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)

A case of 55-year-old male with distal myopathy with rimmed vacuole formation is reported. He first noticed dragging of his legs at the age of forty-three. Two years later, he was evaluated to have muscle wasting and weakness in lower legs. In another ten years, he became unable to stand or walk unaided. On physical examination, proximal limb muscles were more severely affected than distal limb muscles. Notably, muscle strength of the quadriceps femoris muscles were weak (MRC Scale 3/5), compared to hamstrings, tibialis anterior muscle and gastrocnemius muscle (4/5). Serum creatine kinase, electromyography, nerve conduction velocities were all compatible with this diagnosis. A computed tomography of the musculoskeletal system was consistent with physical findings. Muscle biopsy revealed many fibers with typical rimmed vacuoles (approximately 6% of fibers). Additionally, small amount of ragged-red fibers (0.5%) was noted. Histochemical reaction showed a focal deficiency of cytochrome c oxidase. This case suggests that during the longstanding course of the illness, proximal limb muscles may be more severely affected, and quadriceps femoris muscle may be predominantly involved.
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PMID:[A case of distal myopathy with rimmed vacuole formation, progresses into proximal-dominant muscle involvement]. 133 27

The latencies and amplitudes of responses evoked by magnetic brain stimulation (magnetic evoked potentials, MEP) in the first dorsal interosseus and the anterior tibial (TA) muscles were investigated in 15 patients with psychogenic limb weakness and in 50 patients with limb weakness due to established organic central nervous system disease. Of the patients with psychogenic limb weakness, 3 presented with upper limb monopareses, 2 with lower limb monoparesis, 4 with hemipareses, 4 with parapareses and 2 with paraparesis. All patients with psychogenic weakness had MEP in arm and leg muscles with latencies within the normal range. MEP amplitudes were also normal except for 1 patient in whom the response amplitude in the TA of the plegic limb was reduced. In patients with limb weakness due to established organic disease, MEP were frequently but not invariably abnormal. In patients with plegic (i.e. completely paretic, MRC grade 0) muscles due to organic disease, MEP always were clearly abnormal. Normal MEP were sometimes elicited from paretic muscles, more commonly in association with cerebral hemisphere lesions than with spinal lesions. We conclude that psychogenic limb weakness is associated with normal MEP. However, normal MEP in mildly paretic muscles do not definitely exclude organic pathology.
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PMID:Motor responses evoked by magnetic brain stimulation in psychogenic limb weakness: diagnostic value and limitations. 160 85

A 24-year-old carpenter had the shakes and fever on March 13, 1990. He suffered from watery diarrhea on March 14 and 15. He left muscle weakness in his thumbs and fingers when he drove nails with a hammer on March 24. The weakness reached maximum by the 3rd day of illness. He was admitted to our hospital on day 4. Neurological examination revealed symmetrical weakness localized in the intrinsic hand muscles (MRC grade 2-4). The deep tendon reflexes were preserved. Sensation was intact except for mild disturbance of superficial sense on both plantar areas. Campylobacter jejuni was cultured from his stool. A complement fixation test indicated serologically preceding C. jejuni infection. Whereas maximum motor nerve conduction velocities were not reduced and distal latencies were not prolonged, compound muscle action potential recorded in the thenar and hypothenar muscles were remarkably reduced on day 5. Needle EMG showed neuropathic changes in four limbs. Sensory nerve conduction velocities and action potentials were normal. The weakness gradually improved in association with increased compound muscle action potentials in the thenar and hypothenar muscles. His muscle symptom fully resolved 2 months after the onset of his illness. Thin-layer chromatogram with immunostaining revealed that serum IgG from this patient reacted with GM1, GD1a, GD1b, but did not react with GM2 and GT1b. Enzyme-linked immunosorbent assay showed that anti-GM1, GD1a, GD1b antibodies titer (IgG) decreased concurrently with the clinical improvement.
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PMID:[An acute axonal polyneuropathy affecting intrinsic hand muscles following Campylobacter infection--a case report]. 162 53

