Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results presented here strongly suggest that quantitative electroencephalography and event-related potentials are excellent research tools and may be clinically useful as non-invasive monitors of psychotropic drug action and encephalopathies. Our initial data with acute mild alcohol intoxication show that acute tolerance may be reflected in qEEG but not in P3 latency. Since predictably some brain functions may show tolerance, and others not, these approaches may be useful probes. The amplitude of N1-P2 appears to differentiate alcoholics with and without a history of withdrawal seizures. This technique may thus prove useful in determining treatment and monitoring treatment effects in alcohol withdrawal. P3 latency appears to be normal in Korsakoff's syndrome, unlike in Alzheimer's disease. The combination of the event-related potentials with neuropsychology and magnetic resonance imaging scans should be invaluable for future research in these patient groups. Many patients with severe liver disease superficially appear mentally intact. The event-related potential and quantitative electroencephalography findings we have demonstrated may indicate those at greater risk for alterations in brain functioning. These techniques may also prove useful in diagnosing other "subclinical" encephalopathies and further our understanding of the underlying brain pathophysiology.
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PMID:Acute, withdrawal, and chronic alcohol effects in man: event-related potential and quantitative EEG techniques. 229 41

The nervous system is particularly susceptible to the harmful effects of alcohol. These include Wernicke-Korsakoff syndrome, which is related to thiamine deficiency secondary to chronic alcohol abuse. Other neurotoxic effects of alcohol with cognitive impairments include delirium tremens, alcoholic seizures or "rum fits," and alcoholic neuropathies. It has become recognized in recent years that alcohol and its metabolites directly damage the nervous system even in the absence of nutritional deficiencies. Cerebral blood flow (CBF) measurements provide a noninvasive indirect monitor of cerebral metabolic activity. It has been shown conclusively that CBF measured by the 133Xe inhalation method is decreased in chronic alcoholism, correlating well with the amount of alcohol consumed. With abstinence, CBF returns toward normal levels provided the neurotoxic effects of chronic alcoholism are of recent onset. Clinical and pathological studies show significant loss of brain volume with ventricular dilatation after alcohol abuse even among young "social" drinkers. This toxic effect of alcohol is accompanied by varying degrees of cognitive impairments ranging from slight memory loss to frank dementia. Both the decrease in brain volume and the cognitive impairments, which occur with or without nutritional deficiency, are to a large extent reversible with abstinence and nutritional supplementation. Alcohol appears to accelerate age-related declines in CBF while nutritional deficiencies enhance the neurotoxic effects of alcohol. Measurements of local CBF (LCBF) and partition coefficients (L lambda) in deep cerebral structures, including the hypothalamus, thalamus, forebrain nuclei, and limbic system, can be achieved utilizing three-dimensional methods after inhalation of stable xenon as a contrast medium combined with serial computed tomographic imaging of the brain. Among chronic alcoholics, there are significant and diffuse reductions in cortical and subcortical gray matter CBF that are especially remarkable in hypothalamus and substantia innominata, which includes the nucleus basalis of Meynert, a major source of cholinergic input to neocortex and hippocampus. Reductions in LCBF are measurable in cognitively impaired patients with and without Wernicke-Korsakoff syndrome. Reductions of CBF include white matter and are more severe in patients with Wernicke-Korsakoff syndrome. Both types of encephalopathy improve with treatment, but recovery is usually more rapid and complete if nutritional deficiency is absent. Alcohol also appears to be a risk factor for stroke, possibly by depleting neuronal reserves and unfavorably influencing cardiovascular risks.
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PMID:Cerebral hemodynamic and metabolic effects of chronic alcoholism. 270 68

Rats were fed a thiamine-deficient diet for 4 weeks and injected daily with pyrithiamine during the last two weeks of the diet. This regime induced severe neurological anomalies such as ataxia, loss of righting reflex and visual place reflex, and finally full tonic-clonic seizures. These symptoms are reminiscent of the clinical Wernicke-Korsakoff syndrome. Injection of thiamine dramatically reversed these symptoms within one or two hours as seen in Wernicke patients. Six weeks later these rats showed a marked deficit in habituation of exploratory behavior and of the auditory orienting response. To what extent this chronic deficit in habituation contributes to the cognitive dysfunctions seen in Wernicke-Korsakoff patients is discussed. Histological examination of the brains of 6 of the rats revealed a heterogeneous pattern of damage to the brainstem, including mamillary bodies and several thalamic nuclei, reminiscent of that seen in Korsakoff patients. In addition there were many dark abnormal cells in limited fields of hippocampus neocortex and thalamus in almost all animals.
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PMID:Persistence of habituation deficits after neurological recovery from severe thiamine deprivation. 367 33

