PATHOLOGICAL-CHANGES IN MILD HEAD-INJURY

Physical injury of the brain constitutes a major cause of loss of life and productivity. Populations at highest risk for such injuries include children, men in late adolescence and early adult life, and the elderly. Head injuries most commonly result from assaults, vehicular accidents, and falls. The neuropathology of severe injury has been described extensively and constitutes much of the lore of clinical neurosurgery, forensic neuropathology, and critical care neurology.1 The neuropathology of mild head injury is much less well explored, reflecting the low mortality of these injuries. Experimental head injury models originally developed to facilitate research in severe trauma have proven valuable in understanding the neurobiologic basis of the numerous and debilitating symptoms that follow mild head injury and have focused attention on diffuse axonal injury (DAI) as the primary neuropathologic mechanism underlying these symptoms.2 This review sequentially covers experimental models of head injury, neuropathology of human head trauma, with a detailed discussion of DAI, and ends with a discussion of the regenerative response to head injury and possible role of neuroplasticity in the genesis of post-traumatic symptomatology.