Alcohol Withdrawal Syndrome
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
over-activity, typically beginning between 48 and 96 hours after the last
drink (Victor 1983).
Alcohol Withdrawal Syndrome Requires Treatment
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.
Ethanol Plays Important Role in Alcohol 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 over-activation of the central nervous
system when alcohol is withdrawn.
Repeated Alcohol Withdrawals Causes Brain Damage
Clinical researchers have measured this over-activation in patients (Linnoila
et al. 1987). Even patients with moderately severe alcohol
withdrawal can experience sympathetic nervous system over-activity 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 alcohol 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 (sub-threshold),
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
alcohol withdrawals have a cumulative effect and create more serious
future alcohol withdrawals. Only a minority of chronic alcoholics
develop a seizure disorder, so an inherited vulnerability may be
involved.
Non-drug Detoxification Results Successful
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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