Frequently the affected athlete remains on the playing field or walks off under their own power. Indeed, the individual usually remains on their feet for 15 sec to 1 min or so, but appears dazed, like someone suffering from a grade 1 concussion without LOC. The affected athlete may appear stunned, but usually does not experience loss of consciousness (LOC) and in the case of football, he often completes the play. The second blow may be remarkably minor, perhaps involving only a blow to the chest that indirectly injures the athlete's head by imparting accelerative forces to the brain. Before these symptoms resolve, which may take days or weeks, the athlete returns to competition and receives a second blow to the head. Typically, the athlete suffers post-concussion symptoms after the first head injury, which may include headache labyrinthine dysfunction visual, motor, or sensory changes or mental difficulty, especially cognitive and memory problems. The syndrome occurs when an athlete sustains an initial head injury and then suffers a second head injury before the symptoms associated with the first impact have cleared, (Cantu, 1995 Cantu and Voy, 1995 Schnitker, 1949). W hat Saunders and Harbaugh (Saunders and Harbaugh, 1984) called “the second-impact syndrome of catastrophic head injury” was actually first described by Schneider (Schneider 1973). In addition, the imaging similarities between our patients and those with non-accidental head trauma (shaken-baby syndrome) will be discussed. The CT findings included an engorged cerebral hemisphere with initial preservation of grey-white matter differentiation, and abnormal mass effect and midline shift that appeared disproportionately greater than the size of the SDH. The clinical history and the unique neuroimaging features of this entity on CT are described and illustrated in detail. To support our hypothesis, we present 10 additional cases of acute hemispheric swelling in association with small SDHs in athletes who received a second head injury while still symptomatic from a previous head injury. We believe that the brain swelling is due to “second-impact dysautoregulation,” rather than due to the effect of the SDH on the underlying hemisphere. In those cases, the cause of the brain swelling/dysautoregulation was ascribed to the presence of the acute SDH rather than to the acceleration/deceleration forces that caused the SDH. There have been a handful of previously published cases of athletes who were still symptomatic from a prior head injury, and then suffered a second injury in which a thin, acute subdural hematoma (SDH) with unilateral hemisphere vascular engorgement was demonstrated on CT scan.
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