Experimental traumatic brain injury

Albert-Weißenberger, Christiane; Sirén, Anna‐Leena

doi:10.1186/2040-7378-2-16

Cited by 104 publications

(78 citation statements)

References 122 publications

(135 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…32 It is also amenable to the study of repeated concussions and, in terms of reproducibility, incorporates an electromagnetic (EM) coil-based delivery device, which delivers consistent strike velocities. 33,34 To date, published mouse models of CHI have typically investigated the effect of a single mTBI or two mTBIs with an interinjury interval of 24 h. 24,26,31,35 A single mTBI was shown to cause subtle and transient behavioral and immunohistochemical abnormalities, whereas two such injuries 24 h apart worsened the outcome 24,26,27,31 Unfortunately, little is known about the cumulative consequence of more than two brain injuries at multiple time intervals, as investigations of this nature are scarce and have predominantly employed the weight drop model. 25,28,36,37 In this study, we addressed this void by examining mice subjected to a s-mTBI or to a total of five r-mTBIs.…”

mentioning

confidence: 99%

Repetitive Mild Traumatic Brain Injury in a Mouse Model Produces Learning and Memory Deficits Accompanied by Histological Changes

Mouzon

Chaytow²,

Crynen³

et al. 2012

Journal of Neurotrauma

257

255

View full text Add to dashboard Cite

Concussion or mild traumatic brain injury (mTBI) represents the most common type of brain injury. However, in contrast with moderate or severe injury, there are currently few non-invasive experimental studies that investigate the cumulative effects of repetitive mTBI using rodent models. Here we describe and compare the behavioral and pathological consequences in a mouse model of single (s-mTBI) or repetitive injury (r-mTBI, five injuries given at 48 h intervals) administered by an electromagnetic controlled impactor. Our results reveal that a single mTBI is associated with transient motor and cognitive deficits as demonstrated by rotarod and the Barnes Maze respectively, whereas r-mTBI results in more significant deficits in both paradigms. Histology revealed no overt cell loss in the hippocampus, although a reactive gliosis did emerge in hippocampal sector CA1 and in the deeper cortical layers beneath the injury site in repetitively injured animals, where evidence of focal injury also was observed in the brainstem and cerebellum. Axonal injury, manifest as amyloid precursor protein immunoreactive axonal profiles, was present in the corpus callosum of both injury groups, though more evident in the r-mTBI animals. Our data demonstrate that this mouse model of mTBI is reproducible, simple, and noninvasive, with behavioral impairment after a single injury and increasing deficits after multiple injuries accompanied by increased focal and diffuse pathology. As such, this model may serve as a suitable platform with which to explore repetitive mTBI relevant to human brain injury.

show abstract

mentioning

confidence: 99%

Repetitive Mild Traumatic Brain Injury in a Mouse Model Produces Learning and Memory Deficits Accompanied by Histological Changes

Mouzon

Chaytow²,

Crynen³

et al. 2012

Journal of Neurotrauma

257

255

View full text Add to dashboard Cite

show abstract

“…Both surgical patients had a mechanism of injury at a higher velocity than a fall from 3 feet. Higher-velocity head injury could be to our eyes a contributing factor to the failure of conservative management by the following mechanism: as a more important head impact gives rise to more cerebral edema [18,19] , edema associated with higher-velocity head trauma would diminish the capacity to accommodate a large EDH in these patients. Alternatively, a higher impact may lead to an arterial origin of the EDH and a higher likelihood of EDH progression requiring surgery.…”

Section: Discussionmentioning

confidence: 99%

Conservative Management of Large Traumatic Supratentorial Epidural Hematoma in the Pediatric Population

