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

Thiamine deficiency is known to lead to certain neurological sequelae including Wernicke- Korsakoff encephalopathy. Signs attributable to this condition include ataxia, ophthalmoplegia, nystagmus, and mental confusion. Recognised predisposing conditions include alcoholism gastric carcinoma, pyloric obstruction, hyperemesis gravidarum, and prolonged intravenous feeding. We have recently encountered two cases of Wernicke's encephalopathy after vertical banded gastroplasty for morbid obesity . Other neurological sequelae are recognised after vertical banded gastroplasty, including Guillain-Barre syndrome, psychosis, and pseudoathetosis, but the causes are multifactorial.
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PMID:Wernicke's encephalopathy after vertical banded gastroplasty for morbid obesity. 863 78

Pyrithiamine-induced thiamin deficiency has been used in rat as an experimental form of Wernicke-Korsakoff encephalopathy, a disease associated with chronic alcoholism. Although the main etiological factor is known to be the lack of thiamin, the biochemical mechanisms involved in the pathogenesis remain unclear. Thiamin-dependent enzymes were studied in brain mitochondria: alpha-ketoglutarate dehydrogenase activity exhibited 40% reduction, whereas pyruvate dehydrogenase did not change significantly. Polarographic recordings of mitochondrial respiration revealed a decreased State 3, when using pyruvate/malate, alpha-ketoglutarate or glutamine as a substrate, but the respiration rates remained unchanged with glutamate or succinate. This fall in pyruvate oxidation may be due to the impairment of alpha-ketoglutarate dehydrogenase, which follows pyruvate dehydrogenase in the metabolic pathway. A time course of lactate concentration showed dramatic increases in thalamus, mid brain, hypothalamus and colliculli, consistent with the anatomopathological findings. No increases were found before the onset of neurological symptoms.
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PMID:Brain pyruvate oxidation in experimental thiamin-deficiency encephalopathy. 893 Apr 10

Evidence suggests that liver disease per se may contribute to the cognitive and motor impairments encountered in chronic alcoholics. Neuropathologic studies reveal astrocytic changes (Alzheimer type II astrocytosis) in the brains of alcoholic cirrhotic patients who died in hepatic coma. Pathophysiologic mechanisms responsible for hepatic (portal-systemic) encephalopathy in alcoholics include the loss of neuron-astrocytic metabolic trafficking as well as selective alterations of serotoninergic and dopaminergic function. In addition, there is evidence to suggest that endogenous ligands for both central-type (GABA-related) and "peripheral-type" (astrocytic) benzodiazepine receptors are implicated in the pathogenesis of hepatic encephalopathy in these patients. Chronic liver disease may also interfere with brain thiamine homeostasis and thus contribute to the pathogenesis of the Wernicke-Korsakoff syndrome in chronic alcoholism.
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PMID:Cerebral dysfunction in chronic alcoholism: role of alcoholic liver disease. 897 45

Cirrhosis accounts for 60% of liver transplantations that are performed. The main causes are chronic viral hepatitis B and C, and alcoholism. However, all patients with severe cirrhosis are potential candidates for liver transplantation, regardless of the cause. Liver transplantation is indicated when the patient's life expectancy is one year or less. The main criterion for transplantation is severe liver failure (Child-Pugh's stage C). Transplantation is also proposed in patients with intractable ascites, and in patients with spontaneous encephalopathy. Isolated portal hypertension is not an indication for transplantation. Liver transplantation in hepatocellular carcinoma is still a matter of debate. The results of liver transplantation are very satisfactory with survival rates of 70% at 5 years and patient rehabilitation is usually excellent.
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PMID:[Hepatic transplantation for cirrhosis]. 913 14

