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Alcohol-Related Psychosis

  • Author: Zhongshu Yang, MD, PhD; Chief Editor: Iqbal Ahmed, MBBS, FRCPsych(UK)  more...
 
Updated: Dec 03, 2015
 

Background

Alcohol-related psychosis is a secondary psychosis that manifests as prominent hallucinations and delusions occurring in a variety of alcohol-related conditions. For patients with alcohol use disorder, previously known as alcohol abuse and alcohol dependence, psychosis can occur during phases of acute intoxication or withdrawal, with or without delirium tremens. In addition, alcohol hallucinosis and alcoholic paranoia are 2 uncommon alcohol-induced psychotic disorders, which are seen only in chronic alcoholics who have years of severe and heavy drinking.[1] Lastly, psychosis can also occur during alcohol intoxication, also known as pathologic intoxication, an uncommon condition the diagnosis of which is considered controversial.[2, 3]

In chronic alcoholic patients, lack of thiamine is a common condition. Thiamine deficiency is known to lead to Wernicke-Korsakoff syndrome, which is characterized by neurological findings on examination and a confusional-apathetic state. Korsakoff psychosis (or Korsakoff amnesic- or amnesic-confabulatory state) refers to a state that memory and learning are affected out of proportion to other cognitive functions in an otherwise alert and responsive patient.[4]

Alcohol is a neurotoxin that damages 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. Distinguishing alcohol-related psychosis from schizophrenia or other primary psychotic disorders 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 spectrum and other psychotic disorders) and severe mood disorder with psychosis may exist, resulting in the psychosis being attributed to the wrong etiology.

Some characteristics that may help differentiate alcohol-induced psychosis from schizophrenia are that alcohol-induced psychosis shows later onset of psychosis, higher levels of depressive and anxiety symptoms, fewer negative and disorganized symptoms, better insight and judgment, and less functional impairment.[5]

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 attempts to provide as much possible information for adequate knowledge of alcohol-related psychosis and the most up-to-date treatment.

Case examples

Case 1: A 37-year-old white male infantryman stationed in Iraq arrived at a field hospital complaining that his superior officer placed poisonous ants in his helmet. His face is covered with excoriations from persistent scratching. On further examination, he is stuporous and has mildly slurred speech, tremor, and mint odor to his breath. Later his troop leader mentioned that his Humvee was littered with empty bottles of mouthwash and that the man has been reprimanded for falling asleep at his post. After a night of rest, he discussed his excessive use of mouthwash in place of alcohol, which is the only available form of alcohol in Iraq.

Case 2: At 5 pm you are asked to consult on a 44-year-old white female who is 2 days postsurgical hysterectomy. She is complaining of rabbits running across the room and demands the nurses stop intruding "every minute of every hour." She is tremulous, disoriented to time and place, and irritable. A review of her laboratory data shows an elevated gamma-glutamyl transferase (GGT) and slightly elevated liver function test values. White blood cell count is normal. Urinalysis is normal and blood alcohol level is 0.01. Her medications, which were held prior to the surgery, included acamprosate 666 mg thrice daily and clonazepam 1 mg 4 times a day. Her sister later informs the nursing staff that this woman is usually on her fourth Manhattan cocktail by this hour of the day.

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Pathophysiology

Ethanol is a small molecule that readily distributes to the brain and reaches peak levels in blood approximately 30 minutes after ingestion of an alcoholic drink. Ethanol affects proteins that are associated with a wide variety of neurotransmitters and pathways. These include the dopamine pathway, serotonin pathway, proteins associated with GABAA receptor, glutamate receptors (ie, N -methyl-D-aspartate [NMDA]/α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid [AMPA]/Kainate), mGlu receptors, nicotinic receptors, cannabinoid CB1 receptors, voltage-gated calcium ion channels, and calcium-activated potassium channels.[6]

Like other psychotic disorders, the exact etiology of alcohol-related psychosis remains unclear, but most likely it is related to dopamine in the limbic and possibly other systems, such as the glutamatergic neurotransmitter system. 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 the release of dopamine from the neuron. Ethanol acutely disrupts glutamatergic neurotransmission by inhibiting the response of the NMDA receptor. Prolonged inhibition of the NMDA receptor by ethanol leads to supersensitivity. During the phase of withdrawal, acute removal of ethanol causes marked augmentation of activity of postsynaptic neurons, such as those in the noradrenergic system, and, in the extreme, glutamate-induced excitotoxicity.[6, 7]

The pathophysiologies of intoxication, withdrawal, and alcohol idiosyncratic intoxication are all are different, and their exact relationships to psychosis are unclear, but one can certainly postulate the underlying mechanisms are complex, considering alcohol’s broad impact on a variety of neurotransmitter pathways. To some degree, they all involve the neurotoxicity of alcohol and its damage at the genetic, biochemical, and cellular levels leading to physiological and neurological pathology.

