STRIDE LENGTH REGULATION IN PARKINSONS-DISEASE NORMALIZATION STRATEGIES AND UNDERLYING MECHANISMS

Citation
Me. Morris et al., STRIDE LENGTH REGULATION IN PARKINSONS-DISEASE NORMALIZATION STRATEGIES AND UNDERLYING MECHANISMS, Brain, 119, 1996, pp. 551-568
Citations number
50
Categorie Soggetti
Neurosciences,"Clinical Neurology
Journal title
BrainACNP
ISSN journal
00068950
Volume
119
Year of publication
1996
Part
2
Pages
551 - 568
Database
ISI
SICI code
0006-8950(1996)119:<551:SLRIPN>2.0.ZU;2-V
Abstract
Results of our previous studies have shown that the slow, shuffling ga it of Paukinson's disease patients is due to art inability to generate appropriate stride length and that cadence control is intact and is u sed as a compensatory mechanism. The reason for the reduced stride len gth is unclear although deficient internal cue production or inadequat e contribution to cortical motor set by the basal ganglia are two poss ible explanations. In this study we have examined the latter possibili ty by comparing the long-lasting effects of visual cues in improving s tride length with that of attentional strategies. Computerized stride analysis was used to measure the spatial (distance) and temporal (timi ng) parameters of the walking pattern in a total of 54 subjects in thr ee separate studies. In each study Parkinson's disease subjects were t rained for 20 min by repeated 10 m walks set at control stride length (determined from control subjects matched for age, sex and height), us ing either visual floor markers or a mental picture of the appropriate stride size. Following training, the gait patterns were monitored (i) every 15 min for 2 h; (ii) whilst interspersing secondary tasks of in creasing levels of complexity; (iii) covertly, when subjects were unaw are that measurement was taking place. The results demonstrated that t raining with both visual cues and attentional strategies could maintai n normal gait for the maximum recording rime of 2 h. Secondary tasks r educed stride length towards baseline values as did covert monitoring. The findings confirm that the ability to generate a normal stepping p attern is not lost in Parkinson's disease and that gait hypokinesia re flects a difficulty in activating the motor control system. Normal str ide length can be elicited in Parkinson's disease using attentional st rategies and visual cues. Both strategies appear to shave the same mec hanism of focusing attention on the stride length. The effect of atten tion appears to require constant vigilance to prevent reverting to mov e automatic control mechanisms.