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Robert S. Fisher, MD, PhD
Departments of Neurology, Neurosurgery, and The Johns Hopkins Epilepsy Center The Johns Hopkins University School of Medicine 600 N Wolfe St Baltimore, MD 21205

Peter W. Kaplan, BS, MRCP
Department of Neurology and The Johns Hopkins Epilepsy Center The Francis Scott Key Medical Center 4940 Eastern Ave Baltimore, MD 21224

Ronald P. Lesser, MD
Departments of Neurology, Neurosurgery, and The Johns Hopkins Epilepsy Center The Johns Hopkins University School of Medicine 600 N Wolfe St Baltimore, MD 21205

John Repke, MD
Departments of Obstetrics and Gynecology The Johns Hopkins University School of Medicine 600 N Wolfe St Baltimore, MD 21205

Daniel Hanley, MD
Departments of Neurology, Neurosurgery, and Anesthesiology and Critical Care The Johns Hopkins University School of Medicine 600 N Wolfe St Baltimore, MD 21205

Arch Neurol. 1991;48(7):677-678.

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In Reply.

—We would like to thank Brorson for his comments regarding the continuing controversy about the use of magnesium sulfate in the treatment of eclamptic seizures,¹ and take this opportunity to respond to his remarks.

The magnesium ion is known to play a role in blocking the cation channel associated with the N-methyl-D-aspartate (NMDA) receptor subtype of the glutamate receptor.² It is, therefore, not surprising that NMDA antagonists disrupt development or expression of epileptiform activity induced by low magnesium concentrations.³ Reduction of ambient magnesium in bathing medium of in vitro model systems for epilepsy can induce epileptiform activity,⁴ and low serum magnesium concentrations can lead to convulsions.⁵ Nevertheless, these observations do not necessarily imply that magnesium sulfate would be therapeutic for clinical seizures. Magnesium has a special relationship to seizures mediated by the NMDA system; magnesium may not be as effective . . . [Full Text PDF of this Article]

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