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Natural History of Depression in Traumatic Brain Injury Sureyya S 1457 Natural History of Depression in Traumatic Brain Injury Sureyya S. Dikmen, PhD, Charles H. Bombardier, PhD, Joan E. Machamer, MA, Jesse R. Fann, MD, MPH, Nancy R. Temkin, PhD ABSTRACT. Dikmen SS, Bombardier CH, Machamer JE, range of rate estimates likely stems from estimates made at Fann JR, Temkin NR. Natural history of depression in differing times postinjury as well as differences in patient traumatic brain injury. Arch Phys Med Rehabil 2004;85:1457- populations and depression ascertainment methods. Many stud- 64. ies have drawn from small samples and tertiary referral popu- Objective: To examine prospectively the rates, risk factors, lations, thus limiting generalizability of the findings. 5,14,15 and phenomenology of depression over 3 to 5 years after Although some studies have reported a higher rate of traumatic brain injury (TBI). depression among person’s with more severe TBI, the findings Design: Inception cohort longitudinal study. of various other studies6-8,16,17 have been inconsistent with Setting: Level I trauma center. respect to the relations between TBI severity indicators, such as Participants: Consecutive admissions of 283 adults with duration of loss of consciousness and posttraumatic amnesia moderate to severe TBI. (PTA), and the incidence and severity of depression. Stud- Interventions: Not applicable. ies2,3,5,6,18 examining demographic and preinjury risk factors Main Outcome Measure: Center for Epidemiologic Studies have suggested poor social functioning, unstable work status, Depression (CES-D) Scale. lower education, younger age, and past psychiatric history as Results: The rates of moderate to severe depression ranged risk factors for subsequent depression. However, these and from 31% at 1 month to 17% at 3 to 5 years. With 1 exception, other risk factor data have not been consistently replicated in the relation between brain injury severity and depression was the literature.1 negligible. Less than high school education, preinjury unstable Some investigators have suggested that the phenomenology work history, and alcohol abuse predicted depression after of depressive symptoms that arise after TBI differs from that injury. Examination of CES-D factors indicate that, in addition which arises de novo or secondary to other medical conditions, to somatic symptoms, both depressed affect and lack of posi- and that these symptoms may also vary according to the time tive affect contribute to elevated CES-D scores. postinjury.19,20 Although the most prevalent depression-related Conclusions: High rates of depressive symptoms cannot be symptoms include fatigue and concentration difficulties, more dismissed on grounds that somatic symptoms related to brain severe depression and presence of anxiety and vegetative or injury are mistaken for depression. Depressed affect and lack somatic symptoms seem more common in early-onset depres- of positive affect are also elevated in persons with TBI. Pre- sion than in later-onset depression.19,20 Few studies have lon- injury psychosocial factors are predictive of depression and gitudinally examined depression phenomenology beyond 1 knowing them should facilitate efforts to detect, prevent, and year after TBI.21,22 These studies indicate only a general atten- treat depression after TBI. uation of depression symptoms after 1 year. Key Words: Brain injuries; Depression; Risk factors; Re- A better understanding of the magnitude and unique presen- habilitation. tation of post-TBI depression may assist clinicians in commu- © 2004 by the American Congress of Rehabilitation Medi- nicating with patients about their symptoms and recognizing cine and the American Academy of Physical Medicine and and treating depression and associated behaviors in this popu- Rehabilitation lation. The goal of the present study was to examine prospec- tively the rates, risk factors, and phenomenology of depressive EPRESSION CAN SIGNIFICANTLY add to the suffer- symptoms over a 3- to 5-year period in persons with moderate Ding and functional impairment of persons who sustain to severe TBI. traumatic brain injuries (TBI).1 However, rates, risk factors, and phenomenology of depression after TBI may not follow METHODS patterns found in community or other medical populations. Rate estimates for depression after TBI have ranged from Participants 14% to 42% within the first year2-6 and from 11% to 61% at various time points up to 50 years after injury.7-13 The wide The subjects for this study were adult patients with TBI involving intracranial abnormalities consecutively admitted to a level I trauma center. The subjects were enrolled between 1991 and 1995 in the Valproate Prophylaxis Study.23 This was From the Department of Rehabilitation Medicine (Dikmen, Bombardier, Macha- a