Anticonvulsant effects of magnesium sulfate in hippocampal-kindled rats

Standley, Cynthia A.; Irtenkauf, Susan M.; Cotton, David B.

doi:10.1007/bf02257926

Cited by 6 publications

(2 citation statements)

References 25 publications

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“…No effect of Mg was reported against maximal electroconvulsive shock (MES) and pentylenetetrazol (PTZ) 13 , or kainate 14 models of seizures in vivo. Conversely, other experiments have demonstrated that peripherally administered Mg accumulates in the brain and increases amygdala kindling threshold in the rat 15 . It also decreases seizures associated with intracranial NMDA injection when administered both centrally and peripherally 16 and was shown to augment sub-therapeutic VPA in the PTZ model of rat 17 .…”

Section: Discussionmentioning

confidence: 80%

Magnesium as an Effective Adjunct Therapy for Drug Resistant Seizures

Abdelmalik

Politzer

Carlen

2012

Can. J. Neurol. Sci.

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The definitive treatment of eclampsia, a syndrome of pregnancy-induced hypertension, proteinuria and new onset seizures, is magnesium (Mg) supplementation, followed by delivery of the fetus. Magnesium has been the widely accepted treatment since first reported in 1925 1 , and remains the mainstay of treatment for eclampsia. Eclamptic seizures have been compared, both in semiology and electrographically, to generalized tonic-clonic (GTC) "grand mal" seizures, with controlled clinical trials having demonstrated the clear effectiveness of Mg against eclamptic seizures when compared to conventional anticonvulsants 2,3 .Magnesium has been hypothesized to be effective against CNS ischemia and seizures based on its biochemical properties 4 . Magnesium is a known CNS depressant, whose mechanisms of action include: competitive antagonism of N-methyl-D-aspartate (NMDA) receptors, blocking transient receptor potential (TRP) ABSTRACT: Objective: To explore the use of magnesium (Mg), an endogenous ion and enzymatic co-factor used in a variety of medical applications, for the treatment of epileptic seizures resistant to traditional medical therapy. Background: For almost a century, Mg has been used as prophylaxis and treatment of seizures associated with eclampsia. Mg is a CNS depressant, with numerous functions intracellularly and extracellularly. However, because of the availability of well studied anticonvulsant drugs, Mg has not been tested widely in the treatment of epileptic seizures. Methods: A retrospective chart review of 22 cases of drug resistant epilepsy, where a trial of empiric oral Mg supplementation (mainly in the form of Mg-oxide) was conducted. Results: Oral Mg supplementation was associated with a significant decrease in the number of seizure days per month, from 15.3 ± 13.2 (mean ± SD) to 10.2 ± 12.6 at first follow up (3-6 months, p=0.021), and to 7.8 ± 10.0 seizure days/month at second follow up (6-12 months, p=0.004). Thirty-six percent had a response rate of 75% or greater at second follow-up. Two patients reported seizure freedom. Most patients were well maintained on MgO 420mg twice a day, or in 2 cases, Mg Lactate, without significant adverse effects, the most frequent being diarrhea (4/22). Discussion: These results suggest that oral Mg supplementation may prove to be a worthwhile adjunctive medication in treating drug intractable epilepsy. Conclusions: A prospective, double-blinded, placebo controlled study is warranted to evaluate the potential of Mg for the treatment of drug-resistant seizures.RÉSUMÉ: Le magnésium comme traitement d'appoint efficace dans les crises convulsives résistantes au traitement. Objectif : Le but de l'étude était d'explorer l'utilisation du magnésium (Mg), un ion endogène et un cofacteur enzymatique ayant différentes applications en médecine, dans le traitement des crises épileptiques résistantes au traitement médical traditionnel. Contexte : Depuis près d'un siècle, le Mg a été utilisé en prophylaxie et dans le traitement des convulsions associées à l'éclampsie. L'effet...

