Ionized calcium in human cerebrospinal fluid and its influence on intrinsic and synaptic excitability of hippocampal pyramidal neurons in the rat.

It is well-known that the extracellular concentration of calcium affects neuronal excitability and synaptic transmission. Less is known about the physiological concentration of extracellular calcium in the brain. In electrophysiological brain slice experiments, the artificial cerebrospinal fluid traditionally contains relatively high concentrations of calcium (2-4 mM) to support synaptic transmission and suppress neuronal excitability. Using an ion-selective electrode, we determined the fraction of ionized calcium in healthy human cerebrospinal fluid to 1.0 mM of a total concentration of 1.2 mM (86%). Using patch-clamp and extracellular recordings in the CA1 region in acute slices of rat hippocampus, we then compared the effects of this physiological concentration of calcium with the commonly used 2 mM on neuronal excitability, synaptic transmission, and long-term potentiation (LTP) to examine the magnitude of changes in this range of extracellular calcium. Increasing the total extracellular calcium concentration from 1.2 to 2 mM decreased spontaneous action potential firing, induced a depolarization of the threshold, and increased the rate of both de- and repolarization of the action potential. Evoked synaptic transmission was approximately doubled, with a balanced effect between inhibition and excitation. In 1.2 mM calcium high-frequency stimulation did not result in any LTP, whereas a prominent LTP was observed at 2 or 4 mM calcium. Surprisingly, this inability to induce LTP persisted during blockade of GABAergic inhibition. In conclusion, an increase from the physiological 1.2 mM to 2 mM calcium in the artificial cerebrospinal fluid has striking effects on neuronal excitability, synaptic transmission, and the induction of LTP. OPEN SCIENCE BADGES: This article has received a badge for *Open Materials* because it provided all relevant information to reproduce the study in the manuscript. The complete Open Science Disclosure form for this article can be found at the end of the article. More information about the Open Practices badges can be found at https://cos.io/our-services/open-science-badges/. Read the Editorial Highlight for this article on page 435.

[Protective effects of Ginkgo Terpene Lactones Meglumine Injection on focal cerebral ischemia in rats].

To investigate the protective effects of ginkgo diterpene lactone meglumine injection (GDLMI) on cerebral focal ischemia reperfusion injury induced by middle cerebral artery occlusion (MCAO) in rats, and explore its possible mechanism. One hundred and forty male SD rats were randomly divided into sham operation group, model group, ginkgo biloba extract injection (Ginaton, 1.0 mL•kg⁻¹) group, nimodipine (0.4 mg•kg⁻¹) group, and GDLMI (5.2, 2.6, 1.3 mg•kg⁻¹) groups; All of rats received corresponding drugs by tail vein injection 4 days before operation (normal saline in model group and sham operation group). Except the sham operation group, the cerebral ischemic stroke model was established by MCAO method in right brain of the other rats. After 3 h of ischemia, all the animals received intravenous administration again. The neurobehavioral scores of rats after ischemia-reperfusion were evaluated and the infarct rate of brain tissue was observed by TTC staining. The super oxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA) and lactic acid (LA) contents in brain tissue homogenate and the concentration of Ca2+, glutamate (Glu) and aspartate (Asp), creatine phosphate kinase (CK-BB) and lactate dehydrogenase (LDH) content changes in cerebrospinal fluid were measured. As compared with the sham operation group, the cerebral infarction rate was increased significantly in the model group; the content of MDA and LA in the homogenate of brain tissue was increased, and the content of GSH and SOD was decreased; in cerebrospinal fluid, Ca2+ concentration was decreased, and the content of Glu and Asp, CK-BB and LDH increased significantly. As compared with the model group, the high and medium dose GDLMI groups can significantly reduce the cerebral infarction rate and improve the symptoms of neurological impairment; increase SOD and GSH activity, reduce MDA and LA content in serum; increase Ca2+ concentration in cerebrospinal fluid and decrease the content of neurotransmitter Glu and Asp as well as CK-BB and LDH. GDLMI could obviously improve neurologic impairment in model rats, and the mechanism may be related to recovering the blood brain barrier, scavenging free radicals, decreasing free Ca2+ inflow into the cells and the content of excitatory amino acid in cerebrospinal fluid to improve its protective effect on cerebral ischemia.

