Among the social and medical ills of the 20th century, substance abuse -which includes drugs, marijuana, and alcohol- ranks as one of the most devastating and costly.
(E.L. Gardner, 1992). An addictive disorder is defined as the preoccupation with acquiring and consuming alcohol or drugs, the compulsive use of alcohol and drugs despite adverse consequences, and
includes a pattern of relapse to alcohol and drug use despite the recurrence of adverse consequences. Central to addiction is the concept of loss of control over alcohol and drug use which leads to consequences that are harmful to the individual and others associated with him or her. This loss of control is what makes an addiction a disease or disorder similar to other diseases or disorders, such as schizophrenia or diabetes(Miller 1994).
The chemistry of ethanol is relevant to an understanding of the neurobiology of alcohol addiction. Ethyl
alcohol(ethanol) is a small organic molecule consisting of a two-carbon backbone surrounded by hydrogen atoms, with a hydroxyl group attached to one of these carbons. The hydroxyl group provides ethanol with its water soluble properties while the hydrocarbon backbone gives ethanol some of its lipid soluble properties. This composition of ethanol gives it the capacity to interact with and dissolve into both water and lipid. This amphiphilic property of ethanol has been a major impetus for the hypotheses that try to define ethanol's mechanism of action through the perturbation of cell membrane lipids. The small molecular size of ethanol and its lack of isometric carbons supports the theory that ethanol's actions are not expressed through specific recognition sites or receptors for ethanol. The most up to date explanations of ethanol's effects in the central nervous system focus on a nonspecific interaction of ethanol and neuronal membrane lipids. Disorganization of the membrane lipid bilayer is thought to result from this interaction. This perturbation of one of the major structural elements of the neuron is theorized to result in the functional changes seen during alcoholic intoxication.
This “membrane hypothesis” of ethanol's actions may also explain the high-dose anesthetic effects of ethanol. However, the lower dose effects, which include reinforcement, anxiolytic effects, motor
incoordination, and cognitive effects, as well as the development of tolerance and dependence, are not as easily related to ethanol-induced perturbation of membrane lipids. The current conceptualization is that the lower dose effects of ethanol are mediated through the interaction of ethanol with a specific subset of neuronal elements (receptors, enzymes, etc.) that are particularly sensitive to ethanol(Tabakoff & Hoffman,1992). The most recent findings support the hypothesis that alcohol produces its effects by intercollating itself into membranes, resulting in increased fluidity of the membrane with short term exposure to ethanol. It is also theorized that long term use of ethanol results in membrane stiffness. It has long been known that membrane fluidity is critical to the normal functioning of receptors, ion channels, and other membrane
processes.(Keltner, Folks, Palmer, & Powers,1998).
Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the brain. It has been theorized for many years that the depressant effects of ethanol could be mediated by enhancement of the effects of
GABA. The action of GABA at the GABA alpha receptor is modulated by benzodiazepines as well as barbiturates, suggesting that this receptor system may be involved in the anxiolytic and sedative/hypnotic responses to ethanol. Several early studies indicated that the
motor-incoordinating and hypnotic effects of ethanol could be increased by the administration of GABA agonists and attenuated by GABA antagonists.
(Tabakoff & Hoffman, 1992).
Calcium ions have also been investigated in relationship to the mechanism of action of ethanol on neurons. These ions are involved in many aspects of neuronal transmission, and as a result there has been a significant amount of interest in the role that calcium may play in the effects of ethanol in the brain.(Tabakoff & Hoffman,1992)
Adenosine is believed to serve as a neuromodulator rather than a neurotransmitter in the brain, which means that it regulates the response of neurons to other neurotransmitters. Adenosine is believed to play a role in the
motor-incoordinating and hypnotic effects of ethanol. Some biochemical studies have attempted to determine the mechanism by which ethanol influences this system. Ethanol is believed to act directly on the adenosine receptors, and has also been found to enhance cyclic AMP responses to adenosine in human lymphocytes and in neuroblastoma-glioma cells in culture.
(Tabakoff & Hoffman,1992)
The major neurotransmitters thus far thought to be involved in substance abuse and dependence are the opiate, dopamine and GABA systems. The dopaminergic neurons are of specific importance in the ventral tegmental area of the brain, which projects to the cortical and limbic regions - especially the nucleus
accumbens. This particular brain pathway is thought to be involved in the sensation of reward and to be the major mediator of the effects of most substances of abuse. The locus
ceruleus, which is the largest group of adrenergic neurons in the central nervous system, is also believed to be involved in mediating the effects of opiates.
