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)

Solvents were tested for their influence on motivational state, as well as for their sedative effects, after intraperitoneal administration. The following tests were used: open field (exploratory activity, locomotion), activity wheel (running activity), tube test and tilted plane (muscle weakness, incoordination). The agents proved to be similar in causing muscle weakness and ataxia already at low dose levels. Benzene was the most potent in this respect. The three solvents, however, contrasted strongly in influencing motor activity. While benzene and especially toluene exerted CNS stimulation, no such effect could be detected following m-xylene treatment. On the basis of human experiences with these substances it may be suggested that the screening procedure applied in rats might be useful for predicting acute adverse effects in man.
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PMID:Comparative study on the acute effects of benzene, toluene and m-xylene in the rat. 717 Sep 84

The adhesion molecule on glia (AMOG) has been reported to function as cell adhesion molecule and also to constitute the beta 2-subunit of the murine Na,K-ATPase. In order to elucidate these functions in vivo, Magyar et al. have generated mice carrying a targeted deletion of the AMOG gene. These mice exhibit behaviourally normal development till postnatal day P16. At this time, they develop muscular weakness, incoordination, and tremor. Death invariably occurs 24-36 hours after onset of the symptoms. Histological and ultrastructural examination of brain sections show enlarged ventricles, brain edema, and swelling of astrocyte end feet. However, no disturbances of the architecture or cell migration in the brain can be detected. In order to identify long-term consequences of AMOG deficiency which might not yet be detectable at the time of death, we have established a CNS grafting model. The embryonal brain anlage (E10.5-E13.5) was grafted into the caudoputamen of wild type mice. The graft recipients are sacrificed up to 7 months after the procedure. Both wild type and AMOG deficient grafts develop and form solid neural tissue with neurons, myelinated axons, glial cells, and ventricular structures, as shown by histological and immunocytochemical analysis. However, no differences in grafts derived from wild type, heterozygous, and AMOG-deficient donors can be detected. Proliferation has been examined by BrdU immunocytochemistry. The blood-brain barrier as examined by repeated magnetic resonance imaging after injection of Gadolinium-DTPA has been shown to be largely reconstituted five weeks after grafting.
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PMID:[Morphology and development of neural transplants of AMOG-deficient mice]. 753 17

Excessive unexplained mortality was observed in flocks of double-crested cormorants located at Snake Island in Green Bay, Michigan, in June 1992. Clinical signs included weakness, lethargy, diarrhea, respiratory distress, paralysis of the wings and legs, torticollis, and incoordination. The most significant and consistent gross lesions included edema of the eyelids and periocular tissues, pulmonary edema and congestion, marked splenomegaly, hepatic necrosis, and scattered hemorrhages in visceral organs. Histologically, the principal alterations were severe lymphocytic meningoencephalitis and myelitis, as well as splenic lymphoid necrosis with hemorrhage. A type 1 paramyxovirus was isolated from the affected birds and characterized as a velogenic neurotropic strain of Newcastle disease virus. Since the infection occurred in free-living migratory birds, there exists the potential for spread of the virus over a large area, thus posing a hazard to domestic poultry.
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PMID:Neurotropic velogenic Newcastle disease in cormorants in Michigan: pathology and virus characterization. 770 23

An outbreak of neurological disease in 2 1/2-to-3 1/2-week-old male turkey poults was diagnosed morphologically as nutritional encephalomalacia. About 20 to 30% of the flock of 6360 showed clinical signs, which included going down with legs extended or hock-sitting and inability to get up, incoordination, weakness, staggering, trembling, torticollis, and opisthotonus. The most important gross postmortem changes were found in the brain, which consisted of an enlarged and swollen cerebellum with focal and/or diffuse hemorrhages. Major histopathological alterations included congestion, hemorrhages, necrosis, and malacia associated with hyaline capillary thrombi affecting the cerebellar cortex and adjacent white matter. Except for a slightly higher mortality, flock performance compared favorably with performance of other flocks grown in the same farm as well as with the national average for market tom turkeys.
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PMID:Nutritional encephalomalacia in turkeys: diagnosis and growth performance. 783 24

Four 4-5-y-old cows out of a group of 20 developed a toxic myopathy approximately 10 d after being started on a ration contaminated with 21.5% Senna occidentalis beans. Clinical signs included progressive muscle weakness, incoordination of hindlimbs, reluctance to move, dragging of the tip of the hooves of the hindlimbs, and sternal and lateral recumbency. Gross lesions included white to whitish-yellow discolored areas of several groups of skeletal muscle in various regions of the body, but more markedly in the hindlimbs. Significant histopathological changes were restricted to skeletal muscles with variable degrees of segmental degenerative myopathy associated with reparative events. The earliest change seen at electron microscopy of affected skeletal muscles was mitochondrial swelling. More advanced changes ranged from disruption of sarcoplasm and myofibrils to complete lysis of a myofiber segment and early regeneration. Myocardial fibers had swollen mitochondria, disruption of cristae and dense matrical globules. The epidemiology, clinical data and gross, histopathological, and ultrastructural features of S occidentalis poisoning in cattle are presented.
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PMID:Coffee Senna (Senna occidentalis) poisoning in cattle in Brazil. 790 Feb 75

