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 21,692 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two haemodialysis patients with aluminium encephalopathy developed dramatic deteriorations of their neurological symptoms after initiation of desferrioxamine (DFO) therapy. Both patients were treated with relatively large doses of DFO (1 g and 2 g per treatment). In the first case, paranoid delusions, visual hallucinations, seizures and deteriorating speech followed each dialysis treatment with DFO. The second patient experienced increasing confusion, decreasing short-term memory, and deterioration in speech. In both cases the neurological symptoms regressed after decreasing or discontinuing the DFO. These patients demonstrate the potential dangers of using high doses of DFO. The pathogenesis of the exacerbation is not well understood but, may not simply be due to the result of elevated plasma aluminium levels after DFO therapy. We argue in this communication for reducing DFO in patients with aluminium encephalopathy to doses of 1 g three times per week to ensure adequate treatment of aluminium encephalopathy while minimising the risk of exacerbation from overzealous DFO administration.
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PMID:Exacerbation of aluminium encephalopathy after treatment with desferrioxamine. 249 51

Fulminant hepatic failure accompanied by encephalopathy is a rare complication of acute liver disease, especially infection due to hepatitis A virus. We describe a 24-year-old woman and a 27-year-old man who developed this complication. One case presented with loss of consciousness and ended fatally. In the other the presenting symptoms were mental confusion and transient asterixis. Although hepatitis due to virus A is usually mild and the course favorable, one should be aware of the possibility of severe encephalopathy as a complication.
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PMID:[Fulminant hepatic failure due to hepatitis A]. 270 77

A 67-year-old Japanese woman with liver cirrhosis was affected by an unusual acute progressive encephalopathy, presenting mental confusion and slurred speech as its initial symptoms. She died in profound coma, following the entire course of 17 days. Autopsy disclosed bilateral symmetrical, widespread, edematous and necrotic lesions, their centers being located in the basal ganglia, diencephalon and midbrain, and their peripheries expanding into the cerebral white matter, cerebellum, pons and medulla. Diapedesis of erythrocytes and serum plasma was conspicuous, in contrast to paucity of capillary proliferation. Although the lesions were somewhat similar to those of Wernicke's and Leigh's encephalopathies, they were considered to be representative of a more acute metabolic disorder distinct from the latter conditions.
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PMID:Acute necrotizing encephalopathy with widespread edematous lesions of symmetrical distribution. 273 85

D-Lactate-associated encephalopathy is a rare clinical syndrome characterized by dizziness, ataxia, confusion, headaches, memory loss, lethargy, and aggressiveness which may progress to frank but reversible coma. It occurs in patients with profound dysfunction of the short-bowel syndrome and is believed to result from massive carbohydrate malabsorption with resultant over-production of D-lactate and other organic anions by the colonic flora. Extremely elevated serum levels of D-lactate (but not L-lactate) confirm the diagnosis, but currently D-lactate is not clearly established as the putative neurotoxin. We describe a patient who repeatedly developed D-lactate encephalopathy after surgical removal of nearly the entire jejunum and ileum. Markedly elevated D-lactate serum levels were documented during an encephalopathic episode. Potential pathophysiologic mechanisms and the treatment rationale are discussed.
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PMID:D-lactate-associated encephalopathy after massive small-bowel resection. 276 Apr 34

Eighteen consecutive cases of encephalopathy occurring after ifosfamide/mesna chemotherapy were prospectively assessed. No relationship was found with tumour type or chemotherapy response. Onset was from 12 to 146 (mean 46) h after the start of the infusion and median duration was 3 days (range 1-12). In two patients recovery was incomplete. A confusional state and agitation were the major clinical features. Plasma potassium fell from a mean of 4.12 mmol/l before chemotherapy to 2.94 mmol/l at the onset of encephalopathy (P less than 0.001) with plasma potassium less than 3.0 mmol/l in 10 patients. Duration of hypokalaemia was not related to duration of encephalopathy. Median survival following encephalopathy was 25 days. The incidence of encephalopathy in 82 patients treated on two protocols was 11% and the sensitivity of a published nomogram was 18%. It is concluded that ifosfamide/mesna encephalopathy is a serious complication which may be irreversible and remains difficult to predict.
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PMID:Ifosfamide encephalopathy: a reappraisal. 280 53

