1. ¹National Security Technology Department, Johns Hopkins University Applied Physics Laboratory, Laurel, Maryland, USA
2. ²Department of Neurological Surgery and Department of Physical Therapy and Rehabilitation Science, University of California, San Francisco, California, USA

Correspondence: Dr I Cernak, National Security Technology Department, Johns Hopkins University, Applied Physics Laboratory, Biomedicine Business Area, 11100 Johns Hopkins Road, Mail Stop MP2 N108, Laurel, MD 20723, USA. E-mail: ibolja.cernak@jhuapl.edu

Received 5 June 2009; Revised 16 August 2009; Accepted 7 September 2009; Published online 7 October 2009.

Abstract

This review considers the pathobiology of non-impact blast-induced neurotrauma (BINT). The pathobiology of traumatic brain injury (TBI) has been historically studied in experimental models mimicking features seen in the civilian population. These brain injuries are characterized by primary damage to both gray and white matter and subsequent evolution of secondary pathogenic events at the cellular, biochemical, and molecular levels, which collectively mediate widespread neurodegeneration. An emerging field of research addresses brain injuries related to the military, in particular blast-induced brain injuries. What is clear from the effort to date is that the pathobiology of military TBIs, particularly BINT, has characteristics not seen in other types of brain injury, despite similar secondary injury cascades. The pathobiology of primary BINT is extremely complex. It comprises systemic, local, and cerebral responses interacting and often occurring in parallel. Activation of the autonomous nervous system, sudden pressure-increase in vital organs such as lungs and liver, and activation of neuroendocrine-immune system are among the most important mechanisms significantly contributing to molecular changes and cascading injury mechanisms in the brain.