A. Digital EEG is an established substitute for recording, reviewing, and storing a paper EEG record. It is a clear technical advance over previous paper methods. It is highly recommended. (Class III evidence, Type C recommendation). B. EEG brain mapping and other advanced QEEG techniques should be used only by physicians highly skilled in clinical EEG, and only as an adjunct to and in conjunction with traditional EEG interpretation. These tests may be clinically useful only for patients who have been well selected on the basis of their clinical presentation. C. Certain quantitative EEG techniques are considered established as an addition to digital EEG in: C.1. Epilepsy: For screening for possible epileptic spikes or seizures in long-term EEG monitoring or ambulatory recording to facilitate subsequent expert visual EEG interpretation. (Class I and II evidence, Type A recommendation as a practice guideline). C.2. OR and ICU monitoring: For continuous EEG monitoring by frequency-trending to detect early, acute intracranial complications in the OR or ICU, and for screening for possible epileptic seizures in high-risk ICU patients. (Class II evidence, Type B recommendation as a practice option). D. Certain quantitative EEG techniques are considered possibly useful practice options as an addition to digital EEG in: D.1. Epilepsy: For topographic voltage and dipole analysis in presurgical evaluations. (Class II evidence, Type B recommendation). D.2. Cerebrovascular Disease: Based on Class II and III evidence, QEEG in expert hands may possibly be useful in evaluating certain patients with symptoms of cerebrovascular disease whose neuroimaging and routine EEG studies are not conclusive. (Type B recommendation). D.3. Dementia: Routine EEG has long been an established test used in evaluations of dementia and encephalopathy when the diagnosis remains unresolved after initial clinical evaluation. In occasional clinical evaluations, QEEG frequency analysis may be a useful adjunct to interpretation of the routine EEG when used in expert hands. (Class II and III evidence as a possibly useful test, Type B recommendation). E. On the basis of current clinical literature, opinions of most experts, and proposed rationales for their use, QEEG remains investigational for clinical use in postconcussion syndrome, mild or moderate head injury, learning disability, attention disorders, schizophrenia, depression, alcoholism, and drug abuse. (Class II and III evidence, Type D recommendation). F. On the basis of clinical and scientific evidence, opinions of most experts, and the technical and methodologic shortcomings, QEEG is not recommended for use in civil or criminal judicial proceedings. (Strong Class III evidence, Type E recommendation). G. Because of the very substantial risk of erroneous interpretations, it is unacceptable for any EEG brain mapping or other QEEG techniques to be used clinically by those who are not physicians highly skilled in clinical EEG interpretation. (Strong Class III evidence, Type E recommendation).
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PMID:Assessment of digital EEG, quantitative EEG, and EEG brain mapping: report of the American Academy of Neurology and the American Clinical Neurophysiology Society. 922 9

Subacute encephalopathy with seizures in alcoholics (SESA syndrome) is a rare disease entity following chronic alcohol ingestion. It is quite distinct from alcohol withdrawal syndromes, such as delirium, withdrawal seizures or CNS complications of alcohol, such as Wernicke-Korsakow syndrome, central pontine myelinolysis or Marchiafava-Bignami disease, and was proposed in 1981 by Niedermeyer and coworkers. This syndrome consists of multiple neurological deficits, such as hemiparesis or hemianopia, and of recurrent focal and generalized seizures associated with prominent EEG features (periodic lateralized discharges, PLEDs). A 72-year-old Caucasian male with chronic alcoholism and an otherwise unremarkable past medical history was admitted to our hospital because of several secondary generalized simple partial seizures. Laboratory investigations revealed elevated levels of gamma-glutamyltranspeptidase and of mean corpuscular volume. Other laboratory investigations and the CSF examinations on three occasions revealed normal values. Cranial computed and magnetic resonance tomography showed cerebral microangiopathy and generalized atrophy. Despite triple anticonvulsive therapy and an intravenous treatment with acyclovir and thiamine, the epileptic seizures persisted. Several EEGs revealed left parietooccipital periodic lateralized epileptiform discharges (PLEDs). The patient died of an intercurrent pulmonary infection about 3 months after the onset of symptoms. The described clinical picture resembles the symptoms of SESA syndrome.
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PMID:[Subacute encephalopathy with epileptic seizures in a patient with chronic alcoholism (SESA syndrome)]. 955 62

