Dementia is considered a health priority by the World Health Organization (WHO) because it is one of the leading causes of death globally (WHO, 2017). Within the UK, an estimated 944 000 people have been diagnosed with this condition (Luengo-Fernandez and Landeiro, 2023). Dementia is a neurodegenerative syndrome that encompasses several progressive conditions that affect the brain, leading to a deterioration in cognitive function over and above the usual expected biological ageing process (Handing et al, 2015; Langballe et al, 2015).
At present, Alzheimer's disease is the most commonly diagnosed dementia, followed by vascular disease and Lewy bodies dementia (Cunningham et al, 2015). It is well established, however, that there is an association between alcohol use and changes in cognitive function and dementia (Xu et al, 2017). Research suggests that there is a high incidence of alcohol use disorders in patients with dementia, leading to increasing cognitive decline (Rao and Draper, 2018) and significant rates of dementia in people who drink alcohol to excess (Ritchie and Villebrun, 2008). Schwarzinger et al (2018) identified a considerable relationship between alcohol use disorders and all types of dementia. In 2020, the Lancet Commission added excessive alcohol use in mid-life to a list of significant risk factors for developing dementia (Livingston et al, 2020).
Alcohol: a leading cause of death
According to Public Health England (Burton et al, 2016), alcohol is increasingly a leading cause of death in the 50–69 age group in England. This group has the highest rate of alcohol consumption, and it is a particular problem among women (Burton et al, 2016; Nazarko, 2019). With consumption rising rapidly overall, there is an increased risk that young and middle-aged people will develop alcohol-related dementia in the future (Sachdeva et al, 2016; Sabia et al, 2018). There is a significant increase in the risk of early onset dementia in patients with alcohol use disorder (Schwarzinger et al, 2018), yet it is unclear whether this risk is related to developing alcohol-related dementia or other types of dementia.
It is of concern that specific alcohol-related deaths rose by 18.6% in England between 2019 and 2020, the highest rise in 20 years. This is thought to be due to a change in drinking habits and limited access to healthcare services secondary to the COVID-19 pandemic (Office for National Statistics, 2022; Lancet Gastroenterology and Hepatology, 2022). There was also a significant reduction in the rate of dementia diagnoses during this time (Alzheimer's Society, 2021). This indicates that there is likely to be a hidden cohort of undiagnosed patients, and numbers will increase over the coming years.
The incidence and prevalence of alcohol-related dementia varies between studies likely due to a lack of diagnostic criteria (Ridley et al, 2013). It has been reported to account for between 10% and 24% of all cases of dementia in prevalence studies within nursing homes, which is higher when compared with the general population (Ritchie and Villebrun, 2008). However, the number of alcohol-related dementia cases identified in memory and neurology clinics appears to be much lower, which may indicate that this patient group is not being offered referral to such clinics (McMurtray et al, 2006; Bello and Schutz, 2011). Schwarzinger et al (2018) argued that the relationship between dementia and alcohol use disorders is particularly clear in the earlier onset dementias. Historically, studies have not included patients under 60 years of age, subsequently underestimating the prevalence (Ritchie and Villebrun, 2008). Livingston et al (2020) have highlighted the link between excessive alcohol use in midlife and dementia.
Alcohol and the brain
Rao and Draper (2018) identified that there are conflicting reports from public health organisations about whether alcohol consumption has an integral role in the development of dementia. This potentially offers insight into why campaigns about other health risks linked with excessive alcohol consumption, such as liver disease, gain large amounts of public funding but specific health advice about the effect alcohol can have on the brain remains much less publicised and with limited funding for research (Keady et al, 2009).
Post-mortem reviews have shown the pathological effect of heavy alcohol use on the brain's structure and functioning (Sutherland et al, 2014). Verbaten (2009) suggested that even low-to-moderate alcohol consumption has a detrimental effect on brain structure, although one exception might be for elderly light-to-moderate drinkers where less white matter damage was found than in abstainers. Other studies have concluded that even light or moderate alcohol use causes adverse brain outcomes, such as hippocampal atrophy (Topiwala et al, 2017). With excessive levels of alcohol use neuropathological and neuroimaging evidence shows significant white matter loss, particularly within the corpus callosum and the prefrontal cortex of the brain, with significantly reduced neuron density and altered glucose metabolism (Sullivan et al, 2003; Harper, 2009). Harper (2009) concluded that, of the two components of brain pathology found in people with alcohol problems, neuronal loss is permanent, whereas brain volume recovery has been shown after at least 6 weeks' abstinence.