(Tabakoff & Hoffman, 1992)
The structural and neurochemical findings of alcoholic disorders are characterized by the Wernicke-Korsakoff syndrome. In a small percentage of patients with Wernicke's
encephalopathy, punctate hemorrhagic lesions have been found on brain autopsy in the hypothalamus, mamillary bodies, reticular formation, periaqueductal areas of the midbrain, floor of the fourth ventricle, and periventricular areas of the thalamus
(Keltner et al.) The acute phase of Wernicke's syndrome includes ocular disturbances
(nystagmus or 6th nerve palsy), ataxia, and confusion. These symptoms usually clear within a few days, but on occasion may progress to a chronic brain syndrome
(Korsakoff's psychosis). The most characteristic feature of Korsakoff's psychosis is short-term memory loss or anterograde amnesia. “Confabulation” or narration of fanciful tales may occur. This syndrome is associated with necrotic lesions of the mamillary bodies, thalamus, and other brainstem
areas.(Goodman, 1992). The memory loss of Korsakoff's psychosis may result from a breakdown of the functional anatomic linkages between the systems of reward reinforcement and memory. Decreased levels of
norepinephrine, dopamine and serotonin in the central nervous system have been found, the greatest decrements involving norepinephrine levels. One theory suggests that the norepinephrine systems are selectively damaged in Korsakoff's psychosis, resulting in memory deficits but not global dementia.
(Keltner et al.,1998).`
Thiamine corrects early Wernicke signs rapidly and may prevent development of an irreversible Korsakoff's dementia. Once the dementia is established, however, studies have shown that thiamin usually does not help. (Goodwin,1992).
Quantitative studies of the cerebellum in alcoholism have shown a significant loss of cerebellar Purkinje cells and shrinkage of cerebellar molecular and granular cell layers. It has been suggested that alcohol alone may cause cerebellar atrophy. Cerebellar atrophy has been reported to occur in approximately 40% of patients with chronic alcoholism. While generalized brain shrinkage is generally reversible following
prolonged abstinence from alcohol, the loss of cerebellar and cortical neurons and the diencephalic and midbrain damage caused by Wernicke's dementia is often irreversible.
(Keltner et al., 1998).
Deficits in the acetylcholine system have been thought to cause a milder form of damage to the nucleus basalis of Meynert that is similar to that found in Alzheimer's disease. Direct neurotoxicity to this structure may also play a role in Korsakoff's psychosis. Alcoholic hallucinosis is an acute mental syndrome characterized by vivid auditory hallucinations which occur shortly after the cessation or reduction of drinking.
The differential diagnosis of acute alcoholic hallucinosis includes delirium tremens(‘DT's'), paranoid psychosis, borderline transient psychotic episode or other substance-related disorder. It is reported that withdrawal-induced hallucinosis is not a predictor of DT's. In contrast to alcohol-induced delirium and DT's, the hallucinations associated with acute alcoholic hallucinosis usually occur in a clear
sensorium, and are associated with a limited number of autonomic symptoms. The hallucinations may include sounds such as clicks, roaring, humming, or ringing bells to chanting or threatening/maligning voices of friends or enemies(Lishman 1990). Symptoms persisting for six months may become chronic(Franklin and Frances 1992).
The net result of the molecular activities of alcohol is that of a CNS depressant similar to
benzodiazepines, which are cross tolerant and cross dependent with alcohol. An individual with an ethyl alcohol blood level of 0.05% usually manifests loosening of restraint in the areas of thought and
judgement. There are also sometimes disrupted motor functions. Legally defined alcoholic intoxication ranges from the levels of 0.08% to 0.15% in most states. Of interest here is the fact that at 0.2% the function of the entire motor area of the brain is measurably depressed. At 0.3% in the non-tolerant individual there is confusion or stupor. At 0.4% to 0.5% blood alcohol concentration a non-tolerant individual may become comatose, with abnormal breathing, abnormal heart rate and the potential for death from asphyxiation after aspiration of regurgitated gastric contents(Keltner et al, 1998).
