disordres (e.g.,
delusional disorder or schizophreniform disorder), the risk that the adopted child would have one of
these disorders rose to about 22%
Even when raised away from their biological parents, children of parents with schizophrenia have a
much higher chance of having the disorder themselves
At the same time, there appears to be protective factor if these children are brought up in healthy
supportive homes
In other words, a gene-environment interaction was observed in this study, with a good home
environment reducing the risk of schizophrenia
The Offspring A study found that 1.7% of the children with non-schizophrenic parents developed schizophrenia
of Twins “Does this mean you can develop schizophrenia without “schizophrenic genes”?
Or are some people carriers, having the genes for schizophrenia but for some reason not showing
disorder themselves?
An important clue to this question comes from research on children of twins with schizophrenia
Presented by Ms I van Aardt
Summarized by A van Wyngaard
21 identical twins pairs and 41 fraternal twin pairs with a history of schizophrenia were identified, along
with their children
If parent is an identical twin with schizophrenia, have about a 17% chance of having the disorder
A figure that holds if are the child of an unaffected identical twin whose co-twin has the disorder
If parent is the twin with schizophrenia, have about 17% chance of having schizophrenia
If parent does not have schizophrenia but parent’s fraternal twin does, risk is only about 2%
The only way to explain this finding is through genetics
The data clearly indicate that can have genes that predispose to schizophrenia, not show the disorder,
but still pass on genes to children
In other words, can be a “carrier” for schizophrenia
Linkage and Genetic linkage and association studies rely on traits such as blood types (whose exact location on the
Association chromosome is already known) inherited in families with the disorder (schizophrenia) you are looking
Studies for
Researchers have determined the location of the genes for these traits (marker genes), and can make
rough guess about location of disorder genes inherited with them
Three of the most reliable genetic influences that make one susceptible to schizophrenia include
sections on chromosome 8, chromosome 6 and chromosome 22 (COMT)
- The COMT gene is of particular interest to scientists because it plays a role in dopamine
metabolism, which appears to be disrupted in persons with this disorder
Endo- In complex disorders such as this, researchers are not looking for a “schizophrenia gene” or genes
phenotypes Instead, researchers try to find basic processes that contribute to the behaviours or symptoms of the
disorder and then find the gene or genes that cause these difficulties
- A strategy called endophenotyping
One of the more highly researched is called smooth-pursuit eye movement, or eye-tracking
- Keeping head still, typical people are able to track a moving pendulum, back and forth, with
their eyes
The ability to track objects smoothly across the visual field is deficient in many people who have
schizophrenia
Presented by Ms I van Aardt
Summarized by A van Wyngaard
1. A significant number of people with schizophrenia are not helped by the use of dopamine
antagonists
2. Although the neuroleptics block the reception of dopamine activity quite quickly, the relevant
symptoms subside only after several days or weeks, more slowly than we would expect
3. These drugs are only partly helpful in reducing the negative symptoms
- E.g., flat affect ot anhedonia of schizophrenia
♦ A medication called olanzapine
- Along with a family of similar drugs is effective with many people who were not helped with
traditional neuroleptic medications
- The bad news for the dopamine theory is that olanzapine and these other new medications are
weak dopamine antagonists, much less able to block the sites than other drugs
♦ Why would a medication ineddicient at blocking dopamine be effective as a treatment for schizophrenia
if schizophrenia is cause by excessive dopamine activity?
- The answer may be that although dopamine is involved in the symptoms of schizophrenia, the
relationship is more complicated than once thought
♦ Current thinking points to at least three specific neurochemical abnormalities simultaneously at play in
the brains of people with schizophrenia
♦ Strong evidence now leads to believe that schizophrenia is partially the result of excessive stimulation of
striatal dopamine D2 receptors
♦ The striatum is part of the basal ganglia found deep within the brain
- These cells control movement, balance, and walking, and they rely on dopamine to function
♦ Huntington’s disease (which involves a deterioration of motor function) is pointing to deterioration in
this area of the brain
♦ How do we know that excessive stimulation of D2 receptors is involved in schizophrenia?
