Gabapentin for complex regional pain syndrome in Machado-Joseph disease: a case report.

INTRODUCTION: Chronic pain is a common problem for patients with Machado-Joseph disease. Most of the chronic pain in Machado-Joseph disease has been reported to be of musculoskeletal origin, but now there seems to be different chronic pain in patients with Machado-Joseph disease. CASE PRESENTATION: A 29-year-old man (Han Chinese, Hoklo) with Machado-Joseph disease experienced severe chronic pain in both feet, cutaneous thermal change, thermal hypersensitivity, focal edema, and sweating and had a history of bone fracture. These symptoms were compatible with a diagnosis of complex regional pain syndrome. After common analgesics failed to relieve his pain, gabapentin was added and titrated to 2000 mg/day (500 mg every six hours) in less than two weeks. This relieved 40% of his pain and led to significant clinical improvement. CONCLUSIONS: The pathophysiology of complex regional pain syndrome includes peripheral and central sensitizations, the latter of which might be associated with the neurodegeneration in Machado-Joseph disease. In this report, we suggest that gabapentin could inhibit central sensitization as an adjunct for complex regional pain syndrome in patients with Machado-Joseph disease.

Fatigue in colchicine myopathy: a study of transcranial magnetic stimulation.

BACKGROUND: Transcranial magnetic stimulation (TMS) is a noninvasive method to assess brain physiology and plasticity. TMS has shown that nervous system excitability may be altered in myopathy, and it presents with motor disinhibition on cortical and subcortical levels. Eight patients who had colchicine myopathy were observed to have fatigue, but they did not have significant weakness. This study investigated whether there was central reorganization to compensate for their muscle strength. METHODS: TMS was applied to study the central compensative mechanism. The TMS parameters included motor evoked potentials, central conduction time, cortical silent period and intracortical inhibition of paired TMS paradigms. RESULTS: TMS results did not show any significant differences between patient and control groups. CONCLUSION: Although central reorganization may occur in patients with hereditary myopathy to compensate for muscular strength, our study did not find any change in cortical excitabilities in acquired myopathy due to colchicine. Muscle fatigue may precede weakness as an early symptom of myopathy.

Fatigue as the only clinical manifestation of colchicine induced myopathy.

PURPOSE: Fatigue may be induced by drug. Here, we reported that patients had fatigue after medication with colchicines. METHOD: Eight patients (8 Males, age: 42-72 years old) had fatigue but without weakness as their chief complaints. They all described an inability to maintain a sustained effort, which was ameliorated by rest. RESULTS: The course of fatigue was insidious and progressive (mean 3.1 2.3 months, range 1-7 months) along with medication of colchicines (mean 20.3 5.5 months, range 11-28 months). Fatigue severity scale (patient: before drug withdrawal 5.41 0.19; 4 weeks after drug withdrawal 2.46 0.28; control 2.12 0.45) showed fatigue as their most disabling symptom, sometimes preventing them to carry on professional as well as socio-familial activities. The plasma creatine kinase elevated in these 8 patients before withdrawal of colchicines and returned to normal range in each subject 4 weeks after drug withdrawal. A probable diagnosis of drug-induced fatigue was made when symptom subsided after colchicines were discontinued. CONCLUSION: It is emphasized that side effect of drug should be considered as a differential diagnosis of fatigue in patients having colchicines. Early recognition and diagnosis will prevent serious muscle damage.