Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 41 year old man developed a myolysis with myoglobinuria during a period of high fever. The clinical signs were severe myalgia with general muscular weakness without manifest localized paresis. Electromyographically a diffuse generalized floride myopathy was found. Besides the extreme increase of CPK, a myoglobinuria was already macroscopically visible, which caused an acute renal failure. The treatment included corticosteroids and hemodialysis. An illness of several weaks was followed by complete recovery. As other known factors leading to myoglobinuria have been excluded, and the complement fixation reaction for Herpes simplex was more than 1:80, a viral-toxic etiology of this disease might be considered.
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PMID:[Acute myoglobinuria accompanied by renal failure in high febril infection (author's transl)]. 126 94

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

Capillary supply and oxidative and glycolytic enzyme activities were determined in muscle biopsies from the tibialis anterior muscle in six prior polio patients and a control group. The polio patients, who had paresis and atrophy, but were able to walk normally by making maximal use of all remaining anterior tibial motor units, showed type I (slow-twitch) muscle fibre predominance with a mean (SD) of 98 (2%) type I fibres versus 81 (8)% in the controls (p less than 0.01) and muscle fibre hypertrophy, the average type I fibre cross-sectional area being 108% (p less than 0.005) larger than in the controls. The number of capillaries per muscle fibre was not significantly different from that in the control group, but with the increased muscle fibre area in the polio patients, the capillary density was significantly lower. The number of capillaries in contact with type I fibres relative to fibre area was 40% lower in the patients than in the controls (p less than 0.005). The levels of citrate synthase and phosphofructokinase were significantly lower (38% and 33%, respectively, p less than 0.05) in the patients than in the controls, indicating decreased oxidative and glycolytic potentials in the muscle fibres of the polio patients. It is proposed that the abnormal high-frequency activation of all remaining motor units during each step cycle recorded in these patients constitutes a stimulus for type I muscle fibre predominance and hypertrophy but that the overall low muscle usage results in a decreased stimulation of capillary proliferation and mitochondrial enzyme synthesis. The low capillary density and decreased oxidative and glycolytic enzyme potentials might be important factors for the development of muscle weakness, fatigue and muscle pain, which are commonly occurring symptoms in patients with prior poliomyelitis.
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PMID:Prior poliomyelitis-reduced capillary supply and metabolic enzyme content in hypertrophic slow-twitch (type I) muscle fibres. 203 Mar 51

Carnitine is a carrier for the transport of long-chain fatty acids from the cytoplasmic to the mitochondrial space. So far 18 cases of carnitine deficiency myopathy have been recognized, generally occurring as progressive or relapsing myopathy. In contrast episodic exercise-induced myalgia and paresis was found in a 46-year-old patient with carnitine deficiency myopathy which was quickly reversible at rest. As a consequence of this observation carnitine deficiency myopathy must be added to the differential diagnosis of the McArdle syndrome (muscular phosphorylase deficiency) and other "exercise myopathies".
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PMID:[Carnitine deficiency myopathy (author's transl)]. 736 6

Two human ehrlichioses occur in the United States: human monocytic ehrlichiosis (HME), which is caused by Ehrlichia chaffeensis that infects mononuclear phagocytes in blood and tissue, and human granulocytic ehrlichiosis (HGE), an infection of granulocytes that is caused by a similar but phylogenetically distinct organism. The clinical features of both forms of human ehrlichiosis are identical and include nonspecific constitutional manifestations, such as fever, headache, malaise, nausea, vomiting, myalgia, and anorexia; however, rare patients develop neurologic symptoms and signs. Few cases of human ehrlichiosis have been described in detail, and focal neurologic deficits have only rarely been reported in such cases. We describe a patient with HME who developed a trochlear nerve paresis associated with evidence of lymphocytic meningitis during the course of her illness. We believe this to be the first well-documented case of a focal neurologic complication of human ehrlichiosis.
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PMID:Fourth nerve palsy caused by Ehrlichia chaffeensis. 909 62

