Abstract
Introduction: Descending motor pathways, namely the corticospinal (CST) and corticoreticular tracts (CRT), are important for normal gait function and have been implicated in gait recovery after stroke. However, the relationship of structural injury to these tracts and gait function in the acute and chronic stage post-stroke remains unclear.
Methods: Gait velocity was recorded the first week (acute) after stroke (n=127) and one year later (n= 50). CST and CRT injury were measured using weighted lesion load (wLL). The impact of CST and CRT injury on ambulation status (non-ambulatory vs. ambulatory) and gait velocity was assessed with multivariate logistic and linear regression models, respectively, acutely and chronically, controlling for wLL and lesion size.
Results: Greater CRT injury resulted in a higher odds of ambulation loss acutely post-stroke (odds ratio [95% CI, p value]: CRT wLL, 1.06 [1.02-1.12, 0.007]; CST wLL 0.97 [0.95-0.99, 0.04]; lesion volume 1.00 [0.99-1.00, 0.96]). Conversely, greater CST injury had higher odds of ambulation loss at one-year (CST wLL, 1.09 [1.01-1.21, 0.04]; CRT wLL, 0.98 [0.84-1.13, 0.75]; lesion volume, 1.00 [0.99-1.00, 0.81]). For walkers (N=51 [acute] and 46 [chronic]), gait velocity was not significantly associated with CRT nor CST wLL at either time. Multicollinearity results denoted lesion measures provided independent information (maximum variance inflation factors 3.4 (acute), 4.2 (one-year)).
Conclusion: Results suggest CRT injury is the dominant correlate of ambulation loss acutely, with CST the dominant correlate of persistent loss after one-year. Gait velocity is not well explained by damage to either tract. The results imply that the CRT may be the primary cortical projection for normal (pre-stroke) gait. Yet, the nervous system has sufficient redundancy to compensate for unilateral CRT injury, while CST injury may have a more enduring negative impact on gait function.