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
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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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    ABSTRACT: Background/objective: Transient global amnesia (TGA) is a temporary amnestic syndrome characterized by lack of other focal neurological deficits. Cerebrovascular disease, migraine and seizures have been suggested as underlying mechanisms. TGA may be a risk factor for cerebrovascular or other neurological events. We studied the relation of TGA, vascular risk factors, brain magnetic resonance imaging (MRI) indices of subclinical ischemia and neurological events in a community-based sample. Design/setting: A total of 12 TGA cases were ascertained using standard criteria by experienced neurologists, and matched to 41 stroke- and seizure-free controls. Vascular risk factors, brain MRI findings, and subsequent cerebrovascular or seizure events were compared in cases and controls. Participants: Framingham Heart Study (FHS) original and offspring cohort participants were included. Results: No significant differences between the groups were observed in the prevalence of vascular risk factors, or brain MRI measures. Few incident stroke/transient ischemic attacks (TIA) (one event among the cases and four in controls) or subsequent seizures occurred in either group. Head CT during the acute event (n = 11) and brain MRI (n = 7) were negative for acute abnormalities. Electroencephalograms (EEG) (n = 5) were negative for epileptiform activity. Extracranial vascular studies were negative for significant stenosis in all cases. Conclusion: In our community-based study TGA was not related to traditional vascular risk factors, or cerebrovascular disease. However, our study is limited by small sample size and power, and larger studies are required to exclude an association.
    Frontiers in Neurology 05/2013; 4:47. DOI:10.3389/fneur.2013.00047