ARBD Documentation

Please download our ARBD checklist document.

(Download PDF)

There are several terms that are used to describe the potentially damaging effects of alcohol and related vitamin deficiencies on the brain. Read more…

(Download PDF)

It is well established that long term alcohol misuse has a direct effect on nerve cells (neurones) of the brain. What evidence there is indicates that women drinking 30 units or more and men drinking 50 units or more a week for 5 years or longer are likely to experience these changes. These are probably a consequence of disruption of the chemicals that pass messages between neurones but there is also evidence that brain cell volume is also affected; suggesting that there are deleterious effects on the brain structure itself.

These physical changes in the brain are associated with changes in thinking, reasoning and memory, amongst other intellectual changes. This is referred to cognitive damage and may manifest in a very serious and usually permanent disorder called Korsakoff’s Syndrome. Usually, however, in most cases, and provided the individual remains abstinent, cognitive damage may improve.

The brain can take three to four months of abstinence to recover from the direct effects of excessive, long standing alcohol exposure. During this time (depending on the degree of damage), cognitive performance can dramatically improve, and the individual may completely recover. However, longer lasting cognitive damage may have occurred but, research has shown that, provided the individual remains abstinent, the brain can still show signs of recovery and scanning studies clearly show brain growth over a period of three to four years. During this time there may well be evidence of varying degrees of cognitive improvement. Long-term follow-up studies demonstrate that about a quarter of people presenting with severe cognitive damage (including people with Korsakoff’s Syndrome) will remain impaired and show little change over time. The remaining three quarters are likely to show varying degrees of improvement as the brain regrows and heals, with approximately a quarter showing complete or almost complete recovery. These findings will depend on a variety of factors including the nature of the help the individual gets.

Nutritional support is critical to recovery. One of the many characteristics of long-term alcohol dependency are problems with diet. A nutritious diet is frequently the victim of long-term and/or intermittent intoxication. Alcohol provides substantial calories. Consequently, the individual may not eat a good diet. Frequent vomiting due to inflammation of the stomach (caused by alcohol) may compromise the digestion of appropriate vitamins. (A good illustration of this is that Korsakoff’s Syndrome can be bought on by excessive vomiting in pregnancy, unrelated to any alcohol ingestion.)

Many of the vitamins required for the brain to function are water soluble. This means that they cannot be stored by the body, leaving no reserves. A regular and frequent intake is required in order to avoid brain changes. Thiamine (vitamin B1) is one of these vitamins and is critical in maintaining cognitive function. If an individual’s diet is compromised through alcohol dependency, then the shortage of thiamine may become critical. This problem is complicated by a couple of other factors.

Firstly, long term alcohol drinking can affect the gut lining, making it very difficult for the thiamine to be absorbed from the gut into the blood. Consequently, the brain is starved of thiamine even though it is taken in the diet. Secondly, there is some evidence indicating that alcohol can affect the way the brain can use thiamine when the thiamine does reach the brain.

Consequently, the alcohol dependent individual’s brain is highly vulnerable to thiamine starvation through an inadequate diet, poor absorption and changes in how the brain can access the thiamine. There is a very real chance of cognitive damage. It is important to remember that there is also the problem of the direct and toxic effects of alcohol on the brain through damage to neurones and related chemicals. All these changes (and potentially the effect of other vitamin deficiencies) contribute to both Alcohol Related Cognitive Damage and the more well defined Korsakoff’s Syndrome.

When a long-term alcohol dependent individual presents with withdrawal in the context of significant thiamine deficiency, there is a danger that Wernicke’s Syndrome will develop. This is a potentially fatal condition. It can present with confusion, jerky eye movements, double vision and drooping eye lids, tremors and unsteadiness. It can deteriorate into coma and death. Obviously, this is urgent and requires immediate hospitalisation. Apart from stabilising the individual, treatment includes urgent intravenous thiamine. This treatment may be across a few days and is recommended even when the clear signs of Wernicke’s syndrome are not evident, but the clinician considers that there is a risk of them developing.

Permanent brain damage can result in Korsakoff’s Syndrome in which the individual suffers from long standing memory problems often stretching back many years, difficulty in learning new information (short term memory problems), the experience of false memories (confabulations), reasoning problems and residual neurological problems potentially affecting the eye movement and walking. These problems are long lasting and may be irreversible. Long term oral thiamine is recommended after the Wernicke’s syndrome has been treated.

In less severe cases, the onset of signs of thiamine deficiency and direct effects of alcohol can be more subtle and gradual. They can frequently be recognised in high-risk individuals, for example, those attending alcohol treatment services. These include a history of weight loss, vomiting and signs of malnutrition. Other clinical signs include nerve damage, such as numbness and persistent tingling and increasing weakness. Memory/reasoning problems are likely to emerge, and the person may become apathetic, lethargic and increasingly anxious. These features indicate that treatment is advised. In severe cases, this might be intravenous thiamine (undertaken in hospital). However, some alcohol treatment and community services may provide intramuscular thiamine injections that can be given by trained and properly equipped nurses.

It is recommended in most guidelines that if a clinician considers that an alcohol dependent individual is vulnerable to developing thiamine deficiency over a long period, then it is important to encourage oral thiamine supplementation. There is little long-term evidence supporting this approach but despite the potential problems in compliance and thiamine absorption in people that are drinking heavily, it is strongly recommended and generally accepted as good practice.

(Download PDF)

Alcohol Related Brain Damage may present in several ways. Wernicke’s syndrome is well recognised and is characterised in onset by a confusional state in which the individual is disorientated and may be hallucinating. It is frequently (but not always) associated with double vision, drooping eyelids and a staggering or unstable gait. Its sudden onset may be associated with withdrawal from alcohol. The staggering, unstable gait, tremors and double vision may persist as elements of Korsakoff’s Syndrome, after the acute Wernicke’s has been treated. The combination is known as Wernicke-Korsakoff Syndrome. The intellectual (cognitive) changes associated with this condition fall in to two main domains. The more obvious involves memory.

The first major memory problem of someone with Korsakoff’s is disturbance of ‘short term memory’. In this context, this refers to difficulty in learning new information. As a consequence, the individual may be repeatedly given information but cannot remember it and often will deny ever having been told the information. Consequently, the individual is very much living minute by minute. They cannot remember what has just happened and cannot remember what they have been told is going to happen.

The second major memory problem in Korsakoff’s Syndrome are difficulties with long term memory. The individual may lose memories going back to up to 25 years. Sometimes this loss of memory can be patchy. In severe cases the individual may believe that they are 25 years younger than they are; as from their perspective, the last 25 years have not existed. This degree of memory loss becomes evident when speaking to the individual as they appear confused and muddled.

A person suffering from both short- and long-term memory problems will have no understanding or memories of how they have arrived in their current situation and this problem is not easily resolved as they cannot remember any explanations given to them. Usually, such an individual has no understanding or insight into their memory disturbance.

These problems are complicated by false memories (confabulations). One way of trying to understand these are to consider the human brain as always trying to make sense of the world. When there are large gaps in memory, there will be a natural tendency to fill these gaps with ‘memories’ that are unconsciously made up. There are generally two types of confabulations. The first type is a false memory that is held for the short time of the relevant conversation. When asked, a person may ‘remember’ that something has happened when it has not. These transient confabulations are often highly plausible and are easily slipped into the conversation by the individual without realisation. The individual may even contradict themselves a few minutes later when asked a similar question. Individuals with these tendencies are usually suggestible and easily led in conversations.

The second type of confabulation is more complex and permanently held by the individual. These false memories are believed by the individual and the content in frequently slightly grandiose or to the personal benefit of the individual.

Memory is one of the easiest recognised cognitive disturbances found in ARBD. It may not be as obvious as described above but may present more subtly over many months or years. Carers or loved ones will notice repeat conversations, forgetting appointments and denying that things have been said or happened. These early signs are often associated with or follow even more subtle cognitive changes. These very early changes (which get worse as drinking and dependency continues) involve reasoning abilities. These are often described as the dysexecutive syndrome. They include several intellectual features: Planning things and problem solving or sorting out the more complicated aspects of daily living can become problematical. This may well become obvious to relatives, friends and carers. Common examples include difficulty in making joint arrangements and sorting bills. Other features of the dysexecutive syndrome include problems in paying attention and concentrating on things with a tendency to fail to complete tasks. Noticeable changes become evident in speech. More than usual difficulty in finding words and completion of sentences is frequently experienced.

Increasing difficulty in managing day-day tasks and personal environment may become evident. Often here is an impact on the individual’s appreciation of risk relating to decisions and their implications. Impulsive behaviour is common. The individual may become disinhibited. This may be of a sexual nature. Apathy and an increasing lethargy with lack of self-awareness and self-neglect may become more obvious.

These signs are usually couched in the context of loss of emotional and social awareness. The individual loses the ability to understand other people’s emotional states, anticipate their desires, beliefs and knowledge. They lose their ability to empathise.

