Korsakoff’s is ‘an abnormal mental state in which memory and learning are affected out of all proportion to other cognitive functions in an otherwise alert and responsive patient, resulting from nutritional depletion, i.e. thiamine deficiency’ (Kopelman et al, 2009). The emphasis on memory is important but should not overshadow the effect long term misuse and thiamine deficiency has on other domains of intellect.
Approximately 0.5% of the general adult population at death has evidence of brain damage due to alcohol/thiamine deficiency. The prevalence of post mortem damage is as much as 30% in known misusers (Harper et al 1998). These findings are corroborated by a relatively high prevalence of cognitive damage in people attending treatment units (Tuck & Jackson 1991).
Individuals consuming at least 30 units (females) or 50 units (males) for five years, in the context of heavy social drinking, are at risk of cognitive damage (Oslin & Carey 2003). With this degree of alcohol misuse, it takes three months of abstinence for acute cognitive recovery: enabling assessment of, longer term brain damage. Another year of abstinence is required for the brain to regenerate (Sullivan et al 2000). Clinical experience indicates that further adaptation and social recovery may continue over two to three years (Wilson et al 2012) in the context of planned management.
Presentation is often subtle and gradual. Impulsive behaviour, social disinhibition, planning issues, understanding complex conversations and implications of decisions are some, but few, of the frontal cognitive problems which may be mistaken for drunkenness. Memory difficulties become progressively evident with variable confabulation. These cognitive problems may jeopardise ability to memorise, understand and weigh up information, critical in the process of making decisions with regard to further alcohol consumption and the relevant care/treatment that is needed.
Such histories should trigger an assessment of potential B1 deficiency and supplementation. High risk characteristics include: reduced BMI, increased carbohydrate intake, excessive vomiting, weakness, polyneuropathy, eye signs, giddiness, undue fatigue and early cognitive deficits (Thomson et al 2009).
Few alcohol treatment programmes are adapted to accommodate people with these problems, leading to vicious cycle of consumption and cognitive damage (Bowden et al 2001). Routine cognitive examination (as recommended by NICE 2011) is rarely carried out. Assertive engagement, adapting educational programmes and increasing contact are some of the recommended adaptations.
Severe cases are characterised by multiple admissions, undue bed occupancy and difficulty in discharge. Lack of care pathways mean that needs are rarely addressed. The Wirral CCGs commissions services for these patients. The treatment program is a simple, easily transferable program of rehabilitation in which patients are protected from alcohol when incapacitated and encouraged to develop activities of daily living. A series of reviews have been conducted; the first of which has been published (Wilson et al 2012).
Physical, social and psychological health improves across the three year period of active management. Relatively few patients relapse into dependence (10%) and there is a reduction in patient bed days (secondary care) of 85% when compared with the five years prior to referral. In subsequent reviews a minority of patients warranted long term institutional care. The vast majority are returned into community settings, with most living in their own flats or houses. As programme progresses; treatment costs reduce. At first, when the patient may have to be held under a deprivation of liberty order, costs are high, but as autonomy develops; costs reduce by 75% across three years with the majority of patients incurring no on-going treatment costs by the end of the management programme.
Very few health professionals are aware of the implications of ARBD. Non-intervention promotes a cycle of worsening cognition, on-going addiction, deteriorating physical health, increased utilisation of health services and death. In 2014 a national report (Royal College of Psychiatrists CR185) was published. It provides an overview and review of relevant literature and examples of good practice within the UK.
Bowden, S.C.; Crews, F.T.; Bates, M.E.; et al. Neurotoxicity and neurocognitive impairments with alcohol and drug-use disorders: Potential roles in addiction and recovery. Alcohol Clin Exp Res 25(2):317-321, 2001.
Harper C, Kril J, Sheedy D, et al (1998) Neuropathological studies: the relationship between alcohol and aging. In Alcohol Problems and Aging: NIAAA Research Monograph No. 33. (eds ESL Gomberg, AM Hegedus, RA Zucker). National Institute on Alcohol Abuse and Alcoholism.
Kopelman MD, Thomson A, Guerrini I, et al (2009) The Korsakoff syndrome: clinical aspects, psychology and treatment. Alcohol and Alcoholism, 44: 148–54.
National Institute for Health and Clinical Excellence (2011) Alcohol-Use Disorders: Diagnosis, Assessment and Management of Harmful Drinking and Alcohol Dependence (Clinical Guideline CG115). NICE.
Oslin DW, Carey MS (2003) Alcohol related dementia: validation of diagnostic criteria. American Journal of Geriatric Psychiatry, 11: 441–7.
Sullivan, E.V.; Rosenbloom, M.J.; Lim, K.O.; and Pfefferbaum, A. Longitudinal changes in cognition, gait, and balance in abstinent and relapsed alcoholic men: Relationships to changes in brain structure. Neuropsychology 14(2):178-188, 2000b.
Thomson A, Guerrini I, Marshall E (2009) Wernicke’s encephalopathy: role of thiamine. Nutrition Issues inGastroenterology, series 75: 21–30.
Tuck R, Jackson M; (1991) Social, neurological and cogntive disorders in alcoholics The Medical Journal of Australia: Vol 155 August 19, 225-229.
Wilson K, Halsey A, Macpherson H, et al (2012) The psycho-social rehabilitation of patients with alcohol related brain damage in the community. Alcohol and Alcoholism, 47: 304–11.