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

Neurologic complications may appear before the primary disease, alcoholism, is recognized. The common syndromes are polyneuropathy, the withdrawal syndrome and the combination of Wernicke's encephalopathy and Korsakoff's psychosis. Other conspicuous clinical pictures include ataxia of cerebellar origin, convulsions, acute hallucinosis, myopathy and coma. Rarer disorders are Marchiafava-Bignami disease and central pontine myelinolysis.
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PMID:The neurologic complications of alcoholism. 18 91

In spontaneous cerebellar hemorrhage emergency surgical intervention is often life-saving. Clinical features and the operative results of hypertensive cerebellar hemorrhage (18 cases) were compared with those of hemorrhage caused by small angiomas (7 cases). Hypertensive hemorrhage occured most frequently in the seventh decades. Two thirds of the patients developed brainstem compression syndrome within a week from onset. One third remained awake or drowsy throughout their clinical course. Surgical removal of a hematoma was carried out in 13 patients with four deaths. Of note, two comatose patients regained consciousness after surgery, and were discharged with residual ataxia. Rupture of a small angioma occurred in younger patients. Their clinical course was sub-acute or chronic associated with focal cerebellar dysfunction. All seven surgically treated patients subsequently regained independent function. CT findings have been found helpful not only for diagnosis but also in defining appropriate therapy. Hematomas larger than 3 cm in diameter produced signs of rapidly progressing compression of the brainstem. Thereby, regardless of the cause of bleeding, emergency removal of a clot is indicated even in awake patients. Hematomas of 2 to 3 cm produced brainstem compression or prolonged cerebellar dysfunction, and occasionally require surgical decompression. Hematomas smaller than 2 cm can be managed conservatively, since they were absorbed spontaneously in three weeks without residual functional disturbances. However, in case of a young patient exploration should be performed for a probable "cryptic" angioma.
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PMID:[Diagnosis and treatment of cerebellar hemorrhage: comparison of hypertensive hemorrhage with hemorrhage caused by small angiomas, and CT findings (author's transl)]. 49 56

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

Rats were treated by intragastric intubation of a 20% ethanol solution in doses of 9-15 g/kg in 3-5 fractions for 1-7 days. Both tolerance and physical dependence were demonstrated after this treatment with the maximum tolerable doses to only a few days. Tolerance was assessed by signs of severity of intoxication: coma, loss of righting reflex, ataxia-3, ataxia-2, ataxia-1, sedation, and neutrality. During withdrawal, as blood ethanol concentrations approached 100 mg/dl the ethanol dependence phase was characterized by the onset of signs and responses of progressive severity: hyperactivity, tremors, spastic rigidity, and spontaneous convulsive seizures. A significant degree of tolerance was demonstrated for all signs of intoxication after 4 days of treatment, but did not reach maximum level even after 7 days. The severity of the withdrawal reactions intensified progressively to a maximum intensity after 4 days of treatment when as many as 72% of animals exhibited severe withdrawal signs and reactions including convulsive seizures. These different time courses suggest that tolerance and physical dependence are mediated through different mechanisms.
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PMID:Temporal relationship of the induction of tolerance and physical dependence after continuous intoxication with maximum tolerable doses of ethanol in rats. 82 49

Anticholinergic agents may lead to a syndrome described by Longo as the Central Anticholinergic Syndrome (CAS). Patients with this syndrome exhibit one or more of the following: though impairement, disturbance of recent memory, hallucinations, ataxia, excitement, drowsiness of coma. We have reviewed our use of anticholinergics and tried to correlate it with the occurrence of the above symptomatology and have treated 200 cases in which the CAS was diagnosed with physostigmine salicylate (0.04 mg/kg). We also successfully treated 2 cases of apparently central anticholinergic hyperpyrexia in the same way. We would suggest that physostigmine be included in the armamentarium of every anesthetist to combat anticholinergic poisoning by the wide range of presently used anticholinergic drugs. (Act anaesth. belg., 1976, 27, 45-60).
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PMID:Central anticholinergic syndrome in anesthetic practice. 102 54