A 45-year-old woman was administered oral and intravenous diphenhydramine 25 mg for the treatment of an allergic reaction. Within 2 minutes she rapidly developed trismus, dysarthria, tremors of the upper extremities, left-sided weakness, and diminished consciousness. She was treated with intravenous diazepam and benztropine with good response. After approximately 12 hours the patient's condition was completely resolved except for minor subjective weakness of her left extremities. Her hospital stay was uneventful, and she was discharged after 4 days after refusing rechallenge with the drug. Several cases of acute dystonic reactions secondary to antihistamines have been reported in the literature, four of which involved diphenhydramine. Such reactions may occur after short- or long-term therapy. Most patients experienced rapidly developing trismus, facial dystonia, dysarthria, and occasionally, decreases in consciousness, motor incoordination, and weakness. Because of the widespread availability of diphenhydramine and other antihistamines to the general public, awareness of this effect is of great importance.
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PMID:Diphenhydramine-induced acute dystonia. 793 88

A 4-month-old female kitten developed generalized ataxia, mild tremors, weakness, incoordination, and miosis after receiving an injection of ivermectin (0.3 mg/kg of body weight, SC) for treatment of ear mite infestation. The kitten became comatose within 12 hours, and despite supportive treatment, died 7 days after administration of ivermectin. Caution should be exercised when this drug is administered parenterally to kittens.
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PMID:Ivermectin toxicosis in a kitten. 796 Oct 95

A 25-year-old man with symptomatic tethering of the cerebellum is presented. At the age of 8 days, the patient underwent a limited repair of a posterior fossa encephalocele. He was well until the age of 24 when he began to experience paroxysms of extremity weakness, progressive incoordination, and pain at the base of the skull. Imaging demonstrated a connection between the cerebellar vermis and the subcutaneous tissue underlying the site of the previous encephalocele repair. Exploration of the area with the release of a fibrous stalk resulted in the rapid resolution of the patient's symptoms.
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PMID:Symptomatic tethering of the cerebellar vermis: case report. 812 57

In 11 patients with moderately severe multiple sclerosis, lasting 11.2 +/- 7.3 years, in stable condition, and in 10 age- and sex-matched control subjects, we investigated lung function, respiratory muscle strength, and ventilatory control system. Respiratory muscle strength was assessed by measuring maximal inspiratory and expiratory mouth pressures (Pimax and Pemax, respectively). Respiratory central drive was evaluated in terms of neuromuscular (P0.1) and ventilatory (Ve) output, breathing room air and during CO2 rebreathing. In the absence of any significant impairment of lung function, patients showed a reduction of Pimax and Pemax amounting to about 40 percent and 60 percent of the predicted value at functional residual capacity (FRC), respectively; a significant, inverse correlation was found between both Pimax and Pemax at FRC and the severity score of the disease. While at rest Ve was similar to that of control subjects, baseline P0.1 was significantly higher in patients (1.97 +/- 0.79 vs 0.97 +/- 0.20 cm H2O, p < 0.005). Compared with the control group, during CO2 rebreathing P0.1/PetCO2 slope, although less steep, was not dissimilar in patients (0.34 +/- 0.13 vs 0.46 +/- 0.19 cm H2O/mm Hg, NS); on the other hand, Ve/PetCO2 slope was much lower in the patient group (1.93 +/- 0.91 vs 3.27 +/- 1.11 L/min/mm Hg, p < 0.01) and was significantly related to the functional stage of disease and to Pimax and Pemax values at FRC. These results indicate that in patients with clinically stable, moderately severe multiple sclerosis, the respiratory muscle function is abnormal. Moreover, the inspiratory drive at rest is increased and the drive response to CO2 appears normal, while the ventilatory response to CO2 is significantly impaired. Respiratory muscle weakness (and/or lack of coordination) could explain, at least in part, the lower ventilatory response in these patients, whereas the mechanism of increased rate of the initial inspiratory force generation remains unclear.
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PMID:Control of breathing and respiratory muscle strength in patients with multiple sclerosis. 816 44

Cases of melaleuca oil toxicosis have been reported by veterinarians to the National Animal Poison Control Center when the oil was applied dermally to dogs and cats. In most cases, the oil was used to treat dermatologic conditions at inappropriate high doses. The typical signs observed were depression, weakness, incoordination and muscle tremors. The active ingredients of commercial melaleuca oil are predominantly cyclic terpenes. Treatment of clinical signs and supportive care has been sufficient to achieve recovery without sequelae within 2-3 d.
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PMID:Toxicity of melaleuca oil and related essential oils applied topically on dogs and cats. 819 16


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