Locomotion in stroke subjects: interactions between unaffected and affected sides.

Spinal Cord Injury Centre, Balgrist University Hospital, Forchstr. 340, CH-8008 Zurich, Switzerland.
Brain (Impact Factor: 10.23). 02/2011; 134(Pt 3):721-31. DOI: 10.1093/brain/awq370
Source: PubMed

ABSTRACT The aim of this study was to evaluate the sensorimotor interactions between unaffected and affected sides of post-stroke subjects during locomotion. In healthy subjects, stimulation of the tibial nerve during the mid-stance phase is followed by electromyography responses not only in the ipsilateral tibialis anterior, but also in the proximal arm muscles of both sides, with larger amplitudes prior to swing over an obstacle compared with normal swing. In post-stroke subjects, the electromyography responses were stronger on both sides when the tibial nerve of the unaffected leg was stimulated compared with stimulation of the affected leg. This difference was more pronounced when stimuli were applied prior to swing over an obstacle than prior to normal swing. This indicates an impaired processing of afferent input from the affected leg resulting in attenuated and little task-modulated reflex responses in the arm muscles on both sides. In contrast, an afferent volley from the unaffected leg resulted in larger electromyography responses, even in the muscles of the affected arm. Arm muscle activations were stronger during swing over an obstacle than during normal swing, with no difference in electromyography amplitudes between the unaffected and affected sides. It is concluded that the deficits of the affected arm are compensated for by influences from the unaffected side. These observations indicate strong mutual influences between unaffected and affected sides during locomotion of post-stroke subjects, which might be used to optimize rehabilitation approaches.

  • [Show abstract] [Hide abstract]
    ABSTRACT: The purpose of this review is to discuss the achievements and perspectives regarding rehabilitation of sensorimotor functions after spinal cord injury. In the first part we discuss clinical approaches based on neuroplasticity, a term referring to all adaptive and maladaptive changes within the sensorimotor systems triggered by a spinal cord injury. Neuroplasticity can be facilitated through the training of movements with assistance as needed, and/or by electrical stimulation techniques. The success of such training in individuals with incomplete spinal cord injury critically depends on the presence of physiological proprioceptive input to the spinal cord leading to meaningful muscle activations during movement performances. The addition of rehabilitation technology, such as robotic devices allows for longer training times and provision of feedback information regarding changes in movement performance. Nevertheless, the improvement of function by such approaches for rehabilitation is limited. In the second part, we discuss preclinical approaches to restore function by compensating for the loss of descending input to spinal networks following complete spinal cord injury. This can be achieved with stimulation of spinal networks or approaches to restore their descending input. Electrical and pharmacological stimulation of spinal neural networks is still in an experimental stage; and despite promising repair studies in animal models, translations to humans up to now have not been convincing. It is likely that combinations of techniques targeting the promotion of axonal regeneration and meaningful plasticity are necessary to advance the restoration of function. In the future, refinement of animal studies may contribute to greater translational success.
    Brain 10/2013; · 10.23 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Spasticity develops as a consequence of damage to the central nervous system (CNS). Clinically, spasticity is characterized by muscle hypertension and exaggerated reflexes and is associated with varying degrees of paresis. Together this results in the syndrome of spastic paresis. Patients suffer from impeded and retarded movement ability. Electrophysiological investigations of functional arm and leg movements (e.g. in walking) show a reduced activation of arm and leg muscles which can be explained by the loss of activating signals from motor brain centers and functional reflex systems. This effect predominates over the increased tendon-reflex activity. The reduced muscle activation caused by paresis is partially compensated by structural alterations of the muscle fibers (e.g. loss of sarcomeres). For this reason a functional improvement mostly cannot be achieved by antispastic medication which targets the deactivation of tendon-reflexes. However, they are useful in immobilized patients. In mobile patients functional improvement can be achieved by functional training which is accompanied by an adapted, i.e. reduced, spastic muscle tone.
    Der Nervenarzt 11/2013; · 0.80 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective: Gait speed is an important predictor of health that is negatively affected by aging and type 2 diabetes. Diabetes has been linked to reduced vasoreactivity, i.e., the capacity to regulate cerebral blood flow in response to CO2 challenges. This study aimed to determine the relationship between cerebral vasoreactivity and gait speed in older adults with and without diabetes. Research design and methods: We studied 61 adults with diabetes (65 ± 8 years) and 67 without diabetes (67 ± 9 years) but with similar distribution of cardiovascular risk factors. Preferred gait speed was calculated from a 75 m walk. Global and regional perfusion, vasoreactivity and vasodilation reserve were measured using 3-D continuous arterial spin labeling MRI at 3 Tesla during normo-, hyper- and hypocapnia and normalized for end-tidal CO2. Results: Diabetic participants had slower gait speed as compared to non-diabetic participants (1.05 ± 0.15 m/s vs. 1.14 ± 0.14 m/s, p < 0.001). Lower global vasoreactivity (r (2) adj = 0.13, p = 0.007), or lower global vasodilation reserve (r (2) adj = 0.33, p < 0.001), was associated with slower walking in the diabetic group independently of age, BMI and hematocrit concentration. For every 1 mL/100 g/min/mmHg less vasodilation reserve, for example, gait speed was 0.05 m/s slower. Similar relationships between vasodilation reserve and gait speed were also observed regionally within the cerebellum, frontal, temporal, parietal, and occipital lobes (r (2) adj = 0.27-0.33, p < 0.0001). In contrast, vasoreactivity outcomes were not associated with walking speed in non-diabetic participants, despite similar vasoreactivity ranges across groups. Conclusion: In the diabetic group only, lower global vasoreactivity was associated with slower walking speed. Slower walking in older diabetic adults may thus hallmark reduced vasomotor reserve and thus the inability to increase perfusion in response to greater metabolic demands during walking.
    Frontiers in Aging Neuroscience 01/2014; 6:135. · 5.20 Impact Factor