Evidence indicates that experience-dependent cortical plasticity underlies post-stroke motor recovery of the impaired upper extremity. Motor skill learning in neurologically intact individuals is thought to involve the primary motor cortex, and the majority of studies in the animal literature have studied changes in the primary sensorimotor cortex with motor rehabilitation. Whether changes in engagement in the sensorimotor cortex occur in humans after stroke currently is an area of much interest. The present study conducted a meta-analysis on stroke studies examining changes in neural representations following therapy specifically targeting the upper extremity to determine if rehabilitation-related motor recovery is associated with neural plasticity in the sensorimotor cortex of the lesioned hemisphere. Twenty-eight studies investigating upper extremity neural representations (e.g., TMS, fMRI, PET, or SPECT) were identified, and 13 met inclusion criteria as upper extremity intervention training studies. Common outcome variables representing changes in the primary motor and sensorimotor cortices were used in calculating standardized effect sizes for each study. The primary fixed effects model meta-analysis revealed a large overall effect size (E.S. = 0.84, S.D. = 0.15, 95% C.I. = 0.76 -0.93). Moreover, a fail-safe analysis indicated that 42 null effect studies would be necessary to lower the overall effect size to an insignificant level. These results indicate that neural changes in the sensorimotor cortex of the lesioned hemisphere accompany functional paretic upper extremity motor gains achieved with targeted rehabilitation interventions.

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We evaluated the relationship between upper extremity (UE) and lower extremity (LE) motor impairments in Parkinson's disease (PD) to overall disability and quality of life (QoL) measures. A total of 639 patients who were diagnosed with idiopathic PD were administered the Unified Parkinson's Disease Rating Scale (UPDRS), QoL, activities of daily living (ADL), and behavioral scales. Composite UE and LE scores from the motor section of the UPDRS were correlated with ADL, QoL, and behavioral measurement scores while controlling for disease duration. Patients with greater UE and LE motor impairments had lower QoL scores. However, LE impairments had a greater influence than UE impairments across all QoL measures.

At least one small report has suggested the possibility that limb kinetic apraxia (a deficit in deftness) was not dopamine responsive and independent of bradykinesia and rigidity in PD. Quencer et al. (Neurology 68:150-151, 2007) observed that speed of finger tapping (bradykinesia) in optimally medicated persons with PD was largely comparable to healthy controls, yet their ability to manipulate and rotate a coin (deftness) was impaired. The authors concluded that deftness was independent of parkinsonian features. In this study, we measured tasks of deftness in a more objective way in both the ON and OFF dopaminergic state. Further, we evaluated whether finger-thumb force control was compromised in persons with PD. Eleven PD fluctuators (mean age 68 ± 9 years) and ten healthy age-matched controls (68 ± 8 years) were included. The bradykinesia items in the UPDRS and performance on the large box and block (LBB) tests were used to measure bradykinesia. A small box and block test (SBB), small coin rotation task (SCR) and small lock rotation task (SLR) were used as measures of deftness. Statistical analyses revealed a significant improvement in performance for the LBB, SBB, SLR and the bradykinesia items of the UPDRS following medication. Furthermore, our PD cohort's scores were comparable to controls on tests of bradykinesia and deftness (SLR, SBB and LBB) in the ON state, but they performed statistically worse than controls in the OFF state. On the other hand, analyses of the force control tasks revealed no significant difference between the groups. In summary, the improvement in deftness and bradykinesia in the ON state among our PD cohorts (and their comparable performance in the ON but not OFF state compared to healthy controls) suggests the possibility of a more uniform response of these motor features to dopaminergic therapy in PD.