Immediate, but Not Delayed, Microsurgical Skull Reconstruction Exacerbates Brain Damage in Experimental Traumatic Brain Injury Model

Glover, Loren E.; Tajiri, Naoki; Lau, Tsz; Kaneko, Yuji; Loveren, Harry van; Borlongan, Cesario V.

doi:10.1371/journal.pone.0033646

Cited by 32 publications

(34 citation statements)

References 51 publications

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“…CCI without decompressive craniectomy in the mouse has been shown to increase ICP, contusion lesion volume, brain edema, and blood-brain barrier disruption. 24,30,36,37 Its influence on axonal injury, however, has not been previously reported, to our knowledge. In our experiments, the difference in the extent of axonal injury between groups was more pronounced at 1 week post-injury compared with 1 day post-injury.…”

Section: Discussionmentioning

confidence: 85%

Decompressive Craniectomy Reduces White Matter Injury after Controlled Cortical Impact in Mice

Friess

Lapidus

Brody

2015

Journal of Neurotrauma

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Reduction and avoidance of increases in intracranial pressure (ICP) after severe traumatic brain injury (TBI) continue to be the mainstays of treatment. Traumatic axonal injury is a major contributor to morbidity after TBI, but it remains unclear whether elevations in ICP influence axonal injury. Here we tested the hypothesis that reduction in elevations in ICP after experimental TBI would result in decreased axonal injury and white matter atrophy in mice. Six-week-old male mice (C57BL/6J) underwent either moderate controlled cortical impact (CCI) (n = 48) or Sham surgery (Sham, n = 12). Immediately after CCI, injured animals were randomized to a loose fitting plastic cap (Open) or replacement of the previously removed bone flap (Closed). Elevated ICP was observed in Closed animals compared with Open and Sham at 15 min (21.4 -4.2 vs. 12.3 -2.9 and 8.8 -1.8 mm Hg, p < 0.0001) and 1 day (17.8 -3.7 vs. 10.6 -2.0 and 8.9 -1.9 mm Hg, p < 0.0001) after injury. Beta amyloid precursor protein staining in the corpus callosum and ipsilateral external capsule revealed reduced axonal swellings and bulbs in Open compared with Closed animals (32% decrease, p < 0.01 and 40% decrease, p < 0.001 at 1 and 7 days post-injury, respectively). Open animals were also found to have decreased neurofilament-200 stained axonal swellings at 7 days post-injury compared with Open animals (32% decrease, p < 0.001). At 4 weeks post-injury, Open animals had an 18% reduction in white matter volume compared with 34% in Closed animals ( p < 0.01). Thus, our results indicate that CCI with decompressive craniectomy was associated with reductions in ICP and reduced pericontusional axonal injury and white matter atrophy. If similar in humans, therapeutic interventions that ameliorate intracranial hypertension may positively influence white matter injury severity.

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Section: Discussionmentioning

confidence: 85%

Decompressive Craniectomy Reduces White Matter Injury after Controlled Cortical Impact in Mice

Friess

Lapidus

Brody

2015

Journal of Neurotrauma

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“…POMC-GFP mice were used for the GFAP staining and anatomical measurements, and wild-type mice were used for Mac-2 and cFos analyses. TTC staining was performed on acutely prepared live brain slices (Schnell et al, 2012) from wild-type animals 1 week after CHI or sham, and subsequently incubated in 2% TTC in PBS at 37C for 20 minutes, fixed in PBS + 4%PFA, and imaged in accordance with established protocols (Glover et al, 2012). Fluoro-Jade C staining was performed as previously described on wild-type mice (Schmued et al, 2005) with minor modifications.…”

Section: Methodsmentioning

confidence: 99%

Neurologic impairment following closed head injury predicts post-traumatic neurogenesis

Villasana¹,

Westbrook

Schnell

2014

Experimental Neurology

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In the mammalian hippocampus, neurogenesis persists into adulthood, and increased generation of newborn neurons could be of clinical benefit following concussive head injuries. Post-traumatic neurogenesis has been well documented using “open” traumatic brain injury (TBI) models in rodents; however, human TBI most commonly involves closed head injury. Here we used a closed head injury (CHI) model to examine post-traumatic hippocampal neurogenesis in mice. All mice were subjected to the same CHI protocol, and a gross-motor based injury severity score was used to characterize neurologic impairment one hour after the injury. When analyzed 2 weeks later, post-traumatic neurogenesis was significantly increased only in mice with a high degree of transient neurologic impairment immediately after injury. This increase was associated with an early increase in c-fos activity, and subsequent reactive astrocytosis and microglial activation in the dentate gyrus. Our results demonstrate that the initial degree of neurologic impairment after closed head injury predicts the induction of secondary physiologic and pathophysiologic processes, and that animals with severe neurologic impairment early after injury manifest an increase in post-traumatic neurogenesis in the absence of gross anatomic pathology.

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“…In prior studies, AQP4 expression was most commonly evaluated globally, either by Western blot [14][15][16][17][18][19][20][21] or by grading of immunohistochemical staining after TBI. [21][22][23][24] We first quantified changes in global AQP4 expression within the cortex and striatum after mild and moderate TBI. After both mild and moderate TBI, a slight increase in global AQP4 expression was apparent both in the cortex ( Figure 5D) and in the striatum ( Figure 5J) that appeared to peak 7 days post injury, then subside over the subsequent 3 weeks.…”

Section: Evolution Of Aqp4 Dysregulation After Mild and Moderate Tbimentioning

confidence: 99%

‘Hit & Run’ Model of Closed-Skull Traumatic Brain Injury (TBI) Reveals Complex Patterns of Post-Traumatic AQP4 Dysregulation

Ren

Iliff

Yang

et al. 2013

J Cereb Blood Flow Metab

262

197

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Cerebral edema is a major contributor to morbidity associated with traumatic brain injury (TBI). The methods involved in most rodent models of TBI, including head fixation, opening of the skull, and prolonged anesthesia, likely alter TBI development and reduce secondary injury. We report the development of a closed-skull model of murine TBI, which minimizes time of anesthesia, allows the monitoring of intracranial pressure (ICP), and can be modulated to produce mild and moderate grade TBI. In this model, we characterized changes in aquaporin-4 (AQP4) expression and localization after mild and moderate TBI. We found that global AQP4 expression after TBI was generally increased; however, analysis of AQP4 localization revealed that the most prominent effect of TBI on AQP4 was the loss of polarized localization at endfoot processes of reactive astrocytes. This AQP4 dysregulation peaked at 7 days after injury and was largely indistinguishable between mild and moderate grade TBI for the first 2 weeks after injury. Within the same model, blood-brain barrieranalysis of variance permeability, cerebral edema, and ICP largely normalized within 7 days after moderate TBI. These findings suggest that changes in AQP4 expression and localization may not contribute to cerebral edema formation, but rather may represent a compensatory mechanism to facilitate its resolution.

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Immediate, but Not Delayed, Microsurgical Skull Reconstruction Exacerbates Brain Damage in Experimental Traumatic Brain Injury Model

Cited by 32 publications

References 51 publications

Decompressive Craniectomy Reduces White Matter Injury after Controlled Cortical Impact in Mice

Decompressive Craniectomy Reduces White Matter Injury after Controlled Cortical Impact in Mice

Neurologic impairment following closed head injury predicts post-traumatic neurogenesis

‘Hit & Run’ Model of Closed-Skull Traumatic Brain Injury (TBI) Reveals Complex Patterns of Post-Traumatic AQP4 Dysregulation

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