Alcoholic dementia

Alcohol-related dementias refer to all dementia syndromes attributable to alcoholism. Their incidence is difficult to determine (due to unreported consumption, unclear criteria for alcoholism, socially stigmatized diagnosis, and coexistence with other causes of dementia), but they are considered common and may account for up to 20% of all dementias, according to some authors.

Pathophysiology

Between 50% and 70% of long-term alcoholics exhibit cognitive impairments ("mild cognitive impairment"). Progression to full-blown dementia is not uncommon in cases of significant alcohol consumption over more than 5 years.

Their etiology is considered multifactorial: direct alcohol toxicity, nutritional deficiencies, coexistence with vascular or degenerative dementia, repeated trauma, metabolic disorders related to cirrhosis, and other conditions secondary to alcoholism, episodes of Wernicke-Korsakoff, Marchiafava-Bignami, pellagra, etc.

Clinical Presentation

The clinical presentation is variable due to the frequent overlap of different pathological mechanisms, but the classic picture is as follows:

• Onset usually after the age of 50 following massive and regular alcohol consumption (Men: > 35 units/week, Women: > 28 units/week) over more than 5 years
• Insidious progression, with potential worsening in episodes
• Predominance of psycho-behavioral disturbances that may mimic psychiatric pathology or a frontal syndrome:
  • Episodes of aggression and impulsivity
  • Delusional episodes, often with a paranoid theme
  • Ego hypertrophy, anosognosia
  • Excessive familiarity, emotional blunting and lability, lack of motivation, perseveration, reduced verbal fluency, bradypsychia, executive deficits (attention, conceptualization, abstraction, judgment, flexibility, planning), and visuospatial impairments
• Memory disturbances: working memory, long-term memory, etc., variable over time and improved with cues
• Relative preservation of overall functioning (IQ) and verbal abilities

• To establish a diagnosis of probable alcohol-related dementia, a reassessment after a minimum of 60 days of abstinence is required, demonstrating stabilization of symptoms.

The presence of language disorders or focal deficits argues against the diagnosis.

Additional Examinations

Brain MRI may show diffuse cortico-subcortical atrophy (potential frontal predominance) with ventriculomegaly (non-specific), cerebellar atrophy, and sequelae of metabolic encephalopathies, Wernicke-Korsakoff syndrome (++ atrophy of the mammillary bodies), or Marchiafava-Bignami syndrome. After a few months of abstinence, partial regression of the atrophy may sometimes be observed.

Therapeutic Management - Treatment

Alcohol withdrawal, abstinence, re-nutrition, and vitamin supplementation (B vitamins and folates) → stabilization, and often improvement of symptoms (over years and usually incomplete).

Author

Dr Shanan Khairi, MD

Bibliography

Bradley WG et al., Neurology in clinical practice, 5th ed., Butterworth-Heinemann, e-dition, 2007

EMC, Traité de neurologie, 2022

Osborn AG, Diagnostic imaging: brain, Amirsys, USA, 2d ed., 2009