Continually Updated Clinical Reference
  All Sources     eMedicine     Medscape     Drug Reference     MEDLINE
eMedicine - Alcohol-Related Psychosis : Article by

Quick Find
Authors & Editors

Related Articles
Cannabis Compound Abuse

Cocaine-Related Psychiatric Disorders


Delirium Tremens




Wernicke-Korsakoff Syndrome

Patient Education
Mental Health and Behavior Center

Substance Abuse Center

Alcoholism Overview

Alcoholism Causes

Alcoholism Symptoms

Alcoholism Treatment

Alcohol Intoxication Definition and Causes

Substance Abuse Overview

Author: Michael Larson, DO, Clinical Instructor, Department of Child and Adolescent Psychiatry, Harvard University

Michael Larson is a member of the following medical societies: American Academy of Addiction Psychiatry, American Academy of Child and Adolescent Psychiatry, American Medical Association, and Massachusetts Medical Society

Editors: Jennifer S Morse, MD, Assistant Clinical Professor, Department of Psychiatry, University of California at San Diego; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Iqbal Ahmed, MBBS, Professor, Department of Psychiatry, John A Burns School of Medicine, University of Hawaii; Harold H Harsch, MD, Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin; Stephen Soreff, MD, President of Education Initiatives, Nottingham, NH; Faculty, Metropolitan College of Boston University, Boston, MA

Author and Editor Disclosure

Synonyms and related keywords: alcoholic psychosis, alcohol psychosis, alcohol withdrawal, Wernicke-Korsakoff syndrome, Korsakoff psychosis, thiamine deficiency, hallucinations, alcohol idiosyncratic intoxication, Alcoholics Anonymous, AA


Alcohol-related psychosis is a secondary psychosis with predominant hallucinations occurring in many alcohol-related conditions, including acute intoxication, withdrawal, after a major decrease in alcohol consumption, and alcohol idiosyncratic intoxication. Alcohol is a neurotoxin that affects the brain in a complex manner through prolonged exposure and repeated withdrawal, resulting in significant morbidity and mortality. Alcohol-related psychosis is often an indication of chronic alcoholism; thus, it is associated with medical, neurological, and psychosocial complications.

Alcohol-related psychosis spontaneously clears with discontinuation of alcohol use and may resume during repeated alcohol exposure. Although distinguishing alcohol-related psychosis from schizophrenia through clinical presentation often is difficult, it is generally accepted that alcohol-related psychosis remits with abstinence, unlike schizophrenia. If persistent psychosis develops, diagnostic confusion can result. Comorbid psychotic disorders, eg, schizophrenia and bipolar affective disorder, may exist, resulting in the psychosis being attributed to the wrong etiology.

Alcohol idiosyncratic intoxication is an unusual condition that occurs when a small amount of alcohol produces intoxication that results in aggression, impaired consciousness, prolonged sleep, transient hallucinations, illusions, and delusions. These episodes occur rapidly, can last from only a few minutes to hours, and are followed by amnesia. Alcohol idiosyncratic intoxication often occurs in elderly persons and those with impaired impulse control.

Unlike alcoholism, alcohol-related psychosis lacks the in-depth research needed to understand its pathophysiology, demographics, characteristics, and treatment. This article will attempt to provide as much possible information for adequate knowledge of alcohol-related psychosis and the most up-to-date treatment.

For related information, see Medscape's Addiction Resource Center.


Alcohol-related psychosis most likely relates to dopamine in the limbic and possibly other systems. The dopamine hypothesis often is applied to psychosis involving excessive activity of the dopaminergic system. Animal studies have shown dopaminergic activity to increase with increased release of dopamine when alcohol is administered. On the other hand, alcohol withdrawal generates a decrease in the firing of dopaminergic neurons in the ventral tegmental area and a decrease in release of dopamine from the neuron.

The pathophysiological systems of intoxication, withdrawal, and alcohol idiosyncratic intoxication all are different, and their relationships to psychosis are unclear. To some degree, they all involve the neurotoxicity of alcohol with resultant neurological, genetic, biochemical, and physiological pathology.

Alcohol intoxication results in disinhibition, sedation, and anesthesia. Acute depression of the cerebral cortex and reticular activating system results. The pathophysiology of alcoholism involves alterations in short-term membrane regulation and long-term effects on gene expression.

In patients who are dependent on alcohol, alcohol withdrawal results in adrenergic hypersensitivity of the limbic system and brainstem. Thiamine deficiency also is a contributing factor and is known to be associated with more severe episodes of withdrawal psychosis, which may present as a delirious state known as Wernicke-Korsakoff syndrome (WKS). Psychosis is not considered a symptom in uncomplicated alcohol withdrawal in patients who are not dependent on alcohol. The psychosis often is self-limited and recurs with subsequent withdrawals.


United States

Roughly 3% of persons with alcoholism experience psychosis during acute intoxication or withdrawal. Approximately 10% of patients who are dependent on alcohol who are in withdrawal experience severe withdrawal symptomatology, including psychosis. Twins studies have shown concordance rates for alcohol-related psychosis to be 17.3% in monozygotic twins and 4.8% in dizygotic twins.1


In as much as 50% of Japanese, Chinese, and Korean populations, the likelihood of alcohol-related disorders occurring is less because of the absence of aldehyde dehydrogenase. This causes an Antabuse-type reaction involving facial flushing and palpitations.

