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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 ethanol to affect hindlimb ataxia and body weight changes induced by methyl mercury was studied in rats. Animals treated with either water or ethanol increased in body weight during the experiment and showed no impairment of hindlimb movement. Rats treated with methyl mercury also increased in body weight but developed moderate hindlimb ataxia. Animals treated with ethanol and methyl mercury initially gained but subsequently lost weight and exhibited severe hindlimb ataxia. The results provide evidence that ethanol can potentiate methyl mercury toxicity in rats and, by implication, in humans.
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PMID:Ethanol potentiation of methyl mercury toxicity: a preliminary report. 728 7

Diisopropyl methylphosphonate (DIMP), and dicyclopentadiene [3a,4,7,7a-tetrahydro-4,7-methyanoindene] (DCPD), were found as contaminants of groundwater in Colorado. Since there was a potential for cattle to be exposed to these chemicals by drinking well water, a study of their effects was initiated. Eight-to-ten week old calves were given a single dose of either DIMP at 62.5, 125, 250, 500 and 1000 mg/kg of body weight (b.w.) or DCPD at 250, 500, 1000 or 2000 mg/kg of b.w. The calves given DIMP developed tympanitis and ataxia, followed by depression, prostration, and death within two hr after dosing. A slight but significant increase in activated partial thromboplastin time was the only change observed in any of the clinical pathologic parameters. The only gross pathologic changes were acute gastroenteritis with hemorrhages in calves given 1000 mg/kg of b.w. Mild signs of intoxication, ataxia and excess salivation, were observed in calves given 250 mg of DCPD/kg of b.w. At higher doses, these signs were intensified; in addition, calves fell and, while prostrate, exhibited running movements and tonic, clonic spasms. The severity of the signs observed increased as the dose of DCPD increased. All calves given 2000 mg/kg of b.w. and one calf given 1000 mg/kg of b.w. died before seven days after dosing. The only clinical pathologic changes found were increased serum levels of creating phosphokinase, glutamic-oxalacetic transaminase, and glutamic pyruvic transaminase. The only consistent gross pathologic change was congestion in a variety of tissues in calves given 2000 mg/kg of b.w. A variety of histologic changes were observed in tissues from calves treated with both chemicals. However, these changes were not consistent for any one dose level and were not dose dependent. DIMP was slightly toxic for calves, since no signs of intoxication were observed at doses less than 1000 mg/kg of b.w. DCPD exerted detrimental effects on calves at 250 mg/kg of b.w. and was classified as moderately toxic.
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PMID:Toxicologic evaluation of diisopropyl methylphosphonate and dicyclopentadiene in cattle. 730 51

A 59-y-old with a history of chronic renal failure on hemodialysis was diagnosed with herpes zoster and begun on 800 mg acyclovir 5 times daily. Two days later the patient developed visual hallucinations, ataxia, confusion and memory loss along with focal myoclonus, nausea and vomiting. No fever, elevated WBC count or significant electrolyte imbalance was found. CT scan of the brain was unremarkable. The patient was then dialyzed for presumed acyclovir toxicity. Her acyclovir level was later found to have been 3.4 micrograms/ml (normal peak range 0.4-2 micrograms/ml) prior to dialysis. After 3 h of hemodialysis, her post-dialysis acyclovir level was 1.9 micrograms/ml. After a second course of hemodialysis the next day the patient's mental status improved, and she was discharged 5 d later. Due to its low volume of distribution (0.6 L/kg), low protein binding (about 15%) and water solubility, acyclovir is an example of the ideal drug that can be removed by hemodialysis. About 45% of the total body amount can be extracted through a 3-h course of hemodialysis with resultant improvement in symptoms.
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PMID:Hemodialysis removal of acyclovir. 757 52

The developmental toxicity of the anticonvulsant compound, ralitoline, was investigated in Sprague-Dawley rats administered oral doses of 0, 15, 60, 120, 180, or 240 mg/kg on days 6 through 15 of gestation. An untreated control group and a vehicle control group pair-fed to the high dose group were included. Maternal and fetal parameters were evaluated on day 21 of gestation. Fetuses were examined for external, visceral, and skeletal malformations and variations. Maternal death occurred at 180 and 240 mg/kg. Dose-dependent decreases in body weight, food consumption, and water consumption were observed at 60 mg/kg and above. Body weight gain during treatment was similar in the pair-fed and 240 mg/kg groups. Dose-related CNS signs (hypoactivity, ataxia, prostration, and/or convulsions) were observed at 60 mg/kg and above. Decreased numbers of live fetuses and increased postimplantation loss were observed in a dose-related manner at 120, 180, and 240 mg/kg while no changes occurred in pair-fed controls. Fetal body weights and placental weights were decreased in pair-fed controls and in the 120, 180, and 240 mg/kg groups. The percent fetuses per litter, and the percent litters with external/visceral malformations, were significantly increased at 120, 180, and 240 mg/kg compared with vehicle and pair-fed controls. Dose-related increases in cardiovascular malformations, specifically of the aortic arch (interrupted, stenotic, extra vessel), were apparent at 120 mg/kg and above. The incidence of skeletal variations was increased at 120 mg/kg and above.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Developmental toxicity study in rats treated with the anticonvulsant, ralitoline. 759 53