Metallomic Biomarkers in Cerebrospinal fluid and Serum in patients with Parkinson's disease in Indian population.

Parkinson's disease (PD) is a neurodegenerative disease with the absence of markers for diagnosis. Several studies on PD reported the elements imbalance in biofluids as biomarkers. However, their results remained inconclusive. This study integrates metallomics, multivariate and artificial neural network (ANN) to understand element variations in CSF and serum of PD patients from the largest cohort of Indian population to solve the inconsistent results of previous studies. Also, this study is aimed to (1) ascertain a common element signature between CSF and serum. (2) Assess cross sectional element variation with clinical symptoms. (3) Develop ANN models for rapid diagnosis. A metallomic profile of 110 CSF and 530 serum samples showed significant variations in 10 elements of CSF and six in serum of patients compared to controls. Consistent variations in elements pattern were noticed for Calcium, Magnesium and Iron in both the fluids of PD, which provides feasible diagnosis from serum. Furthermore, implementing multivariate analyses showed clear classification between normal and PD in both the fluids. Also, ANN provides 99% accuracy in detection of disease from CSF and serum. Overall, our analyses demonstrate that elements profile in biofluids of PD will be useful in development of diagnostic markers for PD.

Cerebrospinal fluid (CSF) 25-hydroxyvitamin D concentration and CSF acetylcholinesterase activity are reduced in patients with Alzheimer's disease.

BACKGROUND: Little is known of vitamin D concentration in cerebrospinal fluid (CSF) in Alzheimer's disease (AD) and its relation with CSF acetylcholinesterase (AChE) activity, a marker of cholinergic function. METHODS: A cross-sectional study of 52 consecutive patients under primary evaluation of cognitive impairment and 17 healthy controls. The patients had AD dementia or mild cognitive impairment (MCI) diagnosed with AD dementia upon follow-up (n = 28), other dementias (n = 12), and stable MCI (SMCI, n = 12). We determined serum and CSF concentrations of calcium, parathyroid hormone (PTH), 25-hydroxyvitamin D (25OHD), and CSF activities of AChE and butyrylcholinesterase (BuChE). FINDINGS: CSF 25OHD level was reduced in AD patients (P < 0.05), and CSF AChE activity was decreased both in patients with AD (P < 0.05) and other dementias (P < 0.01) compared to healthy controls. None of the measured variables differed between BuChE K-variant genotypes whereas the participants that were homozygous in terms of the apolipoprotein E (APOE) ε4 allele had decreased CSF AChE activity compared to subjects lacking the APOE ε4 allele (P = 0.01). In AD patients (n=28), CSF AChE activity correlated positively with CSF levels of total tau (T-tau) (r = 0.44, P < 0.05) and phosphorylated tau protein (P-tau) (r = 0.50, P < 0.01), but CSF activities of AChE or BuChE did not correlate with serum or CSF levels of 25OHD. CONCLUSIONS: In this pilot study, both CSF 25OHD level and CSF AChE activity were reduced in AD patients. However, the lack of correlations between 25OHD levels and CSF activities of AChE or BuChE might suggest different mechanisms of action, which could have implications for treatment trials.

Concentration of calcium and magnesium and trace elements (zinc, copper, iron and manganese) in cerebrospinal fluid: a try of a pathophysiological classification.

The aim of this study is to analyze the variation of the elements (Ca, Mg, Cu, Fe, Zn and Mn) in normal and pathological CSF and develop a classification basing on the increases in cells and proteins and taking into account these variations. A total of 173 cerebrospinal fluids were analyzed. Of these, 37 fulfilled the criteria of normality and, after clinical exploration, were considered to be healthy (control group). The remaining 136 CSFs (pathological group) belonged to people for whom some neurological pathology had been observed in the clinical exploration and whose CSF analysis presented some abnormality. CSF was extracted by puncture in the lumbar cistern. The analysis of metals was performed by atomic absorption spectrophotometry. The statistical values (mean±standard deviation) obtained for each element analyzed in control group were as follows: Ca (mg/dL): 4.95±0.70; Mg (mg/dL): 2.74±0.10; Cu (µg/dL): 15.70±13.50; Fe (µg/dL): 13.10±3.60; Zn (µg/dL): 17.40±9.50 and Mn (µg/dL): 2.50±0.70. In the pathological CSFs, significant increases were found (p<0.050) in relation to the control group for Ca, Cu, Fe, Zn and Mn in groups with an increase of both cells and proteins. A significant decrease of Mg (p<0.050) was found in the groups with cell and protein increases. Given the results obtained in the different subgroups of the proposed classification, we conclude that it is necessary to further categorize the patients' diagnostics in the different subgroups. This would help to validate the classification.

