Mowment zyxwvutsrqponmlkjihg Di,sordcrs zyxwvutsrqponm Vol. zyxwvutsrqponm 13, No. I, zyxwvutsrqponmlkjihgf 1998, zyxwvutsrqponm p. 195 Q 1998 Movement Disorder Society Letter to the Editor Treatment of Palatal Myoclonus With Sumatriptan We read with interest the recent report by Scott and col- leagues' describing the case of a patient with essential palatal rnyoclonus (EPM) who was successfully treated with either oral or subcutaneous administration of sumatriptan.' The au- thors also pointed out that, in contrast zyxwvutsrq to this EPM patient, a small oral dosage of sumatriptan was ineffective in a second patient with symptomatic palatal myoclonus (SPM).' Based on these findings, Scott and colleagues questioned whether EPM and SPM differ pharmacologically or whether the failure of sumatriptan in SPM may simply have been related to an inad- equately small dosage.' We recently reported in Movement Disorders' the case of a patient who developed palatal myoclonus (PM) (also called palatal while he had a primary intestinal lymphoma. A remarkable feature was that PM was absent at rest and trig- gered only by action, such as attempts at speaking or swallow- ing. Blink reflex study revealed an enhanced recovery curve after stimulation of either side. Magnetic resonance imaging findings in the brain were strongly indicative of hypertrophic degeneration of the inferior olivary nuclei, which are presumed to be the pacemaker of SPM.3 In that patient, we tested the effect of several drugs-including alcohol, clonazepam, suma- triptan, and valproate-on both blink reflex and PM. Only clo- nazepam was effective in reducing action PM and normalizing the blink reflex recovery curve as well.' Most importantly, sumatriptan had no clinical or neurophysiological effect, even if an adequate (6 mg) subcutaneous dosage was injected. - - ~~.__ - Address correspondence and reprint requests to Prof. A. Quattrone at Cattedra di Neurologia, Policlinico Mater Domini, Via T. Campanella, 88 100 Catanzaro, Italy. All these findings suggest that sumatriptan does not affect SPM regardless of the dosage and the character of myoclonus (that is rest or action PM). Therefore, the hypothesis that SPM and EPM represent pharmacologically distinct disorders seems more likely. Accordingly, an exhaustive review of PM patients provides evidence that EPM and SPM are two separate clinical entities' arising from different pathophysiological mecha- nisms."' In SPM, there is presumably a brain stem-release phenomenon resulting from deactivation of GABAergic neu- rons within the olivary nucleL3 On the other hand, the inferior olive does not play a role in EPM, whose pathophysiological characteristics are still ~ n k n o w n . ~ As stated by Scott and col- leagues,' the striking efficacy of sumatriptan may support a major role of serotonin receptors in the pathogenesis of EPM. Antonio Gambardella Aldo Quattrone Institute zyx of Neurology School Qf Medicine Catanzaro Italy References 1. Scott BL, Evans R, Jankovic J. Treatment of palatal myoclonus with sumatriptan. Mov Disord 1996;11:748-750. 2. Gambardella A, Zappia M, Valentino P, et al. Action palatal tremor in a patient with primary intestinal lymphoma. zyxw Mov Disord 1997; 12794-797. 3. Deuschl G, Toro C, Valls-Sole J, Zeffiro T, Zee DS, Hallett M. Symptomatic and essential palatal tremor: clinical, physiological and MRI analysis. Brain 1994:117:775-788. 4. Deuschl G, Mischke G, Schenk E, Schulte-Monting J, Lucking CH. Symptomatic and essential rhythmic palatal myoclonus. Bruin 1990; 1 13: 1645-1672. I 95