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)

Paraneoplastic neurologic syndromes are disorders of the nervous system function caused by cancer but not due to metastatic disease, vascular or metabolic deficits, infections, nutritive deficiency, nor side effects of antineoplastic drugs or irradiation. Immunologic factors probably play the crucial role in the pathogenesis of paraneoplastic neurologic syndromes, but nonimmunologic mechanisms that include metabolic abnormalities and competition for substrate are also involved. Paraneoplastic cerebellar degeneration most commonly occurs in the setting of gynecologic cancers, but it accompanies the small-cell lung cancer too. Other tumors are infrequently associated with cerebellar degeneration. Several paraneoplastic antibodies have been identified in patients with paraneoplastic cerebellar degeneration. Their association with particular cancers may help identify an occult lesion. Anti-Yo antibodies are directed against Purkinje cell antigens and occur in patients with cerebellar degeneration who have breast cancer or gynecologic tumors. A target antigen of anti-Yo antibody is CDR2 protein that is normally expressed only in the brain and testis. Patients with paraneoplastic cerebellar degeneration present with dizziness, nausea and vomiting followed by gait instability, diplopia, gait and appendicular ataxia, dysarthria and dysphagia. Therapeutic options include tumor excision, chemotherapy and/or irradiation, and adjuvant therapy with glucocorticoids, immunoglobulins and plasmapheresis. The role of plasmapheresis in the treatment of paraneoplastic cerebellar degeneration is still uncertain. Reports of its efficacy are anecdotal. We present patient with paraneoplastic cerebellar degeneration with positive anti-Yo antibodies and tumor of the ovaries whose neurologic status significantly improved after four daily plasmaphereses, which was accompanied by a fourfold decrease in the anti-Yo antibodies titer. Further investigations are needed to define a protocol for plasmapheresis in the treatment of patients with paraneoplastic syndromes.
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PMID:[Importance of plasmapheresis in the treatment of paraneoplastic cerebellar degeneration]. 1512 96

Candida meningitis, a previously rare occurrence, has been increasing in prevalence and often is a result of complications of neurosurgery. We describe the case of a 49-year-old man who presented with headache, vertigo, intermittent blurred vision, and multiple episodes of nausea and vomiting. Computed tomography (CT) showed a left cerebellar hemorrhage with obliteration of the fourth ventricle causing hydrocephalus. He had an occipital craniotomy with transcondylar evacuation of the hemorrhage and placement of a temporary ventriculostomy. The hospital stay was prolonged because of postsurgical complications, and Candida tropicalis meningitis developed. Treatment was started with 400 mg of fluconazole administered intravenously every 12 h. In vitro susceptibility testing showed a minimum inhibitory concentration (MIC) to fluconazole of 1 microg/mL. Fluconazole was therefore continued orally for a total of 60 days, and the patient remained asymptomatic for 2 years. He then presented with increased vertigo and ataxia. Cerebrospinal fluid cultures grew C. tropicalis, which again showed susceptibility to fluconazole with a MIC of 1 microg/mL, identical to that in the previous infection. However, a second course of fluconazole failed to control the infection despite adequate cerebrospinal fluid levels.
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PMID:Recurrent Candida tropicalis meningitis. 1582 82

Ethylene glycol is recognised as a potentially lethal poison if ingested. Approximately 100 mls may be fatal in a 70 kg adult. Current Toxbase guidelines are the accepted standard of treatment of such poisonings in the United Kingdom. These guidelines suggest that symptoms of significant poisoning are usually present within 30 minutes of ingestion i.e. ataxia, dysarthria, nystagmus, nausea and vomiting, haematemesis, coma and convulsions. In the absence of these symptoms, metabolic acidosis or ethylene glycol concentration more than 8 mmol/l a single loading dose of ethanol and observation were the recommended course of management until recently. We report a case of a patient who remained relatively asymptomatic for almost 24 hours but then developed clinical symptoms with marked metabolic acidosis and renal impairment requiring intensive treatment including haemodialysis.
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PMID:Toxic alcohol but not intoxicated--a case report. 1616 3

