Magnesium and headache after aneurysmal subarachnoid haemorrhage

Mees, Sanne M. Dorhout; Bertens, D; Worp, H. Bart van der; Rinkel, Gabriël J.E.; Bergh, Walter M. van den

doi:10.1136/jnnp.2009.181404

Cited by 31 publications

(18 citation statements)

References 21 publications

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“…Nevertheless, the potential for gabapentin to produce sedation poses a risk that could limit its use in patients with SAH. Others have examined the effect of magnesium on the pain experienced by SAH patients and reported a mild opioid‐sparring effect . The same group described using tramadol as their preferred analgesic.…”

Section: Discussionmentioning

confidence: 99%

The Longitudinal Course of Pain and Analgesic Therapy Following Aneurysmal Subarachnoid Hemorrhage: A Cohort Study

2016

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Section: Discussionmentioning

confidence: 99%

The Longitudinal Course of Pain and Analgesic Therapy Following Aneurysmal Subarachnoid Hemorrhage: A Cohort Study

2016

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“…Furthermore, low magnesium increases neuronal excitability and triggers cortical spreading depression by increasing NMDA receptor activation, intracellular calcium, glutamate secretion, and the levels of extracellular potassium [ 147 , 149 ]. Intravenous magnesium has been shown to have a beneficial additive effect in alleviating acute migraine [ 150 , 151 ] and other types of acute headaches [ 152 , 153 ]. To this end, oral magnesium supplements have been tried as a prophylactic agent for migraine with a significant beneficial effect [ 154 , 155 ].…”

Section: Hypomagnesemia and Neurological Diseasesmentioning

confidence: 99%

Magnesium and Human Health: Perspectives and Research Directions

Alawi

Majoni

Falhammar

2018

International Journal of Endocrinology

299

223

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Magnesium is the fourth most abundant cation in the body. It has several functions in the human body including its role as a cofactor for more than 300 enzymatic reactions. Several studies have shown that hypomagnesemia is a common electrolyte derangement in clinical setting especially in patients admitted to intensive care unit where it has been found to be associated with increase mortality and hospital stay. Hypomagnesemia can be caused by a wide range of inherited and acquired diseases. It can also be a side effect of several medications. Many studies have reported that reduced levels of magnesium are associated with a wide range of chronic diseases. Magnesium can play important therapeutic and preventive role in several conditions such as diabetes, osteoporosis, bronchial asthma, preeclampsia, migraine, and cardiovascular diseases. This review is aimed at comprehensively collating the current available published evidence and clinical correlates of magnesium disorders.

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“…Experimental studies indicate that the early inhibition of glutamate receptors prevents aSAH associated blood-brain barrier leakage (Palmer et al , 1995) and development of delayed vasospasm (Zuccarello et al , 1994). A number of investigators have used magnesium to block NMDA receptor activity in attempt to prevent the development of delayed vasospasm and DINDs in aSAH patients (Dorhout Mees et al , 2010; Wong et al , 2006). These studies have met little success (Dorhout Mees et al , 2010; Wong et al , 2006).…”

Section: Early Events After Asahmentioning

confidence: 99%

“…A number of investigators have used magnesium to block NMDA receptor activity in attempt to prevent the development of delayed vasospasm and DINDs in aSAH patients (Dorhout Mees et al , 2010; Wong et al , 2006). These studies have met little success (Dorhout Mees et al , 2010; Wong et al , 2006). …”

Section: Early Events After Asahmentioning

confidence: 99%

The importance of early brain injury after subarachnoid hemorrhage

Sehba

Hou

Pluta

et al. 2012

Progress in Neurobiology

492

392

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Aneurysmal subarachnoid hemorrhage (aSAH) is a medical emergency that accounts for 5% of all stroke cases. Individuals affected are typically in the prime of their lives (mean age 50 years). Approximately 12% of patients die before receiving medical attention, 33% within 48 hours and 50% within 30 days of aSAH. Of the survivors 50% suffer from permanent disability with an estimated lifetime cost more than double that of an ischemic stroke. Traditionally, spasm that develops in large cerebral arteries 3-7 days after aneurysm rupture is considered the most important determinant of brain injury and outcome after aSAH. However, recent studies show that prevention of delayed vasospasm does not improve outcome in aSAH patients. This finding has finally brought in focus the influence of early brain injury on outcome of aSAH. A substantial amount of evidence indicates that brain injury begins at the aneurysm rupture, evolves with time and plays an important role in patients’ outcome. In this manuscript we review early brain injury after aSAH. Due to the early nature, most of the information on this injury comes from animals and few only from autopsy of patients who died within days after aSAH. Consequently, we began with a review of animal models of early brain injury, next we review the mechanisms of brain injury according to the sequence of their temporal appearance and finally we discuss the failure of clinical translation of therapies successful in animal models of aSAH.

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Magnesium and headache after aneurysmal subarachnoid haemorrhage

Cited by 31 publications

References 21 publications

The Longitudinal Course of Pain and Analgesic Therapy Following Aneurysmal Subarachnoid Hemorrhage: A Cohort Study

The Longitudinal Course of Pain and Analgesic Therapy Following Aneurysmal Subarachnoid Hemorrhage: A Cohort Study

Magnesium and Human Health: Perspectives and Research Directions

The importance of early brain injury after subarachnoid hemorrhage

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