Schizophrenia is a dissociative disorder whose victims experience paranoid delusions, auditory and visual hallucinations, and an increased separation from reality. Additional symptoms include strange behaviors, scattered and disorganized thought processes, and a acute sense of social withdrawal and sociopathy. Schizophrenia comes in both acute and chronic forms, varying based o repetition and severity of episodes. Some patients with schizophrenia often experience violent behavior due to feelings of danger or risk, and must alleviate their paranoia and anxiety through these actions. The following outlines some of the major etiology and treatment methods of schizophrenia, as well as the rationales behind them.
Our current understanding of the etiology of schizophrenia is not complete, and there is still substantial research that must be conducted in order to fully determine its causes. However, there exist several theories that are supported by evidence, though they are not comprehensive and true of every case. Once cause of schizophrenia is an excess of activity in the brain’s dopamine receptors, which can cause the kinds of visual and auditory hallucinations often found in schizophrenics, as well as paranoia and feelings of distrust in one’s environment (Myers, 2005).
Schizophrenics often experience a dulling of emotions, being unable to generate feelings and compassion for themselves or others; this can be attributed to defects in the anterior cingulated cortex, which is a critical component of emotion generation in the frontal lobe. This kind of damage leads to a distinct sense of apathy, and a lack of concern when they make mistakes or other significant events happen (Eslinger and Damasio, 1985). Another element of brain chemistry affected by schizophrenia are the Von Economo neurons (VENs), which are used to facilitate intuition and emotional value judgments when meeting others; it is theorized that these are responsible for the assumptions and judgments we make about other people, which are altered significantly in patients with schizophrenia.
The hypofrontality hypothesis is another possible explanation for the cause of schizophrenia; this theory comes from preliminary research which indicates that schizophrenics show a decidedly low level of brain activity in the prefrontal cortex. Because of this, when performing activities that require the use of the frontal lobes (e.g. card sorting), schizophrenics cannot focus on other actions, a symptom characteristic of brain damage (Andreasen et al., 1997). Schizophrenics are also shown to have larger ventricles than controls. This theory is almost diametrically opposed to the hyperdopamine theory, although some theorists have linked the two in a concept known as supersensitivity. In this theory, a glutamate-rich pathway that links the prefrontal cortex to the ventral Tegmental area (regulating dopamine release) experiences low basal release. This would cause dopamine receptors to experience supersensitivity, leading to overreactions to stimuli from the patient’s environment (Solomon, 1981).
External factors can exacerbate and intensify the symptoms of schizophrenia; the use of cocaine and amphetamines lead to increased levels of dopamine, which can make symptoms worse (Myers, 2005). Schizophrenics often have a decided inability to filter the sensory input they receive, which if left unattended can lead to the violent behavior schizophrenia victims often display. Given the onslaught of sensory information they receive, they typically do not understand how to process what they are seeing and hearing, which can lead to the deterioration of their mental state and level of control (Myers, 2005).
The current understanding of schizophrenia treatment is just as varied as the understanding of its causes. Neuroleptics are one commonly-used treatment method; neuroleptics are antipsychotic drugs of varying types which are used to alleviate psychotic symptoms. For example, the drug Risperidone acts as a dopamine antagonist, blocking dopamine receptors to prevent oversensitivity. This method of treatment ascribes closely to the dopamine hypothesis, as the goal is to prevent dopamine reception through antagonism, thus diminishing schizophrenia. While these types of medications are showing moderate success, their effects are seen to diminish over time, and a certain amount of the population (~20%) experiences resistance to the treatment (Smith, Weston & Lieberman, 2010).
Apart from antipsychotics and neuroleptics, various types of therapy and rehabilitation are also used in treatment. Cognitive behavioral therapy (CBT) is also used to address feelings of reduced motivation and emotional expression in schizophrenics, with detailed case management being required in order to help patients with emotional responses to the problems of their condition. These should not be considered to be substitutes for antipsychotic medication, but using these psychological treatments in conjunction with medication can provide extra benefits to those suffering from the condition (Lynch, Laws & McKenna, 2010).
In conclusion, our understanding of schizophrenia is not comprehensive, but strongly tied between two opposing theories – dopamine oversensitivity and hypofrontality. The concept of hypersensitivity also links these two theories into a comprehensive causal chain that incorporates both into the etiology of schizophrenia. Treatments include a combination of antipsychotic medication and CBT and other therapies, currently constituting the most effective treatments available to address this chronic dissociative disorder. While these theories are supported by current research in the field, further research is required before more comprehensive etiology and treatment methods can be found.
References
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Myers, D. G. (2005). Exploring psychology (8th ed.). New York, NY: Worth Publishers.
Smith, T; Weston, C; Lieberman, J (2010). "Schizophrenia (maintenance treatment)". American
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Solomon, P. R. (1981). Disrupted latent inhibition in the rat with chronic amphetamine or
haloperidol-induced supersensitivity: Relationship to schizophrenic attention disorder. Biological Psychiatry; Biological Psychiatry.
