Specific influences of cerebellar dysfunctions on gait.
Cerebellar ataxic gait is characterized by unsteady movements and variable gait patterns. Previous studies have successfully identified pathological changes of balance-related gait parameters. However, it has been difficult to demonstrate deficits of joint coordination and the control of limb dynamics. This has motivated the hypothesis that cerebellar ataxic gait might be affected predominantly by balance impairments. We investigated the influences of different types of cerebellar dysfunction on the gait patterns of patients suffering from degenerative cerebellar disease (13 patients, five females, 50.4 +/- 14.4 years). Walking patterns were quantitatively analysed combining standard gait measures and novel measures for the characterization of the spatial and the temporal variability of intra-joint coordination patterns. The temporal variability of gait patterns was significantly correlated with a subscale of the clinical ataxia scale (ICARS) that rates deficits of the control of limb dynamics and intra-limb coordination for goal-directed movements. This suggests that common cerebellar mechanisms might be involved in coordination during voluntary limb control and ataxic gait. The tested standard gait parameters correlated predominantly with clinical measures for balance-related abnormalities. These results imply that ataxic gait is influenced by both balance-related impairments and deficits related to limb control and intra-limb coordination. Applying the same analysis to gait patterns from patients with peripheral vestibular failure (six patients, four females, 47.8 +/- 14.3 years) and Parkinson's disease (eight patients, two females, 60.7 +/- 10.6 years), we found comparable abnormalities in balance-related gait parameters and general gait variability, but significantly lower increases of temporal variability. This implies that increased temporal variability of intra-limb coordination is a specific characteristic of cerebellar dysfunction, which does not arise for other movement disorders that also cause balance deficits and increased gait variability.
Ilg
Winfried
W
Laboratory for Action Representation and Learning/Department of Cognitive Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.
Golla
Heidrun
H
Thier
Peter
P
Giese
Martin A
MA
D000328:Adult; D000368:Aged; D002526:Cerebellar Diseases / Q000150:complications / Q000503:physiopathology*; D004427:Ear Diseases / Q000150:complications / Q000503:physiopathology; D005260:Female; D020234:Gait Ataxia / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D007596:Joints / Q000503:physiopathology; D007866:Leg; D008297:Male; D008875:Middle Aged; D010300:Parkinson Disease / Q000150:complications / Q000503:physiopathology; D004856:Postural Balance / Q000502:physiology; D013997:Time Factors; D014722:Vestibule, Labyrinth / Q000503:physiopathology; D016138:Walking / Q000502:physiology