Alcohol dependent individuals will vary in the degree and combination of features of alcohol related brain damage. This is likely to depend on the degree and duration of alcohol dependency, nutritional status and genetic predisposition. Aspects of the dysexecutive syndrome are likely to present first and may be mild to the extent that the individual can continue to function reasonably well. In fact, these signs are often missed by relatives and carers and mistakenly labelled as ‘wilful behaviour’. As cognitive problems progress, memory disorders may become more evident and features of the dysexecutive syndrome will become more obvious. As drinking continues, ability to remember and to understand deteriorates. Consequently, the individual may lose insight into their own problems and be unable to understand the implications of continued alcohol consumption. It is easy to see how a downward spiral of cognitive damage makes the individual vulnerable to further alcohol consumption and eventual permanent brain damage.

(Download PDF)

Alcohol Related Brain Damage (ARBD) is an umbrella term.  It includes presentations of differing degrees and nature of cognitive damage as a consequence of alcohol dependency and/or thiamine deficiency. As there are no specific instruments validated for the diagnosis of ARBD, this document attempts to provide a pragmatic overview designed to facilitate its recognition.

High risk populations

ARBD may occur after several years of alcohol dependency. Evidence suggests that a significant proportion of individuals attending services for the treatment of alcohol dependency in community settings experience varying degrees of ARBD. There is some evidence suggesting that multiple withdrawals from alcohol are a risk factor for cognitive impairment. ARBD may contribute towards poor compliance with community treatment regimes, due to the undiagnosed cognitive disorders. Other populations that may well have a high prevalence of ARBD include individuals with frequent visits to accident and emergency departments or admissions into acute medical care for the treatment of the physical complications of alcohol dependency. Some surveys have indicated that patients that are ‘difficult to place’, with resultant long-stays in acute hospital care have a high prevalence of ARBD. (This is of course dependent on many other service-related factors as well). Studies in Glasgow have indicated that the homeless population have a high prevalence of ARBD.

Populations at risk of developing Wernicke’s Encephalopathy may be identified through clinical observation. In the case of ARBD, signs of malnutrition, early neurological problems and psychological changes in the context of heavy drinking may all be taken as potential warning signs. These include loss of appetite, weight loss in the past year, decrease in BMI, history of recurrent vomiting and excessive carbohydrate intake. Psychological problems may include insomnia, anxiety, fatigue, weakness and apathy, changes in concentration and early memory loss. Neurological problems may include giddiness, changes in balance, numbness or pins and needles and double vision.

Overview of clinical diagnosis

There are no validated, specific tests for the diagnosis of ARBD. A research project conducted in USA in 2003 found that a combination of a history of heavy alcohol drinking (30 units for women, 50 units for men per week) of at least a duration of five years, combined with evidence of cognitive impairment (of similar degree to that of dementia) and exclusion of cerebrovascular disease identified people with long standing ARBD (described as alcohol dementia).

In diagnosing ARBD, it is important to establish three major issues. Firstly, is there evidence of sustained cognitive damage? The use of the term ‘sustained’ is to exclude those individuals that are suffering from withdrawal. Assessments should be undertaken after a withdrawal regime has ended. In the original research of 2003, the author defined ‘alcohol dementia’ as people suffering from cognitive impairment after three months of abstinence in order to differentiate from those in which cognitive symptoms spontaneously resolved. This occurs quite frequently in the first three months. However, there are problems with this approach in an NHS setting.  It is difficult to maintain someone in an acute hospital bed solely to see if cognition spontaneously improves. Consequently, the pragmatic definition of ARBD includes individuals with cognitive impairment being evident after withdrawal.

Secondly, it is important that there is a history of alcohol dependency that is likely to be the primary cause of the cognitive impairment. As mentioned above, a three-year history of drinking at least 30 (women) or 50 (men) units a week (usually against a background of previous, heavy social drinking) is likely to have a significant effect on cognition. Such a history may be inferred or documented by hospital notes but gaining a corroborative history from carer, family or friend is always useful.

Thirdly, it is important to exclude other causes of cognitive impairment. Up to 25% of ARBD patients presenting through acute care will have some evidence of early cerebrovascular disease or head trauma. In the assessment of a patient, a clinical decision must be made concerning the relevance of these conditions (if present). When there is evidence of sustained and obvious cognitive impairment following the trauma or stroke (vascular event) then it may be appropriate to consider these as the main problem. However, what evidence there is indicates that individuals with ARBD and minor head trauma or early cerebrovascular disease can respond to ARBD management. It is important to note that individuals with a history of heavy drinking are more likely to develop dementia (usually vascular dementia) later in life. A progressive dementia of this nature should be differentiated from ARBD. If there is continued deterioration in the context of abstinence, then a diagnosis of ARBD is unlikely.

Cognitive assessment

There is a wide variety of instruments designed to quantify cognitive deficits. Most of them employ ‘cut-off’ scores that indicate the possibility of dementia. It is not the purpose of this brief document to provide a comprehensive review. We provide a brief critique of a few more commonly used instruments These include the 6-CIT amongst many others. This is an example of a very brief instrument often used in general practice and community settings. Another instrument frequently employed is the Mini Mental State Examination (MMSE). The disadvantage with these instruments is that they fail to capture changes in cognition associated with frontal lobe problems (dysexecutive syndrome) which are very common in ARBD. Slightly longer instruments that do include some aspects of frontal lobe dysfunction include the Montreal Cognitive Assessment (MoCA) ( This test is designed to pick up mild cognitive impairment and can play a useful role in identification of people with ARBD. It is freely available on the web. A slightly longer instrument (in terms of time to administer) is the Addenbrooke’s Cognitive Examination (ACE-R) . It is free to download and easily administered and the scoring instructions are easy to follow. A degree of standardisation and training is recommended and there are now free access on-line training courses available.

When using these tests, it is important to note that these are not diagnostic tests. They are designed to identify people that exhibit some aspects of cognitive dysfunction. They have not been validated in the context of ARBD. Consequently, they certainly exclude important aspects of cognitive dysfunction experienced by people with ARBD and the cut-off scores may not necessarily be applicable. Despite these important issues, the MoCA and the ACE-R offer a structure for conducting a brief cognitive examination for clinicians that have no prior training in undertaking a cognitive examination and provide the context of cut-off scores that have been validated in other conditions.

(Download PDF)

Several of the characteristics of ARBD can be problematical in the assessment of capacity, particularly when complex decisions are being considered.

Firstly, ARBD is frequently characterised by memory impairment. Usually working memory is well preserved. In this context, this refers to that component of memory that enables the immediate processing of information. Consequently, the individual may not, at a superficial level, appear to have a memory problem as they can follow a conversation and answer questions plausibly. However, short- and long-term memories are frequently affected. An attempt should be made to examine the implications of these memory problems in terms of the decision-making process.

Short term memory (STM) refers to the individual’s ability to learn new information and hold it for more than the few seconds or minutes.

Practical suggestions: Other than a formal test of STM, provide the individual with information, (for example: relating to their condition) and encourage them to learn it by repeating it back to you. Having done this, change conversational topic, or better still, take a break in the interview and then when returning, explore whether the individual can recall the information. Individuals with STM problems frequently fail to recall that you had the conversation, or at least, have forgotten its content. STM loss of this degree is likely to incapacitate the person in terms of the decision under examination, even though they may have agreed to an arrangement during the conversation.

Long term memory (LTM) refers to the individual’s ability to recall long-standing memories from the past, usually of a biographical nature. Many individuals with ARBD experience loss of LTM to varying degrees. In many cases the individual’s history of very heavy drinking, multiple hospital admissions, social and financial problems, break-up of family, loss of jobs and a police or criminal record will be lost to the individual in totality or in part. It is very easy for the capacity assessor to assume that the ARBD sufferer can recall these events and has learned from their experiences; potentially influencing future decisions. However, with LTM loss of up to twenty-five years, this may not be the case. The problem of memory loss is frequently complicated by confabulations. These are false memories that the sufferer believes. They may be plausible.

Practical suggestions: It is important to have some familiarity with the individual’s biographical history. An attempt should be made to establish the drinking history and relevant medical and social histories prior to assessing the individual. A corroborative history from a family friend/carer/relative can play a very important role. Long term memory loss can then be informally evaluated and its potential impact on decision making can be judged.  It is important to make the individual aware of his/her past issues, discuss them and see if they are likely to influence the decision under question. It is often the case that the individual may not believe that these problems have arisen in the past.

Secondly: ARBD sufferers will often present with dysexecutive syndrome. This syndrome is characterised by problems in reasoning. Planning things and problem solving and sorting out more complicated aspects of daily living can become problematical. This may be obvious to relatives, friends, and carers. Common examples include difficulty in making joint arrangements and sorting of bills.  Other features of the dysexecutive syndrome include problems in paying attention and concentrating on things with a tendency to fail to complete tasks. In addition to these reasoning problems, noticeable changes become evident in speech. More-than-usual difficulties in finding words and completion of sentences are frequently experienced.

Increasing problems in managing day-day tasks and personal environment may become evident.  Often here is an impact on the individual’s appreciation of risk relating to decisions and their implications. Impulsive behaviour is common. The individual may become disinhibited. This may be of a sexual nature. Apathy and an increasing lethargy with lack of self-awareness and self-neglect may become more obvious.