Phencyclidine (PCP), in a dose of 15 mg/kg, produced delayed cognitive dysfunction (at 24 h) in rats subjected to water maze tasks. At 24 h after PCP administration, ataxia, hyperlocomotion and stereotyped behavior were not induced. NE-100, N,N-dipropyl-2-[4-methoxy-3-(2-phenylethoxy)phenyl]-enthylamine monohydrochloride, a selective and potent sigma receptor ligand, was administered orally 10 min after PCP administration or 15 min before the first trial (24 h after PCP administration). In both cases, NE-100 dose-dependently attenuated the delayed cognitive dysfunction induced by PCP. As these findings show that ingestion of PCP led to delayed cognitive dysfunction similar to the cognitive signs of psychosis seen in humans, NE-100 is being further studied for possible treatment of subjects with schizophrenia.
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PMID:Effect of NE-100, a novel sigma receptor ligand, on phencyclidine- induced delayed cognitive dysfunction in rats. 760 28

The clinical signs of ivermectin toxicity were determined in 6 groups of 10 epileptic and 8 non-epileptic chickens for 72 h after dosing with sc injections of 5.0, 7.5, 10.0, 12.5 or 15.0 mg ivermectin/kg bw. At the 5.0 mg/kg dose, mild diarrhea developed 4 h post-dosing and lasted until the end of the 72-h monitoring period. With higher doses of ivermectin body weight, egg production and feed and water consumption were markedly reduced. Severe diarrhea, mydriasis, bradypnea, ataxia, sedation, coma and death occurred with the highest dose of ivermectin. No differences in the signs of ivermectin toxicity were observed between epileptic and non-epileptic chickens. To assess the efficacy of the antiGABAergic convulsants, methyl-beta carboline-carboxylate (beta-CCM), picrotoxin and pentylenetetrazol (PTZ), as antidotes for ivermectin toxicity, 8 epileptic and 6 non-epileptic chickens/treatment group were given dosages of each convulsant which previously induced convulsions in 50% (ED50) and again in 100% (ED100) of treated chickens. These convulsants were given 6 h after dosing with 15.0 mg ivermectin/kg. The ED100 dosages of picrotoxin and PTZ alleviated mydriasis and sedation, but did not reduce the diarrhea. The ED50 dose convulsants were not effective in reducing or alleviating ivermectin toxicity, nor was alleviation of any sign of ivermectin toxicity obtained with any dosage of beta-CCM. Although the dosages of these antiGABAergic convulsants used normally produced convulsions in epileptic and non-epileptic chickens, no convulsions were observed in chickens with ivermectin toxicity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical signs of ivermectin toxicity and the efficacy of antigabaergic convulsants as antidotes for ivermectin poisoning in epileptic chickens. 763 91

Minamata disease (M. d.) is methylmercury (MeHg) poisoning that occurred in humans who ingested fish and shellfish contaminated by MeHg discharged in waste water from a chemical plant (Chisso Co. Ltd.). It was in May 1956, that M. d. was first officially "discovered" in Minamata City, south-west region of Japan's Kyushu Island. The marine products in Minamata Bay displayed high levels of Hg contamination (5.61 to 35.7 ppm). The Hg content in hair of patients, their family and inhabitants of the Shiranui Sea coastline were also detected at high levels of Hg (max. 705 ppm). Typical symptoms of M. d. are as follows: sensory disturbances (glove and stocking type), ataxia, dysarthria, constriction of the visual field, auditory disturbances and tremor were also seen. Further, the fetus was poisoned by MeHg when their mothers ingested contaminated marine life (named congenital M. d.). The symptom of patients were serious, and extensive lesions of the brain were observed. While the number of grave cases with acute M. d. in the initial stage was decreasing, the numbers of chronic M. d. patients who manifested symptoms gradually over an extended period of time was on the increase. For the past 36 years, of the 2252 patients who have been officially recognized as having M. d., 1043 have died. This paper also discusses the recent remaining problems.
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PMID:Minamata disease: methylmercury poisoning in Japan caused by environmental pollution. 773 58