Propranolol controlled the rage and violent behavior of a man with alcohol withdrawal, Korsakoff's psychosis, and seizures. The authors present evidence linking Korsakoff's psychosis and alcohol withdrawal to pathophysiologic alterations in CNS adrenergic amines and receptors.
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PMID:Propranolol in the treatment of rage and violent behavior associated with Korsakoff's psychosis. 669 26

A female alcoholic presented with Wernicke's encephalopathy subsequent to administration of diazepam and glucose (without thiamine) for treatment of withdrawal seizures. Nystagmus and cerebellar ataxia quickly resolved when administered thiamine, although severe global amnesia consistent with Korsakoff's syndrome persisted. Magnetic resonance imaging (MRI) revealed infarction of the right temporal lobe with hippocampal atrophy, but no lesions of thalamus or atrophy of mammillary bodies. Positron emission tomography (PET) confirmed decreased cerebral metabolic rates for glucose (CMRglu) in the right temporal lobe corresponding to MRI findings, but also significant metabolic asymmetry of dorsal thalamus, i.e. reduced CMRglu in left versus right. This patient is unique in that neuroradiological findings revealed intact mammillary bodies and suggest asymmetrical dysfunctions (structural right temporal and functional left diencephalic) to produce her profound amnesia.
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PMID:Severe global amnesia presenting as Wernicke-Korsakoff syndrome but resulting from atypical lesions. 868 98

A diabetic 66 year old man who presented with pilomotor seizures in his right hemibody is described. The seizures recurred with an increasing frequency, leading to a status-like condition associated with Korsakoff's syndrome. An EEG was performed and several electroclinical seizures were recorded. Brain MRI was negative. The patient, who was treated with carbamazepine, became seizure free after 1 week. Memory and behaviour gradually returned to normal within 3 weeks. There was no further neurological episode during an 8 year follow up. Hyperosmolar, non-ketotic hyperglycaemia was considered to be the cause of the seizures. The pathophysiology of pilomotor seizures is discussed and the literature on the subject reviewed.
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PMID:Status-like recurrent pilomotor seizures: case report and review of the literature. 1076 99

A 10-year-old girl with M2 acute myeloid leukemia underwent an unrelated cord blood transplantation in refractory first relapse. On day +13, after 48 hours with fever, she showed a measles-like rash, and on day +15, she began experiencing neurologic symptoms (headache, tremors, weakness, nystagmus, mild confusion, speaking, taste, and behavior disturbances, and focal seizures). She also had amnesia for recent events with disability to learn, mimicking Wernicke-Korsakoff syndrome. Computed tomography of the brain and cerebrospinal fluid (CSF) and electroencephalogram were nonspecific. We found human herpesvirus 6 (HHV-6) DNA in CSF and cytomegalovirus in bronchoalveolar lavage using polymerase chain reaction techniques. Treatment with ganciclovir and foscarnet was effective, with total resolution of symptoms.
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PMID:Herpesvirus-6 encephalitis complicated by Wernicke-Korsakoff syndrome in a pediatric recipient of unrelated cord blood transplantation. 1190 11

