Neuroleptics have proven effective for the overall treatment of schizophrenia. The neuroleptic therapy of schizophrenia, however, has been limited by tardive dyskinesia and by the relative inability of neuroleptics to ameliorate the negative symptoms of schizophrenia. Intensive research has been conducted to identify atypical neuroleptics which would not cause TD and which would have relatively greater efficacy in treating negative symptoms. Based upon animal models of TD and negative symptoms, four neuroleptics have been identified which may have these properties: clozapine, thioridazine, sulpiride, and molindone. Clinical studies of TD suggest that these four potentially atypical agents may have lower dyskinetic potential than typical neuroleptics. Additionally, clinical studies of negative symptoms suggest that molindone and sulpiride, but not clozapine or thioridazine may preferentially treat depressive-like negative schizophrenic symptomatology. The atypical effects of clozapine, thioridazine, sulpiride and molindone, suggest that they may have a distinct place in the pharmacotherapy of schizophrenia.
Javitt, MD, Daniel C.
"Mechanisms and Therapeutic Implications of Neuroleptic Atypicality,"
Jefferson Journal of Psychiatry: Vol. 7
, Article 4.
Available at: http://jdc.jefferson.edu/jeffjpsychiatry/vol7/iss1/4