Gait variability and basal ganglia disorders: Stride‐to‐stride variations of gait cycle timing in parkinson's disease and Huntington's disease

Abstract

The basal ganglia are thought to play an important role in regulating motor programs involved in gait and in the fluidity and sequencing of movement. We postulated that the ability to maintain a steady gait, with low stride-to-stride variability of gait cycle timing and its subphases, would be diminished with both Parkinson's disease (PD) and Huntington's disease (HD). To test this hypothesis, we obtained quantitative measures of stride-to-stride variability of gait cycle timing in subjects with PD (n = 15), HD (n = 20), and disease-free controls (n = 16). All measures of gait variability were significantly increased in PD and HD. In subjects with PD and HD, gait variability measures were two and three times that observed in control subjects, respectively. The degree of gait variability correlated with disease severity. In contrast, gait speed was significantly lower in PD, but not in HD, and average gait cycle duration and the time spent in many subphases of the gait cycle were similar in control subjects, HD subjects, and PD subjects. These findings are consistent with a differential control of gait variability, speed, and average gait cycle timing that may have implications for understanding the role of the basal ganglia in locomotor control and for quantitatively assessing gait in clinical settings.

Gait dynamics, fractals and falls: Finding meaning in the stride-to-stride fluctuations of human walking

“…These results are consistent with earlier findings that reported increased stride-to-stride variability among patients with PD (Blin et al, 1990;Blin et al, 1991;Hausdorff et al, 1998), but extend these results in a number of ways. These findings demonstrate that the locomotor control system's ability to regulate the stride-to-stride variations in gait timing is especially impaired among PD participants with a history of falls.…”

“…Application of other analysis methods allows one to capture other features of gait time series and generate an array or matrix of outcome measures, each evaluating different aspects of the dynamics. Studies in neurodegenerative disease support the idea that such a matrix of dynamical measures may be helpful in more fully characterizing different pathologic states (Hausdorff, Cudkowicz, Firtion, Wei, & Goldberger, 1998;Hausdorff et al, 2000.…”

“…Patients with PD walk with increased stride-to-stride variability and have a decreased fractal scaling index (Blin, Ferrandez, & Serratrice, 1990;Frenkel-Toledo et al, 2005b;Hausdorff et al, 1998;Hausdorff, Peng et al, 1995;Hausdorff et al, 2000). Increased stride-to-stride variability, both in the stride length and stride time, has been observed in advanced PD (Blin et al, 1990;Hausdorff et al, 1998;Stolze et al, 2001) as well as in patients early in the disease process who have not even begun to take anti-parkinsonian medications (Baltadjieva, Giladi, Gruendlinger, Peretz, & Hausdorff, 2006;Hausdorff, Peng et al, 1995). In fact, in these patients with de novo PD, it has been shown that the increased stride-to-stride variability apparently is independent of a reduced stride length and apparently does not reflect inconsistent motor unit recruitment or muscle force output.…”

“…Gait variability may help to enhance the early identification of potential fallers in PD, as it does in other populations. A few studies have observed increased variability in patients with PD compared to controls, noting that this variability tends to increase with disease severity (Blin et al, 1990;Blin, Ferrandez, Pailhous, & Serratrice, 1991;Hausdorff et al, 1998). In general, however, the relationships between gait variability, fall risk, and other parkinsonian features were not wellstudied and the effect of levodopa on falls and gait variability were also largely unknown.…”

“…Further, one could suggest that because RAS sets the pace, it can act like an external rhythm generator and help to restore neurally controlled rhythmicity, thereby reducing stride-to-stride variability. Conversely, in PD, gait rhythmicity and stride variability often behave differently from stride length, gait speed, and other parkinsonian features (Hausdorff, 2005;FrenkelToledo et al, 2005a;Blin et al, 1991;Hausdorff et al, 1998;Schaafsma et al, 2003). Thus, one could suggest that while RAS restores the ability of PD patients to generate a 'normal' stride length, damage to the circuits that regulate rhythmicity may prevent these patients from walking with a consistent pattern, even in the presence of RAS.…”