Post-traumatic diffuse axonal brain injury. Analysis of 78 patients studied with Computed Tomography

Cordobés, F.; Lobato, R.D.; Rivas, Juán J.; Cabrera, A.; Sarabia, Maria; Castro, S.; C, Cisneros Alonso; Torres, Isabelle; Lamas, Eduardo

doi:10.1007/bf01456261

Cited by 64 publications

(25 citation statements)

References 29 publications

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“…Traumatic axonal injury is a common occurrence in both focal and diffuse brain trauma regardless of injury severity. [19][20][21][22] Traumatic axonal injury has proven to be a reliable predictor of poor survival or poor long-term outcome [23][24][25][26] yet it is frequently underdiagnosed, particularly in mild traumatic brain injury owing to a lack of tools with sufficient thresholds of detection. Importantly, we now understand that there are mechanisms leading to delayed white matter injury beyond the direct initial consequence of shear forces generated at the moment of initial trauma.…”

Section: White Matter Injurymentioning

confidence: 99%

Traumatic brain injury: Can the consequences be stopped?

Park¹,

Bell²,

Baker³

2008

Canadian Medical Association Journal

240

154

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Section: White Matter Injurymentioning

confidence: 99%

Traumatic brain injury: Can the consequences be stopped?

Park¹,

Bell²,

Baker³

2008

Canadian Medical Association Journal

240

154

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“…Diffuse brain injury (DBI) is a significant clinical problem that contributes to poor outcome (Adams et al, 1977;Lobato et al, 1983;Cordobes et al, 1986;Shigemori et al, 1992). In contrast to focal brain injury, in which the brain sustains direct impact, DBI occurs via rapid cranial acceleration-deceleration with or without impact (Adams, 1992).…”

Section: Introductionmentioning

confidence: 99%

Identification and Characterization of Heterogeneous Neuronal Injury and Death in Regions of Diffuse Brain Injury: Evidence for Multiple Independent Injury Phenotypes

Singleton¹,

Povlishock²

2004

J. Neurosci.

107

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Diffuse brain injury (DBI) is a consequence of traumatic brain injury evoked via rapid acceleration-deceleration of the cranium, givingrise to subtle pathological changes appreciated best at the microscopic level. DBI is believed to be comprised by diffuse axonal injury and other forms of diffuse vascular change. The potential, however, that the same forces can also directly injure neuronal somata in vivo has not been considered. Recently, while investigating DBI-mediated perisomatic axonal injury, we identified scattered, rapid neuronal somatic necrosis occurring within the same domains. Moving on the premise that these cells sustained direct somatic injury as a result of DBI, we initiated the current study, in which rats were intracerebroventricularly infused with various high-molecular weight tracers (HMWTs) to identify injury-induced neuronal somatic plasmalemmal disruption. These studies revealed that DBI caused immediate, scattered neuronal somatic plasmalemmal injury to all of the extracellular HMWTs used. Through this approach, a spectrum of neuronal change was observed, ranging from rapid necrosis of the tracer-laden neurons to little or no pathological change at the light and electron microscopic level. Parallel double and triple studies using markers of neuronal degeneration, stress, and axonal injury identified additional injured neuronal phenotypes arising in close proximity to, but independent of, neurons demonstrating plasmalemmal disruption. These findings reveal that direct neuronal somatic injury is a component of DBI, and diffuse trauma elicits a heretofore-unrecognized multifaceted neuronal pathological change within the CNS, generating heterogeneous injury and reactive alteration within both axons and neuronal somata in the same domains.

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“…Primary injury can be induced by a direct contusion to the brain from skull fracture or from shearing and stretching of tissue causing displacement of brain due to movement 3,4 . The resulting hematomas and lacerations cause a vascular response 3,5 , and the morphological and functional damage of the white matter leads to diffuse axonal injury [6][7][8] . Additional secondary changes commonly seen in the brain are edema and increased intracranial pressure 9 .…”

mentioning

confidence: 99%

Lateral Fluid Percussion: Model of Traumatic Brain Injury in Mice

Alder

Fujioka

Lifshitz

et al. 2011

JoVE

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Traumatic brain injury (TBI) research has attained renewed momentum due to the increasing awareness of head injuries, which result in morbidity and mortality. Based on the nature of primary injury following TBI, complex and heterogeneous secondary consequences result, which are followed by regenerative processes 1,2 . Primary injury can be induced by a direct contusion to the brain from skull fracture or from shearing and stretching of tissue causing displacement of brain due to movement 3,4 . The resulting hematomas and lacerations cause a vascular response 3,5 , and the morphological and functional damage of the white matter leads to diffuse axonal injury [6][7][8] . Additional secondary changes commonly seen in the brain are edema and increased intracranial pressure . Following TBI there are microscopic alterations in biochemical and physiological pathways involving the release of excitotoxic neurotransmitters, immune mediators and oxygen radicals [10][11][12] , which ultimately result in long-term neurological disabilities 13,14 . Thus choosing appropriate animal models of TBI that present similar cellular and molecular events in human and rodent TBI is critical for studying the mechanisms underlying injury and repair.Various experimental models of TBI have been developed to reproduce aspects of TBI observed in humans, among them three specific models are widely adapted for rodents: fluid percussion, cortical impact and weight drop/impact acceleration 1 . The fluid percussion device produces an injury through a craniectomy by applying a brief fluid pressure pulse on to the intact dura. The pulse is created by a pendulum striking the piston of a reservoir of fluid. The percussion produces brief displacement and deformation of neural tissue 1,15 . Conversely, cortical impact injury delivers mechanical energy to the intact dura via a rigid impactor under pneumatic pressure 16,17 . The weight drop/impact model is characterized by the fall of a rod with a specific mass on the closed skull 18 . Among the TBI models, LFP is the most established and commonly used model to evaluate mixed focal and diffuse brain injury 19. It is reproducible and is standardized to allow for the manipulation of injury parameters. LFP recapitulates injuries observed in humans, thus rendering it clinically relevant, and allows for exploration of novel therapeutics for clinical translation 20 .We describe the detailed protocol to perform LFP procedure in mice. The injury inflicted is mild to moderate, with brain regions such as cortex, hippocampus and corpus callosum being most vulnerable. Hippocampal and motor learning tasks are explored following LFP. Video LinkThe video component of this article can be found at https://www.jove.com/video/3063/ Protocol 1. Craniectomy 1. A sterile surgical site is prepared including a stereotaxic alignment instrument (Kopf Instruments) for mice with a mouse gas anesthesia head holder (Kopf Instruments) connected to an anesthesia machine with O 2 flush (Parkland Scientific) to allow for continuou...

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Post-traumatic diffuse axonal brain injury. Analysis of 78 patients studied with Computed Tomography

Cited by 64 publications

References 29 publications

Traumatic brain injury: Can the consequences be stopped?

Traumatic brain injury: Can the consequences be stopped?

Identification and Characterization of Heterogeneous Neuronal Injury and Death in Regions of Diffuse Brain Injury: Evidence for Multiple Independent Injury Phenotypes

Lateral Fluid Percussion: Model of Traumatic Brain Injury in Mice

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