eMedicine Specialties > Psychiatry > Addiction

Alcohol-Related Psychosis

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

Updated: Oct 9, 2008

Introduction

Background

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.

Pathophysiology

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.

Frequency

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

International

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

Mortality/Morbidity

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

Race

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.

Sex

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.

Age

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.

Clinical

History

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.

Physical

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.

Causes

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

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