Impairment of neuromuscular transmission in transient global amnesia - does it really exist?

Background: The main hypotheses regarding mechanisms of transient global amnesia (TGA) are ischemia in hippocampal structures, epileptic genesis, and migraine. In accordance with the hypothesis of a shared, common pathophysiological mechanism in both TGA and migraine, neuromuscular transmission (NMT) abnormalities previously found in migraine were also suspected in TGA.

Objective: The aim of our study was to analyze NMT in TGA patients to reveal a subclinical impairment of neuromuscular transmission as a possible indicator of underlying channelopathy, which would point to a shared etiology with migraine.

Materials and methods: The study group consisted of 15 patients (6 males) with TGA (mean age 69.5±7.4yrs). The duration of amnesia ranged from 1 to 6h (mean 4.4h). Single fiber electromyography (SFEMG), the most sensitive tool for NMT assessment, of the voluntarily activated frontal muscle was performed 1-5 days after a TGA incident.

Results: Abnormal SFEMG was found in 1 patient (6.6%). In all other patients, SFEMG was in the normal range.

Conclusion: Our neurophysiological study does not confirm NMT defects in TGA. The role of channelopathy with NMT dysfunction in the pathogenesis of TGA is rather unlikely, whereas subclinical NMT abnormalities were certainly proven in migraine.