Service de neurologie, CHU Grenoble, 38700 La Tronche, France
- Page(s) : 76
- Published in: 2000
Sirs: In a recent issue of Epileptic Disorders, C.T. Lombroso and A. Fischman  reported a case of paroxysmal, non-kinesigenic dyskinesia with both invasive and metabolic findings strongly suggesting dopaminergic striatal dysfunction during clinical episodes. However, not much is described about dopaminergic agents used in this young boy, although the therapeutic issue is discussed. Contrary to the author’s suggestion, it would be of great interest to test dopamine antagonists, i.e. neuroleptics, in this context. In the patient reported, striatal oversensitivity to dopamine might be supported by post-synaptic D2 upregulation as shown on PET images. According to the current model of levodopa-induced dyskinesias, one might propose that paroxysmally higher amounts of endogenous striatal dopamine (compared to a low basic level, according to F-DOPA PET findings) could overstimulate upregulated, post-synaptic D2 receptors. This could transiently lead to subthalamic nucleus inactivation, through the “indirect” striatopallidal pathway. In this case, the tonic drive from subthalamic to GPi will be transiently suppressed, and phasic inactivation of GPi will occur, leading to choreoballic movements. Choreoballism is known to be correlated with silent periods during electrophysiological recording in the internal pallidum (GPi) . Coulter et al. reported a good response to haloperidol in a case with paroxysmal dyskinesia, which might support this view .
1. Lombroso CT, Fischman A. Paroxysmal non-kinesigenic dyskinesia: pathophysiological investigations. Epileptic Disorders 1999; 1: 187-93.
2. Vitek GL, Chockkan V, Zhang JY, et al. Neuronal activity in the basal ganglia in patients with generalized dystonia and hemiballismus. Ann Neurol 1999; 46: 22-35.
3. Coulter DL, Donofrio P. Haloperidol for non-kinesigenic paroxysmal dyskinesia. Arch Neurol 1980; 37: 325-6.