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

The toxicity, uptake, tissue distribution, elimination, and covalent binding of [1-14C]allylnitrile (ALN) in male Sprague-Dawley rats were investigated. Following an oral administration of 57.5 mg/kg body weight (0.5 LD50, 23.4 mu Ci/kg, body weight), the rats exhibited several signs of toxicity, including ataxia, convulsions, mild diarrhea, salivation, lacrimation, and bladder urine retention. The treated animals excreted 41% of the radioactivity in the urine, 6% in the feces, and 34% in the expired air in 10 days. Hydrogen cyanide was not detectable in the expired air. Red blood cells retained significant amount of radioactivity for more than 5 days after treatment. ALN was extensively absorbed through the gastrointestinal tract and distributed in all the tissues of the rats. The major concentrations of the radioactivity were found in bone, kidney, blood, and the gastrointestinal tract. The subcellular fractions of the liver, kidney, heart, lung, and brain showed substantial accumulation of radioactivity from ALN up to 48 hr following dosing. Among the chemical fractions of the liver, the proteins exhibited much higher retention of radioactivity from ALN than the nucleic acid and phospholipid fractions, with a peak at 1 hr. This study indicates that ALN is rapidly absorbed and distributed in the rat and the major route of excretion is urinary followed by the expired air.
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PMID:Toxicokinetics of allynitrile in rats. 810 May 2

At the age of three weeks, two Labrador retriever puppies, out of a litter of nine, suffered from diarrhoea and muscular weakness. One puppy died within two days. The other was killed after a tetraparalysis had developed. Two weeks later a third puppy was killed because of a paretic hind leg. At the age of five months another dog had to be euthanized because of progressive hind limb ataxia. Pathological examination revealed polyradiculoneuritis, multifocal encephalomyelitis and polymyositis. In the lesions, particularly in the nerve roots, free and clustered protozoal tachyzoites were found. In the central nervous system tissue cysts were seen. By use of immunohistochemistry the protozoal organisms were identified as Neospora caninum, a newly recognized protozoan in the dog. Fresh bovine heart, that had been fed to the puppies, is regarded as the possible source of infection.
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PMID:[Neospora caninum as a cause of lameness symptoms in young dogs]. 832 63

In October 1989, an epizootic duckling disease with high mortality occurred in Taiwan. The disease was characterized by droopiness, inappetence, ataxia, ruffled feathers, and watery diarrhea. Affected ducklings were lame, were unable to stand, showed opisthotonos, and often died 3 or 4 days after the onset of the disease. Tolerant maturing ducklings displayed atrophic upper bills with a protruding tongue and became stunted as they reached maturity. No diagnostic histopathologic lesions were found in these ducklings. Fourteen parvovirus isolates, 33 duck viral hepatitis virus (DVHV) isolates, two adenovirus isolates, and two reovirus isolates were obtained and identified from more than 500 sick ducklings in the epizootic. The epizootic was diagnosed as a co-outbreak of duck parvovirus infections and duck viral hepatitis. The high mortality in ducklings and the bill atrophy syndrome were reproduced in ducklings by inoculating the parvovirus isolates alone. The epizootic was controlled by an emergency immunization program of ducklings with sera collected from recovered ducks or a bivalent inactivated vaccine composed of local DVHV and parvovirus isolates.
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PMID:Infectious bill atrophy syndrome caused by parvovirus in a co-outbreak with duck viral hepatitis in ducklings in Taiwan. 839 11

In November 1993, 188 people were admitted to hospital after eating the meat from a single shark (Carcharhinus leucas) in Manakara, a medium-sized town on the south-east coast of Madagascar. This shark and its meat had no unusual characteristics. The attack rate was about 100%. The first clinical signs appeared within 5-10 hr after ingestion. The patients presented with neurological symptoms almost exclusively, the most prominent being a constant, severe ataxia. Gastrointestinal troubles, like diarrhoea and vomiting, were rare. The overall case mortality ratio was close to 30% among the 200 poisoned inhabitants. There were no reports of previous similar poisonings in this area, and fishermen in Manakara usually eat this kind of shark without problems. Bacteriological and chemical causes were eliminated. Two liposoluble toxins were isolated from the liver and tentatively named carchatoxin-A and -B, respectively. They were distinct from ciguatoxin in their chromatographic properties.
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PMID:Fatal mass poisoning in Madagascar following ingestion of a shark (Carcharhinus leucas): clinical and epidemiological aspects and isolation of toxins. 859 86

Forestomach acidosis was diagnosed in 2 llamas and 4 alpacas. All were young, group-housed, sexually intact males. Clinical signs included forestomach atony, lethargy, ataxia, diarrhea, and tachycardia. Forestomach distention was observed in only 1 llama. Clinicopathologic abnormalities included low forestomach fluid pH, hyperchloremia, hypokalemia, and metabolic acidosis. Although camelids differ from domestic ruminants in typical management practices and behavioral, anatomic, and physiologic characteristics, they are, nonetheless, susceptible to forestomach acidosis. Gastric fluid analysis was essential for an accurate diagnosis. Four of 6 camelids recovered after PO and IV treatment with alkalinizing agents and fluids, antibiotics, and thiamine.
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PMID:Forestomach acidosis in six New World camelids. 861 51

