Cerebrospinal Fluid Magnesium Research Articles

Abstracts from Hydrocephalus 2021: The Thirteenth Meeting of the International Society for Hydrocephalus and Cerebrospinal Fluid Disorders

Abstracts from Hydrocephalus 2021: The Thirteenth Meeting of the International Society for Hydrocephalus and Cerebrospinal Fluid Disorders

Anxiolytic effect of chronic intake of supplemental magnesium chloride in rat

Evidence suggest that magnesium dietary supplementation has several health benefits including lowering blood pressure, reducing insulin resistance, and improving symptoms of depression, anxiety, and migraine. Here, we aimed to study the effect of chronic magnesium supplementation on anxiety-like behavior in rats by supplementing with magnesium their drinking water for 30 days. Anxiety-like behavior was induced by subcutaneous injection of veratrin 30 min before performing elevated plus maze and open field tests to measure anxiety levels and locomotion, respectively. We quantify the concentration of magnesium in plasma and cerebrospinal fluid. We used diazepam to compare the efficacy of magnesium supplementation as an anxiolytic agent. Our results show that rats supplemented with magnesium had a statistically significant decrease in anxiety levels with not effects on locomotion and a statistically significant increase in concentration of magnesium in plasma and cerebrospinal fluid. However, the anxiolytic effect of magnesium supplementation washes-out in 12 days. We discuss the advantages of using supplemental magnesium as anxiolytic.

Magnesium Concentration in Cerebrospinal and Brain Interstitial Fluid Correlates with Serum Level in Induced Hypermagnesemia

Being a modulator of the N-methyl-D-aspartate (NMDA) receptor function magnesium has been studied for its neuroprotective and vasodilatative properties in acute and delayed brain ischemia due to vasospasm in aneurysmal subarachnoid haemorrhage (aSAH) and stroke. A number of clinical phase II and III studies have correlated serum magnesium concentrations after intravenous continuous application to clinical outcome and have failed to show a positive therapeutic effect. However, no study supported its conclusion by providing evidence for a local increase in magnesium, i.e. in the cerebrospinal fluid (CSF) and the brain parenchyma. The objective of our observational study was to compare magnesium levels in serum, CSF, and brain microdialysis samples (MDS) in patients with aSAH. Seventeen patients with aSAH at World Federation of Neurosurgeons (WFNS) grade IV and V were included. According to our internal standard treatment protocols, all patients received a ventricular catheter, a frontal intracerebral microdialysis probe, and a continuous intravenous application of 80 mmol MgSO4 per 24 hours. Magnesium concentrations of serum, CSF, and MDS were recorded. We found a positive and significant correlation of increased serum levels of magnesium to CSF and MDS magnesium concentrations. These pharmacokinetic findings may serve as a basis for further discussion of the concept of induced hypermagnesemia in patients with aSAH, especially in the context of recent level A evidence of the lack of clinical benefit.

Possible role of trace elements in epilepsy and febrile seizures: a meta-analysis.

Seizures are among the most common causes of apparent life-threatening events. There are discrepancies among the published reports on the correlation between epilepsy/febrile seizures and deficiency or overload of trace elements. The objective of this review and meta-analysis was to examine the present knowledge on the concentrations of the most investigated trace metals, including zinc, copper, selenium, and magnesium, in patients with epilepsy and febrile seizures. The PubMed and Scopus databases were searched to identify case-control studies that compared the concentration of zinc, copper, magnesium, and selenium in serum, hair, or cerebrospinal fluid between patients with epilepsy/febrile seizures and controls. A total of 60 articles were included in the present study (40 pertaining to epilepsy and 25 pertaining to febrile seizures). The serum concentration of zinc in nontreated patients with epilepsy was significantly higher than in controls (P = 0.034). There were significantly reduced serum concentrations of zinc (P = 0.018) and selenium (P = 0.012) in patients with febrile seizures compared with controls. The concentrations of copper, magnesium, and zinc were all significantly altered in patients with epilepsy who received antiepileptic drugs compared with untreated patients with epilepsy. Designing treatments to selectively restore zinc levels may be a strategy for treating patients with epilepsy. It is still unclear whether these ions are causal to, or a cofactor in, the development of epilepsy. Knowledge of the effects of various antiepileptic drugs on trace element homeostasis could potentially be used to effectively guide appropriate therapeutic strategies in the future.

