The Dopamine Hypothesis Of Schizophrenia

Schizophrenia is not everyday news, but it has had an impact on the world. Schizophrenia is a severe mental disorder in which people interpret reality abnormally. Schizophrenia may result in some combination of hallucinations, delusions, and extremely disordered thinking and behavior that impairs daily functioning, and can be disabling.Doctors and researchers are still studying schizophrenia patients and the effects of medication.
Firstly, the study over schizophrenia unquestionably had a prolonged ride with its time-consuming investigation. ¨The study began in 1986; this report includes data collected until June 1, 1996¨ (241-247). The disease has stricken nerves of team researchers and doctors but they found a way to banish the endless questions
The MEDLINE EMBASE, and Psyc INFO database were searched for studies from January 1,1960 to July 1, 2011 (Howes 776-786). The dopamine hypothesis of schizophrenia was first proposed more than 30 years ago on the basis of indirect evidence (776-786). The hypothesis happened to be a hit so It received support from studies of postmortem brain tissue that found increased striatal D2/3 receptor density and dopamine levels in patients with schizophrenia and from studies of dopamine and its metabolites in cerebrospinal fluid (776-786). Even though the studies of postmortem brain tissues supported the dopamine hypothesis of schizophrenia, it has its negative sides “However, postmortem studies are notable to measure same aspects of the dopaminergic function, such as dopamine release, and potentially biased by the effects of antipsychotic treatment and agonal events,whereas the cerebrospinal fluid studies were inconsistent and unable to provide insights into the regional aspects of dopamine dysfunction” (776-786). The patients were treated with a standard algorithm treatment but there was a sequence with the procedure. Doctors wanted to add the sequence because it was an initial treatment with fluphenazine, up to 20 mg/d; after 6 weeks, the dose for non responders was increased to 40 mg/d for an additional 4 weeks (Robinson 241-247). Patients that had happened to be non responsive to fluphenazine therapy were switched to haloperidol therapy 20 mg/d, for 6 weeks, which was raised to 40 mg/d for 4 additional weeks if needed (241-247). “Treatment response was operationally defined as a CGI global improvement scale rating of “much improved” or “very much improved” and a rating of 3 (mild) or less on all of the following SADs -C+PD psychosis items : severity of delusions, severity of hallucinations, impaired