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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ability of a supralethal dose of chlorpyrifos to produce delayed neuropathy was examined using assessments of clinical signs, electromyography (EMG), motor nerve conduction velocity (MNCV), lymphocyte neuropathy target esterase activity (LNTE), and histologic changes in nervous system tissues. Cats were exposed to a single, im injection of corn oil (vehicle control), DFP (positive control) at 5.0 mg/kg, or chlorpyrifos at 300 mg/kg and observed for 60 days. Atropine and 2-PAM were administered to chlorpyrifos exposed cats one to two times a day for 14 to 24 days in response to the appearance of cholinergic signs. Anorectic cats during the acute toxicosis were force fed by hand and hydration was maintained by administering fluids sc. Onset of ataxia (mean +/- SD) for the positive control and chlorpyrifos exposed cats were 16.2 +/- 1.8 days (range of 14-19 days) and 19.0 +/- 1.4 days (range of 17-21 days), respectively. Functional deficits for both groups were confined to the hindlimbs and characterized by a crouched-waddling gait, hypermetria, and proprioceptive deficits. Maximal inhibition of LNTE activity was 96% at 24 hr postdosing in the positive control group and 46% at 7 days postdosing in the chlorpyrifos group. No EMG or MNCV abnormalities were detected in any of the treatment groups. Axonal degeneration was similar for the positive control and chlorpyrifos exposed cats. Ascending tracts of the cervical spinal cord and descending tracts of the thoracic and lumbar spinal cord were most severely affected and peripheral nerves were only mildly affected. The clinical and histologic effects produced indicate that chlorpyrifos can cause delayed neuropathy in the domestic cat. The moderate but prolonged inhibition of LNTE produced by chlorpyrifos is atypical of classic organophosphorus delayed neurotoxicants.
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PMID:Clinical, biochemical, electrophysiologic, and histologic assessment of chlorpyrifos induced delayed neuropathy in the cat. 128 30

Monensin, lasalocid, salinomycin, narasin and maduramicin are carboxylic ionophores intended for use as anticoccidial drugs for poultry and as growth promotants for ruminants. Generally, ionophores have been found safe and effective in the target animals receiving recommended dosage levels. However, toxic syndromes can result from overdosage and misuse situations. More information and reports of adverse reactions are available for monensin than the other ionophores because of monensin's longstanding and widespread use in the poultry and livestock industries. Care must be exercised in the diagnosis of ionophore toxicoses since clinical signs and lesions are not pathognomic. However, a feed-related problem characterized clinically by anorexia, diarrhea, dyspnea, ataxia, depression, recumbency and death, and pathologically by focal degenerative cardiomyopathy, skeletal muscle necrosis, and congestive heart failure may warrant a presumptive diagnosis of ionophore toxicity. Confirmatory diagnosis will require considerations of differential diagnoses and laboratory assays to determine the specific ionophore involved. Presently, there is no antidote or treatment for toxicoses induced by the ionophores. Judicious use, avoidance of overdosing, and adherence to species recommendation will help prevent the occurrence of adverse effects associated with this class of compounds.
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PMID:The veterinary importance of the toxic syndrome induced by ionophores. 162 67

Three siblings with inhaled elemental mercury toxicity are described, and the signs and symptoms of mercury toxicity, interpretation of mercury concentrations, and management of elemental mercury exposure are reviewed. A 4-year-old girl was admitted to the hospital with a history of fever and increasing irritability, fatigue, malaise, insomnia, headache, anorexia, and ataxia. She was discharged two days later with a diagnosis of acute cerebellar ataxia. During the following 18 days, the child's condition worsened, and she was rehospitalized. Meanwhile her 11-year-old sister was hospitalized for evaluation of fatigue, weakness, lower back pain, and ataxia. The older girl's blood mercury concentration, at 5.5 micrograms/dL, was in the toxic range. Twenty-four-hour urine mercury screening confirmed mercury intoxication in both children. Questioning revealed that the girls' brother had recently spilled 0.5-1 oz of elemental mercury in the house. All family members underwent blood and urine mercury testing. The brother underwent a dimercaprol challenge to determine his tissue mercury burden, which was found to be greater than 2.4 micrograms/dL. The sisters underwent two courses of chelation therapy with dimercaprol. Symptoms persisted in all three children, and they underwent five 10-day cycles of N-acetyl-D,L-penicillamine (NAP) therapy; the youngest underwent a third dimercaprol regimen. All siblings continued NAP chelation therapy because of extensive tissue mercury burden until the results of repeated urine mercury concentration determinations were normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elemental mercury poisoning. 174 59

