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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with sepsis often manifest disorientation, somnolence, asterixis and coma, symptoms also seen in portasystemic encephalopathy. Altered plasma concentrations of the neutral amino acids and in creased blood-brain transport of these acids may play a role in portasystemic encephalopathy. Plasma amino acids and blood-brain barrier transport of neutral amino acids were investigated in a rat model of abdominal sepsis, cecal ligation and puncture. The blood-brain transport was studied by the technique of Oldendorf with carbon-14-amino acids 12 and 24 hours after the induction of sepsis. In similar groups of animals, isolation of brain capillaries was carried out by the technique of Hjelle and the capillaries were incubated with carbon-14-amino acids to study transport activity. Plasma and brain amino acids were deranged in a fashion similar to the derangements seen in portasystemic encephalopathy, with a decrease in plasma branched chain amino acids and an increase in most neutral amino acids in brain. The changes were most pronounced after 24 hours. The brain uptake of several neutral amino acids was increased in the septic rats, while the uptake of lysine, a basic amino acid, was normal. In the brain capillaries isolated from septic rats, tyrosine and leucine transport was also greater than in sham-operated animals. Elevated neutral amino acids may play a role in the encephalopathy encountered in septic patients similar to its role in patients with portasystemic encephalopathy, as similar mechanisms appear to be operating.
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PMID:Blood-brain barrier derangement in sepsis: cause of septic encephalopathy? 745 18

Ifosfamide, a nitrogen mustard derived alkylating agent commonly used in the treatment of solid tumors, has been associated with neurotoxicity in 5-33% of treated patients. Encephalopathy most often occurs during or shortly following drug administration, with increased drowsiness or irritability, confusion, hallucinations, visual blurring, extrapyramidal dysfunction, cranial nerve abnormalities, incontinence, generalized muscle twitching, seizures, and coma reported in infants, children, and older adults. While most reported neurologic abnormalities associated with ifosfamide have been reversible, encephalopathy resulting in death has occurred. We now report an infant who developed ifosfamide-induced encephalopathy, loss of developmental milestones, progressive brain atrophy, and cessation of cranial growth. This is the first case of cerebral atrophy and loss of developmental milestones that has been reported in a pediatric patient treated with ifosfamide. Given the efficacy of this anti-neoplastic agent and its increasing use in pediatrics, further investigation is indicated, especially in infants where brain growth is ongoing.
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PMID:Cerebral atrophy in an infant following treatment with ifosfamide. 805 12

Pyruvate dehydrogenase deficiency is one of the most common causes of encephalopathy associated with lactic acidosis and is known to account for congenital lactic acidosis, recurrent ataxia, and infantile Leigh syndrome. Hitherto, however, peripheral neuropathy has not been regarded as a presenting symptom of pyruvate dehydrogenase deficiency. Here, we report on a boy who presented peripheral neuropathy with severe limb hypotonia, absent deep-tendon reflexes, and reduced motor nerve conduction velocities at 8 months of age. Persistent hyperpyruvicemia with normal lactate/pyruvate molar ratios in plasma were highly suggestive of a pyruvate dehydrogenase deficiency, and the determination of pyruvate dehydrogenase activity in circulating lymphocytes led to the diagnosis of pyruvate decarboxylase (PDH-E1) deficiency in the proband. Based on this observation, we suggest that pyruvate dehydrogenase deficiency should be considered in the diagnosis of peripheral neuropathy in infancy, especially when associated with persistent hyperpyruvicemia, normal lactate/pyruvate molar ratios in plasma, and recurrent episodes of drowsiness and hypotonia of unknown origin.
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PMID:Leigh syndrome: pyruvate dehydrogenase defect. A case with peripheral neuropathy. 815 Oct 84

Neurological complications in bone marrow transplant (BMT) patients include central nervous system (CNS) infection, seizure, cerebrovascular accidents, and CNS disease recurrence. The purpose of this study was to describe the pattern and distribution of CNS complications and responses during BMT and to describe the presentation and outcome of select neurological incidents. The records of 200 BMT patients undergoing transplantation in 1989 were randomly selected and comprise the sampling unit for this study. Generally, the peak occurrence of CNS complications was pretransplant through day 21 posttranplant. Neuropathy and somnolence occurred earliest, peaking on day -13 and -8 pretransplant, respectively; confusion or disorientation peaked around day 12 posttransplant. Fifteen patients (7.5%) experienced seizure or suspected seizure, principally of the tonic-clonic type. Fifty-two patients (26%) experienced coma or encephalopathy. Etiologies included respiratory compromise, renal failure, and hepatic dysfunction, often occurring simultaneously. Coma and encephalopathy were commonly associated with terminal events. Because nurses are often the first to identify sensory and perceptual alterations in BMT patients, these results may assist nurses in the early detection of CNS complications.
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PMID:Pattern of occurrence and clinical presentation of neurological complications in bone marrow transplant patients. 818 Sep 74

