Intervention Review

Magnesium for acute traumatic brain injury

  1. Miguel F Arango*,
  2. Daniel Bainbridge

Editorial Group: Cochrane Injuries Group

Published Online: 8 OCT 2008

Assessed as up-to-date: 27 MAY 2008

DOI: 10.1002/14651858.CD005400.pub3


How to Cite

Arango MF, Bainbridge D. Magnesium for acute traumatic brain injury. Cochrane Database of Systematic Reviews 2008, Issue 4. Art. No.: CD005400. DOI: 10.1002/14651858.CD005400.pub3.

Author Information

  1. University of Western Ontario, Department of Anesthesia and Perioperative Medicine, London, Ontario, Canada

*Miguel F Arango, Department of Anesthesia and Perioperative Medicine, University of Western Ontario, University Hospital , London, Ontario, Canada. Miguel.Arango@lhsc.on.ca.

Publication History

  1. Publication Status: Edited (conclusions changed)
  2. Published Online: 8 OCT 2008

SEARCH

 

Abstract

  1. Top of page
  2. Abstract
  3. Plain language summary
  4. 摘要

Background

Acute traumatic brain injury is a leading cause of death and disability in young adults. Numerous pharmacological and non-pharmacological tools have been investigated and considered as potential mechanisms for improving neurological outcome. Magnesium has been considered as one of these potential therapeutic tools because of its activity on NMDA-receptors, calcium channels and neuron membranes. Animal studies have indicated a beneficial effect of magnesium on outcome after brain injury, but its efficacy in humans is unknown.

Objectives

To quantify the effect of magnesium administration on mortality and morbidity in patients with acute traumatic brain injury.

Search methods

We searched the Cochrane Injuries Group's specialised register, Cochrane Central Register of Controlled Trials, CENTRAL (The Cochrane Library issue 2, 2008), MEDLINE (and PubMed to 28 May, 2008: last 60 days), EMBASE, National Research Register, Current Controlled Trials, SIGLE, LILACS, and Zetoc. Searches were initially conducted in July 2005. The latest search was conducted in May 2008.

Selection criteria

We included all randomized controlled trials comparing any magnesium salt with no magnesium or with placebo, in patients following acute traumatic brain injury.

Data collection and analysis

Two authors independently screened search results and assessed the full texts of potentially relevant studies for inclusion. Data were extracted and methodological quality was examined.

Main results

Four studies met the inclusion criteria; one of which is an ongoing study. Data from three studies were included in the analysis. Data on mortality were only available in one study; RR 1.48 [1.00, 2.19], Test for overall effect: Z = 1.96 (P = 0.05). Glasgow Outcome Score at six months was described in the three studies. The Mean Difference = 0.02 (95% CI -0.38 to 0.041), Test for overall effect: Z = 0.08 (P = 0.94).

Authors' conclusions

There is currently no evidence to support the use of magnesium salts in patients with acute traumatic brain injury.

 

Plain language summary

  1. Top of page
  2. Abstract
  3. Plain language summary
  4. 摘要

Magnesium for acute traumatic brain injury

Traumatic head injury is a leading cause of death and disability in the teenage population, primarily arising from traffic accidents. The estimated annual cost of treating and rehabilitating victims of head injury is approximately US$2Billion in the United States alone. Most of the neurological damage occurs at the time of injury, though the hours or days following the injury account for addition damage. It is believed that excessive calcium entry into the cells is the biggest threat to brain damage, in which the calcium excess ultimately leads to increased free radicals, proteolysis, initiation of apoptosis, and inflammation. As one of the most important ions in the central nervous system, magnesium is important in various physiological effects, such as ischemia, cellular energy metabolism, and protein synthesis. Magnesium is also a potent calcium channel blocker, and helps to control intracellular calcium activity. Magnesium increases cardiac output and cerebral blood flow. Low levels of magnesium can lead to an increase of intracellular calcium levels. Hypomagnesaemia is a risk to head injuries, and this has been associated with poor neurological outcome and increased mortality. Restoring the levels of magnesium may reduce edema, improve neurological and cognitive outcomes, and help with problems associated with ischemia.

 

摘要

  1. Top of page
  2. Abstract
  3. Plain language summary
  4. 摘要

背景

鎂離子對於急性腦外傷的應用

急性腦外傷是種常見的年輕人死亡及失能原因。鎂離子因為可以在NMDA受體、鈣離子通道及神經元膜上產生活性,而被認為是急性腦外傷可能的治療工具。動物實驗已發現對於急性腦外傷病患使用鎂離子是有益的,但對於人類的效果尚未確定。

目標

量化鎂離子用於急性腦外傷病患之死亡率(失敗率)及發病率之成效。

搜尋策略

我們搜尋實證醫學中心登記的特定外傷紀錄及對照試驗文獻,醫學文獻資料庫、生物醫學與藥理學資料庫、國際研究登錄、現今的對照試驗文獻、SIGLE、LILACS、Zetoc等。搜尋從2005年7月開始。最近一次搜尋是2008年5月。

選擇標準

追蹤急性腦外傷後之病患,所採用的文獻皆為隨機控制試驗,去比較使用鎂鹽及不使用鎂或使用安慰劑所得到的結果。

資料收集與分析

兩位作者皆獨立地篩選研究結果,及評估所有可能相關且符合選用原則的研究文章。資料被擷取出來之後使用,並檢查方法學上的品質。

主要結論

4篇研究符合納入標準;其中一篇研究尚在進行中。因此只有3篇資料納入分析。只有一篇可獲得死亡率的資料;RR 1.48 [1.00, 2.19],整體效果試驗:Z = 1.96 (P = 0.05)。6個月的內格拉斯哥結果評分(Glasgow Outcome Score)被描述在此3篇研究。平均差異(Mean Difference) = 0.02 (95% CI −0.38 to 0.041),整體效果試驗:Z = 0.08 (P = 0.94)。

作者結論

目前沒有證據顯示支持鎂鹽於急性腦外傷病患之應用。

翻譯人

本摘要由高雄榮民總醫院畢勇賢翻譯。

此翻譯計畫由臺灣國家衛生研究院(National Health Research Institutes, Taiwan)統籌。

總結

急性腦外傷是種常見的年輕人死亡及失能原因,主因是交通事故。估計在美國每年治療腦外傷與復健的花費就高達20億美金。大部份神經的損壞都發生在受傷當時,雖然接下來的數小時或數天也會有附加的傷害。一般相信大量的鈣離子進入細胞對腦傷是最大的威脅,過量的鈣離子最後會導致游離自由基增加、蛋白質水解、細胞開始自毀、及發炎。鎂是中樞神經系統最重要的離子之一,與不同的生理作用有關,像是組織缺氧、細胞能量代謝、與蛋白質合成。鎂也是有影響力的鈣離子通道阻斷劑,且幫助控制細胞內鈣離子的活動。鎂會增加心輸出量與腦血流量。低濃度的鎂會導致細胞內鈣離子濃度的增加。血鎂低下是腦傷的危險因子,與不良的腦神經預後有關,並且增加死亡率。恢復鎂離子濃度可減少水腫,改善神經學的及認知的結果,且有助於與缺血有關的問題。