Intracranial pressure changes during fluid percussion, controlled cortical impact and weight drop injury in rats.
BACKGROUND
In traumatic brain injury research, the fluid percussion injury (FPI) model in the rat is widely used. The injury is graded based on indirect criteria, such as the extracranial pressure wave and/or physiological responses to the injury. We designed this study to investigate if the extracranially monitored pressure in the FPI-device corresponded to the actual intracranial situation. Severe controlled cortical impact (CCI) and severe weight drop injury (WDI) were studied for comparison.


METHODS
We tested the correlation between the extra- and intracranial pressures during severe FPI in rat (2.6-2.9 atm), using pressure probes (diameter 0.34 mm) with high frequency (500 Hz) and high pressure range (1-5 atm). The probes were inserted into either of the lateral ventricles in FPI and in the contralateral lateral ventricle in CCI and WDI to compare the ictal pressure pulses between the models.


RESULTS
FPI showed a time lag between the extracranial, intracranial ipsilateral and intracranial contralateral pressure curves respectively, reflecting the different distances between the pressure source and the individual pressure probes. There was a high degree of correlation (r = 0.994, p<0.0001) between the extra- and intracranial pressure pulses, once corrected for the time lag. We found no significant differences between the extracranial and the intracranial peak pressure in either ventricle in FPI. In CCI and WDI the contralateral pressure pulses were significantly smaller than in FPI. CCI resulted in higher pressure peaks than WDI, due to higher impact velocity.


CONCLUSIONS
The extracranial pressure pulse appears to be a good estimate of the intraventricular pressure pulse generated during FPI. Severe CCI and WDI generated intraventricular pressure pulses of much lower magnitude than FPI, explaining the lesser degree of brain stem involvement in the former models.
Clausen
F
F
Department of Neuroscience, Neurosurgery, Uppsala University Hospital, Uppsala, Sweden. fredrik.clausen@neurokir.uu.se
Hillered
L
L
D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002245:Carbon Dioxide / Q000378:metabolism; D002540:Cerebral Cortex / Q000293:injuries* / Q000503:physiopathology; D002552:Cerebral Ventricles / Q000502:physiology*; D004195:Disease Models, Animal; D004292:Dominance, Cerebral / Q000502:physiology; D004867:Equipment Design; D016489:Head Injuries, Closed / Q000503:physiopathology*; D006863:Hydrogen-Ion Concentration; D007427:Intracranial Pressure / Q000502:physiology*; D008297:Male; D008365:Manometry / Q000295:instrumentation*; D010101:Oxygen Consumption / Q000502:physiology; D010474:Percussion; D051381:Rats; D017207:Rats, Sprague-Dawley
D002245:Carbon Dioxide