Citation

Effgen GB, Vogel E, Lynch KA, Lobel A, Hue CD, Meaney D, Bass CD, Morrison B. J. Neurotrauma 2014; 31(13): 1202-1210.

Affiliation

Columbia University, Department of Biomedical Engineering, New York, New York, United States ; ge2121@columbia.edu.

Copyright

(Copyright © 2014, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2013.3227

PMID

24558968

Abstract

An increasing number of U.S. soldiers are diagnosed with traumatic brain injury (TBI) following exposure to blast. In the field, blast injury biomechanics are highly complex and multiphasic. The pathobiology caused by exposure to some of these phases in isolation, such as penetrating or inertially-driven injuries, has been investigated extensively. However, it is unclear whether the primary component of blast, a shock wave, is capable of causing pathology on its own. Previous in vivo studies in the rodent and pig have demonstrated that it is difficult to deliver a primary blast (i.e. shock wave only) without rapid head accelerations and potentially confounding effects of inertially-driven TBI. We have previously developed a well-characterized shock tube and custom in vitro receiver for exposing organotypic hippocampal slice cultures (OHSC) to pure primary blast. In this study, isolated primary blast induced minimal hippocampal cell death (on average below 14% in any region of interest), even for the most severe blasts tested (424 kPa peak pressure, 2.3 ms overpressure duration, and 248 kPa-ms impulse). In contrast, measures of electrophysiological function were significantly altered at much lower exposures (336 kPa, 0.84 ms, 86.5 kPa-ms), indicating that functional changes occur at exposures below the threshold for cell death. This is the first study to investigate a tolerance for primary blast-induced brain cell death in response to a range of blast parameters and to demonstrate functional deficits at sub-threshold exposures for cell death.

Language: en