[Physiopathological consequences of blood-brain barrier involvement]

Most of the adverse effects of cerebral injury derive result from the formation of cerebral oedema, which causes brain swelling, brain shift and intracranial hypertension. The mechanisms of cerebral oedema are specific of the type of cerebral injury and the effectiveness of treatments such as corticosteroids depend on the type of cerebral oedema. Recent magnetic resonance imaging studies of the brain in patients with acute intracranial injury have confirmed that anatomical brain shifts accompany the clinical syndromes of brain herniation. In particular, specific neurological syndromes can effectively identify rostro-caudal herniation, both transtentorially (uncal and central syndrome) and through the foramen magnum. Signs of upward transtentorial herniation are less specific. Early detection of these syndromes is essential if therapeutic measures to reduce intracranial pressure are to be taken before secondary neurological injury occurs.