CHARACTERIZATION OF EDEMA BY DIFFUSION-WEIGHTED IMAGING IN EXPERIMENTAL TRAUMATIC BRAIN INJURY

The objective of this study was to use diffusion-weighted magnetic res onance imaging (DWI) to help detect the type of edema that develops af ter experimental trauma and trauma coupled with hypotension and hypoxi a (THH). Reduction in the apparent diffusion coefficients (ADCs) is th ought to represent cytotoxic edema. In a preliminary series of experim ents, the infusion edema model and middle cerebral artery occlusion mo dels were used to confirm the direction of ADC change in response to p urely extracellular and cytotoxic edema, respectively. The ADCs increa sed (p < 0.05) in the case of extracellular edema and decreased (p < 0 .001) in cytotoxic edema. Following these initial experiments, a new i mpact acceleration model was used to induce traumatic brain injury. Th irty-six adult Sprague-Dawley rats were separated into four groups: sh am, trauma alone, hypoxia and hypotension (HH), and THH. Following tra uma, a 30-minute insult of hypoxia (PaO2 of 40 mm Hg) and hypotension (mean arterial blood pressure (MABP) of 30 mm Hg) were imposed and the animals were resuscitated. The DWI was carried out at four 1-hour int ervals postinjury, and MABP, intracranial pressure (ICP), cerebral per fusion pressure (CPP), and cerebral blood flow (CBF) were monitored. T he ADCs in the control and III-I groups remained unchanged. The ADCs i n the THH group rapidly decreased from a control level of 0.68 +/- 0.0 5 x 10(-3) mm(2)/second to 0.37 +/- 0.09 x 10(-3) mm(2)/second by 3 ho urs posttrauma (p < 0.001). In this group, the decreased CBF and CPP d uring secondary insult remained low despite resuscitation, with the IC P increasing to 56 +/- 7 mm Hg by 3 hours. In the trauma alone group, the rise in ICP reached a maximum value (28 +/- 3 mm Hg) at 30 minutes with a significant and sustained increase in CBF despite a gradual de crease in CPP. The ADCs in this group were not significantly reduced. The data lead the authors to suggest that the rise in ICP following se vere trauma coupled with secondary insult in this model is predominate ly caused by cytotoxic edema and that ischemia plays a major role in t he development of brain edema after head injury.