TWEAK is an acronym for Tolerance (T1 number of drinks to feel high; T2, number of drinks one can hold), Worry about drinking, Eye-opener (morning drinking), Amnesia (blackouts), and Cut down on drinking (K/C). In this study, two versions (T1 and T2) of the TWEAK were part of a questionnaire used to detect alcoholism or heavy alcohol intake in three populations, namely, alcoholics in treatment, patients in two outpatient clinics, and the general population. Similar to the CAGE and the 10-item brief MAST, the TWEAK identified most known alcoholics, but the TWEAK had a higher sensitivity and specificity than the CAGE and B-MAST in detecting alcoholism/heavy drinking in the clinical and general populations. Different cut-off values for tolerance (T1 and T2) are recommended for screening different populations.

A new measure of lifetime alcohol consumption, the Cognitive Lifetime Drinking History (CLDH) uses beverage-specific questions on drink sizes and assesses drinking patterns to enhance recall. Two methods of establishing drinking intervals were examined: 1) floating--the respondent's report of when drinking changed, and 2) fixed--defined in terms of decades. Test-retest reliability for lifetime ounces of alcohol consumed and times intoxicated in lifetime estimated at visits 1 week or more apart was assessed in postmyocardial infarction patients (n = 81) and controls (n = 138) who had had at least 12 drinks in a year during their lifetimes. No significant differences in estimates of lifetime ounces of alcohol or times intoxicated were observed. Spearman's r ranged between 0.85 and 0.92 for the floating and fixed versions of the CLDH administered at a single visit and between 0.74 and 0.85 for the floating or fixed administered at both visits. Time between visits did not influence correlations. Intervals reported on the floating CLDH were comparable for postmyocardial infarction patients and controls. It took approximately 5 minutes longer to administer the floating CLDH than the fixed CLDH. Findings support use of the CLDH for case-control studies and suggest that the floating and fixed versions would yield comparable results.

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There is a scarcity of population-based epidemiological investigations concerning the prevalence of epilepsy among alcoholics, and of alcoholism among epileptic patients. Available data seem to suggest that the prevalence of epilepsy among alcoholics is at least triple that in the general population, and that alcoholism may be more prevalent among epileptic patients than in the general population. The term "alcoholic epilepsy" has been used with varying definitions in different investigations. It is suggested that a uniform definition be adopted so as to minimize confusion when comparing data from different laboratories. Although there is general agreement that excessive alcohol intake can increase the frequency of seizures in epileptic patients, limited available data suggest that light to moderate social alcohol drinking may not affect seizure frequency. However, epileptic patients should be warned about the possible adverse effects of alcohol, especially those who have refractory forms of epilepsy. Except for a few anomalous cases, evidence for the direct seizure-provoking effect of alcohol is not strong. This is because it is difficult to pinpoint alcohol as the only etiology; more likely, alcohol is only one factor among others (e.g., head trauma, cerebral infarct, alcohol withdrawal, and metabolic effects of alcohol) in provoking seizures. Because seizures are a symptom and not a disease, it is often difficult to distinguish epileptic seizures from alcohol-withdrawal seizures. Patients with only the latter kind of seizures should not need chronic antiepileptic medication.

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