These signs are usually couched in the context of loss of emotional and social awareness. The individual loses the ability to understand other people’s emotional states, anticipate their desires, beliefs and knowledge.  They lose their ability to empathise.

 It is obvious that some, if not all these issues may impinge upon the process of decision making (depending on the nature of the decision), particularly in disrupting the processes of understanding and the use and weighing up of information.

Practical suggestions: Again, information relating to the individual’s recent past may help to define how problematical these more subtle cognitive deficits are. Examples of difficulty in arranging things, managing household bills and budgets and a frequent history of failing to complete tasks may all provide additional and important information for the assessor to consider. A corroborative history is usually of great value.

Thirdly, the issue of trying to assess whether the cognitive damage is likely to affect future behaviour and compliance with agreed interventions/actions may prove problematical. Apart from the obvious problems of STM difficulty (remembering what has been planned or agreed), there are the more subtle influences of dysexecutive syndrome. Problems of social awareness, increased risk taking and being unable to anticipate implications of actions can cause future difficulties in maintaining compliance with previously agreed arrangements. These issues tend to be less obvious in the context of a structured interview in which prompts, directive questioning, and clear expectations are evident. Likewise, a structured social environment with explicit rules and monitoring  (such as a nursing home, residential setting or hospital setting) will strongly influence behaviour. In the context of the less well-defined rules and obligations of general society, without the obvious imposition of social constraints, people with dysexecutive syndrome will often run into significant difficulties that are not evident in a more structured environment

Practical suggestions: The individual’s personal history, the events and problems they have encountered in the more recent past, prior to any institutionalisation should be considered within the assessment process. Relevant indicators of future problematical behaviour (because of cognitive damage) may include past, recurrent difficulties in managing relationships, evidence of vulnerability (social, financial or physical), self-neglect and other risky behaviours (not necessarily associated with alcohol consumption). This information is best recruited through a corroborative history of a carer/family member or friend.

Lastly, loss of LTM, the inability to learn new information (STM) and problems of reasoning may well contribute to lack of insight. This should be differentiated from the tendency of the alcohol dependent to be in ‘denial’ of their history or drinking behaviour. Denial can be considered as a psychological mechanism by which the individual refuses to accept the problems they have. In denying the issues, the individual protects themselves from anxiety, guilt or other psychologically discomforting experiences they might have if they were to accept responsibility for their problems. In the context of ARBD, lack of insight is a consequence of cognitive damage. The individual is neither consciously nor unconsciously aware of their problems. The relationship between ‘denial’ and ‘lack of insight’ is certainly complicated. As cognitive damage increases over time, it is likely that denial becomes less of a problem and lack of insight becomes more likely.

An individual lacking insight will obviously experience significant problems in understanding and weighing up the pros and cons relating to a decision, particularly if this decision concerns the need for help and future limitation of drinking.

Practical suggestions: When assessing ‘lack of insight’ several pointers are useful: If there is significant evidence of long-term memory problems, reasoning difficulties and problems with learning new information then there is a significant likelihood of some degree of loss of insight.

If a person has difficulty in understanding the implications of on-going drinking (even when it is explained to them) then there may be cognitive problems relating to understanding and self-awareness. Has the individual got alternative explanations regarding their health problems, or do they believe that they have no problems despite the obvious evidence?

The Capacity Assessment

In order to undertake a comprehensive capacity assessment of a person suffering from ARBD it is essential to be familiar with his or her personal history and have access to a corroborative history.

This document refers to the COP3-eng document as a template

The background

Section 4 of the document provides a section for a comprehensive explanation of the circumstances in which the assessment is taking place. This is an often-under-utilised section:

Section 4: ‘Please provide any further information about the circumstances of the person to whom the application relates that would be useful to the practitioner in assessing his or her capacity to make any decision(s) that is the subject of your application’.

It refers the assessor to note 2: Please provide any further information about the circumstances of the person to whom the application relates that would be relevant in assessing their capacity.

Practical suggestions: This section provides an opportunity for the assessor to furnish evidence relating to the individual’s past and issues that might have arisen because of cognitive deficits. It gives financial problems and decision-making difficulties as an example. Other issues known to be affected by cognitive impairment include poor compliance with treatment programs, self-neglect, and other risky behaviours.  Evidence of appropriate behaviour in institutions, compared with decompensated or antisocial behaviour in less structured environments may be a consequence of cognitive damage. Recent/current examples of cognitive damage may be entered here, including observations from nurses, carers and family.

The presence of mental impairment

The next section requires the assessor to provide a diagnosis (where there is one), but the document implies that a general statement of mental impairment is acceptable when there is no formal diagnosis.

Section 7.1: ‘The person to whom the application relates has the following impairment of, or disturbance in the functioning of, the mind or brain. Where this impairment or disturbance arises out of a specific diagnosis, please set out the diagnosis or diagnoses here’ requires.

Practical suggestions: in the case of ARBD, the general term; ‘alcohol related cognitive impairment ‘could be acceptable in the absence of a clear diagnosis such as Wernicke-Korsakoff syndrome.

The next part of 7.1 is the recording of the decision(s) relating to the capacity assessment.

Practical suggestions: An assessor will be aware that an assessment of capacity is decision specific, and these will vary from person to person and situation to situation. However, ARBD sufferers are often confronted with two major decisions when being assessed:

  1. Is the cognitive damage of such a degree that the individual is unable to make a decision concerning further alcohol drinking?
  2. Is the cognitive damage interfering with the person’s capacity to make a decision relating to the care that they need?

Section 7.2 requests information as to why individuals may not be able to make a specific decision. The first subsection requires information regarding the person’s ability to understand the relevant information.

Practical suggestions: It is not usually sufficient to limit the assessment of ‘understanding’ to asking the person if they understand without probing and examining the issue in more depth. Questions might include:

  • What is wrong with you that means you might need help?
    • Explore the person’s understanding of their problem:
    • Do they have any insight into a diagnosed condition and related cognitive difficulties?
    • Explore the possible implications of their decisions/behaviour and the effects on other people/society
  • What are the practical issues with which you need help?
  • Focusing on the practical (related to presentation) for example:
    • Why is there no food in the house?
    • How are you going to get out of debt?
    • How do you feel about your sexual behaviour in public?
    • What do other people feel about your behaviour?
  • What sort of help do you think you need
  • How much help do you need?
  • Who is going to help you?
  • How is this help going to be organised?

The next sub section of 7.2 addresses the issue of memory by asking if the person can retain the information that has been furnished.

Practical suggestions: As already mentioned, it is important not to be misled by a ‘working memory’ when STM may be compromised. Helping the individual to learn the information, providing written material and rehearsal are all aspects of good practice. It is then important to test that the individual can recall the information some few minutes later. This could be done in the context of a second or ‘split’ assessment, incorporating a short period of rest or change of subject. It is now well established that even if an individual makes a decision within the interview context but is later unable to remember the decision that has been made due to cognitive damage, then capacity should be questioned.

The next sub-section asks: ‘Is he or she is unable to use or weigh the following relevant information as part of the process of making the decision(s) (please give details);’

Practical suggestions: as is the case with ‘understanding’, weighing up and using the information not only draws on memory but also requires an intact executive function. It is recommended that the assessor attempts to interrogate the process and ‘depth’ of weighing up the information and the implications and risks associated with the decision. Relevant questions may include:

  • Why would you not want support?

(Are reasons weighty enough to balance against the need for support?)

  • What happens if you do not get support?

(What are the risks you face if you do not get support?)

The last sub section of 7.2 requires a comment regarding the ability of the individual to communicate his/her decision.

Practical issues: Language can be affected in cases of ARBD. In more severe cases, of confusion, attention and concentration problems may prove intrusive and disruptive of normal conversation. ARBD can affect the front part of the brain, rendering difficulty in sentence completion and problems in word finding. In cases in which there are communication difficulties, written material may be helpful.

 Section 7.3 of the document asks for a summary of the issues that have contributed towards the assessor’s decision of incapacity.

Practical issues: This section enables the assessor to present information relating to the history of the patient. A summary of the memory problems and their implications, and evidence relating to understanding, memory, weighing up and communicating the decision. It is an important section in that it brings the evidence together in a reasoned and logical fashion, demonstrating a thorough assessment and substantiated reasoning.


In assessing the capacity of an individual with ARBD, the assessor is likely to make a mistake if the assessment is confined to the information gleaned from the assessment interview alone. Preparatory work is essential and includes familiarity with the individual’s current circumstances and history. A corroborative history is strongly recommended in view of the LTM loss, confabulations, and potential lack of insight. Likewise, due to the issues relating to dysexecutive syndrome, background information will also provide a strong indicator regarding how the individual will cope in the context of general society, outside institutional settings. in addition, clarifying the degree of memory impairment, emphasis should be placed on and exploring problems in understanding and weighing up information as crucial components of the decision-making process.

(Download PDF)

This brief overview does not attempt to provide a comprehensive review of treatment or management approaches. It focuses on two comprehensive reviews of the scientific literature with view to providing an update on contemporary approaches to management. In understanding the management of ARBD, it is important to acknowledge that most patients with ARBD will improve in cognitive function over time. Cognition will recover as the direct effects of alcohol on the brain fades. More serious injuries can be caused through deficiency in thiamine and related nutrients (Hayes, et al 2016). These later effects can take two to three years to recover, and the individual may be left with permanent damage.

