Abstract

We discuss several major related and integrated issues in this two-part series of papers on tardive dyskinesia (TD). In this, the second paper, Part B, the management and mechanisms are emphasized; in Part A the diagnosis and assessment of tardive dyskinesia was discussed. In this Part B series of articles we examine several special important priorities in this condition associated with sometimes permanent involuntary abnormal movements associated with the neuroleptic drugs. We particularly examine the management of this enormously important condition. After the diagnosis and assessment of TD, comes the clinical approach to management and the options and theories behind that approach. There remain no approved medications for the management of tardive dyskinesia. Therefore, all treatments are “out of labeling”. The purpose of this paper is to shed light on high dose buspirone treatment, originally described by the author in 1989 [1], and which after more than a quarter century requires re-evaluation as it still appears, in the author’s opinion, to be the logical and most appropriate management for TD. A major issue focuses, on the updated experience of more than a quarter century with generally almost completely positive effects of high-dose buspirone (HDB) treatment of tardive dyskinesia (TD) and the next issue provides an important, major theoretical demonstration of the mechanism of tardive dyskinesia. The dopamine 2 or 2-3 supersensitivity hypothesis as a cause of TD is strongly supported by HDB. In Part B, the issue of choice of medication for psychosis and related medical conditions becomes pertinent. The choices relate to the newer second generation atypical neuroleptics (SGAs) compared with the older typical, first generation neuroleptics (FGAs). The generally more expensive SGA drugs have become far the most used anti-psychotic agents in wealthy countries such as the United States, because of their efficacy and ostensible safety. Certain maxims are mentioned.

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