The Effect of Controlled Decompression for Severe Traumatic Brain Injury: A Randomized, Controlled Trial

Chen, Junhui; Li, Mingchang; Chen, Lei; Chen, Wei‐Liang; Zhang, Chunlei; Yi, Feng; Wang, Yuhai; Chen, Qianxue

doi:10.3389/fneur.2020.00107

Cited by 21 publications

(26 citation statements)

References 30 publications

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“…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 – 10 ). Hence, studies aiming to further clarify the pathophysiological mechanisms of TBI and search for new and effective pharmacological intervention targets are important and necessary.…”

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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“…Controlled decompression technology can protect nerve cells and function by reducing ischemia-reperfusion damage and maintaining vascular regulation. This clinical study also demonstrated that the 6-months outcomes, the incidence rates of intraoperative acute brain swelling, and delayed intracranial hematoma were significantly better in sTBI patients who underwent controlled decompression than in those who underwent rapid decompression 9 . Rapid craniotomy (opening the skull and dura quickly, without controlled ICP release) causes large amounts of arterial blood to pour quickly into the brain tissue, but without appropriate venous outflow, then lead to brain edema and brain swelling.…”

Section: Discussionmentioning

confidence: 53%

“…These experimental results undoubtedly confirmed that controlled decompression can effectively reduce ICP and inhibit the necroptosis pathway as well. Besides, previous clinical trials also improved surgical patient prognosis and decreased the incidences of postoperative complications 8 , 9 .…”

Section: Discussionmentioning

confidence: 99%

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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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“…DC a life-saving procedure for treatment of refractory raised ICP, in cases of large hemispheric infarction or significant head injury. [ 4 , 6 ] The benefits of aggressive decompression in the context of TBI and malignant supratentorial infarction have been demonstrated,[ 7 ] where the timing to surgical decompression is debated. [ 9 ] Delayed subdural hematoma and intraoperative brain swelling are recognized complications of decompressive surgery;[ 12 ] however, malignant MCA infarction following craniotomy for subacute SDH has not been reported.…”

Section: Discussionmentioning

confidence: 99%

Malignant middle cerebral artery infarction following subacute subdural hematoma: A case report and literature review

Moughal¹,

Uberti

Al-Mousa

et al. 2021

Surgical Neurology International

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Background: Subacute subdural hematomas (ASDH) are only treated surgically when they cause mass effect significant enough to give symptoms. Rarely, sub-ASDH may cause enough pressure to result in a malignant middle cerebral artery (MCA) territory infarction. Decompressive craniectomy (DC) is the last resort to reduce intracranial pressure following malignant MCA infarction. Herein, we review the literature and describe a case of MCA/posterior cerebral artery (PCA) territories infarction following drainage of a sub-ASDH that was treated with DC with good outcome. Case Description: We report a case of malignant right-sided MCA/PCA infarction in a 62-year-old man who presented with progressive headache following a cycling incident leading to a head injury. Initial CT head demonstrated a small right ASDH. He had no neurological deficit, headache settled on analgesia, and there was no expansion of the SDH on the repeat CT; therefore, he was managed conservatively. He was admitted 6-days later with worsening headaches and hyponatremia. Repeat CT revealed an increase in size of the hematoma and mass effect leading to a mini-craniotomy and evacuation of hematoma. He developed left-sided hemiplegia, slurred speech and hyponatremia, and CT head demonstrated a right-sided MCA/PCA infarction with significant mass effect. He underwent emergent DC and subsequent cranioplasty and ultimately recovered to mRS of 2. Conclusion: SDH are frequent neurosurgical entities. Malignant MCA/PCA strokes following mini-craniotomies are rare but need to be considered especially during the consent process.

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The Effect of Controlled Decompression for Severe Traumatic Brain Injury: A Randomized, Controlled Trial

Cited by 21 publications

References 30 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 alleviates early brain injury in rabbit intracranial hypertension model by regulating apoptosis/necroptosis

Malignant middle cerebral artery infarction following subacute subdural hematoma: A case report and literature review

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