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

Selenium poisoning occurs worldwide in nearly all domestic animals. Acute selenium poisoning is associated with feeding high levels or injecting excessive amounts of selenium and is usually fatal. The acute poisoning may cause gastrointestinal disturbance, muscle weakness, depression of the central nervous system, prostration and death (1-2). Chronic selenium poisoning in cattle, sheep and horses may result from the consumption of seleniferous plants over an extended period of time. Chronic selenium results in ataxia, incoordination, partial blindness, paralysis, loss of hair or wool, abnormal hoof growth and possibly abnormal changes in behavior (1). There is little information regarding the clinical signs and pathology of selenium toxicosis in marine mammals. Likewise, there is little information regarding normal tissue levels or toxicologically significant levels of selenium in these species. The results of these investigations in sea lions, based on clinical signs, pathologic findings and tissue levels of selenium, suggest subacute or chronic selenium poisoning was most likely from dietary fish high in selenium.
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PMID:Selenium toxicosis in three California sea lions (Zalophus californianus). 261 40

The lethality of Poa huecu, a plant toxic to cattle and sheep, was followed by injection of chromatographic fractions in mice. The lethal aqueous extract was administered i.p. to Rockland mice of either sex and produced motor incoordination, transient ataxia, rough hair coat, tremors and muscle contractions and, occasionally, blindness. Doses greater than 1.5 g/kg mouse were always lethal. Fractionation of this lethal extract included dialysis, column chromatography on Sephadex G-25 and fractional precipitation with ethanol. Precipitates obtained with 70% and 85% ethanol were further purified on a DEAE-cellulose column. Eight fractions were obtained, each was injected into mice. Only fractions 3-6 were toxic. Fraction 3 produced slight hepatosis and hyperemia in the liver and gliosis in the brain. None of the other tissues exhibited histological lesions. Fractions 4 and 5 caused death of all animals within 30 min to 4 hr after injection. Polyacrylamide gel electrophoresis and acid hydrolysis showed that fractions 4 and 5 contained a glycoprotein of nearly the same mol. wt (67,000-94,000). Microscopic pathology in the mice treated with the lethal glycoprotein of fraction 4 included hyperemia in the kidneys, megakaryocytes in the spleen, slight hepatosis and focal coagulative necrosis with nuclear pyknosis and karyonexis in the liver, gliosis, intracellular brain edema with axon degeneration and swollen astrocytes in the brain. These brain injuries may relate to the motor incoordination of cattle that causes a delayed righting reflex. The major monosaccharides of the lethal glycoprotein are glucose and mannose, while rhamnose, arabinose, xylose and galactose are present in low percentages. Proline and the acidic amino acids (glutamic and aspartic acids) are the most abundant in the peptidic residue.
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PMID:The lethal principle of Poa huecu (coiron blanco): a plant indigenous to Argentina. 262 69

Functional methionine synthase deficiency is generally characterized by homocystinuria and hypomethioninemia in the absence of methylmalonic aciduria. Patients are divided into two classes, cblE and cblG, on the basis of complementation analysis. Presentation has usually been in the first 2 years of life, but one patient came to medical attention at age 21 years with symptoms initially diagnosed as multiple sclerosis. Common findings among 11 patients (4 with cblE and 7 with cblG) have included megaloblastic anemia (all patients) and various neurological deficits including developmental retardation (10 patients), cerebral atrophy (8 patients), hypotonia (7 patients), EEG abnormalities (6 patients), and nystagmus (5 patients). Hypertonia, seizures, blindness, and ataxia were less frequent. All patients have responded to therapy with cobalamin with resolution of anemia and biochemical abnormalities; neurological deficits resolved more slowly and in some cases incompletely. Hydroxycobalamin has been more effective than cyanocobalamin. Fibroblasts from patients with cblE (5 patients) and cblG (6 patients) all showed decreased intracellular levels of methylcobalamin (MeCbl) and decreased incorporation of label from 5-methyltetrahydrofolate into macromolecules, suggesting decreased activity of the MeCbl-dependent enzyme methionine synthase. Methionine synthase specific activity in extracts of all cblE fibroblasts was normal or near-normal under standard reducing conditions; synthase specific activity in extracts of 5 cblG patients was low but was high in a 6th patient measured in another laboratory. Thus, there is heterogeneity among patients with functional methionine synthase deficiency both in clinical presentation and in the results of biochemical studies of cultured cells.
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PMID:Functional methionine synthase deficiency (cblE and cblG): clinical and biochemical heterogeneity. 268 21

