Alcohol and the Adult Brain

Jenny Svanberg, Adrienne Withall, Brian Draper, Stephen Bowden, Jenny Svanberg, Adrienne Withall, Brian Draper, Stephen Bowden

• Publisher: Psychology Press
• Year: 2014
• Print ISBN: 9781848723078
• eBook ISBN: 9781317587576
• Topic: Psicología
• Subtopic: Adicción en psicología

The research literature on the impact of alcohol on the brain has seen a rapid expansion in recent years. Alcohol and the Adult Brain presents an up-to-date overview of some of the issues relevant to understanding and working with people with cognitive impairment as a result of chronic alcohol use.

One issue causing barriers to effective treatment and care is the stigma associated with alcohol dependence, resulting in the belief that difficulties associated with alcohol related brain damage (ARBD) are 'self-inflicted'. Cognitive changes resulting from alcohol excess and poor nutrition can directly affect an individual's ability to motivate themselves, make decisions, and make the informed choices that underlie behaviour change. Attitudes held by professionals, reinforced by societal norms, that a person is 'choosing to drink' and 'not motivated to engage with treatment', in combination with the often subtle cognitive deficits associated with ARBD, can result in a lack of timely intervention, with enormous personal, social and economic cost.

The chapters in this book set ARBD in a social and cultural context, provide discussion of the difficulties in definition and diagnosis, and outline the structural brain changes and neuropsychological deficits associated with chronic alcohol use. The book provides an overview of recent research on ARBD, including impairments associated with Wernicke-Korsakoff Syndrome, and discusses up to date recommendations for managing and working with this complex and varied disorder.

Alcohol and the Adult Brain will be essential for students and researchers working with ARBD and for practitioners in a range of health, social care and voluntary settings.

1

INTRODUCTION

Jenny Svanberg

Alcohol use is common in our society and has been described as the most harmful of the main substances of abuse, when physical, psychological and social harms to the individual and society are considered (Nutt, King and Phillips, 2010). A sizeable proportion of people who drink alcohol to harmful levels experience changes in the structure and functioning of the brain, although some of these changes are reversible in abstinence. “Alcohol-related brain damage” (ARBD) is the umbrella term for the spectrum of neurocognitive changes resulting from long-term excessive alcohol use, particularly in the context of thiamine deficiency. The last decade has seen a rapid expansion in research designed to understand and support people with ARBD. However, there continue to be debates over how to define and diagnose disorders such as Wernicke’s Encephalopathy (WE), Korsakoff’s Syndrome (KS) and alcohol-related dementia (ARD), with corresponding questions around assessment and treatment. These debates reflect the heterogeneity of this population, which spans mild, pervasive cognitive deficits that can occur early in ARBD to potentially severe and variable cognitive impairments associated with Wernicke-Korsakoff Syndrome (WKS). In a majority of those that develop ARBD, impairments will be to some extent reversible in abstinence, highlighting the need to recognize and treat ARBD as early as possible in order to prevent long-term health and social consequences.

Within this book, we recognize WE and KS as acute and chronic stages of WKS, and highlight that both stages can present with heterogeneity of neurological and neuropsychological symptoms. We set out the evidence that shows that ARD is best understood as chronic WKS, and argue that this offers a wider range of options for treatment. The term “alcohol-related brain damage” has become widely used as it reflects the heterogeneity of neurocognitive impairments caused by alcohol excess, and has been described as a pragmatic solution to address the complexity and dual diagnoses common within this group (Royal College of Psychiatrists, 2014).

ARBD can be understood as a form of acquired brain injury in which damage is caused by an external factor, but may be the only one in which the cause of injury is specified in its title (Scottish Executive, 2004). Arguably, this contributes to the considerable stigma that exists around this group, leading at times to a form of “therapeutic nihilism”, where professionals feel that they are unable to intervene effectively or influence longstanding gains. This group also endures the view that their difficulties are “self-inflicted”, adding to marginalization and providing barriers to effective treatment and care. In the context of ARBD, attitudes and beliefs around a person “choosing to drink” and “lacking motivation to engage with treatment”, in combination with the often subtle cognitive deficits seen early in ARBD, deficits which directly impact on the person’s ability to motivate and maintain behavioral change, can result in a lack of timely intervention for this preventable condition, with enormous personal, social and economic costs (Mental Welfare Commission for Scotland, 2006).

