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

In the absence of epidemiological studies, we thought it might be of interest to investigate the relative frequency of first seizures in adults according to age and sex and in comparison with a control population. Our study of 317 patients admitted to hospital a few hours at most after the seizures demonstrated that alcoholism in young adults and vascular pathology in the elderly play an important role in triggering the first seizures, which accounts for the male predominance in epilepsy of the adult. It also showed that the occurrence of first seizures increases with age, especially after 60 years. We found that premonitory symptoms were present in almost one-third of the patients, even when the seizures seemed to be generalized from the start, and that there was a risk of one or several attacks during the hours that followed the first seizures.
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PMID:[Causes of first convulsive seizures in adults. According to age and sex]. 252 94

Four criteria should be fulfilled when establishing an animal model of alcoholism. (1) The animal should voluntarily and selectively consume a solution of the drug to yield pharmacologically significant blood alcohol concentrations. When ethanol is consumed for several weeks under these conditions, (2) the animals should exhibit tolerance to the acute effects of the drug. Furthermore, (3) abrupt termination of drug administration should result in physical signs of drug withdrawal (e.g. audiogenic seizures). (4) Changes in endocrine and liver function would also be expected to occur following the chronic administration of alcohol, such effects being particularly pronounced if the diet of the animal is nutritionally deficient. A number of self-administration, operant conditioning and forced alcohol administration models are critically assessed. A detailed description of the models in which rodents are forced to consume increasing quantities of alcohol as part of a nutritionally enriched milk diet suggests that this method fulfils most of the above criteria.
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PMID:Rodent models of alcoholism: a review. 267 61

Patients with alcohol dependence commonly experience symptoms of anxiety, depression, and insomnia. It is essential that clinicians recognize and treat anxiety disorders in alcoholic patients. Panic attacks with and without agoraphobia are especially prevalent among alcoholics and their families. Treatments of choice for panic disorder are the monoamine oxidase inhibitors, as well as tricyclic antidepressants and the benzodiazepine alprazolam. Benzodiazepines seem to be effective in controlling two pathophysiologic characteristics of alcohol withdrawal--noradrenergic and hypothalamic-pituitary-adrenocortical overactivity. They also can be used to prevent and treat withdrawal seizures and delirium tremens. They are not indicated for the treatment of alcohol dependence per se.
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PMID:Anxiety and alcoholism. 268 Nov 71

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

A limited study of 18 deaths among homeless persons in Atlanta, Georgia, has shown that about two-thirds had utilized public health care facilities prior to their death, often over a period of many years. Utilization of two available, specific clinics for the homeless could not be demonstrated. The county hospital and alcoholism treatment center accounted for all documented episodes of health care. Formal, medical documentation of significant alcohol-related morbidity was shown in 50% of those who died homeless. Other common medical problems included seizure disorders, hypertension, pneumonia, chronic pulmonary disease, and non-lethal trauma. These data may be used practically during medico-legal death investigation and by public health agencies when planning policy and procedure relevant to the homeless population. Paucity of data concerning mortality in the homeless should prompt additional, region-specific studies to determine risk factors in areas where homelessness is manifest.
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PMID:Health care history and utilization for Atlantans who died homeless. 271 46

The possibility of content bias in the MacAndrew's Alcoholism Scale (MAC) from the MMPI was examined in groups of seizure disorder (n = 35), general medical (n = 25), and psychiatric patients (n = 20). Scores above criteria on the MAC were associated with reported alcohol problems only for the psychiatric patients. Almost 50% of the seizure patients with no such history had scores above criteria on the MAC. This classification inaccuracy is even greater than that reported recently in contemporary normal samples. The results suggest that caution should be used when one is administering the MAC to seizure disorder patients and that further investigation of possible content bias in other MMPI scales or subscales should be pursued.
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PMID:Content bias of the MacAndrew's Alcoholism Scale in seizure disorder patients. 272 92

The incidence of cerebral tumors among mentally ill patients was 5.3 per 10,000. In a verified series of brain diseases (131 observations) alcoholism was revealed in 40 cases, which either modified the clinical picture of the disease or provoked a number of mental disorders, such as focal epileptic seizures, Korsakoff, or "frontal" syndromes. Alcohol abuse was regarded as a sign of cerebral tumor in a some patients. Reducing the central nervous system compensation abilities, alcohol promoted the malignant development of species of cerebral tumors causing skyrocketing rapid course.
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PMID:[Alcohol and neoplasms of the brain]. 280 Aug 9

