Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical and epidemiologic analyses of PPMA in Japan based on the nation-wide case survey were reported, and differences between PPMA and ALS were discussed. The present survey covering the years from 1984 through 1991 cited 42 PPMA cases (30 male:12 female). The absolute incidence of PPMA is estimated 0.12/10(5) of the Japanese population (about 150 cases in total), which indicates 0.5% of the polio survivors. In Japan an actual increase of patients is noticed in these 10 years, which reflects the big epidemic of polio around 1950-60. The antecedent poliomyelitis occurred at the mean age of 2.6, mostly between 1940 and 1960. Residual paralysis was generally absent or only minimal. Late muscular atrophy and weakness were noticed at age from 16 to 63 y (mean:41.5), with the mean latency of 40.1 years after polio. Both polio-affected and unaffected site of the limb were equally involved by PPMA, but the left leg tends to be predominantly involved. Neurological symptoms were summarized as an asymmetrical proximal muscular atrophy and flaccid motor paresis in one or two limbs with decreased tendon reflexes. Fasciculation in 45.2%, myalgia in 28.6%, and hypesthesia in 28.5% were noticed. Electromyography and muscle CT scan showed marked selective neurogenic changes. In most cases symptoms are stable or slowly progressive, with some recovery by rest or rehabilitation and deterioration by over work and/or trauma. On regarding these clinical features, PPMA is essentially different from classical ALS. Long-term hyperfunction of survived neurons with potential fragility by polio infection is suspected to mediate PPMA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Post-poliomyelitis late progressive muscular atrophy (PPMA)--clinical analyses of Japanese cases]. 181 99

Postpolio syndrome is a group of related signs and symptoms occurring in people who had paralytic poliomyelitis years earlier. New weakness, fatigue, poor endurance, pain, reduced mobility, increased breathing difficulty, intolerance to cold, and sleep disturbance in various degrees and expressions make up the syndrome. The reported incidence is between 25% and 80%. The origins are multifactorial and can be associated with underexertion, overexertion, inactivity due to intercurrent illness or injury, hypo-oxygenation, sleep apnea, deconditioning, and the failure of sprouted, compensatory large motor units. The exercise question in postpolio syndrome is related to the experience of new weakness or loss of muscle function due to overuse, which is often associated with injudicious repeated challenges to weakened musculature. Carefully prescribed exercise can be used for increasing strength and endurance and improving cardiopulmonary conditioning.
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PMID:Postpolio syndrome and cardiopulmonary conditioning. 186 50

We describe a retrospective study of 42 patients admitted to Sunnaas Rehabilitation Hospital with suspect postpolio syndrome over a period of two years. The patients were 32 females and 10 males aged 28-74 years (mean 54 years). 29 were married or cohabitant, 31 had children, and 20 were in paid employment. The mean age at onset of polio was 12 years, with an average interval of 36 years between onset of polio and onset of new problems. The mean duration of new health problems was seven years. The most common such problems were pain in muscles and joints, general fatigue and new weakness of the muscles. 28 of the patients needed personal assistance to carry out everyday activities. 33 had braces, crutches or wheelchair for ambulation. Lung function was moderately reduced and physical working capacity was severely reduced. Physiotherapy, ergotherapy and technical aids were provided for 38 of the patients, 16 received assistance to organizing social support or help at home, 13 were helped to make practical changes in their homes, and eight were provided with a wheelchair. According to this study, most patients with the postpolio syndrome need interdisciplinary evaluation and management in a rehabilitation hospital.
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PMID:[42 patients with post-polio syndrome. A retrospective study from Sunnaas hospital]. 194 38

Many of the hundreds of thousands of survivors of polio are now developing postpolio syndrome. Symptoms include progressive muscle weakness, fatigue, decreased endurance, joint and muscle pain, weight gain, respiratory difficulties, and sleep disturbance, often precipitated or exacerbated by a Type-A Personality pattern. A postpolio patient with Type-A Personality was taught self-hypnosis as a vital component of treatment. Pre-post testing included the Profile of Mood States, the State-Trait Anxiety Inventory, the State-Trait Anger Inventory, and the Personal Orientation Inventory; the patient's spouse was interviewed during the follow-up. At the 6-month follow-up, improvements were documented in pain level, depression, self-regard, self-acceptance, capacity for intimate contact, time competence (living in the present), confusion, anxiety, insomnia, and in trait and state anger. Only a mild improvement occurred in fatigue, and no improvement was found in weight control. Follow-up at 12 months confirmed the maintenance of improvements. Self-hypnosis training may prove extremely helpful for postpolio patients and may prove helpful in modifying central characteristics of Type-A Personality.
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PMID:Hypnosis for postpolio syndrome & Type-A behavior. 195 Nov 42

