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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