Alcohol-related dementia patients identified through acute hospital admission are predominately male, socially isolated and have comorbid physical and mental health conditions (Oslin and Cary, 2003; Draper et al, 2011). It could be argued that this is a stereotypical profile of someone with an alcohol use disorder so there is potential for cases to be missed because of this. Social isolation, a common factor for people who have an alcohol-related disorder, has been identified as a potential cause for the limited identification of alcohol-related dementia (Oslin and Cary, 2003), which is likely to have increased during the pandemic. People with alcohol-related dementia are potentially faced with a double stigma from society by having an alcohol-related disorder as well as experiencing a decline in cognitive functioning (Boughey, 2003).
There is an ongoing debate regarding the diagnosis of alcohol-related dementia concerning whether it is a subcategory of dementia or whether it is more aligned with Wernicke-Korsakoff syndrome (WKS) (Xu et al, 2017). Cipriani et al (2015) argued that alcohol-related dementia is largely neglected as a diagnosis or that excessive alcohol use is identified as a comorbid factor in the majority of cases.
Little recognition has been given to alcohol-related dementia as a specific clinical diagnosis due to scepticism regarding the cause and how it develops, together with the absence of a typical pathophysiological profile (Anttila et al, 2004). However, Rao and Draper (2018) suggested that it is now emerging as a distinct mental disorder. The debate has focused on whether a primary dementia can be the specific outcome of alcohol neurotoxicity or whether the presentation of clinical symptoms signifies an alternative pathology, for example, a secondary dementia, such as thiamine deficiency (Rehm et al, 2019).
Studies in animals have provided evidence to support alcohol neurotoxicity, showing damage to brain structures that correlate with memory and learning impairment that are alcohol dose related (Brust, 2010; Ridley et al, 2013). However, this is in contrast to earlier findings, which disputed the permanence of the changes and whether they are related purely to neurotoxicity (Harper, 2009).
Wernicke's encephalopathy and Wernicke-Korsakoff syndrome
Ridley et al (2013) argued that the development of alcohol-related dementia is primarily due to a thiamine deficiency. Excessive alcohol use can increase the risk of a thiamine deficiency due to alcohol compromising thiamine metabolism. In combination with a poor diet, this can lead to Wernicke's encephalopathy. The chronic effect of Wernicke's encephalopathy can lead on to WKS, known as a secondary dementia (Moriyama et al, 2002; Tiniakos et al, 2018; Royal College of Psychiatry, 2018).
WKS can vary significantly in presentation, which together with a lack of robust pathological evidence for alcohol-related dementia, has led to the theory that alcohol-related dementia is a variant of WKS (Smith and Atkinson, 1995). However, more than 30 years ago, Harper et al (1989) argued that WKS and alcohol-related dementia are separate disorders with clinical symptoms that overlap, for example, peripheral neuropathology and ataxia. Differences between the disorders have been identified regarding memory, in that WKS often presents with impairment of recent memory after the onset of the condition and confabulation. This is in contrast to alcohol-related dementia, where there is impairment of both short-term memory and other areas of cognitive function (Wiegmann et al, 2020). A further view was suggested by Lishman (1986) that the main underlying pathology in both WKS and alcohol-related dementia is likely to be a chronic or inactive Wernicke's encephalopathy and, despite treatment, the neuropsychiatric consequences may persist (Day et al, 2013).
The Alzheimer's Society has argued that two types of alcohol-related brain damage can cause symptoms of dementia. These, it stated, are:
‘… alcohol-related “dementia” and Wernicke–Korsakoff syndrome. Neither of these are actual types of dementia, because a patient cannot get better from dementia, and there is some chance of recovery in both of these conditions.’
