Effect of gait speed on gait rhythmicity in Parkinson's disease: variability of stride time and swing time respond differently

BACKGROUND: The ability to maintain a steady gait rhythm is impaired in patients with Parkinson's disease (PD). This aspect of locomotor dyscontrol, which likely reflects impaired automaticity in PD, can be quantified by measuring the stride-to-stride variability of gait timing. Previous work has shown an increase in both the variability of the stride time and swing time in PD, but the origins of these changes are not fully understood. Patients with PD also generally walk with a reduced gait speed, a potential confounder of the observed changes in variability. The purpose of the present study was to examine the relationship between walking speed and gait variability. METHODS: Stride time variability and swing time variability were measured in 36 patients with PD (Hoehn and Yahr stage 2–2.5) and 30 healthy controls who walked on a treadmill at four different speeds: 1) Comfortable walking speed (CWS), 2) 80% of CWS 3) 90% of CWS, and 4) 110% of CWS. In addition, we studied the effects of walking slowly on level ground, both with and without a walker. RESULTS: Consistent with previous findings, increased variability of stride time and swing time was observed in the patients with PD in CWS, compared to controls. In both groups, there was a small but significant association between treadmill gait speed and stride time variability such that higher speeds were associated with lower (better) values of stride time variability (p = 0.0002). In contrast, swing time variability did not change in response to changes in gait speed. Similar results were observed with walking on level ground. CONCLUSION: The present results demonstrate that swing time variability is independent of gait speed, at least over the range studied, and therefore, that it may be used as a speed-independent marker of rhythmicity and gait steadiness. Since walking speed did not affect stride time variability and swing time variability in the same way, it appears that these two aspects of gait rhythmicity are not entirely controlled by the same mechanisms. The present findings also suggest that the increased gait variability in PD is disease-related, and not simply a consequence of bradykinesia

Lesion location impact on functional recovery of the hemiparetic upper limb.

The effect of stroke topography on the recovery of hemiparetic upper limb (HUL) function is unclear due to limitations in previous studies-examination of lesion effects only in one point of time, or grouping together patients with left and right hemispheric damage (LHD, RHD), or disregard to different lesion impact on proximal and distal operations. Here we used voxel-based lesion symptom mapping (VLSM) to investigate the impact of stroke topography on HUL function taking into consideration the effects of (a) assessment time (subacute, chronic phases), (b) side of damaged hemisphere (left, right), (c) HUL part (proximal, distal). HUL function was examined in 3 groups of patients-Subacute (n = 130), Chronic (n = 66), and Delta (n = 49; patients examined both in the subacute and chronic phases)-using the proximal and distal sub-divisions of the Fugl-Meyer (FM) and the Box and Blocks (B&B) tests. HUL function following LHD tended to be affected in the subacute phase mainly by damage to white matter tracts, the putamen and the insula. In the chronic phase, a similar pattern was shown for B&B performance, whereas FM performance was affected by damage only to the white matter tracts. HUL function following RHD was affected in both phases, mainly by damage to the basal ganglia, white matter tracts and the insula, along with a restricted effect of damage to other cortical structures. In the chronic phase HUL function following RHD was affected also by damage to the thalamus. In the small Delta groups the following trends were found: In LHD patients, delayed motor recovery, captured by the B&B test, was affected by damage to the sensory-motor cortex, white matter association fibers and parts of the perisilvian cortex. In the RHD patients of the Delta group, delayed motor recovery was affected by damage to white matter projection fibers. Proximal and distal HUL functions examined in LHD patients (both in the subacute and chronic phases) tended to be affected by similar structures-mainly white matter projection tracts. In RHD patients, a distinction between proximal and distal HUL functions was found in the subacute but not in the chronic phase, with proximal and distal HUL functions affected by similar subcortical and cortical structures, except for an additional impact of damage to the superior temporal cortex and the retro-lenticular internal capsule only on proximal HUL function. The current study suggests the existence of important differences between the functional neuroanatomy underlying motor recovery following left and right hemisphere damage. A trend for different lesion effects was shown for residual proximal and distal HUL motor control. The study corroborates earlier findings showing an effect of the time after stroke onset (subacute, chronic) on the results of VLSM analyses. Further studies with larger sample size are required for the validation of these results

Additional file 1: of Personalized upper limb training combined with anodal-tDCS for sensorimotor recovery in spastic hemiparesis: study protocol for a randomized controlled trial

SPIRIT 2013 Checklist: recommended items to address in a clinical trial protocol and related documents. (PDF 152 kb

ENHANCE proof-of-concept three-arm randomized trial: effects of reaching training of the hemiparetic upper limb restricted to the spasticity-free elbow range

Abstract Post-stroke motor recovery processes remain unknown. Timescales and patterns of upper-limb (UL) recovery suggest a major impact of biological factors, with modest contributions from rehabilitation. We assessed a novel impairment-based training motivated by motor control theory where reaching occurs within the spasticity-free elbow range. Patients with subacute stroke (≤ 6 month; n = 46) and elbow flexor spasticity were randomly allocated to a 10-day UL training protocol, either personalized by restricting reaching to the spasticity-free elbow range defined by the tonic stretch reflex threshold (TSRT) or non-personalized (non-restricted) and with/without anodal transcranial direct current stimulation. Outcomes assessed before, after, and 1 month post-intervention were elbow flexor TSRT angle and reach-to-grasp arm kinematics (primary) and stretch reflex velocity sensitivity, clinical impairment, and activity (secondary). Results were analyzed for 3 groups as well as those of the effects of impairment-based training. Clinical measures improved in both groups. Spasticity-free range training resulted in faster and smoother reaches, smaller (i.e., better) arm-plane path length, and closer-to-normal shoulder/elbow movement patterns. Non-personalized training improved clinical scores without improving arm kinematics, suggesting that clinical measures do not account for movement quality. Impairment-based training within a spasticity-free elbow range is promising since it may improve clinical scores together with arm movement quality. Clinical Trial Registration: URL: http://www.clinicaltrials.gov . Unique Identifier: NCT02725853; Initial registration date: 01/04/2016