Traumatic brain injury: classification, models, and markers

Najem, Dema; Rennie, Kerry; Ribecco-Lutkiewicz, Maria; Ly, Dao; Haukenfrers, Julie; Liu, Qing; Nzau, Munyao; Fraser, Douglas D.; Bani‐Yaghoub, Mahmud

doi:10.1139/bcb-2016-0160

Cited by 139 publications

(124 citation statements)

References 192 publications

(214 reference statements)

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Section: Discussionmentioning

confidence: 99%

“…TBIs can be classified into primary and secondary injuries [ 7 ]. Primary injuries result from the initial impact or injury to the head which leads to epidural and subdural hematomas, as well as axonal shearing and cortical contusions [ 7 ]. Secondary injuries present hours to days following the insult and are the result of hypotension, hypoxia, cerebral edema and increased ICP of over 20 mmHg, and include non-mechanical damage that results from cellular disruption [ 5 , 7 ].…”

Section: Discussionmentioning

confidence: 99%

“…As previously mentioned, pediatric patients have widely variable presentations and practitioners often use a combination of associated symptoms and imaging to fully assess the extent of the injury. CT is the most commonly used initial diagnostic test for TBIs due to its speed and ability to detect serious lesions that may require immediate intervention [ 7 ]. CT is specifically useful in detecting hemorrhages, cerebral edema, and bone fractures in TBIs [ 7 ].…”

Section: Discussionmentioning

confidence: 99%

“…CT is the most commonly used initial diagnostic test for TBIs due to its speed and ability to detect serious lesions that may require immediate intervention [ 7 ]. CT is specifically useful in detecting hemorrhages, cerebral edema, and bone fractures in TBIs [ 7 ]. Additionally, the use of MRI allows for complementary visualization of soft tissue structures in addition to CT imaging [ 7 ].…”

Section: Discussionmentioning

confidence: 99%

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Absence of cognitive symptoms in a 6-year-old male with post-traumatic increased intracranial pressure - A case report

Daoud

Drolet

Carto

et al. 2018

Annals of Medicine and Surgery

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IntroductionTraumatic Brain Injuries (TBIs) can range from mild to severe, and may result in increased intracranial pressure (ICP). Increased ICP causes hallmark physical signs, such as diaphoresis, emesis, fixed pupils, and altered mental status. Monitoring the patient's score on the Glasgow Coma Scale (GCS) and cranial CT scans are routine measures used in clinical practice to monitor the development of a TBI.Presentation of the caseA 6-year-old male fell off his father's shoulders and subsequently presented to ED for suspected head trauma. He was transferred to our Level 1 Trauma Center after a head CT scan demonstrated a subdural hematoma. His GCS score remained 15. The next day he began to have episodes of apnea and desaturation. Further imaging indicated expansion of the hematoma with a 5mm midline shift. He remained consistently alert and a neurological exam revealed cranial nerves to be grossly intact. Increased ICP was reduced with several days of hypertonic saline treatment without surgical intervention.DiscussionTBIs can have long-lasting effects in pediatric patients and are typically assessed using both diagnostic imaging and clinical judgment. CT scans are used to assess for hematoma development, while loss of consciousness (LOC) and altered mental status are standard clinical diagnostic indicators of increased ICP. This patient remained alert with a GCS score of 15, although he had clinical signs of increased ICP including apnea and bradycardia with a midline shift confirmed on imaging.ConclusionWhile GCS is an important prognostic indicator in TBI, patients should still be monitored to assure resolution of all symptoms.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Absence of cognitive symptoms in a 6-year-old male with post-traumatic increased intracranial pressure - A case report

Daoud

Drolet

Carto

et al. 2018

Annals of Medicine and Surgery

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“…Traumatic brain injury (TBI) refers to local anatomical and pathological structural damage in the brain due to trauma, which can cause hemiplegia, aphasia, mental retardation, or even coma and death [1][2][3]. Currently, surgery and drugs are commonly used as symptomatic treatments.…”

Section: Introductionmentioning

confidence: 99%

SHED-Derived Exosomes Regulate Microglial Polarization in the Treatment of Traumatic Brain Injury in Rats via miR-330-5p

