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June 2018

Neurobiology of Opioid Use Disorder and Comorbid Traumatic Brain Injury

Author Affiliations
  • 1Menninger Department of Psychiatry and Behavioral Sciences, Baylor College of Medicine, Houston, Texas
  • 2Michael E. DeBakey Veterans Affairs Medical Center, Houston, Texas
JAMA Psychiatry. 2018;75(6):642-648. doi:10.1001/jamapsychiatry.2018.0101

Importance  Treating patients with opioid use disorder (OUD) and traumatic brain injury illustrates 6 neurobiological principles about the actions of 2 contrasting opioid analgesics, morphine and fentanyl, as well as pharmacotherapies for OUD, methadone, naltrexone, and buprenorphine.

Observations  This literature review focused on a patient with traumatic brain injury who developed OUD from chronic morphine analgesia. His treatment is described in a neurobiological framework of 6 opioid action principles.

Conclusions and Relevance  The 6 principles are (1) coactivation of neuronal and inflammatory immune receptors (Toll-like receptor 4), (2) 1 receptor activating cyclic adenosine monophosphate and β-arrestin second messenger systems, (3) convergence of opioid and adrenergic receptor types on 1 second messenger, (4) antagonist (eg, naltrexone)–induced receptor trafficking, (5) genetic μ-opioid receptor variants influencing analgesia and tolerance, and (6) cross-tolerance vs receptor antagonism as the basis of OUD pharmacotherapy with methadone or buprenorphine vs naltrexone.

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