Every year, 1.7 million people in the US sustain a traumatic brain injury (TBI), and nearly 1.1% of Americans live with a disability related to TBI.1 Psychiatric disorders frequently complicate the course of recovery from TBI and occur at rates exceeding those of the general population. Major depression is the most common psychiatric disorder following TBI, affecting an estimated 29.4% of patients in the first year post-injury alone.2 TBI-associated depression contributes to higher suicide risk, altered executive function, poorer social reintegration and vocational outcomes, and decreased quality of life.3
The chronic and relapsing course of TBI-associated depression poses a challenge to the management of afflicted patients. Two-thirds of patients depressed at 1-year post-injury remain so in the second year, and the risk of depression remains elevated for 20 to 30 years after the injury.3 In a small trial (N = 21) of citalopram’s efficacy to prevent relapse in patients with remitted TBI-associated depression, over half of the sample relapsed at a mean time of 6 months.4 The high prevalence, chronicity, and potentially irreversible consequences of post-TBI depression underscore the importance of developing interventions targeting this disorder.
Previous work in the field of TBI-associated depression has focused on treatment strategies. Conflicting results have been seen in randomized controlled trials (RCTs) examining the efficacy of pharmacotherapy for the treatment of TBI- associated depression. Results from a double-blind RCT of patients with TBI-associated depression who received 25 mg to 200 mg sertraline did not show a statistically significant difference in the severity of depressive symptoms compared with placebo after 12 weeks of treatment.5 RCTs of non-pharmacologic treatments have also yielded inconsistent results regarding their efficacy to treat TBI-associated depression.6
In general, preventive strategies are more effective than treatment interventions to decrease the burden of a disease. Our group published preliminary evidence supporting the efficacy of sertraline for the prevention of TBI-associated depression but preventive strategies for TBI-associated depression remain underdeveloped.7
Clinicians may be most familiar with the concepts of primary, secondary, and tertiary prevention. Primary prevention refers to interventions protecting against a disease before its onset, whereas secondary prevention refers to early interventions aimed at preventing disease progression. Tertiary prevention focuses on strategies that reduce the morbidity of a disease after its onset.
Because of the challenges of applying this scheme to the prevention of psychiatric disorders, the Institute of Medicine Committee on the Prevention of Mental Disorders in 1994 recommended a new classification scheme encompassing universal, selective, and indicated preventive strategies. When applied to TBI- associated depression, this scheme emphasizes the prevention of a depressive episode before it begins.
Universal prevention refers to strategies targeting the entire population; in the case of TBI-associated depression, one example would be the enforcement of laws against driving under the influence to reduce the incidence of TBI and hence associated depression. Selective interventions target high-risk groups. Because patients with TBI are at risk for depression, administering an intervention to all patients with a TBI falls under this category. Finally, indicated prevention targets patients with early signs of a disorder, such as those with TBI who have early signs of mood disturbance.
Dr Jones is Assistant Professor, and Dr Jorge is Professor and Acting Director, Beth K. and Stuart C. Yudofsky Division of Neuropsychiatry, Menninger Department of Psychiatry and Behavioral Sciences, Baylor College of Medicine, Houston, TX.
The authors report no conflicts of interest concerning the subject matter of this article.
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