Until now, the pathogenesis of Marchiafava-Bignami disease, an extrapontine myelinolysis, is unknown. Accept an abuse of alcohol for many years additional metabolic and vascular disturbances are supposed. The early performance of magnetic resonance imaging in patients with a sudden encephalopathy and history of alcoholism is essential for an assessment of the diagnosis. The bilateral lack of transcallosal inhibition--a parameter for the integrity of the transcallosal connections between motor cortices--is the consequence of the axonal degeneration of transcallosal fibers. Clinical and neuroradiological features of three patients with extrapontine myelinolysis are reported and possible etiologies of the complex disease are discussed. In two cases a severe alcohol abuse was present with the typical picture of the Marchiafava-Bignami disease. In a third patient an intoxication with methanol was present with a similar clinical picture. Although severe neurological disturbances were initially apparent in the patients, during the follow-up there was a significant amelioration of the clinical course under a high-dose vitamin B supplementation.
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PMID:[Marchiafava-Bignami syndrome. Extrapontine myelinolysis in chronic alcoholism]. 1035 98

We introduce a case of a 66 year-old male with chronic alcoholism who suffered from confusion, Wernicke-aphasia and epileptic seizures. Several EEG revealed periodic lateralized epileptiform discharges. The patient's case resembles the symptoms of a subacute encephalopathy with epileptic seizures which can occur in alcoholics.
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PMID:[Subacute encephalopathy with epileptic seizures in an alcoholic patient]. 1105 Jul 38

Disulfiram is used in the treatment of chronic alcoholism, because of the unpleasant symptoms it provokes after ethanol intake. The underlying mechanism is believed to be the accumulation of acetaldehyde in the blood, due to inhibition of the liver aldehyde dehydrogenases. In addition, it is known that disulfiram also has some neurotoxic properties. The aim of our study was to investigate the relationship between the pharmacological and neurotoxicological properties of disulfiram with respect to the doses applied. Increasing doses of disulfiram (25, 50, 75, 100 and 150 mg/kg) were administered intraperitoneally to Wistar rats and the hepatic enzyme activities of alcohol and aldehyde dehydrogenases were measured. Also, in two brain subregions (midbrain and hypothalamus) the levels of noradrenaline, dopamine, 3,4-dihydroxyphenylacetic acid and homovanillic acid were determined. The higher dose of disulfiram (150 mg/kg) produced lethal effects in all treated animals. Aldehyde dehydrogenase activities were inhibited by disulfiram in a dose-dependent way, while alcohol dehydrogenase was not affected at all. Concerning the levels of brain biogenic amines, disulfiram produced a significant reduction in noradrenaline and an increase in dopamine levels in both structures of the brain, in a dose-dependent way. However, the lowest dose applied (25 mg/kg) had no effects on brain catecholamines. It is known that high doses of disulfiram may cause severe encephalopathy and peripheral neuropathy in humans, which could be attributed to the impairment of the metabolism of brain biogenic amines, due to inhibition of dopamine-beta-hydroxylase. Our experimental data show that disulfiram affects the level of brain biogenic amines at dose levels higher than those inhibiting the activity of aldehyde dehydrogenase. Therefore, in clinical practice 'disulfiram reaction' could still be achieved with a low dosage regimen not producing neurotoxicity
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PMID:Differentiation of disulfiram effects on central catecholamines and hepatic ethanol metabolism. 1116 69

Marchiafava-Bignami disease (MBD) is a rare disorder of an unknown aetiology but strongly associated with alcoholism. MBD primarily affects the corpus callosum leading to confusion, dysarthria, seizures and frequently to death. Over 250 cases from all races and from almost all nationalities have been reported, most cases being alcoholics. We report two cases with a favourable outcome. Magnetic resonance imaging (MRI) demonstrated a typical lesion of the corpus callosum, in both patients. The patients, a 44-year-old male and a 40-year-old female, presented with depressed consciousness and a variety of other symptoms, but finally made a reasonably good recovery leading to home discharge. To the best of our knowledge, only one additional case of MBD from Scandinavia has been published. As alcoholism is a major public health problem in Scandinavia, we assume that MBD is underdiagnosed and/or under-reported. Non-specific general symptoms and encephalopathy in an alcoholic may harbour undiagnosed MBD. We suggest that the incidence of MBD may be higher and its prognosis may be milder than generally believed.
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PMID:Marchiafava-Bignami disease: two cases with favourable outcome. 1132 37


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