We describe a case of a 39-year-old male, who initially presented with severe muscle pain, fever, shortness of breath and tachycardia. He was admitted to hospital with suspected myocarditis. The next days he developed a generalized icterus and acute renal failure. Suspecting leptospirosis an intravenous therapy with penicillin was started. Due to pulmonary and circulatory insufficiency intensive care was necessary. In course the patient developed all known manifestations of leptospirosis including, cardiac arrhythmia and asystolia due to AV-block III degrees, recurrent atelectases of the lungs, hyperbilirubinemia, thrombocytopenia, hepatitis, pancreatitis, very severe rhabdomyolysis and polyradiculitis with areflexia and tetraplegia. Additionally, the patient had a transient hyperthyreosis, which has not been described in the literature so far. After 33 days the patient left the intensive care unit and was discharged out of hospital a fortnight later. 4 weeks later he was able to return to work. The only residuum of this illness is a partial paresis of his right quadriceps muscle.
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PMID:[Fulminant course of leptospirosis complicated by multiple organ failure]. 1155 63

A growing number of therapeutic agents and exogenous toxins are harmful to structure and function of human skeletal muscle. The clinical syndrome encompasses asymptomatic creatine kinase elevation, myalgia, exercise intolerance, muscle paresis and atrophy, and lastly acute rhabdomyolysis. Toxic myopathies are potentially reversible, hence a prompt recognition is particularly helpful for the early diagnosis and in conclusion elimination of a myopathy inducing toxin. Toxic myopathies may be classified as acute or chronic accordingly to the exposition time to a toxin. Main source of an exogenous induced toxic myopathy is chronic alcohol abuse. Alcohol excess induces acute and/or chronic neuropathy and myopathy, consequently muscle wasting and weakness occurs. Drug-induced myopathies are most frequently seen due to amplified utilization of corticosteroids or lipid lowering agents.
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PMID:[Lipid lowering drug and other toxic myopathies]. 1615 87

Myotonic Dystrophy Type 1 (DM1) and 2 (DM2) present with distinct though overlapping clinical phenotypes. Comparative imaging data on skeletal muscle involvement are not at present available. We used the novel technique of whole body 3.0 Tesla (T) Magnetic Resonance Imaging (MRI) to further characterize musculoskeletal features in DM2 and compared the results with DM1.MRI findings of 15 DM1 and 14 DM2 patients were evaluated with respect to patterns of skeletal muscle affection and clinical data using the Muscular Impairment Rating Scale (MIRS) and Medical Research Council scale (MRC). All DM1 patients had pathological MRI compared with only 5 DM2 patients. In contrast to DM2, DM1 patients showed a characteristic distribution of muscle involvement with frequent and early degeneration of the medial heads of gastrocnemius muscles, and a perifemoral semilunar pattern of quadriceps muscle affection sparing the rectus femoris. The most frequently affected muscles in DM1 were the medial heads of gastrocnemius, soleus, and vastus medialis muscles. In DM2, however, the erector spinae and gluteus maximus muscles were most vulnerable to degeneration. MRI data were in line with the clinical grading in 12 DM1 and 3 DM2 patients. In 3 DM1 and 5 DM2 patients, MRI detected subclinical muscle involvement. 9 DM2 patients with mild to moderate proximal muscle weakness and/or myalgias had normal MRI. Pathological MRI changes in DM2 emerged with increasing age and were restricted to women. Whole body 3.0T MRI is a sensitive imaging technique that demonstrated a characteristic skeletal muscle affection in DM1. In contrast, MRI was no reliable indicator for skeletal muscle involvement in mildly affected DM2 patients since myalgia and mild paresis were usually not reflected by MRI signal alterations.
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PMID:Distinct neuromuscular phenotypes in myotonic dystrophy types 1 and 2 : a whole body highfield MRI study. 1651 50