Cerebral spinal fluid and serum ionized magnesium and calcium levels in preeclamptic women during administration of magnesium sulfate.

OBJECTIVE: To study the distribution of ionized and total magnesium (Mg) in serum and cerebral spinal fluid (CSF) in preeclamptic women receiving MgSO(4) and how this treatment affects the ionized calcium (Ca(2+)) and ionized Ca:Mg ratios compared with healthy nonpregnant women and pregnant control women (HP). DESIGN: Controlled clinical study. SETTING: An academic medical center. PATIENT(S): African-American women older than 20 and less than 35 years. The pregnant preeclamptic study and pregnant control groups each consisted of 16 women; the nonpregnant group consisted of 10 subjects. INTERVENTION(S): The preeclamptic women received a 6-g bolus of MgSO(4) IV started at least 4.5 hours before delivery during 15-20 minutes, then 2 g/h baseline. MAIN OUTCOME MEASURE(S): The CSF and serum levels of Ca(2+) and Mg(2+) and total Mg were measured in all three groups of women. The Ca(2+):Mg(2+) ratios were determined. Physiologic monitoring was done and recorded every 4 hours where appropriate. Bloods were drawn every 6 hours for complete blood count, metabolic panel, lactate dehydrogenase, uric acid, and electrolytes. Serum pH, total Mg, Apgar scores, and general health of the infants born to preeclamptic mothers given MgSO(4) were followed. RESULT(S): The HP showed a reduction in mean serum ionized and total Mg, increase in ionized Ca, and a large increase in Ca(2+):Mg(2+) ratios compared with healthy nonpregnant women. Although the CSF ionized and total Mg and Ca(2+):Mg(2+) ratios were not altered with MgSO(4) treatment in the preeclamptic women receiving MgSO(4), the mean serum Mg values increased 3-fold. All infants were full-term, regardless of MgSO(4) treatment, and normal with respect to birth weight, Apgar scores, blood pH, total Mg, and neurologic scores. CONCLUSION(S): The data indicate that there is a direct relationship between the serum and CSF Ca(2+):Mg(2+) ratios in HP and this ratio may be crucial in preventing vascular and neurologic complications in preeclampsia-eclampsia.

CSF Mg and Ca as diagnostic markers for dementia with Lewy bodies.

Accumulating evidence implicates a role for altered metal homeostasis in the pathogenesis of neurodegenerative disorders such as Alzheimer's disease (AD). However, few investigations have addressed this issue in dementia with Lewy bodies (DLB). The aim of the present study was to investigate metal concentrations in cerebrospinal fluid (CSF) and plasma from patients with DLB and other neurodegenerative disorders. To that end, CSF and plasma samples were collected from 29 patients with DLB, 174 patients with AD, 90 patients with AD with minor vascular components, and 51 healthy volunteers. Total concentrations of Mg, Ca, Mn, Fe, Cu, Zn, Rb, Sr, and Cs were determined using mass spectrometry. Patients with DLB had elevated Ca and Mg levels in CSF and Mg levels in plasma as compared to all other groups (p<0.001). Furthermore, a combination of CSF-Mg and CSF-Ca could distinguish DLB from AD with a sensitivity of 93% and a specificity of 85%. Cu levels in both CSF and plasma tended to be higher in DLB compared to the other groups, but these trends failed to reach significance after correction for multiple comparisons. Mn, Fe, Zn, Rb, and Sr concentration in CSF or plasma were similar in all groups. The observed elevations of CSF-Mg, CSF-Ca and CSF-Cu may contribute to or be associated with the neurodegenerative process in DLB. Furthermore, determination of CSF-Mg and CSF-Ca concentration may be a valuable tool in distinguishing DLB from AD.

