Effect of the combination of motor imagery and electrical stimulation on upper extremity motor function in patients with chronic stroke: preliminary results.

BACKGROUND: The combination of motor imagery (MI) and afferent input with electrical stimulation (ES) enhances the excitability of the corticospinal tract compared with motor imagery alone or electrical stimulation alone. However, its therapeutic effect is unknown in patients with hemiparetic stroke. We performed a preliminary examination of the therapeutic effects of MI + ES on upper extremity (UE) motor function in patients with chronic stroke. METHODS: A total of 10 patients with chronic stroke demonstrating severe hemiparesis participated. The imagined task was extension of the affected finger. Peripheral nerve electrical stimulation was applied to the radial nerve at the spiral groove. MI + ES intervention was conducted for 10 days. UE motor function as assessed with the Fugl-Meyer assessment UE motor score (FMA-UE), the amount of the affected UE use in daily life as assessed with a Motor Activity Log (MAL-AOU), and the degree of hypertonia in flexor muscles as assessed with the Modified Ashworth Scale (MAS) were evaluated before and after intervention. To assess the change in spinal neural circuits, reciprocal inhibition between forearm extensor and flexor muscles with the H reflex conditioning-test paradigm at interstimulus intervals (ISIs) of 0, 20, and 100 ms were measured before and after intervention. RESULTS: UE motor function, the amount of the affected UE use, and muscle hypertonia in flexor muscles were significantly improved after MI + ES intervention (FMA-UE: p < 0.01, MAL-AOU: p < 0.01, MAS: p = 0.02). Neurophysiologically, the intervention induced restoration of reciprocal inhibition from the forearm extensor to the flexor muscles (ISI at 0 ms: p = 0.03, ISI at 20 ms: p = 0.03, ISI at 100 ms: p = 0.01). CONCLUSION: MI + ES intervention was effective for improving UE motor function in patients with severe paralysis.

The role of polyol pathway in glucose-induced apoptosis of cultured retinal pericytes.

The pathogenesis of pericyte loss, an initial deficit in the early stage of diabetic retinopathy, remains unclear. Recent studies have suggested that polyol pathway hyperactivity and apoptosis may be involved in pericyte loss. The mechanisms of the glucose-induced apoptosis in retinal pericytes were investigated to evaluate the pathogenesis of diabetic retinopathy. Under the 20 mM glucose condition, intracellular calcium concentrations and caspase-3 activities were significantly increased, and reduced glutathione (GSH) contents were significantly decreased compared with those under the 5.5 mM glucose condition. These abnormalities were all significantly prevented by an aldose reductase inhibitor, SNK-860. Glucose-induced apoptosis was partially but significantly prevented by SNK-860, an inhibitor of calcium-dependent cysteine protease, calpain, or GSH supplementation, and completely normalized by a caspase-3 inhibitor. These observations suggest that glucose-induced apoptosis in retinal pericytes, as one of the pathogenic factors of diabetic retinopathy, would be mediated through an aldose reductase-sensitive pathway including calcium-calpain cascade and increased oxidative stress, and that caspase-3 would be located furthest downstream of these apoptotic signals.