Continuous measurement of intracranial pressure in awake rats after experimental closed head injury

Rooker, Servan; Jorens, Philippe G.; Reempts, Jos Van; Borgers, M.; Verlooy, Jan

doi:10.1016/s0165-0270(03)00233-4

Cited by 30 publications

(17 citation statements)

References 13 publications

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“…In this study, we demonstrated that immediately following a 10% PBBI, the magnitude and duration of the ICP spike produced by the balloon inflation were comparable to the pressures recorded in the brain-simulating material (Zhang et al, 2005), or in the brains of the larger animals injured by handgun projectiles (Carey et al, 1989), supporting the relevance of the PBBI pre-clinical model for studying military-type ballistic wounds of the human brain. More importantly, the second phase of the ICP elevation, although far less dramatic than the first spike, reached a clinically severe level comparable to that seen in other experimental models of closed-head TBI (Prins et al, 1996;Rooker et al, 2003), and consistent with clinical ICP measurements in TBI patients (Abadal-Centellas et al, 2007;Olivecrona et al, 2007). Collectively, our results support the rationale of the use of this rat PBBI model to study military-type penetrating brain injury, and identified the ICP:CPP ratio as a valid pathophysiological marker, as well as a therapeutic target of clinical significance (Carey et al, 1989;Kroppenstedt et al, 1998;Prins et al, 1996).…”

Section: Discussionsupporting

confidence: 67%

Intracranial Pressure following Penetrating Ballistic-Like Brain Injury in Rats

Yang

et al. 2010

Journal of Neurotrauma

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Penetrating ballistic brain injury involves a leading shockwave producing a temporary cavity causing substantial secondary injury. In response to the prevalence of this type of brain trauma in the military, a rat model of penetrating ballistic-like brain injury (PBBI) was established. This study focuses on cerebral physiological responses resulting from a PBBI, specifically the immediate and delayed changes in intracranial pressure (ICP) and cerebral perfusion pressure (CPP). ICP/CPP was measured continuously in rats subjected to PBBI, probe insertion alone, or sham injury. Immediately following the PBBI, a transient (<0.1 sec) and dramatic elevation of ICP reaching 280.0 ± 86.0 mm Hg occurred, accompanied by a profound decrease in CPP to -180.2 ± 90.1 mm Hg. This emergent ICP/CPP response resolved spontaneously within seconds, but was followed by a slowly-developing and sustained secondary phase, which peaked at 24 h post-injury, reaching 37.2 ± 10.4 mm Hg, and remained elevated until 72 h post-injury. The measured decrease in CPP reached 85.3 ± 17.2 mm Hg at 3 h post-injury. By comparison, probe insertion alone did not produce the immediate ICP crisis (28.6 ± 9.1 mm Hg), and only a mild and sustained increase in ICP (13.5 ± 2.1 mm Hg) was observed in the following 3 h post-injury. Injury severity, as measured by lesion volume, brain swelling, and neurological deficits at 1, 3, and 7 days post-injury, also reflected the distinctive differences between the dynamics of the PBBI versus controls. These results not only reinforced the severe nature of this model in mimicking the ballistic effect of PBBI, but also established cerebral pathophysiological targets for neuroprotective therapies.

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Section: Discussionsupporting

confidence: 67%

Intracranial Pressure following Penetrating Ballistic-Like Brain Injury in Rats

Yang

et al. 2010

Journal of Neurotrauma

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“…Previous studies reported that TBI induced by closed-head [34] and fluid percussion injury[35] in rats resulted in immediate (30 min) and late (6–10 h) rises in ICP [34, 36]. The late increase was followed by a slow decline toward control levels, which was reached in about a week [35].…”

Section: Discussionmentioning

confidence: 99%

Effects of Exposure to Blast Overpressure on Intracranial Pressure and Blood-Brain Barrier Permeability in a Rat Model

Kawoos

Lankasky

et al. 2016

PLoS ONE

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Exposure to blast overpressure (BOP) activates a cascade of pathological processes including changes in intracranial pressure (ICP) and blood-brain barrier (BBB) permeability resulting in traumatic brain injury (TBI). In this study the effect of single and multiple exposures at two intensities of BOP on changes in ICP and BBB permeability in Sprague-Dawley rats was evaluated. Animals were exposed to a single or three repetitive (separated by 0.5 h) BOPs at 72 kPa or 110 kPa. ICP was monitored continuously via telemetry for 6 days after exposure to BOP. The alteration in the permeability of BBB was determined by extravasation of Evans Blue (EB) into brain parenchyma. A significant increase in ICP was observed in all groups except the single 72 kPa BOP group. At the same time a marked increase in BBB permeability was also seen in various parts of the brain. The extent of ICP increase as well as BBB permeability change was dependent on intensity and frequency of blast.

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“…However, there are a number of possible causative factors for increased ICP, such as hemorrhage, CSF outflow obstruction and BBB damage (Hoane et al, 2006;Vink et al, 2003). The immediate and late increases in ICP elevation are being attributed to vascular changes and more complex changes, respectively (Engelborghs et al, 1998;Fritz et al, 2005;Jamali et al, 1998;Rooker et al, 2003). ICP measurements seem to be a more sensitive method to detect mTBI than markers for neuropathology (Teranishi et al, 2009), both with respect to the onset of injury and exposure conditions.…”

Section: Discussionmentioning

confidence: 99%