Delirium Tremens DTs: Practice Essentials, Background, Pathophysiology

The periaqueductal gray is thought to trigger clonic seizures, whereas the pontine reticular formation is implicated in the generation of the tonic phase of audiogenic seizures (18). Some evidence suggests that the IC plays a role in alcohol withdrawal seizures in humans, as it does in rodents. Thus, humans with alcohol withdrawal seizures exhibit abnormalities in auditory-evoked potentials that are not observed in other settings, including increased latency to wave V (19,20), whose major source is the IC (21).

Ethanol is a central nervous system depressant that produces euphoria and behavioral excitation at low blood concentrations and acute intoxication (drowsiness, ataxia, slurred speech, stupor, and coma) at higher concentrations. The short-term effects of alcohol result from its actions on ligand-gated and voltage-gated ion channels (2–4). Prolonged alcohol consumption leads to the development of tolerance and physical dependence, which may result from compensatory functional changes in the same ion channels. Abrupt cessation of prolonged alcohol consumption unmasks these changes, leading to the alcohol withdrawal syndrome, which includes blackouts, tremors, muscular rigidity, delirium tremens, and seizures (5,6).

How should I manage alcohol if I have seizures or epilepsy?

Having a bottle of beer or a glass of wine on occasion isn’t likely to cause any problems, and it’s almost certain that it won’t lead to a seizure. That said, as we’ve seen before, some people don’t have the switch in their brain that lets them drink in moderation. Or contact us online to be connected with a compassionate intake specialist who can give https://ecosoberhouse.com/ you more information. Most people will begin to feel better after the acute detox phase of the first week has passed. It is also crucial during this time to develop a long-term strategy to prevent relapses and stay sober. If you are detoxing in a facility, your medical staff will administer medications and help alleviate the worst of the symptoms.

• Someone who does have a seizure during detox will likely be transferred to a hospital setting, as seizures tend to repeat.
• When you have a seizure due to alcohol, you are more likely to develop DTs.
• Choreoathetosis was described in one patient completing withdrawal of clonazepam [14].
• This conclusion is consistent with observations from studies of cerebral glucose metabolism (see previous section entitled Metabolic Changes Following Alcohol Withdrawal).

Interestingly, in humans, phenytoin is not effective in protecting against the recurrence of alcohol withdrawal seizures (Rathlev et al., 1994). The animal model therefore shows a good correspondence with clinical experience. Valproate also has some protective activity against alcohol withdrawal-related HIC in mice (Goldstein, 1979), and topiramate may also protect against enhanced seizure susceptibility in ethanol-dependent rats (Cagetti et al., 2004). Animal studies confirm that gabapentin has protective activity against ethanol withdrawal seizures. For example, in mice undergoing alcohol withdrawal, gabapentin at doses of 50 to 100 mg/kg decreased the incidence of AGS (Watson et al., 1997). Vigabatrin may also be of value in alcohol withdrawal, but data from animal studies are not available as yet (Stuppaeck et al., 1996).

Epilepsy and Seizures 24/7 Helpline

It is estimated that 2 million Americans experience the symptoms of alcohol withdrawal each year (1). Generalized tonic–clonic seizures (rum fits) are the most dramatic and dangerous component of the alcohol withdrawal syndrome. The brain substrates that trigger these seizures are largely in the brainstem and, therefore, are distinct from those believed to be responsible for other clinically important seizure types. Moreover, because alcohol withdrawal seizures are pharmacologically induced, the pathophysiologic mechanisms almost certainly are different from those of the seizures that occur in genetic and acquired epilepsies. This review provides an overview of the current understanding of the cellular and molecular events that lead to alcohol withdrawal seizures. While alcohol withdrawal can cause seizures, they are not guaranteed to happen.

Treatment with these agents may be preferable in patients who metabolize medications less effectively, particularly the elderly and those with liver failure. Lorazepam is the only benzodiazepine with predictable intramuscular absorption (if intramuscular administration is necessary). Thyrotoxicosis, anticholinergic drug poisoning, and amphetamine or cocaine use can result in signs of increased sympathetic activity and altered mental status. Central nervous system infection or hemorrhage can cause seizures and mental status changes. Withdrawal from other sedative-hypnotic agents causes symptoms similar to those occurring in alcohol withdrawal syndrome. The spectrum of withdrawal symptoms and the time range for the appearance of these symptoms after cessation of alcohol use are listed in Table 2.

Causes of Alcohol Withdrawal

However, for those who struggle with alcohol abuse or addiction, stopping drinking can cause serious medical problems. Acute seizure treatment should follow standard protocol, ie, repeated doses of a benzodiazepine (preferably lorazepam or diazepam) until seizures stop. If ineffective (alcohol-related status epilepticus), sodium valproate should be considered before fosphenytoin/phenytoin, alcohol withdrawal seizure as phenytoin has been shown to be ineffective in preventing recurrent seizures in three controlled studies (19). If outpatient treatment is chosen, the patient should be assessed daily. Because close monitoring is not available in ambulatory treatment, a fixed-schedule regimen should be used. Minor withdrawal symptoms can occur while the patient still has a measurable blood alcohol level.

The greatest risk of a seizure during a hangover is not due to the hangover itself but to the long-term blood sugar effects of alcohol. Alcohol causes an initial spike in blood sugar levels, followed by a drop below normal levels for the next 12 hours. Although most people with alcohol-linked seizures experience them during withdrawal, others can get them while drinking heavily. Alcohol acts on receptors in the brain called gamma-aminobutyric acid, or GABA receptors, which are closely linked to seizure risk.

In one case report23 involving five patients, a single 10-mg dose of baclofen resulted in relief of severe withdrawal symptoms. In a preliminary RCT,24 baclofen also reduced craving in alcohol-dependent patients. Diazepam (Valium) and chlordiazepoxide (Librium) are long-acting agents that have been shown to be excellent in treating alcohol withdrawal symptoms. Because of the long half-life of these medications, withdrawal is smoother, and rebound withdrawal symptoms are less likely to occur. Lorazepam (Ativan) and oxazepam (Serax) are intermediate-acting medications with excellent records of efficacy.

Patients with alcohol withdrawal seizures raise a number of management issues. It is important to recognize that not all seizures in alcohol-dependent patients are the result of withdrawal. In epidemiologic studies, the rate of epilepsy and seizures rises in parallel with the amount of an individual’s alcohol intake.

For a comprehensive discussion of seizure types related to alcohol, see McMicken and Liss (37). This article deals only with seizures occurring during alcohol withdrawal in adults. Between 2% and 5% of alcoholics experience withdrawal seizures, which are usually generalized. These seizures typically occur within 48 hours of the last drink but may occur at any time within the first week of withdrawal. Compensatory upregulation of NMDA and kainate receptors (54) as well as calcium channels (55,56) also have been implicated in alcohol dependence and withdrawal seizures. The relevance of this mechanism is highlighted by the fact that NMDA-receptor antagonists are highly effective anticonvulsants in animal models of alcohol withdrawal seizures (59).