Brain damage in non-missile head injury secondary to high intracranial pressure.
ABSTRACT A comprehensive neuropathological analysis was undertaken on 434 patients who died as a result of a non-missile head injury in order to determine the frequency and extent of brain damage secondary to high intracranial pressure (ICP) in head injury. Using the criterion of pressure necrosis in the parahippocampal gyrus as evidence of high ICP due to a supratentorial expanding lesion, it was established that the ICP had been high in 324 cases. In 42 of these there was no other brain damage attributable to a high ICP. There was evidence of secondary brain stem damage in 221 cases and in 44 of these the damage could be seen only microscopically. In 54 cases there was a contralateral peduncular lesion. Other abnormalities were infarction in the territories of various arteries and in the anterior lobe of the pituitary. There was a supracallosal hernia in 80 cases and haemorrhage in the oculomotor nerves in 48 cases. These results further emphasise the frequency and range of brain damage due to secondary vascular factors brought about by high ICP in a patient who has sustained a head injury.
[Show abstract] [Hide abstract]
ABSTRACT: Traumatic brain injury (TBI) is the major cause of death and severe disability in young adults and infants worldwide and many survivors also have mild to moderate neurological deficits which impair their lives. This review highlights the primary and secondary lesions constituting craniocerebral trauma and the main elements of neuroinflammation, one of the most important secondary events evolving after the initial traumatic insult. Neuroinflammation has dual and opposing roles in outcome after TBI, being both beneficial and harmful, its effects often differing between the acute and more delayed phases after injury. Since each patient with TBI has a unique and complex pattern of cerebral damage, developing pharmacological intervention strategies targeted at the multiple cellular and molecular events in the neuroinflammatory cascade is difficult. While there have been very few successful outcomes to date in human clinical trials of drugs developed to treat TBI in general, those that have been devised to modulate neuroinflammation are discussed.Inflammopharmacology 01/2013; 21(4). DOI:10.1007/s10787-012-0164-2