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Secondary Damage after Traumatic Brain Injury: Epidemiology, Pathophysiology and Therapy

Abstract

Traumatic brain injury (TBI) is defined as a microscopic or macroscopic injury to the brain caused by external physical forces. Road traffic accidents, falls, sports injuries (i.e. boxing), recreational accidents (i.e. parachute jumping), the use of firearms, assault, child abuse, and several rare causes e.g. the use of nail guns or lawn mowers have all been described as causes of TBI. The pathology of TBI can be classified by mechanism (closed versus penetrating); clinical severity (Glasgow Coma Scale) and structural damage (imaging e.g. CT-examination). In most cases TBI is graded according to injury severity assessing the level of consciousness of the patient by, most frequently, the Glasgow Coma Scale (GCS). The GCS scores patients based on their ability to open their eyes, perform limb movements and respond adequately to simple questions (Teasdale and Jennett 1974) (see table 1). Mild TBI, e.g. a light concussion, is defined as a patient with a GCS of 13-15 possibly suffering from short-term memory and concentration deficits (Rimel et al., 1981; Mosenthal et al., 2004). Moderate TBI is scored by a GCS of 9-12, e.g. a lethargic and stuporous patient. A comatose patient, unable to open eyes or follow commands has been severely injured and has a GCS of 3-8

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