Abstract

In this review paper, we discuss how the overarching concept of prehabilitation is applicable to alcohol dependence. Central to prehabilitation are the concepts of expected harm, risks, and proactive planning to eliminate the harm or cope with the risks. We review the evidence from animal models, psychological experimental studies, as well as pharmacological studies, on the potential risks and harms associated with medically assisted alcohol detoxification and the current treatment paradigm for alcohol dependence. Animal models provide an approximation mostly of the physical aspect of alcohol withdrawal and detoxification process and make predictions about the development of the phenomena in humans. Despite their limitations, these models provide good evidence that withdrawal from chronic ethanol use induces cognitive impairment, which is worsened by repeated bouts of withdrawal and that these impairments are dependent on the duration of alcohol withdrawal. Initial clinical observations with alcohol-dependent patients confirmed increased incidence of seizures. In recent years, accumulating evidence suggests that patients who have had repeated episodes of withdrawal also show changes in their affect, increased craving, as well as significant deterioration of cognitive abilities, when compared to patients with fewer withdrawals. Alcohol dependence is associated with tolerance and withdrawal, with neuroadaptations in γ-Aminobutyric Acid-A Receptor (GABA-A) and glutamatergic N-methyl-D-aspartate (NMDA) receptors playing key roles. It is suggested that dysregulation of the NMDA receptor system underpins alcohol-related memory impairments. Finally, we discuss the Structured Preparation for Alcohol Detoxification (SPADe) as an example of how prehabilitation has been applied in clinical practice. We discuss the importance of partial control over drinking as an interim step toward abstinence and early introduction of lifestyle changes for both the patient and the immediate environment prior to detoxification and while the patient is still drinking.

Highlights

  • The concept of pre-habilitation has been introduced in the field of orthopedics and describes a set of exercises and training routines for certain groups of patients with the aim to maximize physical strength and reduce the risk of expected harm or frequent injuries, taking a proactive rather than a reactive approach

  • While these models fail to replicate all the complexities of psychosocial and compulsive factors that occur in the human experience of withdrawal, these animal models provide good evidence that withdrawal from chronic ethanol induces cognitive impairment, that this impairment is worsened by repeated bouts of withdrawal, and that these impairments are dependent on the duration of alcohol withdrawal and abstinence

  • These animal models have led to the identification of neuroadaptations and increased levels of corticosterone as potential modifiers of cognitive deficits caused by withdrawal and which brain regions are vulnerable to or involved in these impairments

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Summary

INTRODUCTION

The concept of pre-habilitation has been introduced in the field of orthopedics and describes a set of exercises and training routines for certain groups of patients with the aim to maximize physical strength and reduce the risk of expected harm or frequent injuries, taking a proactive rather than a reactive approach. Alcohol withdrawal induces much more than just physical symptoms with low mood and anxiety evident This negative affective state is thought to contribute to the risk of relapse in alcohol dependence and is a critical area of study (these effects in humans are discussed in detail in Section 5 below). These have been used to demonstrate withdrawal-induced impairments in learning [19, 31], cognitive flexibility [26], memory [20, 24, 25, 31, 36], sociability [38], as well as increasing anxiety [23, 27] and sleep disruption [35]. It is a vital area of research if we are to protect the brain, or at least limit the damage, in alcohol dependence

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