randomized, placebo-controlled and double-blinded investi- mer, Fann), Neurological Surgery (Dikmen, Temkin), Psychiatry and Behavioral Sciences (Dikmen, Fann), and Biostatistics (Temkin), University of Washington, gation of the efficacy of valproate sodium in preventing post- Seattle, WA. traumatic seizures and its neuropsychologic side effects. The Supported by the National Institutes of Health, National Institute of Neurological selection criteria principally required computed tomography Disorders and Stroke (grant no. RO1 NS19643) and the National Center for Medical (CT) evidence or intracranial abnormality, including cortical Rehabilitation Research (grant nos. RO1 HD39415, RO1 HD33677). No commercial party having a direct financial interest in the results of the research contusion, intracerebral, subdural, or epidural hematoma, de- supporting this article has or will confer a benefit upon the author(s) or upon any pressed skull fracture, or penetrating brain injury. Subjects organization with which the author(s) is/are associated. were further required to be at least 14 years old when injured Correspondence to Sureyya S. Dikmen, PhD, Dept of Rehabilitation Medicine, and have no history of preinjury seizures or other significant Box 356490, University of Washington, Seattle, WA 98195, e-mail: dikmen@ u.washington.edu. Reprints are not available from the author. brain injury or neurologic condition. The subjects included in 0003-9993/04/8509-8643$30.00/0 the present study can be described as those hospitalized with doi:10.1016/j.apmr.2003.12.041 severity of brain injury ranging from complicated mild (ie, Arch Phys Med Rehabil Vol 85, September 2004 1458 DEPRESSION IN TRAUMATIC BRAIN INJURY, Dikmen Glasgow Coma Scale [GCS] score, 13–15 with CT abnormal- situations included living alone, with roommates, group home, ities) to severe (GCS score, 3–12). Approximately one third of congregate care facilities, hospital, nursing home, or other hospitalized cases in our series with a GCS score of 13 to 15 institutions. Work stability was examined for those whose had CT abnormalities; for those with more severe injuries, over major preinjury activity was work as opposed to school, home- 90% had CT abnormalities. We believe the cases of this study making, or retirement. Stable workers were defined as those are representative of cases with complicated mild to severe who were working half time or more in the same job in the brain injuries. immediate 6 months before injury. Unstable workers were Subjects who were available for neurobehavioral testing and either unemployed at the time of the injury, employed for less able to take the tests validly (cognitive status did not preclude than half time, or at the same job for less than 6 months. valid testing) were evaluated at 1 month (nϭ213), 6 months Subjects were divided into those with or without a preexisting (nϭ249), 12 months (nϭ193), and 3 to 5 years postinjury psychiatric history. Subjects considered to have a prior psychi- (nϭ175). Tested subjects were oriented times 3, were able to atric history had 1 or more of the following: outpatient help participate at least 1 hour in the testing session, and could show from a psychiatrist, psychologist, social worker, or counselor; that they comprehended the questions and were able to give hospitalization for emotional or psychiatric reasons; or medi- reliable responses to the examiner. This study was approved by cation for emotional problems. Psychiatric history was evalu- the University of Washington Institutional Review Board. ated for the year before the injury and for anytime preinjury. Findings on the impact of valproate on posttraumatic sei- Preinjury alcohol abuse was determined by using the Short zures and neuropsychologic functioning show that valproate Michigan Alcoholism Screening Test38 (SMAST). The does not prevent late posttraumatic seizures and does not have SMAST is a 13-item questionnaire that examines the negative negative or positive effects on neuropsychologic function- consequences of drinking, prior treatment, and dependence ing.23,24 symptoms. Preinjury SMAST scores formed 2 groups, those with little or no alcohol problems (SMAST score, Յ2) and Measures those with scores indicative of significant alcohol problems Depressive symptoms were evaluated by the Center for (SMAST score, Ն3). The SMAST was evaluated for the year Epidemiologic Studies Depression (CES-D) Scale.25 This is a before the injury and for anytime preinjury. well-validated measure that consists of 20 symptoms that are rated by frequency of occurrence in the last week, with 0 being Data Analysis less than 1 day a week, 1 representing 1 to 2 days a week, 2 The data were analyzed to answer the following questions: denoting 3 to 4 days a week, and 3 representing 5 to
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