Depending on the individual and amount consumed, alcohol intoxication can result in disinhibition, sedation, and anesthesia or even coma. 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. The psychosis often is self-limited and recurs with subsequent withdrawals.

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Epidemiology

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 and 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 dizygotictwins.[8]

Those with first-episode psychosis are twice more likely than the general population to present with comorbid substance abuse and are more commonly males than females. The most commonly reported substance is cannabis (51%) followed by alcohol (43%).[9]

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-like 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.[10] Furthermore, there appears to be a close correlation between alcohol psychosis and higher mortality rates compared with alcohol consumption and no psychosis. Studies on alcohol consumption and psychosis are easier to study in Belarus as they are among highest consumers of alcohol in the world, with an annual consumption of 14 liters per capita per year.[11]

Mortality/Morbidity

The appearance of alcohol-related psychosis usually occurs with long-term alcohol use disorder; therefore, it is associated with the same morbidity and mortality of long-term alcoholism. The presence of alcohol-related psychosis is a serious indicator of medical, neurological, and psychosocial complications that can hinder appropriate treatment and lead to negative outcomes. The prognosis for alcohol-related psychosis 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.[12]

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

Alcohol-related psychosis that does not remit with abstinence 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.

Substance abuse is a major contributing factor to the outcome and course of treatment in mentally ill patients with psychosis. The prevalence is up to 87% in those with schizophrenia and 77% in those who are bipolar, with cannabis and alcohol being the most commonly abused.[13]

Some of the medical complications observed with alcohol-related psychosis and chronic alcoholism 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 400 mg/dL in nontolerant individuals can result in lethal respiratory arrest.[14]

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 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.[15]

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 than 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 have an onset in persons aged 35-40 years.

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Contributor Information and Disclosures
Author

Zhongshu Yang, MD, PhD Health Science Assistant Clinical Professor, Department of Psychiatry and Behavioral Sciences, University of California, Davis, School of Medicine; Medical Director, Crestwood Sacramento Psychiatric Health Facility

Zhongshu Yang, MD, PhD is a member of the following medical societies: American Psychiatric Association

Disclosure: Nothing to disclose.

Coauthor(s)

Glen L Xiong, MD Associate Clinical Professor, Department of Psychiatry and Behavioral Sciences, Department of Internal Medicine, University of California, Davis, School of Medicine; Medical Director, Sacramento County Mental Health Treatment Center

Glen L Xiong, MD is a member of the following medical societies: AMDA - The Society for Post-Acute and Long-Term Care Medicine, American College of Physicians, American Psychiatric Association, Central California Psychiatric Society

Disclosure: Received royalty from Lippincott Williams & Wilkins for book editor; Received grant/research funds from National Alliance for Research in Schizophrenia and Depression for independent contractor; Received consulting fee from Blue Cross Blue Shield Association for consulting. for: Received book royalty from American Psychiatric Publishing Inc.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Iqbal Ahmed, MBBS, FRCPsych(UK) Faculty, Department of Psychiatry, Tripler Army Medical Center; Clinical Professor of Psychiatry, Uniformed Services University of the Health Sciences; Clinical Professor of Psychiatry, Clinical Professor of Geriatric Medicine, University of Hawaii, John A Burns School of Medicine

Iqbal Ahmed, MBBS, FRCPsych(UK) is a member of the following medical societies: Academy of Psychosomatic Medicine, American Neuropsychiatric Association, American Society of Clinical Psychopharmacology, Royal College of Psychiatrists, American Association for Geriatric Psychiatry, American Psychiatric Association

Disclosure: Nothing to disclose.

Additional Contributors

Jennifer S Morse, MD Associate Medical Director, Optum Health

Jennifer S Morse, MD is a member of the following medical societies: Academy of Psychosomatic Medicine, Aerospace Medical Association, American Psychiatric Association

Disclosure: Nothing to disclose.

Acknowledgements

Michael F Larson, DO Clinical Instructor, Department of Child and Adolescent Psychiatry, Harvard Medical School; Psychiatrist, Harvard Vanguard Medical Associates and Private Practice

Michael F Larson, DO is a member of the following medical societies: American Academy of Addiction Psychiatry, American Academy of Child and Adolescent Psychiatry, and American Society of Addiction Medicine

Disclosure: Nothing to disclose.

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