Tone-Inhibiting Insoles Enhance the Reciprocal Inhibition of Ankle Plantarflexors of Subjects With Hemiparesis After Stroke: An Electromyographic Study.

BACKGROUND: Spasticity is a common sequela of upper motor neuron pathology, such as cerebrovascular diseases and cerebral palsy. Intervention for spasticity of the ankle plantarflexors in physical therapy may include tone-inhibiting casting and/or orthoses for the ankle and foot. However, the physiological mechanism of tone reduction by such orthoses remains unclarified. OBJECTIVE: To investigate the electrophysiologic effects of tone-inhibiting insoles in stroke subjects with hemiparesis by measuring changes in reciprocal Ia inhibition (RI) in the ankle plantarflexor. DESIGN: An interventional before-after study. SETTING: Acute stroke unit or ambulatory rehabilitation clinic of a university hospital in Japan. PARTICIPANTS: Ten subjects (47-84 years) with hemiparesis and 10 healthy male control subjects (31-59 years) were recruited. METHODS: RI of the spastic soleus in response to the electrical stimulation of the deep peroneal nerve was evaluated by stimulus-locked averaging of rectified electromyography (EMG) of the soleus while subjects were standing. MAIN OUTCOME MEASUREMENTS: The magnitude of RI, defined as the ratio of the lowest to the baseline amplitude of the rectified EMG at approximately 40 milliseconds after stimulation, was measured while subjects were standing with and without the tone-inhibiting insole on the hemiparesis side. RESULTS: Enhancement of EMG reduction with the tone-inhibiting insole was significant (P < .05) in the subjects with hemiparesis, whereas no significant changes were found in controls. CONCLUSION: Tone-inhibiting insoles enhanced RI of the soleus in subjects after stroke, which might enhance standing stability by reducing unfavorable ankle plantarflexion tone. LEVEL OF EVIDENCE: III.

Optimal Reference Electrode Positioning for Electroneurography at the Orbicularis Oculi: A Case Report and Short Review.

Electroneurography is one of the most useful tests for evaluating facial nerve function. Because many patients with peripheral facial palsy complain of difficulty with eye closure, recording compound muscle action potentials (CMAPs) of the orbicularis oculi (OC) is important. However, electromyographers often encounter OC CMAPs that have an initial positivity. In the present study, facial motor potentials of a healthy subject were recorded using an electrode on the acromion and electrical activities over the facial muscles were evaluated.The contralateral OC electrode was the most inactive. A CMAP recorded using two electrodes on the ipsilateral OC showed an initial positivity. It is assumed that the onset discrepancy between electrical activities of the two electrodes on the OC results in an initial positivity. Thus, the authors recommend that electromyographers avoid using a reference electrode on the ipsilateral OC for recording its CMAP. The bilateral OC montage could be useful for recording OC CMAPs.

Reduction in the motor unit number estimate (MUNE) after cerebral infarction.

We examined the relationship between the degree to which motor unit number estimates (MUNEs) decrease in association with the clinical features of patients with the infarction. Using a multiple-point stimulation technique, we obtained the MUNE of the hypothenar muscle group in 13 age-matched control subjects and 30 patients with cerebral infarction. In all patients, we obtained the Japan Stroke Scale (JSS) and head MR images. In 8 patients with acute cerebral infarction, admitted within 24 h after onset, we also obtained head MR angiograms and single-photon emission CT. There was a decrease in the MUNE of the hypothenar muscle group on the affected side of 24 patients with cerebral infarction and hand weakness. The decrease in the MUNE started from 4 to 30 h after the infarction, when T1-weighted MR images of the brain involved were normal. The degree to which the MUNE decreased correlated with the part of the JSS showing the upper extremity weakness. A decrease in the MUNE of the hypothenar muscle group within 30 h after cerebral infarction may be due to transsynaptic inhibition of the spinal alpha motor neurons innervating this muscle.

Reduction in the motor unit number estimate (MUNE) after cerebral infarction.

BACKGROUND: The mechanism of the decrease in motor unit number estimates (MUNEs) after cerebral infarction has not been studied systematically. We examined the relationship between the degree to which MUNEs decreased and the other clinical features of patients with the infarction. METHODS: Using a multiple point stimulation technique, we obtained the MUNE of the hypothenar muscle group in 13 age-matched control subjects and 30 patients with cerebral infarction. In all patients, we obtained the Japan Stroke Scale (JSS) and head MR images. In eight patients with acute cerebral infarction, admitted within 24 h after onset, we also obtained head MR angiograms and single-photon emission CT. FINDINGS: There was a decrease in the MUNE of the hypothenar muscle group on the affected side of 24 patients with cerebral infarction and hand weakness. The decrease in the MUNE started from 4 to 30 h after the infarction, when T1-weighted MR images of the brain involved were normal. The degree to which the MUNE decreased correlated with the part of the JSS showing the upper extremity weakness. INTERPRETATIONS: A decrease in the MUNE of the hypothenar muscle group within 30 h after cerebral infarction may be due to trans-synaptic inhibition of the spinal alpha motor neurons innervating this muscle.

Extracellular signal-dependent nuclear import of STAT3 is mediated by various importin alphas.

The signal transducer and activator of transcription 3 (STAT3) is a transcription factor that is involved in a variety of biological functions. STAT3 is activated by cytokines and growth factors via the phosphorylation of a tyrosine residue, dimerization, and subsequent nuclear translocation. However, the mechanism of its nuclear translocation is unclear. A study of the cytokine-stimulated import of STAT3 into the nucleus is reported herein. An oncostatin M (OSM)-dependent nuclear import assay system was first established in living cells. Using this system, we demonstrated that the microinjection of the importin alpha5/NPI-1 mutant, an anti-importin beta antibody, and the RanQ69L mutant inhibited the nuclear import of STAT3. Second, we showed that tyrosine-phosphorylated STAT3 associates, not only with importin alpha5/NPI-1 but also with other importin alphas, as a result of OSM stimulation, as evidenced by a solution binding assay. These findings suggest that the extracellular signal-dependent nuclear transport of STAT3 is mediated by various importin alphas, importin beta, and Ran.