Protection against Blast-Induced Traumatic Brain Injury by Increase in Brain Volume.

Ming Gu,Mikulas Chavko,Richard McCarron,Usmah Kawoos

doi:10.1155/2017/2075463

Abstract

Blast-induced traumatic brain injury (bTBI) is a leading cause of injuries in recent military conflicts and it is responsible for an increased number of civilian casualties by terrorist attacks. bTBI includes a variety of neuropathological changes depending on the intensity of blast overpressure (BOP) such as brain edema, neuronal degeneration, diffuse axonal damage, and vascular dysfunction with neurological manifestations of psychological and cognitive abnormalities. Internal jugular vein (IJV) compression is known to reduce intracranial compliance by causing an increase in brain volume and was shown to reduce brain damage during closed impact-induced TBI. We investigated whether IJV compression can attenuate signs of TBI in rats after exposure to BOP. Animals were exposed to three 110 ± 5 kPa BOPs separated by 30 min intervals. Exposure to BOP resulted in a significant decrease of neuronal nuclei (NeuN) together with upregulation of aquaporin-4 (AQP-4), 3-nitrotyrosine (3-NT), and endothelin 1 receptor A (ETRA) expression in frontal cortex and hippocampus one day following exposures. IJV compression attenuated this BOP-induced increase in 3-NT in cortex and ameliorated the upregulation of AQP-4 in hippocampus. These results suggest that elevated intracranial pressure and intracerebral volume have neuroprotective potential in blast-induced TBI.

Highlights

Traumatic brain injury (TBI) is of increasing concern in both military and civilian populations due to the long-term health problems and costs related to recovery from such injuries
The pattern of brain damage corresponds with the detailed analysis of brain histopathology previously described in the same blast model [22]
neuronal nuclei (NeuN)-staining showed a significant decrease of immunoreactive neurons in cortex in both blast overpressure (BOP) groups by ∼30% compared with controls (Figures 2(a) and 2(b))

Summary

Introduction

Traumatic brain injury (TBI) is of increasing concern in both military and civilian populations due to the long-term health problems and costs related to recovery from such injuries. The neurological impairment in bTBI may result from different mechanisms including both a direct shock wave effect on brain and an indirect transfer of the shock wave through blood vessels and cerebrospinal fluid (CSF) to the brain [4,5,6,7]. The breakdown of the BBB can result in brain edema and increase in intracranial pressure (ICP), accompanied by activation of secondary brain injury by impairing cerebral perfusion and oxygenation [10]. Activation of oxidative mechanisms and neuroinflammation has been shown to contribute to the neurodegeneration and cell apoptosis in secondary brain injury following bTBI [11, 12]

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