THE RELATIONSHIP BETWEEN GAIT CHANGES AND FALLS

To the Editor: We read with interest the study of the relationship between gait changes and falls by Brian Maki, PhD, and his colleagues. ’ Maki finds that subtle changes in stride-tostride variability are important predictors of falls while other gait variables thought to be altered in fallers (e.g., walking speed and the average values of different temporal and spatial measures) are not. We have results that support these findings and suggest that in other instances as well, the most sensitive measure of walking is variability and not the speed or (average) time spent in different phases of the gait cycle. Our findings also shed light on possible mechanisms for increased variability and its reversibility in certain older populations. Using an ankle-worn footswitch system, we measured the stride-to-stride variability of the gait cycle (stride time) and its subdivisions (e.g., swing time) during a 6-minute, self-paced walk in a group of relatively healthy, communityliving, older men and women.2 When subjects were stratified based on fall history, all measures of gait variability were significantly larger in the fallers compared with the nonfallers ( P < .0002). Subjects in this study walked almost 60% faster, on average, than the subjects in Maki’s study (0.7 dsec) , possibly indicating a higher level of mobility. Nevertheless, even in these subjects, we observed the discriminatory ability of gait variability measures. Again, however, speed and average values were not different in the fallers and non-fallers (e.g., speed was 1.13 d s e c in both fallers and non-fallers). Maki speculates that the increased stride-to-stride variability in older fallers is a manifestation of impaired motor control. We studied subjects with Huntington’s disease and Parkinson’s disease, as well as controls, and found that all measures of gait instability were increased significantly in the neurological subjects compared with controls. However, walking rate and the time spent in many phases of the gait cycle were similar in the three groups. This suggests that central nervous system deficits such as those seen in Huntington’s disease can produce increased stride-to-stride variability without altering the timing of the average gait cycle. We have observed similar gait changes in subjects with heart f a i l ~ r e , ~ suggesting that central cardiovascular effects and/or peripheral weakness may also be responsible for increased variability. Maki questions whether variability in gait is amenable to change, perhaps through interventions such as balance or gait training, changes in footwear, or use of assistive devices. We hypothesized that certain physiological changes common in older people may give rise to increased gait variability and that partial reversal of these processes through exercise should help reduce gait variability. To test this hypothesis, we have been measuring stride-to-stride variability in community-living older women selected for their impaired mobility before and after 6 months of aerobic and progressive resistance muscle training. We have now examined the gait variability of five exercisers. After the exercise program, leg press one repetition maximum increased by 14%, muscle endurance by 130%, and maximal aerobic capacity by 30%. Preliminary analysis shows no change in habitual gait speed. In contrast, gait instability, as measured by the stride interval coefficient variation, was reduced by an average of 40%. Apparently, gait variability is modifiable, at least in certain populations. These findings all support the idea that the mechanisms responsible for gait instability are, to some degree, distinct from those that control walking speed and timing. In the case of some older fallers, stride-to-stride stability is significantly diminished, but speed and gait cycle timing are unchanged. We therefore agree with Maki and encourage further research on the clinical utility and mechanisms behind increased stride-to-stride variability.