Studies of the Soviet Slavic republic of Belarus from 1970-2005 suggest a correlation between cultural and social context of alcohol consumption and alcohol-related suicides and alcohol-induced psychosis.2


The appearance of alcohol-related psychosis occurs with long-term alcohol abuse; therefore, it is associated with the same morbidity and mortality of long-term alcoholism. Alcohol-related psychosis is a serious indicator of medical, neurological, and psychosocial complications, which hinder appropriate treatment and outcome. Prognosis with treatment is considered good, with only 10-20% of psychosis cases becoming chronic. Alcohol-related psychosis itself does not have specific morbidity or mortality; instead, it correlates with a cluster of risk factors that indicate higher morbidity and mortality in patients with alcoholism.3

Psychiatric complications of alcohol-related psychosis include higher rates of depression and suicide. The potential for violence also exists.

Alcohol-related psychosis may indicate undiagnosed schizophrenia or other psychotic disorders. The use of alcohol may potentiate or initiate psychosis through kindling, a process where repetitive neurologic insult results in greater expression of the disease.

Some of the medical complications observed with alcohol-related psychosis include liver disease, pulmonary tuberculosis, diabetes mellitus, musculoskeletal injury, hypertension, and cerebrovascular disease.

  • With intoxication, mortality is associated with the alcohol level in the blood. A blood alcohol level (BAL) greater than 0.30 can result in death.4
  • In withdrawal, auditory hallucinations can be indicative of early-stage withdrawal (6-24 h), the stage associated with withdrawal seizures. Symptoms of visual, auditory, and tactile hallucinations are indicative of late-stage withdrawal (36-72 h), the stage associated with delirium tremens (DT) and a mortality rate of 5-15%.
  • Neurologic abnormalities clear in 20% of patients with Wernicke-Korsakoff syndrome who receive treatment with thiamine and who abstain from consuming alcohol.5


Cultural influences on alcohol-related psychosis stem from cultural norms about alcohol. Irish males who traditionally drink to the point of intoxication are at higher risk, while Jewish males who traditionally shun intoxication have lower risks. Considering the relationship of thiamine to Wernicke-Korsakoff syndrome, cultures that have a low intake of thiamine and high rates of alcohol abuse also are at higher risk for the complication of Wernicke-Korsakoff syndrome.


Alcohol abuse and dependency has a male-to-female ratio of 5:1. Females develop alcohol-related disorders later in life because they start heavy use later then males.


Alcohol-related psychosis occurs after extended periods of alcohol abuse that result in an alteration of neuronal membranes, genetic expression, and thiamine deficiency. Early-onset alcoholism results in a greater chance of complications earlier in life and an outcome that is influenced by psychosocial function. Late-onset alcoholism only delays the onset of complications. As a general rule, alcohol-related psychosis occurs more frequently in older populations. Most alcohol-related disorders occur in persons aged 35-40 years.


Alcohol-related psychosis can be confused with other psychiatric disorders resulting from other substance abuse disorders and from other medical, neurologic, and psychological etiologies. The cause of alcohol-related psychosis can be determined by the patient history and family genealogy.

The Diagnostic Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) provides criteria for the diagnosis of substance-induced psychotic disorder and should be helpful in clarifying etiology.6

  • Developmental history
    • Developmental history is useful for gathering information on in-utero exposure to medication, drugs, alcohol, pathogens, and trauma. As children, patients may have shown prodromal symptoms of a psychotic disorder, such as social isolation, deteriorating school performance, mood lability, amotivation, avolition, and anhedonia.
    • Development suggestive of alcohol-related psychosis involves delinquency, truancy, educational failure, early use of drugs and alcohol, and oppositional or conduct disorder.
  • Psychiatric history
    • Determine whether a psychiatric disorder or symptoms ever occurred when patients were not exposed to alcohol.
    • Determine whether patients ever had a psychiatric disorder or similar symptoms related to any other drug or medication.
  • Recent history: The patient's history of alcohol abuse is extremely significant and is determined by the following questions:
    • Is the patient currently intoxicated?
    • Is the patient at risk for withdrawal?
    • Is the patient in withdrawal?
    • Is the patient homeless?
    • Was the patient outside in the cold?
    • Did the patient fall unconscious?
    • Is the psychosis visual, auditory, and/or tactile hallucinations?
    • When was the patient's last drink?
    • How long has the patient been drinking during the most recent episode?
    • When did the patient first start to drink?
    • How often does the patient drink?
    • How much does the patient drink?
    • Has the patient ever gone through withdrawal, and if so, how many episodes?
  • Substance abuse history: Potentially abused substances include over-the-counter (OTC) sympathomimetics, amphetamines, cocaine, steroids, L-dopa, 3,4-methylenedioxymethamphetamine (ie, MDMA, ecstasy, XTC), and lysergic acid diethylamide (LSD).
  • Family history (including substance abuse, alcoholism, and mental illness)
    • Family history of psychotic disorders in the absence of alcohol suggests a primary psychiatric disorder.
    • If no family history of psychiatric disorders is present, a diagnosis of alcohol-related psychosis can be supported.
  • DSM-IV-TR criteria for substance-induced psychotic disorder include the following:
    • Prominent hallucinations or delusions are present. Hallucinations are false sensations. In this case, they are often visual. Delusions are false ideas. Paranoia and occasionally grandiosity may be the delusions engaged here.
    • Evidence from the history, physical examination, or laboratory findings indicates either (1) the hallucinations or delusions developed during or within a month of substance intoxication or withdrawal or (2) medication use is etiologically related to the disturbance.
    • The disturbance is not better accounted for by a psychotic disorder that is not substance-induced. Evidence that the symptoms are better accounted for by a psychotic disorder that is not substance-induced might include the following:
      • The symptoms precede the onset of the substance or medication use.
      • The symptoms persist for a substantial period of time (eg, a month) after cessation of acute withdrawal or severe intoxication, or the symptoms are substantially in excess of what would be expected given the type or amount of the substance use or the duration of use.
      • Other evidence suggests the existence of an independent non–substance-induced psychotic disorder (eg, a history of recurrent non–substance-related episodes).
    • The disturbance does not occur exclusively during the course of a delirium.


