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

Quantitative autoradiography was used to assess the densities of gamma-aminobutyric acid (GABAA) receptors in the brains of rats with a portacaval end-to-side shunt (PCA). The shunt alone induced only mild encephalopathy with ataxia and decreased locomotion. Aggravation of the encephalopathy was achieved by gavage feeding of packed erythrocytes or by induction of severe hyperammonemia by intraperitoneal injection of urease. Gavage feeding of erythrocytes led to severe encephalopathy in about 50% of the animals with PCA. The combination of PCA and urease treatment caused severe encephalopathy in every animal. The serum ammonia concentration increased 5 times normal by PCA alone, 20 times normal by gavage feeding of erythrocytes and more than 30 times normal by urease-treatment of the PCA-animals. For autoradiography, coronal slices were cut at the level of the hippocampal formation and through the cerebellum. Radioligand binding was measured using as a ligand 3H-muscimol, a specific GABAA receptor agonist. The specific binding of 3H-muscimol was assessed densitometrically in several microregions of cerebral cortex, hippocampus and cerebellar cortex. No significant differences were observed between the magnitude of ligand binding to specific microregions of brains from normal animals, animals with PCA without overt encephalopathy and animals with severe encephalopathy induced by a combination of PCA and gavage feeding of erythrocytes or urease treatment.
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PMID:[Autoradiography determination of the GABA(A) receptor density in the brain of rats with portacaval shunt]. 216 Jul 60

Three patients had neurologic signs due to isopropyl alcohol (IPA) intoxication. Over a several-week period, a known alcoholic developed apathy, confusion, ataxia, and hyperreflexia. During this period, there was no ethanol available to him, and he denied use of other intoxicants. He was found stuporous in the hospital after drinking IPA and admitted to IPA abuse during the preceding weeks. Two other men were admitted in a stupor after large ingestions of IPA. Intoxication with IPA has two different presentations: stupor in a known alcoholic and encephalopathy of unknown cause in individuals who hide their addiction. Ethanol, methanol, IPA, and ethylene glycol intoxications are associated with different clinical and laboratory findings.
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PMID:Isopropyl alcohol intoxication. 198 19

Poisonings resulting from DEET are rarely encountered in companion animals. In human patients, DEET toxicosis has been associated with the development of a toxic encephalopathy characterized by tremors, seizures, behavioral changes, and abnormal movements. Generally, DEET toxicosis in companion animals is of short duration and is characterized by vomiting, tremors, ataxia, and excitation. Treatment for DEET toxicosis includes symptomatic therapy and decontamination.
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PMID:Diethyltoluamide (DEET) insect repellent toxicosis. 218 Jan 85

We report 3 cases of epilepsy with bilateral occipital calcifications followed up for several years. These cases were compared with 21 published cases and were found to differ from the classical Sturge-Weber syndrome on several points: 1) the disease appeared around the age of 5 years and consisted of focal epilepsy without neurological or mental disorders; 2) the epilepsy was easy to control during 2 to 5 years. This was followed by a diffuse encephalopathy with severe, treatment-resistant epilepsy, Gerstmann's syndrome, optic ataxia, cerebellar syndrome and slow activity at EEG. It appears from these 3 cases that: 1) occipital calcifications may be unilateral at the onset of the disease; 2) visual evoked potentials are affected at a late stage, and 3) CT scans are of considerable value in the prognosis of benign epilepsy in childhood.
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PMID:[Epilepsy and bilateral occipital calcifications: 3 cases]. 219 37

Propylene glycol (1,2-propanediol) is a solvent in numerous pharmaceuticals and a major preservative and source of carbohydrates in processed foods. In mammals, propylene glycol is metabolized similar to ethanol, proceeding via hepatic alcohol and aldehyde dehydrogenases to lactate, which can then enter gluconeogenesis. We observed that cats ingesting 1.6 gm of propylene glycol/kg body weight/day developed increased anion gap. To investigate this further, we measured D- and L-lactate concentrations in these cats; we also measured D-lactate in cats ingesting high doses of propylene glycol (8.0 gm/kg). While L-lactate actually decreased throughout the 35-day course of propylene glycol feeding, D-lactate levels were significantly increased on a dose-dependent basis and correlated positively with anion gap. In cats ingesting the high dose of propylene glycol, D-lactate concentrations were as high as 7 mmol/liter, levels associated with encephalopathy in humans. Indeed, this group of cats developed depression and ataxia, consistent with intoxication by D-lactate. These findings are significant not only for animals ingesting diets which contain propylene glycol, but for humans who receive propylene glycol-containing medications.
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PMID:Propylene glycol ingestion causes D-lactic acidosis. 229 57