Cerebrospinal fluid zinc, magnesium, copper and gamma-aminobutyric acid levels in febrile seizures

The exact etiopathogenesis of febrile seizures (FS) is unknown. The present study was conducted to evaluate the cerebrospinal fluid (CSF) zinc (Zn), magnesium (Mg), copper (Cu) and gamma-aminobutyric acid (GABA) levels in children with FS. The study subjects included 20 cases of FS, 26 patients of encephalitis and 22 children of fever with meningismus. The Zn, Mg and Cu levels in CSF and serum were analyzed by atomic absorption spectrophotometry and GABA was estimated by paper chromatography method. The mean CSF Zn, Mg and Cu values were significantly decreased in FS in comparison to encephalitis and fever with meningismus cases ( P P P 37.9°C) had significantly decreased levels of CSF ( P P

The Effect of Intravenous Magnesium Sulphate Treatment on the Spinal Anaesthesia Produced by Bupivacaine in Pre-eclamptic Patients.

In our study, the effect of intravenous magnesium sulphate in normal and pre-eclamptic patients on spinal anaesthesia produced by bupivacaine was investigated. Sixty-four pregnant (32 normal and 32 pre-eclamptic) were accepted in this study. Pregnants were divided into four groups as patients given intravenous magnesium sulphate and as control. Spinal anaesthesia was induced with 12.5 mg 0.5% hyperbaric bupivacaine. Intraoperative and postoperative haemodynamic variables, sensorial block periods, onset times of sensorial and motor block, maximum sensorial block levels, the time to reach maximum block level, Bromage scores, consumptions of intraoperative analgesic and ephedrine, the quality of anaesthesia, the duration of spinal anaesthesia and magnesium levels in blood and cerebrospinal fluid were measured and recorded. The level of magnesium in blood and cerebrospinal fluid was significantly higher in the group given magnesium in pre-eclamptic patients (p<0.01). Onset of sensory block times were significantly longer in intravenous magnesium group than in groups 1, 2 and 3 (p<0.05). Onset of motor block times were significantly longer and the duration of anaesthesia was shorter in groups given magnesium (p<0.05). Although the quality of anaesthesia was similar, supplemental analgesic consumption was significantly higher in pre-eclamptic pregnants given magnesium sulphate than in pre-eclamptic pregnants who were not given magnesium sulphate (p<0.05). Intravenous magnesium sulphate treatment during the spinal anaesthesia produced by bupivacaine extended the onset of sensory and motor block times, shortened the duration of spinal anaesthesia and therefore led to early analgesic requirement.

Magnesium Therapy in Pre-eclampsia Prolongs Analgesia Following Spinal Anaesthesia with Fentanyl and Bupivacaine: An Observational Study.

Magnesium has anti-nociceptive effects and potentiates opioid analgesia following its systemic and neuraxial administration. However, there is no study evaluating the effects of intravenous (IV) magnesium sulphate (MgSO4) therapy on spinal anaesthesia characteristics in severely pre-eclamptic patients. The aim of this study was to compare spinal anaesthesia characteristics in severely pre-eclamptic parturients treated with MgSO4 and healthy preterm parturients undergoing caesarean section. Thus, our primary outcome was regarded as the time to first analgesic request following spinal anaesthesia. Case-control Study. Following approval of Institutional Clinical Research Ethics Committee and informed consent of the patients, 44 parturients undergoing caesarean section with spinal anaesthesia were enrolled in the study in two groups: Healthy preterm parturients (Group C) and severely pre-eclamptic parturients with IV MgSO4 therapy (Group Mg). Following blood and cerebrospinal fluid (CSF) sampling, spinal anaesthesia was induced with 9 mg hyperbaric bupivacaine and 20 μg fentanyl. Serum and CSF magnesium levels, onset of sensory block at T4 level, highest sensory block level, motor block characteristics, time to first analgesic request, maternal haemodynamics as well as side effects were evaluated. Blood and CSF magnesium levels were higher in Group Mg. Sensory block onset at T4 were 257.1±77.5 and 194.5±80.1 sec in Group C and Mg respectively (p=0.015). Time to first postoperative analgesic request was significantly prolonged in Group Mg than in Group C (246.1±52.8 and 137.4±30.5 min, respectively, p<0.001; with a mean difference of 108.6 min and 95% CI between 81.6 and 135.7). Side effects were similar in both groups. Group C required significantly more fluids. Treatment with IV MgSO4 in severe pre-eclamptic parturients significantly prolonged the time to first analgesic request compared to healthy preterm parturients, which might be attributed to the opioid potentiation of magnesium.