A survey was conducted to better understand complaints of fatigue in patients previously diagnosed as having polio. Eighty-six individuals with postpolio syndrome and 20 healthy controls completed a questionnaire about their fatigue, the Beck Depression Inventory, and the CAGE questionnaire. The results showed that fatigue in postpolio syndrome usually occurred on a daily basis and increased in severity as the day progressed. Both the study group and controls described their fatigue as tiredness and a lack of energy. However, physical weakness was reported only in the postpolio group. Minimal physical exercise exacerbated fatigue in 48% of the postpolio group, whereas it diminished fatigue in 70% of the controls and in 15% of the postpolio group. Twenty-seven percent of the postpolio group and none of the controls reported mild to moderate depressive symptoms. However, depression, age, alcohol abuse, and employment status did not significantly affect the differences between groups in reported prevalence or description of chronic fatigue. Criteria to separate psychologic from organic causes of fatigue and treatment interventions are discussed.
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PMID:Fatigue in postpolio syndrome. 199 Oct 11

The effect of age on the ability of motor neurons to develop and maintain an enlarged total axonal and synaptic volume was compared in soleus muscles of 5-8-month and 25-30-month mice, 30-120 d after partial denervation. Before and after partial denervation (transection of the L5 root), the total number of muscle fibers was the same in all muscles. However, in young animals, there was only some transient atrophy and hypertrophy mostly receded by 120 d, whereas in old muscle, a more prominent early atrophy was followed by persistent hypertrophy. Ectopic endplates were not found. In zinc-iodide-osmium (ZIO) stained preparations, muscle fibers with small nerve terminals were present at 60 d and were still present in old muscle at 120 d. Fluorescent staining of nerve terminals and acetylcholine receptors revealed that in young muscle, postsynaptic sites were nearly or completely reoccupied by 60 d. In old muscle, about 22% of former junctions were denervated, with the remainder minimally to fully reinnervated. At 60 d and thereafter, collateral sprouts originated from nodes of Ranvier in both young and old muscle and were remyelinated in young but mainly unmyelinated and remarkably tortuous in old animals. These results, confirmed with immunofluorescent strains for myelin basic protein and neurofilaments, account for many of the physiological findings (Jacob and Robbins, 1990). Motor unit size expanded 2.5 times in young and 2 times in old muscle at 60 d after partial denervation. However, the increment in total quantal output and nerve terminal volume per motor neuron was 60-100% greater than control in young but only 20-25% greater in old muscle, with little further recovery. This inability of the motor neuron in old mice to expand the field of innervation may reflect a limitation imposed by reduced axonal transport. The present findings may elucidate the muscle weakness in postpolio syndrome and amyotrophic lateral sclerosis.
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PMID:Age differences in morphology of reinnervation of partially denervated mouse muscle. 233 95

Eighteen patients with old poliomyelitis were assessed in order to determine the incidence and severity of late complications. Sixty-one percent complained of new weakness, 83% fatigue and 17% muscle pain. After assessment 33% (six patients) were judged to have significant new weakness and muscle fatigue that could not be explained by other causes, and this group may have postpoliomyelitis progressive muscular atrophy or postpolio syndrome. Onset of symptoms was typically about 30 years after the acute illness; new weakness was relatively mild and progression was slow over many years. Clinically and pathologically this disorder is distinct from idiopathic motor neuron disease, and is not life threatening.
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PMID:Neuromuscular symptoms in patients with previous poliomyelitis: a New Zealand study. 252 9

The ventilator management protocol followed over the last 12 years in 23 patients with Duchenne muscular dystrophy (DMD) and six polio survivors with chronic respiratory failure (CRF) secondary to the late effects of poliomyelitis or postpolio syndrome (PPS) is reviewed. After the onset of respiratory failure, patients with DMD continued to show a classic course of progressive, generalized muscle weakness and a steadily declining vital capacity from an average of 482mL to 336mL. The DMD group required an average increase of 0.95 hours in their daily use of assisted ventilation per year. Their overall average length of survival was increased from 19 years 9 months to 25 years 9 months. Members of the postpolio group, to date, have shown no significant decrease in muscle strength nor have they needed more than nocturnal ventilation. Recommended evaluation and pulmonary follow-up for patients with CRF secondary to neuromuscular disease is outlined. Most of these patients can be managed for a number of years with body ventilators before a tracheotomy is necessary.
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PMID:Ventilator management in Duchenne muscular dystrophy and postpoliomyelitis syndrome: twelve years' experience. 264 55

This communication is in response to the article by Michael T Gross and Charles P Schuch entitled "Exercise Programs for Patients with Post-Polio Syndrome: A Case Report" published in the January 1989 issue of Physical Therapy. The investigators examined the effects of a rigorous isokinetic training program on peak torque of the knee flexor and extensor muscles of a post-polio patient. The literature on post-polio syndrome, however, does not support the use of either conventional muscle strengthening regimens or rigorous isokinetic exercise programs in the management of post-polio syndrome. In addition, based on the observation that there was no appreciable increase in muscle strength in either the affected or the apparently unaffected leg, the investigators concluded that their rigorous exercise program was not deleterious. The lack of a normal training response, however, is consistent with bilateral muscle fatigue secondary to overuse rather than muscle weakness secondary to disuse. This result is consistent with the need for a balance between rest and low-intensity exercise, which will help to maintain or enhance function while slowing rather than hastening further deterioration. We hope that this rejoinder clarifies some of the misconceptions that may arise from the Gross and Schuch article and that physical therapists consider very carefully the rationale for any type of exercise program for post-polio patients.
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PMID:A rejoinder to "Exercise Programs for Patients with Post-Polio Syndrome: a case report"--a short communication. 291 19

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


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