Gait apraxia: further clues to localization.
OBJECTIVE
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.
Nadeau
Stephen E
SE
Geriatric Research, Education and Clinical Center, Malcom Randall Veterans Administration Medical Center, Gainesville, Fla. 32608-1197, USA. snadeau@ufl.edu
D000368:Aged; D020235:Gait Apraxia / Q000209:etiology / Q000473:pathology*; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D009044:Motor Cortex / Q000473:pathology*