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From the Mediterranean Neurological Institute (Dr. Ambrosini), IRCCS Neuromed, Pozzilli (Isernia), Italy; and Headache Unit (Drs. Maertens de Noordhout and Schoenen), Department of Neurology, University of Liège, Belgium.
Address correspondence and reprint requests to Dr. J. Schoenen, University Department of Neurology, CHR Citadelle, Bld XIIème de Ligne, 1-B-4000 Liège, Belgium; e-mail: jschoenen{at}ulg.ac.be
OBJECTIVE: To search for impairment of neuromuscular transmission by single-fiber electromyography (SFEMG) in patients with common forms of migraine.
BACKGROUND: P/Q Ca2+ channels are genetically abnormal in most cases of familial hemiplegic migraine (International Headache Society [IHS] code 1.2.3) and may be involved in other types of migraine. Besides in the brain, these channels are found in motor nerve endings, where they control stimulation-induced acetylcholine release. If they are functionally abnormal, the neuromuscular transmission might be impaired.
METHODS: Sixty-two migraineurs (18 without aura, IHS code 1.1; 19 with typical aura, IHS code 1.2.1; 10 with prolonged aura, IHS code 1.2.2; 15 with and without aura) and 16 healthy control subjects underwent stimulation SFEMG. Results were expressed as the mean value of consecutive differences (MCD) and percentage of single-fiber abnormalities (abnormal jitter or impulse blocking).
RESULTS: Average MCD was comparable in control subjects and migraineurs (17.1 ± 2.6 versus 17.5 ± 4.7 µsec). By contrast, single-fiber abnormalities were found in 17 patients but in none of the control subjects (p = 0.036). Most of these patients had unilateral sensorimotor symptoms and/or aphasia and/or loss of balance during the aura. SFEMG abnormalities were significantly correlated with the occurrence of these clinical features and with a diagnosis of migraine with prolonged aura.
CONCLUSIONS: Stimulation SFEMG shows mild abnormalities of neuromuscular transmission in a subgroup of migraineurs with aura, characterized by clinical features frequently found in human P/Q Ca2+ channelopathies. These abnormalities might thus be due to genetically modified P/Q Ca2+ channels.
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