Seven adult mares were used to determine the analgesic, CNS, and cardiopulmonary effects of detomidine hydrochloride solution after epidural or subarachnoid administration, using both regimens in random sequence. At least 1 week elapsed between experiments. A 17-gauge Huber point (Tuohy) directional needle was used to place a catheter with stylet into either the epidural space at the first coccygeal interspace or the subarachnoid space at the lumbosacral intervertebral junction. Catheters were advanced so that the tips lay at the caudal sacral (S5 to S4) epidural space or at the midsacral (S3 to S2) subarachnoid space. Position of the catheter was confirmed radiographically. A 1% solution of detomidine HCl was injected into the epidural catheter at a dosage of 60 micrograms/kg of body weight, and was expanded to a 10-ml volume with sterile water to induce selective caudal epidural analgesia (CEA). A dose of 30 micrograms of detomidine HCl/kg expanded to a 3-ml volume with spinal fluid was injected into the subarachnoid catheter to induce caudal subarachnoid analgesia (CSA). Analgesia was determined by lack of sensory perception to electrical stimulation (avoidance threshold > 40 V, 0.5-ms duration) at the perineal dermatomes and no response to superficial and deep muscular pinprick stimulation at the pelvic limb and lumbar and thoracic dermatomes. Maximal CEA and CSA extended from the coccyx to spinal cord segments T15 and T14 at 10 to 25 minutes after epidural and subarachnoid drug administrations in 2 mares. Analgesia at the perineal area lasted longer after epidural than after subarachnoid administration (142.8 +/- 28.8 minutes vs 127.1 +/- 27.7 minutes). All mares remained standing. Both CEA and CSA induced marked sedation, moderate ataxia, minimal cardiopulmonary depression, increased frequency of second-degree atrioventricular heart block, and renal diuresis. All treatments resulted in significantly (P < 0.05) decreased heart rate, respiratory rate, systemic arterial blood pressure, PCV, and plasma total solids concentration. To the contrary, arterial carbon dioxide tension, plasma bicarbonate, and standard base excess concentrations were significantly (P < 0.05) increased. Arterial oxygen tension, pH, and rectal temperature did not change significantly from baseline values. Results indicate that use of detomidine for CEA and CSA in mares probably induces local spinal and CNS effects, marked sedation, moderate ataxia, mild cardiopulmonary depression, and renal diuresis.
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PMID:Caudal analgesia induced by epidural or subarachnoid administration of detomidine hydrochloride solution in mares. 806 16

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

1,1,1-Trichloro-2-propanone (1,1,1-TCP) has been identified as a chlorination by-product in finished drinking water supplies. Since little was known of its oral toxicity, exposure studies were conducted with male and female Sprague-Dawley rats (10 males and 10 females/group) exposed by corn oil gavage at 0, 16, 48, 161, or 483 mg/kg for 10 d or 0, 30, 90, or 270 mg/kg for 90 d. Evaluations included mortality, clinical signs, body weight, food consumption, ophthalmology, hematology, clinical chemistry, urinalysis, organ weights, gross pathology, and histopathology. In the 10-d study, severe toxicity was observed at the highest dose level, since most treated animals (8/10 males and 7/10 females) died. Toxicity was also noted at 161 and 48 mg/kg. At 161 mg/kg, 2 males died and an increase in liver weights in both sexes was observed. Acanthosis and hyperkeratosis of the forestomach was present in males and females at 48 mg/kg and above. In the 90-d study, toxicity was significant at 270 mg/kg, with acanthosis and hyperkeratosis of the forestomach evident in most animals and ataxia in about one-half of them. Retinal degeneration, increased serum potassium, and increased blood urea nitrogen were present in females and increased blood calcium in males at that same dose level. Acanthosis and hyperkeratosis were observed in both sexes, and retinal degeneration was prominent in 2 females at 90 mg/kg. It was concluded that 16 mg/kg was the NOAEL (no observed adverse effect level) for the 10-d study while 30 mg/kg was the NOAEL for the 90-d exposure of Sprague-Dawley rats to 1,1,1,-trichloro-2-propanone.
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PMID:Toxicity of 1,1,1-trichloro-2-propanone in Sprague-Dawley rats. 835 Mar 84


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