During the initial examination of every psychiatric patient, a full physical and neurological examination is required. When a patient presents as psychotic or intoxicated, also assess the risk of dangerous behavior.

  • Physical
    • The first step in evaluating an intoxicated patient is the initial assessment for medical stability (eg, alertness, breathing, circulation).
    • The second most important step is evaluation of the blood pressure, pulse, and temperature in the event of delirium tremens.
    • This is followed by an assessment for medical complications of alcoholism, eg, blood dyscrasias, liver failure, cardiomyopathy, gastric tumors, and injuries from falls. A comprehensive laboratory evaluation can assist in diagnosing medical complications.
  • Neurologic
    • Head injury may have occurred from a fall, altering the neurological status of the individual.
    • Other complications, such as peripheral neuropathy, amnesia, ataxia, and ophthalmoplegia, also can be evaluated.
  • Mental status: Evaluation of the mental status should focus on orientation, memory, signs of delirium, hallucinations, and delusions. Checking the mental statuses frequently is important, as the affect and level of consciousness may fluctuate dramatically. A Mental Status Examination may appear as follows:
    • General appearance and behavior: Disheveled, withdrawn, malodorous, difficult to engage
    • Poor eye contact
    • Psychomotor agitation
    • Speech: Low volume
    • Thought processes: Thought blocking
    • Disorganized
    • Thought content: Auditory hallucinations
    • Mood: Irritable
    • Affect: Irritable to flat
    • Insight: Poor
    • Judgment: Poor
    • No suicidal or homicidal ideations
  • Dangerous behavior: Assess patients for the potential for assault or self-harm.



Possible causes or contributors to alcohol-related psychosis include the following:

  • Chronic alcoholism
  • Thiamine deficiency (eg, diet, starvation, emesis, gastric tumor)
  • Alcohol-dependent withdrawal early-stage (8-24 h) or late-stage (36-72 h) (Monitor temperature at least every 4 h.)
  • Comorbid substance abuse (Therefore, do an extensive toxicology screen.)
  • Lack of psychosocial supports
  • Comorbid psychotic and mood disorders
  • Alcoholic idiosyncratic intoxication (pathological intoxication)
    • Impulse control disorder
    • Advanced age
    • Early onset of alcohol use

Cannabis Compound Abuse
Cocaine-Related Psychiatric Disorders
Delirium Tremens
Wernicke-Korsakoff Syndrome

Lab Studies

  • The purpose of the workup is to eliminate other possible causes of psychosis, altered mental status, and medical complications. Laboratory evaluation should include the following:
    • Finger-stick blood glucose test for rapid determination of hypoglycemia or hyperglycemia in a patient with diabetes
    • Complete blood cell count to rule out blood dyscrasias, infection, and anemia
    • Electrolytes with magnesium, amylase, albumin, total protein, uric acid, BUN, alkaline phosphatase, and bilirubin
    • Urinalysis to determine the presence of a urinary tract infection and determine renal function
    • Stat urine or serum drug screen to determine if illicit drugs are contributing to psychosis and change in mental status
    • Stat urine or serum toxicology screen for levels of acetaminophen, tricyclic antidepressants, aspirin, and other potential toxins from either an accidental or deliberate overdose
    • Prothrombin time
    • Stool for occult blood
    • BAL measurement (although a patient may appear intoxicated, clinical intoxication can be determined only by BAL)

Imaging Studies

  • If a head injury is suspected, a CT scan is recommended to rule out a subdural hematoma.
  • In those with comorbid schizophrenia and alcoholism, MRIs have shown that the gray matter volume deficits in the prefrontal and anterior superior temporal regions is greater than in those with schizophrenia and alcoholism alone.

