Understanding the intersection between substance misuse and acquired brain injury can assist clinicians in accurately diagnosing and treating these cooccurring conditions.
The relationship between substance misuse and acquired brain injury (ABI) is well documented. Studies examining traumatic brain injury (TBI) model systems data revealed that more than 50% of patients treated for TBI were intoxicated at the time of injury.1 Alcohol misuse is also a risk factor for stroke. Chronic alcohol misuse has been associated with heart arrhythmias, blood clotting disorders, hypertension, and diabetes, all of which are risk factors for stroke.2
Opioids and illicit “street drugs” have also been linked to ABI. Nonfatal opioid overdose is associated with anoxic and hypoxic brain injuries due to the depressive effect of opioids on the respiratory system.3 Use of illicit stimulant drugs (eg, cocaine, methamphetamine, etc) can elevate heart rate and blood pressure to dangerous levels and have been associated with hemorrhagic stroke.4,5
It is important for clinicians to understand the relationship between substance misuse and acquired brain injury, and to accurately diagnose and treat these cooccurring conditions, as a substantial number of individuals with ABI return to risky levels of alcohol and/or drug consumption within the first few years after injury.6 Individuals who continue to misuse substances following discharge from rehabilitation are at higher risk for reinjury, development of mood disorders, increased mortality, and decreased life satisfaction.7
A thorough clinical interview can provide a subjective measure of both the extent and the impact of substance misuse. Evidence demonstrates that using motivational interviewing techniques (eg, asking open-ended questions, reflective listening, and eliciting the patient’s thoughts about change) can help obtain information, build rapport, and begin the process of behavior change.8 Gauging a patient’s readiness for change can also guide treatment planning and selection of appropriate interventions in order to meet the patient where they are in the change process.9
Standardized assessments provide an objective measure of substance use/misuse. Instruments that have been used successfully with the ABI population include the CAGE Assessment10 and the Alcohol Use Disorders Identification Test (AUDIT)11 for alcohol use, and the Alcohol, Smoking, and Substance-Use Involvement Screening Test (ASSIST)12 and the Substance Abuse Subtle Screening Inventory (SASSI)13 for both alcohol and drug use.
Several treatment interventions for cooccurring ABI and substance misuse have been proposed and evaluated. Brief treatment including screening, patient education, and brief interventions may slow the resumption of future alcohol use.14 Other best practices for the treatment of substance use disorders in the ABI population include patient and family education, incentives to encourage treatment attendance and retention, use of motivational interviewing techniques, and interventions to support adaptive coping and adjustment.15-18
Patient and family education with information about the negative effects of continued substance misuse—particularly suppression of cognitive recovery, increased risk for seizures, potential interactive effects of alcohol and prescribed medications, and increased risk for sustaining a second TBI—have been shown to be beneficial in reducing resumption of substance use.19 Some studies suggest that providing firm recommendations regarding abstinence, at least for the first full year following injury, can also impact substance misuse following rehabilitation.
Corrigan20 has suggested tailoring substance misuse treatment and modifying any written materials to account for cognitive and linguistic deficits stemming from brain injury (eg, attention, memory, information processing speed, etc). Additionally, Corrigan21 has recommended a 4-quadrant model that describes the various settings where individuals with ABI can receive treatment, as well as the best treatment based on the severity of the brain injury and severity of substance misuse.
Quadrant I (low severity of brain injury and substance misuse) includes acute medical and primary care settings and interventions that provide screening and brief interventions. Quadrant II (low severity of substance misuse and high severity of brain injury) includes brain injury rehabilitation settings and interventions that provide education, screening, brief interventions, and linkages to community supports and referral for ongoing substance use treatment. Quadrant III (high severity of substance misuse and low severity of brain injury) includes substance use treatment settings and interventions that provide screening, accommodations (for cognitive-linguistic deficits), and service linkage. Quadrant IV (high severity of substance misuse and brain injury) includes specialized brain injury and substance use services, including integrated programming.
Alcoholics Anonymous (AA) and Narcotics Anonymous (NA) have also been suggested as helpful resources in providing education and social support and promoting personal responsibility/accountability.
