Major depression following traumatic brain injury.
BACKGROUND
Major depression is a frequent psychiatric complication among patients with traumatic brain injury (TBI). To our knowledge, however, the clinical correlates of major depression have not been extensively studied.


OBJECTIVE
To determine the clinical, neuropsychological, and structural neuroimaging correlates of major depression occurring after TBI.


METHODS
Prospective, case-controlled, surveillance study conducted during the first year after the traumatic episode occurred. Settings University hospital level I trauma center and a specialized rehabilitation unit.


METHODS
The study group consisted of 91 patients with TBI. In addition, 27 patients with multiple traumas but without evidence of central nervous system injury constituted the control group. The patients' conditions were evaluated at baseline and at 3, 6, and 12 months after the traumatic episode. Psychiatric diagnosis was made using a structured clinical interview and DSM-IV criteria. Neuropsychological testing and quantitative magnetic resonance imaging were performed at the 3-month follow-up visit.


RESULTS
Major depressive disorder was observed in 30 (33%) of 91 patients during the first year after sustaining a TBI. Major depressive disorder was significantly more frequent among patients with TBI than among the controls. Patients with TBI who had major depression were more likely to have a personal history of mood and anxiety disorders than patients who did not have major depression. Patients with major depression exhibited comorbid anxiety (76.7%) and aggressive behavior (56.7%). Patients with major depression had significantly greater impairment in executive functions than their nondepressed counterparts. Major depression was also associated with poorer social functioning at the 6-and 12-month follow-up, as well as significantly reduced left prefrontal gray matter volumes, particularly in the ventrolateral and dorsolateral regions.


CONCLUSIONS
Major depression is a frequent complication of TBI that hinders a patient's recovery. It is associated with executive dysfunction, negative affect, and prominent anxiety symptoms. The neuropathological changes produced by TBI may lead to deactivation of lateral and dorsal prefrontal cortices and increased activation of ventral limbic and paralimbic structures including the amygdala.
Jorge
Ricardo E
RE
Department of Psychiatry, University of Iowa, 500 Newton Road, Iowa City, IA 52242, USA. ricardo-jorge@uiowa.edu
Robinson
Robert G
RG
Moser
David
D
Tateno
Amane
A
Crespo-Facorro
Benedicto
B
Arndt
Stephan
S
D000328:Adult; D000374:Aggression / Q000523:psychology; D001008:Anxiety Disorders / Q000175:diagnosis / Q000453:epidemiology / Q000209:etiology; D001284:Atrophy; D001930:Brain Injuries / Q000150:complications* / Q000453:epidemiology / Q000523:psychology; D020208:Brain Injury, Chronic / Q000150:complications / Q000175:diagnosis / Q000453:epidemiology; D016022:Case-Control Studies; D015984:Causality; D015897:Comorbidity; D003430:Cross-Sectional Studies; D003865:Major Depressive Disorder / Q000175:diagnosis / Q000453:epidemiology / Q000209:etiology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007484:Iowa; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009104:Multiple Trauma / Q000150:complications / Q000453:epidemiology / Q000523:psychology; D009483:Neuropsychological Tests / Q000706:statistics & numerical data; D010555:Personality Inventory / Q000706:statistics & numerical data; D017397:Prefrontal Cortex / Q000293:injuries / Q000473:pathology; D011594:Psychometrics / Q000706:statistics & numerical data; D012307:Risk Factors