Other Tests

  • Some other tests that might be administered include a Brief Psychotic Rating Scale (BPRS), Beck Depression Scale, Violence and Suicide Assessment (VASA), and Mini-Mental State Examination. Other measures also might be useful.
  • If persistent psychosis is noted, neuropsychological testing to assess the level of psychosocial and neurological function can be beneficial for treatment and placement.
  • Projective testing, such as the Rorschach and the Thematic Apperception Test, can clarify a thought disorder.

Medical Care

Because most cases of alcoholic psychosis are self-limiting, removal of alcohol should suffice. Initial treatment should include medically stabilizing the patient by assessing respiratory, circulatory, and neurological systems. A patient intoxicated to the point of psychosis is considered a medical emergency because of the risk of unconsciousness, seizures, and delirium tremens. Medical treatment should focus on the effect of alcohol on the body as a whole. A patient with head trauma may be misdiagnosed with Wernicke-Korsakoff syndrome, and a neurologic examination should always be considered. Alcohol withdrawal requires inpatient hospitalization for more than 72 hours after the risk of delirium tremens has subsided. Remember, although self-limited, it carries with it significant morbidity and mortality.

  • Alcohol-related psychosis is a symptom of alcohol withdrawal and should be treated in the context of alcohol withdrawal. Treatment is initiated with cautious use of PO or IM benzodiazepines. Lorazepam (Ativan) at 1-2 mg or chlordiazepoxide (Librium) at 25-50 mg PO or IM is used commonly.
  • In the event patients are in danger of harming themselves or others, rapid neuroleptization should be initiated with a high-potency antipsychotic drug such as haloperidol (Haldol) at 5-10 mg PO or IM.
  • Antipsychotics may lower the seizure threshold and should not be used to treat withdrawal symptoms unless absolutely necessary and used in combination with a benzodiazepine or antiseizure medications, eg, valproic acid (Depakote) or carbamazepine (Tegretol).
  • Nonmedical treatment includes the use of mechanical wrist and leg restraints if acute danger of assault or self-harm is present.
  • Treatment may include thiamine at 100 mg parentally followed by supplemental thiamine at 100 mg 3 times a day, folic acid at 1 mg, and a daily multivitamin.
  • In case of a suspected opiate overdose, administer naloxone (Narcan) at 0.4-2 mg IV, IM, SC), or endotracheally.
  • In case of diabetic ketoacidosis, administer 50 mL IV dextrose 50% solution.


  • Neurologist: Evaluation of the patient's neurological status should be helpful to rule out neurological consequences of alcohol (ie, peripheral neuropathy, Wernicke-Korsakoff syndrome, seizures, postictal states, encephalitis, subdural hematoma).
  • Internal medicine specialist: An internal medicine specialist can provide extended care to patients with a blood dyscrasia, electrolyte abnormality, thiamine deficiency, gastric tumors, or diabetes.
  • Psychiatrist and social services counselor: Inpatient treatment for substance abuse or further psychiatric stabilization has been the responsibility of psychiatrists and social services counselors.
  • The patient and family need education about alcohol and referral to Alcoholics Anonymous (AA) and family supports.
    • Social services personnel can be used to help with outpatient services (eg, AA, sober houses, provider appointments).
    • Family issues may be involved, and social services counselors can be helpful in providing supportive and directive care.


No specific dietary restrictions are necessary, only the recommendation for a regular diet. However, if a patient has a thiamine-poor diet, further dietary intake should be normalized.


A patient intoxicated with alcohol is dangerous. Limit the activity of such patients until symptoms have been resolved.

Benzodiazepines protect patients from the effects of alcohol withdrawal, and they control psychotic symptoms. Flexibility of administration (eg, PO/IV/IM), rapid onset of action, and efficacy in sedating aggressive patients effectively provide treatment in emergencies. Risk of behavioral disinhibition and liver failure require caution.

Antipsychotics that lower seizure threshold increase risk of seizures associated with alcohol withdrawal. Typical antipsychotics (eg, haloperidol) effectively treat acute psychosis because they have been found to be helpful for rapid tranquilization. Evidence indicating that atypical antipsychotics would have similar rapid effects is insufficient. High-potency antipsychotics are recommended for rapid tranquilization; lower-potency antipsychotics might require higher doses. The medication also should be available in IM form; this eliminates all atypical antipsychotics and some typical antipsychotics (eg, molindone, thioridazine, pimozide). If long-term psychosis develops, the atypical antipsychotics (eg, risperidone, olanzapine, quetiapine) that are more tolerable can be used.

Other medications used in the treatment of alcohol-related psychosis are disulfiram for enforced abstinence, naltrexone or topiramate to dampen cravings, and naloxone if opiate overdose is suspected.

Topiramate doses of up to 300 mg have been studied for treating alcohol dependence. No literature is available to support its use.

Drug Category: Benzodiazepines

By binding to specific receptor sites, these agents appear to potentiate the effects of GABA and facilitate inhibitory GABA neurotransmissions and other inhibitory transmitters.

