Seizure with alcohol withdrawal

The correct answer = B. It is important to treat the seizures associated with alcohol withdrawal. Benzodiazepines, such as chlordiazepoxide, diazepam or or the shorter-acting lorazepam, are effective in controlling this problem. They are less sedating than pentobarbital or phenytoin. 

Use cautiously in patients with alcohol withdrawal or convulsive disorders because of possible lowering of seizure threshold... 

May be useful in decreasing the hypertension, tachycardia, and tremulousness associated with alcohol withdrawal, but not the seizures or delirium tremens In complicated alcohol withdrawal Clonidine may Improve social relationships, affectual responses, and sensory responses In autistic disorder Clonidine may reduce the Incidence of menopausal flushing Growth hormone response to clonidine may be reduced during menses Clonidine stimulates growth hormone secretion (no chronic effects have been observed)... 

Gorwood, P., Limosin, F., Batel, P., Hamon, M., Ades, J., and Boni, C., The A9 allele of the dopamine transporter gene is associated with delirium tremens and alcohol-withdrawal seizure, Biol. Psychiatry, 53, 85, 2003. 

Signs and symptoms of BZ withdrawal are similar to those of alcohol withdrawal, including muscle pain, anxiety, restlessness, confusion, irritability, hallucinations, delirium, seizures, and cardiovascular collapse. Withdrawal from short-acting BZs (e.g., oxazepam, lorazepani, alprazolam) has an onset within 12 to 24 hours of the last dose. Diazepam, chlordiazep-oxide, and clorazepate have elimination half-lives (or active metabolites with elimination half-lives) of 24 to greater than 100 hours. So, withdrawal may be delayed for several days after their discontinuation. 

Alcohol withdrawal seizures do not require anticonvulsant drug treatment unless they progress to status epilepticus. Patients with seizures should be treated supportively. An increase in the dosage and slowing of the tapering schedule of the BZ used for detoxification or a single injection of a BZ may be necessary to prevent further seizure activity. 

Alcoholism is among the major health problems in most countries. Dependence on ethanol, as with other addictive drugs, is expressed as drug-seeking behavior and is associated with a withdrawal syndrome that occurs after abrupt cessation of drinking. The ethanol withdrawal syndrome is characterized by tremors, seizures, hyperthermia, hallucinations, and autonomic hyperactivity. 

Seizures have been reported after withdrawal of high doses of triazolam or relatively low doses combined with alcohol ( 347, 348 and 349). The FDA has reported a signal of an association for withdrawal seizures associated with triazolam ( 350). In a chart review of 150 consecutive patients withdrawn from BZDs, three of 25 triazolam patients experienced seizures, compared with two of 125 given other BZDs ( 351). Psychosis with delirium also has been reported after discontinuation of high triazolam doses (352). 

Heavy drinking—and especially "binge" drinking—are associated with both atrial and ventricular arrhythmias. Patients undergoing alcohol withdrawal syndrome can develop severe arrhythmias that may reflect abnormalities of potassium or magnesium metabolism as well as enhanced release of catecholamines. Seizures, syncope, and sudden death during alcohol withdrawal may be due to these arrhythmias. 

Abrupt alcohol withdrawal leads to a characteristic syndrome of motor agitation, anxiety, insomnia, and reduction of seizure threshold. The severity of the syndrome is usually proportionate to the degree and duration of alcohol abuse. However, this can be greatly modified by the use of other sedatives as well as by associated factors (eg, diabetes, injury). In its mildest form, the alcohol withdrawal syndrome of tremor, anxiety, and insomnia occurs 6-8 hours after alcohol consumption is stopped (Figure 23-2). These effects usually abate in 1-2 days. In some patients, more severe withdrawal reactions occur, with patients at risk of hallucinations or generalized seizures during the first 1-3 days of withdrawal. Alcohol withdrawal is one of the most common causes of seizures in adults. Several days later, individuals can develop the syndrome of delirium tremens, which is characterized by total disorientation, hallucinations, and marked abnormalities of vital signs. 

