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  • Updated 01.23.2021
  • Released 10.09.1997
  • Expires For CME 01.23.2024

Alcohol abuse and its neurologic complications

Introduction

Overview

The topic of alcohol abuse related to acute and chronic exposure covers a wide spectrum of neurologic syndromes involving the central and peripheral nervous system. Historical perspectives, clinical manifestations, clinical vignettes, etiology, pathogenesis, pathophysiology, epidemiology, prognosis, complications, and management are all discussed in this updated article. In addition, the authors discuss select mechanisms of cellular injury by alcohol.

Key points

• Alcohol intoxication has an acute and chronic symptomatology.

• The lethal dose of alcohol varies widely and depends on many external and internal factors. Tolerance develops with repeated exposures.

• Wernicke-Korsakoff syndrome is particularly found in the alcoholic population.

• Alcohol affects almost all areas of the nervous system.

• Alcohol affects the functioning of many systems in the body (heart, liver, muscle, nerve).

Historical note and terminology

Alcohol has been consumed by humans for thousands of years. Indeed, archaeologists have found evidence of nearly 11,000-year-old beer brewing troughs at a site in Turkey called Göbekli Tepe (51).

The term “alcoholism” was first used by a Swedish physician in 1849 to describe adverse systemic effects of alcohol. Also, early psychiatry texts described a syndrome of alcohol-related deterioration characterized by intellectual and behavioral abnormalities (11).

The Diagnostic and Statistical Manual of Mental Disorders, 4th edition, text revision (DSM-IV-Tr) defined alcoholism as “maladaptive pattern of drinking, leading to clinically significant impairment or distress” (12).

The definition of alcoholism by the National Council on Alcoholism and Drug Dependence and the American Society of Addiction Medicine is “a primary, chronic disease characterized by impaired control over drinking, preoccupation with the drug alcohol, use of alcohol despite adverse consequences, and distortions in thinking” (148).

The role of alcoholism in the development of cognitive and functional decline was known in Ancient Greece (99) and has received serious study in Western medicine for more than 250 years.

In Greek mythology, Silenus was the frequently drunken companion and tutor of the wine god Dionysus. Artistic depictions of the drunken Silenus show him supported by satyrs or carried by a donkey.

Some Renaissance artistic depictions of the drunken Silenus show features of alcoholic cirrhosis, perhaps most fully in the painting Drunken Silenus (1626) by Spanish painter Jusepe de Ribera (1591-1652): evident signs of liver disease in this painting include parotid gland swelling, spider angioma (left parasternal area), gynecomastia, and ascites.

Giambattista Morgagni (1682-1771)
Italian anatomist and pathologist Giambattista Morgagni (1682-1771). Line engraving by G. Simoncelli. (Courtesy of the Wellcome Collection.)

A clinic-pathologic description of hepatic encephalopathy from alcoholic cirrhosis was described by Italian anatomist and pathologist Giovanni Battista Morgagni (1682-1771), Professor of Anatomy at the University of Padua, in his De sedibus et causis morborum per anatomen indagatis (Seats and Causes of Diseases Investigated by Anatomy) (147).

John Coakley Lettsom (1744-1815)
English physician and philanthropist John Coakley Lettsom (1744-1815). Lettsom described alcoholic neuropathy. Portrait attributed to Johann Zoffany (1733-1810), circa 1782.

Alcoholic neuropathy was documented at least as early as 1787 by English physician and philanthropist John Coakley Lettsom (1744-1815) (131), but other neurologic complications of alcoholism were probably not recognized until the end of the 19th century or later.

Alcohol-related deficits in memory and intellectual ability were reported in 1878 by British psychiatrist Robert Lawson (1846-1896) of the Wonford House Lunatic Asylum in Exeter (127; 126).

