CONTACT US: Contact info
|
Citation |
Weil ZM, Karelina K, Corrigan JD. Exp. Neurol. 2019; 317: 284-290. |
|
Affiliation |
Department of Physical Medicine and Rehabilitation, Ohio State University Wexner Medical Center, Columbus, OH 43210, USA. |
|
Copyright |
(Copyright © 2019, Elsevier Publishing) |
|
DOI |
|
PMID |
30910407 |
|
Abstract |
Traumatic brain injury (TBI) is closely interrelated with alcohol use disorders. This is mediated, in part, by the large number of individuals who are intoxicated at the time of their injuries. However, there is also evidence, both preclinically and epidemiologically that TBI, particularly when it occurs early in life can increase the incidence of alcohol use disorders later on. This is extremely important because, drinking after TBI has been associated with much poorer long-term outcomes as compared to individuals who do not drink. However, for a number of reasons including, potential confounders and a relatively long time between injury and onset of drinking it has been difficult to definitively assign causality. Here we utilize a framework derived from the toxicology literature to determine whether a causal relationship between pediatric TBI and subsequent alcohol abuse is evident. In order for there to be a high likelihood of a causal relationship between an environmental factor and a health outcome, this framework indicated that an epidemiological relationship be present in humans and that analogous relationship has to exist in a preclinical model system and that the mechanism(s) of action that are identified in the model system must also be plausibly active in humans. In this review we discuss the epidemiological evidence for increased drinking in humans. Further, we discuss, the animal models for increased drinking after TBI and the potential mechanistic insights that have been derived from those animal models. We conclude, based on the framework described, that it is possible that pediatric TBI causes alcohol use disorders in humans. Language: en |