In vitro electrical conductivity of seizing and non-seizing mouse brain slices at 10 kHz

The electrical conductivity of small samples of mouse cortex (in vitro) has been measured at 10 kHz through the four-electrode method of van der Pauw. Brain slices from three mice were prepared under seizing and non-seizing conditions by changing the concentration of magnesium in the artificial cerebrospinal fluid used to maintain the tissue. These slices provided 121 square samples of cortical tissue; the conductivity of these samples was measured with an Agilent E4980A four-point impedance monitor. Of these, 73 samples were considered acceptable on the grounds of having good electrical contact between electrodes and tissue excluding outlier measurements. Results show that there is a significant difference (p = 0.03) in the conductivities of the samples under the two conditions. The seizing and non-seizing samples have mean conductivities of 0.33 and 0.36 S m−1, respectively; however, these quantitative values should be used with caution as they are both subject to similar systematic uncertainties due to non-ideal temperature conditions and non-ideal placement of electrodes. We hypothesize that the difference between them, which is more robust to uncertainty, is due to the changing gap junction connectivity during seizures.

Changes in cerebrospinal fluid magnesium levels in patients undergoing spinal anaesthesia for hip arthroplasty: does intravenous infusion of magnesium sulphate make any difference? A prospective, randomized, controlled study

Most investigators have attributed the reduced postoperative pain or anaesthetic drug requirements in patients receiving i.v. magnesium sulphate (MgSO(4)) infusion during spinal or general anaesthesia to central N-methyl-d-aspartate (NMDA) receptor magnesium (Mg) activity. In this study, we investigated how cerebrospinal fluid (CSF) Mg concentrations change after spinal anaesthesia, and whether peripherally infusing MgSO(4) influences central Mg levels. Forty-five patients undergoing continuous spinal anaesthesia for hip arthroplasty were randomly assigned to receive either i.v. MgSO(4) at a dose of 50 mg kg(-1) diluted in 100 ml 0.9% saline solution followed by 15 mg kg(-1) h(-1) for 6 h or saline at the same volume [mean (sd) 64 (10) ml]. The changes in CSF and serum total and ionized Mg concentrations were assessed at six time points before and after spinal anaesthesia. Secondary outcome variables included serum and CSF electrolytes and proteins. Thirty-five patients completed the study. We found that spinal anaesthesia reduced total and ionized Mg concentrations in CSF by about 10%. Increasing serum Mg concentration over 80% of the baseline value left CSF Mg levels unchanged. Spinal anaesthesia unexpectedly reduced CSF total and ionized Mg concentrations in patients undergoing hip arthroplasty, although the mechanism is unclear. The dose used for peripheral MgSO(4) infusion in this study had no influence on central Mg concentrations in neurologically healthy patients undergoing spinal anaesthesia. If CSF Mg concentration is a reliable marker of Mg brain bioavailability, peripherally infused MgSO(4) during spinal anaesthesia is unlikely to influence central NMDA receptor activity.