Alcohol-related brain injury
The term ‘alcohol-related brain injury’ (ARBI) has been developed more recently to describe the spectrum of cognitive impairment between alcohol-related dementia and WKS (Moriyama et al, 2002; Royal College of Psychiatry, 2018). The term ARBI is often favoured over alcohol-related dementia to emphasise the variability of alcohol-related cognitive disorders in both clinical presentation and aetiology (Jauhar and Smith, 2009). Compounding factors in patients with alcohol disorder such as lifestyle, other comorbidities and higher rates of vascular risk factors have hindered studies in defining alcohol-related dementia (Gupta and Warner, 2008).
Obtaining an accurate and timely diagnosis for people with potential alcohol-related dementia can be difficult for practitioners (Brighton et al, 2013) due to the variety and complexity of symptoms that results in the condition continuing to be misunderstood and under-recognised (Sechi and Serra, 2007; Kopelman et al, 2009). Diagnoses that are inaccurate lead to incongruous treatment and approaches, together with the use of unsuitable medications (Brown et al, 2009).
Classification guidelines
Twenty-five years ago, Oslin et al (1998) attempted to refine the diagnostic criteria of alcohol-related dementia to improve the validity and reliability of identification as they claimed diagnosis was being made entirely on clinical judgement, by practitioners who did not necessarily have the expertise to diagnose. They included measures of severity and duration of alcohol consumption. They defined significant alcohol use as over 52 units per week for men and 42 units for women for a period greater than 5 years within 3 years of the clinical onset of cognitive impairment. They excluded distinctive features of Alzheimer's disease and vascular disease-related dementia, stating that a diagnosis of alcohol-related dementia is probable when clinical symptoms of dementia persist 60 days after the cessation of alcohol. However, the criteria remain to be validated in robust methodical prospective studies, as Rao and Draper (2018) commented.
The two primary classification guidelines, the International Classification of Diseases-10 (ICD-10) (WHO, 2010) and the Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5) (American Psychiatric Association (APA), 2013) provide differing descriptions of alcohol-related dementia. Until recently, the main diagnostic criteria used in England was taken from the ICD-10 (WHO, 2010). Alcohol-related dementia was not classified as an organic disorder but rather as mental and behavioural disturbances secondary to alcohol – a ‘residual and late-onset psychotic disorder’ (WHO, 2010: F10.7) for which the generic criteria for dementia (WHO, 2010: F00–F03) also had to be identified; however, this required the characteristics seen in Alzheimer's dementia rather than alcohol-related dementia for a diagnosis (Cipriani et al, 2021). The release of the ICD-11 (WHO, 2022) will enable a step forward in identifying alcohol-related dementia as a cognitive disorder because there has been a change to the diagnostic criteria. It highlights that impairment is not restricted to memory and may be present in other cognitive domains such as executive and visuospatial functioning.
DSM-5 (APA, 2013) introduced a new term to replace dementia to potentially aid with the diagnosis where many conditions overlap and so allow for alcohol-related dementia to be identified as a neurocognitive disorder (NCD), divided in to two subcategories – minor NCD and major NCD (Cipriani et al, 2021).
It has been suggested that, compared to patients with Alzheimer's disease and vascular dementia, patients with an alcohol-related dementia diagnosis appear less impaired cognitively and functionally. On neuropsychological examination, compared to those with Alzheimer's disease, people with alcohol-related dementia appear to have improved performance on verbal recognition memory and linguistic tests but have reduced ability on visuospatial tasks (Ridley et al, 2013). Frontal lobe damage in the brain, which exhibits as executive dysfunction, is particularly notable in alcohol-related dementia, which may explain an increase in behavioural changes such as carelessness, disorientation, and disinhibition seen in patients with this condition (Rao and Crome, 2016).
