The problem of schizophrenia
remains an urgent challenge to the researcher, clinician, and
sociologist alike. Today, etiological
research is actively exploring four
major factors:
- The genetic, the role of
heredity.
- The biochemical, searching
for a toxic factor that may be result of an innate metabolic
error.
- The psychodynamic, the
effects of early psychic trauma.
- The social, focusing on
the role of a disturbed family structure in the life of a schizophrenic.
Over the centuries there have been many theories about the causes
of psychotic disorders. Among the earliest were the suggestions
that insanity resulted from possession by the devil or evil spirits
or indicated punishment by the Gods. Physical factors in the form
of vapors or pressure on the brain were held responsible by those
who later tried to cure these states by venesection
and purging.
In the 18th century Georg Stahl introduced the idea of a vital
force into the theory of disease. And in the 19th century Heinrich
Neumann suggested that insanity was due to a "loosening of
the togetherness."
These concepts indicated an early awareness of the important role
of dynamic factors and interpersonal relationships in psychotic
disorders.
In fact, during the 19 th
century a violent controversy developed between those psychiatrists
who, as Griesinger had first emphatically proclaimed, believed
that all mental disorders were due to physical brain disease and
those who thought they were due to a dynamic, psychological struggle
between freedom and obstacles, sin and guilt, and other psychological
forces. Heinroth derided his opponents of the somatological school
because they looked on the human mind "as a cadaver which
one could cut pieces with a knife, or as a chemical compound which
could be broken down into elements, or as a mechanical contraception,
the working of which one could calculate with help of mathematics."
The factor of heredity as
a possible cause of psychosis was also considered by psychiatrists
of the early 19th century. Morel describes the case of a psychotic
boy whose mother had been insane and whose grandmother had been
eccentric, suggesting heredity as a definite etiological factor.
Is
all mental disorder constitutional and genetically determined,
or is it acquired through traumatic experiences in early childhood?
The debate between somatogenic and psychogenic schools of thought
on the causes of mental disorder and the nature-nurture controversy
still go on today.
Several risk factors seem to prefigure it, the most notable
of which are genetics and brain structure. And a combination of
these is probably most influential. In addition to these, schizophrenia
occurs with changes in brain chemistry, specifically, excessive
levels of dopamine. Also, significant changes in the activation
of the brains frontal and parietal lobes have been associated
with schizophrenia.
Biological
Cause:
Heredity is the most well
established risk. People who have immediate family members with
schizophrenia have a 10% chance of developing it, ten times that
of the general population. Other personality disorders, including
those with psychotic symptoms, also seem to be more prevalent
in families with schizophrenia. Despite the chance for inheritance,
the number of children born to parents with schizophrenia doubled
in the first 50 years of the 20th century.
A recent study that seems to support a genetic cause of schizophrenia
suggests that identical twins stand a 50% to 85% chance of sharing
the disease. Furthermore, it shows this to be about three times
that for fraternal twins. Still, most studies fail to identify
the exact mechanism and location of genetic transmission, though
they do identify possible genes and chromosomes.
Because not all identical
twins share the disease, and because people without familial history
develop it, it is likely that there are other physiological and
environmental risk factors involved.
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Neurological Cause:
The theory that schizophrenia
is partly a result of abnormal
brain function is useful in understanding its biological
basis. Underactive frontal lobes and overactive parietal lobes
are thought to cause some of schizophrenias associated symptoms.
For example, when frontal lobes are underactive, planning, organization,
and volition are all impaired. Frontal lobe abnormalities are
probably related to schizophrenias negative symptoms.
Parietal lobes are involved
in sensory perception, like voice recognition, the ability to
distinguish patterns, and spatial orientation. Overactive parietal
lobes may cause distortion of these senses, which is seen in many
people with schizophrenia. Parietal lobe abnormalities are probably
more closely related to positive symptoms.
Abnormal brain structure is
found consistently in people with schizophrenia. This includes
enlarged ventricles and asymmetrical hemispheres. Computerized
functional imaging of the brain has found decreased blood flow
to the frontal lobes of people with schizophrenia. These types
of brain abnormalities forecast certain symptoms, like loss of
attention, difficulty with abstract thinking, and the inability
to solve problems.
Some evidence suggests that
infants who experience birth trauma or complications while in
the womb are at greater risk for schizophrenia. Maternal illness
may play a part as well. A mother who contracts a virus like the
flu, especially during her second trimester, may increase the
risk for her child. It is not known, whether the virus itself
or the immune response to it increases the risk.
Some studies have shown that
winter birth may be associated with schizophrenia, especially
during immune response and illness. Furthermore, viruses in the
womb are more common during the winter months. This has led some
researchers to consider intrauterine viral infection during the
winter as a risk factor. The same link, however, is found for
major mood disorders, like bipolar disorder.
The Dopamine Hypothesis:
Dopamine is a neurotransmitter that transports signals between
nerve endings in the brain. It is thought that the brains of people
with schizophrenia and other psychotic disorders produce too much
dopamine. There is evidence that supports and counters the dopamine
hypothesis.
The main support for the theory
that too much dopamine causes schizophrenia is the fact that antipsychotic
medications, which are used to treat schizophrenia, block dopamine
receptors. The medications are designed to bind to dopamine receptors
in the brain, and their effects have helped many people cope with
symptoms. Secondly, drugs that increase levels of dopamine, like
amphetamines, often cause psychotic symptoms and a schizophrenic-like
paranoid state.
However, several factors challenge
the dopamine hypothesis. For example, dopamine-related psychosis
occurs in many disorders, not exclusively in schizophrenia. People
with schizophrenia are not the only ones who respond to antipsychotic
medication.
Antipsychotic medication may
not significantly affect the negative symptoms of schizophrenia,
which suggests that there is more involved than abnormal dopamine
levels alone. Moreover, dopamine levels might actually be lower
rather than higher in the frontal lobes of the brain. At any rate,
antipsychotic medication only treats the symptoms of schizophrenia;
it does not eliminate its underlying causes.
Environmental Cause
Environmental factors and stress
are thought to trigger the onset of schizophrenia. For example,
moving, troubled relationships, problems at work, or substance abuse
may aggravate the constellation of risk factors and lead to psychosis.
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