Citation

Leung LY, Wei G, Shear DA, Tortella FC. J. Neurotrauma 2013; 30(14): 1288-1298.

Affiliation

Walter Reed Army Institute of Research, Brain Trauma Neuroprotection and Neurorestoration Branch, 503 Robert Grant Avenue, Silver Spring, Maryland, United States, 20910; laiyee.leung@us.army.mil.

Copyright

(Copyright © 2013, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2012.2715

PMID

23461630

Abstract

Traumatic brain injury often occurs in conjunction with additional trauma resulting in secondary complications such as hypotension due to blood loss. This study investigated the combined effects of penetrating ballistic-like brain injury (PBBI) and hemorrhagic shock (HS) on physiological parameters including acute changes in regional cerebral blood flow (rCBF), brain tissue oxygen tension (PbtO2), and cortical spreading depolarizations (CSDs). All recordings were initiated prior to injury (PBBI /HS/ both) and maintained for 2.5 hours. Results showed that PBBI alone and combined PBBI and HS produced a sustained impairment of ipsilateral rCBF that decreased by 70% from baseline (p<.05). Significant and sustained reductions in PbtO2 (50% baseline; p<.05) were also observed in the injured hemisphere of the animals subjected to both PBBI and HS (PBBI+HS). In contrast, PBBI alone produced smaller and more transient reductions in PbtO2 levels. The lower limit of cerebral autoregulation was significantly higher in the PBBI+HS group (p<.05 compared to HS alone). Critically, the combined injury resulted in twice the number of spontaneous CSD as in the PBBI alone (p<.05). It also lowered the propagation speed of CSD and the threshold of CSD occurrence (induce CSD at higher MAP). However, rCBF and PbtO2 were not responsive to the depolarizations. Our data suggests that PBBI together with HS cause persistent impairment of CBF and brain tissue oxygen, increasing the probability of CSDs that likely contribute to secondary neuropathology and compromise neurological recovery.

Language: en