Traumatic Brain Injuries during Development: Implications for Alcohol Abuse

Weil, Zachary M.; Karelina, Kate

doi:10.3389/fnbeh.2017.00135

Cited by 16 publications

(11 citation statements)

References 106 publications

(127 reference statements)

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“…Moreover, drinking after TBI is associated with poor rehabilitation outcomes, greater morbidity and a greatly increased chance of future head injuries (Corrigan, 1995; Vaaramo et al, 2014). Given that young TBI patients are less likely to have developed problem drinking prior to injury, increasing evidence suggests that the vulnerability to alcohol abuse later in life is a consequence of TBI-related pathology (Weil et al, 2016a; Weil and Karelina, 2017).…”

Section: Introductionmentioning

confidence: 99%

Minocycline blocks traumatic brain injury-induced alcohol consumption and nucleus accumbens inflammation in adolescent male mice

Karelina

Nicholson

Weil

2018

Brain, Behavior, and Immunity

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Alcohol use is a well characterized risk factor for traumatic brain injury (TBI); however, emerging clinical and experimental research suggests that TBI may also be an independent risk factor for the development of alcohol use disorders. In particular, TBIs incurred early in life predict the development of problem alcohol use and increase vulnerability to neuroinflammation as a consequence of alcohol use. Critically, the neuroinflammatory response to alcohol, mediated in large part by microglia, may also function as a driver of further alcohol use. Here, we tested the hypothesis that TBI increases alcohol consumption through microglia-mediated neuroinflammation. Mice were injured as juveniles and alcohol consumption and preference were assessed in a free-choice voluntary drinking paradigm in adolescence. TBI increased alcohol consumption; however, treatment with minocycline, an inhibitor of microglial activation, reduced alcohol intake in TBI mice to sham levels. Moreover, a single injection of ethanol (2 g/kg) significantly increased microglial activation in the nucleus accumbens and microglial expression of the proinflammatory cytokine IL-1β in TBI, but not sham or minocycline-treated, mice. Our data implicate TBI-induced microglial activation as a possible mechanism for the development of alcohol use disorders.

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Section: Introductionmentioning

confidence: 99%

Minocycline blocks traumatic brain injury-induced alcohol consumption and nucleus accumbens inflammation in adolescent male mice

Karelina

Nicholson

Weil

2018

Brain, Behavior, and Immunity

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“…Second, although our overall sample size was relatively large, the heterogeneity of each individual disease state may have limited our power to detect the smaller effect sizes suggested by current data. Third, TBI can possibly be both a cause and a consequence of AUD (61), and the current sample did not have enough information (i.e., exact date of onset) to resolve these discrepancies. Fourth, patients with severe TBI were intentionally eliminated from the study, which may limit the generalizability of current null findings to a more mild to moderate injury group.…”

Section: Discussionmentioning

confidence: 87%

An Examination of Behavioral and Neuronal Effects of Comorbid Traumatic Brain Injury and Alcohol Use

Mayer

Hanlon

Claus

et al. 2018

Biological Psychiatry: Cognitive Neuroscience and Neuroimaging

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“…These changes explain the adolescents impulsive and novelty-seeking behavior traits [22]. TBI causes disruption to the developing nervous system, which increases the vulnerability to AUD and SUD [23]. TBI increases the risk of addiction by reducing the cognitive ability to perceive negative consequences and increases the perception of gains perceived by drinking and substance abuse [23].…”

Section: Discussionmentioning

confidence: 99%

“…TBI causes disruption to the developing nervous system, which increases the vulnerability to AUD and SUD [23]. TBI increases the risk of addiction by reducing the cognitive ability to perceive negative consequences and increases the perception of gains perceived by drinking and substance abuse [23]. A study by Patel et al found that cannabis abuse among youth increases the risk of intracranial injury by 1.3 times [24].…”

Section: Discussionmentioning

confidence: 99%

Alcohol Use Disorder Increases Risk of Traumatic Brain Injury-Related Hospitalization: Insights From 3.8 Million Children and Adolescent Inpatients

Eskander

Prabhudesai

Imran

et al. 2020

Cureus

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We conducted a cross-sectional study to identify the demographic predictors of traumatic brain injury (TBI), and the risk of association of psychiatric comorbidities including alcohol use disorder (AUD) and TBI-related hospitalizations in the children and adolescent population. Methods We included 3,825,523 children and adolescent inpatients (age 8-18 years) using the nationwide inpatient sample (NIS) database (2010-2014), and 61,948 inpatients had a primary diagnosis of TBI. These inpatients were grouped by comorbid AUD (N = 2,644). Multivariable logistic regression model adjusted for demographics, and psychiatric comorbidities including other substance use disorders (SUDs) was used to evaluate the odds ratio (OR) of AUD as a risk factor for TBI-related hospitalization. Results The majority of the TBI inpatients were adolescents (12-18 years, 82.2%), males (71.2%), and whites (59.2%). Males had three times higher odds (95% CI 3.14-3.26) for TBI-related hospitalization compared to females. Among psychiatric comorbidities, mood (4.1%) and anxiety (2.2%) disorders were prevalent in TBI inpatients, and were not associated with increased odds for TBI-related hospitalization. Among SUD, alcohol and tobacco use (4.4% each), and cannabis use (3.5%) were prevalent, and among all substances, AUD was associated with higher odds (OR 3.5, 95% CI 3.35-3.67) of TBI-related hospitalization. These patients with TBI and comorbid AUD also had higher odds for abusing stimulants (OR 5.11, 95% CI 3.85-6.77), cannabis (OR 4.69, 95% CI 4.12-5.34), and tobacco (OR 3.77, 95% CI 3.34-4.27). Conclusion AUD is an independent risk factor for TBI-related hospitalization with an increased risk of 50% in the children and adolescent population compared to non-alcohol users. TBI inpatients with AUD are prevalent in white, and male adolescents. These at-risk populations are also at higher risk of comorbid mood disorders and increased substance use including stimulants, cannabis, and tobacco.

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Traumatic Brain Injuries during Development: Implications for Alcohol Abuse

Cited by 16 publications

References 106 publications

Minocycline blocks traumatic brain injury-induced alcohol consumption and nucleus accumbens inflammation in adolescent male mice

Minocycline blocks traumatic brain injury-induced alcohol consumption and nucleus accumbens inflammation in adolescent male mice

An Examination of Behavioral and Neuronal Effects of Comorbid Traumatic Brain Injury and Alcohol Use

Alcohol Use Disorder Increases Risk of Traumatic Brain Injury-Related Hospitalization: Insights From 3.8 Million Children and Adolescent Inpatients

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