Drug NameLorazepam (Ativan)
DescriptionPreferred over chlordiazepoxide because half-life in liver disease is more predictable. Does not undergo oxidative metabolism by the liver. Accumulation of drug or its active metabolites does not occur. Available in PO, IV, and IM forms.
Adult Dose5-10 mg/d PO/IV/IM in single or divided doses
Elderly/debilitated: Initial dose of 1-2 mg PO/IV/IM
Detoxification protocol: 1-2 mg PO/IV/IM q6h for 1 d, 1-2 mg PO/IV/IM q8h for 1 d, 1 mg PO/IV/IM bid for 1 d; 1 mg PO/IV/IM qhs on a tapering schedule may be used
Symptom-triggered dosing using structured assessment scales, such as the Clinical Institute Withdrawal Assessment-Alcohol (CIWA-A) withdrawal symptoms, can be well controlled and the total dose of the drug can be reduced
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; acute angle-closure glaucoma
InteractionsToxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, narcotic analgesics, scopolamine, barbiturates, and MAOIs
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsCaution in renal or liver failure, myasthenia gravis, organic brain syndrome, or Parkinson disease; paradoxical excitement resulting in rage behavior; depressed patients with suicidal tendencies

Drug NameChlordiazepoxide (Librium)
DescriptionProvides rapid onset and efficacy in sedating aggressive patients. Longer half-life, providing a steady withdrawal. Available in PO, IV, and IM forms.
Adult Dose50-100 mg/d PO/IV/IM in a single or divided dose
Elderly/debilitated: Initial dose of 10 mg PO/IV/IM
Detoxification protocol: 25 mg PO/IV/IM q6h for 1 d, 25 mg PO/IV/IM q8h for 1 d, 25 mg PO/IV/IM q12h for 1 d, 25 mg PO/IV/IM qhs for 1 d
During taper: If BP is greater than or equal to 140/90 and pulse is greater than or equal to 100, use 25 mg PO/IV/IM prn
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity
InteractionsCoadministration with alcohol, phenothiazines, barbiturates, and MAOIs increases CNS toxicity; cisapride can significantly increase levels
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsCaution in liver failure; paradoxical excitement resulting in rage behavior; depressed patients at risk for suicide; respiratory arrest can occur if doses exceed those needed to control withdrawal; caution in patients receiving other CNS depressants or diagnosed with low albumin levels

Drug Category: Antipsychotics

High-potency agents (eg, haloperidol, droperidol) provide rapid, predictable, and effective sedation in the management of acutely psychotic patients. They are less sedating and are more easily titrated but are more likely to cause EPS than the lower-potency agents. They often are combined in the same syringe with a benzodiazepine (eg, lorazepam, diazepam) for better sedation and anxiolysis and less dystonia or akathisia. They are given IM or IV, or, in a less acute setting, they are given PO (haloperidol only). Haloperidol also has a monthly depot form (Haldol Decanoate). Depot antipsychotics are not intended for use in the acute setting.

Drug NameHaloperidol (Haldol)
DescriptionControls psychosis and provides rapid tranquilization. Administer with a benzodiazepine to protect against lowered seizure threshold.
In emergencies, select high-potency antipsychotic available in tab, liquid, or IM form.
Adult Dose2-5 mg PO/IM
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; extrapyramidal symptoms; Parkinson disease
InteractionsSerum plasma levels decreased by rifampin; potentiates effects of CNS depressants (eg, alcohol, opiates, anesthetics); lithium has induced an encephalopathic syndrome
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsSevere neurotoxicity manifesting as rigidity or inability to walk or talk may occur in patients with thyrotoxicosis also receiving antipsychotics; if administered IV/IM, watch for hypotension; caution in diagnosed CNS depression or cardiac disease; if history of seizures, benefits must outweigh risks; significant increase in body temperature may indicate intolerance to antipsychotics (discontinue if occurs)
Ventricular arrhythmias such as torsade de pointes have been reported in patients, especially those with cardiac disease and in those given high doses of IV haloperidol

Drug NameThiothixene (Navane)
DescriptionBlocks postsynaptic blockade of CNS dopamine receptors, inhibiting dopamine-mediated effects. Provides rapid tranquilization in PO and IM forms.
Adult Dose5-20 mg/d PO/IM in a single or divided dose
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; breastfeeding; CNS depression; blood dyscrasias
InteractionsDecreases effects of guanethidine; increases toxicity of CNS depressants, anticholinergics, and alcohol
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsCaution in narrow-angle glaucoma, severe liver disease, seizures, bone marrow suppression, cardiac disease; extrapyramidal symptoms (eg, muscle rigidity, inability to walk or talk, akathisia, dystonia); opisthotonos and oculogyric crisis; circulatory collapse; coma

Drug Category: Antialcoholic agents

A patient who is highly motivated to participate in an abstinence program may benefit from the use of disulfiram. Disulfiram inhibits the metabolism of alcohol, causing increased levels of acetaldehyde, resulting in flushing, nausea, and multiple other noxious symptoms. Compliance can be determined through detecting diethylamine (disulfiram metabolite) in the urine. Naltrexone is an agent helpful in decreasing the craving for alcohol. It has been shown to be superior to placebo when used in combination with supportive psychotherapy. Naltrexone's mechanism of action is thought to be through blocking the opioid system, which is thought to be involved in alcohol craving. Acamprosate is the newest approved drug. Its mechanism of action is not fully understood, but it is hypothesized to restore neuronal excitation and inhibition balance. In 3 placebo-controlled trials, acamprosate was superior to placebo in maintaining alcohol abstinence as part of a comprehensive management program.

