To support the free and open dissemination of research findings and information on alcoholism and alcohol-related problems. To encourage open access to peer-reviewed articles free for all to view.

For full versions of posted research articles readers are encouraged to email requests for "electronic reprints" (text file, PDF files, FAX copies) to the corresponding or lead author, who is highlighted in the posting.


Wednesday, January 30, 2013

Pathways to alcohol-induced brain impairment in young people: A review

Classically, disorders associated with ‘alcohol-related brain damage’ (ARBD) occur as a result of chronic excessive alcohol misuse and confer significant physical and psychological disability to the individual as well as to the community. These phenotypes are often difficult to detect at early stages and therefore early intervention and treatment is limited. It remains unresolved as to whether there are neurobiological markers of the early stages of such brain damage in young ‘at-risk’ drinkers, who probably experience ‘alcohol-induced brain impairment’ prior to the onset of ARBD, per se.
This review focuses on neurobiological (in particular, neuropsychological and neuroimaging) markers that are associated with alcohol misuse in young people (13–24 years of age).
The findings from this review suggest that a clearer understanding of alcohol misuse (particularly with regards to binge drinking) is needed. Despite this, neurocognitive profile along with supporting neuroimaging evidence appears to be particularly important in the early detection of brain changes that result from excessive alcohol use. In young alcohol misusers, these preventable and potentially reversible deficits may be progressive but if left unresolved such deficits eventually become major contributors to poor outcome (long term) and hamper adherence to treatment.

We address five key themes in this review: (i) there are specific drinking patterns in young people; (ii) youth represents a critical period in brain development that is particularly vulnerable to alcohol misuse; (iii) the extent to which there are pre-existing versus alcohol-induced neurobiological changes remains unclear; (iv) vulnerability markers may be mediated by mental health and substance use comorbidities; and (v) cognitive remediation would be a likely candidate for early prevention and treatment as it could help to develop efficient meta-cognitive skills to prevent relapse in young drinkers.
Request Reprint E-Mail: