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Schizophrenia may be colloquially defined as “the inability to tell what is real from what is imagined” (Begley et al, 2002, p.44). Its major symptoms can be summarized as “an aberrant body awareness” (Lenzenweger, Maher, & Manschreck, 2005, p.1297). A schizophrenic is unable to distinguish between an objective reality and the aberrant auditory and visual sensations of his/her own mind. As schizophrenia is commonly considered a pinnacle of neurological disorders, it is worth reviewing and analyzing certain theories that attempt to focus on its neurological causes.
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The neurological interpretation of schizophrenia has become one of the most influential research approaches. The brain scanning (neuroimaging) of both living and post mortem schizophrenics’ brains demonstrated that “morphological or functional abnormalities” are prevalent in their brains (Iritani, 2007, p.605). The 40 MRI studies’ meta-analysis conducted by Lawrie & Abukmeil (1998) attested to the presence of significant structural abnormalities in the examined schizophrenics’ brains. In particular, average brain volume reduction was found to be near 3%, while temporal lobe and amygdala/hippocampal complex reductions in the left hemisphere amounted to 6% and 6.5%, respectively. The same figures for the right hemisphere were 9.5% and 5.5%. Simultaneously, the lateral ventricles’ volume increased significantly (44% in the left hemisphere, 36% in the right one; & Abukmeil, 1998, pp. 115-119). Hence, the important role of brain abnormalities in schizophrenia’s development may be established.
The origins of these abnormalities are commonly attributed to either the neurodevelopmental or neurodegenerative processes. The former hypothesis is supported by the lack of progressive brain abnormalities in the diagnosed schizophrenia patients, as well as by the cortical cytoarchitecture studies that have found that the schizophrenics’ neuronal structures are rather misplaced and chaotic, which may only be the result of the abnormal prenatal development (Abi-Dargham et al., 1991; Jakob & Beckmann, 1986). However, some studies point at the post-natal brain developments that may be associated with schizophrenia. For instance, excessive extracerebral CSF in schizophrenic brains has been documented in many neuroimaging studies, which means that the brain loss process may be progressive after all (Woods & Yurgelun-Todd, 1991). Therefore, a consensus on the veracity of either neurodevelopmental or neurodegenerative hypothesis cannot yet be reached.
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Still, some other studies emphasize the key role of non-neurological factors in schizophrenia’s development. For instance, Lakhan & Kramer (2009) explore the role of genetic and proteotic factors therein. For instance, in its interaction with interleukin, the DTNBP1 modifier gene was found to increase the schizophrenia’s risk (Lakhan & Kramer, 2009, p.4).
Nevertheless, no singular gene responsible for schizophrenia has been uncovered yet (O’Donovan & Owen, 1999), and the studies of monozygotic twins affected and non-affected by schizophrenia demonstrated that the ventricles and globe grey matter changes in the affected twin are not explained by mere geneticc factors (Reveley et al., 1990). Thus, the purely genetic interpretation of schizophrenia would not suffice to explain its brain symptoms.
The biochemical interpretations may be the useful complement to the neurological and genetic hypotheses. For instance, the dopamine release dysregulation has been frequently observed in schizophrenic patients (Flores et al., 1996). Seaman (2009) observed that the glutamate components’ efficiency in treating psychotic states associated with schizophrenia may lead to the assumption of the causal connection between hypoglutamate condition and schizophrenia (see Gaspar et al., 2009, for the same conclusion). Therefore, at least two biochemical processes may be partially responsible for the disease’s manifestations.
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Furthermore, Baumeister & Hawkins (2004) demonstrated that the original hypothesis of the crucial impact of serotonin imbalance on the schizophrenia development may not be as false as it has been consensually established. In particular, the serotonin disturbance actually has an impact on the severe depression developments and other symptoms that may be observed in schizophrenics as well (Baumeister & Hawkins, 2004, p.286). This may give a more generalist perspective on the connection between schizophrenia and depression.
Therefore, the schizophrenic disorder would appear to be a multifactor phenomenon, with neurological factors having a causal impact on the disease’s development, together with non-neurological one. Hence, further research is needed to consider the interrelationship between schizophrenia’s neurology and biochemistry.
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