Cerebrospinal fluid apolipoprotein E, calcium and cerebral vasospasm after subarachnoid hemorrhage.

Intracellular calcium (Ca++) regulation of cerebral vessels is impaired after subarachnoid hemorrhage (SAH), making secondary pathways, such as that involving apolipoprotein E, potentially more influential. To evaluate cerebrospinal fluid (CSF) apolipoprotein E and Ca++ levels as biomarkers of cerebral vasospasm, we examined changes in levels over time and apolipoprotein E (APOE) epsilon4 allele presence after SAH in individuals with and without vasospasm. We hypothesized that individuals with low apolipoprotein E levels, increased Ca++ levels and/or at least one copy of the APOE epsilon4 allele would have vasospasm. Daily samples from 50 participants, aged 18-75, with SAH were used to quantify apolipoprotein E and Ca++ levels. Vasospasm was verified using cerebral angiogram and/or elevated transcranial Dopplers in combination with clinical neurologic deterioration. Overall apolipoprotein E levels were higher in individuals with the APOE epsilon4 allele (p = .02) or angiographic vasospasm (p = .01), but there were no differences between individuals with and without symptomatic vasospasm. There were no significant changes in apolipoprotein E levels over time. Individuals with the epsilon4 allele had lower Ca++ levels (p = .02) with trends suggesting a different pattern of change over time (p = .07). CSF Ca++ levels were lower in individuals with symptomatic vasospasm (p < .01). Change in apolipoprotein E and Ca++ levels (p = .006) correlated over time regardless of genotype or vasospasm status. These findings suggest that apolipoprotein E and Ca++ may be interacting after SAH, but this interaction does not appear to influence vasospasm.

Speciation analysis of selected metals and determination of their total contents in paired serum and cerebrospinal fluid samples: An approach to investigate the permeability of the human blood-cerebrospinal fluid-barrier.

Neurodegenerative diseases like Alzheimer's disease and Parkinson's disease are gaining increasing relevance in our aging society. However, the complex multifactorial mechanisms of these diseases are not sufficiently understood yet. Several studies indicate that metal ions play an important role in the promotion of these diseases. Consequently, the transport pathways of metals and their species to the brain are of special interest. Following oral or inhalative uptake metals are absorbed and distributed via the blood stream in the body. Transport into the brain requires crossing of the neural barriers. Our study focuses on the investigation of the permeability of the blood-cerebrospinal fluid (CSF)-barrier for selected metals (Mn, Fe, Cu, Zn, Mg and Ca). For the first time paired human serum and CSF samples obtained from a neurological department were characterised for total metal concentrations and metal species. For CSF few data are available in the literature on total metal contents and applications of element speciation analysis in CSF samples are rare. In our study mean CSF/serum ratios (n=29) were 0.7 for Mn, 0.02 for Fe, 0.02 for Cu, 0.03 for Zn, 1.3 for Mg and 0.5 for Ca. Size exclusion chromatography (SEC) online with inductively coupled plasma mass spectrometry was further developed for the size characterisation of the metal species in CSF and serum with limits of detection of 0.4microgL(-1) for Fe, 0.01microgL(-1) for Mn, 0.2microgL(-1) for Cu, 0.2microgL(-1) for Zn, 0.6microgL(-1) for Mg and 3.8microgL(-1) for Ca in the eluate from the HPLC column. Apart from Mn the application of this technique has not been published for metal speciation in CSF, yet. In the case of some Mn species it turned out that methanol, which was contained in the mobile phase of a SEC method previously published from our group on qualitative characterisation of Mn species, was interfering with the quantification. The modified method developed in this work (with NaCl but without methanol in the mobile phase; use of internal standard) allowed reliable quantification. The results clearly indicate changes in the metal species pattern due to different permeation behaviour at the blood-CSF-barrier. As part of the method validation the relative stability of complexes of albumin, transferrin and citrate with Mn, Fe, Cu and Zn was investigated.

alpha-Klotho as a regulator of calcium homeostasis.

alpha-klotho was identified as a gene associated with premature aging-like phenotypes characterized by short lifespan. In mice, we found the molecular association of alpha-Klotho (alpha-Kl) and Na+,K+-adenosine triphosphatase (Na+,K+-ATPase) and provide evidence for an increase of abundance of Na+,K+-ATPase at the plasma membrane. Low concentrations of extracellular free calcium ([Ca2+]e) rapidly induce regulated parathyroid hormone (PTH) secretion in an alpha-Kl- and Na+,K+-ATPase-dependent manner. The increased Na+ gradient created by Na+,K+-ATPase activity might drive the transepithelial transport of Ca2+ in cooperation with ion channels and transporters in the choroid plexus and the kidney. Our findings reveal fundamental roles of alpha-Kl in the regulation of calcium metabolism.

