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

Five patients experienced severe encephalopathy within hours of receiving their initial dose of cranial irradiation for the treatment of central-nervous-system leukaemia. Neurological findings included cranial-nerve palsies, seizures, ataxia, depressed consciousness, increased intracranial pressure, and signs of herniation. Symptoms developed within 3-30 hours of the first radiation treatment of 50-200 rad. Each patient had also received one or more injections of intrathecal chemotherapy before encephalopathy developed. The aetiology of this syndrome is uncertain but may involve transient cerebral oedema and/or an altered blood-brain barrier produced by the combination of intrathecal chemotherapy and cranial irradiation.
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PMID:Acute encephalopathy after initiation of cranial irradiation for meningeal leukaemia. 7 11

Toxic metals encountered industrially or environmentally may produce the following syndromes: 1) Peripheral neuropathy: which is mainly sensory in arsenic and entirely motor with inorganic lead, organophosphorus compounds and tallium produce a mixed form of peripheral neuropathy. 2) Encephalopathy: usually with lead poisoning where ataxia and hemiplegia or optic atrophy may occur. 3) Optic neuritis: transient or permanent impairment of vision in arsenic poisoning and blurring of vision followed by field fedects with thallium poisoning. 4) Cerebellar disturbances: in the form of ataxia in organic mercury. 5) Parkinsonism: extrapyramidal signs occurs in manganese poisoning shown as mask face and rigidity of muscles. 6) Mental changes: as acute psychosis in organic lead and erethism in organic mercury.
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PMID:Neurological syndromes produced by some toxic metals encountered industrially or environmentally. 35 38

Organic mercury compounds have greatest affinity to the central nervous system (cerebellar white matter, basal ganglia, occipital and frontal cortex). Anatomical changes observed in the brain are of degenerative type. Similar changes are found also in the myocardium, liver and kidneys. The authors observed for 2 years a family of three persons who contracted poisoning with organic mercury compounds after easting the meat of pigs and hens fed through negligence with wheat destined for sowing, containing methyl-mercurocyanoguanidine. The level of total mercury determined by the method of cold atomic absorption was in these patients four months after poisoning 650,500 and 175 ng/ml of blood (normal value from 1.56 to 18.72 ng/ml). During the observation it has been established that the severity of poisoning was related to the level of mercury found in the organism. Pharmacological treatment (Cuprenil, Thioctacid, vitamin B complex) and rehabilitation brough slight improvement after 2 years. Two patients with total blood mercury level 650 and 500 ng/ml were completely disabled due to encephalopathy with high grade ataxia, dysarthria and concentric narrowing of the field of vision. In the third patients with less severe poisoning (175 ng/ml) pathological manifestations disappeared completely after short treatment.
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PMID:[Encephalopathy after poisoning with organic mercury compounds]. 48 88

Acute encephalopathy caused by gasoline sniffing is well recognized, but has been thought to be completely reversible. We report a patient who developed a progressive encephalopathy characterized by ataxia, tremor and dementia following repeated, deliberate gasoline inhalation. Blood and urine lead levels were consistently elevated and at autopsy, the formalin-fixed brain lead content was between 5200 and 6500 micrograms/100 gm of tissue. This case shows that repeated gasoline sniffing can result in irreversible encephalopathy and that both the acute and chronic encephalopathy probably result from organic lead intoxication and not from the gasoline itself.
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PMID:Acute and chronic progressive encephalopathy due to gasoline sniffing. 56 91

A toxic encephalopathy characterized by depressed level of consciousness, marked irritability, and ataxia developed in seven children, 5 years of age and younger, following administration of an antiemetic combination of pentobarbital and pyrilamine maleate. Three of the seven patients were given a dosage of medication and exceeding the manufacture's recommendation. All seven patients recovered without sequelae.
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PMID:Toxic encephalopathy related to antihistamine-barbiturate antiemetic medication. 62 61

