Background
Recent evidence from clinical studies and animal models of traumatic brain injury
(TBI) suggest that neuronal and glial loss might progress after the initial insult
in selectively vulnerable regions of the brain such as the hippocampus. There is also
evidence that hippocampal dysfunction plays a role in the pathogenesis of mood disorders.
We examined the relationship between hippocampal damage and mood disorders after TBI
and the effect of hippocampal atrophy on the outcome of TBI patients.
Methods
The study group consisted of 37 patients with closed head injury who were evaluated
at baseline and at 3, 6, and 12 months after trauma. Psychiatric diagnosis was made
with a structured clinical interview and DSM-IV criteria. Quantitative magnetic resonance
imaging scans were obtained at 3-months follow-up.
Results
Patients with moderate to severe head injury had significantly lower hippocampal volumes
than patients with mild TBI. Patients who developed mood disorders had significantly
lower hippocampal volumes than patients without mood disturbance. Furthermore, there
was a significant interaction between mood disorders diagnosis and severity of TBI,
by which patients with moderate to severe TBI who developed mood disorders had significantly
smaller hippocampal volumes than patients with equivalent severe TBI who did not develop
mood disturbance. Finally, reduced hippocampal volumes were associated with poor vocational
outcome at 1-year follow-up.
Conclusions
Our findings are consistent with a “double-hit” mechanism by which neural and glial
elements already affected by trauma are further compromised by the functional changes
associated with mood disorders (e.g., the neurotoxic effects of increased levels of
cortisol or excitotoxic damage resulting from overactivation of glutaminergic pathways).
Finally, patients with greater hippocampal damage were less likely to return to a
productive life 1 year after trauma.
Key Words
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Article info
Publication history
Published online: November 24, 2006
Accepted:
July 19,
2006
Received in revised form:
July 17,
2006
Received:
April 20,
2006
Identification
Copyright
© 2007 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.