There have been several reports describing that immunoadsorption therapy improves the neurologic involvement in Fisher's syndrome (FS). However, few studies have assessed the usefulness of immunoadsorption therapy in view of the removal ability of anti-GQ(1b) antibody, which may function the development of FS. We examined the ability of immunoadsorbents for the anti-GQ(1b) antibody in a patient with FS. A 28-year-old woman developed diplopia and giddiness following a cough, fever and diarrhea. On admission (day 22), neurologic examination showed bilateral moderate oculomotor paralysis and bilateral complete abducens paralysis. She had areflexia, numbness of middle and ring fingers on the left and mild ataxic gait. Her serum had IgG anti-GQ(1b) and anti-GD(1b) antibodies. We examined the absorption of anti-ganglioside antibodies onto a polyvinyl alcohol gel (PVA), a phenylalanine-linked PVA (PH-350) and a tryptophan-linked PVA (TR-350) by the batchwise adsorption method. TR-350 absorbed the autoantibodies, but the removal ability of autoantibody by PVA and PH-350 was not proved. The FS patient was treated with TR-350 (days 29, 34 and 43) and PH-350 (day 39). Anti-GQ(1b) and anti-GD(1b) antibodies were significantly removed by the TR-350, in accordance with the results of the in vivo study. There was little loss of albumin as compared with the immunoglobulins and complements. The numbness and ataxia disappeared on day 44. The diplopia disappeared on day 106. TR-350 would be better than PH-350 in the treatment of FS by immunoadsorption therapy.
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PMID:[Immunoadsorption therapy on Fisher's syndrome--removal ability of anti-ganglioside antibodies by tryptophan-linked immunoadsorbent]. 866 31

Two Japanese male siblings, aged 68 and 59 years, affected by late-onset progressive ataxia distinguished by extensive sensory and mild autonomic disturbances are described. They had global thermoanalgesia, positive Romberg signs, sensorineural deafness, canal paresis and ageusia. Their autonomic disturbances consisted of absence of overflow tears with usual stimuli, dysphagia, blood pressure and vasomotor instability, diarrhoea/constipation, and urinary frequency. Sensory nerve action potentials were completely absent, whereas motor conduction velocity was slightly reduced only in the lower extremities. Sural nerve biopsy on the younger brother demonstrated a marked loss of myelinated fibres and a reduction in the number of unmyelinated axons. Tongue histology revealed absence of fungiform papillae and taste buds. Autonomic function tests showed widespread but mild sympathetic and parasympathetic failures. Neuro-imaging studies revealed atrophy of the spinal cord, cerebellum, brainstem and corpus callosum, and enlargement of the lateral, third and fourth ventricles. These siblings represent a previously unrecognized variant of late-onset hereditary spinocerebellar degeneration with global thermoanalgesia and absence of fungiform papillae on the tongue.
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PMID:Late-onset hereditary ataxia with global thermoanalgesia and absence of fungiform papillae on the tongue in a Japanese family. 867 78

Cisapride is an oral prokinetic agent used to facilitate or restore motility in the gastrointestinal tract. The National Animal Control Center has received 17 reports of accidental overexposure of dogs to cisapride since 1994. Doses of 640 mg/kg in dogs were reported to be lethal, but severe clinical signs have been noted at acute exposures as low as 18 mg/kg. The most common signs include diarrhea, muscle tremors and fasciculations, ataxia and incoordination, and hyperthermia. Available treatment is symptomatic and supportive. Activated charcoal is effective in reducing plasma cisapride levels.
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PMID:Cisapride toxicosis in dogs. 869 86

A case of lithium toxicosis is described in a cow that had consumed grease. Clinical signs included increased salivation, ataxia, reduced consciousness, seizures and diarrhea. No treatment was instituted. The grease did not contain high concentrations of other heavy metals or minerals.
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PMID:Lithium toxicosis in a cow. 869 95

Serotonin syndrome, a condition with numerous clinical neurological manifestations, is the result of central serotonergic hyperstimulation. Features of the syndrome include mental status and behavioral changes (agitation, excitement, hypomania, obtundation), motor system involvement (myoclonus, hemiballismus, tremor, hyperreflexia, motor weakness, dysarthria, ataxia) and autonomic symptoms (fever, chills, diarrhea). Serotonin syndrome has been reported exclusively in patients on medications for psychiatric illness and Parkinsonism, despite the fact that the putative action of many antimigraine agents also involves the serotonin system. We herein report six patients with migraine who developed symptoms suggestive of the serotonin syndrome. Five were taking one or more serotomimetic agents for migraine prophylaxis (sertraline, paroxetine, lithium, imipramine, amitriptyline). In each case the symptoms and signs developed in close temporal proximity with use of a migraine abortive agent known to interact with serotonin receptors. In three instances the agent was subcutaneous sumatriptan and, in three, intravenous dihydroergotamine. In each instance the symptoms were transient and there was full recovery. With the ever increasing use of migraine medications active at serotonin receptor sites, cases of serotonin syndrome will likely occur more frequently. It is important that physicians treating migraine are aware of the serotonin syndrome and are able to recognize its varying presentations.
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PMID:Serotonin syndrome complicating migraine pharmacotherapy. 886 67


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