HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

Correspondence to:

ARTICLES: Anna Ambrosini, Alain Maertens de Noordhout, and Jean Schoenen Neuromuscular transmission in migraine: A single-fiber EMG study in clinical subgroups Neurology 2001; 56: 1038-1043 [Abstract] [Full text] [PDF]

Correspondence: Submit a response to this article

Correspondence published:

Reply to Dr. Jacome's letter

Jean Schoenen, Anna Ambrosini   (17 December 2001)

Neuromuscular transmission in migraine: A single-fiber EMG study in clinical subgroups

Daniel E Jacome   (17 December 2001)

Reply to Dr. Jacome's letter 17 December 2001
Jean Schoenen University of Liege Liege Belgium, Anna Ambrosini Send Correspondence to journal: Re: Reply to Dr. Jacome's letter Jschoenen{at}ulg.ac.be Jean Schoenen, et al.	Dr. Jacome advances the interesting possibility that migraine could be “a multisystem disorder of neuronal hyperexcitability,” going out from our findings of subtle dysfunctions of neuromuscular transmission in migraineurs [1] and from his patients combining headache, blepharoclonus, pseudoasterixis and restless feet. [2] The concept is attractive, considering that the neuronal ion channels thought to be involved in the common form of migraine, such as the P/Q type calcium channel [3], are likely to be involved in various nervous system functions, among which one (or several) may be relevant for recurring migraine attacks and others for other symptoms. We must point out, however, that we found an impairment of neuromuscular transmission in only a minority of migraine with aura patients, especially those having complex neurologic or prolonged auras. We also recently reported subclinical cerebellar signs in migraineurs. [4] Despite genetic heterogeneity, most migraineurs present with the same phenotype. The challenge for research in migraine is to better define the genotype-phenotype correlations with more refined clinical analyses and better neurophysiological tests. At first sight, the patients described by Jacome [2] may not be helpful because they had various types of headaches. Moreover, the motor dysfunction he reports may be somatic expression of anxiety, which coexists with migraine. [5] The association of sommambulism with migraine is well known. [6] Finally, although we agree with the concept that certain migraines are “multisystem channelopathies,” we do not agree with Dr. Jacome’s global assumption that this leads to “neuronal hyperexcitability.” Interictal studies of evoked cortical potentials indicate that dishabituation is the major reproducible functional abnormality in migraineurs and we have recently shown that this is due to a reduced preactivation excitability level in sensory cortices, not to hyperexcitability (Bohotin et al. Brain, in press). Moreover, the very findings in the SFEMG study [1] that prompted this correspondence, show a reduced safety factor at the neuromuscular junction, thus reduced neuronal function instead of hyperexcitability. References: 1) Ambrosini, A, Maertens de Noordhout A, Schoenen J. Neuromuscular transmission in migraine. A single-fiber EMG study in clinical subgroups. Neurology 2001;56:1038-1043. 2) Jacome D. Blepharoclonus, pseudoasterixis and restless feet. Am J Med Sci 2001;322:137-140. 3) Terwindt GM, Opholff RA, van Eijk R, et al. Involvement of the CACNA1A gene containing region on 19p13 in migraine with and without aura. Neurology 2001;56:1028-1032. 4) Sándor PS, Mascia A, Seidel L, De Pasqua V, Schoener J. Subclinical cerebellar impairment in the common types of migraine: A 3- dimensional analysis of reaching movements. Annals of Neurology 2001;49:668-672. 5) Breslau N, Merikangas K, Bowden CL. Comorrbidity of migraine and major affective disorders. Neurology 1994;44:17-22. 6) Barabas G, Ferrari M, Matthews WS. Childhood migraine and somnambulism. Neurology 1983;33(7):948-949.
Neuromuscular transmission in migraine: A single-fiber EMG study in clinical subgroups 17 December 2001
Daniel E Jacome Clinical Neurophysiology Turner Falls, MA Send Correspondence to journal: Re: Neuromuscular transmission in migraine: A single-fiber EMG study in clinical subgroups sandi_moriarity{at}urmc.rochester.edu Daniel E Jacome	I read with interest the article by Ambrosini et al. describing abnormalities in neuromuscular transmission in seventeen patients with migraine with aura. [1] Ambrosini’s group studied a total of sixty-two migraineurs, measuring variation in the mean value of consecutive differences (MCD), abnormal jitter and impulse blocking of single muscle fiber potentials, employing single fiber electromyography (SFEMG). The authors suggested that their findings could be the ultimate result of genetically modified P/Q Ca 2+ channels on these individuals. Mutations in the alpha 1A subunit gene of the neuronal voltage-dependent P/Q Ca 2+ channel are typical of patients with familial hemiplegic migraine and episodic ataxia Type 2. [2] I recently reported a group of thirty patients exhibiting the clinical triad of blepharoclonus (eyelid closure myoclonus), action tremors of the hands on flexion and extension of the wrist, simulating asterixis (pseudoasterixis) and involuntary movements of their feet (restless feet). [3] All these patients suffered from recurrent headaches (seven migraine with aura, eight migraine without aura), eleven tension headache, two with cluster and one with idiopathic stabbing headache). Thirteen of the patients had, albeit limited, abnormalities on standard EMG testing, compatible with axonal motor neuropathy. Eight of the group had restless legs in addition to restless feet and seventeen, had personal or family history of sommambulism. My report and Ambrosini et al. reinforce the notion that migraine is a multisystem disorder of neuronal hyperexcitability, with headache as the cardinal clinical manifestation. In some cases, as exemplified by my series, there is an association between movement disorder (tremors), peripheral neuropathy and migraine. I suggest that sleep walking on the subjects I studied could represent the nocturnal akathisic counterpart of diurnal restless feet and restless legs. Of additional interest is that abnormalities in serotonin and dopamine have been reported in patients with migraine, myoclonus and restless legs. References: 1) Ambrosini A, Maertens de Noordhout A, Schoenen J. Neuromuscular transmission in migraine. A single-fiber EMG study in clinical groups. Neurology 2001;56:1038-1043. 2) Ophoff RA, Terwindt GM, Vergouwe MN, et al. Familial hemiplegic migraine and episodic ataxia type-2 are caused by mutations in the Ca 2+ channel gene CACNLaA4. Cell 1996;87:543-552. 3) Jacome D. Blepharoclonus, Pseudoasterixis, and Restless Feet. Am J Med Sci 2001;322:137-140.