Section 1: Epidemiology and aetiology
Brain damage is a common and potentially severe consequence of long-term, heavy alcohol consumption. Even mild-to-moderate drinking can adversely affect cognitive function.
Significant alcohol use (a minimum of 35 standard drinks per week for males and 28 per week for women) for more than five years and significant alcohol use within three years of onset of cognitive problems can cause alcohol-related dementia.
However, alcohol is often overlooked as a cause of cognitive impairment because Alzheimer's disease, vascular and Lewy body dementia are usually considered more likely causes.
Patients presenting with cognitive impairment may also abuse alcohol as a means to cope with stress, which is itself a potential cause of their impairment.
The presence of multiple potentially contributory factors further complicates determination of the cause of brain damage. Thus, the exact prevalence of alcohol-related brain damage (ARBD) is difficult to ascertain because it often remains undiagnosed.
A study found alcohol-related brain changes in around 1.5% of the general population and 30% in heavy drinkers.1 A study of Wernicke's encephalopathy (WE) found the condition in up to 2.8% of the general population and 12.5% of alcoholics.2
An increase in the heavy drinking that causes ARBD is indicated by the 2011 NHS Alcohol Statistics Report. This states that 160,181 prescription items for drugs for the treatment of alcohol dependency were prescribed during 2010. This is an increase of 6% on the 2009 figure (150,445) and an increase of 56% on the 2003 figure (102,741).
The prevalence of ARBD is likely to increase as alcohol abuse continues to grow.
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Alcohol is a neurotoxin that operates in several ways.
Among the most important of these is degradation of the neuronal myelin sheath, subsequent attenuation of nerve signalling and loss of brain function.
The exact process by which alcohol damages the myelin layer is not fully understood. However, it is known to interfere with the absorption of thiamine, and lack of thiamine inhibits the production of myelin.
In addition to damaging the myelin layer, alcohol can damage the brain, directly and indirectly, in a number of other ways:
- Neuroinflammation has recently been proposed in the pathogenesis of ARBD. Microglia have been known to mediate neuroinflammation.
- Alcohol can cause falls (often unreported by the patient) that can cause subdural haematomas.
- Eating habits and nutrition may be affected, resulting in lack of thiamine in the diet. Thiamine deficiency leads to decreased level of thiamine pyrophosphate in the brain. Thiamine pyrophosphate serves as a co-factor for several enzymes involved in carbohydrate and lipid (myelin) metabolism. If thiamine deficiency lasts for two to three weeks, axonal conduction and cellular metabolism are affected, leading to impaired conduction of action potential. DNA microarray technology has shown that expression of genes that encode myelin proteins becomes affected, which affects the structure of the myelin sheath.
Section 2: Making the diagnosis
The first stage in diagnosis is to determine whether brain damage is real and long term, and not simply short-term impairment due to intoxication. The second stage, which is often more difficult, is to identify the cause of the damage.
Early detection and intervention produces a better outcome; however, a full needs assessment of ARBD is best undertaken after three months of abstinence.
As a result, a preliminary diagnosis may have to be made when a patient is suffering short-term effects of alcohol abuse.
ARBD encompasses a range of conditions with subtly different combinations of symptoms, so making an accurate diagnosis can be difficult (see table below). The Caine criteria clarify the diagnosis of WE and Korsakoff's psychosis.
|DIFFERENTIATING ALCOHOL-RELATED CONDITIONS|
|Alcohol-related brain damage||Clinical features|
||Caine criteria – two of the following four should be present.
a) Ocular abnormality, for example, nystagmus or ophthalmoplegia.
b) Cerebellar dysfunction, for example, loss of equilibrium, inco-ordination of gait, dysdiadochokinesis, limb ataxia or dysarthria.
c) Altered mental state, for example, mental sluggishness, apathy or impaired awareness of immediate situation.
d) Nutritional deficiency.
MRI should be used to support the diagnosis of acute WE.
||Clinical diagnosis of dementia at least 60 days after the last exposure to alcohol and significant alcohol use. There are other supporting physical, neurological and investigational criteria.|
These two disorders are often referred to as Wernicke-Korsakoff syndrome. WE is the acute stage which can progress in a proportion of cases to Korsakoff's syndrome, which is a chronic amnestic state.
Patient history and drinking habits can give useful indicators of the cause of their brain damage.
Ask if there were signs of cognitive impairment before alcohol abuse began and if there is a history of Alzheimer's disease or dementia in the family.
Specialist neuropsychometric testing can reveal deficits in working memory, cognitive flexibility, problem solving and perseveration.
Blood tests can be ordered if one suspects underlying Alzheimer's disease (FBC including MCV, MCHC, LFTs, liver enzymes, B12, folate, RBC and transketolase) and MRI should be used to support diagnosis. Structures that are affected include mammillary bodies, corpus callosum, frontal lobe, thalamus and cerebellum.
Specific sequences are required and an expert opinion should be sought from a neuroradiologist.
Having established the presence of brain damage, diagnosis of ARBD can be assisted by a process of eliminating other potential causes of the damage.
Wernicke-Korsakoff syndrome involves damage to specific areas in the brain, for example, petechial haemorrhage in the periaqueductal grey matter and volume changes in the mammillary bodies.
Neuropathological studies have revealed that damage to the anterior nucleus of the thalamus accounts for Korsakoff's psychosis and patients with non-amnestic WE also have damage to this area, but it is less severe.
Amnesia is probably caused by interruption to the diencephalic-hippocampal circuit including thalamic nuclei and mammillary bodies, rather than a single lesion in the anterior thalamic nucleus.
Section 3: Managing the condition
Despite its prevalence, guidelines relating to alcohol dependence do not address the specific issue of ARBD.