Within this book, we hope to challenge some of these attitudes, and aim to present some of the key issues relevant to understanding and working with people with ARBD. We begin in Chapter 2 with an overview of WKS. Simon Scalzo, Stephen Bowden and Matti Hillbom highlight that WE and KS can be seen as acute and chronic phases of WKS with a common underlying neuropathology, complicated by the heterogeneity within both the acute and chronic phases. The authors address problems of diagnosis, and argue that the term “alcohol-related dementia” can be seen as a misdiagnosis of severe WKS, which can result in inadequate or inappropriate treatment and therefore poorer prognosis. The chapter outlines approaches to assessment designed to minimize misdiagnosis, and describes the guidance on prevention and treatment of WKS, covered from different perspectives in later chapters.

In Chapter 3, Nicole Ridley and Brian Draper describe the epidemiology of ARBD, recognizing the difficulties in obtaining accurate epidemiological data when there has been a historical lack of consensus in diagnostic criteria and classification of ARBD. The authors therefore consider international data on alcohol consumption and alcohol-use disorders. Carly Johnco and Brian Draper then place ARBD in a cultural context in Chapter 4, looking at some of the social and cultural factors influencing alcohol consumption and excess, and the risk factors associated with ARBD.

When considering a whole-life perspective on the development of cognitive changes as a result of prolonged alcohol excess, it should be immediately apparent that comorbidity and heterogeneity are likely to be the norm rather than the exception. From the genetic factors or adverse early life experiences that may predispose someone to alcohol dependence, to the physical, psychiatric, neurological and societal consequences of chronic alcohol excess, the complexity of ARBD requires individually designed, multidisciplinary assessment and treatment approaches. In Chapter 5, Apo Demirkol and Nicholas Lintzeris consider comorbidities and consequences of alcohol-use disorders and ARBD, presenting an update of the literature on treatment approaches for concurrent alcohol use, mental health problems and cognitive impairments.

One of the recent advances in the field has been the emergence of a new cohort of older adults who are more likely to use alcohol and other substances to excess. Adrienne Withall and Samaneh Shafiee address this in Chapter 6, which calls for new models of care to respond to this group, who often have additional general health issues and may be uncomfortable in an addiction setting that is more suited to younger clients, but may also be excluded from memory clinics as a result of alcohol use. Issues around assessment and management of this group are presented, and the authors again highlight the need for integrated systems of care.

There remain questions over the underlying pathology of ARBD and its relation to neuropsychological functioning. Chapters 7, by Lisa Savage, and 8, by Hélène Beaunieux, Francis Eustache and Anne-Lise Pitel, address the neuropathological and behavioral changes associated with chronic alcohol use and dependence, drawing on animal models, post-mortem studies and in-vivo imaging studies to specify the structural changes to focal brain regions and the resulting behavioral changes. The authors in this section emphasize recent research into the alcohol-influenced disruption of reward and motivational brain networks, outlining the trap of ARBD: focal brain damage that directly affects the areas of the brain associated with recognizing the need to make behavioral changes, making those changes and maintaining new patterns of behavior. These chapters also illustrate the resilience and adaptability of those with ARBD, describing the mechanisms of recovery and compensation that can occur in abstinence.

The last chapters of the book provide more detail on prevention, assessment and rehabilitation of ARBD. Adrian Bonner, in Chapter 9, describes the nutritional issues and deficiencies associated with alcohol use, which are key in the development of WKS, and considers nutritional interventions that may mitigate cognitive decline.

Chapter 10 covers issues around cognitive screening and neuropsychological assessment with this population, considering questions such as when it may be appropriate to offer neuropsychological assessment to individuals continuing to use alcohol (Svanberg, Morrison and Cullen, 2015). The chapter provides a structure for assessment, and gives guidance on how neuropsychological assessment can be used to support assessment of decision-making capacity where necessary. This latter issue is addressed in detail in Chapter 11, by Chris Perkins and John Hopkins, which describes the ethical and legal issues that are vital to consider with this population. The authors provide a compassionate summary of the ethical dilemmas inherent in finding a balance between autonomy and protection. This is all the more difficult for this population for whom alcohol use may begin as a conscious and informed choice, but through subtle cognitive changes may be robbed of the ability to make and act on the decision to stop drinking. Ironically, in these cases, earlier use of legislation may be the least restrictive option to enable assertive treatment, prevent further deterioration and promote self-determination to the greatest degree.

