Like the majority of central nervous system (CNS) disorders, the initial understanding of the factors causing schizophrenia was based on serendipity, in this instance, the finding that chlorpromazine, the first drug used for the treatment of the disease, was a dopamine (DA) receptor antagonist.3 Since then it has been well established that schizophrenia is a multifactorial disease involving both genetic and epigenetic factors7 that may also exist in several distinct subtypes. Identified risk factors for schizophrenia include: winter birth; low socioeconomic status; cannabis use; obstetric complications and intrauterine infection related to birth; immigration; living in a city (urbanicity) and the neighborhood cognitive social capital8; low intelligence quotient; and a family history of the disorder. There is increasing data81 that schizophrenia can be associated with autoimmune diseases, e.g., celiac disease, acquired hemolytic anemia, thyrotoxicosis, interstitial cystitis, and Sjogren's syndrome, and that this association resulted in a 45% increase in risk for schizophrenia. The antipsychotics used to treat schizophrenia can be divided into two distinct classes, typical and atypical. The distinction between the two can be based on their time of introduction to market, typicals preceding atypicals; their receptor-binding profile, the atypicals antagonizing both D2 and 5HT2 receptors with additional binding to D3 and D4 receptors; but most importantly, the ability, albeit limited, of the atypical neuroleptics to address the negative symptoms of schizophrenia together with a lower risk of developing the tardive dyskinesia associated with the older, typical antipsychotic agents. A more controversial distinction is that typical antipsychotics are neurotoxic while atypical agents are metabolic poisons.9
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