The effect of intravenous magnesium therapy on the duration of intrathecal fentanyl labor analgesia

BackgroundMagnesium has been reported to augment the analgesic effects of opioids when co-administered into the cerebrospinal fluid. The purpose of this study was to determine the influence of intravenous magnesium therapy administered for preeclampsia on the duration of intrathecal fentanyl analgesia for labor. MethodsThirty-four nulliparous parturients having labor induced for preeclampsia and receiving intravenous magnesium therapy were recruited. Thirty-four nulliparous patients having labor induced for elective or medical reasons were recruited as controls. At request for analgesia, baseline serum magnesium levels were obtained and combined spinal–epidural analgesia was initiated with intrathecal fentanyl 25μg. Before injection of fentanyl, a sample of cerebrospinal fluid was obtained for magnesium assay. An epidural catheter was sited but no additional medications were administered until the second request for analgesia. The primary outcome was duration of intrathecal fentanyl analgesia. ResultsThere was no difference in the median duration of analgesia between the magnesium [79min (95% CI 76 to 82)] and control groups [69min (95% CI 56 to 82)] (difference between medians: 10min (95% CI −4 to 21min; P=0.16). There was neither a relationship between the serum and cerebrospinal fluid magnesium concentrations nor the cerebrospinal magnesium concentration and duration of intrathecal fentanyl analgesia. ConclusionsIntravenous magnesium therapy at doses typically used for seizure prophylaxis in preeclampsia did not influence the duration of intrathecal fentanyl labor analgesia. However, this study may have been underpowered to detect a difference and future study is warranted.

Effect of intrathecal magnesium sulfate solution injection via a microcatheter in the cisterna magna on cerebral vasospasm in the canine subarachnoid haemorrhage model

Objective. To evaluate intracisternal injection of magnesium sulfate (MgSO4) solution via a lumbar catheter for the treatment of cerebral vasospasm in the canine subarachnoid haemorrhage (SAH) model. Materials and methods. SAH was induced in 7 beagle dogs using the dual haemorrhage model. Vertebral angiography was repeated on Day 1 (before SAH), and on Day 7 (during cerebral vasospasm) before and 1.5 hours after injection of 0.5 mL/kg of 15 mmol/L MgSO4 in Ringer solution via the tip of a microcatheter placed in the cisterna magna from the lumbar spine. Results. After injection of MgSO4 solution, the cerebrospinal fluid magnesium ion concentration significantly increased to 3.89 ± 0.97 mEq/L (P < 0.01) from the baseline value (1.49 ± 0.07 mEq/L). The arterial diameters of the basilar artery (BA), vertebral artery (VA), and superior cerebral artery (SCA) on Day 1 were 1.26 ± 0.19 mm, 1.10 ± 0.13 mm, and 0.74 ± 0.21 mm, respectively. On Day 7 before injection, the arterial diameters of the BA, VA, and SCA significantly decreased to 0.75 ± 0.27 mm, 0.74 ± 0.25 mm, and 0.36 ± 0.21 mm, respectively (P < 0.01), due to vasospasm, and were significantly increased to 0.91 ± 0.27 mm (P < 0.01), 0.91 ± 0.31 mm (P < 0.05), and 0.54 ± 0.14 mm (P < 0.01), respectively, after intracisternal injection of MgSO4 solution. Conclusions. Intracisternal MgSO4 therapy using a microcatheter from the lumbar spine may be effective against vasospasm in the clinical setting of endovascular treatment of ruptured aneurysm.

Optimal cerebrospinal fluid magnesium ion concentration for vasodilatory effect and duration after intracisternal injection of magnesium sulfate solution in a canine subarachnoid hemorrhage model

