Transcranial Magnetic Stimulation (TMS) induces inhibition at a cortical level

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<ul><li><p>A REPLY</p><p>We are pleased to learn of another case of colchicine myo-neuropathy with myotonic discharges on electromyogra-phy. This patient has many similarities to the 4 individualswe presented, including the presence of chronic renal in-sufficiency, mild progressive weakness, and rapid improve-ment in strength and resolution of myotonic dischargeswith discontinuation of the drug. Like the majority of ourcases, this patient had neither signs nor symptoms of myo-tonia. This case helps underscore the usefulness of recog-nizing these discharges in patients with possible colchicinemyoneuropathy.</p><p>Seward B. Rutkove, MDElizabeth M. Raynor, MDDepartment of NeurologyBeth Israel Deaconess Medical Center330 Brookline AvenueBoston, MA 02215, USA</p><p>FAMILIAL AUTOSOMAL-DOMINANTCARPAL TUNNEL SYNDROMEPRESENTING IN A 5-YEAR-OLD CASE</p><p>With interest we have read the report by Vadasz et al.3 ona family with autosomal-dominant carpal tunnel syndrome(CTS). In the course of their study, they have analyzedDNA samples for the presence or absence of the 1.5-Mbduplication or deletion on chromosome 17p11.2, whichare causative for CharcotMarieTooth syndrome(CMT)1A or hereditary neuropathy with liability to pres-sure palsies (HNPP), respectively. This indicates that theythink that it is possible that familial CTS is a clinical variantof these disorders.</p><p>Recently the peripheral myelin protein-22 gene(PMP22) has been identified as the HNPP-causing gene,since the deletion of PMP22 as well as point mutations inPMP22 lead to the clinical phenotype.1,5 Clinical studieshave demonstrated that there is in fact a large variation inthe clinical phenotype of affected individuals.2 The con-clusion of the authors that the disease in the reportedfamily is primary familial CTS rather than a variant ofHNPP thus appears premature. Only after an exclusion ofPMP22 as the disease-causing gene, e.g., by direct sequenc-ing5 or with indirect markers,4 should the disease in thereported kindred be termed familial CTS.</p><p>Florian Stogbauer, MDPeter Young, MDKlinik und Poliklinik fur NeurologieUniversitat MunsterAlbert Schweitzer Str. 33D-48129 Munster, Germany</p><p>Harald Funke, MDInstitut furArterioskleroseforschung undInstitut fur Klinische Chemie undLaboratoriumsmedizinUniversitat MunsterMunster, Germany</p><p>1. Chance PF, Alderson MK, Leppig KA, Lensch MW, Matsu-nami N, Smith B, Swanson PD, Odelberg SJ, Disteche CM,Bird TD: DNA deletion associated with hereditary neuropathywith liability to pressure palsies. Cell 1993;72:143151.</p><p>2. Pareyson D, Scaioli V, Taroni F, Botti S, Lorenzetti D, SolariA, Ciano C, Sghirlanzoni A: Phenotypic heterogeneity in he-reditary neuropathy with liability to pressure palsies associ-ated with chromosome 17p11.2 deletion. Neurology 1996;46:11331137.</p><p>3. Vadasz AG, Chance PF, Epstein LG, Lou J-S: Familial autoso-mal-dominant carpal tunnel syndrome presenting in a 5-year-old-case. Report and review of the literature. Muscle Nerve1997;20:376378.</p><p>4. Young P, Wiebusch H, Stogbauer F, Ringelstein EB, AssmannG, Funke H: Four frequently observed polymorphisms in the38UTR of the human peripheral myelin protein 22 (PMP22)gene. Clin Genet 1996;49:321322.</p><p>5. Young P, Wiebusch H, Stogbauer F, Ringelstein EB, AssmannG, Funke H: A frameshift mutation in PMP22 accounts forhereditary neuropathy with liability to pressure palsies(HNPP). Neurology 1997;48:450452.</p><p>TRANSCRANIAL MAGNETICSTIMULATION (TMS) INDUCESINHIBITION AT A CORTICAL LEVELWe read with great interest the recent article by Cruccuand colleagues on the mechanisms mediating the inhibi-tory period after magnetic stimulation of the facial motorcortex.1 In the introduction, the authors acknowledge thatthey carried out the experiments because None of thestudies dedicated to the motor inhibition after TMS hasaddressed the cranial nerve motor system. This is incor-rect. We studied in detail the effect of the inhibitory phe-nomenon following TMS on cranial motor neuron excit-ability and on the cortical control of brain stem reflexes.Our findings were published in Muscle &amp; Nerve.2</p><p>The results of Cruccu and colleagues confirm our origi-nal observations; both studies provide compelling evi-dence that the inhibition following TMS originates rostralto the facial nucleus, at a cortical level.</p><p>A. Arturo Leis, MDThe University of Mississippi Medical CenterSection of EEG/EMGDepartment of Neurology2500 North State StreetJackson, MS 39216-4505, USA</p><p>Markus Kofler, MDDepartment of NeurologyUniversity Hospital InnsbruckInnsbruck, Austria</p><p>Dobrivoje S. Stokic, MDMMRC-Mississippi Methodist Rehabilitation CenterJackson, MS 39216</p><p>1. Cruccu G, Inghilleri M, Berardelli A, Romaniello A, ManfrediM: Cortical mechanisms mediating the inhibitory period aftermagnetic stimulation of the facial motor area. Muscle Nerve1997;20:418424.</p><p>2. Leis AA, Kofler M, Stokic DS, Grubwieser GJ, Delapasse JS:Effect of the inhibitory phenomenon following magneticstimulation of cortex on brainstem motor neuron excitabilityand on the cortical control of brainstem reflexes. Muscle Nerve1993;16:13511358.</p><p>Letters to the Editor MUSCLE &amp; NERVE April 1998 551</p></li></ul>

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