Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Escherichia coli O157:H7 was isolated from a fatal case of haemorrhagic colitis with haemolytic uraemic syndrome and neurological symptoms. This strain induced diarrhoea and neurological symptoms including incoordination, ataxia, and convulsions in piglets after oral inoculation. Similar neurological signs were seen in piglets inoculated intraperitoneally with bacterial extracts containing a shiga-like toxin that is elaborated by the bacteria. Histological examination of the brains from these piglets showed vascular damage and small infarcts confined to the cerebellum. Comparable lesions were also seen in the brain of the child from whom E coli O157:H7 was isolated. We suggest that the cerebral changes in the piglets and in the patient were caused by the shiga-like toxin elaborated by E coli O157:H7. The shiga-like toxin is thought to cause neurological abnormalities by damage to cerebral blood vessels rather than by a direct effect on the neurones.
 ...
PMID:Cerebral infection with Escherichia coli O157:H7 in humans and gnotobiotic piglets. 305 80

The pharmacological actions of N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate (SUN 1165), a new antiarrhythmic agent, on the central nervous system were studied in various experimental animals as compared with those of disopyramide, mexiletine and lidocaine, and the following results were obtained. 1. Acute toxicity of SUN 1165 in mice was similar to that of mexiletine, and twice as potent as compared with that of disopyramide and lidocaine. Main acute toxic symptoms of SUN 1165 were muscle relaxation, ataxia, clonic convulsions, tremor and a decrease in spontaneous activity in mice, rats and rabbits. In addition to these symptoms, vomiting in dogs was observed. These toxic symptoms were similar to those of lidocaine. In the case of disopyramide, ataxia, tremor and a decrease in spontaneous activity were observed in mice and rats. On the other hand, mexiletine caused central nervous excitatory symptoms, that is, tremor, Straub tail, clonic convulsions, jumping, running and opisthotonus in mice and rats, and vomiting in dogs. 2. SUN 1165 even at large doses (50-100 mg/kg p.o.) exerted no significant effects on the following changes: hexobarbital-induced induced hypnosis, oxotremorine-induced tremor, apomorphine-induced hypothermia, reserpine-induced ptosis and hypothermia, 5-hydroxytryptophan syndrome and fighting behavior in mice, and conditioned avoidance response in rats. 3. An ineffective dose of SUN 1165 (12.5 mg/kg p.o.) on spontaneous locomotor activity was lower than of disopyramide and lidocaine, however, higher than that of mexiletine. 4. SUN 1165 at large doses showed antagonistic action on toxic extensor seizures induced by maximal electroshock, picrotoxin, or strychnine in mice, but anticonvulsive effects of SUN 1165 were less potent than those of mexiletine and lidocaine. SUN 1165 had no effect on clonic convulsions induced by pentetrazol and pictrotoxin in mice, while both mexiletine and lidocaine prolonged the duration of clonic convulsions. 5. The muscle relaxant effect of SUN 1165 (50%-toxic dose, TD50 = 30 mg/kg p.o.) was more marked than that of lidocaine (TD50 = 92 mg/kg p.o.) on traction test in mice. However, effect of SUN 1165 (TD50 = 62 mg/kg p.o.) on motor incoordination was similar to that of disopyramide, mexiletine and lidocaine on the rotarod test in mice. 6. The analgesic effect of SUN 1165 was as weak as that of disopyramide, mexiletine and lidocaine on chemically and mechanically-induced pain response in mice.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:General pharmacological studies on N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate. 1st communication: effect on the central nervous system. 319 80

When fertilized eggs (50 g) are injected on day 1 with 100 mumol taurine (0.2 ml), 15-day-old embryos exhibit increased taurine content in heart and brain. Lethal toxicity was no higher than with equimolar injections of NaCl (50 mumol) or valine (100 mumol) of the same volume. That same dose of taurine injected either on embryonic day 1 or 7 produced in hatchlings a typical syndrome of ataxia, reduced muscle strength and motor incoordination. When injected on embryo day 15 (E15) most chicks appeared incapable of pecking out of the egg, and the resulting delay in hatching, if if did occur, precluded presuming that the poor condition of such chicks was exclusively due to the late taurine injections. In view of the tendency of Friedreich's ataxia patients to exhibit increased alimentary absorption of taurine, and to demonstrate an excessive accumulation of taurine in the cerebellum and heart tissue on autopsy, fetal exposure to high taurine levels or neonatal high taurine milk ingestion may, by analogy, contribute to the slowly progressing disease process.
 ...
PMID:Embryonic exposure to high taurine: a possible nutritional contribution to Friedreich's ataxia. 322 74

Epidermoid tumors located in the fourth ventricle are exceedingly rare. Seven cases of this pathological condition were observed during a 10-year period. Patients were mostly middle-aged men, with a clinical history of relatively short duration (5 months). Clinical symptoms consisted of vertigo and ataxia, followed by incoordination, dysmetria, and tremor at a later stage. Computed tomography scanning represented the main diagnostic technique for these lesions, and typically showed a highly hypodense, round-shaped area within the fourth ventricle, occasionally accompanied by hydrocephaly. Subtotal surgical removal of the cysts produced excellent results in 86% of the cases. The implications of these findings are discussed.
 ...
PMID:Epidermoid cysts of the fourth ventricle. 334 62