Studies have shown that the significant difference between alcohol-related dementia and Alzheimer's disease or vascular dementia is the potential for stability and possible improvement in some cognitive domains over time if abstinence from alcohol is maintained, particularly for late-onset alcohol misuse, where the latter patients experience a general decline (Woodburn and Johnstone, 1999; Oslin and Cary, 2003; Gazdzinski et al, 2005). Smith and Hillman (1999) identified that with accurate diagnosis and support 75% of people with alcohol-related dementia make some form of cognitive improvement, with up to 20% regaining previous levels of cognitive functioning.
Magnetic resonance imaging studies have shown neuroplasticity and early reversibility of white matter shrinkage in the brain is an important process for structural and cognitive recovery (Munro et al, 2001; Bartsch et al, 2007). However, Kopelman et al (2009) suggested that, with increasing age, there is a reduction in the brain's resilience against the neurotoxic effects of alcohol as studies have shown that older people who drink alcohol excessively show more alcohol-related cognitive decline and their functioning is less likely to return on abstinence.
Due to the potential for cognitive improvement, differentiating between reversible and irreversible brain damage is highly important, to enable individualised treatment, focusing on the best outcome for the person (Crews, 2008). Sachdeva et al (2016) suggested that recovery is often faster in females than in males. Positive involvement from friends and family is foremost in achieving abstinence; however, numerous studies have indicated that social isolation is a factor for those with alcohol-related dementia, which may hamper recovery.
Not all people with alcohol-related dementia will improve or recover with abstinence. Approximately 20% of patients will require long-term institutionalised care. Studies show that cognitive rehabilitation can help to slow down cognitive decline and improve the development of new cognitive capabilities (Bernardin et al, 2014). However, engagement with rehabilitation can be difficult due to decreased self-efficacy and poor compliance with treatment (Sachdeva et al, 2016).
An improvement in cognitive functioning has been shown in patients with alcohol-related dementia and WKS following treatment with memantine, a glutamate receptor antagonist used in moderate-to-severe Alzheimer's disease, together with significant improvements in quality of life and behavioural symptoms (Cheon et al, 2008), although, these findings require further study to ensure the results are methodologically sound (Copersino et al, 2009; Bernardin et al, 2014).
Current evidence-based treatment guidance and policy is lacking worldwide for alcohol-related dementia or alcohol-related brain impairment. The National Institute for Health and Care Excellence (2011) only refers to WKS and within this there is no emphasis on the potential for cognitive improvement with appropriate rehabilitation, only a suggestion of 24-hour care. A key report published by the Mental Welfare Commission for Scotland (MWCS) has highlighted a severe lack of appropriate rehabilitation, with many younger people being forced to live in care homes with residents who are decades older. It also stated that their human rights were being breached because they were compelled to live in a setting which they would never choose (MWCS, 2021).
Patients with alcohol-related dementia have often fallen between the cracks in services, and it has been known for many years that there is a lack of clinical services, treatment programmes and suitable accommodation for such patients in England (Thomson and Marshall, 2006). However, there are often repeated opportunities for interventions by healthcare practitioners (Kopelman et al, 2009).
Regardless of the highly detrimental biopsychosocial effects of alcohol-related dementia, significant issues remain regarding the provision of care, support and clinical management. Service provision for diagnosis and treatment is often fragmented due to disputes about which service should provide the care (Boughey, 2003; Keady et al, 2009). Establishing a suitable care package is often unnecessarily convoluted as some health professionals feel alcohol-related dementia is self-inflicted, that an individual does not deserve treatment, or they refuse to deliver appropriate care but rather promote abstinence from alcohol (MacRae and Cox, 2003; Rota-Bartelink and Lipmann, 2010). A person-centred, respectful and compassionate approach is often believed not to be required in the care of individuals with alcohol-related dementia (North et al, 2010).
Importance of the nurse's role
Nurses across the healthcare system are in a good position to drive a preventive approach regarding the increased risk of dementia with excessive alcohol use through screening and brief interventions (Kaner et al, 2018; Livingston et al, 2020). Brief interventions have been shown to be effective in prompting behaviour change among people who engage in harmful drinking. Nurses can use their communication, relationship-building and partnership-working skills to support people to consider behaviour change (Webb, 2023).