Drug NameDisulfiram (Antabuse)
DescriptionUsed to enforce abstinence but does not cure alcoholism. Often used in conjunction with psychotherapy and AA meetings.
Adult Dose500 mg PO qd for up to 2 wk; 250 mg PO qd; not to exceed 500 mg PO qd
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; ethanol intoxication; psychosis; cardiac disease, coronary occlusion
InteractionsIncreases effects of diazepam and chlordiazepoxide; metronidazole, isoniazid, and phenytoin may increase toxicity; coadministration with warfarin may increase prothrombin time
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsRequires >12 h abstinence before administration; caution in hypothyroidism, diabetes, hepatic cirrhosis or insufficiency, and seizure disorders
Because disulfiram also inhibits dopamine-beta-hydroxylase activity, caution should be used in those with comorbid schizophrenia.

Drug NameNaltrexone (ReVia)
DescriptionUsed primarily to block the opioid receptors and prevent euphoria (thus decreasing craving) in those who abuse opiates. Theoretically, when a person with alcoholism craves alcohol, the opioid system is stimulated and the opioid receptors are antagonized, thus, the craving is dampened.
Adult Dose25-50 mg PO qd
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; patients who have had opiates within past 7-10 d
InteractionsInhibits effects of opiates
PregnancyB - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
PrecautionsLiver function should be established prior to use; higher than approved doses have led to hepatotoxicity; caution in those at risk for suicide (overdose can lead to liver failure)

Drug NameAcamprosate (Campral)
DescriptionSynthetic compound with a chemical structure similar to that of the endogenous amino acid homotaurine (structural analogue of gamma-aminobutyric acid [GABA]). The mechanism of action to maintain alcohol abstinence is not completely understood. Hypothesized to interact with glutamate and GABA neurotransmitters centrally to restore neuronal excitation and inhibition balance. Not associated with tolerance or dependence development. Use does not eliminate or diminish alcohol withdrawal symptoms. Indicated to maintain alcohol abstinence as part of a comprehensive management program that includes psychosocial support. Available as a 333-mg tab.
Adult Dose666 mg PO tid; initiate as soon as possible after alcohol withdrawal when abstinence has been achieved; if <60 kg, may need to decrease dose by 333-666 mg/d
CrCl 30-50 mL/min: 333 mg PO tid
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; severe renal impairment (ie, CrCl <30 mL/min)
InteractionsCoadministration with naltrexone increases acamprosate Cmax and AUC, but no dosage adjustments are necessary
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsCommon adverse effects include headache, diarrhea, flatulence, and nausea; depression and anxiety incidence slightly higher than that of placebo in 1 study

Drug Category: Atypical antipsychotics

These agents provide a number of major improvements over the traditional agents, including the following: fewer adverse anticholinergic effects, less dystonia and parkinsonism, very low risk of tardive dyskinesia, and potential reversal of many negative symptoms (eg, affective blunting, alogia, withdrawal, avolition). These agents affect dopamine receptors but also affect serotonin receptors involved with frontal lobe functions.

Drug NameAripiprazole (Abilify)
DescriptionImproves positive and negative schizophrenic symptoms. The mechanism of action is unknown but is hypothesized to work differently than other antipsychotics. Aripiprazole is thought to be a partial dopamine (D2) and serotonin (5HT1A) agonist, and antagonize serotonin (5HT2A). Additionally, no QTc interval prolongation was noted in clinical trials. Available as tab, orally disintegrating tab, or oral solution.
Adult Dose10-15 mg PO qd; if needed, may increase dose gradually q2wk, not to exceed 30 mg/d
Alternatively, 9.75 mg IM initially (dose range 5.25-15 mg); may give second dose after minimum of 2 h; not to exceed total cumulative dose of 30 mg/d; replace injection with oral dose (10-30 mg/d) as soon as possible
Pediatric Dose<13 years: Not established
>13 years: 2 mg PO qd initially; after 48 h, may titrate upward to 5 mg/d and then after another 48 h to 10 mg/d; subsequent dose increases should be in 5 mg/d increments; not to exceed 30 mg/d
ContraindicationsDocumented hypersensitivity
InteractionsCYP450 3A4 and 2D6 isoenzyme substrate, thus, inhibitors (ie, ketoconazole, quinidine, fluoxetine, paroxetine) or inducers (ie, carbamazepine) may increase or decrease serum levels respectively; decrease dose by one-half when coadministered with strong CYP450 3A4 inhibitors (eg, ketoconazole, clarithromycin) or 2D6 inhibitors (eg, quinidine, fluoxetine, paroxetine); dose should be doubled when coadministered with strong CYP3A4 inducers (eg, carbamazepine, rifampin)
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsCommon adverse effects include headache, anxiety, somnolence, or insomnia; rare reports of tardive dyskinesia and neuroleptic malignant syndrome; may cause orthostatic hypotension, seizure, dysphagia, or suicidal ideation; hyperglycemia may occur and in some cases be extreme, resulting in ketoacidosis, hyperosmolar coma, or death

