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Traumatic brain injury (TBI) is considered an epidemic that continues to compromise the welfare of humankind. Despite the extensive efforts invested in countering this clinical health problem, current clinical science and technology still fall short of providing a pharmacological cure for TBI rendering tens of thousands of TBI patients vulnerable to its detrimental sequelae. Over the past 30 years, the understanding of the pathophysiological mechanisms of TBI indicates that the pathology of TBI is biphasic. It comprises 2 injuries; the primary and the secondary injuries. The primary injury occurs simultaneously with the impact that caused the injury, which explains why this injury is not amenable to acute intervention. Whereas the secondary injury is a composite of interwoven pathophysiological responses that commence after the initial trauma leading to delayed, non-mechanical impairment of neuronal structure and function. In this review, we aim to highlight the main pathophysiological mechanisms that take place in the primary and secondary phases of traumatic brain injury.
Department of Anatomy and Cell Biology, College of Medicine, Jordan University of Science and Technology, PO Box 3030, Irbid 22110, Jordan. Tel. +962 772040491. Fax. +962 (2) 7201064. E-mail: firstname.lastname@example.org.
This article was published in the following journal.
Name: Neurosciences (Riyadh, Saudi Arabia)
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Prolonged unconsciousness from which the individual cannot be aroused, associated with traumatic injuries to the BRAIN. This may be defined as unconsciousness persisting for 6 hours or longer. Coma results from injury to both cerebral hemispheres or the RETICULAR FORMATION of the BRAIN STEM. Contributing mechanisms include DIFFUSE AXONAL INJURY and BRAIN EDEMA. (From J Neurotrauma 1997 Oct;14(10):699-713)
Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.
Traumatic injuries to the cranium where the integrity of the skull is not compromised and no bone fragments or other objects penetrate the skull and dura mater. This frequently results in mechanical injury being transmitted to intracranial structures which may produce traumatic brain injuries, hemorrhage, or cranial nerve injury. (From Rowland, Merritt's Textbook of Neurology, 9th ed, p417)
Bleeding within the brain as a result of penetrating and nonpenetrating CRANIOCEREBRAL TRAUMA. Traumatically induced hemorrhages may occur in any area of the brain, including the CEREBRUM; BRAIN STEM (see BRAIN STEM HEMORRHAGE, TRAUMATIC); and CEREBELLUM.
Bleeding into structures of BRAIN STEM, including the MIDBRAIN; PONS; or MEDULLA OBLONGATA, as the result of CRANIOCEREBRAL TRAUMA. DIFFUSE AXONAL INJURY is commonly associated. Clinical manifestations may include OCULAR MOTILITY DISORDERS; ATAXIA; PARALYSIS; PERSISTENT VEGETATIVE STATE; and COMA.
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