Finally, pharmacological treatments of substance misuse in the ABI population have been recommended as an adjunct to traditional therapies, or when therapy alone has been unsuccessful.22 Naltrexone, acamprosate, and disulfiram (Antabuse) are US Food and Drug Administration (FDA)-approved medications for the treatment of alcohol use disorder. Naltrexone and acamprosate act to reduce alcohol cravings, whereas disulfiram operates via aversive counterconditioning. It is recommended that these medications be initiated after a period of abstinence, and they may require liver function tests. Naltrexone, methadone, and buprenorphine are FDA-approved to treat opioid dependence. These medications also reduce cravings by binding with opioid receptors.
Dr Seale is the regional director of clinical services at the Centre for Neuro Skills, which operates post-acute brain injury rehabilitation programs in California and Texas. He is licensed in Texas as a chemical dependency counselor and psychological associate with independent practice. He also holds a clinical appointment at the University of Texas Medical Branch (UTMB) in Galveston in the Department of Rehabilitation Sciences.
1. Corrigan JD. Substance abuse as a mediating factor in outcome from traumatic brain injury. Arch Phys Med Rehabil. 1995;76(4):302-309.
2. Gorelick PB. Alcohol and stroke. Stroke. 1987;18(1):268-271.
3. Schirmer DM, Seale GS. Non-lethal opioid overdose and acquired brain injury: a position statement of the Brain Injury Association of America. Brain Injury Association of America; 2018.
4. Sordo L, Indave BI, Barrio G, et al. Cocaine use and risk of stroke: a systematic review. Drug Alcohol Depend. 2014;142:1-13.
5. Lappin JM, Darke S, Farrell M. Stroke and methamphetamine use in young adults: a review. J Neurol Neurosurg Psychiatry. 2017;88(12):1079-1091.
6. Ponsford J, Whelan-Goodinson R, Bahar-Fuchs A. Alcohol and drug use following traumatic brain injury: a prospective study. Brain Inj. 2007;21(13-14):1385-1392.
7. Zgaljardic DJ, Seale GS, Schaefer LA, et al. Psychiatric disease and post-acute traumatic brain injury. J Neurotrauma. 2015;32(23):1911-1925.
8. Miller WR, Rollnick S. Motivational Interviewing: Helping People Change. Guilford Press; 2013.
9. DiClemente CC. Addiction and Change: How Addictions Develop and Addicted People Recover. Guilford Press; 2018.
10. Ewing JA. Detecting alcoholism. the CAGE questionnaire. JAMA. 1984;252(14):1905-1907.
11. World Health Organization. AUDIT: The Alcohol Use Disorders Identification Test: Guidelines for Use in Primary Health Care. 2nd Edition. World Health Organization; 2001.
12. World Health Organization. The Alcohol, Smoking and Substance Involvement Screening Test (ASSIST). World Health Organization. January 1, 2010.
13. Miller GA. The Substance Abuse Subtle Screening Inventory (SASSI) Manual, Second Edition. The SASSI Institute; 1985, 1999.
14. Bogner J, Corrigan JD, Peng J, et al. Comparative effectiveness of a brief intervention for alcohol misuse following traumatic brain injury: a randomized controlled trial. Rehabil Psychol. 2021;66(4):345-355.
15. Jones GA. Substance abuse treatment for persons with brain injuries: identifying models and modalities. Neurorehabilitation. 1992;2(1):27-34.
16. Bombardier CH, Rimmele CT. Motivational interviewing to prevent alcohol abuse after traumatic brain injury: a case series. Rehabil Psychol. 1999;44(1):52-67.
17. Corrigan JD, Bogner J. Interventions to promote retention in substance abuse treatment. Brain Inj. 2007;21(4):343-356.
18. Vungkhanching M, Heinemann AW, Langley MJ, et al. Feasibility of a skills-based substance abuse prevention program following traumatic brain injury. J Head Trauma Rehabil. 2007;22(3):167-176.
19. Seaton JD, David CO. Family role in substance abuse and traumatic brain injury rehabilitation. J Head Trauma Rehabil. 1990;5(3):41-46.
20. Corrigan JD. Substance abuse. In: High WM, Sander AM, Struchen MA, Hart KA, eds. Rehabilitation for Traumatic Brain Injury. Oxford University Press; 2005:133-155.
21. Corrigan JD. The treatment of substance abuse. In: Zasler ND, Katz DL, Zafonte RD, et al, eds. Brain Injury Medicine: Principles and Practice. Demos Publications; 2013.
22. Corrigan JD, Mysiw WJ. Substance abuse among persons with TBI. In: Zasler ND, Katz DL, Zafonte RD, et al, eds. Brain Injury Medicine: Principles and Practice. Demos Publications; 2013.