John M. Barkley
L. Anne Hayman
Pedro J. Diaz-Marchan
The term cerebral edema is often misused or misunderstood. Global cell injury or cell swelling has been called cerebral edema in the past. Multiple injuries to the brain or anoxic insult may present as diffuse abnormality, or brain swelling. Brain swelling occurs because of increased cerebral blood volume, loss of autoregulation of cerebral blood flow, or a generalized increase in tissue fluid. This manifests clinically as elevated intracranial pressure. Radiologically, brain swelling manifests as diffuse effacement of sulci, ventricles and cisterns. The normal appearing gray/ white matter interface is also lost and the brain appears somewhat featureless throughout (Figure 11-8). As mentioned earlier, severe brain swelling may lead to herniation syndromes in the craniocaudal axis—transtentorial, or inferiorly through the foramen magnum.
The prior confusion of the term cerebral edema stems from the fact that there are many different types of edema that have specific pathophysiology. Cytotoxic edema occurs when there is cell injury, ischemia or death.
Ion gradients that maintain cell homeostasis are lost, due to inactivation of the sodium/potassium ATP-ase. When ion gradients cannot be maintained, the cells eventually swell with fluid. An increase in water within the cell results in cytotoxic edema. This may be seen on CT as areas of subtle low density or loss of the normal gray/white interface—usually in a focal area or vascular territory. The visual density of gray and white matter on CT is abnormally uniform. Diffusion-weighted MRI (DWI) is very sensitive for areas of cytotoxic edema. Cytotoxic edema manifests as high signal on DWI sequences, or restricted diffusion (1).
DWI has gained widespread use in the work-up of acute stroke, among other abnormalities that demonstrate restricted diffusion. An emerging role for DWI in predicting outcome of patients presenting with traumatic brain injury will be discussed later.
Vasogenic edema occurs when there is an increase in extracellular free water. This often occurs around masses, abscesses or hemorrhages. It manifests on CT and routine MRI sequences as fingerlike areas of hypodensity extending from the mass/hemorrhage into the adjacent white matter. Because vasogenic edema is free extracellular water, there is no restricted diffusion on diffusionweighted
MRI sequences. The diffusion MRI sequence and apparent diffusion coefficient (ADC) map, a calculated parameter, can distinguish between cytotoxic edema (irreversible) and vasogenic edema (reversible). Cytotoxic edema is high in signal intensity on DWI and low in signal intensity on the ADC map, while free water or vasogenic edema is low in signal intensity on DWI. DWI has properties that reflect relative T2 weighting. Thus, anything that is bright on T2 or FLAIR sequences, may be bright on DWI. This is termed T2 shine-through. The ADC map image is devoid of T2 weighting, and should always be checked in the setting of bright foci on DWI, to confirm that restricted diffusion of water is actually present.
Interstitial edema is seen in the setting of hydrocephalus and increased intracranial pressure. There is transependymal resorption of CSF from the dilated ventricles into the periventricular regions. There is also an increase in extracellular free water. On imaging, interstitial edema appears as hypodensity in the periventricular locations.
Original: Brain Injury Medicine. Principles and Practice
- Mukherji SK, Chenevert TL, Castillo M. Diffusion-weighted magnetic resonance imaging. J Neuroophthalmol. 2002; 22(2): 118–22.