The association of pineal calcification with drug-induced dystonic movements

Abstract

There is evidence that reduced melatonin secretion is associated with the pathophysiology of neuroleptic-induced movement disorders including tardive dyskinesia and Parkinsonism. It has been recently reported that pinealectomized rats developed increased incidence and severity of spontaneous chewing movements compared to normal controls. Increased chewing movements in rats has been suggested to reflect acute drug-induced dystonias in humans. To investigate the relationship between melatonin secretion and the pathophysiology of neuroleptic-induced dystonic movements, the presence and size of pineal calcification (PC) on CT scan was studied in relation to the severity of dystonic movements in 34 neuroleptic-treated chronic schizophrenic patients. The incidence of pathologically enlarged PC (greater than 1 cm in diameter) in the schizophrenic patients was 8-9 times greater than the incidence reported in the literature among nonpsychiatric patients. In addition, there were significant differences (p less than .0001) between the severity of dystonic movements in patients with no PC and those with pathologically enlarged PC, and between the severity of the dystonic movements in patients with PC of less than 1 cm and those with PC of greater than 1 cm diameter. These findings indicate an association between the pathophysiology of neuroleptic-induced dystonic movements and the presence of enlarged PCs and suggest that disturbances of melatonin secretion is associated with the emergence of neuroleptic-induced dystonic movements in schizophrenic patients. Further studies using direct measurements of plasma melatonin levels are required more precisely to confirm the association between pineal melatonin secretion and the pathophysiology of drug-induced dystonic movement disorders.