Journal of neurotrauma
-
Journal of neurotrauma · Oct 2002
ReviewRoller coasters, g forces, and brain trauma: on the wrong track?
There has been enormous attention in the general press on the possibility that high G force roller coasters are inducing brain injury in riders. Armed with a handful of anecdotal case reports of brain injuries, the U. S. ⋯ With this model, we calculated peak head rotational accelerations in three directions. Even for a conservative worst-case scenario, we found that the highest estimated peak head accelerations induced by roller coasters were far below conventional levels that are predicted for head injuries. Accordingly, our findings do not support the contention that current roller coaster rides produce high enough forces to mechanically deform and injure the brain.
-
Journal of neurotrauma · Oct 2002
Age-dependent NOC/oFQ contribution to impaired hypotensive cerebral hemodynamics after brain injury.
Previous studies have observed that the newly described opioid, nociceptin/orphanin FQ (NOC/oFQ), contributed to age dependent reductions in cerebral blood flow (CBF) and pial artery diameter after fluid percussion brain injury (FPI). Unrelated studies have noted a similar age dependency in impaired hypotensive cerebral autoregulation after FPI. This study was designed to compare the role of NOC/oFQ in impaired hypotensive cerebral autoregulation after FPI in newborn and juvenile pigs equipped with a closed cranial window. ⋯ In contrast, blunted hypotensive pial artery dilation was protected significantly less by this NOC/oFQ antagonist in the juvenile (32 +/- 2 vs. 7 +/- 2 vs. 13 +/- 2% for sham control, FPI and FPI-NOC/oFQ antagonist, respectively). Similarly, [F/G] NOC/oFQ (1-13) NH(2) had less protective effect on normotensive and hypotensive CBF values post FPI in the juvenile. These data indicate that NOC/oFQ contributes to impaired hypotensive cerebral hemodynamics following brain injury in an age-dependent manner.
-
Journal of neurotrauma · Oct 2002
Continuous cerebral autoregulation monitoring by cross-correlation analysis.
In order to validate cross-correlation analysis between spontaneous slow oscillations of arterial blood pressure (aBP) and intracranial pressure (ICP) or flow velocity as a means to assess the status of cerebral autoregulation continuously, we compared its results with different autoregulation bedside tests. The second aim was to check the method's stability over longer time periods. aBP, ICP, and flow velocity in the middle cerebral artery (FV(MCA)) was measured continuously in 13 critically ill comatose patients. Cross-correlation analysis was performed online and offline between aBP and ICP (CC [aBP --> ICP]) and aBP/FV(MCA) (CC [aBP --> FV(MCA)]). ⋯ Comparison between the cross-correlation test results and the bedside tests showed a sensitivity of 44-73% for CC [aBP --> FV(MCA)], whereas CC [aBP --> ICP] was more specific (60-80%). Long-term monitoring revealed stable cross-correlation tests in about 45% of the measurement time. It is concluded that cross-correlation between aBP, ICP, and FV(MCA) is a valid means to monitor the autoregulation status continuously, although further improvement of sensitivity and specificity is needed to make it reliable for clinical decision making.
-
Journal of neurotrauma · Oct 2002
Temporal profile of changes in brain tissue extracellular space and extracellular ion (Na(+), K(+)) concentrations after cerebral ischemia and the effects of mild cerebral hypothermia.
Cerebral ischemic cellular swelling occurs primarily in astrocytes. This water influx into the intracellular space is believed to result from osmotic water movement after disruption of membrane ionic homeostasis. However, cellular swelling occurs earlier than expected after ischemia and new ionic and water channels have been discovered. ⋯ With mild hypothermia, the ECS started to decrease at 75 +/- 35 sec after ischemia and reached half the maximum change at 123 +/- 44 sec, [K(+)](e) started to increase initially at 80 +/- 24 sec (phase 1) and then increased rapidly at 120 +/- 32 sec (phase 2), and [Na(+)](e) started to decrease at 172 +/- 70 sec. The present study shows that ischemic cellular swelling (decreased ECS) occurs concomitantly with the phase 1 increase of [K(+)](e) but precedes the disruption of ionic membrane homeostasis (phase 2). Mild hypothermia prolongs the onset of these phenomena but does not affect the magnitude of the changes in ECS and ion concentrations.