Phenytoin toxicity may result from intentional overdose, dosage adjustments, drug interactions, or alterations in physiology. Intoxication manifests predominantly as nausea, central nervous system dysfunction (particularly confusion, nystagmus, and ataxia), with depressed conscious state, coma, and seizures occurring in more severe cases. Cardiac complications such as arrhythmias and hypotension are rare in cases of phenytoin ingestion, but they may be seen in parenteral administration of phenytoin or fosphenytoin. Deaths are unlikely after phenytoin intoxication alone. A greatly increased half-life in overdose due to zero-order pharmacokinetics can result in a prolonged duration of symptoms and thus prolonged hospitalization with its attendant complications. The mainstay of therapy for a patient with phenytoin intoxication is supportive care. Treatment includes attention to vital functions, management of nausea and vomiting, and prevention of injuries due to confusion and ataxia. There is no antidote, and there is no evidence that any method of gastrointestinal decontamination or enhanced elimination improves outcome. Activated charcoal should be considered if the patient presents early; however, the role of multiple-dose activated charcoal is controversial. Experimental studies have proven increased clearance rates, but this effect has not been translated into clinical benefit. There is no evidence that any invasive method of enhanced elimination (such as plasmapheresis, hemodialysis, or hemoperfusion) provides any benefit. This article provides an overview of phenytoin pharmacokinetics and the clinical manifestations of toxicity, followed by a detailed review of the various treatment modalities.
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PMID:Phenytoin poisoning. 1617 88

A 76-year-old man suddenly experienced floating sensation, transient vertigo, and nausea. Neurological examination was unremarkable except for hypotonia and mild ataxia in the limbs, but orthostatic nausea and vomiting forced him to take a quiet, recumbent position. Magnetic resonance imaging of the brain showed cerebellar infarction restricted to the bilateral inferior vermis. During a course of recovery, he fell down in any directions while standing unattended. He was unable to keep the center of gravity on the feet base in an upright posture. The inferior vermis may participate in maintaining the center of gravity while standing.
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PMID:[Cerebellar infarction restricted to bilateral inferior vermis presenting with floating sensation and then astasia]. 1664 35

A review of national poison center data from 1990 through 2003 showed approximately 10,000 annual ingestion exposures to camphor-containing products. A guideline that determines the threshold dose for emergency department referral and need for pre-hospital decontamination could potentially avoid unnecessary emergency department visits, reduce health care costs, optimize patient outcome, and reduce life disruption for patients and caregivers. An evidence-based expert consensus process was used to create the guideline. Relevant articles were abstracted by a trained physician researcher. The first draft of the guideline was created by the primary author. The entire panel discussed and refined the guideline before distribution to secondary reviewers for comment. The panel then made changes based on the secondary review comments. The objective of this guideline is to assist poison center personnel in the appropriate out-of-hospital triage and initial management of patients with suspected exposures to camphor-containing products by 1) describing the manner in which an exposure to camphor might be managed, 2) identifying the key decision elements in managing cases of camphor exposure, 3) providing clear and practical recommendations that reflect the current state of knowledge, and 4) identifying needs for research. This guideline applies to camphor exposure alone. Co-ingestion of additional substances, such as in commercial products of camphor combined with other ingredients, could require different referral and management recommendations depending on the combined toxicities of the substances. This guideline is based on an assessment of current scientific and clinical information. The expert consensus panel recognizes that specific patient care decisions may be at variance with this guideline, and are the prerogative of the patient and the health professionals providing care, considering all of the circumstances involved. This guideline does not substitute for clinical judgment. Recommendations are in chronological order of likely clinical use. The grade of recommendation is in parentheses. 1) Patients with stated or suspected self-harm or who are the recipients of malicious administration of a camphor-containing product should be referred to an emergency department immediately, regardless of the amount ingested (Grade D). 2) Patients who have ingested more than 30 mg/kg of a camphor-containing product or who are exhibiting symptoms of moderate to severe toxicity (e.g., convulsions, lethargy, ataxia, severe nausea and vomiting) by any route of exposure should be referred to an emergency department for observation and treatment (Grade D). 3) Patients exhibiting convulsions following a camphor exposure should be transported to an emergency department by pre-hospital emergency medical care providers (Grade D). A benzodiazepine should be used to control convulsions (Grade C). 4) Patients who have been exposed to a camphor product and who remain asymptomatic after 4 hours can be safely observed at home (Grade C). 5) Induction of emesis with ipecac syrup should not be performed in patients who have ingested camphor products (Grade C). 6) Activated charcoal administration should not be used for the ingestion of camphor products. However, it could be considered if there are other ingredients in the product that are effectively adsorbed by activated charcoal or if other substances have been co-ingested. (Grade C). 7) For asymptomatic patients with topical exposures to camphor products, the skin should be thoroughly washed with soap and water and the patient can be observed at home for development of symptoms (Grade C). 8) For patients with topical splash exposures of camphor to the eye(s), the eye(s) should be irrigated in accordance with usual poison center procedures and that referral take place based on the presence and severity of symptoms (Grade D). 9) Patients with camphor inhalation exposures should be moved to a fresh air environment and referred for medical care based on the presence and severity of symptoms. It is unlikely that symptoms will progress once the patient is removed from the exposure environment (Grade D).
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PMID:Camphor Poisoning: an evidence-based practice guideline for out-of-hospital management. 1680 37

