Alcohol Dementia

This diagnosis has always been difficult to distinguish from Korsakoff syndrome and Victor, Adams and Collins thought it part of  the Wernicke-Korsakoff Syndrome. However in the 1980s it was established that alcohol itself is neurotoxic and can cause a partially reversible dementia through the work of Harper and of Lishman. In most cases therefore two causes of brain damage are at work i.e. alcohol and thiamine deficiency. Alcohol can be a risk factor for late life dementia such as Alzheimer’s disease. (Lancet Public Health, February, 2018)

Dementia – “loss”

    • AGNOSIA –   cannot recognise familiar things
    • APHASIA –   circumlocutions, cliches, circumstantiality
    • APRAXIA –   senses intact, understand what asked, physically able to do it BUT STILL CAN’T DO IT
    • LOSS OF EXECUTIVE FUNCTIONING – Poor planning and poor organising of simple actions into more complicated sequences of action (like dressing), and very poor adaptability.  OK in familiar place but cannot cope with change in circumstance or surroundings.  DEPENDENT ON THE FAMILIAR

Tests for mental status

There are several ways to assess dementia that can be used in this context

  • MMSE. (Mini Mental State Examination)
  • MoCA(Montreal Cognitive Assessment)
  • ACE-III (Addenbrookes Cognitive Evaluation –Version 3-Has attention , memory, language , fluency and visuospatial sub components and generates a total score out of 100)

You can also assess changes in brain structure using Magnetic resonance imaging (MRI). This is safe and requires no injections. MRI is able to show small brain parts. These imaging techniques can be used to identify shrinkage in ventricles. In the image below it is possible to see the difference between the ventricles of someone with alcohol use disorder and someone without.

Non-alcohol use disorder
Alcohol use disorder

And here the shrinkage of the cerebellum in the lower right portion of the brain of a healthy control and someone with alcohol use disorder.

Healthy control
Alcohol use disorder

Lishman’s hypothesis on aetiology of alcohol related brain damage

Non-alcohol related forms of Wernicke-Korsakoff syndrome due to thiamine depletion alone usually show full recovery with time.(If underlying medical condition allows for this). Alcohol neurotoxicity on its own leads to a slowly reversible form of global cognitive impairment/dementia  provided abstinence from alcohol is achieved. The combination of susceptibility to alcohol neurotoxicity and thiamine depletion can lead to irreversible cognitive impairment involving damage to cortical (alcohol-induced) and sub-cortical (alcohol and thiamine depletion induced) structures.This forms a spectrum of disorders from a classic amnestic syndrome to  dementia.