In 2020, Cabelleria et al undertook a systematic review of the treatment of ARBD. The authors identified 26 studies, 12 referring to pharmacological and 14 to neuropsychological interventions. Of the neuropsychological interventions, computerised treatments, errorless learning, and various interventions showed positive effects on working memory and general cognitive function. In errorless learning the individual is asked to repeat the learned material as soon as it is presented. He or she is encouraged to learn by avoiding trial and error (testing), presenting the learning experience as a positive experience through gradually increasing the difficulty as learning is achieved. General cognitive stimulation was also found to have benefitted the cognitive profile of participants (Oliveira et al 2015).
Regarding drug interventions, thiamine (vitamin B1 IM/IV), memantine (a drug licenced in UK to treat Alzheimer’s Dementia) and methylphenidate (often known as ‘Ritalin’ and used to treat ADHD) improved working memory, long term memory and general cognitive function. All these studies were small and require replication.
Other than thiamine treatment the evidence is not strong enough to recommend routine treatment of ARBD with these drugs. Notably, thiamine was used in people undergoing withdrawal treatment (Ambrose, et al 2001) and found to be beneficial. In another recent review of six publications, Smith et al (2021) were unable to demonstrate a consensus regarding dosage and suggest that doses > 100mg of parenteral thiamine should be given in cases of confirmed Wernicke’s Encephalopathy. Thiamine remains the main stay of treatment in an acute setting.
Patients presenting with acute WE should receive intravenous thiamine treatment: for between 3-5 days or even longer in order to achieve improvement (Royal College of Psychiatrists 2014). However, the treatment is usually more complicated than solely relying on parental thiamine, involving physical stabilisation and other interventions (NICE 2011) and should be carried out in acute hospital settings. Delay in treatment may cause more permanent brain damage. In cases of dependent drinkers who have responded to parenteral thiamine, oral prophylactic thiamine should be prescribed. Likewise, oral thiamine should be prescribed in cases of decompensated liver disease; acute or medically assisted withdrawal; or before and during a planned medically assisted alcohol withdrawal (NICE 2010).
As in Cabelleria’s review, Svanberg & Evans, in their 2013 review indicate that a variety of neuropsychological techniques may potentially be of use in helping improve cognition. This review included studies involving errorless learning, studies utilising assistive technology, behavioural reinforcement, CBT approaches and specific psychological interventions targeting the executive and reasoning aspects of cognition.
The review includes three studies exploring the role of specialist rehabilitation and specialist institutions. Blansjaar et al (1992) found that social functioning improved in specialised sheltered accommodation and deteriorated in those in a nursing home environment, however cognitive dysfunction was stable in all three groups. In 2008 Irvine and Mawhinney studied patients living in a supported living unit over 12 months. General health improved over the study time, and it was noted that lack of insight was associated with an increase in challenging behaviour and lowered engagement. Lastly, Wilson et al (2012) followed up 41 patients manged through a phased rehabilitation programme. It is important to note all that these are small studies. Wilson’s study of 2012 was an uncontrolled naturalistic follow up study (based on the published guidance manual: : reference documents). Consequently, any conclusions concerning interventional efficacy can only be made with caution. Despite this, from a service delivery perspective, Price et al. (1988) compared outcomes of patients managed by specialist services with those managed by generic psychiatric services and found that specialist services performed better.

This summary focuses on two literature reviews. These provide a general impression of the literature. It is evident that most studies are too small and need replication. The lack of larger qualitative studies and randomised controlled trials means that it is impossible to make definitive statements concerning the value of specific interventions. Despite this, cumulative evidence and clinical consensus indicates a modest optimism in terms of the advantages of targeted psychological interventions and holistic, specialised service provision (Royal College of Psychiatrists 2014). This web site ( : reference documents) includes a guidance manual for the management of ARBD generated through a follow up study (Wilson et al 2012) and
a self-help manual currently being used in the context of an alcohol treatment service in Wales.

Ambrose M, Bowden S, Whelan G (2001) Thiamine treatment and working memory function of alcohol dependent people: preliminary findings. Alcohol Clin Exp Res 25, (1) 112-6
Blansjaar BA, Takens H, Zwinderman AH (1992) The course of alcohol amnestic disorder: a three-year follow-up study of clinical signs and social disabilities Acta Psychiatr Scand vol. 86. 240-6
Caballeria E, OLiveras C, Nuno L et al. (2020) A systematic review of treatments for alcohol- related cognitive impairment: lessons from the past and gaps for future interventions. Psychological Medicine 50,13,2113-2127
Hayes, V., Demirkol, A., Ridley, N., Withall, A. & Draper, B. (2016). Alcohol-related cognitive impairment: current trends and future perspectives. Neurodegenerative Disease Management, 6, 509-523.
Irvine C, Mawhinney, S (2008) Functioning of individuals with Korsakoff syndrome: a
pilot study of supported group living in Northern Ireland. Ment Health Rev J, 13 16- 23. NICE (2011) Alcohol use disorders: diagnosis and management Quality Standards QS.
Oliveira J, Bento B, Gamito P. et al (2015) Cognitive stimulation of alcoholics through  VR-based Instrumental Activities of Daily Living. Conference paper
Price J, Mitchell S, Wiltshire B et al. (1988) A follow up study of patients with alcohol related brain damage in the community. Aust Drug Alcohol Rev 7:83–7.
Royal College of Psychiatrists College Report 185 (2014) Alcohol and brain damage in adults with reference to high-risk groups
Smith H, McCoy M, Varughese K et al (2021) Thiamine dosing for the treatment of alcohol induced Wernicke’s Encephalopathy: A review of the Literature. J Pharm Technol. 37 (2) 107-113
Svanberg J, Evans J, (2013) Neuropsychological rehabilitation in alcohol-related brain damage: a systematic review. Alcohol Alcohol. Nov-Dec ;48(6):704-11.
Wilson K, Halsey A, Macpherson H et al. (2012) The psycho-social rehabilitation of patients with alcohol-related brain damage in the community. Alcohol Alcohol 47, 304-11
Wilson K (2021) A clinical management guide for the psycho-social rehabilitation of people presenting in secondary care with severe alcohol related brain damage.

(Download PDF)

Overall prevalence (amount of ARBD in a population at any one time)

Galvin and colleagues (2010) combined the data from 20 autopsy studies (n=37,783) and found a prevalence (percent that suffered from ARBD) of 1.3% with an increased prevalence of 9.3% in people with a history of alcohol misuse disorders. A more recent compilation of autopsy studies has been described by Scalzo et al (2015). These 12 studies range from 1961 to 1998 and represent data from USA, Australia, Brazil, France, Germany and Norway. The authors note some difficulty in combining the results and two studies were not confined to adult populations. Of the 40,783 autopsies 1.4% had Wernicke’s Korsakoff’s (WK) pathology but only 5% had reported histories of alcohol misuse disorders in their medical documents. The authors point out that 83% of people with WK did not receive a clinical diagnosis during lifetime. ARBD is widespread among patients with problems linked to excessive alcohol use and is detected in up to 78% of autopsies of heavy drinkers (Ridley et al 2013). These post-mortem studies suggest an overall prevalence rate of between 1 and 1.4 % in the general population and a dramatic increase in alcohol dependent individuals.

When examining the overall drinking habits of a living population, a ‘J’ shaped curve is found. This implies that small amounts of alcohol (less than 20 grams a day: one small glass of wine (UK) contains approximately eight grams) may be protective. However, this finding may be a consequence of population sampling techniques or study design (Public Health England 2016) and may not reflect reality. It is evident that these large population studies show that heavier drinking is associated with increasing cognitive problems (Sachdeva et al., 2016).

Cumulative lifetime drinking has been thought to influence the likelihood of developing cognitive damage (Ryback RS 1971) particularly in the case of alcohol dependent individuals (Woods et al.2016). However, a history of more recent heavy drinking, length of dependence, recurrent binge drinking, multiple withdrawals, and poor nutrition, are now thought to be more important in terms of risk factors for ARBD (Beatty et al 2000, Pitell et al 2009, Green et al 2010, Woods et al 2016, Duka et al 2003, Ritz et al 2016).

High Risk populations:

Alcohol dependent individuals

As larger population and postmortem studies imply, there is an increased prevalence of ARBD in alcohol dependent individuals. Pitel et al (2011) found that 16% had clinical signs of Wernicke’s Encephalopathy and as many as 57% had at least one sign as defined by the European Federation of Neurological Sciences.  Notably, people with diagnosed Korsakoff’s Syndrome (thiamine deficiency related) present with more severe damage than those presenting with damage solely a direct effect of alcohol (Hayes, et al 2016), without evidence of thiamine deficiency. Several authors have demonstrated that up to 50% of detoxified alcohol dependent individuals demonstrate varying signs of cognitive damage (Zahr et al 2011, Moretti et al., 2017; Ridley et al., 2013; Zahr & Pfefferbaum, 2017, Seddon et al 2021). These findings are consistent with findings in more long-term abstinent alcohol dependent individuals. Bernardin et al (2014) and Le Berre et al (2019) found 50% and 80% of abstinent dependent inndividuals showed a variety of cognitive and motor deficits. There is emerging evidence indicating that there may be a genetic vulnerability, as the presence of the ε4 allele ( a form of a gene found on a chromosome) may contribute towards the deleterious effects of heavy alcohol consumption on cognition (Slayday et al 2021).

