Nutrition and Traumatic Brain Injury Improving Acute and Subacute Health Outcomes in Military Personnel (2011) / Chapter Skim
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12 Magnesium
12 Magnesium
Pages 157-187
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From page 157... ...
. Following traumatic brain injury (TBI)
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From page 158... ...
Symptoms of magnesium toxicity are more likely to occur in individuals suffering from renal failure, when the kidney loses its ability to remove excess magnesium (Fleet and Cashman, 2001; IOM, 1997) .2 EVIDENCE INDICATING EFFECT ON RESILIENCE Human Studies The committee's review of the literature found no clinical trials investigating the effects of magnesium on resilience for TBI or related diseases or conditions (i.e., subarachnoid hemorrhage, intracranial aneurysm, stroke, anoxic or hypoxic ischemia, or epilepsy)
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From page 159... ...
controlled trial for 10–14 days plasma magnesium level in the treatment group was between 1.59–1.84 mmol/L, n=22 patients while the average in the control group who were ranged from 0.85–1.02 mmol/L. simultaneously participating Although the treatment group had higher in an levels of cerebrospinal fluid magnesium intravenous overall, the difference was significant only on day 2 and days 5–8 (p ≤ 0.035)
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From page 160... ...
experienced hours) intra-operative brain swelling during surgical decompression than patients in the MgSO4 group (29.4%, OR=0.15, 95% CI: 0.03–0.71, p=0.01)
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From page 161... ...
, but not the risk of developing delayed cerebral ischemia. PTH's effect on risk of poor outcome increased after adjusting for age and gender (OR=16.3; 95% CI: 2.2–119.2)
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From page 162... ...
. Patient with serum magnesium levels of > 1.28 mmol/L at day 8 (categorized as quartiles 2nd–4th)
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delayed cerebral ischemia than patients with normal calcium level (HRf=2.1; 95% CI: 1.0–4.3)
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From page 164... ...
. Patients with WFNS grades 4–5 in MgSO4 group also had a higher level of S-100 in cerebrospinal fluid, as well as higher levels of neuron-specific enolase in both serum and cerebrospinal fluid (p < 0.05)
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From page 165... ...
However, patients without cortical ischemic stroke had significantly fewer poor outcomes if treated with magnesium (OR=0.75, 95% CI: 0.58–0.97; p=0.026) ; analysis showed a significant interaction between magnesium treatment and the group of patients with non-cortical syndromes (p=0.011)
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From page 166... ...
of patients participating in other neuroprotective trials at UCLA Chia et al., Aneurismal Non- Nimodipine (20 No adverse event was associated with μg/kg/hr) alone 2002 SAH randomized, magnesium treatment.
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From page 167... ...
. Ischemic stroke patients who died 7 days after stroke onset had significantly lower Mg2+ levels than controls (p=0.002)
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From page 168... ...
. Further multivariable analysis of highest and lowest magnesium intake showed that higher intake in men younger than 60 was associated with lower risk of cerebral infarction (RR=0.67, 95% CI: 0.64–0.89)
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From page 169... ...
McKee Acute brain Prospective Postinjury, i.v. Compared to baseline, there was a et al., 2005b injury resulting study MgSO4 (bolus significant increase of mean total and ionized Mg2+ in serum and in CSF in intracranial of 20 mmol over n=30 patients throughout the study period (p < 0.008)
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From page 170... ...
No adverse effects were mentioned and serum levels of Mg2+ remain lower than those producing toxicity. Iso et al., Stroke Prospective Dietary and No significant association was observed 1999 cohort supplementary between dietary or supplementary study (part magnesium magnesium intake and risk of total or of Nurses' intake ischemic stroke in women.
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From page 171... ...
However, compared diffuse TBI minutes after to untreated rats, MgSO4-treated rats had injury decreased AQP4 activity and increased labeling of micro-vessels. Labeling in treated rats was restored to the level of sham-injured controls and uninjured rats.
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From page 172... ...
; Evaluation of tissue loss in the sham-injured hippocampus showed that rats treated rats were treated with MgSO4 had significantly reduced with saline 90 loss (14%) compared to rats treated with minutes after NPS 1506 (38%)
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and faster model of Dawley rats kg of MgSO4, cognitive recovery (p < 0.05) compared to diffuse TBI magnesium gluconate, saline-treated rats.
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, magnesium treatment restored the rats' performance to the level of sham injured rats. On the Barnes Maze testing spatial learning abilities, saline-treated rats showed significantly slower improvement in performance than sham-injured rats (p < 0.05)
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. All injured rats had decreased free magnesium concentration immediately after injury.
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From page 176... ...
CA3 region was the same in all injured or saline at 10 rats. minutes after At –3.3 mm Bregma, MgCl2-treated rats injury; rats fed had smaller spectrin breakdown area in a magnesium the cortex than rats fed with magnesium deficient deficient diet (p < 0.05)
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From page 177... ...
compared to or 24 hours after injury, saline-treated rats, but the rate of their or initial dose improvement was slower than rats treated at 30 minutes at 30 minutes. postinjury, then For up to 2 days after injury, blood additional doses free-Mg2+ level was significantly every 12 hours lower in untreated rats (p < 0.05)
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From page 178... ...
or i.m. bolus performance on Rotarod test was better in Dawley rats of MgSO4 or rats treated with i.m.
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From page 179... ...
. Analysis of recovery rate showed that rats treated for 5 or 2 days recovered significantly faster than saline-treated rats (treatment/days interactions for vibrissae-forelimb test: p < 0.0001; for forelimb-forelimb: p < 0.009)
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From page 180... ...
Brain Mg2+ level in rats treated with MgSO4 for 48 hours was significantly higher when compared to sham-injured, untreated rats (p < 0.01) , but not when compared to injured, untreated rats.
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From page 181... ...
. Enomoto and colleagues reported in 2005 that intravenous administration of magnesium 5 to 20 minutes before the induction of traumatic brain damage by a lateral fluid percussion brain injury model prevented injury-induced neuronal loss in the hippocampus, as well as injury-induced impairments in working and reference memory on the Morris water maze, a test of spatial memory.
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From page 182... ...
reported that TBI in laboratory rodents was associated with a decline in intracellular free magnesium and further noted that the greater the reduction in magnesium, the more severe the trauma-induced neurological deficits. In subsequent work, these investigators demonstrated that magnesium deficiency exacerbated the physiological and behavioral outcomes of traumatic brain injury, while pretreatment with magnesium improved them (McIntosh et al., 1988, 1989)
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From page 183... ...
. As mentioned in the earlier section on resilience, a significant reduction in ipsilateral hippocampal cell loss was seen when magnesium therapy was admin istered prior to fluid percussion brain injury; accordingly, the magnesium therapy prevented injury-induced cognitive dysfunction in the Morris water maze (Enomoto et al., 2005)
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From page 184... ...
is comparing the effects of magnesium given intravenously by paramedics within 1 to 2 hours of symptom onset on scales of global handicap, neurological deficits, quality of life, and mortality, to placebo three months following injury.4 Results of this study have yet to be published. Results of studies employing experimental animals have shown that magnesium can protect against a number of the secondary consequences of traumatic brain injury.
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From page 185... ...
2005. Pre-injury magnesium treatment pre vents traumatic brain injury-induced hippocampal ERK activation, neuronal loss, and cognitive dysfunction in the radial-arm maze test.
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From page 186... ...
2001. Subdural hematoma following traumatic brain injury causes a secondary decline in brain free magnesium concentration.
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From page 187... ...
2007. Magnesium sulfate for neuroprotection after traumatic brain injury: A randomised controlled trial.
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