Seizures in alcohol-dependent patients: epidemiology, pathophysiology and management

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NBAC effects on glutamatergic and GABAergic neurotransmission may help combat the symptoms of the protracted abstinence syndrome by restoring proper neurotransmission in the ventral striatum and its neurocircuitry. Anticonvulsants may facilitate homeostasis and restorative changes once a subject has obtained sobriety. Glutamate and dopamine interactions are likely necessary components of addiction maintenance 61. However, there have been reports that the risk of seizure increases in an alcohol-dependent person who misuses a sedative and takes nonsedative AEDs.

  • Additionally, there is a shocking 4.8x increase in the mortality rate of those who experience seizures compared to those who do not experience seizures during withdrawal.
  • Alcohol affects brain chemistry by slowing down its activity through neurotransmitters that regulate mood and behavior.
  • Case-control studies convincingly demonstrate the association of first seizures to alcohol use in a dose-dependent manner.
  • It won’t be long after alcohol reaches its half-life that you start to experience withdrawal symptoms.

What Actually Triggers Alcohol Withdrawal Symptoms in Your Brain?

Individuals with a history of alcohol misuse presenting with these symptoms should be evaluated for alcohol withdrawal seizures, especially if they occur within 6 to 48 hours after the last drink. Alcohol withdrawal seizures are serious and potentially life-threatening complications that can occur during the withdrawal phase from chronic heavy alcohol use. These seizures typically manifest between 6 to 48 hours after the cessation of heavy drinking, though they can sometimes occur several days later. Medical detoxification is the safest and most effective way to manage alcohol withdrawal.

alcohol withdrawal seizure

The Role of Laboratory Tests and Imaging in Diagnosing Alcohol Seizures

The serious disorder of central pontine myelinolysis is thought to be triggered by osmotic gradients in the pons, a situation that might result from attempts to correct electrolyte disturbances too Sober living home rapidly (32). If parenteral treatment is considered necessary, according to a retrospective study, the rate of serum sodium correction should not exceed 10 mmol/l per day (57). For detection of alcohol overuse, questionnaire-based interviews are reported to be more sensitive than any biomarker (04). However, in cases where information on recent alcohol consumption is unavailable or considered unreliable, markers of alcohol consumption can increase accuracy of clinical diagnosis (06; 08).

When someone quits drinking without medical support, they face risks like severe dehydration, confusion, or even seizures. Without proper care, these symptoms can quickly escalate and become life-threatening. Long-term drinking reduces the brain’s ability to function without alcohol, creating a dependency. When drinking stops, the brain becomes overstimulated, leading to symptoms like restlessness, anxiety, or, in severe cases, alcohol seizures.

Multiple Detoxifications Kindle Susceptibility to Alcohol Withdrawal Seizures

One retrospective chart review suggested that a symptom-triggered protocol may decrease total doses of benzodiazepines administered, however, this finding would need to be replicated in a prospective, controlled study 40. A professional health sciences librarian (MDW) developed our search strategy. We searched MEDLINE and CENTRAL using concepts emergency department AND alcohol withdrawal AND (drugs OR drug subheadings). We searched EMBASE using concepts emergency department AND alcohol withdrawal (focused) AND (drugs OR drug subheadings), as well as concepts emergency department AND alcohol withdrawal AND drugs AND drug subheadings. Subheadings and keywords were included in the searches to increase sensitivity. Patients who experience harms from alcohol and other substance use often seek care in the emergency department (ED) 1, 2.

Inpatient Treatment

Alcohol use reduces the levels of glutamate in the brain which produces depressant effects. After prolonged exposure to alcohol, the brain will increase sensitivity to glutamate to compensate for the reduced levels. Along with the increased sensitivity to glutamate, this produces a dangerous state of hyperarousal in the brain. The tonic phase is fairly short, typically lasting less than 30 seconds, while the clonic phase may last around 2 minutes on average. The period of greatest seizure risk is between 6-48 hours after someone has taken their last drink of alcohol.

alcohol withdrawal seizure

alcohol withdrawal seizure

In these models, animals are exposed to alcohol by intragastric intubation, inhalation, or feeding in a nutritionally complete liquid diet for periods of 2 to 21 days. The animals exhibit sound-evoked audiogenic seizures or handling-induced convulsions during the 1- to 3-day period after cessation of alcohol intake and may also experience spontaneous generalized seizures. A 3-week randomized flexible-dose pilot study was completed comparing zonisamide with diazepam for the treatment of AWS in 40 alcohol-dependent subjects 60.

alcohol withdrawal seizure

CLINICAL RELEVANCE

alcohol withdrawal seizure

Sudden cessation of alcohol, especially after prolonged use, increases the risk of seizures from alcohol withdrawal. The most typical and severe type of seizure that happens is called tonic-clonic seizures, also called what is alcoholism convulsions. Seizures, while scary on their own, can also be a warning sign of the DTs, and those who experience alcohol withdrawal seizures are at a higher risk . Someone who does have a seizure during detox will likely be transferred to a hospital setting, as seizures tend to repeat.

alcohol withdrawal seizure

There have been many effective treatments developed in the last few decades which greatly reduce the dangers. This most likely tends toward the lower end (1-4%) of the scale, but further definitive studies are needed to hone in on a more precise number. GABA is an inhibitory neurotransmitter that is responsible for dampening or slowing down signals in the brain.