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Modulation of muscle activation in superficial and deeper regions may be induced by tactile stimulation. The purpose of this study was to examine changes in muscle activation with skin friction. Subjects performed an isometric elbow flexion at 30% maximal voluntary cotraction (MVC) with skin friction at different frequencies (0.5-2.7 Hz). Surface electromyography (S-EMG) and intramuscular EMG were obtained from the elbow flexor muscles (BBS: short head of biceps brachii, BBL: long head of biceps brachii, BRA: brachialis). S-EMG activity decreased at a higher frequency of 2.7 Hz and increased linearly with an increase in skin friction frequency (0.5-2.7 Hz) in BBS. A decrease in high-threshold motor unit (HT-MU) firing rate in superficial regions and an increase in low-threshold motor unit (LT-MU) firing rate in deeper regions were observed with skin friction (2.7 Hz) in BBS. The actions of inhibitory interneurons may be influenced by cutaneous afferent input with skin friction. Muscle activation of BBS depended on the intensity of the stimulus. Skin friction over BBS results in an inhibitory response in superficial regions of BBS, most likely due to the increase in firing rate of low-threshold cutaneous mechanoreceptors.

We concluded that LLLT at the wavelength and parameters used in the present study was effective for chronic pain of the elbow, wrist, and fingers.

Spasticity following cerebral vascular accidents (CVAs) is a common occurrence, but remains a problematic entity to treat and interferes with mobility and self-care activities which are critical for successful rehabilitative outcomes. Low reactive-level laser therapy (LLLT) has attracted attention in a number of areas including spasticity associated with cerebral palsy. In the case of post CVA therapy, LLLT has been reported for pain treatment, but not spasticity. The present study examined the efficacy of LLLT in attenuating triceps surae muscle spasticity in CVA patients. The study subjects comprised 15 chronic CVA patients with spasticity, treated at our university hospital between 2002 and 2006. The LLLT device we used was a near infrared (830 nm) semiconductor laser device delivering 1 W in continuous wave (irradiance, 670 mW/cm 2). The laser probe was applied with mild pressure to the skin over the tibial nerve on the affected side, 30 sec/point (dose/point 20.1 J/cm 2) repeated 3 times with a 5 sec interval between irradiations. Two sessions were given per week for 1 week. At the end of the week, we recognized LLLT effects in 11 cases out of 15. The other 4 patients had little or no effect but were in their fifties, and had successive bouts of ankle clonus. LLLT is a promising medical treatment for the attenuation of CVA-related spasticity of the triceps surae muscle spasticity, and facilitate voluntary movements in such patients. Further studies are warranted to elucidate the mechanisms by which LLLT can attenuate spasticity.