The dog with an end-to-side portacaval shunt (PCS) has been extensively used as a model to investigate hepatic encephalopathy (HE) as it demonstrates a plasma amino acid pattern similar to patients with chronic liver disease. In adult mongrel dogs, the effect of PCS on plasma and CSF amino acids, octopamine (OCT), phenylethanolamine (PEA) and CSF 5-hydroxyindolacetic acid (5-HIAA), were studied. Moreover, the effect of correction of plasma amino acids by infusional techniques was investigated.Tyrosine, tryptophan and phenylalanine levels increased dramatically during the development of HE in plasma and CSF, while valine, leucine and isoleucine decreased in plasma only, but CSF levels remained stable. Plasma and CSF octopamine and phenylethanolamine and CSF 5-HIAA increased markedly as clinical features in the dogs' behavior, characteristic of hepatic encephalopathy occurred, including hypersalivation, ataxia, flapping tremor, somnolence and finally coma. Once in coma, the dogs were infused with an amino acid mixture (F080) calculated to normalize the plasma amino acid pattern. After one to eight hours, the dogs began to awake. Simultaneously, blood, and CSF aromatic amino acids returned to their control values, as did OCT, PEA and CSF 5-HIAA. If F080 infusion was stopped, biochemical alterations would appear within one week, again accompanied by clinical hepatic encephalopathy.The results indicate that the altered levels of aromatic and branched chain amino acids, octopamine and PEA in plasma and CSF correlate well with the development of HE and that correction of the plasma amino acid abnormalities improves encephalopathy simultaneously with correction of neurotransmitter derangements in CSF.
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PMID:Alterations in plasma and CSF amino acids, amines and metabolites in hepatic coma. 63 94

A fatal case of toxic encephalopathy due to ingestion of bismuth salts is reported in a twenty year old female patient. The clinical features were characterized by a confusional state, ataxia, myoclonic jerks, and epileptic seizures. Despite supportive therapy and administration of chelating agents, there was an irreversible evolution towards coma. The immediate cause of death was an intercurrent septicaemia. The anatomo-pathological study showed non specific anoxic lesions including a widespread loss of Purkinje cells in the cerebellum. Despite a drastic decrease of bismuth levels in blood, the concentration of bismuth in visceral organs and different parts of the central nervous system remained very high.
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PMID:Bismuth encephalopathy. A clinical and anatomo-pathological report of one case. 71 34

Similar movement disorders developed in two 8-year-old retarded children while they were receiving phenytoin. Seizures subsequent to a diphtheria-pertussis-tetanus immunization had developed in each child at 1 to 2 months of age. A static encephalopathy ensued, characterized by mental retardation, ataxia, spasticity, and a mixed seizure disorder. Intermittent dystonia and choreoathetosis developed insidiously while serum phenytoin concentrations were in the therapeutic range. Sustained dystonia and choreoatheosis developed 2 hours after an oral provocation with phenytoin. The baseline abnormalities on the electroencephalogram remained unchanged during the choreoathetosis. Recognizable metabolic abnormalities known to be associated with similar movement disorders were excluded. It was concluded from these studies that the movement disorder is secondary to phenytoin and can occur at therapeutic serum concentrations. Phenytoin is a central anticholinergic agent and a central stimulant of serotonin, and may induce movement disorders as a result of altering these neurotransmitters in the brain. The variable expression of these movement disorders may relate to the nature of the preexisting striatal insult.
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PMID:Phenytoin-induced dystonia and choreoathetosis in two retarded epileptic children. 94 1

Bismuth encephalopathy, characterized by the constant association of acute confusion, myoclonus, severe ataxia and dysarthia has reached "epidemic" proportion since its first description in 1974. The clinical aspects the pathogenic hypothesis, the diagnostic criteria as well as the report of a typical case are described by the authors, who stress the similarities with encephalopathies induced by other metals.
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PMID:Bismuth encephalopathy. 100 97

Scrapie and transmissible mink encephalopathy were studied in hamsters; clinical signs, pathology, and the replication of the agents of each disease in brain and spleen were compared. The most noticeable clinical sign in scrapie-affected hamsters was a distinct cerebellar ataxia beginning 16 weeks after inoculation. Ataxia was not prominent in animals affected with transmissible mink encephalopathy; these animals gradually became more and more lethargic. The pathology in the central nervous system in both diseases consisted of astrocytic hypertrophy, microvacuolation of the neuropil, and neuronal degeneration. The scrapie agent appeared to have a greater effect on nuclear masses, especially those present in brain stem and the central white matter of the cerebellum. The earliest lesions in both diseases were detected near pia arachnoid surfaces and adjacent to the ventricular system. These initial sites of involvement suggest that the cerebrospinal fluid may be an important route by which inocula are disseminated to susceptible cells after intracerebral inoculation. Both agents multiplied rapidly in brain, reaching titers greater than 10-8 ld-50/0.05 ml before the onset of clinical signs. Titers in spleen were 4-6 logs lower than titers in brain at every point measured during the asymptomatic or clinical course of disease.
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PMID:Comparison of scrapie and transmissible mink encephalopathy in hamsters. II. Clinical signs, pathology, and pathogenesis. 116 84


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