Value of Ventricular Intracranial Pressure Monitoring for Traumatic Bifrontal Contusions

Chen, Junhui; Li, Peipei; Yang, Likun; Chen, Lei; Zhu, Jie; Hu, Xu; Wang, Yuhai

doi:10.1016/j.wneu.2018.02.122

Cited by 14 publications

(26 citation statements)

References 43 publications

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“…TBI has a high incidence in low-income and middle-income countries, as well as developing countries such as Iran and China (3)(4)(5). The incidence of TBI is increasing rapidly due to the significant increase in road traffic collisions, including motor vehicle accidents (5). Although an increasing number of randomized controlled trials including intracranial pressure monitoring, therapeutic hypothermia, surgical methods and drug administration have been performed in recent years and the long-term outcome has substantially improved, a significant benefit is not observed following drug interventions (4)(5)(6)(7)(8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine alleviates early brain injury following traumatic brain injury by inhibiting autophagy and neuroinflammation through the ROS/Nrf2 signaling pathway

Feng

Zhu

et al. 2021

Mol Med Rep

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Traumatic brain injury (TBI) is a major public health problem and a major cause of mortality and disability that imposes a substantial economic burden worldwide. Dexmedetomidine (DEX), a highly selective α-2-adrenergic receptor agonist that functions as a sedative and analgesic with minimal respiratory depression, has been reported to alleviate early brain injury (EBI) following traumatic brain injury by reducing reactive oxygen species (ROS) production, apoptosis and autophagy. Autophagy is a programmed cell death mechanism that serves a vital role in neuronal cell death following TBI. However, the precise role of autophagy in DEX-mediated neuroprotection following TBI has not been confirmed. The present study aimed to investigate the neuroprotective effects and potential molecular mechanisms of DEX in TBI-induced EBI by regulating neural autophagy in a C57BL/6 mouse model. Mortality, the neurological score, brain water content, neuroinflammatory cytokine levels, ROS production, malondialdehyde levels and neuronal death were evaluated by TUNEL staining, Evans blue extravasation, ELISA, analysis of ROS/lipid peroxidation and western blotting. The results showed that DEX treatment markedly increased the survival rate and neurological score, increased neuron survival, decreased the expression of the LC3, Beclin-1 and NF-κB proteins, as well as the cytokines IL-1β, IL-6 and TNF-α, which indicated that DEX-mediated inhibition of autophagy and neuroinflammation ameliorated neuronal death following TBI. The neuroprotective capacity of DEX is partly dependent on the ROS/nuclear factor erythroid 2-related factor 2 signaling pathway. Taken together, the results of the present study indicated that DEX improves neurological outcomes in mice and reduces neuronal death by protecting against neural autophagy and neuroinflammation.

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Section: Introductionmentioning

confidence: 99%

Dexmedetomidine alleviates early brain injury following traumatic brain injury by inhibiting autophagy and neuroinflammation through the ROS/Nrf2 signaling pathway

Feng

Zhu

et al. 2021

Mol Med Rep

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“…After conservative treatment fails to control refractory intracranial hypertension (e.g., ICP >25 mmHg for a long period of time), there is sufficient evidence to support the use of decompression as a life-saving intervention [17]. Rapid decompressive craniectomy can reduce ICP, thus improving cerebrovascular compliance [18], cerebral oxygenation [19,20], and cerebral perfusion [21,22], and can also reduce postoperative brain edema [11], but it also leads to a high probability of rebleeding and brain swelling during surgery or post-operatively. Flint et al reported that 58% of patients (n=40) experienced acute encephalocele and ipsilateral or contralateral rebleeding with rapid decompressive craniectomy [23], which sharply increases ICP and aggravates cytotoxicity and angiogenic brain edema [24,25].…”