The optimal CSF Mg(++) concentration for vasodilation of spastic cerebral arteries after subarachnoid hemorrhage (SAH) and its duration are unknown. The temporal profile of the vasodilatory effect and optimal CSF Mg(++) concentration after the intracisternal injection of MgSO(4) solution were investigated in an SAH model in canines. Cerebral vasospasm was induced by experimental SAH using a 2-hemorrhage model in 26 female beagles. On Day 7, 0.5 ml/kg of 15, 10, 5, or 0 mmol/L MgSO(4) in Ringer solution was injected into the cerebellomedullary cistern. Angiography was performed on Day 1 (before SAH) and before and 1, 3, and 6 hours after the intracisternal injection on Day 7 to measure arterial diameters of the basilar artery (BA), superior cerebellar artery (SCA), and vertebral artery (VA). Cerebrospinal fluid Mg(++) was also measured at the same time. Arterial diameters of the BA, SCA, and VA were significantly decreased by vasospasm on Day 7. Arterial diameter ratios (ratio of arterial diameter after MgSO(4) injection to diameter before injection on Day 7) of the BA and SCA at 1 and 3 hours after and the VA at 1 hour after intracisternal injection of the MgSO(4) solution were positively correlated with the CSF Mg(++) concentration. All arterial diameter ratios, except 1 point of the SCA, exceeded 1 if the CSF Mg(++) concentration was > 3 mEq/L at 1 hour after injection. Animals with CSF Mg(++) concentrations > 3 mEq/L at 1 hour after injection (11 dogs) showed significantly increased arterial diameters of the BA at 1 and 3 hours after and of the SCA and VA at 1, 3, and 6 hours after injection, as compared with the diameters before injection. The CSF Mg(++) concentration significantly increased at 1 hour (3.73 ± 0.69 mEq/L, p < 0.01) and 3 hours (2.05 ± 0.35 mEq/L, p < 0.01) after the intracisternal injection as compared with the baseline value (1.41 ± 0.20 mEq/L). The reversible effect of an intracisternal injection of MgSO(4) solution on the spastic artery requires CSF Mg(++) concentrations > 3 mEq/L. The vasodilatory effect continues for 3-6 hours after injection. These results suggest that the continuous infusion or intermittent intracisternal injection of MgSO(4) is needed to maintain the optimal CSF Mg(++) concentration and constantly ameliorate cerebral vasospasm.

The effect of hypermagnesemic treatment on cerebrospinal fluid magnesium level in patients with aneurysmal subarachnoid hemorrhage

Preliminary evidence has suggested that magnesium sulfate infusion reduces delayed ischemic neurological deficit and improves clinical outcome after aneurysmal subarachnoid hemorrhage. However, little is known about its site of action in vivo. We studied 22 aneurysmal subarachnoid hemorrhage patients with or without magnesium sulfate infusion for 10-14 days. Thirteen patients had external ventricular drains inserted for hydrocephalus and daily cerebrospinal fluid magnesium levels were measured. For patients given magnesium sulfate infusion, the aim was to raise the plasma magnesium level to double the baseline level. We found that the magnesium sulfate infusion bought an 11% to 21% increase in cerebrospinal fluid magnesium. The elevation of cerebrospinal fluid magnesium was sustained for at least nine days. Whether this mild elevation in cerebrospinal fluid magnesium level was adequate for neuroprotection awaits the results of ongoing clinical trials.

Serum and Cerebrospinal Fluid Magnesium Levels, Glasgow Coma Scores, and In-Hospital Mortality in Patients with Acute Stroke

The aim of this study was to determine the relationship between serum and cerebrospinal fluid (CSF) magnesium(Mg+2) levels, Glasgow Coma Scores (GCS), and 7-day mortality in acute stroke patients. Patients with acute ischemic or hemorrhagic stroke arriving within the first 3 h of symptoms were included in the study. The control group consisted of healthy volunteers. GCS was determined, and blood and CSF samples were taken in order to establish serum and CSF glucose, Mg+2, sodium, potassium, calcium, and chlorine levels.Mortality was recorded at 7 days after admission. CSF Mg+2 in the ischemic infarct group was significantly lower than in the control group (p=0.006). CSF Mg+2 in the ischemic infarct patients with a GCS < or = 8 were significantly lower (p=0.002) than controls and in ischemic infarct patients with a GCS > or = 9. In the ischemic stroke patients, CSF Mg+2 and GCS were significantly correlated (r=55, p=0.031). CSF Mg+2 levels in ischemic stroke patients who died within 7 days were significantly lower than controls, ischemic stroke patients who survived, and hemorrhagic stroke patients who died (p=0.002, p=0.042, and p=0.005,respectively). Low CSF Mg+2 levels in patients with acute ischemic stoke at admission predicted a higher 1-week mortality.

