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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alcohol withdrawal syndromes in humans lie on a continuum of increasing severity, from the acute hangover to delirium tremens. Early mild reactions consist primarily of hyperexcitability phenomena such as tremor, insomnia, hyperreflexia and hyperventilation. In more severe degree, the same process gives rise to hallucinations and seizures. These early reactions are mimicked closely by alcohol withdrawal signs in experimental animals. Late reactions in humans are characterized by marked sympathetic nervous system overactivity, profound disorientation and hallucinations. Analogous reactions have not yet been observed clearly in other species. The problem may be one of finding appropriate techniques for detecting such changes, rather than a true species difference in their occurrence.
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PMID:Alcohol withdrawal syndromes in the human: comparison with animal models. 33 82

Periodic brain stimulation, particularly in the limbic system, at stimulus intensities initially too low to produce any behavioural or EEG effects, progressively produces EEG changes, motor automatisms, and eventually convulsions, an effect called kindling. Data are presented and reviewed that suggest that the severity of alcohol withdrawal symptoms progressively increases over years of alcohol abuse in a stepwise fashion similar to the kindling process. The model is presented that the limbic system hyperirritability which accompanies each alcohol withdrawal serves over time to kindle increasingly widespread subcortical structures. These long-term changes in neuronal excitability might relate to the progression of alcohol withdrawal symptoms from tremor to seizures and delirium tremens, as well as the alcoholic personality changes between episodes of withdrawal.
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PMID:Kindling as a model for alcohol withdrawal syndromes. 35 67

We determined zinc, copper, magnesium, and calcium concentrations by atomic absorption spectrophotometry in the plasma of 30 patients hospitalized for treatment of seizures during a period of alcohol withdrawal. Those patients who developed delirium tremens or a prolonged hallucinatory state had significantly higher plasma copper concentrations (P = 0.026), significantly lower zinc concentrations (P = 0.004), and significantly higher copper/zinc ratios (P = 0.001) than the patients who recovered uneventfully. Zinc deficiency may be one of the factors that contribute to the neurologic complications of alcoholism. A determination of the plasma copper/zinc ratio early in the course of alcohol withdrawal could be of value in indicating which patients have the most substantial underlying disease or metabolic imbalance and therefore may be at greatest risk of developing delirium tremens or prolonged hallucinosis.
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PMID:Plasma calcium, copper, magnesium, and zinc concentrations in patients with the alcohol withdrawal syndrome. 68 16

Ventricular irritability and ventricular fibrillation developed in an alcoholic patient who had withdrawal seizures and delirium tremens; he was successfully resuscitated. Potassium and magnesium level were low; therefore replacement of these electrolytes was carried out, as well as intravenous administration of lidocaine hydrochloride; however, ventricular tachycardia developed again and required countershock. No further arrhythmias occurred after additional potassium chloride and procainamide hydrochloride therapy was given. Hypokalemia and possibly hypomagnesemia are implicated as important factors in the development of ventricular ectopy. Delirium tremens is a potential medical emergency, and in the presence of low potassium and/or magnesium levels, or ventricular irritability, patients with this condition should be treated expectantly in an intensive care unit, with close monitoring and aggressive therapy for life-threatening arrhythmias.
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PMID:Life-threatening ventricular tachyarrhythmias in delirium tremens. 90 Oct 94

The following neuropsychiatric disorders have been briefly described: alcohol withdrawal syndrome, delirium tremens, alcohol hallucinosis, Wernicke-Korsakow syndrome, seizures, tremor, Marchiafava-Bignami disease, central pontine myelinolysis, alcoholic amblyopia, alcoholic cerebellar degeneration cerebral atrophy, alterations of personality in chronic alcoholics, alcoholic polyneuropathy. The pathogenetical aspects as well as the pathological findings have been reviewed with special emphasis on nutritional factors.
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PMID:Neuropsychiatric disorders of alcoholism. 91 47

Acid-base changes in arterial blood and lumbar cerebrospinal fluid were correlated with simultaneously determined lactate levels in patients admitted after alcohol withdrawal seizures. Arterial and cerebrospinal fluid lactate was elevated in association with a marked respiratory alkalosis in 13 patients studied 5 to 12 hours after the seizure. Similar elevations of arterial and cerebrospinal fluid lactate were found in five patients during delirium tremens without antecedent withdrawal seizure. The cerebrospinal fluid lactate determined on admission appeared to correlate best with the length and severity of the alcohol withdrawal syndrome that developed in patients after a withdrawal seizure.
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PMID:Cerebrospinal fluid acid-base and lactate changes after seizures in unanesthetized man II. Alcohol withdrawal seizures. 123 4