Brain changes due to alcohol damage are regionally specific and some of these changes are reversible with abstinence (white matter is capable of regeneration).
This is often complemented by medications to decrease cravings and neuroprotection with thiamine.
It is common practice to refer patients to a psychiatrist to determine the causes and the extent of their cognitive impairment.
A study found that the average length of stay in hospital was 84 days due to the absence of appropriate care pathways.4 These circumstances reflect much of the current situation in England.
Acute Wernicke’s encephalopathy: axial FLAIR images show abnormal high signal in the periventricular region of third ventricle (arrows)
The University of Stirling has led the way in exploring the needs of patients with ARBD and has drawn together a comprehensive framework for development of services.
The framework emphasises the importance of:
a. Early detection and intervention to prevent further damage.
b. A full needs assessment to be undertaken after three months of abstinence.
c. A named person or service with responsibility to support the person via an assessment by a multidisciplinary team.
d. Referral to specialists in the field of neurorehabilitation psychiatry.
e. Treatment includes training in specific cognitive domains and rehabilitation programmes. Targeted computerised practice has been shown to improve performance in a number of cognitive domains. This also improves activities of daily living. Ward-based specialist neurorehabilitation programmes also have a good evidence base. This should be integrated with alcohol treatment programmes.
There are five stages in recovery for patients with Wernicke-Korsakoff syndrome.
- Medical stabilisation following management of encephalopathy.
- Quick recovery of ataxia, abducent gaze palsy in few weeks.
- Adaptation stage where strategies are employed to optimise independence using cognitive strategies.
- Gradual improvement of other neurological deficits, such as nystagmus, may take a few years.
- Progressive socialisation and relapse prevention.
As they are treated for ARBD, patients should be considered for CBT, acceptance commitment therapy and motivational interviewing to break the cycle of alcohol abuse to alleviate fear of mental deterioration.
Section 4: Prognosis
Any improvement usually occurs within two years. The Alzheimer's Society estimates that about a quarter of those affected make a very good recovery. About half make a partial recovery and need support to manage their lives. A further quarter make no recovery and may need long-term care. If the patient continues to drink heavily and has poor nutrition, Korsakoff's syndrome is likely to continue to progress. Patients need long-term follow-up for their cognitive deficits.
Vertical nystagmus may persist for months. Fine horizontal nystagmus may persist indefinitely in as many as 60% of patients. Patients completely recover from sixth nerve palsy, ptosis and vertical gaze palsy.
Prognosis of ataxia
Approximately 40% of patients completely recover from ataxia. The remainder have varying degrees of incomplete recovery.
This often resolves gradually after thiamine is started. Only 20% patients who persist with amnestic deficits even after treatment has been initiated recover fully. The remainder have a varying degree of persistent deficits with new learning and memory.
Section 5: Case study
A 79-year-old single man with a strong history of alcohol dependence and type 2 diabetes was admitted via A&E after being found confused and wandering the streets with a knife.
He was unable to give a coherent history and was found to be dysarthric, having severe truncal ataxia and cerebellar signs. His finger-nose test was impaired and he failed on most cerebellar tests. He was diagnosed as suffering from WE and received IM thiamine.
CT and blood tests
He had a brain CT and blood tests. The CT showed prominent sulci and gyri with deep white matter changes. There were no other abnormalities. After a week he still appeared confused and scored 11/30 on the mini mental state examination. He revealed heavy alcohol use and admitted he had spent all his money on alcohol.
The man admitted to starting drinking at the age of eight and increased his drinking habits by age 22 when he started working at sea. He admitted drinking seven pints of beer a day and has had alcohol withdrawal symptoms in the past, including visual hallucinations.
He also admitted having poor memory characterised by being forgetful of locations, mislaying his belongings and failing to recognise family and friends.
Owing to the global nature of cognitive impairment, he was diagnosed as suffering from alcohol-related dementia. A differential diagnosis of Korsakoff's psychosis was considered.
Section 6: Evidence base
- Sechi G, Serra A. Wernicke's encephalopathy: new clinical settings and recent advances in diagnosis and management. Lancet Neurol 2007; 6: 442-55.
- NICE. Alcohol-use disorders: Diagnosis and clinical management of alcohol-related physical complications. CG100. London, NICE, 2010.
Section 4.5 Wernicke's encephalopathy
- SIGN: The Management of Harmful Drinking and Alcohol Dependence in Primary Care. Guideline No 74, 2004.
- CKS. Alcohol - problem drinking - Management.
- McCabe L. Working with People with Alcohol Related Brain Damage. University of Stirling, 2006.
This site aims to bridge the gap between the scientific evidence on alcohol and the wider public by making evidence accessible to health professionals and other interested groups.
Alcohol Concern website
This site provides information and articles on a range of topics surrounding alcoholism.
It includes 18 excellent fact sheets for professionals, a search engine and a good list of alcohol-related links.
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1. Cook CCH, Hallwood PM, Thomson AD. B-vitamin deficiency and neuropsychiatric syndromes in alcohol misuse. Alcohol 1998; Supplement 33 (4): 317-36.
2. Cook CCH, Thomson AD. B-complex vitamins in the prophylaxis and treatment of Wernicke-Korsakoff syndrome. Br J Hospital Med 1997; 57(9): 461-5.
3. Oslin D, Atkinson RM, Smith DM et al. Alcohol-related dementia: proposed clinical criteria. Int J Geriatr Psychiatry 1998; 13(4): 203-12.
4. Popoola A, Keating A, Cassidy E. Alcohol cognitive impairment and the hard to discharge acute hospital inpatients. Ir J Med Sci 2008; 2: 141-5.