Alcohol withdrawal seizures

Geir Brathen MD PhD (Dr. Brathen of Trondheim University Hospital in Trondheim, Norway, has no relevant financial relationships to disclose.)
Maurizio A Leone MD (Dr. Leone of Ospedale Maggiore della Carita in Novara, Italy, has no relevant financial relationships to disclose.)
C P Panayiotopoulos MD PhD, editor. (Dr. Panayiotopoulos of St. Thomas' Hospital has no relevant financial relationships to disclose.)
Originally released June 19, 2006; last updated October 12, 2015; expires October 12, 2018
Notice: This article has expired and is therefore not available for CME credit.

This article includes discussion of alcohol withdrawal seizures and rum fits. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


Alcohol withdrawal seizures are frequently encountered in the emergency room. Such seizures comprise acute and serious complications to alcohol abuse that need immediate attention. Benzodiazepines should be the first choice in the pharmacological management of such seizures. There is a risk of mistakenly making an epilepsy diagnosis if a thorough alcohol anamnesis is omitted. Any patient with withdrawal seizures should be given thiamine during hospitalization, regardless of nutritional state. In this article, the authors explain the clinical presentation, pathophysiology, diagnostic work-up, and management of alcohol withdrawal seizures and provide clues to the differentiation of withdrawal seizures from seizures due to epilepsy.

Key points


• Alcohol withdrawal is a major seizure-precipitating factor.


• Drinking history is essential; biomarkers such as GGT and CDT may be useful supplements.


• Investigation of first seizures must include neuroimaging.


• Benzodiazepines are safe and effective in alleviating both seizures and general withdrawal symptoms as well as preventing further seizures. High initial doses may be necessary, but treatment should be discontinued within less than a week.


• Parenteral thiamine should be given before any carbohydrate-containing fluids or food.


• The recommended initial preventive thiamine dose is 200 mg; if Wernicke encephalopathy is suspected, give 200 mg three times daily for at least 2 days.

Historical note and terminology

The relation of alcohol to seizures was appreciated by Hippocrates (Lloyd 1978), as well as by the Romans, who even put a name to it, morbus convivialis, or “disorder related to partying” (Lennox 1941). Minimal progress was made to knowledge in this field during the centuries until Magnus Huss introduced the term “alcoholismus chronicus” in 1851 and showed that after prolonged intoxication, alcoholics may have seizures (Huss 1851). He also established that epileptic patients who drink must be differentiated from alcohol abusing patients having epileptic seizures during withdrawal (Jellinek 1943). In 1953 the first systematic article describing the alcohol withdrawal syndrome appeared (Victor and Adams 1953), and later an article exploring the nature of alcohol withdrawal seizures (Victor and Brausch 1967). These have remained landmark articles, forming a basis for our current knowledge.

The lack of a comprehensive definition of clinical entities or a unanimous classification of alcohol-related seizures have been major obstacles to gaining evidence-based knowledge about alcohol and seizures.

“Alcohol-related seizures” describes all types of interrelation between seizures and alcohol use. “Alcoholic epilepsy,” is a confusing term with many different meanings and should be abandoned. “Alcohol-provoked seizures” is a useful term for seizures directly precipitated by a drinking bout, when other etiologies than withdrawal are suspected, eg, metabolic or toxic effects of acute alcohol intoxication, sometimes complicated by drug abuse, head trauma, or epilepsy. For a comprehensive discussion of seizure types related to alcohol, see (Mattson 1990). The present article deals only with seizures occurring during alcohol withdrawal.

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