Two hundred dogs with pituitary dependent hyperadrenocorticism (PDH) were treated with mitotane at an initial daily dosage of 21 to 69 mg/kg (mean = 45.2 mg/kg) for 5 to 14 days. During the induction period, 194 of the dogs also were given daily maintenance dosages of a glucocorticoid. Fifty of the dogs exhibited one or more adverse effects during initial induction, including weakness, vomiting, anorexia, diarrhea, and ataxia. After completion of the induction period, repeat ACTH stimulation testing revealed significant decreases in mean serum cortisol concentrations when compared with initial values. Twenty-five dogs, however, still responded to exogenous ACTH with serum cortisol concentrations above normal resting range, necessitating daily treatment for an additional 5 to 55 days. In contrast, 70 of the 200 dogs had low post-ACTH serum cortisol concentrations after the induction period. These subnormal serum cortisol concentrations generally increased spontaneously to within normal resting range 2 to 6 weeks after cessation of mitotane. In 184 dogs, mitotane was continued at an initial mean maintenance dosage of 49 mg/kg administered weekly in two to three divided doses. Of these dogs, 107 had one or more relapses of hyperadrenocorticism during treatment. In the 75 dogs that had one relapse, the median maintenance dosage was increased by approximately 35%, whereas the median maintenance dosage in the 32 dogs having two or more relapses was eventually increased by 225% over the initial dosage. After a mean maintenance treatment time of 2.0 years, the final maintenance dosage required in the 184 dogs ranged from 26.8 to 330 mg/kg/week.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mitotane (o,p'-DDD) treatment of 200 dogs with pituitary-dependent hyperadrenocorticism. 165 32

The literature contains about 500 cases of equine leucosis, though the reports are deposited in a great number of journals and vary considerably concerning particular topics. During the last years there has been a remarkable increase of publications about this syndrome in the equine. The clinical leucosis key recommended by us has been confirmed in principle considering the latest literature. In about 70 individual symptoms which can be clinically observed in equine with leucosis 11 can be considered as main symptoms because of their frequency; they are again classified in primary (lymph node tumours including splenomegaly--loss of condition, weakness--cachexia, weight loss, periphery oedema), secondary (anorexia, inappetence--fever--paleness of mucous membrane--anaemia--tachycardia) and accessory (incoordination--tachypnoea, dyspnoea--apathy, lethargy) main symptoms. Furthermore in future it will be necessary to take into more consideration the symptoms "recurrent colic" and "hydrothorax" within differential diagnosis. The main symptom "incoordination" (ataxia, asynergy, paresis, paralysis) is used by us more precisely only in case of impairment of nervous system by neoplastic infiltrations and does not signify as possible symptoms of general physical weakness, for example faltering, staggering, tumbling or lameness. The morphological classification follows further on our previous recommendation. There exist generalized forms with tumour infiltrations in abdominal and in thoracic cavity as well as especially in peripheral lymph nodes. On the other hand there are characteristic manifestations in certain regions of the body, which establish distinctly the clinical symptomatology. They are marked as regional multicentric forms with the main localizations "mediastinal", "splenic", "mesenteric" or "intestinal".(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical diagnostic keys and special manifestations in equine leukosis]. 195 30

A herd of 15 mature riding horses with a history of anorexia, weight loss, and lethargy was examined. The animals had been fed a 50/50 mixture of commercial sweet feed and corn screenings contaminated with a heavy growth of Fusarium moniliforme. Thirteen of the horses had one or more neurologic signs. The most characteristic signs were profound depression and mild ataxia. Over the 19-day course of the epizootic, the horses had increasing severe neurologic deficits, including unilateral blindness and delirium. Despite the clinical appearance of dehydration, 12 horses had low PCV (16 to 27%), hematocrit (21.2 to 31.0%; determined by automated cell counter), and RBC counts (3.76 to 5.5 x 10(6) RBC/microliters). White blood cell counts were variable (4,900 to 17,000 WBC/microliters). Necropsy findings included diffuse malacia of the white matter of the frontal cortex and severe multifocal perivascular hemorrhage in the white matter of the temporal cortex, basal ganglia, anterior medulla, and pons. One horse had a hepatic lesion consisting of a mixed inflammatory cell infiltrate and bile duct proliferation. The attack rate of this epizootic was 100%. The course of disease was unusually long in some animals. In an experiment, the fusarium-infected corn screenings were fed to horses and did not cause clinical signs or alterations in blood or serum biochemical values.
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PMID:Clinical and epidemiologic features of an epizootic of equine leukoencephalomalacia. 204 19