Nursing expertise is also required to carry out a holistic biopsychosocial assessment including cognitive screening of individuals with potential alcohol-related dementia due to the complexity and potential risk of acute physical health problems such as alcohol withdrawal (Latt and Dore, 2014). Using validated assessment tools when planning and then reviewing care on an ongoing basis can identify any improvement, stabilisation or deterioration (Pelletier et al, 2016).
Nurses can lobby for this group of patients, acting as advocates to lead and develop care responsive to the changing requirements of this population (Health Education England, 2017). This patient group is often socially isolated and may then present to hospital for another health condition; this provides an ideal opportunity for screening for alcohol use and cognitive impairment to aid identification and subsequent intervention, including support to patients' families where appropriate (Davis et al, 2022).
The prospective reversibility of alcohol-related dementia has significance for early detection and intervention within substance misuse and mental health services specifically. As there is the potential for cognitive impairment at a younger age with alcohol-related dementia, routine cognitive testing, together with brief interventions on alcohol within substance misuse and mental health services, would also help to promote the primary and secondary prevention of alcohol-related dementia (Rao and Draper, 2018). Increasing the focus on prevention of alcohol-related dementia in the community may provide an opportunity for early detection. However, wider public education regarding the potential long-term effects of excessive alcohol use on the brain is required (Davis et al, 2022).
Recommendations for practice
To advance practice within alcohol-related dementia there is a need for future randomised controlled trials on prevention and secondary prevention to enable the development of evidence-based guidelines to support diagnosis and management. Nurses could be at the forefront of such research. Trials situated within the primary healthcare system, focusing on underused areas of analysis for alcohol-related dementia such as genetic profiles, cognition, mood and behavioural assessments, together with the analysis of brain function, would be beneficial (Rehm et al, 2019). If the limited amount of healthcare-related research and fragmented service provision remains, people with alcohol-related dementia will continue to be socially excluded and marginalised (Keady et al, 2009; MWCS, 2021). The updating of the diagnosis criteria within the ICD-11 (WHO, 2022) and the MWCS report (2021) potentially signifies the start of a shift in culture. Much of the literature surrounding this topic dates from the late 20th and early 21st century, showing the need for more current research.
Collective service provision across substance misuse, mental health and older age specialties, including physical health, would further improve access to services and reduce stigma (MacRae and Cox, 2003). Parity of esteem needs to be established for alcohol-related dementia with other alcohol-related physical health disorders such as liver disease; however, problems with identification and access to treatment needs to be overcome to enable this (Rao and Draper, 2018). There is a requirement, through training and promotion, to increase the awareness of the risk of dementia within the health and social care system. Dawber (2010) has identified that people living with alcohol-related dementia were found to benefit from specialist clinicians, in particular nurses and advanced practitioners with experience in substance misuse and mental health, as they are able to assist the person to navigate complex care pathways.
Conclusion
Knowledge regarding the risks of excessive alcohol use and dementia appears to be increasing. However, research specifically focusing on alcohol-related dementia continues to be lacking compared to the other dementias. This article has highlighted the historical and ongoing challenges involved in the care of people with alcohol-related dementia and the need for this to change to enable the development of evidence-based practice supporting proactive nursing care.
Finally, and most importantly, nurses can bring the voice of the patient to the forefront; the lived experiences of people with alcohol-related dementia are absent in the literature. Future research should investigate what people with alcohol-related dementia need, using their perspective to enable the co-production of service developments in the future.
KEY POINTS
- There is an association between alcohol use and changes in cognitive function and dementia
- Historically, there has been debate about whether alcohol-related dementia should be classified as a dementia or as a mental and behavioural disturbance secondary to alcohol
- Patients with alcohol-related dementia have often fallen between the cracks in services
- Nurses are well placed to drive a preventive approach through screening and brief interventions
- More research is needed, focusing specifically on alcohol-related dementia
CPD reflective questions
- Think about the different types of dementia and consider why alcohol-related dementia is different
- As a prescribing clinician, when would you consider prescribing thiamine?
- What is a brief intervention and when would you consider using this approach?
- What validated assessment tools would you consider using with someone who admits to drinking more than the recommended weekly units?