Most studies suggest that the main acute effect of ethanol on memory is to impair the acquisition of new information, with little effect on retrieval of previously stored material. There is even some evidence that ethanol can enhance the consolidation of memory under some circumstances. This has been suggested to be a consequence of the stimulatory effect that is sometimes observed after ingestion or administration of low doses of ethanol. The impairing effect of ethanol on learning is a process which occurs when the individual is asked to perform a task while they are intoxicated. This could reflect deficits in attention, perception, motivation, or performance. Ethanol affects the function of at least two neurotransmitter systems that play important roles in learning and memory. The cholinergic systems in various brain areas have been linked to learning and memory in a number of studies and appear to be playing an important role in “working memory”. “Working memory” is the memory necessary to perform the task on the particular day of the test, as opposed to memory of the test situation in general. Acetylcholine release in the brain is very sensitive to inhibition by ethanol, and it appears that this action of ethanol would be expected to influence some aspects of memory(Tabakoff & Hoffman, 1992).
Individuals with longstanding histories of alcohol abuse sometimes appear to be less intoxicated than they really are because of their acquired ability to tolerate higher concentrations of ethanol due to their chronic and repeated exposure. It is a myth that drinking alcohol aids sleep; alcohol is actually associated with decrease in rapid eye movement sleep and a disruption of normal sleep architecture. There is a decrease in deep sleep and an increase in sleep fragmentation which includes more or longer episodes of awakening(Keltner,et al., 1998). Because small amounts of alcohol may have transient sedative effects at night, poor sleep may be associated with relapse into active alcoholism in previously abstinent patients with alcoholism. The conclusion in this study was that alcoholic relapse within 3 month after discharge from a one month inpatient alcohol treatment program may be predicted on admission by short REM density in patients with uncomplicated alcoholism. This study suggests that evaluation of self-medication from the resulting sleep disturbance of addiction may be a significant factor in relapse
Recent research by Blum, Cull, Braverman and Comings has suggested an association between certain genes and various behavioral disorders, including alcoholism; other substance abuse;
cigarette smoking; compulsive overeating and obesity; attention-deficit disorder; Tourette's syndrome, and pathological gambling. These researchers believe that the disorders listed are linked by a common substrate in the brain, consisting of cells and signaling molecules that provide pleasure in the process of rewarding certain behavior. An example might be how normal people respond to safety, warmth and a full stomach. If these needs are threatened or are not met, an individual may experience discomfort and anxiety. An inborn chemical imbalance that alters the intercellular signaling in the brain's reward processes could theoretically supplant an individual's feelings of well being with anxiety, anger or a craving for a substance that can alleviate the negative emotions. This chemical imbalance manifests itself as one or more behavioral disorders which have been termed “reward deficiency syndrome”(Blum, Cull, Braverman and Comings, 1996).
During the past several decades, research on the biological basis of chemical dependency has established some of the brain regions and neurotransmitters involved in central reward mechanisms. In particular, it appears that dependence on alcohol, opiates, and cocaine relies on common biochemical mechanisms(Cloninger 1983, Blum et al 1989). A neuronal circuit deep in the brain involving the limbic system, and two regions called the nucleus accumbens and the globus pallidus appear to be critical in the expression of reward for people taking drugs of abuse(Wise and Bozarth 1984). Although each substance of abuse appears to act on different parts of this circuit, the end result is the same: dopamine is released in the nucleus accumbens and the hippocampus(Koob and Bloom 1988). Dopamine appears to be the primary neurotransmitter of reward at these reinforcement sites. (Blum, et al., 1996, paragraph 7). Although the system of neurotransmitters involved in the biology of reward is complex, at least three other neurotransmitters are known to be involved at several sites in the brain: serotonin in the hypothalamus, the enkephalins
(opioid peptides) in the ventral tegmental area and the nucleus accumbens, and the inhibitory neurotransmitter GABA in the ventral tegmental area and the nucleus accumbens (Stein and Belluzi 1986, Blum 1989). Interestingly, the glucose receptor is an important link between serotonergic system and the opioid peptides in the hypothalamus. An alternative reward pathway involves the release of norepinephine in the hippocampus from neuronal fibers that originate in the locus coerulus(Blum et al., 1996, paragraph 8).
These neurotransmitters appear to work together in a cascade of excitation or
inhibition-between complex stimuli and complex responses-leading to a feeling of well-being in the normal person, the ultimate reward. In the cascade theory of reward, a disruption of these intercellular interactions, results in anxiety, anger and other “bad
feelings,” or in a craving for a substance that either helps relieve or alleviate these negative emotions. Alcohol is known to activate the norepinephrine system in the limbic
circuitry through an intercellular cascade that includes serotonin, opioid peptides and dopamine. Alcohol may also cause a direct effect through the production of neuroamines that interact with opioid receptors or with dopaminergic systems. In the cascade theory of reward, it is postulated that genetic anomalies, prolonged stress or long-term abuse of alcohol can lead to a self-sustaining pattern of abnormal cravings
in both animals and human beings(Blum et al., 1996).