Champagne¹,

He²,

Mercier³

et al. 2017

Pediatr Neurosurg

View full text Add to dashboard Cite

Background/Aims: Conservative management of traumatic epidural hematomas is being recognized as a safe alternative to surgical treatment in asymptomatic children. There is still debate about the maximal size of epidural hematoma that should be tolerated before deciding for surgery. Methods: We report - through a retrospective cohort study from a single institution - a series of 16 conservatively managed traumatic epidural hematomas of more than 15 mm thickness. Results: 14 patients (88%) were successfully treated using conservative management. Two patients required surgery. These 2 patients had the only 2 documented high-velocity injury mechanisms. All patients had a Glasgow Outcome Scale of 5/5 on follow-up. Conclusion: Conservative management with close observation is a safe alternative even in this population of voluminous hematomas. Injury velocity may be a contributing factor for failure of conservative management in this population.

show abstract

“…The pathology of TBI is multifaceted and may include contusion, hemorrhage and diffuse axonal damage. Cerebral edema is an additional acute complication of brain injury and results from excess accumulation of water in the intra-and extracellular can be varied by using different weights and/or heights of the weight-drop (50). Weight loss models to produce closed head traumas have been used to create diffuse lesions through the energy transfer between the weight in free fall and the experimental animal head.…”

Section: The Histopathological Changes In Tbimentioning

confidence: 99%

“…

ABSTRACT spread neurodegeneration and is still a major worldwide health problem (2,33,44,50,51). TBI causes not only direct mechanical damage to the brain, but it also induces biochemical changes that lead to delayed neural cell loss.

…”

mentioning

confidence: 99%

See 1 more Smart Citation

Effectiveness of gfap in determining neuron damage in rats with induced head trauma

Çıkrıklar¹,

Uysal²,

Ekici³

et al. 2015

Turkish Neurosurgery

View full text Add to dashboard Cite

spread neurodegeneration and is still a major worldwide health problem (2,33,44,50,51). TBI causes not only direct mechanical damage to the brain, but it also induces biochemical changes that lead to delayed neural cell loss. These biochemical changes are called secondary injury. The primary █ INTRODUCTION O ne common form of acute brain injury, traumatic brain injury (TBI), is the result of an outside force causing immediate mechanical disruption of brain tissue and delayed pathogenic events that collectively mediate wideAIm: To determine whether the serum level of glial fibrillary acidic protein (GFAP), an important indicator of neuron damage, correlates with the extent of tissue damage in the rat with induced head trauma and to obtain data in order to avoid unnecessary cranial computed tomography analyses. mATERIAl and mEThODS: Three-month-old male Sprague-Dawley rats were used. Rats were divided into 5 groups. The experimental head trauma model was examined in five groups (n=8) as follows: The control group had no intervention; Group 1: Head trauma was induced by dropping a 25 mg ball from a height of 20 cm; Group 2: Head trauma was induced by dropping a 50 mg ball from a height of 20 cm; Group 3: Head trauma was induced by dropping a 50 mg ball from a height of 80 cm; Group 4: Head trauma was induced by dropping a 100 mg ball from a height of 80 cm. Thus, according to the Newton's Law, respectively 0.05, 0.1, 0.2 and 0.4 N trauma was created. Serum GFAP levels were analyzed and the damage to cerebral tissues was evaluated in all groups. RESUlTS:We determined that number of apoptotic cells and particularly the number of GFAP (+) protoplasmic astrocytes at the perilesional region of the cortex increased in association with the increased serum GFAP level as long as the severity of the trauma increased.CONClUSION: Serum GFAP concentration can be used as a marker of the severity of head trauma and traumatic brain injury. However, more animal studies are required to reflect this result in clinical practice.

show abstract

Experimental traumatic brain injury

Cited by 104 publications

References 122 publications

Repetitive Mild Traumatic Brain Injury in a Mouse Model Produces Learning and Memory Deficits Accompanied by Histological Changes

Repetitive Mild Traumatic Brain Injury in a Mouse Model Produces Learning and Memory Deficits Accompanied by Histological Changes

Conservative Management of Large Traumatic Supratentorial Epidural Hematoma in the Pediatric Population

Effectiveness of gfap in determining neuron damage in rats with induced head trauma

Contact Info

Product

Resources

About