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Query: UMLS:C0004134 (ataxia)
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The toxic effects of oral administration of Cassia occidentalis to goats was evaluated. The prominent signs of Cassia poisoning were diarrhea, inappetence, dyspnea, staggering, ataxia and recumbency. Lesions consisted of hemorrhages and congestion in the heart, lungs, abomasum and spleen, catarrhal enteritis, hepatic fatty change and necrosis, splenic hemosiderosis, pulmonary emphysema, necrosis and/or degeneration of the epithelial cells of the renal convoluted tubule, and packing of the glomeruli with endothelial and small round cells. These changes were accompanied by increases in GOT activity and in the serum concentrations of ammonia and urea, as well as by decreases in the total protein and calcium in serum. There were decreases in Hb, PCV and RCB, and increased leucocyte counts. Total lipids were higher in the liver, kidneys and heart of the Cassia-poisoned goats.
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PMID:The toxicity of Cassia occidentalis to goats. 713 98

Buflomedil was administered intravenously to rats at dosages of 1, 4, 12 or 30 mg/kg/day for up to three months. The no-adverse-effect dosage was considered to be 12 mg/kg/day. At 30 mg/kg/day several deaths and clinical signs, including ataxia, decreased activity, dyspnea and jerking movements after dosing, were observed. These were considered to result from the acute, exaggerated pharmacologic effects of buflomedil. Body weight gain and food consumption were decreased after six weeks in males at 30 mg/kg/day. Increases in the relative weights of the kidneys, brain and testes of males at 30 mg/kg/day were correlated with decreased body weight gain in this group. There were no effects on hematology or serum chemistry parameters, and no morphologic changes were found.
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PMID:Buflomedil: three month intravenous safety evaluation in rats. 716 13

In singly- and group-housed cats, an intraventricular injection of 6-hydroxydopamine (6-OHDA) in doses up to 1.0 mg, after a latent period of 1 to 3 days, evoked motor responses including tremor, ataxia, rigidity, weakness with adynamia and clonic-tonic convulsions. However, the intraventricular administration of 6-OHDA in a dose of 2.0 mg in group-housed cats, also after a latent period of 1 to 3 days, caused aggression, a restlessness, irritability, rage, fear, threat, attack, fighting and flight. These responses were accompanied by autonomic signs of mydriasis and dyspnoea and motor changes including tremor, ataxia, rigidity, weakness with adynamia and clinic-tonic convulsions. In the singly-housed cat only the latter motor phenomena were observed after the higher dose. Intraventricular injection of reserpine (0.5-1.0 mg) in both singly- and group-housed cats produced catalepsy, sedation, miosis, ptosis, defecation and micturition as well as motor responses of tremor, rigidity and akinesia. It is concluded that although 6-OHDA and reserpine evoke different behavioral effects, the motor changes are similar.
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PMID:Comparison of behavioral changes in cats treated with intracerebroventricular 6-hydroxydopamine and reserpine. 719 23

The effect of 6-hydroxydopamine (6-OHDA) injected into the cerebral ventricles on behaviour of singly- and group-housed cats was investigated. 6-OHDA in doses of 0.5, 1 and 2 mg was administered every morning for 5 to 8 days. In small doses 6-OHDA in singly- and group-housed cats evoked motor phenomena such as tremor, ataxia, rigidity, weakness and sometimes clonic-tonic convulsions. Occasionally restlessness, irritability and rage were observed. Large doses of 6-OHDA in group-housed cats, after a short latent period (2-3 days) produced aggression which intensified on subsequent injections, and thereafter, on repeated administrations, no longer occurred. The aggression consisted of restlessness, irritability, anger, rage, apprehension, threat, attack, fighting, flight and crying. Of autonomic phenomena mydriasis, dyspnea and sometimes piloerection were observed. The aggression was initiated by the most restless cat, or by disturbing the animals, such as by moving the cage. When 6-OHDA no longer produced aggressive behaviour, motor changes such as tremor, ataxia, rigidity, walking on broad base, weakness with adynamia and clonic-tonic convulsions developed. These latter symptoms were produced by large doses of 6-OHDA in singly-housed cats. In these animals spontaneous signs of aggressive behaviour usually were not observed, although if handled they showed rage, snarling and hissing. When singly-housed cats were kept in the same cage with group-housed animals, the singly-housed cats usually became aggressive. It appears that hyperactivity induced aggression in 6-OHDA-treated cats.
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PMID:6-hydroxydopamine and aggression in cats. 719 85

