Schizophrenia Is a Form of Term Paper

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This view has one advantage in that it goes toward explaining why the same general disease - schizophrenia - can vary significantly from person to person. The Vulnerability Model suggests to us that schizophrenia is caused by a combination of interacting factors including physical, psychological and environmental events that work dysfunctionally together to produce what we call "schizophrenia."

This does not mean the brains of schizophrenics are identical to those without schizophrenia, however. Some evidence persuasively points to brain development that goes wrong before a baby is ever born. During gestation, brain cells have to migrate from one central location to become the different parts of the brain. In the process, some brain cells are redundant, and the brain "prunes," or destroys them. Some researchers believe that in some people who later develop schizophrenia, brain cells group together that should not be together, resulting in a baby that is born with a dysfunctional brain from the beginning (Bower, 1996).

Research suggests that fetal development of the brain malfunctions about halfway through the pregnancy, when large numbers of neurons are traveling to the place they belong in the baby's brain. Research has found disorganized clumps of neurons both in the cerebral cortex and in other parts of the brain (Bower, 1996). Whether this problem is caused or worsened by viral infections during pregnancy isn't known, but some studies suggest that schizophrenia is more common in babies whose mothers had some kind of viral illness during pregnancy. For example, in a Finnish study, schizophrenia was more common in babies when their mothers had influenza during the second trimester of their pregnancies (Bower, 1996). Other researchers have noted schizophrenia occurring more commonly in people who were born prematurely (Bower, 1996), (Ratey, 2001).

Other studies show neurons that are abnormally large, and malformation of the myelin, a fatty substance that insulates neurons and allows electrical impulses to travel along neurons more efficiently and effectively (Bower, 1996).

At the same time, several twin studies point to a strong genetic component. The exact mechanism is not known, but a number of mental illnesses and neurochemical disorders appear to have genetic tendencies (Bower, 1996), (Ratey, 2001).

In identical twin studies, when one twin develops schizophrenia, the other twin develops it about 50% of the time (Bower, 1996). In some of those studies, the twin who developed schizophrenia showed damage to the brain not related to the schizophrenia (Bower, 1996). This provides strong support for the Vulnerability model, because it suggests that the twin who developed schizophrenia may have done so because of the additional brain

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Other studies show neurons that are abnormally large, and malformation of the myelin, a fatty substance that insulates neurons and allows electrical impulses to travel along neurons more efficiently and effectively (Bower, 1996).

At the same time, several twin studies point to a strong genetic component. The exact mechanism is not known, but a number of mental illnesses and neurochemical disorders appear to have genetic tendencies (Bower, 1996), (Ratey, 2001).

In identical twin studies, when one twin develops schizophrenia, the other twin develops it about 50% of the time (Bower, 1996). In some of those studies, the twin who developed schizophrenia showed damage to the brain not related to the schizophrenia (Bower, 1996). This provides strong support for the Vulnerability model, because it suggests that the twin who developed schizophrenia may have done so because of the additional brain

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