Motor recovery following capsular stroke

Abstract

SUMMARYThe functional anatomy of motor recovery was studied by assessing motor function quantitatively in 23 patients following capsular or striatocapsular stroke. While selective basal ganglia lesions (caudate and/or putamen exclusively) did not affect voluntary movements ofthe extremities, lesions ofthe anterior (plus caudate/putamen) or posterior lirnb of the internal capsule led to an initially severe motor impainnent followed by excellent recovery, hand function included. In contrast, lesions of the posterior limb of the internal capsule in combination with damage to lateral thalamus compromised motor outcome. In experimental tracing of the topography of the internal capsule in macaque monkeys, we found axons ofprimary motor cortex passing through the middle third ofthe posterior lirnb ofthe internal capsule. Axons ofpremotor cortex (dorsolateral and post-arcuate area 6) passed through the capsular genu, and those of supplementary motor area (mesial area 6) through the anterior lirnb. Small capsular lesion can therefore disrupt the output of functionally and anatomically distinct motor areas selectively. The clinica1ly similar motor deficits with a similar course of functional restitution following disruption of these different descending motor pathways indicate a parallel operation of cortical motor areas. They may have the further capability of substituting each other functionally in the process of recovery from hemiparesis.

The role of ipsilateral premotor cortex in hand movement after stroke

“…Further experiments are needed to establish the anatomical route by which iPMd influences the spinal cord in these patients Involvement of iPMd was greatest in the more impaired patients. Therefore, the present results cannot be interpreted as showing that the undamaged premotor cortex is functionally substituting for the injured contralateral motor system in a complete and simple way (8). What seems clear, however, is that increased activity in iPMd is not maladaptive (16), because the effects of TMS disruption have demonstrated that iPMd activity is functionally significant.…”

“…A popular interpretation of such activation is that areas in the intact hemisphere adaptively compensate for damaged regions (8). However, identification of movement-related activation with functional imaging does not establish the functional significance of this ipsilateral activation.…”

“…For example, ipsilateral activation could be a correlate of mirror movements (9), reflect potentially maladaptive disinhibition of the intact motor cortex due to reduced transcallosal influences (10), or reflect increased attention to movement (11). An additional possibility is that ipsilateral activation reflects compensation rather than adaptive recovery, i.e., it may reflect use of a different cognitive strategy for movement after stroke, rather than new recruitment of these areas to some functional equivalence with damaged or disconnected contralateral motor regions (8).…”

Evolution of Cortical Activation During Recovery From Corticospinal Tract Infarction

“…Even in cases in which there is autopsy-or image-documented damage to the corticospinal tract, recovery from severe hemiparesis to near-normal function is possible. [2][3][4] Many lines of investigation have attempted to define the mechanisms for stroke recovery in the hope that understanding these mechanisms will improve our ability to enhance the recovery process. With the development of functional imaging methods, it has become possible to identify anatomic regions of the brain that show increased metabolic activity when a patient with recovered hemiparesis performs a motor task such as repetitive finger-thumb opposition.…”

Interlimb Coordination During Step-to-Step Transition and Gait Performance

“…This can probably be explained by the fact that walking is an energy-cheap activity for healthy subjects, because interlimb coordination is optimised and integrated. Yet, this interlimb coordination can be impaired directly or indirectly as a consequence of lesions in specific supraspinal neuronal structures (Fries, Danek, Scheidtmann, & Hamburger, 1993;Marque, Simonetta-Moreau, Maupas, & Roques, 2001;Maupas, Marque, Roques, & Simonetta-Moreau, 2004;Nardone & Schieppati, 2005). Also, the interlimb coordination is affected by gait symmetry (Krasovsky & Levin, 2009).…”