Apart from dependent drinking and genetic vulnerability, demographic characteristics are associated with increased risk of developing ARBD. Women are more susceptible and may take longer to recover in the short term (Fama et al 2020).  A higher level of educational attainment appears to be protective (Ridley et al., 2013). Age seems to be of importance with middle aged and older people being particularly vulnerable (Piumatti et al 2018).

Acute hospital patients

It is well established that ARBD presents acute hospitals with significant clinical and management problems. Thompson et al (2020) screened 1276 patients admitted into an acute hospital. Of these, 205 patients were identified as being of high risk of suffering from ARBD. The screening criteria included more than three alcohol-related admissions in one year: two alcohol-related admissions in any given 30-day period and patient or their ‘significant other’ having concerns regarding cognitive function. This high-risk group was examined using the Montreal Cognitive Assessment Tool. A period prevalence of 36.1% of patients fulfilling the criteria for ARBD was found (percentage of people identified as suffering from ARBD during the study period). Homeless patients and those staying in hostels were of higher risk than those living with families (Thompson et al 2020).

In reviewing a series of patients that had been identified as ‘hard to discharge’ from acute hospital settings Popoola et al (2008) found that 34.1% had significant alcohol problems with a high prevalence of ARBD.

In a subsequent review of the literature MacPhail et al (2013) identified several risk factors associated with delayed acute hospital discharge in patients with ARBD. These included complex clinical profiles, challenging behaviors, limited social support and lack of appropriate accommodation. The authors recommend the development of pathways of care and specialised service provision.


A recent survey found that 42% of homeless people accessing accommodation providers need support for mental health issues (Homeless Link Annual Review 2020). More specific research suggests that cognitive damage may be a significant variable. Forty studies were included in a systematic review (Stone et al 2018) of the prevalence and potential causes of cognitive impairment in homeless people. The authors conclude that there is an over representation of cognitive impairment in the homeless population. The variability in prevalence that was found in this review is certainly influenced by the design and differing populations examined. A good example of the studies included is that of Nishio et al. (2015), finding that 34.2% of a homeless sample experienced varying degrees of cognitive impairment. This was a prevalence study and did not examine the causative factors. Notably, the review included studies examining traumatic brain injury, Attention Deficit/Hyperactivity Disorder and learning disabilities. The authors acknowledge the potential importance of substance misuse and quote a sub study of the Brown et al (2017) paper describing an association between high use of alcohol and cognitive impairment in homeless people.

More specifically, Gilchrist and Morrison (2005), estimated that 21% of the Glasgow homeless showed evidence of ARBD. In a more recent study of 350 homeless individuals, 25% were found to have significant cognitive impairment and severe alcohol misuse was associated with both global impairment and executive (reasoning) problems (Hurstak et al 2017).


What research there is indicates that ARBD related changes in the brain may be found in as many as 1-1.5% of the general population. Genetic issues may play a part. Women and older people are particularly vulnerable. Recognised high-risk groups include alcohol dependent individuals, those attending alcohol treatment services and abstinent dependents. The homeless population are of particular risk and those that are hard to discharge from acute medical care are likely to have a relatively high prevalence. Other populations that may be of high risk include frequent hospital attenders and prison populations, but the research/surveys have not yet been undertaken.


Beatty WW, Tivis R, Stott HD, Nixon SJ, Parsons OA. (2000) Neuropsychological deficits in sober alcoholics: influences of chronicity and recent alcohol consumption. Alcohol Clin Exp Res;24 (2):149–154. doi:10.1111/j.1530-0277.2000.tb04584.

Bernardin F, Maheut-Bosser A, Paille F. (2014). Cognitive impairments in alcohol-dependent subjects. Front Psychiatry.;5:78. doi:10.3389/fpsyt.2014.00078

Brown, R. T., Hemati, K., Riley, E. D., Lee, C. T., Ponath, C., Tieu, L. Kushel, M. B. (2017). Geriatric conditions in a population-based sample of older homeless adults. The Gerontologist, 57, 757–766.

Duka T, Townshend JM, Collier K, Stephens DN. (2003) Impairment in cognitive functions after multiple detoxifications in alcoholic inpatients. Alcohol Clin Exp Res. 27(10):1563–1572. doi:10.1097/01.ALC.0000090142.11260.D7

Fama, R., Le Berre, A.-P., & Sullivan, E. V. (2020). Alcohol’s unique effects on cognition in women: A 2020 (re)view to envision future research and treatment. Alcohol Research: Current Reviews, 40(2), 1–17.

Galvin R, Brathen G. Ivashynka A, Hillbom M, Tanescue R, Leone M. (2010) EFNS guidelines for diagnosis, therapy, and prevention of Wernicke Encephalopathy. European Journal of Neurology 17, 1408-18.

Gilchrist G, Morrison DS (2005) Prevalence of alcohol related brain damage among homeless hostel dwellers in Glasgow. European Journal of Public Health 15 (6) 587-8

Green A, Garrick T, Sheedy D, Blake H, Shores EA, Harper C. (2010) The effect of moderate to heavy alcohol consumption on neuropsychological performance as measured by the repeatable battery for the assessment of neuropsychological status. Alcohol Clin Exp Res ;34(3):443–450.

Hayes, V., Demirkol, A., Ridley, N., Withall, A. & Draper, B. (2016). Alcohol-related cognitive impairment: current trends and future perspectives. Neurodegenerative Disease Management, 6, 509-523.

Homeless Link: (2020) Support for Single Homeless People in England: Annual Review.

Hurstak E, et al (2017), Factors associated with cognitive impairment in a cohort of older homeless adults: Results from the Hope Home study. Drug and Alcohol Dependency 1: 178: 562-570.

Le Berre AP, Laniepce A, Segobin S, Pitel AL, Sullivan EV. (2019): Alcohol use disorder: permanent and transient effects on the brain and neuropsychological functions. In: Stern RA, Alosco ML, editors. The Oxford Handbook of Adult Cognitive Disorders. Oxford, UK: Oxford University Press; 302–332.

MacPhail A, l McDonough M, Ibrahim J (2013) Delayed discharge in alcohol-related dementia: consequences and possibilities for improvement. Australian Health Review 37(4) 482-487.

Moretti, R., Caruso, P., Dal Ben, M., Gazzin, S. & Tiribelli, C. (2017). Thiamine and Alcohol for Brain Pathology: Super-imposing or Different Causative Factors for Brain Damage? Current Drug Abuse Reviews, 10, 44-51.

Nishio, A., Yamamoto, M., Ueki, H., Watanabe, T., Matsuura, K., Tamura, O., Shioiri, T. (2015). Prevalence of mental illness, intellectual disability, and developmental disability among homeless people in Nagoya, Japan: A case series study. Psychiatry and Clinical Neurosciences, 69, 534–542

Pitel AL, Rivier J, Beaunieux H, Vabret F, Desgranges B, Eustache F. (2009) Changes in the episodic memory and executive functions of abstinent and relapsed alcoholics over a 6-month period. Alcohol Clin Exp Res.;33(3):490–498.

Pitel AL, Zahr Nm, Jackson K, sasson SA, Rosenbloom MJ, Pfefferbaum A, Sullivan EV. (2011) Signs of preclinical Wernicke’s Encephalopathy and thiamine levels as predictors of neuropsychological deficits in alcoholism without Korsakoff’s syndrome. Neuropsychopharmacology 36,580-8.

Piumatti G et al. (2018) The relationship between alcohol use and long-term cognitive decline in middle and late life: a longitudinal analysis using UK Biobank. Journal of Public Health, Volume 40, Issue 2, June, Pages 304–311,

Popoola A, Keating A, Cassidy E.  (2008) Alcohol, cognitive impairment and the hard to discharge acute hospital inpatients. Irish Journal of Medical Science 177(2):141-5

Public Health England (2016) The Public Health Burden of Alcohol and the Effectiveness and Cost-Effectiveness of Alcohol Control Policies. An Evidence Review.

Ridley, N. J., Draper, B. & Withall, A. (2013). Alcohol-related dementia: an update of the evidence. Alzheimer’s Research and Therapy, 5, 3. doi:10.1186/alzrt157.

Ritz L, Coulbault L, Lannuzel C, et al. (2016) Clinical and biological risk factors for neuropsychological impairment in alcohol use disorder. PLoS One.;11(9):e0159616. doi:10.1371/journal.pone.0159616

Ryback RS. (1971) The continuum and specificity of the effects of alcohol on memory; a review.Q J Stud Alcohol.;32(4):995–1016. doi:10.15288/qjsa.1971.32.995

Sachdeva, A., Chandra, M., Choudhary, M., Dayal, P. & Anand, K. S. (2016). Alcohol-Related Dementia and Neurocognitive Impairment: A Review Study. International Journal of High Risk Behaviours and Addiction, 5, e27976. doi:10.5812/ijhrba.27976.