The final chapter provides an overview of the psychosocial rehabilitation of people with ARBD, from diagnosis to longer-term management, drawing together the earlier chapters and reflecting recent recommendations made by a group of medical associations in the UK (Royal College of Psychiatrists, 2014; Wilson, 2015). The chapter outlines a successful service model embedded in an evidence base that draws on the cognitive and psychosocial rehabilitation literature, describing the considerable benefits of a flexible, staged framework for managing ARBD. The author emphasizes that timely and appropriate care involving abstinence, nutritional support and assertive follow-up can provide an optimal environment to enhance recovery from ARBD, and points out that although specialist services can be cost effective in preventing hospital admissions and improving individual outcomes, all services can provide an element of prevention and early treatment.

We hope that a number of particular themes stand out within this book. First, that ARBD is preventable, and that some level of recovery is possible for a majority, even for those with severe cognitive impairments as a result of alcohol excess. Second, that the historically narrow diagnostic criteria for WKS have resulted in under-diagnosis, with enormous costs to individuals, families and society. A broader recognition of the heterogeneity of cognitive impairments within ARBD, and at both the acute WE and chronic KS stages of WKS, will allow better targeting of appropriate treatment for both cognitive impairment and alcohol-use disorders. Third, that people with ARBD can present with complex needs which impact on multiple levels of their functioning and ability to participate in their lives. Considering treatment from the point of view of these needs rather than their aetiology may reduce the stigma around this population, and emphasizes the need to draw on expertise from multiple disciplines and at multiple tiers of health and social care, as well as within the community. Neuropsychology has a key role to play at every stage of the journey experienced by people with ARBD, from supporting earlier recognition and assessment of specific cognitive impairments to using assessment feedback to explain difficulties in functioning and influencing the design of multidisciplinary rehabilitation packages for individuals to maximize their independence and participation in their lives.

References

Mental Welfare Commission for Scotland. (2006). Investigation into the care and treatment of Mr H. Edinburgh: MWCScot. Available at http://www.mwcscot.org.uk/media/51999/Mr_H_Inquiry.pdf. Accessed 8 July 2014.

Nutt, D. J., King, L. A. and Phillips, L. D. (2010). Drug harms in the UK: a multicriterion decision analysis. Lancet, 376, 1558–65.

Royal College of Psychiatrists. (2014). Alcohol and brain damage in adults, with reference to high-risk groups. College Report CR185. Available at http://www.rcpsych.ac.uk/files/pdfversion/CR185.pdf. Accessed 8 July 2014.

Scottish Executive. (2004). A Fuller Life: Report of the Expert Group on Alcohol Related Brain Damage. Stirling: Dementia Services Development Centre.

Svanberg, J., Morrison, F. and Cullen, B. (2015). Neuropsychological assessment of alcohol-related cognitive impairment. In J. Svanberg, A. Withall, B. Draper and S. Bowden (eds), Alcohol and the Adult Brain. Hove: Psychology Press.

Wilson, K. (2015). The clinical rehabilitation of people with alcohol-related brain damage. In J. Svanberg, A. Withall, B. Draper and S. Bowden (eds), Alcohol and the Adult Brain. Hove: Psychology Press.

