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Over the last 25 years, there has been considerable literature drawing attention to neuropathological, neuroimaging, and neuropsychological evidence of disproportionate frontal lobe involvement in chronic alcoholism. There is copious evidence of disproportionate volume loss and reduced neuronal count in the frontal lobes at autopsy. On neuroimaging in vivo, the frontal lobes are characteristically atrophied on CT (computed tomography) and MRI (magnetic resonance imaging), and they show reduced perfusion and metabolism on positron emission tomography (PET). Likewise, patients with a history of chronic alcohol misuse show characteristic impairments on executive or ‘frontal lobe’ tests, such as Card-Sorting, Trailmaking, FAS verbal fluency, and the Brixton and Hayling tests. Moreover, specific aspects of memory impairment have been attributed to damage in the frontal lobes. These include a disproportionate impairment in recall memory (relative to recognition memory), an impairment in identifying the temporal context or temporal sequence of memories, and so-called ‘spontaneous confabulation’ when it occurs concurrently with severe amnesia in the alcoholic Korsakoff syndrome.

This does not, of course, mean that damage elsewhere is unimportant. The neuropathological and neuroimaging studies show widespread cortical atrophy, and indeed more recent studies of diffusion-weighted tensor imaging (DTI) show widespread white-matter change following chronic alcohol misuse. Subtle changes in visuo-perceptual function have commonly been reported. Moreover, the characteristic impairment in anterograde memory function, which is sometimes a precursor to the onset of a frank Korsakoff syndrome, may be associated with subtle changes within the mammillary bodies, thalamus, and related diencephalic-thalamic structures. Some fluoro-deoxy-glucose (FDG)-PET investigations have found hypometabolism within these memory circuits.

What Uekermann and Daum [1] have done in their excellent paper is to specify in more detail the ways in which frontal lobe dysfunction affects social cognition. For example, they have reviewed evidence that alcoholics take longer to decode emotional facial expressions than healthy comparison groups. Not only that, but alcoholics over-estimate the intensity of emotions, and they show a clear bias towards mislabelling sad expressions as hostile. They tend to judge a happy face as reflecting a negative mood state, and fear responses are enhanced. There is some evidence that the decoding of facial expressions improves following abstinence in parallel with improvements in cognitive function, but this is not always seen. Somewhat similarly, alcoholic patients show deficits in identifying the affective component of speech prosody. The association between such impairments and interpersonal problems may predispose to relapse.

In studies of ‘mentalising’ or ‘theory of mind’, Uekermann et al.[2] showed that alcoholic patients were impaired in processing humour. Other studies have also looked at humour processing [3], finding that alcoholics commonly chose endings to cartoons which were unrelated to the main topic of the cartoon, and that they often failed to select an appropriate punchline to jokes. As the present authors comment, humour has been associated with ‘good health and well-being’, although it is also true, of course, that a number of humourists have led particularly miserable lives, such as Tony Hancock and Kenneth Williams. In the first of these, alcohol may well have contributed to his depressed mood state.

Uekermann and Daum [1] have also discussed the putative consequences of this impaired social cognition on alcohol misuse. Problems in social perception may lead to ‘discomfort and stress in social situations’, which may predispose in turn to alcohol consumption and relapse. The authors go on to say that existing knowledge does not allow us to disentangle whether the impaired social cognition in alcoholism is a consequence of the neurotoxic effects of alcohol, or whether it in fact predisposes to heavy drinking. However, the authors speculate that alcoholics’ deficits in social cognition may both contribute to interpersonal problems and play a role in relapse. Further investigations of these interactions may help us design and develop new social skills interventions in alcoholism.

One aspect of the paper which intrigued me derives from the fact that heavy drinkers commonly get into fights and commit violent or acquisitive offences whilst under the influence of alcohol. In English law, and in many other jurisdictions, the fact of being intoxicated does not in any way diminish responsibility for an action, because the law rules that the act of taking the first drink of the day was entirely voluntary and intentional. The main exception to this rule (in English law) occurs if the alleged offender can be shown to have ‘the disease of alcoholism’, broadly interpretable as ‘the alcohol dependence syndrome’, in which case the lawyers have ruled (in their black and white fashion) that the act of taking the first drink of the day was involuntary. One wonders what will be the legal implications of arguing that, not only do chronic alcoholics have frontal pathology, but that this gives rise to social misperceptions, such as that they may mislabel sad expressions as being hostile, judge a happy face as reflecting a negative mood, and misperceive the emotional prosody in conversation. Such misperceptions may well give rise to aggressive and violent acts, but will these now be regarded as evidence of underlying brain dysfunction, sufficient in cases of homicide to constitute an ‘abnormality of mind’ with resulting impairment of mental responsibility for the act?

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