Scalzo S, Bowden S, Hillborn M. (2015) Wernicke-Korsakoff Syndrome in Alcohol and the Adult brain. Current Issues in Neuropsychology  Psychological Press, East Sussex. ISBN: 978-1-84872-307-8

Seddon J, Wadd S, Elliott L, Madoc-Jones I. Cognitive impairment and treatment outcomes amongst people attending an alcohol intervention service for those aged 50+.  Advances in Dual Diagnosis, Vol. 14 No. 2, pp. 58-69.

Slayday R et al (2021), Interaction between Alcohol Consumption and Apolipoprotein E (ApoE) Genotype with Cognition in Middle-Aged Men. Journal of the International Neuropsychological Society 27,1,56-68

Stone B, Dowling S, Cameron A. (2018) Cognitive impairment and homelessness: A scoping review. Health and Social Care 13 nov.

Thompson A, Richardson P, Pirmohamed M, Owens L. (2020), Alcohol-related brain injury: An unrecognized problem in acute medicine. Alcohol, 88, 49-53

Woods AJ, Porges EC, Bryant VE, et al. (2016) Current heavy alcohol consumption is associated with greater cognitive impairment in older adults. Alcohol Clin Exp Res.;40(11):2435–2444. doi:10.1111/acer.13211

Zahr NM., Kaufman KL., Harper CG (2011) Clinical and pathological features of alcohol related brain damage. Nature Reviews Neurology 7, 284-94

Zahr, N. M. & Pfefferbaum, A. (2017). Alcohol’s Effects on the Brain: Neuroimaging Results in Humans and Ani- mal Models. Alcohol Research: Current Reviews, 38, 183- 206.

(Download PDF)


Working with ARBD sufferers in the community

This Document is informed by the current literature and clinical work undertaken by Dr Julia Lewis and the clinical team of the Gwent Specialist Substance Misuse Service

The four constituent nations of the UK have legal frameworks catering for the management of people who are incapacitated in decision making because of mental impairment. Within these frameworks it is feasible to generate a pathway of care for people suffering from incapacitating ARBD. Typical patients may present with acute withdrawal, Wernicke’s encephalopathy and other confusional states secondary to alcohol dependency in hospital settings. Such patients can be protected under the relevant legislation from further alcohol exposure and high-risk behaviours until it is deemed that capacity to make the relevant decisions has returned.

Despite a significant proportion of alcohol dependents experiencing some degree of ARBD, the great majority are usually assessed as having capacity to make their own decisions. These decisions include further exposure and consumption of alcohol and care and treatment that might be needed. Consequently, there is a significant proportion of alcohol dependents with ARBD continuing to drink alcohol to excess. It is the purpose of this paper to bring together some of the recommendations relating to the provision of alcohol treatment services for these individuals.

Common cognitive problems encountered in people with ARBD in the community
A comprehensive review (and meta-analyses) of the literature (143 papers from 250 countries covering 1997-2011) identified four profiles of cognitive impairment in heavy drinkers (Ihara H et al, 2000).
1. No cognitive impairment
2. Isolated executive deficits with normal memory and global cognitive efficiency
3. Mild executive dysfunction with memory impairment and preserved global efficiency
4. Global impairment (problems with executive function, memory impairment and impaired cognitive efficiency)

These problems manifest through difficulties in mental flexibility, ability to pay attention, problem solving and decision making, slowness in intellectual processing and difficulties in planning. Other problems of executive dysfunction include disinhibition and problems in multitasking. Short term memory is affected through problems in encoding (registering information) and recall (Pitel AL et al, 2007, Noel X. et al, 2012).

Frequently there are visuo-spatial impairments, problems in visual learning and undertaking constructional tasks (Oscar-Berman N. et al, 2007, Ratti MT. et al 2002).
There is an increased risk of developing dementia.

Examples of studies include:
Problems in concentration (DeFranco et al, 1985)
Problems in learning new information (short term memory) (Alterman et al, 1989; Mann et al, 1999; Zinn et al, 2004; Schmidt et al, 2005)
Problems in reasoning (Beatty et al, 1996; Mann et al, 1999; Zinn et al, 2004)
Problem-solving difficulties (Beatty et al, 1996; Mann et al, 1999)
Difficulties in explaining actions and reasons (Beatty et al, 1996)
Problems in understanding complex information and concepts (such as alcohol dependency and implications for behaviour) and difficulty in acquiring drink refusal strategies (Smith & McCrady, 1991)
Reduced ability to change from one stream of thought to another with normal degrees of flexibility (difficulty in working in groups or following complex discussions) (Beatty et al, 1996)
Increased proneness to make impulsive decisions and less awareness of the longer-term implications of decisions and actions (Weissenborn & Duka, 2003; Davies et al, 2005; Parks et al, 2010)
Problems in understanding risk related to actions and decisions (Blume et al, 2005)
Reduced organisational skills (Parks et al 2010), planning, and managing arrangements (Weissenborn & Duka, 2003)
Poor compliance to treatment programs (Copersino et al, 2012)
Lower confidence (Bates & Pawlack 2006)
Breakdown of interpersonal relationships (Patterson et al, 1988)
Cognitive problems of this nature have a significant impact on attendance, compliance, and outcome in terms of interventions intended to reduce or manage alcohol dependence. (Bates & Pawlak 2006)
Screening and recognition of ARBD in community settings
It is recommended that all clients referred to alcohol treatment services undergo a mental health screening. (National Institute for Health and Clinical Excellence, 2011). As part of this, cognitive screening can be carried out using simple texts which include the MoCA (Nasreddine et al 2005) or the ACE R . (Mioshi E, et al. 2006)
Individuals of high risk of developing severe cognitive damage may be identified through a history of weight loss, low BMI, recurrent vomiting, and an increase in carbohydrate intake.
Obvious signs include early memory loss. As ARBD is associated with thiamine deficiency (which can affect the neurological system), a history of pins and needles, numbness and periods of double vision are all potential warning signs (Thomson 2000). Cognitive impairment is also associated with problems in attendance and compliance in treatment programs, suggesting that people that drop out or fail to attend may be of high risk (Bates & Pawlak 2006).

Adaptations in service provision
The literature provides examples of a variety of modifications that can be made to cater for these cognitive deficits. Engagement and planning
There should be a focus on achieving abstinence (McCrady and Smith 1986). Strategies to achieve this and drinking strategies in general should be made as simple as possible. Community alcohol treatment services frequently follow protocols relating to the engagement of referred clients. Poor compliance or appointment failure may be due to cognitive impairment. An active engagement strategy should be considered (Wilson et al 2011, McCrady & Smith, 1986). This could include more frequent visits to the individual’s home, phone contact, leaving written messages, and contacting carers or friends (when
appropriate). Transport and social support may be indicated. Staff introduction at each interview, the use of name badges, (McCrady & Smith, 1986), preferably with a photograph of the therapist (Drinkwise age well 2020) is advised. When working with the cognitively impaired, collaborative, and structured scheduling and planning is recommended (Acquired Brain Injury Services 2011). This may involve enhanced support and planning, and the provision of a timetable may be useful (Arbias 2007). As cognition is likely to improve (if drinking can be reduced or managed) more complex
interventions and educational approaches can be delayed until the individual is more receptive (McCrady & Smith, 1986). In the first few weeks, particular emphasis should be placed on reducing exposure to risk as there is an increased likelihood of impulsive decision making (Weissenborn & Duka 2003, Davies et al 2005, Parks et al 2010). Individuals with cognitive impairment frequently require longer contact sessions because of the cognitive
problems (VanDamme & d’Ydrewalle, 2008) and the clinician should allow for a cognitively individual to take longer to benefit from interventions (McCrady & Smith 1986).

Therapeutic adaptations
The simplification of educational materials is recommended (McCrady & Smith, 1986) and providing information through a varying media, (written, visual, etc) (McCrady & Smith, 1986) and memory aids can be useful. Learning texts and materials can be used to ensure that one concept is understood and learned before going on to another (McCrady & Smith, 1986).

In ARBD, powers of concentration maybe reduced, consequently, educational discussions should be time limited (DeFranco et al 1985) and focus on clearly defined, single topics at a time (Beatty et al 1996). Frequent changes in topics of conversation may lead to confusion.
As already mentioned, cognitively impaired sufferers may take longer to learn and undertake tasks (DeFranco. et al 1985). Learning may be facilitated by encouraging individuals to repeat information (Kessels 2007) and explain it as soon as it is given to them (Zinn, S 2004). If the individual is unable to remember the information, guessing should be discouraged (Mann et al. 1999). Memory cues have been advocated (Morgan et al 1990). Diary keeping may help in memory prompting and may also be used for the planning of activities (Wilson et al 2012). Learning can be facilitated through reinforcement and role play. The provision of rewards for appropriate behaviour may be of benefit. Rewards may be psychological or social and tailored for the individual (Hochalter & Joseph 2001).