Section: Discussionmentioning

confidence: 99%

Controlled Decompression Attenuates Brain Injury in a Novel Rabbit Model of Acute Intracranial Hypertension

et al. 2019

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This work was supported by Key Disciplines of Wuxi (ZDXK005) and Major Projects of Wuxi Health and Family Planning Commission (Z201705) Background: In the past, standard rapid decompressive craniectomy was used to alleviate the secondary damage caused by high intracranial pressure. Recent clinical studies showed that controlled decompression may have a better curative effect than rapid decompression. However, the effect on controlled decompression in animals is unclear. Material/Methods: Totally 80 healthy male New Zealand rabbits were randomly divided into a sham group (n=20), a rapid decompression group (n=30), and a controlled decompression group (n=30). An intracranial hypertension model was induced by injecting saline into an epidural balloon catheter and reducing ICP slowly and gradually by use of a pressure pump. The model was evaluated and analyzed by general observations, imaging examination, ICP values, behavioral score, brain water content, Nissl staining, and caspase-3 protein detection. Results: The mortality rate was 36.7% (11/30) in the rapid group, 20% (6/30) in the controlled group, and 5% (1/20) in the sham group. The incidence of epidural hematoma in the controlled group was lower than in the rapid group (p<0.01). The ICP was significantly lower in the controlled group than in the rapid group (p<0.001), and the behavioral score in the rapid group was higher than in the controlled group (p<0.05). There was a marked difference in brain water content between the controlled group and the rapid group (p<0.01). Nissl staining demonstrated that the ratio of Nissl body in the controlled group was significantly higher than in the rapid group (p<0.01). WB detection showed the expression of Caspase-3 in the controlled group was lower than in the rapid group (p<0.05). Conclusions: The results show the advantages of use of controlled decompression with intracranial hypertension. The animal model we developed provides a platform for further research on controlled decompression.

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“…According to the epidemiological statistics, the incidence of sTBI is considerably high, which can account for about 10–20% of the total number of surgical traumas, and has a higher wartime incidence 1 , 2 . The increased intracranial pressure (ICP) is one of the main causes of death after sTBI 3 , 4 . The standard decompressive craniotomy is currently the conventional surgery for sTBI in neurosurgery, since it rapidly decreases ICP to minimize brain damage 5 .…”

Section: Introductionmentioning

confidence: 99%

Controlled decompression alleviates early brain injury in rabbit intracranial hypertension model by regulating apoptosis/necroptosis

et al. 2021

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Purpose To evaluate the effects of controlled decompression and rapid decompression, explore the potential mechanism, provide the theoretical basis for the clinical application, and explore the new cell death method in intracranial hypertension. Methods Acute intracranial hypertension was triggered in rabbits by epidural balloon compression. New Zealand white rabbits were randomly put into the sham group, the controlled decompression group, and the rapid decompression group. Brain water content, etc., was used to evaluate early brain injury. Western blotting and double immunofluorescence staining were used to detect necroptosis and apoptosis. Results Brain edema, neurological dysfunction, and brain injury appeared after traumatic brain injury (TBI). Compared with rapid decompression, brain water content was significantly decreased, neurological scores were improved by controlled decompression treatment. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and Nissl staining showed neuron death decreased in the controlled decompression group. Compared with rapid decompression, it was also found that apoptosis-related protein caspase-3/ tumor necrosis factor (TNF)-a was reduced markedly in the brain cortex and serum, and the expression levels of necroptosis-related protein, receptor-interacting protein 1 (RIP1)/receptor-interacting protein 1 (RIP3) reduced significantly in the controlled decompression group. Conclusions Controlled decompression can effectively reduce neuronal damage and cerebral edema after craniocerebral injury and, thus, protect the brain tissue by alleviating necroptosis and apoptosis.

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Value of Ventricular Intracranial Pressure Monitoring for Traumatic Bifrontal Contusions

Cited by 14 publications

References 43 publications

Dexmedetomidine alleviates early brain injury following traumatic brain injury by inhibiting autophagy and neuroinflammation through the ROS/Nrf2 signaling pathway

Dexmedetomidine alleviates early brain injury following traumatic brain injury by inhibiting autophagy and neuroinflammation through the ROS/Nrf2 signaling pathway

Controlled Decompression Attenuates Brain Injury in a Novel Rabbit Model of Acute Intracranial Hypertension

Controlled decompression alleviates early brain injury in rabbit intracranial hypertension model by regulating apoptosis/necroptosis

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