Initial Clinical Experience of Vasodilatory Effect of Intra-cisternal Infusion of Magnesium Sulfate for the Treatment of Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage

The vasodilatory effect of intra-cisternal infusion of magnesium sulfate solution was evaluated in 10 patients with symptomatic vasospasm after aneurysmal subarachnoid hemorrhage (SAH) who underwent early clipping surgery. Cisternal drainage was installed in the prepontine and/or sylvian fissures. Carotid angiography was performed immediately after the onset of symptomatic vasospasm, then intra-cisternal infusion of 15 mmol/l magnesium sulfate in Ringer solution was started at 20 ml/hr and continued until day 14. Irrigation was performed from the cisternal tube (inlet) to the spinal drainage (outlet). The cerebrospinal fluid magnesium ion concentration (1.2 +/- 0.2 mEq/l) significantly increased after the infusion therapy (6.0 +/- 1.7 mEq/l, p < 0.001). Repeat angiography showed vasodilatory effect on the spastic cerebral arteries at 3 hours after the infusion, especially in the arteries near to the site of cisternal drainage placement. The magnesium infusion also caused decreased mean arterial blood velocity in the spastic arteries in 6 of the 7 measured patients (162 +/- 38 cm/sec to 114 +/- 42 cm/sec, p < 0.001). Finally, 5 of the 10 patients achieved good recovery, 1 patient had moderate disability, 1 patient became severely disabled due to meningitis, and 3 patients were vegetative or dead, due to failure of magnesium irrigation in 1 patient and advanced age in the other 2 (more than 80 years old). This preliminary study indicates that intra-cisternal infusion of magnesium sulfate solution has vasodilatory effect on the spastic cerebral arteries after aneurysmal SAH.

The efficacy of intrathecal administration of a very low dose potirelin after acute spinal cord injury

The objective of this study was to determine the effect of a very low dose protirelin in cerebrospinal fluid (CSF) glucose, magnesium and lactate levels after spinal cord trauma (SCT) in rabbits. We also aimed to evaluate whether this very low dose might induce analeptic effect. Twenty rabbits were divided equally into two groups: group I (n=10) was the control group, suffered from SCT but received only saline after SCT. Group II (n=10) (treatment group), received a very low dose of 0.05 mg/kg thyrotropin releasing hormone (TRH), analogue protirelin intratechally after SCT. The basal CSF glucose, magnesium and lactate levels were recorded in both groups. CSF lactate, glucose and magnesium contents were recorded at the same time (an hour before and after) SCT. Serum thyroid stimulating hormone (TSH), freetriiodothyronine (FT3) and freethyroxine (FT4) were measured in all rabbits before and after SCT. Before spinal cord trauma, there were not any significant differences in glucose, lactate and magnesium levels between group I and II whereas, after spinal cord trauma in group II, the significant suppression in elevation of lactate and glucose depletion (p<0.05) were observed while no significant suppression was observed in magnesium level (p>0.05) as compared with group I (Table 3). In respect of serum TSH levels, there were not any significant differences between two groups before and after SCT. This study showed that intratechal TRH has no analeptic effect on serum TSH, FT3 and FT4 levels but can attenuate the increase of lactate levels following spinal cord trauma. No significant decrease in magnesium level and also suppression of glucose decline in group II, may be related to the neuroprotective effects of TRH.

Serum and Cerebrospinal Fluid Magnesium in Severe Traumatic Brain Injury Outcome

Serum magnesium concentration has a neuroprotective effect in experimental models of traumatic brain injury (TBI). This study was designed to assess the relationship between initial serum magnesium, cerebrospinal fluid (CSF) magnesium, neurological outcome and the efficacy of magnesium replacement therapy (MgSO4). A retrospective analysis was performed on a prospectively collected dataset from 216 patients admitted during 1996-2006 to the University of Pittsburgh Medical Center with severe TBI. Admission serum and CSF magnesium were dichotomized into low and normal magnesium concentration groups for serum and normal and high concentration groups for CSF. A logistic-regression analysis was performed with 6-month Glasgow Outcome Scale (GOS) scores as outcome variable. The outcome of a subset of 31 patients who presented with low serum magnesium and who were rapidly corrected within 24 h of admission was also analyzed. Low initial serum magnesium was measured in 56.67% of all patients. Patients with an initial serum magnesium of <1.3 mEq/L were 2.37 times more likely to have a poor outcome (CI: 1.18-4.78, p = 0.016). The prognostic significance of depressed serum magnesium remained, even in patients whose serum magnesium levels were corrected within 24 h (OR = 11.03, CI: 1.87-68.14, p = 0.008). Patients with an initial high CSF magnesium were 7.63 more likely to have a poor outcome (p = 0.05). Elevated CSF magnesium correlated with depressed serum magnesium only in patients with poor outcome (p = 0.013). Patients with low serum magnesium and high CSF magnesium are most likely to have poor outcome after severe TBI. Rapid correction of serum magnesium levels does not reverse the prognostic value of these markers.