Idiopathic hypoparathyroidism was diagnosed in five young to middle-aged cats of mixed breeding. Three of the cats were male and two were female. Historic signs included lethargy (n = 5), anorexia (n = 5), muscle tremors (n = 4), weakness (n = 4), generalized seizures (n = 3), ataxia (n = 3), mental dullness or disorientation (n = 3), panting (n = 2), pruritus (n = 1), ptyalism (n = 1) and dysphagia (n = 1). Weakness (n = 4), dehydration (n = 2), cataracts (n = 2), hypothermia (n = 1), and bradycardia (n = 1) were found on physical examination. Results of electrocardiography revealed a prolonged Q-T interval in two cats. Results of initial laboratory tests revealed profound hypocalcemia and severe hyperphosphatemia with normal renal function. The diagnosis of hypoparathyroidism was made on the basis of the history, clinical signs, and results serum biochemical testing (i.e., severe hypocalcemia and hyperphosphatemia); in two cats, the diagnosis was also confirmed by histologic examination of parathyroid glands. Initial treatment included intravenous administration of 10% calcium gluconate and oral administration of large loading doses of calcium and vitamin D (dihydrotachysterol). Successful long-term management with dihydrotachysterol and calcium was achieved in all cats. The final dosage of dihydrotachysterol required to maintain normocalcemia in the five cats ranged from 0.004 to 0.04 mg/kg/day (mean = 0.015 mg/kg/day). Long-term calcium supplementation was given to three of the cats in dosages ranging from 29 to 53 mg/kg/day (mean = 42 mg/kg/day) of elemental calcium. One cat died after 28 months of therapy from widely metastatic hemangiosarcoma; the other three cats are still alive and well after 5 to 37 months of treatment.
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PMID:Idiopathic hypoparathyroidism in five cats. 202 14

The subacute toxicity of compound 1 was investigated in rats and dogs. Compound 1 was administered orally to rats of both sexes at daily doses of 0.5, 1.0 or 2.5 g/kg for 3 months. No change attributable to the administration of compound 1 was found either in blood count or in histopathological examination. Decreases in SGPT, alkaline phosphatase and lactic acid dehydrogenase and an increase in serum cholesterol were detected. Compound 1 was mixed with food and given to dogs of both sexes daily at doses of 0.2 or 0.5 g/kg for 3 months. Severe toxic symptoms including anorexia, emesis, ataxia and convulsive seizures were observed. A decrease in SGPT and increase in alkaline phosphatase were also detected. Hyperemia of the duodenal mucosa and severe kidney lesions were found in histopathological examination. Neither abnormality of appearance nor histopathological change was found in a pig receiving compound 1 at the daily dose of 0.1 g/kg for 3 months. The results suggest that there are differences of compound 1 metabolism among the species used in this study.
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PMID:[Species differences in subacute toxicity of pyrrole aldehyde N4-(4-methoxyphenyl) semicarbazone]. 215 Dec 66

Two hundred forty-one elderly depressed patients entered the 8-week, double-blind phase of this parallel-group, multicenter study; 161 patients were randomized to receive sertraline (50-200 mg/day) and 80 were randomized to receive amitriptyline (50-150 mg/day). Among evaluable patients, there were no statistically significant differences between treatments in any of the primary efficacy variables: change in total Hamilton Rating Scale for Depression (HAM-D) score (17 items), percentage change in HAM-D score, change in HAM-D Item 1, change in Clinical Global Impressions (CGI) Severity score, change in the Depression Factor of the 56-item Hopkins Symptom Checklist, and the CGI Improvement score at the last visit. Similar results were obtained using data from all patients (intention-to-treat analysis), except that amitriptyline was superior in HAM-D Total score (p = .044). The two drugs produced a similar degree of response: on the basis of the HAM-D criterion, 69.4% of sertraline patients and 62.5% of amitriptyline patients responded, and, on the basis of CGI criterion, 79.5% of sertraline and 73.4% of amitriptyline patients responded. Twenty-eight percent of the sertraline patients withdrew from the study because of a treatment-related side effect and 2.5% (4) because of a laboratory abnormality. In comparison, 35% of the amitriptyline patients withdrew because of treatment-related side effects. Sertraline was associated with a statistically lower frequency of somnolence, dry mouth, constipation, ataxia, and pain and a higher frequency of nausea, anorexia, diarrhea/loose stools, and insomnia; thus, anticholinergic effects were less common and gastrointestinal effects were more common with sertraline than with amitriptyline.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Double-blind, multicenter comparison of sertraline and amitriptyline in elderly depressed patients. 225 79

A case of amoebic meningoencephalitis in a sheep, suspected of being caused by Acanthamoeba sp., is described. An adult ewe was necropsied 5 days after it had developed anorexia and nervous signs, which included ataxia and walking in circles. Significant gross lesions were restricted to the central nervous system and consisted of thickening of the meninges and extensive necrosis of the cerebrum and cerebellum. The cerebral changes were characterised microscopically by a multifocal to coalescent necrotising granulomatous meningoencephalitis as well as choroid plexitis, ventriculitis and diffuse vasculitis. Numerous amoebic trophozoites and a few encysted forms morphologically compatible with Acanthamoeba sp. were present in the affected areas, particularly in the walls of blood vessels and perivascular spaces.
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PMID:Amoebic meningoencephalitis in a sheep. 226 87


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