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)

A total of 383 cases of incident panic attack were identified among 12,823 participants in the Epidemiologic Catchment Area Program over various 12-month periods in 1980-1983. These cases not phobia-stimulated were compared with 766 controls. Risk factors were examined for the onset of panic attacks, with attacks categorized as panic disorder, severe and unexplained panic attacks, or other panic attacks. Risk factors were also examined for the onset of attacks in which cardiovascular symptoms were experienced and those in which psychologic symptoms were experienced. Females were at greater risk than males for each category of attacks (relative odds ranged from 1.36 to 2.25). Persons aged 65 years or older were at lower risk than younger persons (relative odds, compared with 30- to 44-year-olds, ranged from 0.26 to 0.71). A history of cardiac symptoms, shortness of breath, depression or a major grief episode, drug abuse or dependence, alcohol abuse or dependence, and seizures were each strongly associated with panic attacks. A history of cardiac symptoms was more strongly associated with attacks in which cardiovascular symptoms were experienced than with attacks in which psychologic symptoms were experienced (relative odds, 8.36 vs. 2.23). A history of seizures was more strongly associated with attacks with psychologic symptoms than with attacks with cardiovascular symptoms (relative odds, 5.21 vs. 1.58).
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PMID:Risk factors for the onset of panic disorder and other panic attacks in a prospective, population-based study. 229 82

To determine if there is an increase in the risk of seizure activity when patients experience recurrent alcohol detoxifications, we reviewed the detoxification and seizure histories of 256 men and 45 women voluntarily admitted to a 5-day in-patient detoxification program. Structural brain damage, focal neurologic deficits, epileptogenic findings on electroencephalograms, and provocative drug use were all considered pertinent variables for seizure risk. Seizures did not occur during alcohol detoxification in any of the study patients, despite a high incidence of antecedent seizures and provocative drug use. Oral chlordiazepoxide use during detoxification was associated with the elimination of withdrawal seizures. Of all 301 patients, 64 had a history of seizures, 42 had significantly abnormal electroencephalograms during detoxification, and 30 had focal slowing on the electroencephalogram. There was no correlation between the duration of alcohol abuse or lifetime consumption of alcohol and seizure activity. There was, however, a significant correlation between the number of inpatient alcohol detoxifications and the prevalence of seizure disorders. This correlation held true even when provocative drug use was taken into consideration.
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PMID:Seizure risk with recurrent alcohol detoxification. 233 1

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

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

The records of 46 patients who were admitted to a general hospital with the diagnosis of phenytoin toxicity were retrospectively studied to identify factors present at the time of admission which correlated with severity of illness and which would therefore be of prognostic value. Length of hospital stay was used as a measure of severity of illness. Correlations were made between the length of hospital stay and 18 variables studied at the time of admission, including severity of symptoms, use of other drugs (sedative hypnotics, anticonvulsants and phenothiazines), history (seizures, cardiac arrhythmias, and alcohol abuse), laboratory evidence of liver disease or renal disease, electrolyte abnormalities, coagulopathies, prior suicide attempts, glucose levels, and white blood cell counts. Significant correlations related the length of hospital stay with the severity of symptoms, concurrent phenothiazine usage, and the presence of abnormal liver function tests on admission, but not with other factors studied. Admission phenytoin serum levels following an overdose were not a useful predictor of length of hospital stay in this series of patients.
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PMID:Phenytoin toxicity: predictors of clinical course. 292 26