Changes in immune and glial markers in the CSF of patients with Complex Regional Pain Syndrome.

Complex Regional Pain Syndrome is a severe chronic pain condition characterized by sensory, autonomic, motor and dystrophic signs and symptoms. The pain in CRPS is continuous, it worsens over time, and it is usually disproportionate to the severity and duration of the inciting event. This study compares cerebrospinal fluid (CSF) levels of pro- and anti-inflammatory cytokines, chemokines and several biochemical factors (glial fibrillary acidic protein (GFAP), the nitric oxide metabolites (nitrate plus nitrite), the excitatory amino acid neurotransmitter glutamate, calcium, total protein and glucose) in patients afflicted with CRPS to levels found in patients suffering with other non-painful or painful conditions. The aim of the study is to determine the degree of involvement of glial cells and immune system mediators in the pathophysiology of CRPS. There was no elevation or reduction of a CSF marker that was specific for CRPS patients. However, there were several patterns of markers that could be helpful in both elucidating the mechanisms involved in the disease process and supporting the diagnosis of CRPS. The most common pattern was found in 50% (11 out of 22) of the CRPS patients and consisted of; elevated IL-6, low levels of IL-4 or IL-10, increased GFAP or MCP1 and increases in at least two of the following markers NO metabolites, calcium or glutamate. The results from this and other similar studies may aid in elucidating the mechanisms involved in the pathophysiology of CRPS. A better understanding of these mechanisms may lead to novel treatments for this very severe, life-altering illness.

Extracellular calcium and magnesium in preeclampsia and eclampsia.

The cause of preeclampsia remains unknown and calcium and magnesium supplement are being suggested as means of prevention. The objective of this study was to assess magnesium and calcium in the plasma and cerebrospinal fluid of Nigerian women with preeclampsia and eclampsia. Setting was University of Benin Teaching Hospital, in Nigeria. It was a cross-sectional study comprising of eleven patients and twenty-three controls. The mean, standard deviation and Standard Error of Mean (SEM) were calculated. Student 't' test method was applied. Plasma calcium was significantly lower in patients than controls (9.2 +/- 1.02 Vs 9.98 +/- 0.87mg/dl, P 0.043) "t" test. The CSF calcium and magnesium levels were lower in patients than controls, (5.66 +/- 1.22 vs 6.67 +/- 1.15 mg/ dl, P 0.043 and 1.75 +/- 0.56 vs 1.91 +/- 0.19 mg/dl, P 0. < 0.0001) respectively. There is extracellular calcium and magnesium reduction in patients with preeclampsia and eclampsia. This reduction may have a cause and effect relationship with these disorders.

Cerebrospinal fluid sodium increases in migraine.

BACKGROUND: 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. OBJECTIVE: To compare levels of sodium, calcium, potassium, and magnesium in cerebrospinal fluid (CSF) and blood plasma between migraineurs and controls. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Effects of potassium concentration on firing patterns of low-calcium epileptiform activity in anesthetized rat hippocampus: inducing of persistent spike activity.