Drug NameOlanzapine (Zyprexa)
DescriptionMay inhibit serotonin, muscarinic, and dopamine effects. Efficacy similar to risperidone, fewer dose-dependent adverse effects but more concern about weight gain.
Adult Dose5-20 mg/d PO in divided doses
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity
InteractionsFluvoxamine may increase effects; antihypertensives may increase risk of hypotension and orthostatic hypotension; levodopa, pergolide, bromocriptine, charcoal, carbamazepine, omeprazole, rifampin, and cigarette smoking may decrease effects
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsCaution in narrow-angle glaucoma, cardiovascular disease, cerebrovascular disease, prostatic hypertrophy, seizure disorders, hypovolemia, and dehydration

Drug NameQuetiapine (Seroquel)
DescriptionMay act by antagonizing dopamine and serotonin effects. Efficacy similar to risperidone and olanzapine. Fewer dose-dependent adverse effects and less concern of weight gain.
Adult Dose25 mg PO bid; titrate to 150-750 mg/d PO; not to exceed 800 mg/d
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity
InteractionsMay antagonize levodopa and dopamine agonists; phenytoin, thioridazine, and other liver enzyme inducers may reduce levels
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsMay induce orthostatic hypotension associated with dizziness, tachycardia, and syncope; neuroleptic malignant syndrome has been associated with this treatment; cataracts may develop (perform eye examination every 6 mo)

Drug NameRisperidone (Risperdal)
DescriptionUnlike haloperidol, has serotonergic blocking effects that alleviate negative symptoms of psychosis (eg, anhedonia, avolition, amotivational, flat effect). Well tolerated with fewer adverse extrapyramidal effects than with typical antipsychotics. Doses > 6 mg/d increase risk of extrapyramidal effects. No atypical antipsychotic agent is preferred in treating alcohol-related psychosis.
Adult Dose2-14 mg/d PO in divided doses
Pediatric DoseChildren: Not established
Adolescents: Administer as in adults
ContraindicationsDocumented hypersensitivity
InteractionsCoadministration with carbamazepine may decrease effects; may inhibit effects of levodopa; clozapine may increase levels
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsMay cause extrapyramidal reactions, hypotension, tachycardia, and arrhythmias

Drug Category: Narcotic antagonists

Naloxone acts similar to naltrexone as an opiate receptor antagonist but has significant differences, restricting it to emergency situations of opiate overdose. Also should be considered in patients with alcoholism who have altered mental status due to overdose of opiates. Naloxone is poorly absorbed PO and should be administered IM or IV.

Drug NameNaloxone (Narcan)
DescriptionUsed in emergencies in which narcotic overdose results in respiratory depression. Available in IV, IM, and SC forms.
Adult Dose0.4-2 mg IV; if no improvement, repeat q2-3min; not to exceed 10 mg; if no response observed after 10 mg, question the diagnosis; if IV unavailable, use IM or SC route
Pediatric Dose<20 kg or < 5 years: 0.1 mg/kg IV; if no improvement, repeat q2-3min
>20 kg or > 5 years: 2 mg IV; if no improvement, repeat q2-3min
If IV unavailable, use IM or SC route
ContraindicationsDocumented hypersensitivity
InteractionsDecreases effects of narcotic analgesics
PregnancyB - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
PrecautionsCaution in cardiovascular disease; may precipitate withdrawal symptoms in patients addicted to opiates

Further Inpatient Care

Admit for observation if further withdrawal, cognitive impairment, psychosis, and medical complications occur.

Further Outpatient Care

  • A day treatment program or partial hospitalization can be used for those who do not require a highly structured inpatient environment. Daily individual, group, and weekly family therapy provide intensive treatment that is similar to inpatient settings. Programs specifically designed for substance abuse also provide daily substance abuse meetings and education. Medication evaluations and monitoring assure stabilization in the least restrictive environment.
  • Institute a psychiatric follow-up visit within 2 weeks of the initial evaluation to assure compliance.
  • Consider a follow-up examination with a neurologist or internal medicine specialist, depending on the complications of alcohol abuse.
  • Carefully monitor patients for recurring psychosis, depression, and relapse of alcohol use.

In/Out Patient Meds

  • If the psychosis has resolved and the patient is medically stable, no further medication is needed.
  • If psychosis persists beyond elimination of the offending substance, an atypical antipsychotic drug (eg, risperidone, olanzapine, quetiapine) may be considered. No single atypical antipsychotic drug has been proven most beneficial for treatment of persistent alcohol-related psychosis.
  • Once thiamine levels have been restored, daily multivitamins are recommended to maintain appropriate levels of essential vitamins that often are depleted in patients with alcoholism.
  • Disulfiram (Antabuse) is an agent indicated to facilitate abstinence from alcohol. This can be started 12 hours after a patient consumes alcohol (125-500 mg/d).
  • Continue thiamine (100 mg PO tid).


