Citation

Salzar RS, Treichler D, Wardlaw A, Weiss G, Goeller J. J. Neurotrauma 2016; 34(8): 1589-1602.

Affiliation

Advanced Technology & Research Corp. , 6650 Eli Whitney Dr. , Columbia, Maryland, United States , 21046 ; jgoeller@atrcorp.com.

Copyright

(Copyright © 2016, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2016.4600

PMID

27855566

Abstract

The potential of blast induced traumatic brain injury from the mechanism of localized cavitation of the cerebral spinal fluid is investigated. While the mechanism and criteria for non-impact blast-induced TBI injury is still unknown, this study demonstrates that local cavitation in the CSF layer of the cranial volume could contribute to these injuries. The cranial contents of three post mortem human surrogate cephali were replaced with both a normal saline solution, and a ballistic gel mixture with a simulated CSF layer. Each were instrumented with multiple pressure transducers and placed inside identical shock tubes at two different research facilities. Sensor data indicates that cavitation may have occurred in the PMHS models at pressure levels below those for a 50% risk of blast lung injury. This study points to skull flexion, the result of the shock wave on the front of the skull leading to a negative pressure in the contrecoup, as a possible mechanism that contributes to the onset of cavitation. Based on observation of intracranial pressure transducer data from the PMHS model, cavitation is thought to occur from around a 190 kPa incident blast.

Language: en