Risks, signs, symptoms & presentation


ARBD Part 1

Dr Wilson

In this short video, learn about ARBD, its effect on cognitive function, Wernicke Korsakoff’s syndrome and its treatment

ARBD Part 2

Dr Wilson

In this short video, learn more about ARBD, its effects and treatment from Professor Kenneth Wilson

Alcohol and the brain

David Nutt

Recorded at the ARBD network and ACUK online conference September 2023

Warning signs, recognition and diagnosis

Grant Brand

Recorded at the ARBD network and ACUK online conference September 2023

Examination of reasoning

Dr Wilson

In this short video learn about the examination of reasoning in capacity assessment


Signs and Symptoms of ARBD

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.

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The Clinical Diagnosis of ARBD

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) (https://www.mocatest.org/the-moca-test/). 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) https://advancemed.com.au/wp-content/uploads/2019/01/ace-r_aus_versiona1.pdf . 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.

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