Intracranial Pressure in a Modified Experimental Model of Closed Head Injury

Engelborghs, K.; Verlooy, Jan; Deuren, Bruno Van; Reempts, Jos Van; Borgers, M.

doi:10.1007/978-3-7091-6837-0_38

Cited by 9 publications

(10 citation statements)

References 2 publications

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“…Preliminary results of this study were published in the proceedings of the 10th Brain Edema Congress. 6 …”

mentioning

confidence: 97%

Temporal changes in intracranial pressure in a modified experimental model of closed head injury

Engelborghs¹,

Verlooy²,

Reempts³

et al. 2001

FOC

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Object The authors describe an experimental model of closed head injury in rodents that was modified from one developed by Marmarou and colleagues. This modification allows dual control of the dynamic process of impact compared with impulse loading that occurs at the moment of primary brain injury. The principal element in this weight-drop model is an adjustable table that supports the rat at the moment of impact from weights positioned at different heights (accelerations). The aim was to obtain reproducible pathological intracranial pressure (ICPs) while maximally reducing the incidence of mortality and skull fractures. Methods Intracranial pressure was investigated in different experimental settings, including two different rat strains and various impact-acceleration conditions and posttrauma survival times. Identical impact-acceleration injuries produced a considerably higher mortality rate in Wistar rats than in Sprague–Dawley rats (50% and 0%, respectively). Gradually increasing severity of impact-acceleration conditions resulted in findings of a significant correlation between the degree of traumatic challenge and increased ICP at 4 hours (p < 0.001, R2 = 0.73). When the impact-acceleration ratio was changed to result in a more severe head injury, the ICP at 4, 24, and 72 hours was significantly elevated in comparison with that seen in sham-injured rats (4 hours: 19.7 ± 2.8 mm Hg, p = 0.004; 24 hours: 21.8 ± 1.1 mm Hg, p = 0.002; 72 hours: 11.9 ± 2.5 mm Hg, p = 0.009). Comparison of the rise in ICP between moderate and severe impact-acceleration injury at 4 and 24 hours revealed a significantly higher value after severe injury (4 hours: p = 0.008; 24 hours: p = 0.004). Continuous recordings showed that ICP mounted very rapidly to peak values, which declined gradually toward a pathological level dependent on the severity of the primary insult. Histological examination after severe trauma revealed evidence of irreversible neuronal necrosis, diffuse axonal injury, petechial bleeding, glial swelling, and perivascular edema. Conclusions This modified closed head injury model mimics several clinical features of traumatic injury and produces reliable, predictable, and reproducible ICP elevations with concomitant morphological alterations.

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“…Preliminary results of this study were published in the proceedings of the 10th Brain Edema Congress. 6 …”

mentioning

confidence: 97%

Temporal changes in intracranial pressure in a modified experimental model of closed head injury

Engelborghs¹,

Verlooy²,

Reempts³

et al. 2001

FOC

Self Cite

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“…Intuitively, the closest model to this type of aggression is skull contusion with solid objects. However, this aggression often generates intracranial hematomas and bone fractures, which have unpredictable effects on brain compliance 17 . So, animal models allowing gradual and controlled ICP increase, thus more predictable, are the most widely used.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, ICP in severe traumatic brain injury is increased to a critical value enough to impair brain perfusion 6 . This extremely high intracranial pressure has not always been controlled in ICP studies 17 , which not always had brain perfusion pressure decreased to these critical levels to the point of impairing vascular reactivity and brain blood flow. In this model, we have tried to maintain ICP above 30 mmHg for group SB, as seen during severe traumatic brain injuries, and this has significantly decreased brain perfusion pressure from mean baseline value of 87 mmHg in M0 to 60 mmHg in M2 (p < 0.001).…”

Section: Discussionmentioning

confidence: 99%

Efeitos da hipertensão arterial induzida sobre a complacência e pressão de perfusão encefálica em hipertensão intracraniana experimental: comparação entre lesão encefálica criogênica e balão subdural

Mizumoto¹,

Tango²,

Pagnocca³

2005

Rev. Bras. Anestesiol.

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“…Injury is produced after exposing the skull and performing a trephination by the impact of a rapid fluid bolus which strikes the intact dural surface and then moves in the epidural space concentrically from the injection area leading to diffuse loading to the brain [22,54]. This model has been subsequently used and modified over Arterial spin-labeled magnetic resonance imaging [25,187] Microsphere technique [167,188] Autoradiography [78,189,190] Hydrogen clearance technique [183] Increase in Intracranial inserted probes intracranial pressure [24,102,153,169,170] Metabolic alterations Microdialysis and chromatography of metabolites [191][192][193][194][195] Staining for respiratory function [58,131] Determination of local cerebral glucose utilization [190,[196][197][198] Nuclear magnetic resonance spectroscopy [91,183,199] Assess mitochondrial function and integrity [98,101,200] Direct measurement of oxygen consumption [201] Genomic changes…”

Section: A Fluid Percussion Brain Injurymentioning

confidence: 99%

“…Second to these macroscopically detectable anatomical differences, more subtle alterations in the animals physiology, neurotransmitter receptor distribution, signal transduction or genomic differences may lead to a substantially different response to trauma of comparable magnitude or type [9]. The situation becomes even more complex since, third, a number of investigations has described profound differences in the behavioral and histopathological responses to TBI within different rodent strains, additionally influenced by the age of the animal and its laboratory environment [82,102,[152][153][154][155].…”

Section: A Species Differencesmentioning

confidence: 99%

Models of Traumatic Brain Injury

Laurer

Lenzlinger

McIntosh

2000

European Journal of Trauma

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We present a review of the currently popular preclinical models of non-penetrating traumatic brain injury (TBI). This article focuses on animal models that cause TBI by applying mechanical energy to the head, skull or dura. It attempts to provide a compendium of the main characteristics of each of these experimental models of TBI in respect to acute and chronic histological findings and behavioral impairment in neurologic motor and cognitive function. Finally, several limitations of the described models are discussed briefly.

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Intracranial Pressure in a Modified Experimental Model of Closed Head Injury

Cited by 9 publications

References 2 publications

Temporal changes in intracranial pressure in a modified experimental model of closed head injury

Temporal changes in intracranial pressure in a modified experimental model of closed head injury

Efeitos da hipertensão arterial induzida sobre a complacência e pressão de perfusão encefálica em hipertensão intracraniana experimental: comparação entre lesão encefálica criogênica e balão subdural

Models of Traumatic Brain Injury

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