Backgroud
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.
Design
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.