Social cognition in alcoholism: a link to prefrontal
Jennifer Uekermann & Irene Daum
Institute of Cognitive Neuroscience, Ruhr-University of Bochum, Bochum, Germany
Aims Alcoholism is associated with a range of cognitive deficits. These deficits might be explained by the ‘frontal lobe hypothesis’ which suggests a specific vulnerability of the prefrontal cortex (PFC) to the neurotoxic effects of alcohol. Social cognition is thought to be processed in the PFC, but so far only few studies have addressed the issue of social cognition deficits in alcoholism. This review aims to evaluate the deficits in social cognition in alcoholic patients. In addition an outline for future perspectives is given. Methods Medline and Psyclit searches were performed for a 30-year period (1977–2007). Results Alcoholism is associated clearly with social cognition impairments which include emotional face and prosody perception problems, theory of mind deficits and humour processing difficulties. Conclusions In summary, the social cognition impairments are consistent with the frontal lobe hypothesis of alcoholism. Future studies should focus on (i) the delineation of the basic cognitive processes which underlie social cognition deficits; and (ii) their relevance as predictors of treatment outcome in alcoholism. Keywords
Alcoholism, frontal lobe, prefrontal cortex, social cognition.
Correspondence to: Jennifer Uekermann, Faculty of Psychology, Institute of Cognitive Neuroscience GAFO 05/607, Ruhr-University of Bochum, Bochum 44780, Germany. E-mail: email@example.com Submitted 12 July 2007; initial review completed 4 October 2007; final version accepted 11 January 2008
Alcoholism is associated with a range of cognitive impairments such as attention, memory and executive deficits. Different neuropsychological models have been postulated to explain the cognitive profile of alcoholics . Empirical support for the ‘right hemisphere hypothesis’
or the ‘premature aging hypothesis’ is sparse . The
‘mild generalized dysfunction hypothesis’ of alcoholism
suggests a variable pattern of impairments . The
‘frontal lobe hypothesis’, on the other hand, is based on the idea of a specific vulnerability of the prefrontal cortex (PFC) to the neurotoxic effects of alcohol. This leads to
pronounced executive function impairments in people
who suffer from alcoholism. The latter hypothesis has
received strong support from clinical and neuroimaging
studies to account for social cognition disorders in alcoholics . Skilled social interaction is critically dependent upon
our capacity to understand other people’s minds.
Humans are excellent in drawing conclusions from a person’s facial expression, prosody or body posture upon the
person’s emotional stage or intentions. Social cognition is severely disrupted in disorders such as autism , schizophrenia , dementia  and in patients with PFC injury . Given the link between alcoholism, executive control
impairments and PFC dysfunction, on one hand, and
social cognition and PFC function on the other hand, only
little is known about social cognition in alcoholism.
The present review aims (i) to evaluate the available
evidence of social cognition problems in alcoholism in
the context of the frontal lobe hypothesis; (ii) to discuss
the clinical implications of such deficits; and (iii) to
outline suggestions for future research in this area. First, brain changes during the course of alcoholism are summarized; then, deficits in facial affect perception and impaired perception of emotional prosody in alcoholism
are focused upon, following which deficits of theory of
mind abilities, empathy and humour processing will be
discussed. In the concluding section, the clinical implications of social cognition problems will be discussed with respect to interpersonal problem...
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