Sixty-six hospitalized patients suffering from chronic methylmercury poisoning were examined in Baghdad during 1972. The poisoning was attributed to consumption of home-made bread prepared from seed wheat treated with mercurial fungicide. The age incidence ranged between 4 and 70 years.Of the various clinical features encountered, neurological symptoms and signs were predominant and included muscular weakness, numbness, unsteady gait, paraesthesia, dysarthria, mental disturbances and, in severe cases, blindness, partial deafness, stupor, coma, and death. Involvement of the cardiovascular, urinary, gastrointestinal and haemopoietic systems, which was commonly encountered in ethylmercury poisoning in the 1960 outbreak in Iraq, was unusual.The severity of symptoms and signs was, broadly speaking, dose-dependent; high exposure led to severe clinical manifestations, but variations existed. Criteria, based on the clinical manifestations, were set for grading the severity of cases. The series included 2 asymptomatic cases, 20 mild, 20 moderate, 14 severe, and 10 very severe. In the latter group 5 patients died from failure of the central nervous system.The severely poisoned patients died irrespective of the medical treatment received. After 2 years of observation, most patients graded as mild or moderate cases lost their symptoms completely. Severe cases improved slowly, although ataxia, diminution of visual field and acuity and paraesthesia were still present. Thus, the previously accepted view that neurological signs were irreversible has been disproved.
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PMID:Intoxication due to alkylmercury-treated seed--1971-72 outbreak in Iraq: clinical aspects. 108 68

Five-week-old broilers were submitted to the diagnostic laboratory showing sudden onset of incoordination, ataxia, anorexia, dehydration and coma. Groups of birds were being fed the New England Conference (NECC) broiler diets in which scallop viscera was added. Moribund birds receiving thiamine hydrochloride recovered without complications.
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PMID:Observations of possible thiaminase activity in scallop viscera fed in broiler diets. Case report. 116 88

Two cases of acute meningoencephalitis, presumably viral in origin, with brainstem involvement are reported. Common to both patients during the course of their illness was coma, downbeat nystagmus, and ataxia. Although both reached what appeared to be a terminal state, recovery began following treatment with corticosteroids. The significance of the neurologic signs, particularly the unusual occurrence of downbeat nystagmus, is discussed, as is the appropriate management of the disorder.
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PMID:Downbeat nystagmus as a sign of brainstem involvement in acute meningoencephalitis. 116 35

This paper reports findings relative to a simple, rapid and reproducible technique for the induction of physical dependence upon ethanol in the rat. The dependence was induced by intragastric intubation of 20% (w/v) ethanol solutions at 9-15 g/kg in 3-5 fractional doses daily for 4 days, maintaining blood ethanol concentrations above a threshold level sufficient to sustain observable sedation throughout the entire period of intubation. Two phases were distinguished during the withdrawal period: 1. Prodromal detoxication, characterized by a spectrum of signs and responses of diminishing severity, related to the decline in blood ethanol concentrations (mg/dl): death, greater than 640; coma, 780-460; loss of righting reflex, 640-400; ataxia 3-1, 570-250; sedation 340-190; neutrality, 220-130; 2. Ethanol dependence, characterized by a spectrum of withdrawal signs and reactions of progressively increasing severity as blood ehtanol concentration approached 100 mg/dl: hyperactivity, tremors, akinesia, spastic rigidity, and induced and spontaneous convulsions. A rapid sucession of two diverse clusters of signs and reactions represents a reversal of the central nervous system function from the extremes of ethanol intoxication (CNS depression) to the extremes of ethanol dependence (CNS hyperexcitability) during the withdrawal period. Both extremes may terminate in death.
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PMID:Induction of physical dependence upon ethanol and the associated behavioral changes in rats. 123 14


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