When confronted with problems, simple rules can be applied in order to `offer help (Bardenhagen et al. 2007). These include five steps (D’Zurilla & Goldfried 1971)
• Identify the problem
• Collect information concerning the problem
• Generate solutions
• Select the appropriate solution
• Implement the solution

Prescribing in ARBD for Alcohol Dependence
Medication has two main roles in the management of alcohol dependence:
1. The medical management of alcohol withdrawal
2. Prescribing to support abstinence

Medically Managed Alcohol Withdrawal (MMAW)
NICE Clinical Guidance 100 states that individuals considered at risk of complicated alcohol withdrawal (such as seizures, delirium tremens and Wernicke’s encephalopathy) should be receive MMAW as an inpatient. (NICE, 2010). The presence of ARBD is a risk factor for complicated withdrawal and so individuals with ARBD requiring MMAW should be admitted to an inpatient facility where staff can identify and appropriately manage any emerging
As with any medical procedure, fully informed consent must be obtained prior to MMAW. If, as a result of cognitive impairment, the patient lacks the capacity to make this decision, then the appropriate legal framework must be employed (e.g., Mental Capacity Act, 2005). It is important to present the necessary information in a clear way, delivering it in short chunks and asking the patient to repeat what they have been told, in order to maximise understanding. Patients must be supported to make their own decisions as much as possible and being sensitive to their cognitive needs when discussing treatments options with them is very important. The duty of clinicians to ensure that patients have accurate information
and adequate space and time to make decisions has been highlighted by recent case law (Thefaut vs Johnson, 2017).

When using standardised assessments of alcohol withdrawal symptoms (e.g., Clinical Institute Assessment of Withdrawal, CIWA-Ar, Sullivan et al, 1989), consideration must be given to how cognitive impairment can impact on these. For instance, short term memory impairment may affect the recollection of withdrawal symptoms experienced since the previous assessment. Patients may be aware that they have felt tremulous and sweaty but may not recall exactly when that was during the withdrawal process. Difficulty with describing abstract concepts can mean that they struggle to articulate the level of anxiety they are experiencing. If it is felt that the patient will find it difficult to engage with such standardised assessment scales, then protocols for MMAW that do not rely on such measures of withdrawal need to be employed (e.g., fixed reduction schedules).

All patients with a history of ARBD will need appropriate nutritional support during MMAW which will include thiamine supplementation (most likely to be parenteral) (Thomson et al, 2002; Lingford-Hughes et al, 2012). It is important to avoid a carbohydrate load and magnesium supplementation may be required (Glen, 1994; Turner et al, 1989). Hydration can be overlooked; patients who have been taking almost the entirety of their daily fluid intake in the form of alcohol may neglect to replace this with other fluids, especially where there is dysexecutive syndrome. Prescribing to Support Abstinence NICE Clinical Guidance 115 (NICE, 2011) recommends that, after successful withdrawal from alcohol, individuals with moderate to severe dependence can appropriately be offered either acamprosate or naltrexone alongside psychosocial interventions. If these drugs are not suitable, or if the patient prefers, the guidance then suggests the use of disulfiram. Increasingly in practice, baclofen is also being used as relapse prevention medication,
especially in those with hepatic impairment (Gache et al, 2014).

Once again, informed consent must be obtained before commencing relapse prevention medication. In addition, the prescriber needs to be assured that the patient understands the way in which the medication is taken and the expected outcomes. This is particularly important for disulfiram and, if there is any concern that the patient does not fully understand the risks, then it should not be prescribed.

If there are issues with short term memory, then consideration should be given to the use of a dosette box if not already being used for other medication and the use of prompting (such as the use of smart phone apps).

It is evident that a variety of cognitive impairments can manifest in individuals that are under the care of alcohol treatment services. These can vary from subtle reasoning problems through to an obvious global impairment. Hence, it is necessary for the therapist to assess the specific needs of an individual in designing interventions. This can be aided through formal and repeat assessments using the mini-Ace or ACE-111 for cognitive testing. The informal clinical identification of high-risk individuals is likely to play an important role. Indicators have already been mentioned but include physical issues such as weight loss and self-neglect, poor diet and vomiting and neurological disorders. Other practical warning signs may include memory and reasoning problems, poor compliance, difficulty in managing group settings and understanding the educational issues. Evidence of an on-going history of impulsive or antisocial history may be considered to warrant further investigation.

Appropriate adaptations to prescribing policies may be required in catering for patient with ARBD.

Flexibility is the key in terms of adaptation of therapeutic interventions. The modification of engagement, support and educational and drug treatment approaches should be driven by the need of the individual.

Alterman AI, Holahan JM, Baughman TG, et al (1989) Predictors of alcoholics’ acquisition of treatment related knowledge. Journal of Substance Abuse Treatment, 6: 49–53.
ARBIAS. (2007) Looking Forward: General Information Book on Alcohol Related Brain Impairment, 3rd edn. Victoria, Australia: Arbias Ltd.
Bardenhagen FJ, Oscar-Berman M, Bowden SC (2007) Rule knowledge aids performance on spatial and object alternation tasks by alcoholic patients with and without Korsakoff’s amnesia. Neuropsychiatric Disease and Treatment, 3: 907–18.
Bates ME, Pawlak AP, Tonigan JS, et al (2006) Cognitive impairment influences drinking outcome by altering therapeutic mechanisms of change. Psychology of Addictive Behaviors, 20: 241–53.
Beatty WW, Hames KA, Blanco CR, et al (1996) Visuospatial perception, construction and memory in alcoholism. Journal of Studies on Alcohol, 57: 136–43.
Blume AW, Schmaling KB, Marlatt GA (2005) Memory, executive cognitive function, and readiness to change drinking behaviour. Addictive Behaviours, 30: 301–14.
Copersino ML, Schretlen DJ, Fitzmaurice GM, et al (2012) Effects of cognitive impairment on substance abuse treatment attendance: predictive validation of a brief cognitive screening measure. American Journal of Drug and Alcohol Abuse, 38: 246–50.
D’Zurilla TJ, Goldfried MR (1971) Problem solving and behaviour modification. Journal of Abnormal Psychology, 78: 107–26.
Davies SJC, Pandit SA, Feeney A, et al (2005) Imbalance between neuroexcitatory and neuroinhibitory amino acids causes craving for ethanol. Addictive Behaviors, 29: 1325–39.
DeFranco C, Tarbox AR, McLauglin EJ (1985) Cognitive deficits as a function of years of alcohol abuse. American Journal of Drug and Alcohol Abuse, 11: 279–93.
Drink Wise Age Well. (2020). Supporting older adults who have an alcohol problem and cognitive impairment: A good practice guide. Retrieved from and-cognitive-impairment-a-good-practice-guide/
Gache , de Beaurepaire, Jaury P, et al (2014). Presscribing guide for baclofen in the treatment of alcoholism – for use by physicians. Br J Med and Med Res.;4:1164-1174.
Glen I et al (1994) The management of alcohol withdrawal & delirium tremens: A good practice statement. CRAG/SCOTMEG Working Group on Mental Illness.
Hochalter AK, Joseph B (2001) Differential outcomes training facilitates memory in people with Korsakoff and Prader-Willi syndromes. Integrative Physiological and Behavioral Science, 36: 196–204.
Ihara H et al, 2000 Group and case study of the dysexecutive syndrome in alcoholism without amnesia. JNNP 2000 68: 731-7.
Kessels RPC, van Loon E, Wester AJ (2007) Route learning in amnesia: a comparison of trialand- error and errorless learning in patients with the Korsakoff syndrome. Clinical Rehabilitation, 21: 905–11.
Lingford-Hughes, A. R., Welch, S., Peters, L., & Nutt, D. J. (2012). BAP updated guidelines: evidence-based guidelines for the pharmacological management of substance abuse, harmful use, addiction and comorbidity: recommendations from BAP. J Psychopharmacol, 26(7), 899-952.
Mann K, Gunther A, Stetter F, et al (1999) Rapid recovery from cognitive deficits in abstinent alcoholics: a controlled test-retest study. Alcohol and Alcoholism, 23: 567–74.
McCrady BS, Smith DE (1986) Implications of cognitive impairment for the treatment of alcoholism. Alcoholism: Clinical and Experimental Research, 10: 145–9.
Mioshi E, Dawson K, Mitchell J et al. (2006) The Addenbrooke’s Cognitive Examination Revised (ACE-R): a brief cognitive test battery for dementia screening. Int J Geriatr Psychiatry 21:1078–85.
Morgan J, McSharry K, Sireling L (1990) Comparison of a system of staff prompting with a programmable electronic diary in a patient with Korsakoff’s syndrome. International Journal of Social Psychiatry, 36: 225–9.
Nasreddine Z. et al. 2005. The Montreal Cognitive Assessment, MoCA: A Brief Screening Tool for Mild Cognitive Impairment. Journal of American Geriatric Med Society 53,4, 695- 699
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.
NICE. (2010). Alcohol-use disorders: diagnosis and management of physical complications (CG100) National Institute for Health and Care Excellence. London.
Noel X. et al, The contribution of executive functions deficits to impaired episodic memory in individuals with alcoholism. Psychiatry Research 2012: 198: 116-22.
Oscar-Berman N. et al, 2007, Alcohol: effects on neurobehavioral functions and the brain. Neuropsychological review 2007 17:239-57
Parks M, Greenberg D, Nickel M, et al (2010) Recruitment of additional brain regions to accomplish simple motor tasks in chronic alcohol dependent patients. Alcoholism: Clinical and Experimental Research, 34: 1098–109.
Patterson BW, Parsons OA, Schaeffer KW, et al (1988) Interpersonal problem solving in alcoholics. Journal of Nervous and Mental Disease, 176: 707–13.
Pitel AL et al, 2007, Genuine Episodic memory deficits and executive dysfunction in alcohol subjects early in abstinence. Alcohol Clinical Experimental Research. 2007 31; 1169-78)
Ratti MT. et al, Chronic Alcoholism and the frontal Lobe: which executive functions are impaired? Acta Neurol Scand 2002; 105 276-81.
Schmidt K, Gallo J, Ferri C, et al (2005) The neuropsy- chological profile of alcohol related dementia suggests cortical and subcortical pathology. Dementia and Geriatric Cognitive Disorders, 20: 286–91.
Smith DE, McCrady BS (1991) Cognitive impairment among alcoholics: impact on drink refusal skill acqui- sition and treatment outcome. Addictive Behaviours, 16: 265–74.
Sullivan JT, Sykora K, Schneiderman J, Naranjo CA, Sellers EM (1989) Assessment of alcohol withdrawal: the revised clinical institute withdrawal assessment for alcohol scale (CIWA-Ar).
Br J Addiction 84: 1353-1357.
Thomson AD (2000) Mechanisms of vitamin deficiency in chronic alcohol misusers and the development of the Wernicke-Korsakoff syndrome. Alcohol and Alcoholism Supplement, 35: 2–7.
Thomson, AD, Cook, C. C., Touquet, R., & Henry, J. A. (2002). The Royal College of Physicians report on alcohol: guidelines for managing Wernicke’s encephalopathy in the accident and Emergency Department. Alcohol Alcoholism, 37(6), 513-521.
Turner RC, Lichstein PR, Peden JG Jnr, Busher JT and Waivers LE (1989) Alcohol withdrawal syndromes: a review of pathophysiology, clinical presentation, and treatment J General Int Medicine 4: 432-444.
VanDamme I, d’Ydewalle G (2008) Elaborative process- ing in the Korsakoff syndrome: context versus habit. Brain and Cognition, 67: 212–24.
Weissenborn R, Duka T (2003) Acute alcohol effects on cognitive function in social drinkers: their relationship to drinking habits. Psychopharmacology, 165: 306–12.
Wilson K (2011) Alcohol-related brain damage: a 21st-century management conundrum.
British Journal of Psychiatry, 199: 176–7.
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.
Zinn S, Stein R, Swartzwelder HS (2004) Executive func- tioning early in abstinence from alcohol. Alcoholism: Clinical and Experimental Research, 28: 1338–46.

