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Table of Contents
Vol. 58, No. 3, 2007
Issue release date: October 2007
Section title: Original Paper
Eur Neurol 2007;58:142–145
(DOI:10.1159/000104714)

Gait Apraxia: Further Clues to Localization

Nadeau S.E.
Geriatric Research, Education and Clinical Center and the Brain Rehabilitation Research Center, Malcom Randall Veterans Administration Medical Center, and the Department of Neurology, University of Florida College of Medicine, Gainesville, Fla., USA

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: January 03, 2007
Accepted: February 09, 2007
Published online: June 29, 2007
Issue release date: October 2007

Number of Print Pages: 4
Number of Figures: 2
Number of Tables: 0

ISSN: 0014-3022 (Print)
eISSN: 1421-9913 (Online)

For additional information: http://www.karger.com/ENE

Abstract

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.

© 2007 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: January 03, 2007
Accepted: February 09, 2007
Published online: June 29, 2007
Issue release date: October 2007

Number of Print Pages: 4
Number of Figures: 2
Number of Tables: 0

ISSN: 0014-3022 (Print)
eISSN: 1421-9913 (Online)

For additional information: http://www.karger.com/ENE


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