The responses of apparently healthy newborn foals to neurologic testing differ significantly from those of adult horses. These responses and the diagnostic techniques pertinent to neurologic problems are reviewed as a basis for evaluation of the compromised neonatal foal. The more frequently encountered neurologic diseases are discussed in a problem-oriented format. These clinical problems include behavioral abnormalities, convulsions, changes in consciousness, blindness, ataxia without loss of strength, ataxia with weakness and paralysis, and the floppy foal.
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PMID:Neurologic diseases. 300 May 43

We have found a group of individuals with the late infantile, the early juvenile variant, and juvenile neuronal ceroid-lipofuscinosis (NCL) in Newfoundland, an island with a population of 500,000. In the past 25 yr, we have ascertained 44 cases of NCL in 32 sibships: 32 cases of late infantile NCL (LINCL) in 24 sibships, 11 cases of the early juvenile variant in 7 sibships, and one patient with the juvenile form (JNCL). The clinical presentation of the LINCL patients is very characteristic, with onset of seizures at age 2 1/2 to 3 1/2 yr, frequently with drop attacks and myoclonic jerks, followed by mental deterioration, ataxia, visual loss, and death by the end of the first decade. Typical curvilinear profiles are seen on electron microscopy (EM). The second group of patients mainly have the early juvenile variant with onset of seizures at age 5 to 6 yr and fingerprint profiles with occasional curvilinear profiles on EM. However, a child with the juvenile form presenting with blindness was also encountered. In both of these types, death occurs in the second decade of life. There is no overlap of these three clinical forms within sibships, although both late infantile and early juvenile variant types may occur in the same small fishing village. All three forms appear to be inherited as autosomal recessive traits. Although the early juvenile variant has been postulated to represent a double heterozygote between LINCL and JNCL, this cannot be confirmed on the basis of the present study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The Newfoundland aggregate of neuronal ceroid-lipofuscinosis. 314 10

Portosystemic shunt was diagnosed in a 6-month-old Quarter Horse filly with acute onset of apparent blindness and a 3-month history of depression, lethargy, and ataxia. Clinicopathologic test results indicated slightly high gamma-glutamyl transpeptidase activity and serum total bilirubin concentration. Sulfobromophthalein half time was prolonged, and plasma ammonia and serum bile acid concentrations were high as well. Histopathologic findings of percutaneous liver biopsy included widespread hepatocyte atrophy and numerous prominent small arterioles in the area of the portal triad. On the basis of history, clinical findings, and clinicopathologic abnormalities, a presumptive diagnosis of portosystemic vascular anomaly was made. To confirm the tentative diagnosis, nuclear hepatic scintigraphy and operative mesenteric portography were performed. Medical treatment was unsuccessful, and the foal was euthanatized. Portosystemic shunts have been described in dogs and cats, but few cases have been reported in large animal species. Other, more common causes of neurologic abnormalities in foals, such as trauma, vertebral body abscesses, brain abscesses, and meningitis, must be ruled out before portosystemic shunt is considered.
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PMID:Clinical and diagnostic features of portosystemic shunt in a foal. 335 82

