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child is left in a confused state and must choose to obey
either the verbal or the non- verbal messages. This leads
to a weakening of the child's understanding of reality
wherein the child must develop his or her own creative
explanation of events.
One criticism of this theory centers on new evidence indicating
that a mother's relationship with a troubled child often
differs from the way she acts with other children within
the family. Disturbances in her relationship with a troubled
child can therefore also be a result of situational influences,
such as the behavior of that child. Expressed emotion
(EE), which consists of the dimensions of criticism and
emotional over-involvement, has also been shown to be
a valid vulnerability risk for developing schizophrenia
and indicative of the course outcome of the disorder;
high levels of expressed emotion have been shown to predict
greater chances of relapse.
Biological Causes of
Schizophrenia
There is strong evidence that schizophrenia may be heritable.
The degree of genetic information shared with a relative
with schizophrenia is correlated with an individual's
risk for developing the disorder. (This means that, for
example, there is a higher risk for developing the disorder
if one's father is affected than if one's uncle has been
diagnosed with schizophrenia.)
Evidence for a possible biological basis for schizophrenia
include the following: Studies have found that the concordance
rate for schizophrenia is also twice as high for monozygotic
twins than dizygotic twins, and if an individual is reared
away from his or her biological parents, the likelihood
of developing the disorder is associated with the appearance
of schizophrenia in the biological parents, not the adoptive
parents. Further evidence comes from genetic studies which
indicate that when the liability for developing schizophrenia
is on the father's side of the family and more than one
child has schizophrenia, the children are all likely to
be of the same sex.
The dopamine hypothesis states that schizophrenia is caused
by the over- activity of dopamine neurons in the brain
in the pathway between the ventral tegmental area (VTA)
and the nucleus accumbens (NA). Support for this theory
comes from evidence that indicates dopamine antagonists,
or drugs that decrease dopamine activity, also decrease
psychotic, or positive, symptoms of schizophrenia. In
addition, drugs that increase dopamine activity in the
brain, such as amphetamines and cocaine, increase psychotic
behavior. The pathway from the VTA to the NA plays a role
in reinforcement; chances are that when an individual
engages in a certain action or thought that he or she
likes, dopamine is firing. The basic rules of operant
conditioning, then, say that the likelihood of the individual
continuing to engage in that type of action will increase.
Everyone experiences seemingly random or out of context
thoughts, but when this occurs in individuals with schizophrenia,
a corresponding increase in dopamine levels creates a
surge of positive reinforcement in the brain and increases
the chances that they will have such thoughts again.
Schizophrenia may also be the result of a neurological
deficit in the dorsolateral prefrontal cortex of the brain.
In the prefrontal cortex, dopamine gives us the ability
to inhibit learned responses and to switch to a new response
when required. Individuals with schizophrenia seem to
exhibit symptoms of hypofrontality, or low dopamine activity
in that part of the brain. One measure of hypofrontality
is the Wisconsin Card Sort Test (WCST). Individuals with
schizophrenia tend to perform at very low levels on the
WCST, persisting in committing preservative errors; these
results indicate that dopamine may be acting differently
than normal in the prefrontal cortex. In an attempt to
understand the contradictions concerning the level of
dopamine activity in the brain and its subsequent relation
to schizophrenia, a new argument has been offered, positing
a chain of malfunction started by some unknown lesion
that causes decreased dopamine functioning in the prefrontal
cortex, leading to low dopamine levels in neurotransmitters.
The low level of dopamine functioning leads to reduced
glutamate activity, producing a low tonic or steady-state
release of dopamine and leading to super-sensitivity of
post- synaptic dopamine receptors and overreaction in
the nucleus accumbens. In simpler terms, low dopamine
leads to over-sensitivity to tonic releases and, therefore,
too much neuronal action during phasic releases.
Anti-psychotic drugs, which inhibit the post-synaptic
dopamine receptors, can then lead to a decrease in the
positive symptoms associated with schizophrenia, but not
necessarily the negative symptoms.
Treatment for Schizophrenia
There have been vast improvements in medications for schizophrenia
over the past twenty years. However, the possibility of
serious side effects makes it necessary for every individual,
in conjunction with a physician, to find the right balance
in his or her medication. Chlorpromazine, which is similar
to an antihistamine, reduces anxiety without causing mental
confusion. However, the side effects can be quite frightening:
extrapyramidal symptoms, which include muscular rigidity,
tremors, and restless agitation, result from the high
levels of dopamine antagonists. These symptoms appear
quite similar to symptoms of diseases associated with
low dopamine activity such as Parkinson's disease. Another
side effect of Chlorpromazine, known as tardive dyskinesia,
causes arm flapping, tongue rolling, and grimacing. Clozapine,
another drug used for treating schizophrenia, has been
associated with less severe side effects.
Social therapy, with a psychosocial basis, also plays
a key role in helping individuals diagnosed with schizophrenia
to learn, regain, and maintain skills essential in coping
with a stressful environment.
Potential Causes of the Neurodevelopmental
Disorders Apparent in Schizophrenia
Several observations have suggested that neurodevelopmental
problems associated with schizophrenia represent antecedents
rather than consequences of the disorder. The concept
of an unknown brain legion is a hypothetical construct
that has been supported by evidence such as the latitude
effect, which indicates that individuals who live at higher
latitudes show an increased risk for developing more malignant
forms of schizophrenia. The prenatal environment and gestation
period may also play an important role. The seasonality
effect describes findings that births occurring in late
winter or early spring are associated with a higher risk
for developing schizophrenia, especially when temperatures
were very low the previous fall. Both the latitude effect
and the seasonality effect, however, may point to the
mother having contacted some viral infection, or developed
some autoimmune response.
Support for this theory can also be drawn from the evidence
that the influenza epidemic of 1957 was associated with
an increased rate of schizophrenia. Also, in times of
severe food shortage, such as during the Hungerwinter
of 1945 in the Netherlands, children show an increased
risk of developing schizophrenia (though this was true
only for female offspring whose mothers were in their
first trimester during the Hungerwinter). Further proof
of the importance of the gestation period is seen by the
fact that monozygotic twins who are discordant for schizophrenia
are also discordant for fingerprint ridge count, which
is formed in the second trimester.
Certain qualities are associated with a better course
and outcome. Individuals who had a good pre-morbid adjustment
or who were doing well before the onset of the disorder
tend to have a higher chance of recovery. Other qualities
associated with a better outcome include: later age of
onset, acute rather than a gradual, insidious onset, brief
duration of active phase symptoms, good inter-episode
functioning, minimal residual symptoms, no structural
brain abnormalities, and no family history of schizophrenia
or mood disorder
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