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

Acute cerebellar toxicity with ataxia and dysarthria is a well-known side effect during high-dose cytarabine therapy. Dose, age, previous neurological disorders, hepatic dysfunction, and renal insufficiency have been inconsistently reported as risk factors. The present paper presents a patient with renal insufficiency who developed severe cerebellar toxicity following treatment with a dose of cytarabine (8 g/m2 over 5 days) not generally expected to be associated with neurotoxicity. Together with a review of the literature, the present case gives evidence of renal insufficiency as a major risk factor in the development of cerebellar toxicity during cytarabine therapy. Reduced doses of cytarabine should be considered in patients with renal impairment.
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PMID:Cerebellar toxicity during cytarabine therapy associated with renal insufficiency. 224 95

Amantadine and rimantadine are recommended for the treatment and prophylaxis of influenza A infections, and constitute an integral component of influenza control measures in the nursing home setting. However, optimal use necessitates a thorough understanding of the toxicity profiles of these agents, as well as strategies to reduce the risk of adverse reactions. Adverse reactions of these compounds predominantly involve the gastrointestinal tract and the central nervous system (CNS), including hyperexcitability, slurred speech, tremors, insomnia, dizziness, mood disturbance, ataxia, psychosis and fatigue. Based on data from comparative trials, rimantadine appears to exhibit a lesser propensity to cause adverse CNS reactions than amantadine, but a similar propensity to cause adverse gastrointestinal reactions. Factors enhancing the risk of adverse reactions to these agents include reduced renal function (especially for amantadine), drug-drug interactions with cationic drugs, which inhibit amantadine renal tubular secretion (e.g. trimethoprim, triamterene, and possibly cimetidine and procainamide), elevated peak and trough plasma concentrations, and a history of seizures. Careful attention to published dosage adjustment guidelines for these compounds, avoidance of interacting drugs and avoiding these agents in patients with a history of seizures may be the best means to reduce the risk of toxicity in elderly patients. Rimantadine may have an advantage over amantadine in the elderly population in light of its lesser propensity to cause adverse reactions, less complex dosage adjustment in the case of renal impairment and probable lack of drug-drug interaction potential with cationic drugs.
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PMID:Amantadine and rimantadine prophylaxis of influenza A in nursing homes. A tolerability perspective. 791 41

We report the case of a 44 year old man who presented with a two-month history of dysarthria, ataxia and leg weakness whilst on maintenance lithium for bipolar disorder. Examination revealed significant cerebellar and pyramidal dysfunction. Serum lithium was 1.5 mmol/l, a moderate elevation above his usual stable levels of 0.4-0.8 mmol/l. The patient's past history included hypertension and chronic renal impairment and the development of neurological symptoms coincided with the recent onset of heart failure. On cessation of lithium he partially recovered, the main residuum being persistent cerebellar ataxia. The case is an example of lithium neurotoxicity developing insidiously in the absence of an overt acute phase syndrome, and highlights the need for keen observation of the patient in the hope of preventing permanent deficits.
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PMID:Lithium neurotoxicity: the development of irreversible neurological impairment despite standard monitoring of serum lithium levels. 1209 41

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

An 84-year-old male with stage III chronic kidney disease and a history of multiple psychiatric and medical disorders presented to the emergency department (ED) with new onset proximal leg weakness with tremor upon standing, truncal ataxia, and myoclonic jerks of the upper extremity that had progressively worsened over three weeks. Magnetic resonance imaging and head computed tomography showed no acute change from baseline. After admission, the patient reported visual hallucinations, vertigo, and slurred speech, and displayed nocturnal agitation/delirium. These symptoms were managed with risperidone. Prior to admission, the most recent medication change was the initiation of bupropion 100 mg extended-release twice daily. Bupropion was titrated to 150 mg twice daily over the three weeks prior to the ED visit. Gradual tapering of the bupropion dose was started after admission. Symptoms of agitation, delirium, speech, and motor disturbances decreased 36 to 48 hours after bupropion dose was lowered to 75 mg daily, and risperidone was changed to quetiapine. The patient was discharged to short-term rehabilitation with return of mental status to baseline. Bupropion and quetiapine were discontinued at discharge from the rehabilitation center. Case reports exist for acute psychotic and parkinsonian symptoms after administration of bupropion and bupropion extended-release, but none exist for the combination of focal neurologic deficits and psychotic symptoms found in this patient's presentation. Limited pharmacokinetic data in the elderly and those with renal impairment suggest that this patient population may have reduced clearance of bupropion. Dose adjustment should be considered in such patients and signs of toxicity closely monitored. Adverse reactions to bupropion should be considered if a patient presents with acute neurologic or psychotic symptoms after initiation or dose modification of bupropion.
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PMID:Progressive tremor, truncal ataxia, and acute mental status changes after use of bupropion. 2189 73

