Dopamine hypothesis is a theory that links schizophrenia or psychosis to the dopamine levels in the brain. This theory is derived from several clinical observations and otherwise symptom related results of medication from different patients. The significant presence of dopamine level in a patient’s brain may be the strongest link in the study of patient psychosis. However, since the theory is still in clinical studies; and other factors are now being studied in relation to the change in mental state.
There are several evidences supporting the dopamine hypothesis. Firstly, the evidence comes from pharmacological studies of a group of drug called phenothiazine more specifically chlorpromazine. This drug is used in as a treatment for schizophrenic patients (Delay, Deniker and Harl). The therapeutic use of this drug is known to block dopamine receptors. Blocking of the dopamine receptors has been the main focus of treating psychosis. The dopamine function is one of different neurotransmitters located in the brain. Another evidence of dopamine hypothesis is from another group of drug called amphetamine. The function of this drug is to produce an excess of dopamine in the brain. However, with the abuse of this drug so is the eventual effect of amphetamine-induced psychosis. Amphetamine-induced psychosis is recognized as a possible consequence of chronic amphetamine use (Young and Scoville). With the substance abuse of amphetamine, abusers experience psychosis and schizophrenic episode until the effect of the drug has subsided. At times, with prolonged use, abusers may still experience hallucinations and psychosis even after the drug subsided in the person’s body. And, another evidence is raised by another drug called L-DOPA. Patients with Parkinson’s disease are treated with this drug. But, the significant problem with this treatment is that it induces psychosis. From these three evidences, there is a stronger proof supporting the dopamine hypothesis.
However, there are several evidences against the dopamine hypothesis. In recent experiments where modern methods are developed to examine the correlation of dopamine blockage and psychosis. PET scanning is used to examine how the drug works in the patient’s brain and the results have shown that increase in antipsychotic drug results to an insignificant reduction on the patient’s psychosis. Also, new generation of atypical antipsychotic drug which had limited relation to dopamine blockage is also as effective as the previous antipsychotic drug. There is also the evidence of glutamate being associated with schizophrenia. Ketamine which is known to block glutamate receptors can cause psychosis. This means that dopamine function is not the only one associated with psychosis. It may involve other neurotransmitter as well, aside from dopamine function. However, some study also relates structural formation of the brain to schizophrenia and other psychosis. In the study, individuals have distributed gray matter mostly around the front and median temporal lobe (McDonald et al.). Genetics also plays an important role in psychosis. In a separate study, it has shown the particular gene could cause schizophrenia. Though, it may not be solely based on the influence of the genes of an individual to be prone to schizophrenia. This may involve different factors to activate the genes and schizophrenia would be observed (Schwab et al.).
It can be noted that medication and treatment of psychosis must not be concentrated in one aspect. Rather, treatment involves a different approach to ensure the patient’s response to each one of them. This is also essential in determining the most effective approach for the patient. Although there has been a significant proof linking dopamine hypothesis of psychosis, further studies and examinations need to be done on other neurotransmitters in the brain.
Delay, J, P Deniker, and JM Harl. 'Therapeutic Use in Psychiatry of Phenothiazine of Central Elective Action (4560 RP)'. 110.2 1 (1952): 112. Print.
McDonald, Colm et al. 'Regional Volume Deviations Of Brain Structure In Schizophrenia And Psychotic Bipolar Disorder Computational Morphometry Study'. The British Journal of Psychiatry 186.5 (2005): 369--377. Print.
Schwab, Sibylle G et al. 'Support for Association of Schizophrenia with Genetic Variation in the 6P22. 3 Gene, Dysbindin, In Sib-Pair Families with Linkage and In an Additional Sample of Triad Families'. The American Journal of Human Genetics 72.1 (2003): 185--190. Print.
Young, D., and W.B. Scoville. 'Paranoid Psychosis in Narcolepsy and the Possible Danger of Benzedrine Treatment'. The Medical clinics of North America 22 (1938): 637-46. Print.