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

Citation
A. Ambrosini et al., Neuromuscular transmission in migraine - A single-fiber EMG study in clinical subgroups, NEUROLOGY, 56(8), 2001, pp. 1038-1043
Citations number
41
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
NEUROLOGY
ISSN journal
00283878 → ACNP
Volume
56
Issue
8
Year of publication
2001
Pages
1038 - 1043
Database
ISI
SICI code
0028-3878(20010424)56:8<1038:NTIM-A>2.0.ZU;2-D
Abstract
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 fam ilial hemiplegic. migraine (International Headache Society; [IHS] code 1.2. 3) and may be involved in other types of migraine. Besides ill the brain, t hese channels are found in motor nerve endings, where they control stimulat ion-induced acetylcholine release. If they are functionally abnormal, the n euromuscular 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 w ith prolonged aura, IHS code 1.2.2; 15 with and without aura! and 16 health y control subjects underwent stimulation SFEMG. Results were expressed as t he mean value of consecutive differences (MCD) and percentage of single-fib er abnormalities (abnormal jitter or impulse blocking). Results: Average MC D was comparable in control subjects and migraineurs (17.1 +/- 2.6 versus 1 7.5 +/- 4.7 mu sec). By contrast, single-fiber abnormalities there 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 o f balance during the aura. SFEMG abnormalities were significantly correlate d with the occurrence of these clinical features and with a diagnosis of mi graine with prolonged aura. Conclusions: Stimulation SFEMG shows mild abnor malities of neuromuscular transmission in a subgroup of migraineurs with au ra, characterized by clinical features frequently found in human P/Q Ca2+ c hannelopathies. These abnormalities might thus be due to genetically modifi ed P/Q Ca2+ channels.