- One clue is that the most effective antipsychotic drugs all share dopamine D2 receptor
antagonism – meaning they help block the stimulation of the D2 receptors
♦ Using brain-imaging techniques, scientists can view the living brain of a person with schizophrenia and
can observe how the newer, “second generation” antipsychotic medications work on these specific
dopamine sites
♦ A second area of interest to scientists investigating the cause of schizophrenia is the observation of a
deficiency in the stimulation of prefrontal dopamine D1 receptors
♦ Therefore, while some dopamine sites may be overactive (e.g., striatal D2), a second type of dopamine
site in the part of the brain that we use for thinking and reasoning (prefrontal D1 receptors) appears to
be less active and may account for other symptoms in common with schizophrenia
♦ People with schizophrenia display a range of deficits in the prefrontal section of the brain, and this area
may be less active in people with schizophrenia (a condition known as hypofrontality)
♦ Finally, a third area of neurochemical interest involves research on alterations in prefrontal activity
involving glutamate transmission
- Glutamate is an excitatory neurotransmitter that is found in all areas of the brain and is only
now being studies in earnest
- Glutamate has different types of receptors, and the ones being studied for their role in
schizophrenia are N-methy-d-aspartate (NMDA) receptors
♦ The effects of certain drugs that affect NMDA receptors point to clues to schizophrenia
♦ A deficit in glutamate or blocking of NMDA sites may be involved in some symptoms of schizophrenia
♦ Two recreational drugs
- Phencyclidine (PCP) and ketamine – can result in psychotic-like behaviour in people without
schizophrenia and can exacerbate psychotic symptoms in those with schizophrenia
♦ Both PCP and ketamine are also NMDA antagonists, suggesting that a deficit in glutamate or blocking of
NMDA sites may be involved in some symptoms of schizophrenia
Brain ◊ Many children with a parent who has the disorder, and who are therfore at risk, tend to show subtle but
Structure observable neurological problems, such as abnormal reflexes and inattentiveness
◊ Adults who have schizophrenia show deficits in their ability to perform certain tasks and to attend
during ability to perfrom certain tasks and attend during reaction time exercises
◊ Such findings suggest that brain damage or dysfunction may cause or accompany schizophrenia,
although no one site is probably responsible for the whole range of symptoms
◊ One of the most reliable observations about the brain in people with schizophrenia involves the size of
the ventricles
◊ These liquid-filled cavities showed enlargement in some brains examined in people with schizophrenia
◊ In the dozens of studies conducted on ventricle size, the great majority show abnormally large lateral
and third ventricles in people with schizophrenia
◊ Ventricle size may not be a problem, but the dilation (enlargement) of the ventricles have not
developed fully or have atrophied, thus allowing the ventricles to become larger
◊ Ventricle enlargement is not seen in everyone who has schizophrenia
- Several factors seem to be associated with this finding
- E.g., enlarged ventricles are observed more often in men than in women
◊ Also ventricles seem to enlarge in proportion to age and to the duration of the schizophrenia
◊ Onse study found that individuals with schizophrenia who were exposed to influenza prenatally may be
more likely to have enlarged ventricles
◊ In a study of ventricle size, researchers investigated the possible role of genetics
- Invesitgators compared brain structure among people with schizophrenia, their same-sex
siblings who did not have schizophrenia, and healthy volunteers
- Both the people with schizophrenia and their otherwise unaffected siblings had enlargement of
the third ventricle compared with the volunteers
◊ Suggests that the enlargement of ventricles may be related to susceptibility to schizophrenia
◊ The frontal lobes of the brain have also interested researchers looking for structural problems
associated with schizophrenia
◊ This area may be less active in people with schizophrenia than in people without the disorder, a
phenomenon sometimes known as hypofrontality (hypo means “less active”, or “deficient”)
◊ Deficient activity in a particular area of the frontal lobes, the dorsolateral prefrontal cortex (DLPFC), may
be implicated in schizophrenia
◊ When people with and without schizophrenia are given tasks that involve the DLPFC, less activity
(measured by cerebral blood flow) is recorded in the brains of those with schizophrenia
◊ Follow-up studies show that some individuals with schizophrenia show hyperfrontality (too much
activity), indicating that the dysfunction is reliable, but hyperfrontality displays itself differently in
different people
◊ It appears that several brain sites are implicated in the cognitive dysfunction observed among people
with schizophrenia, especially the prefrontal cortex, various related cortical regions, and subcortical
circuits, including the thalamus and the stratum
◊ Remember that this dysfunction seems to occur before the onset of schizophrenia
◊ In other words, brain damage may develop progressively, beginning before the symptoms of the
disorder are appharent, perhaps prenatally
Prenatal and ♦ There is evidence that the prenatal (before birth) and perinatal (around the time of birth) environment
Perinatal are correlatedc with the development of schizophrenia
Influences ♦ Fetal exposure to viral infection, pregnancy complications, and delivery complictions are among the
environmental influences that seem to affect whether or not someone develops schizophrenia
