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Compensatory Limb Use and Behavioral Assessment of Motor Skill Learning Following Sensorimotor Cortex Injury in a Mouse Model of Ischemic Stroke
Published on: July 10, 2014
[Movement alterations following cerebrovascular damage in the intact hemisphere ipsilateral to the affected upper
M J Díaz-Arribas1, M Ramos-Sánchez, M Ríos-Lago
1Departamento de Medicina Física y Rehabilitación, Facultad de Medicina, Universidad Complutense de Madrid, Madrid, Spain. mjdiazar@med.ucm.es
Objective:
We analyze the explanatory hypotheses proposed in most relevant studies on the different altered movements (AM) in the unaffected part of the body following a stroke. We report 25 cases of AM patients whose clinical signs do not correspond with the AM described in previous studies. A possible explanation could be established from a different neuroplastic hypothesis.
Development:
To review the main hypotheses which try to explain the presence of AM in the part of the body ipsilesional to the injured hemisphere of the brain. To this end we overview some updated studies concerning the corticospinal tract function, and the neuroplastic capacity after a stroke. Simultaneously, we study 25 cases of patients with cerebrovascular disease and some clinical findings which present a different type of AM from those previously reported.
Conclusions:
Motor alterations described in most studies concerning stroke patients correspond well to a diminished selectivity of movements of the unaffected hand, to associated movements in both upper limbs or to mirror movements. Explanations of these hypothesis are: the effect of injured fibres of the uncrossed corticospinal tract and neuroplastic reorganization of the ipsilateral pathways. The existence of different AM is observed in some clinical cases which we found to be scarcely studied in published research. These movements appear in the non-affected part of the body throughout cerebrovascular disease evolution, and which could be caused by maintained hypersolicitation of the unaffected part of the body and the neuroplastic process following a stroke. Further functional neuroimaging investigations are needed to confirm this clinical hypothesis.
