Characterizing edema associated with cortical contusion and secondary insult using magnetic resonance spectroscopy.

It is traditionally believed that edema associated with brain contusion is vasogenic. The objective of this study was to quantify and characterize the edema in cortical contusion coupled with early hypoxia and hypotension. Sprague-Dawley rats were randomised into six groups: Sham, Trauma moderate (Tm), Trauma severe (Ts), Hypoxia and Hypotension (HH), Tm and Ts with HH (THHm; THHs). Trauma was induced with controlled cortical impact; associated secondary insults lasted 30 minutes. Water content was measured using tissue longitudinal relaxation time (T1). Apparent diffusion coefficient of water (ADC) was calculated from diffusion-weighted imaging and single voxel spectroscopy. In the trauma groups ICP increased at 30 minutes post trauma (p < 0.05) and then gradually decreased. Only in the THH groups, ICP showed a trend to continually rise. No ICP variations were seen in the others groups. The increase in water content at 4 hours post trauma was inversely related to ADC variation (p < 0.0001). A significant increase in water content with low ADC, developed in the injured region in Ts, THHm (p < 0.05) and THHs (p < 0.01) compared to Sham. Intracellular water rose in the whole brain in THH groups although more severely in the THHs (p < 0.01). Immediately after trauma ADC fell in the THH groups, but gradually increased in the THHm, whereas there was no recovery in THHs. The results indicate that the type of edema in the injured area, with and without superimposed secondary insult, is predominantly cytotoxic (cellular). Moreover, secondary insults act synergistically with focal injury to increase cellular water in both injured tissue and remote regions.