Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0392674 (exhaustion)
 13,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with late effects of poliomyelitis, i.e., PPS, are being seen at an ever increasing frequency by general physicians, neurologists, and orthopedists. An appropriate time interval for the onset of late manifestations has elapsed since the major epidemics of poliomyelitis in the 1940s and 1950s. Post-polio neurological manifestations primarily include new weakness, atrophy, muscle pain, and fasciculations. Fortunately, the weakness is of a very slow, progressive nature. Abnormal laboratory studies include routine EMG, demonstrating chronic denervation; SFEMG, demonstrating increased fiber density, increased jitter, and blocking; and muscle biopsy most often revealing fiber-type grouping of chronic denervation and small isolated angular (or angulated) fibers and group atrophy in some series, both suggestive of active denervation. Unfortunately, both EMG and muscle biopsy studies suffer from a lack of specificity as they do not appear to distinguish asymptomatic from symptomatic (new weakness, PPMA) patients with prior poliomyelitis. Although the cause of PPMA is unknown, electrophysiological (SFEMG) and muscle biopsy studies suggest that the process involves a loss or dropout of axon terminals of reinnervated motor units. The axons terminal dropout could be due to dysfunction in the cell soma, the axon, or the terminals themselves. Whether motor neuron exhaustion, a persistent viral infection, or immune-mediated mechanisms play a role in the pathogenesis of the late weakness is unclear at present and will require further investigation. Treatment at this time is of a supportive nature. A major controversy involves the role of strengthening exercises in these patients since experimental animal studies suggest that excessive exercise of denervated muscles leads to increased weakness. Clearly, a better understanding of PPS and PPMA will allow more effective management of these patients' problems and might also provide insight into other motor neuron and neuromuscular junction diseases.
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PMID:Neurological manifestations of the post-polio syndrome. 331 37

The PPS is now a well-recognized entity encompassing the late manifestations that occur because of previous poliomyelitis. Common signs and symptoms include fatigue, cold intolerance, joint deteriorations with pain, and prominent neurologic problems that include new weakness, muscle pain, atrophy, respiratory insufficiency, dysphagia, and sleep apnea. It is estimated that there are 1.63 million polio survivors in the United States and that half of them will develop PPS. PPS and PPMA usually begin 30 to 40 years after the acute illness and are very slowly progressive. The etiology is unclear, although premature exhaustion of the new sprouts that develop after acute poliomyelitis and of their motor neurons appears most likely. Less likely is a persistent polio-virus infection or an immune-mediated problem. Treatment is primarily supportive, although nonfatiguing strengthening exercise may improve strength over the short term. The long-term effects of this type of exercise remain to be clarified.
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PMID:Post-polio syndrome: an update. 827