European neurology · 2007
Gait apraxia: further clues to localization.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Nadeau Stephen E
Аннотация
BACKGROUND/AIMS: Gait apraxia characterized primarily by gait ignition failure has been linked to lesions involving the dorsomedial frontal lobes, but the precise locus within this general region has not been determined. It has previously been hypothesized by Thompson and Marsden that disease, disconnection, or dysfunction of supplementary motor area (SMA) may account for the similarities in the gait disorders observed in Binswanger's disease, hydrocephalus, frontal lobe lesions, and Parkinson's disease. We reevaluate this hypothesis.
METHODS: Clinical description and MRI of 2 subjects with gait apraxia characterized primarily by gait ignition failure.
RESULTS: Both subjects had incapacitating gait disorders characterized by particular difficulty with initiating gait and making turns. Both had MRI-demonstrated lesions of the SMA region, parasagittal convexity premotor cortex, or subjacent white matter bilaterally, one due to primary CNS lymphoma, one due to a lobar atrophy.
CONCLUSIONS: In both these cases, the lesions were substantially more limited and focal than any reported heretofore in the literature on gait apraxia or freezing of gait. The clinicopathologic correlation in these cases provides partial support for the Thompson and Marsden hypothesis, but also may implicate parasagittal convexity premotor cortex in the genesis of gait apraxia.
METHODS: Clinical description and MRI of 2 subjects with gait apraxia characterized primarily by gait ignition failure.
RESULTS: Both subjects had incapacitating gait disorders characterized by particular difficulty with initiating gait and making turns. Both had MRI-demonstrated lesions of the SMA region, parasagittal convexity premotor cortex, or subjacent white matter bilaterally, one due to primary CNS lymphoma, one due to a lobar atrophy.
CONCLUSIONS: In both these cases, the lesions were substantially more limited and focal than any reported heretofore in the literature on gait apraxia or freezing of gait. The clinicopathologic correlation in these cases provides partial support for the Thompson and Marsden hypothesis, but also may implicate parasagittal convexity premotor cortex in the genesis of gait apraxia.