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)

Bismuth subsalicylate preparations are over-the-counter products for gastrointestinal complaints. Bismuth toxicity causes delirium, psychosis, ataxia, myoclonus, and seizures and is reversible over several weeks or months, when bismuth intake is stopped. We report a 54-year-old man with a 6-week history of progressive confusion and memory difficulty and a 2-3-week history of involuntary movements and gait impairment. His encephalopathy was further characterized by marked multifocal myoclonic jerks, coarse postural tremors, postural instability, and gait ataxia. He gradually improved. Extensive toxic, metabolic, and infectious workup demonstrated bismuth toxicity. Spinal tap and brain magnetic resonance scan were normal. Electroencephalography showed bihemispheric slowing. As his encephalopathy cleared, he reported using bismuth subsalicylate long term (daily intake of 8 oz). Bismuth levels 5 weeks after cessation of bismuth were elevated and normalized after 12 weeks. He followed a typical course for bismuth toxicity with subacute progressive encephalopathy and gradual recovery. Creutzfeldt-Jakob was strongly considered due to his rapidly progressive encephalopathy, multifocal myoclonus, and ataxia. Due to its rarity, bismuth toxicity is often overlooked. We hope this presentation will increase recognition of bismuth toxicity. We believe more detailed labeling of bismuth products is needed to avoid similar toxicity from this readily available product.
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PMID:Bismuth subsalicylate toxicity as a cause of prolonged encephalopathy with myoclonus. 775 66

Up to now, clinical predictors for the course of the alcohol withdrawal syndrome, especially for the occurrence of a delirium, are lacking. Thus, this study was undertaken to examine whether clinical routine investigations at admission before the withdrawal syndrome can reveal factors indicating a higher risk for the development of a delirium. Our results showed that decreased serum electrolyte concentrations (i.e., chloride and potassium), elevated ALT, and gamma-glutamyltransferase serum levels, as well as ataxia and polyneuropathy at the neurological examination, indicate a higher risk for the development of an alcohol withdrawal delirium.
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PMID:Clinical predictors of alcohol withdrawal delirium. 784 90

Psychiatric medications cause side effects in several organ systems that need emergency evaluation and treatment. Serious cardiovascular side effects include postural hypotension, cardiac conduction blockade, and SA mode dysfunction; serious neurological side effects include extrapyramidal reactions, seizures, delirium, catatonia, pseudotumor cerebri, ataxia, and glaucoma; serious genitourinary side effects include urinary retention, nephrotic syndrome, and priapism, and the serious hematological side effect of agranulocytosis. Also potentially fatal syndromes secondary to psychiatric drugs are the neuroleptic malignant syndrome, hyperandrenergic crisis, the serotonin syndrome, and lithium toxicity. Individual psychiatric drug classes most notorious for causing side effects with high morbidity and mortality are low potency neuroleptics, clozapine, tertiary tricyclics, monoamine oxidase inhibitors, and lithium.
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PMID:Emergencies caused by side effects of psychiatric medications. 816 98

We reviewed the records and radiologic studies of eight patients who developed new focal neurologic abnormalities while receiving interleukin-2 (IL2)-based immunotherapy for malignancy or HIV infection. Initial confusion and delirium in the patients evolved into coma, ataxia, hemiparesis, seizures, and cortical syndromes including aphasia, apraxia, and cortical blindness. Imaging studies showed multiple white and gray matter lesions with a predilection for the occipital poles, centrum semiovale, and cerebellum. After cessation of IL2 treatment, seven patients improved to normal or near-normal neurologic function paralleled by resolution of the lesions on scans. One patient improved only minimally. Possible etiologies for the lesions include an IL2-induced cerebral vasculopathy, a direct toxic effect of IL2, or immunologically mediated damage.
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PMID:Multiple cerebral lesions complicating therapy with interleukin-2. 875 14

Aging is a physiological process that shares many behavioral, biochemical and neuroendocrine phenomena with the pathophysiological situation of unresolved stress, as well as with a pharmacologically induced syndrome resulting from chronic benzodiazepine (BZ) consumption. Behavioral findings include symptoms such as drowsiness, ataxia, fatigue, confusion, weakness, dizziness, vertigo, syncope, reversible dementia, depression, impairment of intellectual, psychomotor and sexual function, agitation, auditory and visual hallucinations, paranoid ideation, panic, delirium, depersonalization, sleepwalking, aggressivity, orthostatic hypotension, and insomnia. Neuroendocrine findings include: central depletion of noradrenaline (NA), dopamine, adrenaline (AD), and serotonin (5-HT); reduction in the ratio of circulating NA/AD as well as platelet 5-HT and increase of AD, plasma free 5-HT and cortisol. These disturbances together with the increased platelet aggregability observed in the three groups are typical of unresolved-stress situations. Immunological findings include significant reduction of peripheral T lymphocytes (CD3, CD4, CD8) and the CD4/CD8 ratio, CD16 and gamma-delta cells. On the other hand, the three groups (elderly subjects, subjects faced with unresolved stress, and BZ consumers) show increase of the CD57 lymphocyte subset as well as natural killer cytotoxicity. Alterations of several biological markers have also been found, specifically in the oral glucose tolerance test, the intramuscular clonidine test, and the supine/orthostasis/exercise test. From a clinical point of view, the three groups appear to be more susceptible to the appearance and progression of many acute and chronic diseases (infectious and malignant diseases). As a result, chronic consumption of BZs should be avoided in both the elderly and subjects in unresolved-stress situations.
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PMID:Benzodiazepines: tolerability in elderly patients. 884 97