Tick-borne borreliosis (Borrelia burgdorferi) is a common and complex disorder affecting the skin, the joints and the nervous system. It progresses through different clinical stages. The clinical spectrum of neuroborreliosis has expanded since the introduction and widespread application of specific serological tests. We have investigated 41 patients with Bannwarth's meningopolyneuritis (MPN) as the classical form of neuroborreliosis, in a prospective (26 patients) and a retrospective (15 patients) study. When questioned, 19/41 patients reported a tick bite and only 15/41, erythema migrans as the characteristic early skin lesion. In 34/41 patients typical MPN characterized by painful radiculoneuritis and/or cranial neuritis, especially facial palsy, were seen. Among these, 3 had a complicated form with a progressive remitting relapsing course or focal central nervous system involvement (hemiparesis, cerebellar syndrome); 2 had mild meningitis and facial nerve palsy bilaterally without radicular pain; and in 5 radicular pain was the only symptom. MPN associated with Lyme arthritis was observed only once. In 2 patients in the retrospective study (no antibiotics in the acute stage) we saw a chronic spinal cord disorder with spastic paresis several years after uncomplicated MPN, accompanied in 1 of them by acrodermatitis chronica atrophicans (ACA), the typical late-onset borrelia-induced dermatosis. In the acute stage of the disease 40/41 patients had a cerebrospinal fluid (CSF) syndrome compatible with MPN (mononuclear pleocytosis, blood-brain barrier dysfunction, elevated IgG and/or oligoclonal bands). IgG antibody titers against borrelia antigen were elevated in all patients in the serum and in 21/30 also in the CSF. In all patients pain was an early and prominent symptom; the first symptoms are usually felt in the region of the tick bite or the erythema, initially as diffuse myalgia, arthralgia or pain in the connective tissue. In the further course the migrating pain becomes more radicular in character, without being limited to defined dermatomic areas or peripheral nerves. The intense, burning pain is characterized by exacerbation during the night. Peripherally and centrally acting analgesics have only minor effects. Often neurological deficits are still absent at this time. Erythema migrans with radicular pain in the region of the dermatological lesion was observed in 2 patients. This is an early manifestation of MPN. After MPN and/or Lyme arthritis a sympathetic reflex dystrophy (SRD) developed in 2 patients. In a further patient SRD was observed right at the beginning of the illness, immediately before MPN. There is a close clinical similarity between SRD and the acute stage of ACA. Therefore, borreliosis can be assumed to produce a painful skin dystrophy like SRD or ACA by direct injury to the sympathetic nerves even in the early clinical stage of the infection. The main conditions to be considered in the differential diagnosis are polymyalgia rheumatica; lumbar disk herniation; inflammatory radiculopathies of other origin (e.g. herpes zoster); painful neuropathies, including the diabetic thoraco-abdominal form; internal disorders of chest and abdomen with referred pain; lymphocytic meningitis of other origin, encephalomyelitis; and sympathetic reflex dystrophy. High-dose penicillin G i.v. is a potent analgesic in all patients with tick-borne neuroborreliosis.
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PMID:[Pain syndromes in tick-borne neuroborreliosis. Clinical aspects and differential diagnosis.]. 1841 56

Propylthiouracil (PTU) is a frequently prescribed drug in the treatment of hyperthyroidism. The use of PTU is, however, accompanied by numerous potentially serious side effects including vasculitis. PTU-related vasculitides can present as haematuria, pulmonary haemorrhage, or cutaneous lesion together with aspecific symptoms such as fever, myalgia, arthralgia, and fatigue. Cerebral involvement is seldom observed. We present a 49-year-old female with Graves' disease and asthma, who developed paresis of the proximal extremities, eosinophilia, pulmonary, and cutaneous lesions following treatment with PTU. A cerebral vasculitis consistent with Churg-Strauss syndrome (CSS) was suspected. Although cerebral involvement is seldom observed with PTU treatment, cerebral vasculitis should be considered in patients developing CNS symptoms.
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PMID:Churg-Strauss Syndrome following PTU Treatment. 2010 67


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