Three formulations of 2,4-D were tested in rats for their ability to increase landing foot splay, a measure of ataxia. When administered for three to four consecutive days, 2,4-D-n-butyl ester (150 mg/kg/day SC) produced significant increases in landing foot splay while 2,4-D acid (120 mg/kg/day SC) and 2,4-D mixed butyl esters (150 mg/kg/day SC) did not. The ability of acute n-butanol, 2-butanol, and a 50:50 mixture of both (2.13 mM/kg SC) to increase landing foot splay was then assessed. Only n-butanol significantly increased landing foot splay. Similarly, when n-butanol was administered daily, at doses corresponding to 150 mg/kg/day of the 2,4-D-n-butyl ester, significant increases in landing foot splay were evident. The pattern of splay increases was remarkably similar to that observed for 2,4-D-n-butyl ester. When locomotor activity was the dependent variable, daily n-butanol had no effect. These results suggest that in vivo formation of n-butanol after administration of 2,4-D-n-butyl ester is responsible for the motor incoordination but not the depression of locomotor activity observed following 2,4-D-n-butyl ester administration. These data demonstrate that different formulations of the same herbicide can produce differential behavioral effects.
 ...
PMID:2,4-D-n-butyl ester (2,4-D ester) induced ataxia in rats: role for n-butanol formation. 335 73

Two unrelated females, age 15 and 5 years respectively, were studied cytogenetically because of severe mental retardation, seizures and ataxia-like incoordination. A similar deletion of the proximal long arm of chromosome 15 was found in both patients. Re-evaluation showed no voracious appetite or obesity; normal size of hands and feet, minimal to no hypotonia by history or examination and facial features not typical of the Prader-Willi syndrome. However, the facial appearance of the girls was similar to each other with mild hypertelorism. The similarity of these girls and dissimilarity to Prader-Willi syndrome suggest a different syndrome, perhaps the result of deletion of a different segment of 15q. The findings of ataxic-like movements, frequent, unprovoked and prolonged bouts of laughter and facial appearance are more compatible with the diagnosis of Angelman syndrome.
 ...
PMID:Is Angelman syndrome an alternate result of del(15)(q11q13)? 368 21

Approximately 250 sheep were poisoned and died from ingesting death camas (Zygadenus paniculatus) within a 2-day period on a foothill range in southeastern Idaho. Sixty to 70% of the poisoned sheep were 80-90 lb lambs and the rest were mature ewes. Poisonings were confirmed by field investigation, microhistological analysis of plant fragments from rumen contents of dead sheep, clinical signs, gross and microscopic analysis of tissues, and by experimentally feeding death camas collected on the poisoning site to 3 ewes at the Poisonous Plant Research Laboratory at Logan, UT. Clinical signs and gross and microscopic analysis of tissues were similar in ewes from the field investigation to those in ewes experimentally fed death camas. Ataxia, muscular weakness, trembling, incoordination, discharge of frothy saliva from the mouth and nose, vomition, dyspnea, collapse and death were the most common clinical signs. Gross changes included severe pulmonary congestion and subcutaneous hemorrhage. Microscopic lesions were those of severe pulmonary congestion.
 ...
PMID:Death camas poisoning in sheep: a case report. 382 76

Observations on patients with frontal lesions including the premotor cortex but not the primary motor cortex as shown by CT scans have shown a slight or moderate weakness of the contralateral shoulder or hip muscles which remained as a permanent deficit. The second deficit was an incoordination between movements requiring temporal adjustment between proximal muscle activities of both sides (limb-kinetic apraxia). From the clinical examination there was no evidence for deficient sensory guidance of movement. Visual control of hand and finger movements was normal as long as the arm could be supported during the tasks. In contrast, gross abnormalities of visually guided reaching (visuomotor ataxia) or somesthetic movement control (tactile apraxia) are seen after parieto-occipital lesions. On the basis of clinical observations it is therefore more likely that sensory-motor integration and transformation already takes place at the posterior lobes, where corresponding disturbances are pronounced but are absent after frontal lobe lesions.
 ...
PMID:Clinical aspects of premotor function. 391 45

Lithium toxicity can produce persistent and possibly permanent neurologic damage involving multiple areas of the nervous system, often including the cerebellum. Such cases, though rare, may continue to occur since lithium salts are widely used. In this report we describe the neurologic presentation, rehabilitation management, and outcome of treatment in such a patient. Her persistent neurologic syndrome was dominated by features of cerebellar dysfunction. Deficits in speech, swallowing, activities of daily living, transfers, and ambulation were identified and a rehabilitation program was implemented. Therapeutic rehabilitative techniques focused on compensatory mechanisms for ataxia and incoordination. Though her basic neurologic status did not change substantially, she did respond well to rehabilitative measures with significant functional gains and the patient was returned to her prior living arrangement.
 ...
PMID:Rehabilitation in lithium toxicity: case report. 406 31

Chronic states of methylmercurialism were induced in squirrel monkey subjects. Principal neurological signs included ataxia, abnormal gait, incoordination and amaurosis. Although slight to moderate vacuolization occurred in supporting cell layers of the cristae and maculae, receptor cell function was essentially normal. Except for a lowered cold threshold, bithermal caloric-induced nystagmus was not significantly different from control values. Pre and postrotatory (Barany chair) tests revealed a reduction only in frequency related variables. The development of spontaneous and positional nystagmus (sometimes with eyes open) coupled with the behavioral signs and the evidence of normal receptor response suggested cerebellar dysfunction. Severe pathologic changes were present in the cerebral cortex, but no lesions were found in the cerebellar cortex. Substantial neuronal degeneration and gliosis, however, were observed in several subcortical nuclei, including cerebellar and vestibular nuclei.
 ...
PMID:Horizontal nystagmus in methylmercury poisoned squirrel monkeys. 613 46


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>