Creutzfeldt-Jakob disease is relatively poorly documented in psychiatry. An observation will be presented concerning a 69 years old patient admitted for conduct disorder and prosecution delirium. In fact, the symptomatology associated dementia, transient confusion, parkinsonism, ataxia and abnormal movements. In the checkup the electroencephalogram gave us an important orientation for diagnosis. After a thoracic trauma the patient was admitted in an intensive care unit with a positive pressure ventilation. His general condition worsened until he died. Brain histic exploration and PRP gene analysis confirmed the diagnosis. Even if there is no efficient treatment, such a diagnosis has to be done in order to take prophylactic measures and conduct epidemiological surveys.
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PMID:[Creutzfeldt-Jakob disease and psychiatry. Apropos of a case]. 917 71

A 60-year-old diabetic male presented with transient ischemic attacks. Initial neurological examination and head CT were normal. Dysarthria, ataxia, delirium, and lethargy developed. A diagnosis of cryptococcal meningitis was made after lumbar puncture and treatment with intravenous amphotericin B and 5-fluorcytosine was begun. A repeat head CT showed an anterior cerebral artery territory infarct. His condition worsened and he died of associated complications three weeks after admission. The case is used to discuss the association between cryptococcal meningitis and diabetes, transient ischemic attacks, and vasculitis with cerebral infarction.
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PMID:Case of the month: July 1997--diabetic male with transient ischemic attacks. 945 81

A case of Creutzfeldt-Jakob disease (CJD) with presenting Wernicke encephalopathy (WE)-like symptoms and severe insomnia is presented. An 80-year-old alcoholic man with a 6 month history of tremors, ataxia, memory loss and confabulation, developed profound insomnia, confusion, and delirium with vivid hallucinations. Polysomnography revealed a marked reduction of sleep time, with central-type sleep apnea. Neither myoclonus nor periodic synchronous discharge (PSD) was observed. An autopsy revealed diffuse spongiform changes and astrocytosis throughout the cerebral gray matter, with severe involvement of the mammillary bodies and thalamus. Prion protein (PrP) immunostaining was positive in kuru plaques in the cerebellum, PrP polymorphism at codon 129 was heterozygous Met/Val, and proteinase K resistant PrP (PrP(res)) was demonstrated by Western blotting. The lack of necrotizing lesions in the mammillary bodies, thalamus, and periaqueductal gray matter could rule out WE. The data suggest that the present case of CJD is consistent with PrP(res) type 2 (CJD M/V 2), but was unique in the lack of some typical CJD signs and the presence of signs of WE and sleep abnormalities.
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PMID:Wernicke encephalopathy-like symptoms as an early manifestation of Creutzfeldt-Jakob disease in a chronic alcoholic. 1037 Oct 84

The term Morvan's disease, first coined in 1890, is still in use, although the generic term neuromyotonia--which is not exempt from criticism--has largely superseded it. Symptoms and signs are variable, ranging from benign painful fasciculations, pseudomyotonic cases, rigid forms, cases in which central nervous system features are also present (with, in addition to nerve hyperexcitability, agitation, confusion, delirium, insomnia, hyperhidrosis and tachycardia). A distal peripheral motor nerve is the origin of nerve hyperexcitability. There is growing evidence that autoimmunity is involved in the pathogenesis of many cases. Antibodies to voltage-gated potassium channels are detected in the serum of many patients with peripheral nerve hyperexcitability. Other cases are probably genetic. Inherited disorders are related to episodic dominant ataxia type 1, with the same mutation of a gene coding for potassium channel subunit Kv 1-1. Many inappropriate or non specific names are used to refer to peripheral nerve hyperexcitability. Isaacs syndrome, voltage-gated potassium channelopathy, or Morvan's syndrome are suggested.
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PMID:[From Morvan's disease to potassium channelopathies]. 1550 15

A postherpetic-neuralgia patient abruptly discontinued pregabalin. Thirty hours later, unexplained nausea, headache, and ataxia developed, progressing to delirium 8 days later. Magnetic resonance imaging indicated T2-hyperintense lesions of her splenium. Similar magnetic resonance imaging abnormalities, interpreted as focal vasogenic edema, develop in some epileptic patients after rapid anticonvulsant withdrawal. Patients with high-altitude cerebral edema have similar splenial-predominant magnetic resonance imaging abnormalities that accompany these same neurological symptoms. This case is the first to associate anticonvulsant-withdrawal splenial abnormalities with neurological symptoms, with gabapentin-type anticonvulsants, and is among the first in nonepileptic patients, suggesting that sudden anticonvulsant withdrawal alone, unaccompanied by seizures, can initiate symptomatic focal brain edema. The similarity of this syndrome to high-altitude cerebral edema suggests a possible common pathophysiology and offers potential therapies.
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PMID:Pregabalin-withdrawal encephalopathy and splenial edema: a link to high-altitude illness? 1637 25


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