Major depression is common following traumatic brain injury and often complicated by anxiety or another psychiatric disorder

Major depression is common in the first year after a traumatic brain injury and is often associated with anxiety and executive dysfunction, according to an article in the January issue of the Archives of General Psychiatry.

Although previous work has suggested depression is a common psychiatric sequel to traumatic brain injury, research has not focused on the clinical implications, if any, of mood disorder following central nervous system insult. In the current study, 91 patients with traumatic brain injury and 27 patients treated at the same university center for multiple trauma excluding central nervous system injury were evaluated 3, 6, and 12 months after injury. At the 3-month visit, neuropsychological testing and magnetic resonance imaging of the brain were conducted.

Of the 91 patients with traumatic brain injury, 30 people (33 percent) were diagnosed with major depression during the first post-injury year, a statistically significant difference from the rate seen in the control trauma patients. The researchers also found that patients with brain injury and depression were more likely to have a history of mood and anxiety disorders than patients with brain injury who did not experience depression after their trauma.

Among the 30 patients with traumatic brain injury and depression, 76.7 percent also had anxiety and 56.7 percent exhibited aggressive behavior. Major depression was also associated with significantly greater impairment in executive functions during the follow-up period as well as worse social functioning at the 6- and 12-month follow-up.

On imaging, patients with major depression were more likely to have significantly decreased gray matter volume in the left prefrontal region, particularly in the ventrolateral and dorsolateral areas. The authors hypothesize that the neuropathological changes triggered by traumatic brain injury can lead to deactivation of the lateral and dorsal prefrontal cortex and increased activation of ventral limbic and paralimbic structures, including the amygdala.


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