(Download PDF)


There are several principal issues that are worth summarising

1. One of the first issues to consider is whether the individual has the capacity to make decisions. Pertinent decisions may include:
deciding about:
a. Future alcohol drinking

b. The care and help that is needed regarding the management of his or her health and safety.

Issues regarding capacity assessment in cases of ARBD can be found under ‘resources’ on this web site ( If the individual is deemed not to have capacity with regard to the relevant decision, then the employment of the Mental Capacity Act should be considered.

2. Individuals that are deemed to be capacitated should be referred to the appropriate alcohol treatment services. Recovery hinges on the maintenance of abstinence, support for this is vitally important and that, as long as treatment services can adapt their approach to the needs of someone with cognitive impairment, there’s no reason why community services wouldn’t be able to work with them (see document Working with ARBD sufferers in the community: : resources).

3. Provided a person with ARBD maintains abstinence and receives a well-balanced nutrition, (supplemented by oral thiamine in the first few months) then there is a very good chance that cognition will improve.
a. Rapid improvement may occur within the first three months of abstinence (Cox et al 2004).

b. Residual cognitive deficits may continue to improve over the following 1-3 years as the brain re-grows. (Sullivan & Pfefferbaum, 2005; Bartels et al, 2007)

4. Improvement in cognition can be expected in 75% of cases, with a significant majority living relatively independently after this time (Wilson et al 2012). Smith and Hillman (1999) reported that 25% make a complete recovery, 25% make a significant recovery, 25% make a slight recovery, and the remaining 25% make no recovery.

5. Therapeutic and rehabilitative processes have been informed by the rehabilitation of patients with acquired brain injury. However, it is important to note that the active management of a person with severe ARBD may take an average of 1-3 years and in complex cases, longer periods of time may be required. (Wilson et al 2012)

6. Management is best undertaken in the context of a multidisciplinary team with some experience in working with patients with cognitive damage. A close working relationship with social services is required.

7. Principal themes of intervention include:
a. Development of the individual’s optimum level of autonomy (Ylvisaker and Feeney 1998). This is a holistic approach including the development of the emotional, intellectual, social, physical, financial and behavioural function of the individual in the context of natural recovery process (Prigatano, et al 1996).

b. The programme should be facilitative; the individual should be given as much control of the management of their own rehabilitation as possible in the context of on-going risk management (Ylvisaker and Feeney 1998, Bates, et al. 2002).

c. The rehabilitation of the individual’s life skills must be tailored to the individual’s needs and priorities and is carried out in the context of the development of a therapeutic relationship (Ylvisaker and Feeney 1998, Bates et al. 2002).

d. Rehabilitation is an active process, and may demand therapeutic time, on-going re-assessment (with defined goals), care planning and long-term engagement (Wilson et al 2012).

e. Rehabilitation should focus on life skill development and can take place in the home, institutions and other ‘real world’ settings (Ylvisaker and Feeney 1998).

f. Non-experienced, care workers, family and community agents can be supervised in facilitating the rehabilitation process (Wilson et al 2012).

g. Baddeley et al (2002) advocates memory and orientation aids as playing an important role in rehabilitation.

8. Five management phases have been described (Wilson et al 2012)
a. Stabilisation Phase: This concerns the acute physical management and stabilisation of the individual going through withdrawal or being treated for encephalopathy and other alcohol related problems.

b. Assessment Phase: during the first three months cognition is likely to improve, during which on-going assessment is undertaken.

c. Therapeutic phase: This can last up to three years during which the brain regrows, and cognition can further improve. During this phase alcohol education and facilitating progression in activities of daily living are emphasised.

d. Adaptive Phase: Rate of cognitive and behavioural improvement has slowed or ceased; social and physical environment is adapted to optimize independence.

e. Social integration and relapse prevention phase. This phase may require long term follow-up.

A detailed description of the five therapeutic phases can be found in the reference document section of this website (

9. Flexible accommodation and support: The patient may have been placed in a highly supportive and structured environment after phase 1 (Physical stabilisation and treatment) (e.g. a mental health nursing home). As cognition improves, independence increases, and protective and support needs will change. These changes should be reflected in changes in the living circumstances of the patient, with transfer to less dependent environments, such as residential, supported living or return to their own homes.

10. On-going assessment of Mental Capacity: The patient’s capacity to make critical decisions concerning their management is likely to change over time. Consequently, it is necessary to frequently re-assess capacity, and facilitate decision making.


Baddeley AD, Kopelman MD, Wilson BA. (2002) Handbook of Memory Disorders. 2nd edn. Chichester: Wiley;.
Bartels C, Kunert H, Stawicki S, et al (2007) Recovery of hippocampus-related functions in chronic alcoholics during monitored long-term abstinence. Alcohol and Alcoholism, 42: 92–102.
Bates M, Bowden S, Barry D (2002) Neurocognitive impairment associated with alcohol use disorders: implications for treatment. Experimental and Clinical Psychopharmacology, 10: 193–212.
Cox S, Anderson I, McCabe L (eds) (2004) A Fuller Life: Report of the Expert Group on Alcohol Related Brain Damage. Dementia Services Development Centre, University of Stirling.
Prigatano GP, Glisky EL, et al (1996) Cognitive rehabilitation after traumatic brain injury. In PW Corrigan and S C. Yudofsky (eds) Cognitive rehabilitation for neuropsychiatric disorders. Washington DC: APA
Smith I, Hillman A. (1999) Management of Alcohol Korsakoff ’s syndrome. Advances in Psychiatric Treatment, 5, 271–8.
Sullivan EV, Pfefferbaum A (2005) Neurocircuitry in alcoholism: a substrate of disruption and repair. Psychopharmacology, 180: 583–94.
Wilson K., Halsey A., Macpherson H., Billington J., Hill S., Johnstone G, Rajue K., Abbot P (2012) The psychosocial rehabilitation of patients with alcohol-related brain damage in the community. Alcohol and Alcoholism 47, (3) 304-11.
Ylvisaker M. Feeney TJ. (1998) Collaborative brain intervention: positive Everyday routines. San Diago, CA: Singular.

(Download PDF)


Discover all our resources.

Discover all our resources.

Fill the form

Connect with our network

To register your interest in this network please contact us by completing the form