We read with interest the recent article by Martı -Masso and Poza 1 but we were surprised that our previous paper 2 on the same topic was not quoted by the authors. In fact, the prospective follow-up study 2 we have carried out over a median 5-year period in a small population of patients with cinnarizine (CNZ)-and flunarizine (FNZ)-induced parkinsonism represents, to our knowledge, the first report attempting to characterize possible patterns of clinical course and the long-term prognosis of this syndrome, according to well-defined (although arbitrary) criteria. The same is true for the occurrence and the outcome of coexisting iatrogenic dyskinesias. The overoptimistic results reported by Martı -Masso and Poza 1 showing a complete recovery of parkinsonism in 89% of 74 patients with drug-induced parkinsonism (45 of whom were taking CNZ as the sole drug) are at variance with those of our study 2 and with those of another shorter, prospective follow-up study. 3 Indeed, in our series, 2 a diagnosis of "persistent and not progressive" parkinsonism was still made in 10 of 13 (76.9%) patients at the end of the follow up. This discrepancy may be the result of a less rigorous collection of data which failed to provide evidence of the course of clinical recovery in the patients described by Martı -Masso and Poza, 1 a drawback from which all retrospective studies commonly experience. In fact, it has not been clarified by the authors if their results of completely recovered parkinsonism found at the end of the follow up were obtained indirectly by consultation of medical records or by interviewing patients and/or their family members rather than by personal examination of the affected subjects. In addition, possibly lower cumulative dosages of the offending drug, not reported in their article, could account for the different results of the two studies. Moreover, contrary to published literature, 4 it appears strange enough that completely reversible parkinsonism could be observed in such a high proportion of elderly patients who had been taking neuroleptics in addition to CNZ. Regarding the late development of a progressive syndrome resembling idiopathic parkinsonism, a direct comparison between the results of our study 2 and those of Martı -Masso ànd Poza 1 is impossible because they did not separate the patients who had been previously exposed to CNZ given as monotherapy from those taking other antidopaminergic drugs concurrently. The lower percentage of patients with persistent dyskinesias at the final assessment of the follow up found in the study of Martı -Masso `and Poza, 1 in comparison with the figures reported by us, 2 may also have a bearing on the interpretation of the finding.
In short, we defend our view that the evolution of CNZ-FNZ-induced parkinsonism is not so benign although we recognize that the residual extrapyramidal signs are commonly mild and do not determine significant impairment in motor function.