• Jonathan Lifshitz, Brian Joseph Kelley, and John Theodore Povlishock.
• Spinal Cord and Brain Injury Research Center, University of Kentucky Chandler Research Center, Lexington, Kentucky, USA. jlifshitz@uky.edu
• J. Neuropathol. Exp. Neurol. 2007 Mar 1;66(3):218-29.

AbstractMorbidity and mortality associated with traumatic brain injury (TBI) stem from diffuse axonal injury (DAI) throughout subcortical and brainstem white matter and subcortical nuclei. After midline fluid percussion brain injury, DAI in the thalamus includes perisomatic axotomy and resembles human post-traumatic pathology where the degree of morbidity correlates with thalamic damage. After axotomy, acute somatic perturbations resolve and appear compatible with cell survival; however, the long-term fate of neurons in an area with perisomatic axotomy is unknown. From brain-injured and uninjured rats at 1, 7 and 28 days after injury (injury, n = 5/group; sham, n = 4), alternate sections were immunostained for amyloid precursor protein (APP) to detect perisomatic axotomy or Giemsa stained for quantification of neuronal number, neuronal density, regional volume, and neuronal nuclear volume using design-based stereology. One day postinjury, APP-immunoreactive axons were identified consistently within the perisomatic domains of thalamic neurons of the ventral basal complex. Bilateral systematic-random quantification of the ventral basal complex indicated a significant reduction in neuronal density (number per mm, but not number alone) at 1 week after injury, compared with sham and 1 day postinjury. Furthermore, by 1 day and persisting through 1 week after injury, the mean neuronal nuclear volume was atrophied significantly compared with sham. Therefore, diffuse TBI results in early perisomatic axonal injury followed by neuronal atrophy in the ventral basal complex, without gross degeneration. Enduring atrophy in thalamic relays could underlie circuit disruption responsible for post-traumatic morbidity.

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