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Section: Discussionmentioning

confidence: 80%

Magnesium as an Effective Adjunct Therapy for Drug Resistant Seizures

Abdelmalik

Politzer

Carlen

2012

Can. J. Neurol. Sci.

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“…This is in good agreement with the results of BORGES and GÜCER (1978) who have reported that MgSO 4 is able to suppress epileptic neuronal activity induced by topical application of penicillin on motor cortex in cats, dogs and primates. STANDLEY et al (1995) also found that intraperitoneal injection of MgSO 4 significantly shortens seizure duration in hippocampal-kindled rats. On the other hand, lowering of extracellular Mg 2+ concentration leads to epileptiform activity in many parts of the central nervous system (WALTHER et al 1986).…”

Section: Discussionmentioning

confidence: 80%

Magnesium Effects on Nonsynaptic Epileptiform Activity in Leech Retzius Neurons

Stanojević

Lopičić

Jovanović

et al. 2015

folia biol (krakow)

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The effects of Mg 2+ on Ni 2+-induced epileptiform bursting activity and input membrane resistance during this activity of leech Retzius neurons were examined using intracellular recordings. To induce epileptiform activity, 3 mmol/l NiCl 2 was added into superfusing Ringer (Ri) saline. To test for dose-dependence of the effects of Mg 2+ on the induced epileptiform activity, MgCl 2 was added in concentrations from 1 mmol/l to 20 mmol/l Mg 2+ to the Ni 2+-containing Ri saline. Input membrane resistance (IMR) was measured in standard Ri, Ni 2+ Ri and 20 mmol/l Mg 2+ Ni 2+ Ri saline. Superfusion with Ni 2+ Ri induced epileptiform bursting activity characterized by generation of paroxysmal depolarization shifts (PDSs). Parameters of epileptiform activity including PDS frequency, PDS duration, PDS amplitude and the number of spikes/PDS were measured. Magnesium suppressed Ni 2+-induced epileptiform activity, significantly reducing values of all parameters observed in a concentration-dependent manner. The highest concentration applied of 20 mmol/l Mg 2+ completely eliminated epileptiform activity. To test for the effect of Mg 2+ on membrane conductance during bursting, IMR was measured. Magnesium significantly increased IMR during bursting suppression.

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Magnesium and Affective Disorders

Murck¹

2002

Nutritional Neuroscience

128

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There are several findings on the action of magnesium ions supporting their possible therapeutic potential in affective disorders. Examinations of the sleep-electroencephalogram (EEG) and of endocrine systems point to the involvement of the limbic-hypothalamus-pituitary-adrenocortical axis as magnesium affects all elements of this system. Magnesium has the property to suppress hippocampal kindling, to reduce the release of adrenocorticotrophic hormone (ACTH) and to affect adrenocortical sensitivity to ACTH. The role of magnesium in the central nervous system could be mediated via the N-methyl-D-aspartate-antagonistic, gamma-aminobutyric acidA-agonistic or a angiotensin II-antagonistic property of this ion. A direct impact of magnesium on the function of the transport protein p-glycoprotein at the level of the blood-brain barrier has also been demonstrated, possibly influencing the access of corticosteroids to the brain. Furthermore, magnesium dampens the calciumion-proteinkinase C related neurotransmission and stimulates the Na-K-ATPase. All these systems have been reported to be involved in the pathophysiology of depression. Despite the antagonism of lithium to magnesium in some cell-based experimental systems, similarities exist on the functional level, i.e. with respect to kindling, sleep-EEG and endocrine effects. Controlled clinical trials examining the effect of Mg in affective disorder are warranted.

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Anticonvulsant effects of magnesium sulfate in hippocampal-kindled rats

Cited by 6 publications

References 25 publications

Magnesium as an Effective Adjunct Therapy for Drug Resistant Seizures

Magnesium as an Effective Adjunct Therapy for Drug Resistant Seizures

Magnesium Effects on Nonsynaptic Epileptiform Activity in Leech Retzius Neurons

Magnesium and Affective Disorders

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