The Activity-Function-Structure Relationship and Rehabilitation…Masahiko MUKAINO 96

Molecular Biological Study on Muscle Strengthening and Functional Recovery on the Infarction Model…Satoshi IKEDA, Yurie KAMIKAWA, Katsuhiro HARADA, Akihiko OHWATASHI, Akira YOSHIDA 101

Molecular Mechanisms for Competitive Synaptic Circuit Development in the Cerebellum…Masahiko WATANABE 104

Sensory Input-regulated Mechanisms of Neuronal Turnover in the Adult Brain…Kazunobu SAWAMOTO 108

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The Interdisciplinary Rehabilitation Team Model in China Rehabilitation Research Center…Fubiao HUANG 111

Rehabilitation Team Perspective in Thailand…Chompunut PONGAKKASIRA 114

Rehabilitation Teamwork in Japan…Kozo HANAYAMA 117

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In two cases of poststroke shoulder-hand syndrome, the patients complained of hemi-paretic shoulder pain. Both cases showed characteristic findings on magnetic resonance imaging (MRI) of the paretic shoulder. Case 1 underwent MRI before the syndrome occurred, while Case 2 underwent MRI after the syndrome occurred. In both cases, chemical saturation T2-weighted images revealed high intensity signals mainly anterior to the scapula, but also surrounding the articular capsule of the shoulder joint. Also, the subscapular muscle and subscapular bursa appeared damaged, and bloody fluid extended into the connective tissue. In Case 2, chemical saturation T2-weighted images revealed high intensity signals in the axillary fat. The paretic hands of both patients showed conscious and objective allodynia, edema, and decreased range of finger flexion and carpal extension. Observed symptoms were consistent with a diagnosis of complex regional pain syndrome (CRPS). Adherence of the posterior brachial plexus to the subscapular muscle may result in positional relationship changes and tears to the cords when the paretic shoulder is moved. The resultant small fiber neuropathy may result in edema by conduction block. Furthermore, aseptic synovitis from neurogenic inflammation may also occur. In Case 1, the arthritis of the shoulder appeared before the neuropathy. This indicates that damage to the subscapular bursa rather than neuropathy may be the underlying cause of the arthritis.

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Botulinum toxin type A (BTXA) has been shown to be an effective treatment in reducing muscle tone and managing spasticity in poststroke patients. However, its effectiveness in improving function in lower limb spasticity has been more controversial. In this report, we present our findings in three cases of chronic stroke patients with lower limb spasticity wherein we examine the effectiveness of a 4-week intensive rehabilitation program following BTXA treatment. For each patient, BTXA was injected into spastic muscles of the affected lower limb and a rehabilitation program was provided for the patient in-hospital for 4 weeks. Before BTXA treatment (baseline) and at 2 and 4 week follow-ups after each treatment, the Stroke Impairment Assessment Set (SIAS), the Modified Ashworth Scale (MAS) and the Range of Motion (ROM) of the ankle, the 10 Meter Walking Test (10MWT), the 6 minutes walking distance (6MD), the Timed Up and Go Test (TUG), the Berg Balance Scale (BBS), and the Functional Independence Measure (FIM) were all assessed. In each patient, ankle MAS and ROM, 10MWT, 6MD, TUG, and BBS after 4 weeks improved from the baseline. Furthermore, the ankle MAS and ROM improved significantly within 2 weeks, as did the 10MWT and 6MD over the total 4 weeks. In conclusion, it is suggested that a better improvement of ambulation and balance, as well as spasticity, would be found with intensive rehabilitation following BTXA treatment for lower limb spasticity.

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