There are several clinically distinct forms of neuronal ceroid lipofuscinosis whose presentation and pathology are usually homogeneous within families. Several atypical variants have also been reported. We have studied an inbred sibship in which neuronal ceroid lipofuscinosis appeared to present in two completely different ways. In the proband, the course was compatible with a somewhat atypical juvenile variant. Ataxia and spasticity started at 4.5 years, followed by blindness with optic atrophy, intractable seizures, dementia, and death at 14 years. Atypical features included areflexia, hypotonia, and ataxia. Electron microscopic studies of her skin and her rectal ganglion cells showed lucent, dense, and fingerprint inclusions that were also found in the central nervous system at autopsy. Her brother and sister developed difficulty walking at ages 8.5 and 10.5 years and are alive at 24 and 18 years. They presented with slowly progressive spinocerebellar degeneration with sensorimotor neuropathy without dementia, seizures, or visual impairment. Lysosomal enzymes and lipoprotein analysis were normal in all three siblings and their parents. Elevated dolichol in the urine and lucent, dense, and fingerprint inclusions in skin, cutaneous nerve, buffy coat lymphocytes in both siblings and in the sural nerve of the brother suggest that their disease may represent a novel phenotype of neuronal ceroid lipofuscinosis. While it is possible that two different recessive genes may be segregating in this consanguineous family, we cannot dismiss the possibility that variability of gene expression may account for the divergent phenotypes.
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PMID:Spino-cerebellar degeneration with polyneuropathy associated with ceroid lipofuscinosis in one family. 342 77

The currently recognized toxic effects of quinine in humans are identified and the problems of management of overdosage of quinine are discussed. Quinine, available therapeutically as sulphate or hydrochloride salts, also is widely used in tonic water, and there are several case reports of allergic reactions to the drug when a patient has consumed the drug in this way. Another unintentional source of poisoning is its use as an adulterant in heroin for "street" use. This appears to be a problem in the US. Quinine, termed a "general protoplasmic poison" is toxic to many bacteria, yeasts, and trypanosomes, as well as to malarial plasmodia. Quinine has local anesthetic action but also is an irritant. The irritant effects may be responsible in part for the nausea associated with its clinical use. In addition it has a mild antipyretic effect. Several features are common to both an acute single overdose in self-poisoning and accumulation of quinine during therapy for malaria: together they are termed cinchonism. Auditory symptoms, gastrointestinal disturbances, vasodilatation, sweating, and headache occur with moderately elevated plasma quinine concentration. As these rise, increasingly severe visual disturbances and then cardiac and neurologic features occur. Mild nausea may be the only symptom, but with large overdoses profuse vomiting, abdominal pain, and diarrhea may occur. These result from a combination of the local irritant effect of quinine on the gut and the central effects of quinine on the chemoreceptor trigger zone. Vasodilatation and sweating are well recognized, and tinnitus is common. Visual symptoms usually are delayed, and blindness may not be discovered for a day or more. Aspirin-sensitive patients, and others, may develop angioedema by nonimmunological mechanisms in response to drugs, and quinine has been reported to produce pseudo-allergic reactions in aspirin-sensitive patients. Quinine also can cause drug-induced thrombocytopenia and purpura. In patients suffering with malaria due to "Plasmodium falciparum," anemia and acute intravascular hemolysis with renal failure are recognized complications. There appears to be little evidence in the literature in support of the folk tradition of quinine as an inducer of abortion. Quinine is known to cause deterioration in patients with myasthenia gravis and erythema multiforme, to stimulate insulin release in patients receiving treatment for falicparum malaria, and to be responsible at times for ataxia following moderate overdosage. Clinically, quinine poisoning is observed in 3 situations: self-poisoning; accidentally; and following use of quinine in excessive doses in the hope of achieving abortion. Treatment courses are reviewed.
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PMID:Quinine toxicity. 354 70

Hypovitaminosis A was diagnosed in a group of feedlot cattle that had been fed a diet low in carotene for 18 months. The primary signs of disease in the cattle were poor weight gain, ataxia, convulsions, night blindness, and total blindness. Serum vitamin A concentrations were used to confirm the diagnosis. The cattle were treated orally and intramuscularly with vitamin A, and the less severely affected herd members recovered rapidly.
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PMID:Hypovitaminosis A in feedlot cattle. 358 85

A 2-year-old Duroc boar was examined because of weakness, ataxia, and blindness. During hospitalization, fever spikes of about 41.6 C (107 F) were recorded every 24 hours. The tentative diagnosis was a space occupying mass in the diencephalon. The boar's condition deteriorated rapidly, so the boar was euthanatized and necropsied. On the basis of gross and histopathologic findings, as well as cell marker-specific-staining characteristics, astrocytoma was diagnosed.
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PMID:Astrocytoma in a boar. 405 5


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