Cerebrospinal Fluid Sodium Increases in Migraine

Pharmaceuticals with calcium- or sodium-channel-blocking activity have proven useful for migraine prophylaxis, and calcium channel, sodium transporter, and sodium channel gene mutations have been found in familial hemiplegic migraine. However, it is not known whether calcium or sodium homeostasis is altered in migraine. To compare levels of sodium, calcium, potassium, and magnesium in cerebrospinal fluid (CSF) and blood plasma between migraineurs and controls. We recruited 20 migraineurs without aura and 11 controls prospectively, and studied migraineurs in sick (MH(+)) and well (MH(-)) states. We collected lumbar CSF and venous blood plasma, quantified elements with ion-selective electrodes or colorimetry, and determined osmolality by depression of freezing point. We compared levels of Na(+), Ca(2+), K(+), and Mg among and also within subjects who were studied in both MH(+) and MH(-) states. Mean CSF Na(+) levels were increased by 3 mmol/L in MH(+) compared with MH(-) and by 4 mmol/L compared to controls (P < 0.005). In 4 subjects who were sampled in both MH(+) and MH(-) states, mean CSF Na(+) concentration increased by 2 mmol/L in the MH(+) state compared with the MH(-) state (P < 0.05). Simultaneous plasma Na(+) levels did not differ among the 3 clinical groups, nor did osmolality, total Ca and Ca(2+), K(+), and total Mg levels in CSF. Compared to both controls and the MH(-) state, CSF Na(+) concentration increased in MH(+) independently from other clinical or pharmacological fluctuations, CSF concentrations of Ca(2+), Mg, and K(+), and blood plasma Na(+) levels. These results implicate a deviation of Na(+) homeostasis in migraine. The modestly elevated extracellular Na(+) in MH(+) may cause the neural changes that underlie clinical features of migraine.

Neuroprotective effects of magnesium on metabolic disturbances in fetal hippocampal slices after oxygen-glucose deprivation: mediation by nitric oxide system.

We investigated the effects of magnesium on metabolic disturbances in hippocampal slices prepared from fetal guinea pigs after oxygen-glucose deprivation (OGD). Metabolic disturbances were assessed by measuring changes in energy metabolism and protein synthesis. In addition we determined cyclic guanosine monophosphate (cGMP) concentrations in the slices after OGD, as a measure of nitric oxide (NO) production, to clarify whether a possible neuroprotective effect of magnesium is mediated in part through the NO system. Twelve hours after oxygen-glucose deprivation, adenosine triphosphate (ATP) concentration and protein synthesis in the hippocampal slices were significantly reduced depending on the severity of OGD. A higher magnesium concentration in the incubation medium from 1.3 mM to 3.9 mM 2 hours before OGD significantly improved the recovery of ATP and protein synthesis, whereas treatment after OGD was ineffective. The cGMP concentrations increased dramatically in hippocampal slices 10 minutes after OGD, indicating a significant increase in NO production. When the concentration of magnesium in the artificial cerebrospinal fluid was increased 2 hours before OGD the rise in tissue levels of cGMP was considerably reduced. Again, treatment after OGD had no effect. We conclude that increasing magnesium concentration in the artificial cerebrospinal fluid before OGD alleviated metabolic disturbances in hippocampal slices from mature fetal guinea pigs, whereas treatment after OGD had no effect. This neuroprotective property of magnesium might be mediated in part through the inhibition of NO production shortly after OGD.

Postmortem biochemical markers of experimentally induced hypomagnesaemic tetany in cattle

Severe hypomagnesaemia and tetany were induced in 10 lactating cows by feeding them semi-synthetic low magnesium diets and the animals were used to study the stability of postmortem markers of...