Transient global amnesia and migraine.

Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Headache The Journal of Head and Face Pain (Impact Factor: 3.19). 11/2005; 45(10):1408-10. DOI: 10.1111/j.1526-4610.2005.00275.x
Source: PubMed
  • Cambridge University Press, New York.
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    ABSTRACT: This book presents papers on the ethical aspects of nuclear weapons. Topics considered include the concept of a ''just'' war, national defense, political aspects, religion and politics, the failure of deterrence, conventional warfare, nuclear deterrence and democratic politics, the future of the nuclear debate, non-proliferation policy, arms control, national security, and government policies.
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    ABSTRACT: 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 ± 7.4 yrs). The duration of amnesia ranged from 1 to 6 h (mean 4.4 h). 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.
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