Patients presenting with subacute amnesia are frequently seen in acute neurological practice. Amongst the differential diagnoses, herpes simplex encephalitis, Korsakoff's syndrome and limbic encephalitis should be considered. Limbic encephalitis is typically a paraneoplastic syndrome with a poor prognosis; thus, identifying those patients with potentially reversible symptoms is important. Voltage-gated potassium channel antibodies (VGKC-Ab) have recently been reported in three cases of reversible limbic encephalitis. Here we review the clinical, immunological and neuropsychological features of 10 patients (nine male, one female; age range 44-79 years), eight of whom were identified in two centres over a period of 15 months. The patients presented with 1-52 week histories of memory loss, confusion and seizures. Low plasma sodium concentrations, initially resistant to treatment, were present in eight out of 10. Brain MRI at onset showed signal change in the medial temporal lobes in eight out of 10 cases. Paraneoplastic antibodies were negative, but VGKC-Ab ranged from 450 to 5128 pM (neurological and healthy controls <100 pM). CSF oligoclonal bands were found in only one, but bands matched with those in the serum were found in six other patients. VGKC-Abs in the CSF, tested in five individuals, varied between <1 and 10% of serum values. Only one patient had neuromyotonia, which was excluded by electromyography in seven of the others. Formal neuropsychology testing showed severe and global impairment of memory, with sparing of general intellect in all but two patients, and of nominal functions in all but one. Variable regimes of steroids, plasma exchange and intravenous immunoglobulin were associated with variable falls in serum VGKC-Abs, to values between 2 and 88% of the initial values, together with marked improvement of neuropsychological functioning in six patients, slight improvement in three and none in one. The improvement in neuropsychological functioning in seven patients correlated broadly with the fall in antibodies. However, varying degrees of cerebral atrophy and residual cognitive impairment were common. Over the same period, only one paraneoplastic case of limbic encephalitis was identified between the two main centres. Thus, VGKC-Ab-associated encephalopathy is a relatively common form of autoimmune, non-paraneoplastic, potentially treatable encephalitis that can be diagnosed by a serological test. Establishing the frequency of this new syndrome, the full range of clinical presentations and means of early recognition, and optimal immunotherapy, should now be the aim.
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PMID:Potassium channel antibody-associated encephalopathy: a potentially immunotherapy-responsive form of limbic encephalitis. 1496 Apr 97

Disease processes or events that accompany acute alcohol withdrawal (AW) can cause significant illness and death. Some patients experience seizures, which may increase in severity with subsequent AW episodes. Another potential AW complication is delirium tremens, characterized by hallucinations, mental confusion, and disorientation. Cognitive impairment and delirium may lead to a chronic memory disorder (i.e., Wernicke-Korsakoff syndrome). Psychiatric problems associated with withdrawal include anxiety, depression, and sleep disturbance. In addition, alterations in physiology, mood, and behavior may persist after acute withdrawal has subsided, motivating relapse to heavy drinking. Recent advances in neurobiology may support the development of improved medications to decrease the risk of AW complications and support long-term sobriety.
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PMID:Complications of alcohol withdrawal: pathophysiological insights. 1570 35

Alcohol dependence is a chronic, relapsing biobehavioral disease mediated by various parts of the brain, including reward systems, memory circuits, and the prefrontal cortex. It is characterized by loss of the ability to drink alcohol in moderation and continued drinking despite negative consequences. The alcohol withdrawal syndrome is a common but not universal diagnostic feature of alcohol dependence. Benzodiazepine detoxification of the alcohol withdrawal syndrome prevents the development of withdrawal seizures and delirium tremens, and makes patients more comfortable, which promotes engagement in treatment. Symptom-triggered dosing, based on a withdrawal rating scale such as the Clinical Institute Withdrawal Assessment of Alcohol Scale, Revised, is optimal for minimizing the total benzodiazepine dosage. Use of a long-acting benzodiazepine (eg, chlordiazepoxide) is preferred in uncomplicated patients. Thiamine should be administered routinely before the administration of intravenous fluids to prevent the development of Wernicke's encephalopathy and Wernicke-Korsakoff syndrome. In combination with psychosocial treatment, disulfiram, naltrexone, and acamprosate can reduce the frequency of relapse. Naltrexone may be more effective for reduction of loss of control with the first drink and cue-related craving, and acamprosate may be more effective for stabilizing the physiology of post-acute withdrawal. Disulfiram, an aversive deterrent, can be useful if administration can be monitored and tied to meaningful contingencies or when used prophylactically for situations anticipated to carry high risk of relapse. Psychiatric comorbidity, especially depression, is common and is best addressed concurrently, although definitive diagnosis may have to await a period of prolonged sobriety. Prescription of addictive substances, including benzodiazepines beyond the period of acute detoxification, should be avoided, and if necessary should be closely monitored (eg, by frequent visits with small prescriptions, clinic-administered disulfiram, and/or urine or breath alcohol screenings). Abstinence from alcohol is recommended for persons with alcohol dependence. Psychosocial treatment and participation in Alcoholics Anonymous can help patients achieve and maintain abstinence.
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PMID:The psychiatric management of patients with alcohol dependence. 1771 2


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