Article

Paresis in stroke is largely a result of damage to descending
corticospinal and corticobulbar pathways. Recovery of paresis predominantly
reflects the impact on the neural consequences of this white matter lesion by
reactive neuroplasticity (mechanisms involved in spontaneous recovery) and
experience-dependent neuroplasticity, driven by therapy and daily experience.
However, both theoretical considerations and empirical data suggest that type of
stroke (large vessel distribution/lacunar infarction, hemorrhage), locus and
extent of infarction (basal ganglia, right-hemisphere cerebral cortex), and the
presence of leukoaraiosis or prior stroke might influence long-term recovery of
walking ability. In this secondary analysis based on the 408 participants in the
Locomotor Experience Applied Post-Stroke (LEAPS) study database, we seek to
address these possibilities. Methods Lesion type, locus, and extent were
characterized by the 2 neurologists in the LEAPS trial on the basis of clinical
computed tomography and magnetic resonance imaging scans. A series of regression
models was used to test our hypotheses regarding the effects of lesion type,
locus, extent, and laterality on 2- to 12-month change in gait speed, controlling
for baseline gait speed, age, and Berg Balance Scale score. Results Gait speed
change at 1 year was significantly reduced in participants with basal ganglia
involvement and prior stroke. There was a trend toward reduction of gait speed
change in participants with lacunar infarctions. The presence of right-hemisphere
cortical involvement had no significant impact on outcome. Conclusions Type,
locus, and extent of lesion, and the loss of substrate for neuroplastic effect as
a result of prior stroke may affect long-term outcome of rehabilitation of
hemiparetic gait.
CI - (c) The Author(s) 2015.

Langue : ANGLAIS