Internal medicine (Tokyo, Japan) · 2011
Transient myoclonic state with asterixis: primary motor cortex hyperexcitability is correlated with myoclonus.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Hitomi Takefumi, Ikeda Akio, Inouchi Morito, Imamura Hisaji, Nakagawa Tomokazu, Fumuro Tomoyuki, Matsumoto Riki, Takahashi Ryosuke
Аннотация
OBJECTIVE: To clarify the clinical features and mechanism of the transience of myoclonus in patients with a transient myoclonic state with asterixis (TMA).
METHODS: We investigated the clinical and eletrophysiological profiles of 6 patients with TMA (age: 84±3 years). During an asymptomatic period, somatosensory evoked potentials (SEPs) were recorded in all 6 patients and motor evoked potentials (MEPs) were examined in 1 patient. SEPs were recorded and jerk-locked back averaging (JLA) was performed in 2 patients while symptomatic. SEPs were also recorded from 8 aged control subjects (age: 68±5 years).
RESULTS: All TMA patients had mild chronic systemic diseases. During an asymptomatic period, SEP amplitudes were not significantly enlarged in comparison with control subjects, and MEPs were normal. Examination of 2 patients during symptomatic period indicated no enlargement of SEP amplitudes and JLA disclosed a positive spike preceding myoclonic jerks. In one of these patients, the amplitude of the positive spike decreased once myoclonus improved.
CONCLUSION: TMA occurred in aged patients with mild chronic systemic diseases. JLA findings and the absence of giant SEPs further support that TMA is a cortical non-reflex myoclonus. In addition, transient hyperexcitability at the primary motor cortex disclosed by JLA correlated well with its transient symptoms.
METHODS: We investigated the clinical and eletrophysiological profiles of 6 patients with TMA (age: 84±3 years). During an asymptomatic period, somatosensory evoked potentials (SEPs) were recorded in all 6 patients and motor evoked potentials (MEPs) were examined in 1 patient. SEPs were recorded and jerk-locked back averaging (JLA) was performed in 2 patients while symptomatic. SEPs were also recorded from 8 aged control subjects (age: 68±5 years).
RESULTS: All TMA patients had mild chronic systemic diseases. During an asymptomatic period, SEP amplitudes were not significantly enlarged in comparison with control subjects, and MEPs were normal. Examination of 2 patients during symptomatic period indicated no enlargement of SEP amplitudes and JLA disclosed a positive spike preceding myoclonic jerks. In one of these patients, the amplitude of the positive spike decreased once myoclonus improved.
CONCLUSION: TMA occurred in aged patients with mild chronic systemic diseases. JLA findings and the absence of giant SEPs further support that TMA is a cortical non-reflex myoclonus. In addition, transient hyperexcitability at the primary motor cortex disclosed by JLA correlated well with its transient symptoms.