Abstract Schizophrenia is a psychotic disorder, which affects 1.1% of the population around the world. Schizophrenia is a disorder of the mind and brain that severely impairs ones thinking, emotions and behaviors. Schizophrenia is highly treated with antipsychotic medications and psychosocial therapies, however it is incurable. This disorder generally onsets during early adulthood and tends to be chronic. Through the course of many decades, research on possible causes, risk factors and potential strategies of prevention, have led researchers to have multiple perspectives on the disorder. This review of studies will discuss the symptoms, etiology and treatment of schizophrenia from a cognitive and psychodynamic perspective of the disorder.
The DSM-IV-TR diagnostic criterion for schizophrenia includes, two or more: delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behavior and negative symptoms. For a significant portion of the time one or more major areas of functioning such as work, interpersonal relations, or self-care are markedly below the level achieved prior to the onset. Schizophrenia consists of positive and negative symptoms; positive symptoms consist of delusions and hallucinations, whereas negative symptoms include affective flattening, alogia, avolition, anhedonia and asociality (Nasrollahi, Bigdelli, Mohammadi & Hosseini, 2012). Different types of schizophrenia include paranoid type, where delusions and auditory hallucinations are especially prominent; disorganized type, where disorganized speech and behavior as well as flat affect are present; catatonic type, two of the following must be present: increased motor movement without purpose, negativism, peculiar movements, echolalia, echopraxia and lastly where one cannot move from set posture; undifferentiated type, where positive and negative symptoms are prominent; residual type where negative symptoms are most prominent.
Etiology: Cognitive Perspective
In a research article by Cornblatt, Obuchowski, Roberts, Pollack & Erlenmeyer-Kimling (1999), the basic biological error that leads to schizophrenia can occur as early as the prenatal periods in life, but are not triggered until late adolescence-early adulthood. These biological errors may not involve further major deterioration in the brain functioning after the initial symptoms have appeared. Results of several studies have indicated that structural anomalies, such as enlarged ventricles, are found in schizophrenic patients at their initial episode of illness and do not appear to increase as the illness progresses (Cannon, 1991; Degreef et al., 1991; Delisi et al., 1992; Hoffman, Ballard, Turner & Casey, 1991). In addition to enlarged ventricles found in schizophrenic patients, abnormalities on the cellular level, including abnormal synaptic pruning, defects in embryonic cell migration, and abnormal myelination of axons have been reported that support the neurodevelopmental model (Kovelman & Scheibel, 1984; Jakob & Beckmann, 1986; Falkai, Bogerts, & Rozumek, 1988). The neurodevelopmental hypothesis is an alternative view of schizophrenia as a neurodegenerative illness, which states at least some aspects of schizophrenia are neurodevelopmental. The neurodevelopmental model states that one is born with this disease gene, which consists of brain abnormalities such as structural, functional and biochemical abnormalities, that lead to potential marker deficits such as attention, eye movements and memory deficits. However, the nature of which remains unknown, is what triggers the clinical expression of illness relatively late in the process, generally in late adolescence-early adulthood (Cornblatt et al, 1999).
Along with the previous study, Cannon, Van Erp, Bearden, Loewy et al. (2003) investigated early brain development in the etiology of schizophrenia. These brain disturbances can occur as early as during