Alcohol abuse after traumatic brain injury: Experimental and clinical evidence. (March 2016)

• Record Type: Journal Article
• Authors: Weil, Zachary M.; Corrigan, John D.; Karelina, Kate
• Is Part Of: Neuroscience and biobehavioral reviews. Volume 62(2016)
• Page Start: 89
• Page End: 99
• Publication Date: 2016-03
• Subjects: Traumatic brain injury -- Alcohol -- Inflammation -- Substance abuse -- Rehabilitation -- Reward; Psychophysiology -- Periodicals; Human behavior -- Periodicals; Animal behavior -- Periodicals; Neurology -- Periodicals; Behavior -- Periodicals; Ethology -- Periodicals; Neurology -- Periodicals; Psychophysiologie -- Périodiques; Comportement humain -- Périodiques; Animaux -- Mœurs et comportement -- Périodiques; Neurologie -- Périodiques; Animal behavior; Human behavior; Neurology; Psychophysiology; Periodicals; Electronic journals; 573.8
• DOI: 10.1016/j.neubiorev.2016.01.005
• Languages: English
• ISSNs: 0149-7634

Abstract

Highlights: Traumatic brain injury is bidirectionally linked to alcohol abuse. Brain injury patients may be more likely to abuse alcohol. Alcohol abuse after brain injury results in poorer long-term outcomes. We have developed an animal model of increased drinking after brain injury. Inflammation may link brain injury to alcohol abuse. Abstract: Brain injury survivors, particularly those injured early in life are very likely to abuse drugs and alcohol later in life. Alcohol abuse following traumatic brain injury (TBI) is associated with poorer rehabilitation outcomes and a greatly increased chance of suffering future head trauma. Thus, substance abuse among persons with brain injury reduces the chances for positive long-term outcomes and greatly increases the societal costs. In this review, we discuss the evidence for modulation of drinking behavior after TBI and the costs of problem drinking after TBI from both a biomedical and economic perspective. Further, we review the existing animal models of drinking after brain injury and consider the potential underlying psychosocial and neurobiological mediators of this phenomenon. In particular, we highlight the potential interactions among TBI, neuroinflammation and alcohol abuse. Substance abuse is a major problem in this vulnerable patient population and a greater understanding of the underlying biology has the potential to greatly improve outcomes.