Subsequently, in a series of 3 articles from 1887 to 1889, Russian neuropsychiatrist Sergei Sergeievich Korsakoff (sometimes spelled Korsakov; 1853/1854-1900) gave a comprehensive description of the persistent amnestic confabulatory state now known as Korsakoff psychosis, occurring in conjunction with peripheral polyneuropathy, a combination he initially labeled either as “psychosis associated with polyneuritis” or “polyneuritic psychosis” (Korsakoff 1887; 114; 113; 112; 244; 239; 240; 238; 119; 122; 123). Korsakoff based his conclusions on at least 46 patients, about two-thirds of whom were alcoholics, whereas the remainder suffered from a diverse group of disorders associated with protracted vomiting.

Carl Wernicke
German neuropsychiatrist Carl Wernicke (1848-1905). Photograph by J.F. Lehmann in Munich. (Courtesy of the U.S. National Library of Medicine, a public domain.)

Korsakoff was apparently unaware of the syndrome incorporating a confusional state, ophthalmoparesis and other oculomotor findings, ataxia, and neuropathic features, which had been described by German neuropsychiatrist Carl Wernicke (1848-1905) in 1881 and labeled as “Die acute, hämorrhagische Poliencephalitis superior” (acute hemorrhagic superior polioencephalitis) and is now generally called Wernicke encephalopathy (248; 109; 110). The clinico-pathologic overlap between Wernicke encephalopathy and Korsakoff psychosis was ultimately recognized in the late 1920s and early 1930s (67; 101; 31), and the 2 terms became linked as Wernicke-Korsakoff syndrome.

The term “alcoholic hallucinosis” (also known as “alcohol hallucinosis” and “alcohol-related psychotic disorder”) refers to a disorder of acute onset, with a predominance of auditory hallucinations (although delusions and hallucinations in other sensory modalities may also be present), no disturbance of consciousness, and a history of heavy alcohol consumption (71).

Paul Eugen Bleuler (1857-1939)
Swiss psychiatrist Paul Eugen Bleuler (1857-1939), circa 1900. (Courtesy of the U.S. National Library of Medicine.)

This syndrome has often been attributed to Swiss psychiatrist Paul Eugen Bleuler (1857-1939), who labeled it alcoholic hallucinosis (Alkoholhalluzinose) and considered it as an alcoholic madness (Alkoholsahnsinn) (23); Bleuler was also responsible for other psychiatric terms, including schizophrenia, schizoid, and autism. However, in his textbook, Bleuler acknowledged the earlier description by Wernicke, who labeled the disorder as “chronic hallucinosis in alcoholism” (chronische Halluzinose beim Alkoholismus) (249). Even earlier, in 1847, the French author Claude-Nicolas- Séraphin Marcel described a similar symptom complex under the label of folie d'ivrogne (ie, drunken madness) (139).

Although alcoholic intoxication was long recognized in art, portrayals of delirium tremens in caricatures (217) and health propaganda posters became particularly prominent in the early 20th century, in the years before and during Prohibition (1920-1933) in the United States.

Marchiafava-Bignami disease is a progressive alcoholism-related neurologic disease characterized by corpus callosum demyelination and necrosis and subsequent atrophy. The disease was first described in 1903 by the Italian pathologists Ettore Marchiafava (1847-1935) and Amico Bignami (1862-1929) in an Italian Chianti drinker (140). In the autopsy of this patient, the middle two-thirds of the corpus callosum were necrotic.

In the last century, through careful observation and description, American neurologist and neuropathologist Raymond Delacy (“Ray”) Adams (1911-2008) made the most prodigious contributions in understanding the neurologic complications of alcohol abuse, in conjunction with various protégés, notably Boston-born neurologist Joseph Michael (“Joe”) Foley (1916-2012) and, subsequently, Canadian-American neurologist Maurice Victor (1920-2001) (01; 02; 03; 04; 64; 05; 241; 240; 242; 236; 243). Foley began to work with Adams on the neurologic manifestations of liver disease in the late 1940s after Foley returned from his military service during World War II (Lanska and Sommer 2011; 120). In a series of reports from 1949 to 1953, Adams and Foley described the clinical (neurologic), electroencephalographic, and neuropathologic features of alcoholic liver disease, including the clinical and electrophysiologic features of asterixis (01; 02; 03; 04; 64).

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