Abstract
BackgroundNeuroanatomical determinants of motor skill recovery after stroke are still poorly understood. Although lesion load onto the corticospinal tract is known to affect recovery, less is known about the effect of lesions to cortical sensorimotor areas. Here, we test the hypothesis that lesions of somatosensory cortices interfere with the capacity to recover motor skills after stroke.MethodsStandardized tests of motor skill and somatosensory functions were acquired longitudinally over nine months in 29 patients with stroke to the pre- and postcentral gyrus, including adjacent areas of the frontal, parietal and insular cortices. We derived the recovery trajectories of each patient for five motor subtest using least-squares curve fitting and objective model selection procedures for linear and exponential models. Patients were classified into subgroups based on their motor recovery models. Lesions were mapped onto diffusion weighted imaging scans and normalized into stereotaxic space using cost-function masking. To identify critical neuranatomical regions, voxel-wise subtractions were calculated between subgroup lesion maps. A probabilistic cytoarchitectonic atlas was used to quantify of lesion extent and location.ResultsTwenty-three patients with moderate to severe initial deficits showed exponential recovery trajectories for motor subtests that relied on precise distal movements. Those that retained a chronic motor deficit had lesions that extended to the center of the somatosensory cortex (area 2) and the intraparietal sulcus (areas hIP1, hIP2). Impaired recovery outcome correlated with lesion extent on this areas and somatosensory performance. The rate of recovery, however, depended on the lesion load onto the primary motor cortex (areas 4a, 4p).ConclusionsOur findings support a critical role of uni-and multimodal somatosensory cortices in motor skill recovery. Whereas lesions to these areas influence recovery outcome, lesions to the primary motor cortex affect recovery dynamics. This points to a possible dissociation of neural substrates for different aspects of post-stroke recovery.
Highlights
Stroke is one of the leading causes of long-term disability in adult life
Recent neuroanatomical studies in stroke patients show that the amount of corticospinal tract (CST) injury correlates well with chronic motor status [1,2], but prospective studies that analyze lesion topography, its anatomical relationship to cortical structures and behavioural implications are missing
Since we were interested in the recovery of skilled motor function, we focused our analysis on the time courses of the Jebsen-Taylor Test (JTT) subtests
Summary
Stroke is one of the leading causes of long-term disability in adult life. Outcomes are highly heterogeneous, with 50–88% of survivors suffering from permanent sensorimotor sequelae, while others regain almost complete functionality. Many clinical predictors have been defined, but less is known about the effect of biological determinants, e.g. degree and localization of structural lesions, on longitudinal post–stroke recovery. Recent neuroanatomical studies in stroke patients show that the amount of corticospinal tract (CST) injury correlates well with chronic motor status [1,2], but prospective studies that analyze lesion topography, its anatomical relationship to cortical structures and behavioural implications are missing. Two recent cross-sectional studies and one longitudinal study have used cytoarchitectonic information to infer structure-function relationships in patients with focal ischemic lesions [5,6,7]. Neuroanatomical determinants of motor skill recovery after stroke are still poorly understood. Lesion load onto the corticospinal tract is known to affect recovery, less is known about the effect of lesions to cortical sensorimotor areas. We test the hypothesis that lesions of somatosensory cortices interfere with the capacity to recover motor skills after stroke
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