T-2 toxin was given to cats every other day per os to evaluate the suitability of this species as a model for the human disease, alimentary toxic aleukia. The chronic lethal intoxication resulting was characterized by pancytopenia, hemorrhagic diatheses, bone marrow aplasia, diminished hemostasis, severe lymphatic tissue alterations, and histopathologic changes in proliferative tissue. Clinical signs included vomiting, bloody feces, weakness, lassitude, ataxia, dyspnea, dehydration, loss of weight, and pre-terminal anorexia. The clinical course, hematologic picture, and the gross and microscopic tissue changes seen in the experimentally produced disease in cats were similar to alimentary toxic aleukia, a frequently fatal mycotoxin induced disease of man.
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PMID:Experimental alimentary toxic aleukia in cats. 719 59

Clinical signs and lesions of levamisole toxicosis include: nausea, vomiting, increased salivation, frequent urination and defecation, colic, dizziness, headache, muscle tremors, ataxia, anxiety, hyperesthesia with irritability, clonic convulsions, depression, rapid respiration, dyspnea, prostration, collapse, hemorrhages in the subepicardium and thalamus, enteritis, hepatic degeneration and necrosis, and splenic congestion. Most of these signs and lesions are similar to those observed in nicotine poisoning. Levamisole causes vasopressor and panting effects which are blocked by ganglionic blocking agents hexamethonium and mecamylamine but are not blocked by atropine. The vasopressor effect of levamisole is blocked by alpha-adrenergic antagonists phentolamine and dibenamine; however, the respiratory effect of levamisole is not affected by these alpha-adrenergic antagonists. Repeated IV injections of levamisole cause a tachyphylactic response. With levamisole-induced tachyphylaxis, the effects of other ganglionic stimulants dimethylpiperazinium and nicotine are also abolished. Levamisole causes an electroencephalographic arousal which is antagonized by atropine sulfate and mecamylamine. There is also a structural similarity of levamisole to nicotine. These studies suggest that levamisole is a nicotine-like compound. Possible treatment of levamisole poisoning is discussed. Drug interactions of levamisole with organophosphates and anthelmintics, eg, pyrantel, methyridine, and diethylcarbamazine, are also discussed.
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PMID:Toxicity and drug interactions of levamisole. 721 95

We report a 55-year-old man with papilledema and multiple cranial nerve palsies. He was well until 52 years of age when there was an onset of progressive difficulty in initiating urination; he visited the urology service of our hospital where a diagnosis of prostate cancer was made; the cancer was invading the bladder and was metastasizing to lymph nodes and bones. He was treated with oochiectomy and estrogen preparations with some improvement in his symptoms. Two years later, he developed difficulty in urination again, and transurethral resection of the tumor was performed in 1991. In December 1991, he noted tingling and numb sensation in his left face, which had become progressive worse within the next one month, and he developed blepharoptosis and deafness all on the left side. He was admitted to the urology service on February 4, 1992, and a neurological consultation was asked. On physical examination, general findings were unremarkable, except for lymph node enlargements of about 0.5 to 1.0 mm in size in cervical and inguinal regions. On neurologic examination, he was alert with normal mental activities; higher cerebral functions were intact. He had normal vision and visual fields, however, papilledema was present bilaterally; pupils and light reactions were normal. Extraocular muscles were intact on the right side, however, moderate restriction was noted in the left eye in that all the extraocular muscles except for the medial rectus were weak; blepharoptosis was noted on the left; no nystagmus was present. The sensation was diminished in the left face, and left facial paresis of the peripheral type was also noted; the taste sensation was also diminished in the left anterior two thirds of the tongue. He had sensorineural deafness on the left side. The other cranial nerves appeared intact. He walked normally; no weakness or muscle atrophy was noted; muscle tone was normal and no ataxia was observed. Deep reflexes were normally elicited and symmetric; the plantar response was flexor. No meningeal signs were present. Laboratory examination revealed following abnormalities: Hb 7.1 g/dl, platelet 47,000/cmm, WBC3,800/cmm, LDH 950IU/l, PAP232ng/ml (normal less than 1.6), PA2.631ng/ml (normal less than 7.4); a small amount of effusion was noted in the left pleural cavity; cytological examination of the fluid was class V. A cranial CT scan as well as MRI were entirely normal, as was the spinal tap. He was treated with glycerol, however, there was progressive increase in the pleural effusion, and he developed dyspnea; moist rale had become audible in the end of February.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 55-year-old man with prostate cancer, papilledema, and multiple cranial nerve palsies]. 794 37

