Introduction

With a few exceptions, epidemiological studies of akathisia have been limited for the following reasons.

While extrapyramidal side-effects of drugs have attracted attention ever since neuroleptic drugs were introduced (Delay and Deniker, 1952; Steck, 1954), in most early investigations akathisia was lumped together with other extrapyramidal reactions. Some early authors (eg, Freyhan, 1958; Ayd, 1961) did attempt to describe akathisia separately, but it was not until the mid-1970s that akathisia received serious attention in its own right and the 1980s that incidence and prevalence estimates became available from well-conducted studies. As stated in Chapter 1, this neglect has been difficult to understand. It is possible that EPSE and TD, by virtue of their more definite clinical features, received most of the attention at the expense of akathisia. Moreover, akathisia was a paradoxical response that was inconsistent with the notion that neuroleptics produced tranquillization, resulting in some resistance to its acceptance. Especially in the United States, akathisia was until recently (Van Putten and Marder, 1986) conceptualized as a subjective response, and since AA occurs in acutely psychotic individuals, it is likely that the subjective report would be misattributed to agitation or anxiety or, even worse, ignored. On the other hand, TA is generally overshadowed by TD, or subsumed by it, especially as the two often co-occur.

Until recently, no definite diagnostic criteria for akathisia had been proposed.