Alcohol-Related Dementia (Alcohol-Induced Dementia; Alcohol-Related Brain Damage)
Jane Marshall
Introduction
Long-term heavy alcohol consumption causes significant brain abnormalities and impairs cognitive functioning. A number of terms have been used to describe these effects, including: ‘alcohol-related dementia’, ‘alcohol-induced dementia’, and ‘alcoholic dementia’.(1) The more pragmatic umbrella term ‘alcohol-related brain damage’ (ARBD) is also used. The literature is beset with limitations, in particular the lack of a diagnostic gold standard, and the difficulty in making a clinical diagnosis. Many individuals labelled as having an alcohol-related dementia are, in fact, suffering from the Wernicke-Korsakoff syndrome (WKS).(2) (This is a specific neuropathological disease caused by thiamine deficiency, which can occur secondary to alcohol misuse. It is considered in Chapter 4.1.12.) When considering the topic of ‘alcohol-related dementia’ it is probably sensible to take a broad clinically-based diagnostic view that includes both WKS and other cases of ‘dementia’ that appear to be alcohol-related.(3)
Diagnostic criteria
Diagnostic criteria for ‘substance-induced persisting dementia’ are included in DSM-IV(4) (Table 4.1.11.1), which also states that there must be evidence from the history, physical examination, or laboratory findings that the deficits are aetiologically related to the persisting effects of substance use (in this case alcohol). No specific inclusion criteria are offered to distinguish alcohol-related dementia from other dementias. In ICD-10,(5) the Korsakoff syndrome is listed separately under the amnesic syndrome heading (F10.6) whereas alcohol-induced ‘dementia’ and ‘other persisting cognitive impairment’ are included under the ‘residual and late-onset psychotic disorder’ category (F10.73 and F10.74 respectively), where diagnostic guidelines can be found.
Diagnostic criteria for establishing a diagnosis of ‘alcohol-related dementia’ have been proposed, conceiving it as a spectrum of alcohol-related intellectual and neurological syndromes, ranging from moderate deficits to the more severe Wernicke-Korsakoff syndrome.(3) ‘Alcohol-related dementia’ is thus defined as a syndrome that results from several aetiological mechanisms including the direct neurotoxic effects of alcohol, metabolic dysfunction during intoxication and withdrawal, trauma, vascular injury and thiamine or other nutritional deficiencies.
Table 4.1.11.1 DSM-IV diagnostic criteria for substance-induced persisting dementia | ||||||||||||||||||||||||||||||||||||||||
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Prevalence
Adequate epidemiological studies to determine the size of the problem have not been carried out. It has been estimated that ‘alcohol-related dementia’ accounts for 10 per cent of the dementia population.(1) Indeed alcohol misuse may contribute to as many as 21-24 per cent of all cases of cognitive impairment in mid-adulthood.(6) The prevalence is likely to be higher in areas of socio-economic deprivation, with most cases presenting between the ages of 50 and 60 years.(7) Early onset has been associated with poorer prognosis and potential for recovery. Recent evidence suggests that the prevalence of the Wernicke-Korsakoff syndrome, caused by thiamine deficiency, may be increasing.(8,9) Early identification and intervention can help to maximize optimum recovery.
Causal mechanisms
There is no single cause of ‘alcohol-related dementia’. Individual susceptibility may be influenced by age; age of onset of drinking and the drinking history; gender; genetic background; family history of alcohol dependence; nutrition; alcohol exposure before birth; and general health status.(10) Causal mechanisms include: the neurotoxic effect of alcohol and its metabolite acetaldehyde; repeated episodes of intoxication and withdrawal; dietary neglect and vitamin deficiencies; repeated episodes of head trauma; cerebrovascular events; and liver damage. In particular, thiamine depletion, and metabolic factors, such as hypoxia, electrolyte imbalance, and hypoglycaemia, all of which result from acute or chronic intoxication and withdrawal, are important and interrelated. It is difficult to determine the relative contributions of these mechanisms. A number of theories have been advanced by Lishman and others to explain the mechanisms by which chronic alcohol use might lead to dementia.(1, 6)
The brain might be vulnerable to both thiamine depletion and alcohol neurotoxicity, the former affecting the basal brain regions and the latter both the basal brain and the frontal cortex.(1) Individual genetic vulnerability is likely to have a role in influencing these processes.
Wernicke-Korsakoff pathological processes in the basal brain have the potential to damage nearby cholinergic fibres projecting to the cerebral cortex: the so-called cholinergic hypothesis.(1,6)
Alcohol-induced brain pathology couples with other processes including ‘ageing, trauma, vascular changes, and hepatic dysfunction’ leading to cognitive decline: the coupling hypothesis.(1,6)
Ethanol stimulates pituitary corticotrophin leading to elevated corticosteroid levels and possible injury to the hippocampus.
Recurrent alcohol withdrawal has been hypothesized to have a kindling effect.(11) During alcohol withdrawal there is increased N-methyl-d-aspartate (NMDA) function which is postulated to lead to increased neuronal excitability and to glutamate-induced neurotoxicity.(12) The way in which alcohol interferes with glutamatergic neurotransmission, especially through the NMDA receptor, is probably central to an understanding of its long-term effects on the brain.
Alcohol might lead to an accelerated ageing process.
Areas of the brain affected
There is evidence that the frontal lobes and sub-cortical areas such as the limbic system, the thalamus and the basal forebrain are particularly vulnerable to alcohol-related damage. The cerebellum is also vulnerable. Alcohol-related brain changes in the frontal lobes become more prominent with age.(13) Emotional processing is affected by long-standing heavy alcohol use and dependence, and probably reflects abnormalities in the limbic system and the frontal lobes.(14) This is manifested as difficulty with interpreting non-verbal emotional cues and recognizing facial expressions of emotion.
Alcohol-related brain damage has been studied using a variety of methods, ranging from the neuropathology of the post-mortem alcoholic brain to neuro-imaging techniques focusing on structural, functional and biochemical changes. There is also a considerable neuropsychological literature.
Neuropathology
Early neuropathological studies of the alcoholic brain described fairly uniform cerebral atrophy, mainly over the dorso-lateral frontal regions, widened sulci, a narrowed cortical ribbon, and enlargement particularly of the anterior horns of the lateral ventricles.(1)
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