Alcohol Withdrawal

The alcohol withdrawal syndrome is a cluster of symptoms observed in persons who stop drinking alcohol following continuous and heavy consumption. Milder forms of the syndrome include tremulousness, seizures, and hallucinations, typically occurring within 6-48 hours after the last drink. A more serious syndrome, delirium tremens (DTs), involves profound confusion, hallucinations, and severe autonomic nervous system overactivity, typically beginning between 48 and 96 hours after the last drink (Victor 1983). Estimates vary on the incidence of serious consequences of alcohol withdrawal. Regardless of actual incidence, recent evidence suggests that it may be important to treat everyone who is suffering from alcohol withdrawal.

In a classic study that has shaped our understanding of alcohol withdrawal for many years, Isbell et al. (1955) found that alcohol-related seizures occur only after stopping heavy drinking. In a recent study that looked primarily at seizures, Ng et al. (1988) challenged Isbell's concept and reported that the risk of first seizure is related to current alcohol use rather than to withdrawal. They concluded, based on self-reports given retrospectively by seizure patients, that the relationship of alcohol use to seizures is causal and dose-dependent. However, emerging neurophysiological findings lend support to Isbell's interpretation of withdrawal.

In the central nervous system, ethanol (in concentrations high enough to intoxicate humans) interferes with the processes that tell certain nerve cells to activate or become excited (Hoffman et al. 1989; Lovinger et al. 1989). It also enhances those processes that tell certain nerve cells to be restrained (Suzdak et al. 1986). Thus, ethanol acts as a nonspecific biochemical inhibitor of activity in the central nervous system. During withdrawal, a person's central nervous system experiences a reversal of this effect: Excitatory processes are enhanced while inhibitory processes are reduced (Morrow et al. 1988). Such changes can result in overactivation of the central nervous system when alcohol is withdrawn.

Clinical researchers have measured this overactivation in patients (Linnoila et al. 1987). Even patients with moderately severe alcohol withdrawal can experience sympathetic nervous system overactivity and increased production of the adrenal hormones cortisol and norepinephrine. Both of these hormones can be toxic to nerve cells. Moreover, cortisol can specifically damage neurons in the hippocampus (Sapolsky et al. 1986)--a part of the brain that is thought to be particularly important for memory and control of affective states. Thus, repeated untreated alcohol withdrawals may lead to direct damage to the hippocampus.

Ballenger and Post (1978) did a retrospective chart review that led them to postulate that repeated inadequately treated withdrawals could produce future withdrawals of increased severity. These authors suggested that this phenomenon may be analogous to kindling as described in the animal literature. In kindling, repeated, weak (subthreshold), electrical or pharmacological stimulation of certain parts of the central nervous system leads to increased sensitivity; an animal eventually exhibits behavioral changes (including seizures) that are more severe on each occasion. The implication is that repeated untreated withdrawals from alcohol have a cumulative effect and create more serious future withdrawals. Only a minority of chronic alcoholics develop a seizure disorder, so an inherited vulnerability may be involved.

However, Whitfield et al. (1978) reported success with non-drug detoxification of a group of ambulatory patients with uncomplicated alcoholism. The treatment consisted of screening and providing extensive social support during withdrawal. The authors concluded that non-drug detoxification offers a reduced need for medical staff, a shortened detoxification period, and no sedative interference with a patient's alertness for participating in an alcohol treatment program.

Several researchers have developed scales for assessing the severity of the alcohol withdrawal syndrome: the Total Severity Assessment and Selected Severity Assessment (Gross et al. 1973), the Abstinence Symptom Evaluation Scale (Knott et al. 1981), and the Clinical Institute Withdrawal Assessment Scale [CIWA] (Shaw et al. 1981) Originally developed as research tools for studying treatment efficacy, such scales are now finding clinical use. Foy et al. (1988) demonstrated that a modified version of the CIWA can assist in guiding treatment and predicting patients at risk for severe alcohol withdrawal. However, rating procedures are not infallible, and an occasional patient will have a more severe reaction than the scale predicts. Rating procedures cannot replace the clinical judgment of medical staff.

One final point deserves mention. A recent study by Hayashida et al. (1989) compared outpatient with inpatient detoxification. However, the data from this study indicate that inpatient detoxification was more effective than outpatient detoxification: At the 6-month follow-up those treated as inpatients reported significantly greater improvement in their drinking behavior, despite having been measured as more impaired than the outpatient group at the time of admission. This point is not emphasized in the report. Whereas outpatient detoxification may be cheaper for some alcoholics, it is not clear to what extent serious conditions may lead to more severe and expensive problems later.

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