Chapter 20 - Comparing radiation and traumatic brain injuries: New insights

Abstract

This chapter will identify similar mechanisms that may account for the changes in brain structure and function resulting from Traumatic Brain Injury and Radiation-Induced Brain Injury. The similar mechanisms are important because the management of the patient may include similar pharmaceuticals even while the insult to the brain from TBI results from the interaction of shear pressure forces, whereas the injury from RBI result from absorption of ionizing radiation and vascular injury on brain parenchyma. The organization of the chapter progresses from a consideration of the major anatomic changes observed following TBI and radiation exposure, to the common mechanisms (oxidative and nitrosative stress) associated with each of these shearing and ionizing stresses on neural function, to intracellular compartmental stresses (endoplasmic reticulum stress, unfolded protein response events and the renin angiotensin response). Both insults affect the endothelial cell of the microvascular structure of the brain, increase the permeability of the blood-brain barrier (BBB), cause neuronal apoptosis, glial responses, and microglial activation including major inflammatory responses in the interface between the gray/white matter. The increased permeability of the BBB has as a consequence the exposure of brain parenchyma to toxicants and infectious agents that may be in the vascular compartment and thereby compromise the integrity of neural function. The pharmacological approaches to mitigate the neuropathological events associated with TBI and RBI utilize similar drugs including atorvastatin (inhibitor of HMG-CoA reductase) and Ramipril (ACE 2 inhibitor) which are administered systemically.