Muscle & nerve · 2011
Nerve compression, membrane excitability, and symptoms of carpal tunnel syndrome.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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.
Han S Eric, Lin Cindy S-Y, Boland Robert A, Kiernan Matthew C
Аннотация
INTRODUCTION: In this study we investigated the changes in axonal excitability and the generation of neurological symptoms in response to focal nerve compression (FNC) of the median nerve in carpal tunnel syndrome (CTS).
METHODS: Sensory excitability recordings were undertaken in 11 CTS patients with FNC being applied at the wrist using a custom-designed electrode.
RESULTS: During FNC, refractoriness increased significantly (62.4 ± 3.4%; P < 0.001), associated with a rapid reduction in superexcitability (16.9 ± 2.8%; P < 0.001) and sensory nerve action potential amplitude (SNAP) (32.4 ± 3.9%; P < 0.001), consistent with axonal depolarization. Associated with these changes, paresthesiae steadily increased throughout FNC, as did numbness. Reductions in SNAP amplitude and superexcitability developed more rapidly for CTS patients during FNC compared with controls, and these changes were associated with more marked symptoms.
CONCLUSIONS: Axonal responses to compression are impaired in CTS. This may suggest a greater reliance on axonal membrane Na(+) /K(+) -ATPase function.
METHODS: Sensory excitability recordings were undertaken in 11 CTS patients with FNC being applied at the wrist using a custom-designed electrode.
RESULTS: During FNC, refractoriness increased significantly (62.4 ± 3.4%; P < 0.001), associated with a rapid reduction in superexcitability (16.9 ± 2.8%; P < 0.001) and sensory nerve action potential amplitude (SNAP) (32.4 ± 3.9%; P < 0.001), consistent with axonal depolarization. Associated with these changes, paresthesiae steadily increased throughout FNC, as did numbness. Reductions in SNAP amplitude and superexcitability developed more rapidly for CTS patients during FNC compared with controls, and these changes were associated with more marked symptoms.
CONCLUSIONS: Axonal responses to compression are impaired in CTS. This may suggest a greater reliance on axonal membrane Na(+) /K(+) -ATPase function.