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Owaki et al. revealed that auditory feedback conveyed through foot pressure sensors can improve the short-term walking performance of stroke patients [13].
Data derived from transcranial magnetic stimulation (TMS) studies suggest that transcallosal inhibition mechanisms between the primary motor cortex of both hemispheres may contribute to the reduced motor performance of stroke patients.
Primary objective of our study is, by differentiating pathological performance from the healthy performance and identifying the kinematic metrics that best evaluate the impairment, to demonstrate the robustness/usability of Microsoft Kinect in kinematic analysis of motor performance of stroke patients.
However, the huge variety in measuring the performance of stroke care hampers comparisons [ 43].
In particular, a more effective integration of ipsilesional M1 into the motor network architecture might constitute a key factor for improving motor performance of stroke patients by means of repetitive TMS (Grefkes et al., 2010 a ).
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The two correlations are combined to form a directed connection correlation, which is applicable in comparing the performance of different stroke sequence recovery algorithms.
Most of the parameters that can affect the performance of four stroke spark ignition engines, such as equivalence ratio, spark timing, heat release rate, compression ratio, compression index and expansion index are studied.
Preserved inter-hemispheric connectivity was also indicative of better performance of aphasic stroke patients in language tasks (Warren et al., 2009).
Furthermore, Lotze et al. (2006) have shown that disrupting contralesional M1 activity by means of TMS may cause a deterioration in motor performance of the stroke-affected hand of chronic stroke patients (>8 months) with internal capsule infarcts.
However, other studies have demonstrated that inhibition of contralesional M1 excitability using repetitive TMS protocols may lead to improved motor performance of the stroke-affected hand in the subacute (Nowak et al., 2008; 1–4 months post-stroke), subacute to chronic (Mansur et al., 2005; <12 months) or chronic phase after an infarct (Takeuchi et al., 2005; 7–54 months).
Similar to the findings of the dynamic causal modelling analyses, these pathological effects were especially present in patients with stronger deficits, and might hence contribute to the reduced performance of the stroke-affected hand (Murase et al., 2004; Duque et al., 2005).
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