Acta neurochirurgica. Supplement
-
Acta Neurochir. Suppl. · Jan 2000
Distinguishing between cellular and vasogenic edema in head injured patients with focal lesions using magnetic resonance imaging.
Having determined that edema and not vascular engorgement is the major factor leading to traumatic brain swelling, the objective of this study was to determine which type of edema, cellular or vasogenic, is responsible for increased tissue water in patients with focal lesions. Severely head injured patients (GCS 8 or less) were transported to imaging suites for measurement of brain water and apparent diffusion coefficient (ADC) using magnetic resonance technique. Cerebral blood flow by stable Xenon method was also measured in the regions of interest. ⋯ The increase in water was associated with reduced ADC signifying a predominant cellular edema. The ADC in the contralateral hemisphere was near normal value. Cerebral blood flow values in the regions of interest were above ischemic levels suggesting that factors other than ischemia are responsible for the cytotoxic swelling in patients with focal injury.
-
Acta Neurochir. Suppl. · Jan 2000
Does an increase in cerebral perfusion pressure always mean a better oxygenated brain? A study in head-injured patients.
The adequate management of cerebral perfusion pressure (CPP) continues to be a controversial issue in head-injured patients. The purpose of our study was to test two hypotheses. The first was that in patients with a CPP below 70 mm Hg, oxygen delivery is compromised and that therefore signs of tissue hypoxia would be reflected in low PtiO2 measurements. ⋯ In our study a low PtiO2 was not observed in patients with marginally low CPPs (48-70 mm Hg) and readings below 15 mm Hg were observed in cases with both normal or supranormal CPPs. We conclude that episodes of low PtiO2 could not be predicted on the basis of CPP alone. On the other hand, raising CPP did not increase oxygen availability in the majority of cases, even if the CPP was markedly improved.
-
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 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.
-
Acta Neurochir. Suppl. · Jan 2000
Effects of hypothermia on intracranial hemodynamics and ischemic brain damage-studies in the rat acute subdural hematoma model.
Brain ischemia is the leading pathophysiological mechanism in the development of secondary brain damage after subdural hematoma (SDH). Hypothermia has been used as the effective neuroprotective treatment in clinical and laboratory studies of ischemic brain injury. In this study, we have examined the rat acute SDH model to assess the effect of hypothermia upon intracranial hemodynamics and also upon ischemic brain injury 4 hours after the induction of hematoma. ⋯ This reduction in brain edema formation was comparable to the result of MK-801 (2 mg/kg) treatment (80.95 +/- 0.35%; p < 0.01). Ischemic brain damage detected by H-E staining was also significantly reduced in the hypothermia and MK-801 treated groups (59.1 +/- 12.3 mm3 and 66.4 +/- 13.8 mm3; p < 0.01 and p < 0.05) compared with the normothermic control group (86.6 +/- 20.7 mm3). In conclusion, the present study demonstrates that hypothermia is a potent neuroprotective method and an inhibition of the glutamate excitotoxic process may contribute the protective mechanisms of hypothermia in this rat acute SDH model.