The criteria for diagnosing alcoholic withdrawal include the development of two or more of the following symptoms within several hours or a few days after cessation or marked decrease of alcohol consumption: autonomic hyperactivity (e.g., sweating or pulse rate greater than 100); hand tremor; insomnia; nausea or vomiting; transient visual, tactile, or auditory hallucinations or illusions; psychomotor agitation; anxiety; or grand mal seizures. These symptoms should cause clinically significant distress or impairment in social, occupational or other important areas of functioning. Observed autonomic hyperactivity during withdrawal, which is mediated by the sympathetic nervous system, has produced a focus on the noradrenergic neurotransmitter system. Increased CSF norepinephrine has been associated with the intensity of withdrawal symptoms. The by-products of alcohol metabolism include acetaldehyde, which may have an inhibitory effect on the adrenergic receptors. Increased cyclic adenosine monophosphate in neurons with long term alcohol exposure may increase norepinephrine receptor sensitivity and norepinephrine turnover(Keltner,et al., 1998).
A kindling model developed in rats has shown that repeated mild withdrawal
from alcohol increases subcortical neuronal spiking. This increased spiking
may serve as a kindling focus for the limbic, hypothalamic, and thalamic
areas, thereby increasing the severity of withdrawal and the potential for
seizures(Keltner,et al., 1998,pg.143).
Enlargement of the cortical sulci, fissures, and ventricles is commonly observed in the cerebral CT scans of alcohol addicted patients. The reduction of the brain
volumes of these patients results from the loss of white matter in the cerebral hemispheres and not from the volume changes in the cortex.
(Keltner, et al, 1998).
The identification of the “reinforcement” area in the brain that is activated by alcohol and drugs has suggested a biochemical explanation to support the substantial genetic evidence that alcoholics are born, not made(Miller,1992). An alteration in any of the genes that are involved in the expression of the molecules in the reward cascade might predispose an individual to alcohol addiction. Evidence for a genetic basis for alcohol addiction has accumulated progressively over the past five decades, beginning in 1972 when scientists at the Washington University School of Medicine in St.Louis found that adopted children whose biological parents were alcoholics were far more likely to have a drinking problem than those born to nonalcoholic parents. They found that the sons born to alcoholic fathers were three times more likely to become alcoholic than the sons of non-alcoholic fathers. Research is ongoing to discover the exact genetic marker for alcoholism, with interesting results emerging in genetic studies of the A1 allele marker. To date, 14 independent laboratories have supported the finding that the A1 allele is a causative factor in severe forms of alcoholism, though perhaps not in milder forms. It was pointed out that these findings do not prove that the A1 allele of the dopamine D2 receptor gene is the only cause of severe alcoholism, but they are a powerful indication that the A1 allele is somehow involved with
alcoholism(Blum, et al., 1996).
Further evidence for the role of biology in alcoholism comes from efforts to discover electrophysiological markers that could indicate a predisposition to alcoholism.
A marker of this type is the latency and the magnitude of the positive 300-millisecond
(P300) EEG wave, which is an indicator of the general electrical activity of the brain that is evoked by a specific stimulus such as an audible tone. Abnormalities in the electrical activity of the brain are evident in the EEGs of young sons of alcoholic fathers. Their P300 waves are markedly reduced in amplitude compared to the P300 waves of sons of nonalcoholic fathers. These results raised the question as to whether this deficit had been transferred from father to son and whether this deficit could predispose the son to substance abuse in the
future(Begleiter, Porjexa, Bihari, and Kissin, 1984).
Several experiments have been carried out since then to answer both questions.
The alcoholic fathers had the same P300 EEG wave deficit found in their sons - and the sons showed increased drug-seeking behaviors (including alcohol and nicotine) compared to sons of nonalcoholic fathers. In addition, the sons of alcoholic fathers had an atypical neurocognitive
profile(Whipple, Parker and Noble1988). Evidence now shows that children with P300 EEG abnormalities are more likely to abuse drugs and tobacco in later
years(Berman, Whipple, Fitch and Noble 1993).
