Acute responses to experimental blunt head trauma

Abstract

Anesthetized cats subjected to impact followed by acceleration and rotation of the skull were sacrificed at 15 minutes or 6 hours after injury and were selected for study if unilateral cerebral contusion was present. Widespread areas of cerebral cortex were examined bilaterally for edema, using measurement of tissue density with an organic gradient, and for breakdown of the blood-brain barrier to plasma protein tagged with Evans blue dye. At both times tested, a halo of vasogenic edema (Evans blue stain plus decreased density) was present in the cortex surrounding areas of contusion. At 15 minutes after injury, animals with deep contusions also had a slight decrease in density without Evans blue staining, interpreted as cytotoxic edema, in some gyri neighboring the contusion. At 6 hours, cytotoxic edema was not evident, but some animals had vasogenic edema in the gyri adjoining the contusion. Most gyri contralateral to contused areas had neither Evans blue staining nor changes in tissue density. These findings suggest that, with the present head-injury model, acute changes in tissue density and vascular permeability occur in the cerebral cortex of hemispheres with contusion. These responses are related topographically to contusion sites, and change over the two times studied. The authors conclude that events in addition to spread of fluid from areas of contusion contribute to the edema of head injury, and that more than one form of edema can follow mechanical trauma to the brain.

An Unexpected Transient Breakdown of the Blood Brain Barrier Triggers Passage of Large Intravenously Administered Nanoparticles

“…Additionally, BBB dysfunction is a hallmark of several neurological conditions including multiple sclerosis and stroke 10 . BBB disruption is associated with concomitant spread of vasogenic brain oedema and axonal injury from a primary brain lesion to areas neuroanatomically connected to the injured region 11 12 . Moreover, both traumatic and inflammatory brain injuries are directly associated with increased inter- and intracellular transport making the BBB tight junctions leaky 13 .…”

Changes in Local Microvascular Permeability and in the Effect of Intervention with 21-Aminosteroid (Tirilazad) in a New Experimental Model of Focal Cortical Injury in the Rat

“…Although abnormal microvascular permeability is a common feature in many models of brain trauma in which hemorrhage occurs (Cortez et al, 1989;Mitchell et al, 1979;Persson and Hansson, 1979;Tornheim et al, 1984), there are few reports of vasogenic edema occurring in experimental trauma not associated with traumatic disruption of vessels and consequent hemorrhage. Wei et al (1986) demonstrated increased permeability to HRP localized to vessels in the brain stem, occurring in the first 2 h from injury in a feline fluid-percussion model.…”