Traumatic Brain Injuries in Early Life Linked to Alcohol Abuse
24th August 2017
By Elliot Miller
The relationship between traumatic brain injuries (TBI) and alcohol abuse has long been considered to be unidirectional, with drinking a significant risk factor for TBI. While drunk, people are at an increased risk of head injuries. In the US, up to 50% of TBI emergency department admissions involve alcohol use. But could the opposite – that TBI is a risk factor for the development of alcohol use disorders (AUDs) – also be true?
There is limited evidence that TBI may serve as an independent risk factor for alcohol abuse, because problem drinking in adults is a significant predictor of TBI. Therefore, the TBI population is disproportionately made up of heavy drinkers, making it difficult to discern whether alcohol use increases post-TBI. However, when studies have examined individuals injured in early life, TBI has been consistently and repeatedly associated with the development of AUDs, as found in a new study published in Frontiers in Behavioural Neuroscience.
Researchers at Ohio State University examined previous studies to investigate the relationship between TBI and alcohol abuse. They found evidence that TBIs in children and adolescents could lead to alcohol abuse in later life. For example, children who suffer a TBI before age 5 are over 3.6 times more likely to display substance abuse as teenagers, compared with uninjured children. The review also revealed similar discrepancies between age of injury and post-TBI drinking behaviour in animal studies. An experiment – involving the co-authors of this study – found that mice injured as juveniles, but not as adults, drink significantly more alcohol in adulthood.
To summarise, the converging evidence suggests that brain injuries may in fact lead to the development of AUDs, especially among patients that suffer TBIs in early life. So, what are the potential mediators of alcohol abuse after TBI?
First, TBI reduces the effects of psychosocial factors that protect against alcohol abuse. For instance, participation in extracurricular activities, likelihood of educational success/full time employment and forming stable romantic relationships are associated with reduced risk of alcohol abuse, yet are all less likely in brain injury survivors. Also, TBI often results in cognitive dysfunction – making individuals more impulsive and less able to perceive the negative consequences of their actions – increasing the likelihood of AUDs. Furthermore, there is the possibility that brain injury survivors drink to self-medicate – reducing negative emotions or pain induced by brain injury.
Second, TBI can cause neuroinflammation. The interaction between neuroinflammation and alcohol intake – whereby inflammatory responses drives alcohol intake and vice versa – creates a vicious cycle in which inflammatory responses promote drinking behaviours and subsequent drinking further exacerbates inflammatory responses.
Lastly, a common consequence of TBI is the presence of neurochemical abnormalities. There is evidence that dysfunction in dopaminergic signalling is a risk factor for the development of AUDs. As the dopaminergic system undergoes significant developmental changes during childhood development, this can explain why early life injuries are more strongly related to later alcohol abuse.
Although the explicit mechanisms that link TBI and alcohol abuse are unclear, evidence suggests the presence of psychosocial and neuroanatomic risk factors, during important developmental periods, may underlie increased alcohol intake in children and adolescents. This is an important problem to address because drinking after TBI is associated with poor long term outcomes; thus reducing alcohol abuse in this population will help to improve the efficacy of rehabilitation programs, and decrease the likelihood of future TBI.
The full article can be read here: http://journal.frontiersin.org/article/10.3389/fnbeh.2017.00135/full