Magnesium Sulfate for Acute Traumatic Brain Injury

Li, Wen; Bai, Yin-An; Li, Yajun; Liu, Kaige; Wang, Maode; Xu, Gaoran; Shang, Hong-Li; Li, Yanfeng

doi:10.1097/scs.0000000000001339

Cited by 24 publications

(12 citation statements)

References 49 publications

(57 reference statements)

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“…A Cochrane systematic review including three randomized controlled trials (RCTs) published in 2008, found no beneficial role for magnesium treatment in acute TBI patients in terms of improving neurological outcomes or mortality and therefore did not support its use [ 42 ]. Another methodical review of the use of magnesium sulfate in acute TBI management, including eight RCTs published in 2015, also found no significant improvement in mortality but did report a nonsignificant improvement in GOS and GCS scores with magnesium therapy [ 43 ].…”

Section: Excitotoxicitymentioning

confidence: 99%

Revisiting Traumatic Brain Injury: From Molecular Mechanisms to Therapeutic Interventions

et al. 2020

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Studying the complex molecular mechanisms involved in traumatic brain injury (TBI) is crucial for developing new therapies for TBI. Current treatments for TBI are primarily focused on patient stabilization and symptom mitigation. However, the field lacks defined therapies to prevent cell death, oxidative stress, and inflammatory cascades which lead to chronic pathology. Little can be done to treat the mechanical damage that occurs during the primary insult of a TBI; however, secondary injury mechanisms, such as inflammation, blood-brain barrier (BBB) breakdown, edema formation, excitotoxicity, oxidative stress, and cell death, can be targeted by therapeutic interventions. Elucidating the many mechanisms underlying secondary injury and studying targets of neuroprotective therapeutic agents is critical for developing new treatments. Therefore, we present a review on the molecular events following TBI from inflammation to programmed cell death and discuss current research and the latest therapeutic strategies to help understand TBI-mediated secondary injury.

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Section: Excitotoxicitymentioning

confidence: 99%

Revisiting Traumatic Brain Injury: From Molecular Mechanisms to Therapeutic Interventions

et al. 2020

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“…A number of other experimental compounds have been successfully used to reduce edema formation in experimental TBI studies, including more recently progesterone and magnesium (4, 82), both of which have been unsuccessful in clinical trials to date (83, 84). Notably, when tested in our sheep model of TBI, our preliminary results also showed that both compounds had little effect on ICP or P bt O 2 after TBI (unpublished results).…”

Section: Icp and Brain Oxygenation After Tbimentioning

confidence: 99%

The Role of Substance P in Secondary Pathophysiology after Traumatic Brain Injury

2017

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It has recently been shown that substance P (SP) plays a major role in the secondary injury process following traumatic brain injury (TBI), particularly with respect to neuroinflammation, increased blood–brain barrier (BBB) permeability, and edema formation. Edema formation is associated with the development of increased intracranial pressure (ICP) that has been widely associated with increased mortality and morbidity after neurotrauma. However, a pharmacological intervention to specifically reduce ICP is yet to be developed, with current interventions limited to osmotic therapy rather than addressing the cause of increased ICP. Given that previous publications have shown that SP, NK1 receptor antagonists reduce edema after TBI, more recent studies have examined whether these compounds might also reduce ICP and improve brain oxygenation after TBI. We discuss the results of these studies, which demonstrate that NK1 antagonists reduce posttraumatic ICP to near normal levels within 4 h of drug administration, as well as restoring brain oxygenation to near normal levels in the same time frame. The improvements in these parameters occurred in association with an improvement in BBB integrity to serum proteins, suggesting that SP-mediated increases in vascular permeability significantly contribute to the development of increased ICP after acute brain injury. NK1 antagonists may therefore provide a novel, mechanistically targeted approach to the management of increased ICP.

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“…It interrupts a number of secondary factors involved in pathophysiology of TBI, the principal action that has been suggested by animal models is by NMDA receptor blockade and decreasing glutamate release. The other neuroprotective mechanisms proposed are improvement of cerebral blood flow, calcium channel blockage and inhibition of apoptosis [15, 31, 32]. A recent meta-analysis of existing randomized controlled trials did not identify a significant beneficial effect in the mortality of traumatic brain injury patients; however, it suggests that magnesium sulfate shows a tendency to improve the GOS and GCS scores, which is a promising result for traumatic brain injury therapy [33].…”

Section: Discussionmentioning

confidence: 99%

Efficacy of Simultaneous Administration of Nimodipine, Progesterone, and Magnesium Sulfate in Patients with Severe Traumatic Brain Injury: A Randomized Controlled Trial

Abdoli¹,

Rahimi–Bashar²,

Torabian³

et al. 2019

BEAT

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Objective: To investigate the safety and efficacy of simultaneous administration of nimodipine, progesterone, magnesium sulfate in patients suffering from severe traumatic brain injury (TBI). Methods: Overall, 90 patients with blunt head trauma who were admitted to the Besat hospital, Hamadan University of Medical Sciences, Iran through the Emergency Department in 2017 to 2018 were randomly assigned to the study or control groups each containing 45 patients. In the study group, intravenous nimodipine 60 mg every 12 hours for 5 days, intramuscular progesterone 1 mg/kg daily for 5 days, and magnesium sulfate 5 grams stat followed by 2.5 grams every 4 hours for 21 days were administered. Daily GCS and jugular venous oxygen saturation (SjvO2) of the patients were measured on admission day (day 0) through hospitalization day 4 at the intensive care unit. Then, all patients were visited at three months after discharge. Results: The mean age of the patients was 31.4 ± 12.8 years including 59 (65.6%) men with no significant difference between the groups. The baseline GCS and SjvO2 of the patients were comparable in both groups, however, GCS of the patients in the study group were significantly higher in the next 4 hospitalization days compared to the controls. Whereas, the SjvO2 of the patients were not significantly different between the groups during these days. Three-month mortality rate of the patients in the study group was significantly lower than the three-month mortality rate of the patients in the control groups (22.2% vs. 42.2%, p =0.042). Conclusion: Administration of combined protocol of magnesium sulfide, progesterone and nimodipine may be safe and effective in patients suffering from severe TBI. Clinical Trial Registry: IRCT201210229534N2

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Magnesium Sulfate for Acute Traumatic Brain Injury

Cited by 24 publications

References 49 publications

Revisiting Traumatic Brain Injury: From Molecular Mechanisms to Therapeutic Interventions

Revisiting Traumatic Brain Injury: From Molecular Mechanisms to Therapeutic Interventions

The Role of Substance P in Secondary Pathophysiology after Traumatic Brain Injury

Efficacy of Simultaneous Administration of Nimodipine, Progesterone, and Magnesium Sulfate in Patients with Severe Traumatic Brain Injury: A Randomized Controlled Trial

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