Time course of events during the alcohol withdrawal syndrome. The signs and symptoms that manifest earliest are tremor, anxiety, and insomnia as well as (in severe syndromes) hallucinations and seizures. Delirium tremens—with its associated delirium, hallucinations, and autonomic instability—develops 48-72 hours after alcohol discontinuation. 

The major objective of drug therapy in the alcohol withdrawal period is prevention of seizures, delirium, and arrhythmias. Potassium, magnesium, and phosphate balance should be restored as rapidly as is consistent with renal function. Thiamine therapy is initiated in all cases. Persons in mild alcohol withdrawal do not need any other pharmacologic assistance. 

Dependence becomes apparent 6-12 hours after cessation of heavy drinking as a withdrawal syndrome that may include tremor (mainly of the hands), nausea and vomiting, excessive sweating, agitation, and anxiety. In some individuals, this is followed by visual, tactile, and auditory hallucinations 12-24 hours after cessation. Generalized seizures may manifest after 24-48 hours. Finally, 48-72 hours after cessation, an alcohol withdrawal delirium (delirium tremens) may become apparent in which the person hallucinates, is disoriented, and shows evidence of autonomic instability. Delirium tremens is associated with 5-15% mortality. 

Humans who hit the wall of alcohol withdrawal show the more complex picture of toxic-delirium, consisting of visual hallucinations (often with stereotyped insect and animal imagery like the bugs and pink elephants of barfly lore), disorientation and confusion, confabulation, and memory loss as their seizure propensity increases. 

Sleep lab recordings reveal that in the first three days following alcohol withdrawal, the REM sleep rebound becomes so intense as to practically displace the NREM sleep that alcohol had initially enhanced at the expense of REM. This is REM debt payback with a vengeance. As the subject becomes more and more tremulous, more and more delirious, and more and more seizure prone, REM sleep levels go to 100 percent of sleep, indicating a marked shift in brain excitability that we assume is related to a desperate attempt of the system to restore neuromodulatory equilibrium. 

BZDs such as chlordiazepoxide (Librium) or diazepam (Valium) may be prescribed to treat anxiety, seizures, acute stress reactions, and panic attacks, or to alleviate the side effects of drug or alcohol withdrawal. Those BZDs with a more sedating effect, such as estazo-lam (ProSom) or triazolam (Halcion), may be prescribed for short-term treatment of sleep disorders. However, the newer generation of non-BZD agents—zolpidem (Ambi-en) and (Sonata)—are less potentially addictive hypnotic drugs than the BZDs. 

Phenothiazine medications for alcohol withdrawal have potentially serious adverse effects (eg, increasing seizures) that probably outweigh their benefits. Antihistamines have been used but with little justification. 

Tiapride appears to be useful in alcohol withdrawal as an alternative to the benzodiazepines (2). It facilitates the management of ethanol withdrawal, but its use in patients at risk of severe reactions in acute withdrawal should be accompanied by adjunctive therapy for hallucinosis and seizures. Since it may prove difficult to identify such patients and since there is also a small risk of the neuroleptic malignant syndrome (particularly with parenteral administration), the usefulness of tiapride in this setting is likely to be limited. The potential risk of tardive dyskinesia at the dosage used in alcoholic patients following detoxification (300 mg/day) requires evaluation and necessitates medical supervision. It is unlikely to produce problems of dependence or abuse. 

Tramadol, phenothiazine antipsychotics and the majority of antidepressants, as well as a number of other drugs, can lower the seiznre threshold and are associated with an increased risk of convnlsions [6]. Again, these drugs may accumulate in patients with liver impairment such as cirrhosis or acute liver failure, and care must be taken if choosing to use them. This is especially important in alcoholics, who have an increased risk of seizures from acute alcohol withdrawal [7]. Examples of drugs that can lower the seizure threshold and should be used with caution/avoided are ... 

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