Beriberi is a disease caused by thiamine (vitamin B1) deficiency. Peripheral and central nerve involvement causes psychosis and memory loss as well as cardiocirculatory effects. We report the case of a 35-year-old woman 8 weeks pregnant who came to the emergency department after bouts of nausea and vomiting over a period of 6 days, with intolerance of both solids and liquids. The initial diagnosis of gastroenteritis was later changed to hyperemesis gravidarum. Episodes of vomiting and nausea continued 48 hours after admission, accompanied by vertical nystagmus, ataxia, and diminished osteotendinous reflexes. Evaluation of the clinical picture confirmed vitamin B1 deficiency, leading to a diagnosis of Wernicke-Korsakoff syndrome. Symptoms improved with thiamine therapy but did not entirely disappear. The patient was admitted for elective cesarean section at 37 weeks' gestation. Examination revealed neurological involvement (horizontal and vertical nystagmus) and general anesthesia was therefore chosen to assure adequate hemodynamic control given the possibility of cardiocirculatory alteration.
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PMID:[Anesthetic management for elective cesarean section for a woman with beriberi]. 1739 Jun 94

Schistosomiasis is a parasitic disease caused by blood flukes of the genus Schistosoma. Currently more than 200 million people worldwide are affected. Neuroschistosomiasis constitutes a severe presentation of the disease. Neurological symptoms result from the inflammatory response of the host to egg deposition in the brain and spinal cord. Neurological complications of cerebral schistosomiasis include delirium, loss of consciousness, seizures, dysphasia, visual field impairment, focal motor deficits and ataxia. Cerebral and cerebellar tumour-like neuroschistosomiasis can present with increased intracranial pressure, headache, nausea and vomiting, and seizures. Myelopathy (acute transverse myelitis and subacute myeloradiculopathy) is the most common neurological complication of Schistosoma mansoni infection. Schistosomal myelopathy tends to occur early after infection and is more likely to be symptomatic than cerebral schistosomiasis. The conus medullaris and cauda equina are the most common sites of involvement. Severe schistosomal myelopathy can provoke a complete flaccid paraplegia with areflexia, sphincter dysfunction and sensory disturbances. Schistosomicidal drugs, steroids and surgery are the currently available treatments for neuroschistosomiasis. Rehabilitation and multidisciplinary team care are needed in severely disabled patients.
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PMID:Neurological complications of Schistosoma infection. 1790 71

Simultaneous bilateral cerebellar infarctions in posterior inferior cerebellar arterial (PICA) territory, without brain stem involvement are rare. We herein report a 51-year-old man developed sudden dizziness, nausea and vomiting. CT revealed hypodense bilateral lesions over the cerebellum corresponding to the medial PICA (mPICA) branch territory. His mental state deteriorated 2 days after onset; repeated CT showed severe third and lateral ventricular dilation. Endoscopic third ventriculostomy (ETV) was done to relieve the acute obstructive hydrocephalus. The patient was later discharged with only mild residual ataxia. Compared with conventional surgical treatments (external ventricular drainage, craniectomy and cerebellectomy), ETV has several advantages, including less risk and minimal invasiveness. However, further study is needed on its safety and efficacy under such circumstances.
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PMID:Bilateral cerebellar infarction in the medial branches of posterior inferior cerebellar arterial territory--using endoscopic third ventriculostomy to relieve acute hydrocephalus. 1791 47

Neurotoxic shellfish poisoning (NSP) is caused by consumption of molluscan shellfish contaminated with brevetoxins primarily produced by the dinoflagellate, Karenia brevis. Blooms of K. brevis, called Florida red tide, occur frequently along the Gulf of Mexico. Many shellfish beds in the US (and other nations) are routinely monitored for presence of K. brevis and other brevetoxin-producing organisms. As a result, few NSP cases are reported annually from the US. However, infrequent larger outbreaks do occur. Cases are usually associated with recreationally-harvested shellfish collected during or post red tide blooms. Brevetoxins are neurotoxins which activate voltage-sensitive sodium channels causing sodium influx and nerve membrane depolarization. No fatalities have been reported, but hospitalizations occur. NSP involves a cluster of gastrointestinal and neurological symptoms: nausea and vomiting, paresthesias of the mouth, lips and tongue as well as distal paresthesias, ataxia, slurred speech and dizziness. Neurological symptoms can progress to partial paralysis; respiratory distress has been recorded. Recent research has implicated new species of harmful algal bloom organisms which produce brevetoxins, identified additional marine species which accumulate brevetoxins, and has provided additional information on the toxicity and analysis of brevetoxins. A review of the known epidemiology and recommendations for improved NSP prevention are presented.
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PMID:Neurotoxic shellfish poisoning. 1900 78


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