In 1985 a 5-year multicenter Veterans Administration Cooperative Study was completed that compared the efficacy and toxicity of phenobarbital, carbamazepine, phenytoin, and primidone in a double-blind prospective study design. A total of 622 patients, either previously untreated or undertreated, were entered into the study. Strict exclusion criteria limited confounding factors such as drug or alcohol abuse. Results showed that each of the four drugs used as monotherapy were similarly effective in the treatment of generalized tonic clonic seizures, but carbamazepine was significantly more effective in the treatment of complex partial seizures as measured by 100% control. When the results for all four drugs were combined, the data showed that approximately 80% of the patients were adequately managed on monotherapy. Differences in toxicity were the most significant factor that discriminated between these four drugs. Both carbamazepine and phenytoin were associated with significantly lower incidences of intolerable side effects than were primidone or phenobarbital. A behavioral toxicity battery was performed whenever possible prior to administration of any antiepileptic drug and at 1, 3, 6, and 12 months after initiation of monotherapy. Significant differences in performance on all subtests of the battery were found between patients with epilepsy and a control group matched by age, sex, and education. When the differential effects of all four drugs on behavioral toxicity were compared, few statistically significant differences emerged. However, carbamazepine consistently produced fewer adverse effects on tests of attention/concentration and motor performance than did the other three antiepileptic drugs.
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PMID:Results of a nationwide Veterans Administration Cooperative Study comparing the efficacy and toxicity of carbamazepine, phenobarbital, phenytoin, and primidone. 331 43

We obtained CTs in 259 patients with a first alcohol-related convulsion. Each subject had generalized convulsions, recent abstinence from alcohol abuse, and no obvious etiology for seizures other than alcohol withdrawal. Patients with only focal seizures, major head injury, coma, or a severe toxic-metabolic disorder were excluded. We recorded history and signs of minor head injury, presence of headache, level of consciousness, neurologic signs, routine medical examination findings, and subsequent clinical course. Sixteen patients (6.2%) had intracranial lesions on CT. Eight had subdural hematomas or hygromas, two had vascular malformations, two had neurocysticercosis, and one each showed a Berry aneurysm, possible tumor, skull fracture with subarachnoid hemorrhage, and probable cerebral infarction. In ten cases (3.9%), clinical management was altered because of the CT result. History or signs of minor head trauma, headache, level of consciousness, or focal neurologic signs did not significantly correlate with CT abnormality.
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PMID:Intracranial lesions shown by CT scans in 259 cases of first alcohol-related seizures. 341 99

Approximately 25% of patients with epilepsy will have their first seizure after the age of 25 years. These individuals will need special attention with regard to etiology. Brain tumor is one of several causes that may be suspected. The present study of 221 patients with late-onset epilepsy from the University Clinic of Neurology, Hvidovre Hospital, Copenhagen, Denmark, was undertaken to look for means to select those cases in which computerized tomography (CT) scan should be performed. Brain tumor was the cause in 16% and cerebrovascular infarctions in 14%. The major etiological group was the one in which no cause could be detected (38%). Alcohol abuse as the etiology--defined as cases with a history of long-standing alcohol overuse, concomitant signs of alcohol intoxication, and spontaneous recurrent epileptic seizures--made up a group of one-fourth of all the patients with late-onset epilepsy. Comparison of the history, clinical symptoms and signs, EEG abnormalities, and CT scan speaks in favor of some consideration being given to the first three parameters before the CT scan is performed.
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PMID:Late-onset epilepsy: etiologies, types of seizure, and value of clinical investigation, EEG, and computerized tomography scan. 400 82

The authors studied 286 patients with epilepsy with disease onset past the age of 20 years (176 males, 110 females) from the urban and rural populations. In 57% of cases the aetiology of epilepsy was undetermined. Among the known aetiological factors head trauma accounted for 15.5% of cases, inflammatory processes in the central nervous system for 4.5%, alcoholism for 7%, vascular lesions for 6%, tumours for 5.2%, degenerative and atrophic changes for 1.5%. Over 40% of patients had had attacks for up to 15 years and over 18% for over 20 years. In 80% of cases grand mal seizures occurred, and in 33% of these cases more than 12 attacks occurred annually. Six cases of status epilepticus were observed with 2 deaths. The attacks were precipitated by menstruation, alcohol abuse, infection, stressed, television watching. Among the signs accompanying or following the seizures tongue biting and urination prevailed. Neurological signs were demonstrated in 21% of cases, encephalopathy in 65%, other psychic disturbances in 9.5%. Systematic treatment was received by 75% of the patients (over 80% in urban population), and therapy with multiple drugs was most frequent. Drug-resistant epilepsy was found in 34% of cases. The patients from the rural population had a lower educational level and had more children. About 70% of the patients were in employment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Analysis of clinico-social features of epilepsy]. 404 96


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