1. Staff

2. Rehabilitation and health consultation for Minamata disease patients

　Once nerve cells in the brain or spinal cord are damaged, their regeneration still remains difficult even today. The brain, however, can compensate for damage in one region by enlisting help from other regions. Rehabilitation promotes such brain plasticity. The main treatment for Minamata disease in the chronic stage where the symptoms become stable is to control those symptoms with drugs or rehabilitation.
　Our institute is open to Minamata disease patients for daycare and rehabilitation (occupational therapy and physical therapy). In order to maintain and improve the power of skeletal muscle and to prevent contracture of the joints, training by a therapist or exercising on various equipment is available. Medication needed to improve high muscle tonus is also provided. Standing and walking training are important in order to improve balance and prevent contracture of the Achilles tendon. In addition, low-frequency electrical stimulation therapy and transcutaneous electrical stimulation therapy are effective for relief from pain. The patients with fetal type of Minamata disease (patients damaged during gestation) have difficulty in fine movements of the hands and fingers caused by disturbed brain function. In such cases, occupational therapy including handicrafts is provided to improve finger movements.
　Some patients visit our room to consult whether their symptoms might be related to Minamata disease. Consultations concerning mercury and its health effects have also been performed.

　Additionally, we conduct experimental research to investigate the mechanism of methylmercury (MeHg) cytotoxicty and its treatment. We have clarified the central role of oxidative stress in the pathogenesis of MeHg intoxication in vitro and in vivo. We found that the addition of the antioxidant Trolox, a water soluble vitamin E analog, protected the cells against apoptosis, and have confirmed the in vivo effectiveness of Trolox on MeHg-intoxication using MeHg-intoxicated model rats.

3. References:

Matsumoto M, Miyamoto K, Usuki F (1997) The effect of rehabilitation on ADL improvement in a case with action myoclonus. Sogo Rehabiriteshon 25：753ｰ756.

Usuki F and Ishiura S (1998) Expanded CTG repeats in myotonin protein kinase increases susceptibility to oxidative stress. NeuroReport 9: 2291-2296.

Usuki F, Yasutake A, Matsumoto M, Umehara F, Higuchi I (1998) The effect of methylmercury on skeletal muscle: a histopathological study. Toxicol Lett 94: 227-232.

Usuki F ＆ Maruyama K (2000) Ataxia caused by mutation in theα-tocopherol transfer protein gene. ＪNeurol Neurosurg Psychiatry 69:254-256.

Usuki F, Takahashi N, Sasagawa N, Ishiura S (2000) Differential signaling pathways following oxidative stress in mutant myotonin protein kinase cDNA-transfected C2C12 cell lines. Biochem Biophys Res Comm 267: 739-743.

Usuki F, Yasutake A, Umehara F, Tokunaga H, Matsumoto M, Eto K, Ishiura S, Higuchi I (2001) In vivo protection of a water-soluble derivative of vitamin E, Trolox, against methylmercury-intoxication. Neurosci Lett, 304: 199-203.

Usuki F, Yasutake A, Matsumoto M, Higuchi I (2001) Chronic low-dose methylmercury administration decreases mitochondrial electron transport system enzyme activities and induces myopathic changes in rats. J Health Science 47: 162-167.

Matsumoto M, Miyamoto K, Usuki F (2002) Analysis of subjective well-being in Minamata disease patients using PGC Morale Scale. Sogo Rehabiriteshon 30:81-85.