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Gross-motor impairments are common after stroke, but efficacious and motivating therapies for these impairments are scarce. We present a novel musical sonification therapy especially designed to retrain gross-motor functions. Four stroke patients were included in a clinical pre-post feasibility study and were trained with our sonification training. Patients' upper-extremity functions and their psychological states were assessed before and after training. The four patients were subdivided into two groups, with both groups receiving 9 days of musical sonification therapy (music group, MG) or a sham sonification training (control group, CG). The only difference between these training protocols was that, in the CG, no sound was played back. During the training the patients initially explored the acoustic effects of their arm movements, and at the end of the training the patients played simple melodies by moving their arms. The two patients in the MG improved in nearly all motor function tests after the training. They also reported in the stroke impact scale, which assesses well-being, memory, thinking, and social participation, to be less impaired by the stroke. The two patients in the CG did benefit less from the movement training. Taken together, musical sonification may be a promising therapy for impairments after stroke. [ABSTRACT FROM AUTHOR]

Recent neurophysiological studies have associated focal-task specific dystonia (FTSD) with impaired inhibitory function. However, it remains unknown whether FTSD also affects the inhibition (INH) of long-term overlearned motor programs. Consequently, we investigated in a Go/NoGo paradigm the neural correlates associated with the activation (ACT) and inhibition of long-term overlearned motor memory traces in pianists with musician's dystonia (MD), a form of FTSD, during a relevant motor task under constraint timing conditions with multichannel EEG. In NoGo trials, the movement related cortical potentials showed a positive shift after the NoGo signal related to inhibition and was significantly smaller over sensorimotor areas in musicians with MD. Further, we observed an increase at 850-900 ms in the power of beta oscillations which was significantly weaker for the patient group. The role of the inter-electrode phase coupling in the sensorimotor integration of inhibitory processes turned out to be the most relevant physiological marker: the global phase synchronization during INH exhibited an increase between 230 and 330 ms and 7-8 Hz, increase which was significantly smaller for pianists with MD. This effect was due to a weaker phase synchronization between the supplementary motor cortex and left premotor and sensorimotor electrodes in patients. Thus, our findings support the hypothesis of a deficient phase coupling between the neuronal assemblies required to inhibit motor memory traces in patients with MD. EMG recorded from the right flexor pollicis longus muscle confirmed that patients with MD had a disrupted INH in NoGo trials. Hum Brain Mapp 2009. © 2008 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]