Academic journal article Alcohol Health & Research World

Kindling in Alcohol Withdrawal

Academic journal article Alcohol Health & Research World

Kindling in Alcohol Withdrawal

Article excerpt

In many alcoholics, the severity of withdrawal symptoms increases after repeated withdrawal episodes. This exacerbation may be attributable to a kindling process. Kindling is a phenomenon in which a weak electrical or chemical stimulus, which initially causes no overt behavioral responses, results in the appearance of behavioral effects, such as seizures, when it is administered repeatedly. Both clinical and experimental evidence support the existence of a kindling mechanism during alcohol withdrawal Withdrawal symptoms, such as seizures, result from neurochemical imbalances in the brain of alcoholics who suddenly reduce or cease alcohol consumption. These imbalances may be exacerbated after repeated withdrawal experiences. The existence of kindling during withdrawal suggests that even patients experiencing mild withdrawal should be treated aggressively to prevent the increase in severity of subsequent withdrawal episodes. Kindling also may contribute to a patient's relapse risk and to alcohol-related brain damage and cognitive impairment. KEY WORDS: AOD withdrawal syndrome; AODR (alcohol and other drug related) seizure; symptom; disease severity; neurotransmission; neurotransmitter receptors; cell electrophysiology; sensory stimuli; biochemical mechanism; AOD abstinence; AODD (alcohol and other drug dependence) relapse; brain damage; cognitive process; detoxification; treatment; animal model; clinical study; literature review

Alcohol dependence and alcohol abuse frequently involve drinking patterns in which bouts of heavy drinking (i.e., binge drinking) are interspersed with periods of abstinence. During the binge-drinking episode, the body, particularly the brain, adapts to the presence of alcohol by compensating for alcohol's effect on the central nervous system (CNS). Alcohol has an overall suppressing effect on CNS activity. Accordingly, the adaptation process involves several mechanisms to increase the excitability of nerve cells (i.e., neurons) in the brain-that is, their ability to become activated in response to signals from other neurons. When the alcohol is eliminated from the body during abstinence, this compensatory activation of the CNS remains in effect for several more days, resulting in excessive excitability of the CNS (i.e., hyperexcitability). This hyperexcitability manifests itself as alcohol withdrawal (AW), with symptoms ranging from tremors and agitation to seizures and delirium tremens. As a result of the bingeing-abstaining consumption pattem, many alcoholics experience numerous withdrawal episodes during the course of their illness (Hillbom 1990).

The severity of AW symptoms can differ widely among alcoholics and even among different withdrawal episodes in the same person. Both the amount of alcohol consumed and the duration of intoxication just before cessation of drinking are important determinants of the severity of a withdrawal reaction. In addition, a history of withdrawal episodes appears to be a critical factor in the intensity of withdrawal symptoms. Accordingly, some researchers have suggested that repeated AW may sensitize a person to subsequent withdrawal episodes. This hypothesis implies that the severity of withdrawal-- related symptoms may increase in a cumulative fashion, with more severe symptoms becoming evident after years of alcohol abuse and numerous periods of abstinence.

The mechanisms underlying the exacerbation of withdrawal symptoms following repeated withdrawal episodes are currently unknown. One hypothesis proposes that the phenomenon may result from a "priming" effect, in which each consecutive episode of alcohol exposure evokes stronger compensatory (i.e., withdrawal) responses. In contrast, Ballenger and Post (1978) have hypothesized that the progressive exacerbation of AW is the manifestation of a "kindling" mechanism, which has been observed in other neurological conditions. According to this model, it is the repeated experience of AW, rather than repeated alcohol exposure, that underlies the progressive intensification of symptoms. …

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