2

WERNICKE-KORSAKOFF SYNDROME

Simon Scalzo, Stephen Bowden and Matti Hillbom

A syndrome resulting from thiamine deficiency was described in ancient China as Jiao Qi disease, now known as Beriberi, but in the late 1880s Carl Wernicke and Sergei Korsakoff independently described the different aspects of the syndrome still carrying their names (Fan, 2004; Victor, Adams and Collins, 1989; Wernicke, 1881). Vitamins were discovered at the beginning of the 20th century and thiamine deficiency was not shown to be the primary reason for Wernicke-Korsakoff Syndrome (WKS) until the middle of the 20th century (for review see Victor, Adams and Collins, 1971). WKS is a frequent cause of cognitive impairment among those with alcohol-use disorders (DSM-5 Codes 305.00 or 309.90 (American Psychiatric Association, 2013) or ICD-10 Codes 10.1 harmful use of alcohol, or 10.2 dependence on alcohol (World Health Organization, 2010)) and the most important preventable and treatable vitamin deficiency syndrome still frequently seen worldwide. This chapter provides an overview of the conditions leading to WKS and its prevalence, and addresses difficulties encountered in prevention, diagnosis and management of the disease.

Throughout this review, the unified term of “Wernicke-Korsakoff Syndrome” (WKS) will be used to refer to the neuropathological condition caused by thiamine deficiency, although the term “Korsakoff’s Syndrome” (KS) is sometimes used to describe clinical amnesias due to other aetiologies. However, we would recommend that the term “Korsakoff’s Syndrome” be restricted to description of cases of cognitive impairment caused by thiamine deficiency, the chronic or recovering phase of WKS, in line with Korsakoff’s original descriptions and the usage recommended by Victor (1994; Victor, Adams and Collins, 1989). Aspects of these alternative definitions will be discussed below. Nevertheless, to preserve accuracy in citing previous authors’ work, the separate terms of “Wernicke’s Encephalopathy” (WE) and KS will be used as synonyms for the acute and chronic phases of WKS, respectively.

Conditions leading to Wernicke-Korsakoff Syndrome

The cornerstone in the prevention of WKS is to consider the conditions that predispose to thiamine deficiency. This is particularly important because the onset of the disease is often insidious. Signs and symptoms are often slight or mild and easily missed.

Thiamine is a water-soluble vitamin absorbed from the intestines. Much remains to be understood regarding the role of thiamine in metabolism. About half of the thiamine in the body is stored in the muscles and liver, and thiamine functions as a coenzyme in the metabolism of carbohydrates, lipids and branched-chain amino acids (Hoyumpa, 1980). A healthy adult eating an average diet needs about 0.66mg thiamine per 1,000kcal per day (Hoyumpa, 1980). The requirement may be tripled during pregnancy. High caloric and carbohydrate intakes increase the daily demand for thiamine due to the great role of thiamine in carbohydrate metabolism. Major reasons for thiamine deficiency are poor absorption of thiamine, lack of thiamine in ingested food and thiamine depletion from body stores if alcohol or fat are primary energy sources (Hoyumpa, 1980). Among those who eat carbohydrate-containing food the deficiency state may develop within approximately three weeks after total cessation of thiamine supply and WE may manifest as an acute confusional syndrome with nystagmus, and ataxia leading to coma (Bergin and Harvey, 1992; Hillbom et al., 1999). Three weeks is a very short precipitating period when compared with the development of deficiencies due to other vitamins. The period of time required to develop thiamine deficiency may even be less than three weeks if the stores are poor when intake is totally stopped. Thiamine deficiency also develops rapidly if associated with severe prolonged vomiting.

Table 2.1 shows the variety of clinical situations that may predispose to thiamine deficiency, whether through increased thiamine requirements, or nutritional risk factors (Kumar, 2010). As can be inferred, WKS can be seen among patients treated in medi...

Table of contents

• Cover
• Half Title
• Title Page
• Copyright Page
• Table of Contents
• Contributors
• Acknowledgements
• 1 Introduction
• 2 Wernicke-Korsakoff Syndrome
• 3 Alcohol-related dementia and brain damage: a focus on epidemiology
• 4 Cultural considerations in alcohol use and misuse
• 5 Comorbidity and complexity in chronic alcohol misuse
• 6 Alcohol and cognitive impairment: considerations with the older client
• 7 Alcohol-related brain damage and neuropathology
• 8 The relation of alcohol-induced brain changes to cognitive function
• 9 Alcohol, ageing and cognitive function: a nutritional perspective
• 10 Neuropsychological assessment of alcohol-related cognitive impairment
• 11 Ethical issues associated with alcohol-related cognitive impairment
• 12 The clinical rehabilitation of people with alcohol-related brain damage
• Index