Innovations In Clinical Neuroscience

MAR-APR 2018

A peer-reviewed, evidence-based journal for clinicians in the field of neuroscience

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43 ICNS INNOVATIONS IN CLINICAL NEUROSCIENCE March-April 2018 • Volume 15 • Number 3–4 T Traumatic brain injury (TBI) has a complex pathophysiology. The damage has great variability in the severity of injury and the neuroanatomical location. At the cellular level, the neurobiological response to TBI is divided into acute and chronic phases. 1 Acutely, the mechanical forces from an injury can cause local depolarization, leading to glutamate excitotoxicity. 1,2 Locally compromised vasculature can also result in areas of ischemia. The resultant inability to remove waste products or deliver energy substrates causes dissolution of local ion gradients and tissue acidification by lactate buildup. Additionally, N-methyl- D-aspartate (NMDA)-dependent increases in intracellular calcium activate inflammatory and apoptotic pathways. 1 These biochemical processes play an important role in injury- associated cell death. In the chronic phase of TBI, there is persistent inflammation with increased levels of proinflammatory cytokines in peripheral blood. 3,4 Astrocyte activation results in altered gene expression and astrogliosis. Cell death can continue for weeks to months after a TBI. 5 The mechanisms of neuroplasticity and tissue remodeling reinforce existing neuronal connections to maintain circuit function. 3,6 H O T To p i c s in Neuroscience This ongoing column explores off-label or emerging treatment options, drug development trends, and theoretical concepts in the field of neuroscience. by ANJA SRIENC, PhD, MD; PUNEET NARANG, MD; SIMRAT SARAI, MD; YEE XIONG, MD; and STEVEN LIPPMANN, MD Dr. Srienc is with the Medical Scientist Training Program & Graduate Program in Neuroscience at the University of Minnesota in Minneapolis-St. Paul, Minnesota. Dr. Narang is Assistant Professor at the University of Minnesota, and Staff Physician, Lead ECT Psychiatrist at the Regions Hospital in Minneapolis-St. Paul, Minnesota. Dr. Sarai is Research Scholar at the University of Louisville School of Medicine in Louisville, Kentucky. Dr. Xiong is Psychiatry Resident, HCMC-Regions Psychiatry Residency Program in Minneapolis, Minnesota. Dr. Lippmann is Professor of Psychiatry at the University of Louisville School of Medicine in Louisville, Kentucky. Innov Clin Neurosci. 2018;15(13–4):43–46 A B S T R A C T Traumatic brain injury (TBI) can be caused by blunt or penetrating injury to the head. The pathophysiological evolution of TBI involves complex biochemical and genetic changes. Common sequelae of TBI include seizures and psychiatric disorders, particularly depression. In considering pharmacologic interventions for treating post-TBI depression, it is important to remember that TBI patients have a higher risk of seizures; therefore, the benefits of prescribing medications that lower the seizure threshold need to be weighed against the risk of seizures. When post-TBI depression is refractory to pharmacotherapy, electroconvulsive therapy (ECT) could provide an alternative therapeutic strategy. Data remain sparse on using ECT in this seizure-prone population, but three case reports demonstrated good outcomes. Currently, not enough evidence exists to provide clinical recommendations for using ECT for treating post-TBI depression, and more research is needed to generate guidelines on how best to treat depression in TBI patients. However, the preliminary data on using ECT in patients with TBI are promising. If proven safe, ECT could be a powerful tool to treat post-TBI depression . KEY WORDS: Traumatic brain injury, TBI, mood disorders, depression, treatments, electroconvulsive therapy, ECT FUNDING: Research reported in this publication was supported by the National Center for Advancing Translational Sciences of the National Institutes of Health Award Number UL1TR000114. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. DISCLOSURES: The authors have no conflicts of interest relevant to the content of this article. CORRESPONDENCE: Puneet Narang, MD; Email: Puneet.d.Narang@healthpartners.com Is Electroconvulsive Therapy a Treatment for Depression Following Traumatic Brain Injury?

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