The effects of alcohol on the central nervous system can be subdivided into three main categories: the effects of acute intoxication (drunkenness, acute encephalopathy, stroke), the effects of tolerance and ethanol withdrawal (delirium tremens, seizures) and the delayed manifestations of chronic alcohol consumption (cerebellar degeneration, Wernicke's encephalopathy, dementia).
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PMID:[Main involvement of the central nervous system in alcoholism]. 141 Sep 80

Delirium tremens is linked with a chronic depression of the central nervous system by alcohol and a compensatory hyperactivity of neurotransmitters. A sudden stoppage of alcohol intake induces excessive production of these transmitters. Firstly appearing is a noradrenergic hyperactivity which may be responsible not only for reducing the magnesium blood level but also for activating the other transmitter systems. A magnesium blood level lower than 1 mmol.l-1 involves a risk of seizures and requires IV magnesium sulfate. Noradrenergic hyperactivity can be prevented by IV alcohol associated with sedation best achieved by IV clomethiazole in alcoholic solution. Should these preventive measures fail, noradrenaline action in the central nervous system can be blocked by clonidine. Should hallucinations become manifest, linked to dopaminergic hyperactivity, haloperidol is indicated. Benzodiazepines may be useful, particularly carbamazepine, for their depressing effect on gaba-ergic hyperactivity.
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PMID:[Delirium tremens. Recent neurophysiologic concepts and therapeutic outlook]. 151 60

Narcolepsy is clinically associated with cataplexy, sleep paralysis and hypnagogic hallucinations. It is treated by reassurance (that there is no physical disease) and by stimulants such as ephedrine and amphetamine on an intermittent basis. The special tricyclic antidepressant clomipramine is also used, and mono-amine oxidase inhibitors (MAOIs) are useful in theory. Obstructive sleep apnoea is an important and often unrecognised cause of daytime somnolence. It is treated by weight reduction (pickwickian syndrome), hormones, or recently, with continuous positive pressure apparatus. Night terrors (pavor nocturnus) and sleepwalking typically occur during deep sleep (stage 3 and 4 throughout the episode) in children. In a night terror the child sits up with a scream, with eyes open, but inaccessible. He eventually falls asleep calmly. Sleepwalking, too, shows the features of inaccessibility and subsequent amnesia for the episode. Both conditions are normally treated with reassurance (to the parents) but may occasionally warrant benzodiazepines. Enuresis usually occurs in non-rapid eye movement (NREM) sleep, especially stages 3 and 4. The reason for the efficacy of tricyclic antidepressants is not precisely known. Delirium tremens (DT) is treated as a rebound excess of REM sleep, with benzodiazepines and other drugs. It is the withdrawal syndrome (with or without major seizures) to the barbiturate-alcohol group of drugs, which includes alcohol, chloral, paraldehyde, glutethimide, methylprylone, ethchlorvynol, meprobamate and meprobamate-diphenhydramine. Insomnia may be treated by the above drugs, by analgesics, antidepressants, major tranquillisers (neuroleptics) and miscellaneous other compounds. For the majority of patients, however, the most suitable group seems to be the benzodiazepines. The benzodiazepines are much safer than their predecessors, in both acute and chronic usage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The treatment of sleep disorders. 158 14

This paper examines severity of depressive symptoms, as measured by the Beck Depression Inventory, in chronic alcoholics with and without a history of hallucinations. We found a) alcoholics entering alcohol treatment who have experienced hallucinations during detoxification report higher levels of subjective depression than alcoholics who have never experienced hallucinations, b) the level of subjective depression in alcoholics with a history of hallucinations remains higher at the end of inpatient alcohol treatment than in alcoholics without hallucinations, and c) hallucination is the important variable; alcoholics with blackouts, seizures, and delirium tremens, do not experience higher levels of depression during detoxification. The reporting of a significantly higher level of depressive symptoms by alcoholics with a history of experiencing hallucinations during withdrawal suggests that in some alcoholics, there exists a vulnerability for mood abnormalities which includes a predisposition toward other abnormal mental phenomena such as perceptual distortions.
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PMID:Dysphoria in male alcoholics with a history of hallucinations. 186 70


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