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Introduction to Alcohol Withdrawal

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Introduction to Alcohol Withdrawal Introduction to Alcohol Withdrawal Richard Saitz, M.D., M.P.H. Heavy drinkers who suddenly decrease their alcohol consumption or abstain completely may experience alcohol withdrawal (AW). Signs and symptoms of AW can include, among others, mild to moderate tremors, irritability, anxiety, or agitation. The most severe manifestations of withdrawal include delirium tremens, hallucinations, and seizures. These manifestations result from alcohol-induced imbalances in the brain chemistry that cause excessive neuronal activity if the alcohol is withheld. Management of AW includes thorough assessment of the severity of the patient’s symptoms and of any complicating conditions as well as treatment of the withdrawal symptoms with pharmacological and nonpharmacological approaches. Treatment can occur in both inpatient and outpatient settings. Recognition and treatment of withdrawal can represent a first step in the patient’s recovery process. KEY WORDS: AOD withdrawal syndrome; biochemical mechanism; neurotransmission; neurotransmitter receptors; central nervous system; symptom; tremor; anxiety state; delirium tremens; AODR (alcohol and other drug related) hallucinosis; AODR seizure; AOD abstinence; disease severity; patient assessment; treatment method; alcohol withdrawal agents; drug therapy; detoxification; addiction care; literature review very year more than one-and- clinical syndrome that affects people a-half million people in the accustomed to regular alcohol intake RICHARD SAITZ, M.D., M.P.H., is an EUnited States either enter alco- who either decrease their alcohol assistant professor of medicine in the holism treatment or are admitted to consumption or stop drinking com- Clinical Addiction Research and a general hospital because of medical pletely. In these people, the central Education Unit, Section of General consequences resulting from alcohol nervous system (CNS) has adjusted to Internal Medicine, Department of dependence. These patients, as well as the constant presence of alcohol in the Medicine, at Boston Medical Center a substantial number of other people body and compensates for alcohol’s and Boston University School of Medicine; who stop drinking without seeking depressive effects on both brain func- a faculty fellow in the Center for professional treatment, experience tion and the communication among Substance Abuse Prevention Faculty alcohol withdrawal (AW). AW is a nerve cells (i.e., neurons). Consequently, Development Program; and a generalist when the alcohol level is suddenly physician faculty scholar of the Robert 1Clinicians generally distinguish between signs and lowered, the brain remains in a hyper- Wood Johnson Foundation. symptoms of a disorder or syndrome. “Signs” are changes in the patient’s condition that can be active, or hyperexcited, state, causing objectively observed by an examiner (e.g., temperature, withdrawal syndrome. Support for this work was provided a rash, or high blood pressure). Conversely, symp- AW syndrome varies significantly by National Institute on Alcohol toms are changes that are subjectively perceived by among alcoholics in both its clinical Abuse and Alcoholism grant the patient (e.g., irritability or craving for alcohol). manifestations and its severity. These 5RO1–AA–10870 and by Center The term “manifestations of alcohol withdrawal,” 1 which is used in this article, can refer to either signs manifestations can range from mild for Substance Abuse Prevention grant or symptoms. insomnia to severe consequences, 1T15–SPO7773. Vol. 22, No. 1, 1998 5 such as delirium tremens (DT’s) and toms. Moreover, the symptoms of AW Of these neurotransmitters, scientists even death. Substantial variability also were dose dependent: The men who best understand the roles of GABA exists in the incidence with which had consumed the largest amounts of and glutamate. For example, researchers symptoms occur in various drinkers. alcohol developed the most severe have demonstrated that alcohol Some people who regularly consume manifestations of withdrawal, such as enhances (i.e., potentiates) GABA’s alcohol never experience any withdrawal hallucinations, seizures, and DT’s. inhibitory effects on signal-receiving symptoms. Conversely, in some alco- These findings support the association neurons, thereby suppressing neuronal holics withdrawal symptoms can occur between alcohol intake and the clinical activity. With chronic alcohol exposure, at blood alcohol concentrations (BAC’s) manifestations of withdrawal syndrome. however, GABA receptors become less that would be intoxicating in non- responsive to the neurotransmitter, alcohol-dependent people but which and higher alcohol concentrations are for the dependent patients represent