Li¹,

Wang²,

Cao³

et al. 2020

Preprint

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Background: Traumatic brain injury (TBI) causes structural damage and impairs motor and cognitive function of the brain. Our previous study suggested that exosomes (EXs) secreted by stem cells from human exfoliated deciduous teeth (SHED) extenuated motor damage in TBI rats by regulating microglia. The molecular mechanism of SHED-EXs was investigated in the present study. Methods: The miRNA array was performed to determine the differential miRNA expression in SHED-EXs treating microglia. The key miRNA was selected. Flow cytometry, immunofluorescence, enzyme linked immunosorbent assay (ELISA) and Griess assay were performed to detect the function of key miRNA. Real-time PCR, Western blotting and dual luciferase reporter assay were used to confirm the relationship between key miRNA and the target gene. Chromatin immunoprecipitation (ChIP) was performed to determine the downstream pathway of EXs-miRNA. Traumatic brain injury rat model was established and local injection of EXs-miRNA was performed to evaluate the effect.Results: SHED-EXs delivery of miR-330-5p was the key in the regulation of microglia polarization by inhibiting M1 polarization and promoting M2 polarization. Mechanistically, miR-330-5p had an inhibitory effect on Ehmt2, and miR-330-5p/Ehmt2 promoted the transcription of CXCL14 through H3K9me2. In vivo data showed that SHED-EXs/miR-330-5p reduced neuro-inflammation and repaired neurological function of TBI rats. Conclusions: SHED-EXs/miR-330-5p improved the motor function of rats after TBI by inhibiting M1 polarization and promoting M2 polarization of microglia through Ehmt2/H3K9me2/CXCL14 pathway.

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Nicorandil attenuates cognitive impairment after traumatic brain injury via inhibiting oxidative stress and inflammation: Involvement of BDNF and NGF

Tu,

Han,

Liu

et al. 2023

Brain and Behavior

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Background and purposeCognitive impairment is a prevalent adverse consequence of traumatic brain injury (TBI). The neuroprotective effects of nicorandil (N‐(2‐hydroxyethyl)‐nicotinamide nitrate) has been previously documented, yet its protective effects against cognitive dysfunction post‐TBI remain unclear. Hence, the present study was aimed to evaluate whether nicorandil attenuates cognitive dysfunction in TBI rats and the underlying mechanism behind this process.MethodsThe TBI model was established with a controlled cortical impact (CCI). The effects of nicorandil on cognitive dysfunction of rats with TBI were examined through Novel object recognition (NOR) test, Y‐maze test, and Morris water maze (MWM) task. After behavioral tests, hippocampal tissue was collected for Quantitative real‐time PCR, Western blot analysis, and Enzyme‐linked immunosorbent assay (ELISA) assay.ResultsWe observed that nicorandil administration effectively ameliorates learning and memory impairment in TBI rats. Alongside, nicorandil treatment attenuated oxidative stress in the hippocampus of TBI rats, characterized by the decreased reactive oxygen species generation, malondialdehyde, and protein carbonyls levels, and concurrent promotion of antioxidant‐related factors (including superoxide dismutase, glutathione peroxidase, and catalase) activities. Additionally, nicorandil treatment attenuated the inflammatory response in the hippocampus of TBI rat, as evidenced by the upregulated levels of interleukin (IL)‐1β, IL‐6, and tumor necrosis factor‐α (TNF‐α), as well as the downregulated level of IL‐10. Mechanistically, nicorandil treatment significantly enhanced the mRNA and protein levels of neurotrophic factors, brain‐derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the hippocampus of TBI rats.ConclusionThese findings suggest that nicorandil mitigates cognitive impairment after TBI by suppressing oxidative stress and inflammation, potentially through enhancing BDNF and NGF levels.

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Traumatic brain injury: classification, models, and markers

Cited by 139 publications

References 192 publications

Absence of cognitive symptoms in a 6-year-old male with post-traumatic increased intracranial pressure - A case report

Absence of cognitive symptoms in a 6-year-old male with post-traumatic increased intracranial pressure - A case report

SHED-Derived Exosomes Regulate Microglial Polarization in the Treatment of Traumatic Brain Injury in Rats via miR-330-5p

Nicorandil attenuates cognitive impairment after traumatic brain injury via inhibiting oxidative stress and inflammation: Involvement of BDNF and NGF

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