Prospects for research advances in alcoholism are very promising, because of the explosion in the neurosciences and advances in epidemiology and typology of the disorder. For example, the field is now ready for molecular genetics studies of the early onset form of alcoholism that is transmitted from father to son with high penetrance. Leading neuroscientists are being recruited into alcoholism research. Paradoxically, this time of new hope coincides with challenges to the scientific enterprise, such as the animal rights movement and impatience with the scientific process in the face of the public health emergencies represented by acquired immunodeficiency syndrome (AIDS) and drug abuse. The emergence of genetically based subtypes of alcoholism suggests that at least two discrete illness processes are involved. Mounting evidence from spinal fluid studies has rekindled interest in a key role for serotonin in the early onset form of alcoholism. One hypothesis now being explored is that genetically low brain serotonin function may be part of the predisposition to this form of alcoholism. It is known that acute alcohol intake transiently increases brain serotonin turnover. Thus, drinking might be viewed as an attempt to correct a deficit, only to produce further serotonin depletion as the drug's effect wears off, setting up a vicious cycle of repeated attempts to self-medicate. Impulsive, violent, and suicidal behavior as well as alcohol abuse are associated with the low brain serotonin activity. Persons with these problems suffer from circadian rhythm and glucose metabolism disturbances that may also be mediated by serotonin. New pharmacological probes are now available to tease out the mechanisms of altered serotonin function. The progressively deteriorating course of severe episodic alcoholism in many ways parallels the process of electrically kindled seizures in experimental animals. There is evidence that repeated withdrawal episodes may kindle a worsening course, including phobic disorders, perhaps by triggering a hyper-reactive noradrenalin system.
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PMID:Alcoholism research: delivering on the promise. 284 8

From 1984 to 1988, 195 male alcoholics aged 30-64 years who died outside hospitals and nursing homes in Oslo were autopsied at the Institute of Forensic Medicine, the National Hospital, Oslo. Of the 127 brains neuropathologically examined, 86 (67.7%) showed abnormalities, and 28 contained lesions of more than one type. One or two lesions associated with alcoholism were found in 61 cases (48%). Thus, 18 (14.2%) showed Wernicke's encephalopathy, 47 (37%) cerebellar atrophy, two central pontine myelinolysis, and one hepatic encephalopathy. Subdural haematoma and/or cortical contusions were found in 30 (23.6%), and cerebrovascular lesions in 19 (15%). Of the 195 cases, 22 had a history of repeated epileptic seizures. Nineteen of them were examined neuropathologically, and 13 had focal damage that might have been responsible for their fits. The results indicate that the frequency of Wernicke's encephalopathy and cerebellar atrophy in male alcoholics who die outside hospital is similar to that previously observed in cases who died in hospital. Although cerebral damage was even more frequent among vagrants and others dependent on social support, half the men living in their own homes were also affected.
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PMID:[Pathologic brain damage in male alcoholics dying outside of hospitals]. 291 77

Clinically, patients with Delirium Tremens (DT) and acute alcohol hallucinosis (impending DT) appear excited with vivid false perception. Cerebral blood flow and eeg correspondingly point to hyperexcitability in the CNS during these conditions. Clinical trials with barbital treatment in alcohol withdrawal shows that the amount of drug and the drug plasma concentration is the same no matter whether the physical signs of withdrawal are accompanied by hallucinations and clouding of consciousness. The psychotic signs in DT and acute alcoholic hallucinosis develops after many years of alcoholism as does seizures. We hypothesize that physical withdrawal is determined by the degree of physical dependence developed during the most recent drinking period whereas the psychotic signs and seizures are due to a cumulated CNS hyperactivity developed over many years of repeated alcohol intoxication and withdrawal. Changes of electrolyte concentrations in plasma or CSF do not play an important role in the pathogenesis of DT and related clinical states except that changes in calcium and inorganic phosphate metabolism indirectly point to changes in membrane excitability. A new model for a study of rapidly repeated intoxication and withdrawal episodes in rats has shown that repetition of episodes augments the convulsive component of withdrawal whereas the non-convulsive signs are dependent on the most recent episode only. The augmentation of the convulsive component correlates with regional differences in brain glucose consumption. Furthermore, synaptic proteins and acidic phospholipids may be involved in the development of CNS hyperexcitability during alcohol withdrawal. In conclusion both clinical and experimental studies indicate that severe alcohol withdrawal reactions may consist of two components: 1) Physical withdrawal signs determined by recent physical dependence. 2) A long term cumulated CNS hyperexcitability relating to seizures and psychotic signs during withdrawal. This state is elicited by alcohol withdrawal but it represents a cumulated and permanent or long lasting CNS dysfunction in alcoholics. The precise biochemical/pathophysiological mechanisms for the development of the two-component dysfunction still remain to be clarified in detail.
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PMID:Delirium tremens and related clinical states: psychopathology, cerebral pathophysiology and psychochemistry: a two-component hypothesis concerning etiology and pathogenesis. 306 44


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