required to achieve the same level of a decline from their usual BAC’s. Most manifestations suppression. This clinically observed This article briefly reviews the mech- of withdrawal adaptation is referred to as tolerance. anisms, clinical features, and man- When alcohol is removed from this agement of AW. The article also discusses will resolve after adapted system, the GABA receptors how the treatment of AW can be linked several hours to remain less responsive, leading to an to the treatment of alcohol dependence imbalance in favor of excitatory neu- and any co-occurring or underlying dis- several days. rotransmission. This imbalance is orders. For more in-depth discussions of enhanced further by an alcohol- some of these issues, the reader is referred induced increase in the number of to subsequent articles in this issue. one type of receptor for the excitatory To better understand the mecha- neurotransmitter, glutamate. Even nisms underlying withdrawal, one when alcohol is removed, the number Mechanisms of Alcohol must briefly review some of the prin- of these receptors remains elevated, Withdrawal ciples of neuronal communication in leading to enhanced excitatory neuro- the CNS. The transmission of nerve transmission. Both of these mechanisms Historically, several mechanisms have signals from one neuron to the next is contribute to the neuronal hyperex- been suggested to play a role in the achieved, in general, through small citability that is characteristic of AW. development (i.e., etiology) of AW. For molecules called neurotransmitters, (For more information on the neuro- example, researchers initially thought which are secreted by the signal- chemical mechanisms underlying with- that withdrawal might be caused by emitting neuron. The neurotransmitter drawal, see the article by Littleton, nutritional deficiencies (Isbell et al. 1955; molecules traverse the small gap (i.e., pp. 13–24.) Victor and Adams 1953) and that some the synapse) between adjacent neurons complications of withdrawal (e.g., seizures) and interact with docking molecules might result directly from alcohol use (i.e., receptors) on the signal-receiving Clinical Features of or intoxication (Ng et al. 1988). Although neuron. The interaction between a Alcohol Withdrawal alcoholic patients exhibit many metabolic neurotransmitter and its receptor and nutritional disturbances, overwhelm- initiates a cascade of chemical and Despite this current understanding of ing laboratory and clinical evidence electrical reactions in the signal- the mechanisms underlying AW syn- now indicates that the constellation of receiving cell that depending on the drome, some controversies still exist signs and symptoms known as AW are neurotransmitter involved, results in regarding the risk, complications, and caused by interrupting the constant the activation or inhibition of that cell. clinical management of withdrawal. exposure of the CNS to alcohol. Thus, excitatory neurotransmitters These controversies likely arise from The hypothesis that withdrawal (e.g., glutamate) stimulate the signal- the varied clinical manifestations of occurs as a result of “insufficient” alco- receiving neuron, whereas inhibitory the syndrome in alcoholic patients hol intake or abstinence in dependent neurotransmitters (e.g., gamma- and from the diverse settings in which patients rather than because of nutri- aminobutyric acid [GABA]) inhibit these patients are encountered. For tional deficiencies was supported by an the neuron. Under normal conditions, example, some alcoholic patients who early study of men who received large a tight balance is maintained between cut down or stop drinking may expe- daily doses of alcohol (Isbell et al. excitatory and inhibitory influences. rience no withdrawal symptoms, 1955). The study participants, who Regular alcohol intake affects whereas others experience severe man- also were well fed, each consumed up numerous excitatory and inhibitory ifestations. In fact, even in clinical to almost 30 standard drinks per day neurotransmitter systems in the brain studies of patients presenting for for up to 3 months. Upon abstaining (Begleiter and Kissin 1996). Similarly, alcohol detoxification, the proportion from this alcohol intake, these men many neurotransmitters and mecha- of patients who developed significant invariably developed withdrawal symp- nisms probably are involved in AW. symptoms ranged from 13 to 71 6 Alcohol Health & Research World Introduction to Alcohol Withdrawal percent (Victor and Adams 1953; the first seizure (Victor and Brausch • Abnormal liver function Saitz et al. 1994). What is the reason 1967). Although multiple seizures are for this variability? Likely, individual not common, AW is one of the most • Prior detoxification patients differ in their underlying common causes in the United States
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