The authors report the development of a rapidly progressive encephalopathy marked by confusion, myoclonus, seizures, coma, and death in a group of women with renal failure who received an oral solution of citrate and aluminum hydroxide gel concurrently. Two patients were documented as having marked hyperaluminemia far exceeding blood aluminum levels encountered in the chronic state of aluminum intoxication. We ascribe the toxicity to enhanced gastrointestinal absorption of aluminum when complexed with citrate.
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PMID:Acute aluminum toxicity associated with oral citrate and aluminum-containing antacids. 291 1

5'-dFUrd (doxifluridine) is a new fluoropyrimidine that may have a higher antitumor effect and less side effects than 5-FU. In this study 15 patients with advanced colorectal carcinoma, one with renal carcinoma, one with carcinoid and one with advanced carcinoma of unknown origin, were randomly assigned to receive 5'-dFUrd 5 g/m2 or 3 g/m2 as a 1-h infusion for 5 days in 3 cycles at intervals of 4 weeks. The patients had repeated neurological and neurophysiological examinations before and during the treatment. Ten patients developed symptoms of toxicity of the central nervous system (CNS), with cerebellopathy and encephalopathy resembling a Wernicke-Korsakoff syndrome. The neurotoxicity was dose related, affecting 7 of 8 patients in the high dosage group and 3 of 9 patients in the low dosage group. The symptoms generally started at the end of the second week of the cycle with unsteadiness and diplopia, and progressed to the fourth week with ataxia, confusion and EEG-changes, becoming more pronounced with increasing number of cycles. After the treatment there was normalisation within 4-8 weeks. Cachectic patients and patients with a pathological EEG before treatment seem to represent a high-risk group for CNS-symptoms. EEG may be helpful in early diagnosis of CNS-toxicity.
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PMID:Wernicke-Korsakoff-like syndrome in patients with colorectal carcinoma treated with high-dose doxifluridine (5'-dFUrd). 294 66

Eight patients with acquired immune deficiency syndrome (AIDS) presented complications affecting the nervous system. The complaints were headache, seizure, confusion or hallucination. Neurologic manifestations included meningitis, focal deficits, cranial nerve palsy, and dementia. Cerebrospinal fluid exhibited a decrease in the percentage of T helper lymphocytes with an inverted helper-to-suppressor cell ratio. The neurologic manifestations of AIDS may depend on multiple factors, such as HIV infection of the central nervous system, concomitant infections with other agents or meningeal invasion by systemic lymphoma or Kaposi's sarcoma. Many patients develop a diffuse encephalopathy which characteristically begins with impaired concentration and mild memory loss, and progresses to severe global cognitive impairment and dementia. Perivascular infiltrates and scattered microglial nodules, consisting of aggregates of microglia and astrocytes, are the most common findings in these patients.
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PMID:[Neurologic complications accompanying acquired immunodeficiency syndrome (AIDS): study of a group of 8 cases]. 295 8

A case is reported in which tocainide, a relatively new cardiac antiarrhythmic for oral use, is believed to have caused a delirium. The patient had been admitted to a coronary intensive care unit for the treatment of ventricular arrhythmia and had developed confusion, impairment in concentration and severe anxiety. Her EEG was compatible with metabolic encephalopathy. The clinical picture varied with the use of tocainide so closely that it appeared to be the most likely cause of the delirium. Other factors were taken into consideration but did not seem to adequately disprove this impression. Tocainide has been known to cause minor, transient and treatable side effects in the form of gastrointestinal and central nervous symptoms--mainly nausea, tremor and dizziness. There have also been three case reports of paranoid psychoses. It is suggested that psychiatrists be aware of the above complications as they may have occasion to see patients taking tocainide, especially in consultation-liaison work. A table with the more common side effects and their frequencies is included.
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PMID:Mental changes associated with tocainide, a new antiarrhythmic. 310 61

Acute confusional state following metrizamide myelography has been reported to occur in up to 2% of patients. These patients have been diagnosed as having toxic encephalopathy. Recently, various cases have been reported to have a nonconvulsive status (absence status or complex partial status) who responded well to diazepam or clonazepam therapy. However, some authors have described cases of nonresponders to anticonvulsive therapy. Failure of therapy can be dose-related. For this reason, our patient was closely monitored by EEG to determine if dose adjustment was warranted, thereby achieving good results.
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PMID:Absence status following metrizamide myelography: management of nonresponders. 314 84


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