Alcoholism is a behavioral disorder. The most recent definition of alcoholism was produced by a committee of distinguished alcohologists of the American Society of Addiction
Medicine(ASAM) published in the ASAM News in March-April, 1990:
Alcoholism is a primary, chronic disease, characterized by.....impaired control
over drinking, preoccupation with alcohol, use of alcohol despite adverse
consequences, and distortions in thinking, most notably denial (Goodwin 1992,
The specific behavior that characterizes alcoholism is the consumption of significant quantities of alcohol on repeated occasions. The subjective motivating factor underlying this behavior is often obscure. When alcoholics are asked why they drink excessively, they will occasionally attribute their drinking to a particular mood such as depression or anxiety or to situational problems. Many times they simply describe an overpowering “need” to drink, variously described as a craving or compulsion. Just as often, however, the alcoholic is unable to give any plausible explanation for his or her excessive drinking(Goodwin 1993). Drinking relieves guilt and anxiety; however, it then also produces anxiety and depression(Davis 1971). The symptoms associated with depression and anxiety disorders, such as terminal insomnia, low mood, irritability, and anxiety attacks with chest pain, palpitations, and dyspnea often occur. Alcohol seems to relieve these symptoms, resulting in a vicious cycle of drinking followed by depression followed by drinking that ultimately leads to a withdrawal syndrome. Sometimes the patient succeeds in stopping drinking for several days or weeks only to “fall off the wagon” again (Goodwin 1981). Despair and hopelessness are common. By the time the patient contacts the physician, they have often reached rock bottom. Their problems have become so numerous that they feel nothing can be done for them. At this point they may finally be ready to acknowledge their alcoholism but feel powerless to stop drinking(Goodwin 1993).
Alcohol occasionally produces an amnesia which can be particularly distressing to the alcoholic because of the fear that they have harmed someone or acted imprudently while intoxicated (Goodwin 1971). The amnesia is retrograde
(Tamerin,Weiner,Poppen, Steinglass & Mendelson 1971). When an individual has a blackout, they have relatively intact remote and immediate memory but experience a specific short-term memory deficit in which they are unable to recall events that happened 5 or 10 minutes before.
Since other intellectual faculties are well-preserved, they can perform complicated acts and appear normal to the casual observer.
Blackouts probably represent impaired consolidation of new information rather than some form of purely psychological repression motivated by a desire to forget events that happened while drinking (Goodwin 1997). Sometimes a curious thing happens: the alcoholic recalls things that happened during a previous drinking period that, when sober they had forgotten. An example would be that alcoholics often report hiding money or alcohol when drinking, and having their memory return when drinking again (Goodwin 1971).
Benzodiazepines combined with alcohol frequently increase the likelihood of blackouts with smaller amounts of alcohol than are usually required for such disturbances of memory(Morris & Estes 1987).
Identifying a drinking problem in a patient can sometimes be done by a physical exam and laboratory tests, which may reveal the following:
1. Arcus senilis-a ringlike opacity of the cornea-occurs commonly with age
and is considered an innocent condition. The ring forms from fatty material
in the blood. Alcohol increases fat in the blood and more alcoholics have
the ring than do non-alcoholics the same age.
2. A red nose (acne rosacea) suggests that the owner may have a weakness for
3. Red palms(palmar erythema) are suggestive but not diagnostic of
4. Cigarette burns between the index and middle fingers or on the chest
and contusions and bruises suggest periods of alcoholic stupor.
5.Painless enlargement of the liver suggests a larger alcohol intake than
the liver can cope with. Severe, constant upper abdominal pain and
tenderness radiating to the back may indicate pancreatic inflammation,
of which alcohol is a frequent cause.
6. Reduced sensation and weakness in the feet and legs may occur as a result of polyneuropathy secondary to chronic alcoholism.
7. Laboratory tests provide other clues. More than half of active alcoholics
have increased amounts of gamma-glutamyl transpeptidase (GTT)
in their blood, which is unusual in non alcoholics. After
in the following tests are most often associated with heavy drinking:
mean corpuscular volume, uric acid, triglycerides, aspartate amino-
transferase, and urea (Goodwin,1993,pg.146).
