CONCLUSIONS

There are two major findings from this investigation.

First, neurons survive for at least three days in the area of contused cortex destined to evolve into a fluid filled cyst in the subsequent three weeks.
Second, neuronal death begins in the deep lamina at the lateral edge of the directly traumatized cortex. This is likely due to the rupture of distal arterioles which are at their finest caliber and adjacent to the stiff corpus callosum in these lamina ( 3) and the sheering forces generated by the edge of the footplate.

These data indicate the very slow cyst development represents the spread of pancellular necrotic processes, a "tertiary" neuronal injury process of unknown mechanisms. Note that the ischemic area measured 1 day after injury closely follows the cortical area that will evolve over weeks into a cyst (Compare Figure 1 and Figure 3). Tissue along the midline of contused cortex is always spared and yet much of this region is directly underneath the footplate. Perhaps midline sparing is due to the cushioning by the contralateral hemisphere. Conversely, in the lateral aspect of the contused cortex extends beyond the edge of the footplate. Most likely this displaced tissue is compressed against the skull, exacerbating the injury and producing the asymmetric shape of the cyst.

The prolonged ischemia in the compromised environment of contused cortex, may contribute to the slow panecrosis. Other data indicate that despite the ischemia, neurons in contused cortex are viable for at least 14 days after 400 mg/cm impact. We previously reported (2) that microstimulation of contused cortex evoked appropriate movements for up to 2 weeks following TBI. Stimulation after 2 weeks was unsuccessful in evoking any movements. Together with this histological work, the data indicates that neurons in contused cortex appearing viable for days after TBI are also functional for up to two weeks following cortical contusion despite severe ischemia. Whether this is an extended "therapeutic window" when surviving neurons could be rescued from the progressive panecrosis is unknown.

References
1. Auer RN, Olsson Y, Siesjo BK (1984) Hypoglycemic brain injury in the rat: correlation of density of brain damage with the EEG isoelectric time: a quantitative study. Diabetes 33:1090-1098.
2. Boyeson MG, Feeney DM, Dail WG (1991) Cortical microstimulation thresholds adjacent to sensorimotor cortex injury. J. Neurotrauma 8(3):205-217.
3. Feeney DM, Boyeson MG, Linn RT, Murray HM, Dail WG (1981) Responses to cortical injury: I. Methodology and local effects of contusions in the rat. Brain Res 211:67-77.
4. Paxinos G, Watson C (1982) The rat brain in stereotaxic coordinates. Academic Press, New York.
5. Weisend, M.P. and Feeney, D.M. The relationship between traumatic brain injury-induced changes in brain temperature and behavioral and anatomical outcome. Journal of Neurosurgery, 80, 120-132, 1994.
6. Feeney, D. M. Rehabilitation Pharmacology:Noradrenergic Enhancement of Physical Therapy. In: Ginsberg, M. and Bogousslavsky, J. (Editors) Cerebrovascular Diseases, Vol. I.. Blackwell Scientific Press Cambridge MA (In Press.).

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