In the present study, the toxic and immunosuppressive effects of three isolates of Fusarium moniliforme (MRC 826, MRC 1069, and RRC 408) in male White Leghorn chickens were investigated. Chickens were fed diets containing .5, 5.0, or 25% of F. moniliforme corn cultures for 6 wk. About 30% of the chickens fed RRC 408 had leg weakness. Relative weights of bursae of Fabricius were lower in birds fed all doses of MRC 826. Birds fed 5.0 or 25% MRC 1069 had lower relative spleen weights. Thymus weights were lower in birds fed .5 and 5.0% RRC 408, but not in those fed 25%. Immunosuppressive effects were determined by measuring serum levels of primary and secondary agglutinin responses to SRBC and Brucella abortus. Birds fed 5.0 or 25% MRC 826 were immunosuppressed, as shown by low antibody titers to B. abortus in both the primary and secondary responses. Isolate MRC 1069 caused a decrease in secondary response to SRBC at 25% and B. abortus at the 5.0 and 25% of culture material. The RRC 408 isolated reduced the secondary response to SRBC at all doses and response to B. abortus at 5.0 and 25% of culture material. These results appear to be the first report that feed contaminated with F. moniliforme can produce deficiencies in the immune system of chickens.
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PMID:Immunosuppressive effects of Fusarium moniliforme corn cultures in chickens. 178 Feb 60

Using standard electrophysiologic techniques motor conduction velocity (MCV), motor action potential amplitude (Mmax), minimum F latency (Flat), maximum F amplitude (Fmax), F chronodispersion (Fdisp), Fmax/Mmax, and F persistence (Fpers) were measured in median, ulnar, peroneal, and tibial nerves (N = 60) in 15 patients with myotonic muscular dystrophy (DM). The results were compared to data from 80 nerves in 20 healthy controls. The DM group (mean age = 39.7 yrs, mean duration of symptoms = 20.8 yrs) had diminished or absent biceps, triceps, knee, and ankle reflexes but retained 4- or better strength (modified MRC Scale) in the respective muscles. Thirteen nerves in 6 patients had absent F waves. For the remaining 47 nerves, no statistically significant difference was noted in parameters primarily related to conduction through peripheral nerve fibers (MVC, Flat, Fdisp) or Fmax/Mmax. Fmax, Fpers and Mmax were significant (p less than or equal to .02) diminished in all nerve subgroups in the DM patients. The results indicate that in DM there is altered excitability of the motorneuron pool. This may underlie the early loss of DTR's and produce the characteristic distal pattern weakness.
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PMID:Altered motor neuron excitability in myotonic dystrophy. 179 41

A 76-year-old man had progressive low back pain, leg weakness, and sensory loss. Radiology showed changes consistent with wide-spread Paget's disease, but no cord compression or involvement of nerve roots was detected by myelography or computerised axial tomography. His symptoms were relieved within 12 days of starting 100 MRC units of subcutaneous salmon calcitonin and recurred when calcitonin was discontinued for 5 days. The improvement continued on calcitonin treatment for 1 year, with falls in serum alkaline phosphatase and urinary hydroxyproline excretion. It is suggested that calcitonin treatment, in reducing the abnormally high metabolic activity of the diseased bone, and hence its vascular perfusion, allows more blood to reach the spinal cord.
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PMID:Spinal-cord syndrome due to non-compressive Paget's disease of bone: a spinal-artery steal phenomenon reversible with calcitonin. 610 24

