Second-impact Syndrome - Pathophysiology

Pathophysiology

Concussion temporarily changes the brain's function. It is believed that the brain is left in a vulnerable state after concussion and that a second blow is linked to SIS. The actual mechanism behind the catastrophic brain swelling is controversial. A second injury during this time is thought to unleash a series of metabolic events within the brain. Changes indicative of SIS may begin occurring in the injured brain within 15 seconds of the second concussion. Pathophysiological changes in SIS can include a loss of autoregulation of the brain's blood vessels, which causes them to become congested. The vessels dilate, greatly increasing their diameter and leading to a large increase in cerebral blood flow. Progressive cerebral edema may also occur. The increase of blood and brain volume within the skull causes a rapid and severe increase in intracranial pressure, which can in turn cause uncal and cerebellar brain herniation, a disastrous and potentially fatal condition in which the brain is squeezed past structures within the skull.

Studies on animals have shown that the brain may be more vulnerable to a second concussive injury administered shortly after a first. In one such study, a mild impact administered within 24 hours of another one with minimal neurological impairment caused massive breakdown of the blood brain barrier and subsequent brain swelling. Loss of this protective barrier could be responsible for the edema found in SIS.

Animal studies have shown that the immature brain may be more vulnerable to brain trauma; these findings may provide clues as to why SIS affects only people under age 18.