Pathologic Changes in Mild Head Injury

Abstract

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. T h e neuropathology of severe injury has been described extensively and constitutes much of the lore of clinical neurosurgery, forensic neuropathology, and critical care neurology.' T h e 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 sympt o m~.~ 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 posttraumatic symptomatology.

Injury risks of heading in young football players

“…Babbs By means of neuropsychological tests they arrived at conclusion that heading does not have any influence on worsening these functions. These result, however, differ from neuropsychicologocal literature which states that repeated minor head injuries results in structural damage, tracable in neuropsychic tests (Elson & Ward 1994;Goodman, 1994).…”

“…Symptoms of mild traumatic brain injury fade away quickly in most cases, nevertheless, long-term repetitive strain may induce permanent health problems (Gronwall & Wrightson, 1975;Rieder & Jansen, 2011). Neuropsychological literature puts it that permanent mild head injury results in a structural damage that can be detected via neuropsychological tests (Elson & Ward 1994;Goodman, 1994). Rutherford et al (2003) mention two causes of cumulative injuries in football.…”

Diffusion tensor imaging and white matter lesions at the subacute stage in mild traumatic brain injury with persistent neurobehavioral impairment

“…Brain movements against the skull and dura matter result in stretching and distortions rather than breaking of the axons [Gennareli and Graham, 1998;Smith et al, 2003]. DAI has been evidenced in pathological studies as well as using neuroimaging [Aihara et al, 1995;Blumbergs et al, 1994;Blumbergs et al, 1995;Gennarelli, 1996;Goodman, 1994;Inglese et al, 2005;Mittl et al, 1994]. Conventional T 1 -weighted brain imaging has not contributed to the understanding of persistent PCS as most often it shows no brain abnormalities and does not detect DAI [Adams et al, 1982;Adams et al, 1991;Bazarian et al, 2007;Fork et al, 2005;Medana and Esiri, 2003;Nakayama et al, 2006;Parizel et al, 2005;Scheid et al, 2006].…”

Posttraumatic headache

“…Neuronal compression also has been advocated [25]. Brain electrical activity perturbations, cerebral edema, cerebral blood flow abnormality with loss auto-regulation and ischemic damage [26,27] all have been implicated. Ancillary investigations show abnormal magnetic resonance imaging (MRI) findings, abnormality on positron emission tomographic scans with glucose metabolism, and cerebral blood flow changes on single photon emission computed tomographic scans as many as 3 years later [28].…”