The PEHO syndrome (progressive encephalopathy with oedema, hypsarrhythmia, and optic atrophy) is a recently recognised disorder of unknown biochemical background. Diagnostic features have been found in neuroradiological and neuropathological studies, which show characteristic severe cerebellar atrophy. In combined neuroradiological and ophthalmological studies, 10 out of 21 possible PEHO patients fulfilled the criteria for true PEHO syndrome. All were abnormal at birth showing hypotonia, drowsiness, or poor feeding. Head circumference was normal, but usually dropped to 2 SD below average during the first year of life. Visual fixation was either absent from birth or lost during the first months of life. Nine patients had peripheral oedema in early childhood. The mean age of onset of infantile spasms was 4.9 months. All patients were extremely hypotonic and no motor milestones were reached. Patellar reflexes were brisk. Brain stem and somatosensory evoked potentials were abnormal in each case studied, cortical responses of somatosensory evoked potentials could not be elicited, and motor conduction velocities became delayed with age. Altogether 19 PEHO patients were found in 14 Finnish families. Autosomal recessive inheritance is likely.
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PMID:Diagnostic criteria and genetics of the PEHO syndrome. 830 48

A high prevalence of sleep apnoea was found in a group of men occupationally exposed to organic solvents. Workers with long term exposure to organic solvents often report symptoms such as fatigue, forgetfulness, and concentration difficulties. These symptoms are strikingly similar to those reported by patients with obstructive sleep apnoea syndrome (OSAS). This is a frequently diagnosed disorder characterised by disturbed sleep causing psychic or somatic complications and daytime sleepiness. A study was undertaken to evaluate whether people with long term occupational exposure to organic solvents have a higher prevalence of sleep apnoea than the general population. Patients exposed to solvents (66 men) were invited to participate in a screening for sleep apnoea. A static charge sensitive bed was used for the monitoring of respiration movements and pulse oximetry during one night. A classical sleep apnoea was diagnosed if periodic respiration movement exceeded 45% of estimated sleep time and the oxygen desaturation index exceeded 6. The prevalence of sleep apnoea among the men exposed to solvents was compared with the prevalence in the general population (1.4%). The prevalence among the participating exposed men was 19.7% which gave a conservative relative risk estimate of 14.1 (95% confidence interval (95% CI) 7.5-24.2). The results indicate that exposure to organic solvents causes sleep apnoea. An alternative possibility is that people with sleep apnoea are misdiagnosed as cases of solvent induced toxic encephalopathy. The interpretation has importance for the caring of the patient.
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PMID:Occupational exposure to organic solvents as a cause of sleep apnoea. 845 96

A case of acute hepatic failure following ingestion of the veterinary euthanasia drug T61 is described. Presenting symptoms were drowsiness, disorientation, muscle hypertonia, and upper limb myoclonus, which faded within a few hours. Two days later, acute liver failure occurred, manifested as encephalopathy, jaundice, and a severe coagulopathy. The hepatic damage was thought to be due to the solvent dimethylformamide, which is the only known hepatotoxin included in the preparation utilized in the suicide attempt. High-dose (1.2 g/day) intravenous reduced glutathione was administered, with a rapid improvement of liver function. The patient was discharged after 17 days. Normalization of all liver function tests was achieved within two months. The favorable outcome in this case stands in contrast to the report of a previous case of lethal T61-induced hepatic failure. Although a different amount of dimethylformamide was ingested in each case (0.45 vs 0.60 ml/kg body wt) and individual differences in susceptibility to the effects of the hepatotoxic agent may have played a major role in these two cases, it is not unlikely that the infusion of high doses of glutathione to our patient contributed to her survival and hepatic recovery.
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PMID:Severe hepatic failure occurring with T61 ingestion in an attempted suicide. Early recovery with the use of intravenous infusion of reduced glutathione. 846 75

Some non-steroid anti-inflammatory drugs, and especially diclofenac, may, in some susceptible patients bring about the appearance of segmentary myoclonic symptoms, which in some cases where there is kidney failure may cause real myoclonic encephalopathy. We present the case of a patient admitted into the nephrology service suffering from prerenal kidney failure as a result of dehydration. Once her kidney problems had been overcome and analytical parameters normalized, during treatment with diclofenac for inflammation of the lower left extremity arthritic in origin, she showed generalized myoclonic symptoms of action and attitude especially in the upper extremities. Neurologic examination showed no abnormalities other than certain drowsiness. General analysis and kidney function were normal, as was brain CT scan, EEG showed only a general tendency towards slowing down. Myoclonic symptoms completely disappeared in the next 24 hours after giving diclofenac up, the patient remaining neurologically asymptomatic and not showing a similar clinical picture in any subsequent check-up.
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PMID:[Myoclonic encephalopathy induced by diclofenac treatment]. 855 23

During an epidemic of dengue type 2 virus in the rural community of Charters Towers, North Queensland, Australia, in 1993, 210 cases presented to the local hospital with signs and symptoms of classic dengue fever. Two cases were noteworthy because of neurologic complications, which included drowsiness, short term memory loss, agitation, and seizure. The cases are presented in detail because they are the first cases of dengue-associated encephalopathy to be documented in Australia. An increasing number of cases of encephalopathy associated with classic dengue fever is being reported world wide, but the etiology of this clinical syndrome remains unknown.
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PMID:Dengue fever with encephalopathy in Australia. 860 Jul 60

Children appear particularly susceptible to severe but reversible neurological symptoms and/or signs after minor head injury; these include headache, confusion, drowsiness, vomiting, hemiparesis, cortical blindness, or seizures. Significantly, these neurological episodes are not associated with any identifiable structural brain abnormality on neuro-imaging. We propose that the cause of this condition is a reactive hyperaemia, a 'benign hyperaemic encephalopathy' mediated via activation of the trigeminovascular system.
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PMID:Neurological episodes after minor head injury and trigeminovascular activation. 918 32


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