RSS-Feed abonnieren
DOI: 10.1016/S0973-0508(05)80023-1
Serum ionic magnesium in traumatic brain injury
Verantwortlicher Herausgeber dieser Rubrik:
Publikationsverlauf
Publikationsdatum:
05. April 2017 (online)
Abstract
Magnesium is an important ion in the body milieu, being a component of several enzymatic processes in the intra- and extracellular compartments. We have compared serum ionic magnesium levels between patients of severe closed traumatic brain injury and normal volunteers, so as to correlate the magnesium levels to severity of head injury. The study was carried out on fifty four patients of closed head injury with GCS 5–8. Biochemical analysis of serum for ionic magnesium was done at admission. The test was also performed on 20 normal volunteers and the results were studied for significant differences. Magnesium levels were compared between various subgroups defined by age, sex, admission interval, alcohol dependence, GCS, CT findings and appropriate statistical analyses done. Serum ionic magnesium levels in patients of severe head injury were in the range 0.15 to 0.45 mmol/ L (Mean 0.37 mmol/L) as compared with control range 0.4 to 0.6 mmol/L (Mean 0.44 mmol/L) which was statistically significant. Additionally it was found that patients presenting earlier than 6 hrs had significantly lower serum ionic magnesium levels compared with those presenting later. Other subgroup differences were not statistically significant. Admission serum ionic magnesium levels of patients with severe closed TBI appear to be significantly lower than those of normal controls, more so within the first 6 hours after injury.
-
References
- 1 Vink R, Nimmo AJ, Cernak I. An overview of new and novel pharmacotherapies for use in Traumatic Brain Injury. J Exp Pharm Phy 28 2001; 919-921
- 2 Reilly PL. Brain injury: the pathophysiology of the first hours. ‘Talk and Die revisited’. J Clin Neurosci 08 2001; 398-403
- 3 Marshall LF, Marshall SB, Klauber MR. A new classification of head injury based on computerized tomography. J Neurosurg 75 Suppl 1991; S14-S20
- 4 Kaye P, O’Sullivan I. The role of magnesium in the emergency department. Emerg Med J 19 2002; 288-291
- 5 Fox C, Ramsoomair D, Carter C. Magnesium: Its proven and potential clinical significance. South Med J 94 2001; 1195-1201
- 6 Ozgurtas T, Kahraman S. State of the art of new data on the role of magnesium in brain injury: clinical interest of measurements of total and ionized magnesium. Magnes Res. 17 2004; 327-334
- 7 Vink R, McIntosh TK, Demediuk P, Faden AI. Decrease in total and free magnesium concentration following traumatic brain injury in rats. Biochem Bioph Res Comm 149 1987; 594-599
- 8 Vink R, McIntosh TK, Demediuk P, Weiner MW. Decline in intracellular free magnesium is associated with irreversible brain injury following brain trauma. J Biol Chem 263 1988; 757-761
- 9 Polderman KH, Bloemers FW, Peerdeman SM, Girbes AR. Hypomagnesemia and hypophosphatemia at admission in patients with severe head injury. Crit Care Med 28 2000; 2022-2025
- 10 Bareyre FM, Saatman KE, Helfaer MA, Sinson G, Weisser JD, Brown AL, McIntosh TK. Alterations in ionized and total blood magnesium after experimental traumatic brain injury: relationship to neurobehavioral outcome and neuroprotective efficacy of magnesium chloride. J Neurochem 73 1999; 271-280
- 11 Memon ZI, Altura BT, Benjamin JL, Cracco RQ, Altura BM. Predictive value of serum ionized but not total magnesium levels in head injuries. Scand J Clin Lab Invest 55 1995; 671-677
- 12 Andersen BJ, Marmarou A. Post-traumatic selective stimulation of glycolysis. Brain Res 585 1992; 184-189
- 13 Kuroda Y, Inglis FM, Miller JD, McCulloch J, Graham DI, Bullock R. Transient glucose hypermetabolism after acute subdural hematoma in the rat. J Neurosurg 76 1992; 471-477
- 14 McIntosh TK, Faden AI, Yamakami I, Vink R. Magnesium deficiency exacerbates and pretreatment improves outcome following traumatic brain injury in rats: 31P magnetic resonance spectroscopy and other studies. J Neurotrauma 05 1988; 17-31
- 15 Mendez DR, Corbett R, Macias C, Laptook A. Total and ionized plasma magnesium concentrations in children after traumatic brain injury. Pediatr Res 57 2005; 347-352
- 16 Johnson JW, Ascher P. Voltage-dependent block by intracellular Mg2+ of N-methyl-D-aspartate-activated channels. Biophys J 57 1990; 1085-1090
- 17 Iseri LT, French JH. Magnesium: nature’s physiologic calcium blocker. Am Heart J 108 1984; 188-193
- 18 Smith DAS, Connick JH, Stone TW. Effect of changing extracellular levels of magnesium on spontaneous activity and glutamate release in the mouse neocortical slice. Br J Pharmacol 97 1989; 475-482
- 19 Chi OZ, Pollak P, Weiss HR. Effects of magnesium sulfate and nifedipine on regional cerebral blood flow during middle cerebral artery ligation in the rat. Arch Int Pharmacodyn Ther 304 1990; 196-205
- 20 Okiyama K, Smith DH, Gennarelli TA, Simon RP, Leach M, McIntosh TK. The Sodium channel blocker and glutamate release inhibitor BW1003C87 and Magnesium attenuate regional cerebral edema following experimental brain injury in the rat. J Neurochem 64 1995; 802-809