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The word schizophrenia means

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Schizophrenia
The word schizophrenia means splitting of personalities and has its origin in the Greek language and was coined by Eugene Bleuler in 1908. Other researchers who did pioneering work in the field include Kurt Schneider, who described the diagnostic features of the disease. This illness is one of the most debilitating psychiatric illnesses known to man and has the capacity to affect all aspects of the affected person’s life. Extensive research has been done to identify the causative factors of the disease. Genetic factors, environmental insults, perinatal insults and psychological stresses have all been explored as possible etiological agents for the diagnosis of the disease (Hirsch and Weinberger 21)
Physiological and anatomical effects of schizophrenia
Recent research has shown that schizophrenia cannot simply be explained by the interplay of genetic and environmental factors. The neuro developmental hypothesis has been put forward to explain the occurrence of the disease with certain characteristic structural changes in the brain present in schizophrenic patients along with altered blood flow to certain areas of the brain and altered function or amount of neurotransmitters.
Structural changes in brain in context to symptoms in patients
With the help of advanced imaging techniques, scientists have discovered certain consistent alterations in brain morphology seen in a majority of schizophrenic patients. The schizophrenic brain shows a decreased amount of grey matter most prominently seen in temporal and frontal areas.

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This loss of grey matter begins posteriorly and then goes on to involve the front of the brain. It has been postulated that the involvement of frontal and temporal lobes in this pathology leads to symptoms like auditory and visual hallucinations, abnormal thoughts and delusions with the severity of symptoms being directly proportional to the amount of brain matter lost. An increased volume of ventricles is also seen in patients (Fauci et al.,2008 p 2721).
Prefrontal cortex is the area of the brain which helps in planning tasks and also governs self-care, in schizophrenics there is decrease in the activity of the prefrontal cortex thus making these patients incapable of understanding the extent of their disease or its symptoms. Since prefrontal cortex is involved, the thought pattern is quite disorganized.
The schizophrenic brain also has decreased volume of amygdala, limbic system and superior temporal gyrus; these are the areas of the brain which regulate mood, language and emotion thus explaining the various mood abnormalities and speech disturbances seen in such patients. Heschel’s gyrus which is the location of the primary auditory cortex is also decreased in size, and there is evidence to suggest that the severity of auditory hallucinations is dependent on the damage suffered by this area.
MRI and PET imaging has also shed light on changes in the cerebral blood flow in schizophrenic patients. There is decreased blood flow to the frontal lobes along with decreased supply to the cingulated and temporal areas but the same areas have increased flow if seen when the patient is having active hallucinations (Shenton ME, 2001) This can explain the delusions and hallucinations occurring in these patients.
The role of inhibitory interneuron has also come under the scanner in the pathogenesis of schizophrenia. These neurons generally act in a manner by which they help the brain to filter out unnecessary stimuli thus preventing brain overloading. It has been postulated and the theory has found support via imaging that in schizophrenic patients the number of inhibitory interneurons is decreased considerably thus leading to all stimuli being processed by a damaged brain thus causing inappropriate perceptions and responses which may manifest as hallucinations, delusions or illogical thinking or irrelevant talking. Researchers have also found evidence to link a change in the way astrocytes and glutaminergic neurons communicate with each other thus leading to a different perception of any stimulus by a schizophrenic patient (Taylor 411-13).
Various neurotransmitters have also been pinpointed as the cause of the manifestations of schizophrenia. According to the dopamine hypothesis of schizophrenia, there is some abnormality in the dopamine pathway in the brain which leads to the so-called positive symptoms of the disease. Studies have shown an increased amount of dopamine receptors in the putamen, caudate nucleus and nucleus accumbens. Different ligands were used to identify dopamine receptor binding in PET imaging, and it does seem that there is a definite increase in this binding in schizophrenic patients. Imaging has also shown that in patients with schizophrenia the structure of the dopamine receptor itself seems to be altered by presence of an extra fragment. The role of glutamate is also being investigated in the pathogenesis of the disease. Glutamate is a very important amino acid that interacts with dopamine pathways and has an excitatory role in the brain. Decreased function of glutamate receptors and change in its interaction with dopamine and dopamine pathway can also explain certain symptoms of the disease. Long-term potentiation of thoughts up to an abnormal extent may be the result of this altered dopamine glutamate interaction.
In a nutshell it can be said that there is still loads of work that needs to be done in order to pinpoint the exact causative factors related to the occurrence of schizophrenia and understand the changes in human brain that lead to this disease.
Work Cited
Hirsch SR; Weinberger DR. Schizophrenia. Wiley-Blackwell. 2003. Print.
Taylor DM. Refractory Schizophrenia and atypical antipsychotics. J Psychopharmacol. 2000. Print. BIBLIOGRAPHY l 1033

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