Archives of neurology · 1996
Pallidal lesions. Structural and functional magnetic resonance imaging.
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.
Bucher S F, Seelos K C, Dodel R C, Paulus W, Reiser M, Oertel W H
Аннотация
OBJECTIVE: To study noninvasively the functional anatomy and pathophysiologic characteristics of the globus pallidus external (GPe) and internal (GPi) divisions.
DESIGN: Structural and functional neuroimaging using high-resolution magnetic resonance imaging.
SETTING: University medical center research facility. SUBJECTS. Seven patients with pallidal lesions, 4 with an akinetic-rigid syndrome and 3 with a dystonic syndrome, and 15 age-matched volunteers.
MAIN OUTCOME MEASURES: T2-weighted anatomical magnetic resonance imaging and number of activated voxels in the GP during rapid supination and pronation of the hand.
RESULTS: T2-weighted images showed hyperintense bilateral lesions in the GP of all patients. Patients with dystonic syndromes had isolated lesions in the GPi. Patients with signs of akinetic-rigid syndromes showed abnormalities in the GPe or in central portions of the GP (GPc). Patients with lesions in both parts of the GP had akinetic-rigid or dystonic syndromes. All patients showed activation in the areas of the lesions. The number of activated voxels in the GP was significantly smaller (P < .005, Wilcoxon signed rank test) in patients than in control subjects. Activation of the GP was predominantly contralateral to the moving hand.
CONCLUSIONS: Lesions in the GPi result in a loss of inhibitory pallidal projections to the thalamus, which may explain the hyperkinetic signs. Lesions in the GPe lead to an increased inhibition of the thalamus, which may explain the hypokinetic signs. Neuronal activation in lesion sites suggests the presence of remaining functionally vital tissue.
DESIGN: Structural and functional neuroimaging using high-resolution magnetic resonance imaging.
SETTING: University medical center research facility. SUBJECTS. Seven patients with pallidal lesions, 4 with an akinetic-rigid syndrome and 3 with a dystonic syndrome, and 15 age-matched volunteers.
MAIN OUTCOME MEASURES: T2-weighted anatomical magnetic resonance imaging and number of activated voxels in the GP during rapid supination and pronation of the hand.
RESULTS: T2-weighted images showed hyperintense bilateral lesions in the GP of all patients. Patients with dystonic syndromes had isolated lesions in the GPi. Patients with signs of akinetic-rigid syndromes showed abnormalities in the GPe or in central portions of the GP (GPc). Patients with lesions in both parts of the GP had akinetic-rigid or dystonic syndromes. All patients showed activation in the areas of the lesions. The number of activated voxels in the GP was significantly smaller (P < .005, Wilcoxon signed rank test) in patients than in control subjects. Activation of the GP was predominantly contralateral to the moving hand.
CONCLUSIONS: Lesions in the GPi result in a loss of inhibitory pallidal projections to the thalamus, which may explain the hyperkinetic signs. Lesions in the GPe lead to an increased inhibition of the thalamus, which may explain the hypokinetic signs. Neuronal activation in lesion sites suggests the presence of remaining functionally vital tissue.