PURPOSE: It has been shown that a low-calcium high-potassium solution can generate ictal-like epileptiform activity in vitro and in vivo. Moreover, during status epileptiform activity, the concentration of [K+]o increases, and the concentration of [Ca2+]o decreases in brain tissue. Therefore we tested the hypothesis that long-lasting persistent spike activity, similar to one of the patterns of status epilepticus, could be generated by a high-potassium, low-calcium solution in the hippocampus in vivo. METHODS: Artificial cerebrospinal fluid was perfused over the surface of the exposed left dorsal hippocampus of anesthetized rats. A stimulating electrode and a recording probe were placed in the CA1 region. RESULTS: By elevating K+ concentration from 6 to 12 mM in the perfusate solution, the typical firing pattern of low-calcium ictal bursts was transformed into persistent spike activity in the CA1 region with synaptic transmission being suppressed by calcium chelator EGTA. The activity was characterized by double spikes repeated at a frequency approximately 4 Hz that could last for >1 h. The analysis of multiple unit activity showed that both elevating [K+]o and lowering [Ca2+]o decreased the inhibition period after the response of paired-pulse stimulation, indicating a suppression of the after-hyperpolarization (AHP) activity. CONCLUSIONS: These results suggest that persistent status epilepticus-like spike activity can be induced by nonsynaptic mechanisms when synaptic transmission is blocked. The unique double-spike pattern of this activity is presumably caused by higher K+ concentration augmenting the frequency of typical low-calcium nonsynaptic burst activity.

Changes in magnesium concentration in the serum and cerebrospinal fluid of neuropathic rats.

BACKGROUND: Central sensitization of neuropathic pain is associated with an influx of extracellular calcium via the opening of N-methyl-D-aspartate (NMDA) receptor-gated ion channels, which are usually blocked by magnesium plugs. As magnesium-deficient rats develop a mechanical hyperalgesia and intrathecal or intraperitoneal magnesium suppresses neuropathic pain, the magnesium concentrations in serum and cerebrospinal fluid may be altered in neuropathic pain. We therefore compared the magnesium concentrations in serum and cerebrospinal fluid of neuropathic rats with those in injured rats without symptoms of neuropathic pain and normal rats. METHODS: Mechanical allodynia was induced in male Sprague-Dawley rats by tight ligature of the left lumbar fifth and sixth spinal nerves. The threshold of paw withdrawal was evaluated by the up-down method using withdrawal response to stimulus with a von Frey filament on the third, seventh and 14th days. Rats with a threshold of less than 4 g were selected as the symptomatic group and compared with an asymptomatic group, an unoperated control group and a sham-operated group. On the 16th day, the Mg2+ concentrations in serum and cerebrospinal fluid were measured. RESULTS: The magnesium concentrations in the serum and cerebrospinal fluid of symptomatic neuropathic rats did not differ from those in the injured rats without symptoms of neuropathic pain, sham-operated rats and normal rats. CONCLUSION: Our results suggest that physiologic homeostasis is maintained by active transport through the blood-brain barrier despite the activation of NMDA receptor-gated ion channels. However, rats with neuropathic pain may be in a magnesium-deficient condition at the effector site, such that magnesium treatment can decrease neuropathic pain.

Ionized magnesium in the cerebrospinal fluid of patients with head injuries.

BACKGROUND: In head injury patients, a decrease in the serum ionized magnesium (iMg) concentration is considered to be related to the severity of the injury, however, this phenomenon is still not completely understood. The cerebrospinal fluid (CSF) iMg concentration has not been well documented under such conditions and, moreover, its normal value has not yet been established. We hereby intended to investigate the role of the iMg concentration and other parameters in both the serum and CSF of head injury patients and identify any relationship with other parameters. MATERIALS AND METHODS: The subjects consisted of head injury patients without any other serious injuries. Ten healthy volunteers were selected as control subjects. Arterial blood and CSF specimens were simultaneously obtained and measured. We measured the Glasgow Coma Scale scores (GCS), the intracranial pressure (ICP), pH, po2, pco2, sodium, potassium, iCa, iMg, glucose, lactate, urea nitrogen. All data are expressed as the mean+/-SD and the units of iMg and iCa (corrected under pH 7.40) are given in mmol/L. RESULTS: In the healthy subjects, the iMg concentration in the serum/CSF was 0.48 +/- 0.02 / 0.66 +/- 0.14, and iCa was 1.14 +/- 0.05 / 0.94 +/- 0.07. The GCS of the 15 head injury subjects at examination was 8.7 +/- 4.5. When the subjects were divided into 3 groups according to the GCS level (3 and 4, 5-8, and > or =9) at the time of examination, the serum iMg concentration was thus found to be related to the severity of injury based on the GCS level (p = 0.028), but not the CSF iMg concentration (p = 0.89). No relationship was observed between the iMg concentration in the serum and CSF when all specimens were compared, but an extremely close correlation was seen in the group with GCS 3 and 4 (p < 0.0001, r = 0.995), although no such correlation was seen in the other 2 groups (p = 0.12, r = -0.56 in the group with GCS 5-8, and p = 0.26, r = -0.35 in the group with GCS > or = 9). There was a significant correlation between the serum iMg and iCa (p = 0.0093, r = 0.47), and also between the CSF iMg and iCa concentrations (p < 0.0001, r = 0.67). CONCLUSION: The serum iMg concentration has been suggested to possibly affect the neurologic state through CSF iMg in patients with the most severe head injury. In patients with moderate or mild head injuries, however, the ionized magnesium concentration is also probably associated with the degree of neurologic deficit based on the ionized calcium level. The CSF and serum ionized magnesium dissociation may thus result from the slow movement of ionized magnesium through the blood brain barrier.