  • If psychosis persists past initial treatment, the patient may be suffering from an undiagnosed psychotic disorder, such as schizophrenia or bipolar affective disorder. Inpatient psychiatric hospitalization may be required for diagnosis and psychopharmacological treatment.
  • If a risk of delirium tremens or suicide is present, transferring the patient to a psychiatric inpatient unit might be required.
  • A day treatment program or partial hospitalization can be used for those who do not require a highly structured inpatient environment. Daily individual, group, and weekly family therapy is provided. Programs specifically designed for substance abuse also provide daily substance abuse meetings and education. Medication evaluations and monitoring assure stabilization in the least restrictive environment.


  • Prevention is a result of abstinence and is the primary treatment of choice. Some patients may achieve success by attending 90 AA meetings in 90 days.
  • A sponsor (a recovering alcoholic committed to sobriety) helps provide a support network for attending meetings and seeking community resources.


  • Theoretically, alcohol may potentiate or initiate a psychotic disorder, such as schizophrenia, through kindling, a process where repetitive neurological insult results in greater expression of disease.
  • In some instances, psychosis may persist and may be considered by DSM-IV-TR criteria as a substance-induced psychotic disorder.
  • Other complications may include the following:
    • Increased risk of suicide
    • Increased risk of depression
    • Increased psychosocial impairment


  • Alcohol-related psychosis is indicative of severe alcohol abuse and suggests a poor prognosis. The prognosis is similar to that of severe alcoholism.
  • Of all psychosis cases, 10-20% tend to become permanent.
  • Symptoms of any accompanying Korsakoff syndrome (amnestic disorder) are highly resistant to treatment because of the irreversible neurological damage.

Patient Education

Medical/Legal Pitfalls

  • Failure to recognize and treat associated conditions, delirium tremens, Wernicke-Korsakoff syndrome, subdural hematoma, and medical complications
  • Failure to evaluate for ingestion of potentially dangerous illicit drugs or medications
  • Failure to evaluate patient's potential for suicide and homicide
  • Discharging an intoxicated patient
  • Allowing an intoxicated patient to drive

  1. Reed T, Page WF, Viken RJ, Christian JC. Genetic predisposition to organ-specific endpoints of alcoholism. Alcohol Clin Exp Res. Dec 1996;20(9):1528-33. [Medline].
  2. Razvodovsky YE. Suicide and alcohol psychoses in Belarus 1970-2005. Crisis. 2007;28(2):61-6. [Medline].
  3. Soyka M. [Alcohol-induced hallucinosis. Clinical aspects, pathophysiology and therapy]. Nervenarzt. Nov 1996;67(11):891-5. [Medline].
  4. Kaplan HI, Sadock BJ, eds. Pocket Handbook of Emergency Psychiatric Medicine. Baltimore, Md: Lippincott Williams & Wilkins; 1993:93-4.
  5. Preuss UW, Soyka M. [Wernicke-Korsakow syndrome: clinical aspects, pathophysiology and therapeutic approaches]. Fortschr Neurol Psychiatr. Sep 1997;65(9):413-20. [Medline].
  6. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Text Revision. Washington, DC: American Psychiatric Association; 2000.
  7. Fogel B, Schiffer R, Rao S. Neuropsychiatry. Baltimore, Md: Lippincott Williams & Wilkins; 1996:309-310, 336, 378, 685-7, 704.
  8. Galanter M, Kleber HD, eds. The American Psychiatric Press Textbook of Substance Abuse Treatment. 2nd ed. Washington, DC: American Psychiatric Press; 1999:7-8,155, 283-5.
  9. Guze BH, Ferng H, Szuba MP, Richeimer SH. The Psychiatric Drug Handbook. 2nd ed. St. Louis, Mo: Mosby-Year Book; 1995:14-15, 178-9, 222 -5.
  10. Johnson BA, Rosenthal N, Capece JA, Wiegand F, Mao L, Beyers K, et al. Topiramate for treating alcohol dependence: a randomized controlled trial. JAMA. Oct 10 2007;298(14):1641-51. [Medline].
  11. Kaplan HI, Sadock BJ, eds. Comprehensive Textbook of Psychiatry. 6th ed. Baltimore, Md: Lippincott Williams & Wilkins; 1995:784-5, 792-5, 1046, 1053.
  12. Krausz M, Mass R, Haasen C, Gross J. Psychopathology in patients with schizophrenia and substance abuse: a comparative clinical study. Psychopathology. 1996;29(2):95-103. [Medline].
  13. Mayo-Smith MF. Pharmacological management of alcohol withdrawal. A meta-analysis and evidence-based practice guideline. American Society of Addiction Medicine Working Group on Pharmacological Management of Alcohol Withdrawal. JAMA. Jul 9 1997;278(2):144-51. [Medline].

Alcohol-Related Psychosis excerpt

Article Last Updated: Oct 9, 2008