The treatment of alcoholism and the management of alcohol withdrawal present separate issues for the treating professional. In the absence of serious medical complications, alcohol withdrawal syndrome is usually transient and self-limited. The patient recovers within several days regardless of the treatment given. Treatment for withdrawal is symptomatic and prophylactic. Relief of agitation and tremulousness can
be achieved with a variety of drugs, including barbituates, paraldehyde, chloral hydrate, the
phenothiazines, and the benzodiazepines. Currently, the benzodiazepines are widely
considered the drugs of choice for withdrawal (Miller 1995). Benzodiazepines have little, if any, synergistic action with alcohol. When compared with barbiturates and paraldehyde, they have relatively little abuse potential. There is some evidence that
mortality is increased when the phenothiazines are used which is reportedly from hypotension or hepatic encephalopathy (Goodwin 1993).
Associated mood disturbances many times are directly related to alcohol and can be resolved within 2 to 3 weeks after the patient is detoxified. Depressive symptoms that persist beyond this period need evaluation for a comorbid psychiatric disturbance that may require specific treatment in its own right, e.g. psychotherapy and/or antidepressants. Drugs such as benzodiazepines and other dependence-producing agents should generally be avoided with these patients. Patients with severe chronic anxiety may be safely treated with
buspirone, an anxiolytic agent not known to be habit forming (Keltner et al. 1998).
Administration of large doses of vitamins--particularly B vitamins--is obligatory, given the role of these vitamins in preventing peripheral neuropathy and the Wernicke-Korsakoff syndrome(Adams 1953). The vitamins are water-soluble and there is no apparent danger to the patient in giving them in high doses(Goodwin 1993).
If patients develop delirium, they should be considered possibly dangerous to
themselves and others, and protective steps should be taken. Ordinarily, tranquilizers will calm the patient sufficiently. Administration of intravenous barbiturates may be necessary for severe agitation. More important, if delirium occurs, the caregiver should explore further to rule out serious medical illness(Goodwin 1988).
The actual treatment of alcoholism itself does not really begin until physical withdrawal symptoms subside. Treatment usually has two goals. The first is sobriety and the second is amelioration of psychiatric conditions that are often associated with alcoholism(Castaneda & Cushman 1989). Most relapses occur within 6 months of discharge from the hospital and tend to become less frequent after that(Glatt 1959).
For many patients, disulfiram (Antabuse) is helpful in maintaining abstinence.
By inhibiting aldehyde dehydrogenase, this drug leads to an accumulation of the intermediary alcoholic metabolic product, acetaldehyde when alcohol is consumed. Acetaldehyde is highly toxic and causes flushing,
dyspnea, palpitations, nausea and hypotension in the alcoholic who drinks while taking
disulfiram. Discontinuation of Antabuse after its administration for several days or weeks still deters drinking for a 3 to 5 day period because the drug requires that long to be excreted (Goodwin 1993).
Serotonin reuptake inhibitors(SSRIs) have been reported to reduce drinking in animals and also in some heavy drinking individuals
(Liskow and Goodwin 1987). Fluoxetine is one SSRI being used(Goodwin 1993). Research has shown that serotonin uptake inhibitors may reduce alcohol intake in certain alcoholics. The mechanism of this effect is not completely understood. It may be mediated by changes in the desire to drink and in the alcohol
effects(Naranjo,Poulos,Bremner, Lanctot 1992).
The drug naltrexone has also recently been used in the pharmacologic treatment of alcoholism. The effectiveness of this drug is in reducing alcohol craving and alcohol intake. In one study naltrexone lowered levels of alcohol craving, decreased the mean number of drinking days by alcoholics, and lowered the relapse rates compared to placebo. The mechanism of these effects is not
clear(Volpicelli, Alterman, Hayashide, OBrian 1992).
Both psychological and somatic approaches have long been and continue to be used to treat alcoholism. There is no convincing evidence that in-depth ‘exploratory' or ‘Freudian' psychotherapy helps most alcoholics. Nor is it believed that major or minor tranquilizers are effective in maintaining abstinence from alcohol(Smith & Frawley 1990). Although it is not known how many alcoholics benefit from participation in Alcoholics Anonymous, most clinicians agree that alcoholics should be encouraged to attend meetings at least on a trial basis(Goodwin 1993). Psychotherapy and counseling adjunctive with other forms of inpatient or outpatient treatment as inpatient or outpatient have yielded very positive results(Miller 1995).
The field of alcoholism and addiction is currently in rapid change both in regard to the basic science and pathophysiology of drug dependence and also to the newest and most effective methods of treatment. New scientific advances can be expected to shed still more light on the complex etiologies of these age-old human maladies, while providing more specific and therapeutically efficacious treatments for individuals suffering from all forms of addiction.
back to top