Cerebrospinal fluid: postmortem biochemical study.

UNLABELLED: Postmortem phenomena can change and alter biochemical components in body fluids such as blood and as cerebrospinal fluid (CSF). AIMS OF THE STUDY WERE: (a) to analyse urea, glucose, potassium, chloride, protein, creatinine, calcium, alkaline phosphatase and cortisol in CSF fluid and (b) to compare results between two age groups, between groups with or without mental or degenerative neurological illness and between a group reported as dying from natural causes and a group that had a violent death. MATERIALS AND METHODS: The study was carried out in Hospitalet de Llobregat (Barcelona) of 55 corpses. Samples were obtained following section of the corpus callosus, through the lateral ventricles and frozen to -80 degrees C until processed. RESULTS: Significant differences were found in urea levels between the two age groups, in protein between natural and violent death groups and in alkaline phosphatase between the two age groups and between the natural and violent death group. Cortisol levels revealed significant difference between the two age groups and is those supplying natural and violent death. CONCLUSIONS: The study indicates to the need for further studies designed to include groups with defined diagnose of mental or degenerative disorders as well as different age groups.

Studies on cerebrospinal fluid ionized calcium and magnesium concentrations in convulsive children.

BACKGROUND: The concentrations of ionized calcium (iCa) and ionized magnesium (iMg) were measured in the cerebrospinal fluid (CSF) of convulsive and non-convulsive children, to investigate the relationship between seizure manifestation and CSF iCa and iMg concentrations. Standard concentrations of CSF iCa and iMg were also established. METHODS: CSF samples from 23 patients, ages 0-15 years, with various forms of seizures and 26 age-matched non-convulsive children were collected by lumbar puncture. CSF was obtained anaerobically and the concentrations of CSF iCa and iMg were measured with an electolyte analyzer (Stat Profile Ultra M1, NOVA, USA) immediately after the lumbar puncture. RESULTS: The concentrations of CSF iCa were significantly higher in non-convulsive children younger than 11 months old compared with children older than 12 months. The concentrations of CSF iMg in non-convulsive children did not differ significantly with aging. The concentrations of CSF iCa in convulsive children did not differ significantly from the concentrations of non-convulsive children. The concentrations of CSF iMg in convulsive children were significantly lower than in non-convulsive children. CONCLUSION: These results suggest that seizure manifestation is related to age-dependent changes in iCa and decreased iMg in the developing brain.

[Role of calcium and magnesium ions in cerebrospinal fluid in alcoholic-traumatic coma]. / Rolul determinarii ionilor de calciu si magneziu în LCR în coma etilico-traumatica.

The goal of investigation was to determine the role of calcium and magnesium ions in the cerebrospinal fluid in ethylic-traumatic coma. We measured the level of calcium in the cerebrospinal fluid within simple photometric test and the magnesium level within xylidyl blue photometric test. We found a high mortality in patients with high level of calcium in cerebrospinal fluid and low level of magnesium in cerebrospinal fluid. At patients with ethylic-traumatic coma high levels of calcium in cerebrospinal fluid are caused by the excitatory amino acids cascade and increased of hematoencephalic barrier permeability. Decreased levels of magnesium in cerebrospinal fluid are associated with convulsions and a poor prognosis of the patients. These analyses are very important for establishment of prognosis in patients with ethylic-traumatic coma.