Between 1983 and 1990 a total of 74 freestyle mountaineers and 88 mountaineers with skis attempted to climb Mount Agri (Ararat). From the freestyle group two mountaineers were affected by acclimatisation disorder at 3200 m and seven at 4200 m above sea level. Acute mountain sickness (AMS) affected four mountaineers at 4200 m, eight at 4700 m, two at 5000 m and two at 5165 m, while 49 reached the summit. Only one of the mountaineers with skis was affected by AMS (at 4200 m), while all the others reached the summit. The symptoms of acclimatisation disorder and AMS, according to their degree of frequency, were headache, weakness, dyspnoea and palpitation, anorexia, nausea, vomiting, giddiness, ataxia and insomnia. Pulse rates varied between 115 and 124/min, and breathing between 30 and 38/min.
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PMID:Cases of acute mountain sickness on Mount Agri. 803 91

The authors' primary purpose was to identify home healthcare needs of adults (N = 244) living with HIV disease/AIDS. The study followed a retrospective chart review of a stratified random sample of cases discharged during 1991 from a certified home health agency (CHHA) in New York City. Frequently observed signs and symptoms included dyspnea, weakness, fatigue/lethargy, pain, ataxia, cough, skin lesions, and memory deficit. Additional problems identified included inadequate nutrition, issues related to compliance with prescribed medications, inadequate in-home support systems, inadequate facilities/utilities in the home, financial concerns and lifestyles that included drug/alcohol abuse and tobacco use. The results suggest that the health care needs of people living with HIV disease/AIDS in the home care setting are multifaceted and extend beyond the clinical manifestations of HIV disease.
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PMID:Home healthcare needs of adults living with HIV disease/AIDS in New York City. 803 11

Toxic effects and excretion in urine of 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX), the potent mutagenic compound in chlorinated drinking water, was evaluated in male Wistar rats by the up-and-down method. MX was dosed by gavage in deionized water at doses between 200 mg/kg and 600 mg/kg, for one animal at a time, and effects were observed for 14 days. Urine was collected in metabolism cages up to 72 h after dosing for chemical analysis of MX in urine. The animals receiving 200 mg/kg did not display clear clinical signs but at higher doses the signs of ill effects included dyspnea, laborious, wheezing and gasping breathing, decreased spontaneous motor activity, ataxia, nostril discharges, catalepsia and cyanosis. In necropsy bronchi contained foamy liquid and the lungs appeared edematous and spongy. The stomach cavity was expanded due to accumulation of fluid and gas and the gastrointestinal tract from stomach to caecum was reddish. Microscopically, the main target organ of toxicity was the gastrointestinal tract (diffuse congestion and necrosis in the mucosa). Signs of toxicity were recorded also in lungs (slight edema) and kidneys (dilated tubules, thin tubular epithelium, brownish tubular and interstitial concretion). The LD50 in 48 h was 230 mg/kg. Only 0.03-0.07% of the dose (200 mg/kg or 300 mg/kg) was excreted in urine as intact MX. The results indicate that at high doses MX has a strong local irritating effect in the gastrointestinal tract and it probably increases liquid permeability in lungs. MX may also cause tubular damage in kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Toxic effects and excretion in urine of 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX) in the after a single oral dose. 809 31


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