A retrospective analysis of telephone enquiries to the Veterinary Poisons Information Service found 772 cases with follow-up concerning suspected metaldehyde slug bait ingestion in dogs between 1985 and 2010. Half the enquiries occurred in the summer months. The amount and strength of the slug bait ingested was rarely known. In 56, cases the quantity consumed was estimated and was on average 229.6 grams of bait. Clinical signs developed in 77.3 per cent of dogs; common signs were convulsions, hypersalivation, twitching, hyperaesthesia, tremor, vomiting, hyperthermia and ataxia. Only 4.6 per cent of dogs developed hepatic changes, and only one developed renal impairment. The average time to onset of signs was 2.9 hours post-ingestion, with 50.3 per cent of dogs developing effects within one hour. Increased muscle activity (twitching, convulsions) lasted on average 15.2 hours. Recovery time was reported in 61 cases and occurred on average at 39.3 hours. Common treatments were gut decontamination, anticonvulsants, anaesthetics and intravenous fluids. Of the dogs that were treated with sedatives, 45.8 per cent required more than one sedative or anaesthetic agent. Methocarbamol was rarely used, probably due to unavailability. The outcome was reported in 762 dogs; 21.7 per cent remained asymptomatic, 61.7 per cent recovered and 16 per cent of dogs died or were euthanased. Where known (only six cases), the fatal dose of bait ranged from 4.2 to 26.7 g/kg (average 11.8 g/kg).
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PMID:Suspected metaldehyde slug bait poisoning in dogs: a retrospective analysis of cases reported to the Veterinary Poisons Information Service. 2285 14

Listeriosis is a rare food borne infection which, in the invasive form, presents as bloodstream infection, central nervous system infection, materno-fetal infection, or focal infection. Certain immunosuppressive conditions have been identified as risk factors for severe invasive disease. The invasive forms of listeriosis are associated with a high case fatality rate. We present the case of a 62-year-old male with an unremarkable medical history admitted to the Iasi Infectious Diseases Hospital for fever. headache, ataxia, and diplopia. Physical examination revealed high temperature, confusion, relative bradycardia, and signs of meningeal irritation. Laboratory test showed leukocyt osis with neutrophilia. pathological CSF findings (high WBC count with predominance of neutrophils, low glucose and high protein levels), increased liver enzymes (ALAT, ASAT, AP, gammaGT), and important renal impairment (normal levels at presentation). No abnormalities at chest x-ray, cranial CT and abdominal ultrasound. CSF and blood cultures were positive for Listeria monocytogenes. Under antibiotics (ampicillin and ciprofloxacin), the course was marked by respiratory failure requiring mechanical ventilation, coma, hypotension, tachycardia. and death 12 days after admission. The particularity of this case consists in the association of the two classical forms of invasive listeriosis, meningitis and bacteriemia, with a focal infection. acute hepatitis, and a course marked by multiple organ dysfunction syndromes and exitus in a previously apparently healthy individual.
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PMID:Severe invasive listeriosis--case report. 2327 33

Impaired renal function increases the risk for cefepime-induced neurotoxicity. Symptoms include disorientation, myoclonus, status epilepticus, ataxia, gait disturbance, coma, and death. A high index of suspicion and early recognition of symptoms can minimize the risk of progression of symptoms to permanent neurologic impairment or death.
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PMID:Cefepime-induced neurotoxicity in a pediatric patient on chronic hemodialysis: a case report. 2922 28

Movement disorders often emerge from the interplay of complex pathophysiological processes involving the kidneys and the nervous system. Tremor, myoclonus, ataxia, chorea, and parkinsonism can occur in the context of renal dysfunction (azotemia and electrolyte abnormalities) or they can be part of complications of its management (dialysis and renal transplantation). On the other hand, myoglobinuria from rhabdomyolysis in status dystonicus and certain drugs used in the management of movement disorders can cause nephrotoxicity. Distinct from these well-recognized associations, it is important to appreciate that there are several inherited and acquired disorders in which movement abnormalities do not occur as a consequence of renal dysfunction or vice versa but are manifestations of common pathophysiological processes affecting the nervous system and the kidneys. These disorders are the emphasis of this review. Increasing awareness of these conditions among neurologists may help them to identify renal involvement earlier, take timely intervention by anticipating complications and focus on therapies targeting common mechanisms in addition to symptomatic management of movement disorders. Recognition of renal impairment in a patient with complex neurological presentation may narrow down the differentials and aid in reaching a definite diagnosis.
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PMID:Movement Disorders and Renal Diseases. 3304 74