Comparative analysis of gait in Parkinson's disease, cerebellar ataxia andsubcortical arteriosclerotic encephalopathy

Citation
G. Ebersbach et al., Comparative analysis of gait in Parkinson's disease, cerebellar ataxia andsubcortical arteriosclerotic encephalopathy, BRAIN, 122, 1999, pp. 1349-1355
Citations number
36
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
BRAIN
ISSN journal
00068950 → ACNP
Volume
122
Year of publication
1999
Part
7
Pages
1349 - 1355
Database
ISI
SICI code
0006-8950(199907)122:<1349:CAOGIP>2.0.ZU;2-H
Abstract
Quantitative gait analysis has been used to elucidate characteristic featur es of neurological gait disturbances. Although a number of studies compared single patient groups with controls, there are only a few studies comparin g gait parameters between patients with different neurological disorders af fecting gait. In the present study, gait parameters were compared between c ontrol subjects, patients with parkinsonian gait due to idiopathic Parkinso n's disease, subjects suffering from cerebellar ataxia and patients with ga it disturbance due to subcortical arteriosclerotic encephalopathy, In addit ion to recording of baseline parameters during preferred walking velocity, subjects were required to vary velocity from very slow to very fast. Values of velocity and stride length from each subject were then used for linear regression analysis. Whereas all patient groups showed slower walking veloc ity and reduced step length compared with healthy controls when assessed du ring preferred walking, patients with ataxia and subcortical arteriosclerot ic encephalopathy had, in addition, increased variability of amplitude and timing of steps. Regression analysis showed that with changing velocity, su bjects with Parkinson's disease changed their stride length in the same pro portion as that measured in controls. In contrast, patients with ataxia and subcortical arteriosclerotic encephalopathy bad a disproportionate contrib ution of stride length when velocity was increased. Whereas the findings in patients with Parkinson's disease can be explained as a reduction of force gain, the observations for patients with ataxia and subcortical arterioscl erotic encephalolpathy reflect an altered spatiotemporal gait strategy in o rder to compensate for instability. The similarity of gait disturbance in s ubcortical arteriosclerotic encephalopathy and cerebellar ataxia suggests c ommon mechanisms.