Three patients with Hypokalemic Periodic Paralysis (HOPP)-associated progressive interattack muscle weakness, who became unresponsive or worsened by acetazolamide, responded favorably to dichlorophenamide, a more potent carbonic anhydrase inhibitor. Dichlorophenamide in single-blind placebo-controlled trials, considerably improved functional strength in two of the patients and had a moderate but definite effect in the third. Muscle groups graded 4/5 (MRC scale)returned to normal; very weak (0-3/5) atrophic muscles, improved to a minor degree. In one patient with acetazolamide-resistant paralytic attacks, dichlorophenamide also diminished the frequency and severity of the acute attacks. Dichlorophenamide had, in the present study, less effect than acetazolamide in reducing serum HCO3(-) and elevating Cl-. Its effectiveness may be related to the degree of sensitivity of certain HOPP patients to alterations of Cl- and/or HCO3(-) serum levels or to a different action of the drug unrelated to carbonic anhydrase inhibition or acidosis. Dichlorophenamide should be considered as an alternate to acetazolamide in the treatment of patients with HOPP-associated interattack muscle weakness who have become unresponsive or worsened by acetazolamide.
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PMID:Treatment of "permanent" muscle weakness in familial Hypokalemic Periodic Paralysis. 685 4

In most of the cases previously described, the defect on complex II was suggested by low activity of succinate cytochrome C reductase (SCCR). The clinical pattern of the previous 10 cases is heterogeneous and may be limited to one particular tissue or be of a more general nature. We report a 22-year-old-woman, daughter of consanguineous parents, with generalized muscle weakness, easy fatigability and benign course, who showed a decrease of SCCR activity in mitochondria of muscle fibers. Free carnitine (FC) concentration was decreased in muscle as well. The muscle biopsy showed a mild variation in fiber size, with fiber type I predominance, subsarcolemmal oxidative DPNH accumulations, excess of neutral lipids and abnormally large mitochondria with paracrystalline inclusions. A possible inheritance pattern is discussed. Coenzyme Q10 therapy in this patient induced a significant increase of global MRC index score and a decrease of the turns-mean amplitude ratio in the automatic analysis of the EMG.
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PMID:Benign mitochondrial myopathy with decreased succinate cytochrome C reductase activity. 783 16

The effect of asbestos-related pleural disease (ARPD) on the generation of maximum respiratory pressure was investigated in 11 male patients with ARPD mean age 57 years, range 45-74, and mean duration of asbestos exposure of 9.9 years, range 5-16. There were three smokers, seven ex-smokers and one non-smoker. Breathlessness ranged from grade 1-3 on the MRC score. The extent of pleural disease was calculated using a score based on the ILO score for pleural disease. Full respiratory function tests, global respiratory muscle strength and diaphragmatic strength were assessed. Respiratory muscle strength, including diaphragm strength, was normal. Recoil pressure was high or at the upper limit of normal in four patients and correlated with chest radiograph score for pleural disease (r = 0.65, P < 0.02). There was no difference in either global respiratory muscle or diaphragmatic strength between patients with and without involvement of one or both costophrenic angles or between patients with mild or severe breathlessness. We conclude that respiratory muscle strength is not importantly reduced in ARPD, and it is unlikely that weakness contributes to breathlessness in these patients. By contrast reduced chest wall compliance is likely to be an important factor in breathlessness in some cases.
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PMID:Respiratory muscle function in patients with asbestos-related pleural disease. 814 8

Based on the known trophic effects of growth hormone (GH) on nerve and muscle 75 patients with ALS were treated for up to 18 months with synthetic human growth hormone (Protropin) or a placebo. The course of ALS was assessed serially using a quantitative (TQNE) neuromuscular and manual exam (MRC) and laboratory chemistries. Average insulin-related growth factor (IGF-I) values increased from 1.2 to 2.3 U/mL in the treated group. Surprisingly, serum insulin levels did not increase. Hyperglycemia was noted in only 2 patients of the 38 patients receiving hGH, and this resolved with cessation of treatment. Over the 12 months of treatment there were 11 deaths (6 controls, 5 treated). Survival analysis, performed approximately 12 months following cessation of treatment, did not reveal a difference between the treatment and placebo group. The TQNE scores declined inexorably in both the control and treated group. Retrospective analysis of the TQNE data indicated a poor prognosis for patients who lost arm strength early. A correlation between the TQNE and MRC scores was evident at early stages of motor unit loss, less so when muscle weakness was advanced.
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PMID:Recombinant growth hormone treatment of amyotrophic lateral sclerosis. 850 60


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