Infants and children with symptomatic human immunodeficiency virus (HIV) infection frequently develop neurologic disease with symptoms and signs of acquired microcephaly, developmental delays, encephalopathy, pyramidal tract signs, and less often, movement disorders and ataxia. However, clinical courses vary and, based upon progression of neurologic findings, we have classified them into 2 broad categories; progressive (loss of previously acquired language and cognitive skills) and plateau (failure to acquire additional developmental skills). We have used immunocytochemistry to localize HIV within the brains of neurologically involved children with AIDS. Interestingly, the brains of those children with a progressive neurologic course showed readily detectable HIV antigen, while those with a plateau course showed little or no detectable HIV. These findings suggest that in children with symptomatic HIV infection, the progressive neurologic deterioration is due to continued presence of HIV within deep white matter and gray matter, while the plateau neurologic course is due to HIV induced damage followed by either limited penetration of virus into the central nervous system, or clearance of virus below detectable limits.
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PMID:Human immunodeficiency virus within the brains of children with AIDS. 230 89

Five children with subacute or acute onset of cerebellar ataxia and opsoclonus are described. Two had cerebrospinal fluid pleocytosis at the onset of ataxia and were initially thought to have acute parainfectious cerebellar ataxia of childhood. All were found to have tumors of neural crest origin (two neuroblastomas, three ganglioneuroblastomas). Tumors were small and only found by computed tomographic techniques. Urinary catecholamine metabolites were elevated in only two of the patients. Four of the five failed to improve neurologically with resection of the tumor. All four have had a steroid-sensitive chronic ataxic syndrome that worsens with acute nonspecific illnesses and has resulted in long-term deficits, particularly in speech and gross motor function. This is a metabolic encephalopathy associated with permanent residual neurologic deficits but without visible lesions on neuroimaging studies. We stress the frequency of cerebrospinal fluid pleocytosis in patients with tumor-associated opsoclonus and the clinical difficulty in separating tumor-associated cases from those due to other causes [corrected].
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PMID:Opsoclonus-ataxia due to childhood neural crest tumors: a chronic neurologic syndrome. 234 82

Acute cerebellar encephalopathy (ACE)--ataxia often associated with opsoclonus, polymyoclonus, and irritability--may be associated with neuroblastoma and should be suspected in a child who presents with ACE. The survival in ten children with ACE associated with neuroblastoma was 100%. Most of the tumors were ganglioneuroblastomas. The abdomen was the most common location for the tumor in this study although it also can be found in the mediastinum. All patients with this syndrome had a localized tumor. With ACTH therapy, ACE may resolve early postoperatively, but it tends to recur in most patients, continuing for as long as 3 years after the initial operation. Treatment with ACTH or prednisone modifies and rapidly clears the symptoms during the acute episode of recurrent ACE as well as helps to resolve subsequent neurologic sequelae. Significant neurologic sequelae persisted in seven of ten patients and included deficits in cognition or intellect, hyperactivity, impulsivity, emotional lability, and mild motor deficits. Seizures were seen in one patient.
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PMID:Clinical outcome in children with acute cerebellar encephalopathy and neuroblastoma. 272 81

Ureterosigmoidostomy, a urinary diversion procedure performed for treatment congenital urologic defects or bladder cancer, may be associated with hyperammonemia. A delayed periodic encephalopathy, characterized by dysarthria, ataxia, and coma, developed in a 44-year-old woman who had undergone this procedure. Hyperammonemia-associated neurotoxicity resolved after surgical revision of the ureterosigmoidostomy to a uretero-ileostomy. Therefore, a treatable episodic encephalopathy may occur in association with hyperammonemia in patients who have undergone ureterosigmoidostomy.
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PMID:Periodic hyperammonemic encephalopathy associated with a ureterosigmoidostomy. 274 94

D-Lactate-associated encephalopathy is a rare clinical syndrome characterized by dizziness, ataxia, confusion, headaches, memory loss, lethargy, and aggressiveness which may progress to frank but reversible coma. It occurs in patients with profound dysfunction of the short-bowel syndrome and is believed to result from massive carbohydrate malabsorption with resultant over-production of D-lactate and other organic anions by the colonic flora. Extremely elevated serum levels of D-lactate (but not L-lactate) confirm the diagnosis, but currently D-lactate is not clearly established as the putative neurotoxin. We describe a patient who repeatedly developed D-lactate encephalopathy after surgical removal of nearly the entire jejunum and ileum. Markedly elevated D-lactate serum levels were documented during an encephalopathic episode. Potential pathophysiologic mechanisms and the treatment rationale are discussed.
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PMID:D-lactate-associated encephalopathy after massive small-bowel resection. 276 Apr 34


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