Acta neurochirurgica. Supplement
-
Acta Neurochir. Suppl. · Jan 2000
Increased adrenomedullin in cerebrospinal fluid after traumatic brain injury in children: a preliminary report.
Adrenomedullin is a recently discovered 52-amino-acid peptide that is a potent vasodilator. Infusion of adrenomedullin increases regional cerebral blood flow and reduces infarct volume after vascular occlusion in rats. Adrenomedullin may represent an endogenous neuroprotectant since it is increased after focal brain ischemia. ⋯ All 36 case samples had an adrenomedullin concentration above the median value for the controls (1.52 fmol/ml). We conclude adrenomedullin is elevated in the CSF of children following severe TBI. We speculate that it participates in the endogenous response to cerebral hypoperfusion after TBI.
-
Acta Neurochir. Suppl. · Jan 2000
The permissive nature of blood brain barrier (BBB) opening in edema formation following traumatic brain injury.
The contribution of blood brain barrier opening to traumatic brain edema is not known. This study compares the course of traumatic BBB disruption and edema formation, with the hypothesis that they are not obligately related. Sprague-Dawley rats were divided into three groups: Group A (n = 47)--Impact Acceleration (IAM); Group B (n = 104)--lateral cortical impact (CCI); Group C (n = 26)--IAM + hypoxia & hypotension (THH). ⋯ Edema formation clearly does not correspond with BBB opening and an open BBB is clearly not required for edema formation. However we hypothesize that a permeable BBB permissively worsens the process, by acting as a low resistance pathway for ion and water movement. These findings are consistent with our general hypothesis that edema formation after TBI is mainly cytotoxic.
-
Acta Neurochir. Suppl. · Jan 2000
The use of decompressive craniectomy for the management of severe head injuries.
The aim of Neurosurgical care is to minimise the secondary brain damage that occurs after a severe head injury. This includes the evacuation of an intracranial space occupying haematoma, the reduction of intracranial volume, external ventricular drainage with hydrocephalus, and conservative therapy to reduce intracranial pressure (ICP) and to maintain tissue oxygen p(ti)O2. When conservative treatment fails, a decompressive craniectomy might be successful in lowering ICP. ⋯ The prognosis after decompression depends on clinical signs and symptoms on admission, patients' age and the existence of major extracranial injuries. Our guidelines for decompressive craniectomy after failure of conservative intervention and evacuation of space occupying hematomas included: a patient's age below 50 years without multiple trauma or a patient's age below 30 years in the presence of major extracranial injuries; severe brain swelling on CT scan (primary brainstem injuries were excluded). In 8 patients conservative 1TU treatment had failed.
-
Acta Neurochir. Suppl. · Jan 2000
Time profile of neuron specific enolase serum levels after experimental brain injury in rat.
The aim of this study was to investigate the time course of NSE serum levels after traumatic brain injury in rats. 65 male Wistar rats were subjected to severe cortical impact injury (100 PSI, 2 mm deformation). Blood samples were drawn directly after trauma, after 1 h, 6 h, 12 h, 24 h, and 48 h in the trauma group as well as in sham operated animals directly after craniotomy, after 6 h and after 48 h. NSE serum levels were estimated with a commercially available enzyme immuno assay (LIA-mat Sangtec). ⋯ We demonstrated a time dependent release of NSE into the serum after trauma. The highest NSE serum values were detected six hours after trauma (31.5 micrograms/l, mean, n = 10). NSE serum level seems to reflect neuronal damage after cortical contusion in the rat in a time dependent manner.
-
Acta Neurochir. Suppl. · Jan 2000
The synergistic effect of acute subdural hematoma combined with diffuse traumatic brain injury on brain edema.
It is well-documented that acute subdural hematoma (ASDH) following diffuse traumatic brain injury (dTBI) contributes to severe disability and high mortality. The objective of this study was to characterize edema formation in a model of ASDH and ASDH following dTBI. Eighteen Sprague-Dawley rats were separated into three groups: Sham operated (n = 6), ASDH (n = 6), ASDH following dTBI (n = 6). ⋯ We conclude that edema formation in ASDH is worsened by the combination of dTBI and ASDH. Furthermore a diffuse and focal injury in combination retain the features of the diffuse injury, but with increased severity. Further studies are required to elucidate the synergistic mechanisms involved in these pathological processes.