♦ Several studies have shown that schizophrenia may be associated with prenatal exposure to influenza
♦ Those whose mothers were exposed to influenza during the second trimester of pregnancy were more
likely to have schizophrenia than others
♦ The indications that virus-like diseases may cause damage to fetal brain, which later may cause the
symptoms of schizophrenia, are suggestive and may help explain why some people with schizophrenia
behave the way they do
♦ The evidence of pregnancy complications (e.g., bleeding) and delivery complications (e.g., asphyxia or
lack of oxygen) and their relationship to later schizophrenia suggest, on the surface, that this type of
environmental stress may trigger the expression of the disorder
♦
Psychological ◊ That one identical twin may develop schizophrenia and the other may not suggests that schizophrenia involves something
and Social in addition to genes
Influences Stress ◊ It is important to learn how much and what kind of stress makes a person with a predisposition for
schizophrenia develop the disorder
◊ Researchers have studies the effects of a variety of stressors on schizophrenia
- Living in a large city is associated with an increased risk of developing schizophrenia –
suggesting the stress of urban living may precipitate its onset
◊ Otherwise healthy people who engage in combat during a war often display temporarry symptoms that
resemble those of schizophrenia
◊ In a classic study, Brown and Birley examined people whose onset of schizophrenia could be dated
within a week
◊ These individuals had experienced a high number of stressful life events in the 3 weeks before they
started showing signs of the disorder
◊ In a large-scale study sponsored by the World Health Organization in the onset of schizophrenia
◊ This cross-national study confirmed the findings of Brown and Birley across eight research centres
◊ The retrospective nature of such research creates problems
- Each study relies on after-the-fact reports, collected after the person showed signs of
schizophrenia
◊ One always wonders whether such reports are baised in some way and therefore misleading
◊ At the same time, there are strong individual differences in how people experience the same life events,
and people with schizophrenia may experience events differently than those without the disorder
◊ Do the symptoms of schizophrenia become worse as a result of stressful life experiences?
- This vulnerability – stress model of schizophrenia suggests that this is the case, and may be
helpful in predicting problems
◊ One research study used a natural disaster – the 1994 Northridge, California, earthquake – to assess
how people with schizophrenia would react to this stress when compared with those bipolar disorder
and healthy controls
◊ Both patient groups reported more stress-related symptoms compared with the controls
◊ However, the people with schizophrenia reported lower levels of self-esteem after the disaster and
were more likely to engage in avoidance coping (not thinking about the problem or becoming resigned
to difficulties) than the other two groups
◊ Research on sociocultural stress, such as poverty, homelessness, and the stress of being in a new
country, extends the types of psychosocial stressors influential in schizophrenia
◊ Important research has begun to isolate the gene – environment interactions in this area
- E.g., some studies now show that particular gene variances may predict which individuals with
schizophrenia will be more likely to react negatively (such as relapse) with increased stress
◊ These types of studies point to how stress can impact people with schizophrenia and amy suggest useful
treatments (such as cognitive-behavioural therapy to help them cope more appropriately)
Family ♦ A great deal of research has studies how interactions within the family affect people who have
schizophrenia
- E.g., the term schisophrenogenic mother was used for a time to describe a mother whose cold,
dominant, and rejecting nature was though to cause schizophrenia in her children
♦ In addition, the term double bind communication was used to portray a communication style that
produced conflicting messages, which, in turn, caused schizophrenia to develop
- Here, the parent presuambly communicates messages that have two conflicting meanings; e.g.,
a mother respons coolly to her child’s embrace but says “Don’t you love me anymore”? when
the child withdraws
♦ Although these theories are no longer supported, they have been – and in some cases continue to be –
destructive, producing guilt in parents who are persuaded that their early mistakes caused devastating
consequences
♦ Recent work has focused more on how family interactions contribute not to the onset of schizophrenia
but to replapse after initial symptoms are observed
♦ Research has focused on a particular emotional communication style known as expressed emotion (EE)
♦ This concept was formulated by George W. Brown and his colleagues in London
♦ Following a sample of people who had been discharged from the hospital after an episode of
schizophrenic symptoms, the researchers found that former patients who had limited contact with their
relatives did better than the patients who spent longer periods with their families
♦ Additional research results indicated that if the levels of criticism (disapproval), hostility (animosity),
and emotional over-involvement (intrusiveness) expressed by the families were high, patients tend to
relapse
♦ Other researchers have since found that ratings of high expressed emotion in a family are a good
predictor of relapse among people with chronic schizophrenia
♦ If have schizophrenia and live in a family with high expressed emotion, are 3.7 times more likely to