Clinical Studies of Magnesium Deficiency in Epilepsy

By Lewis B. Barnett, MD

Summary: In this article from the pioneering mid-twentieth-century journal Clinical Physiology, Dr. Lewis Barnett summarizes his laboratory and case-study findings correlating magnesium deficiency and epilepsy. Dr. Lewis spent many years studying this essential mineral and its profound relationship to the utilization of calcium. From Clinical Physiology, 1959. Lee Foundation for Nutritional Research reprint 114.

The following is a transcription of the original Archives document. To view or download the original document, click here.

Clinical Studies of Magnesium Deficiency in Epilepsy[spacer height=”20px”]

Interest in the physiology and chemistry of the mineral magnesium has gradually increased over the past ten years. As early as 1944, a correlation between magnesium, tetany, and petit mal seizures was reported. Numerous studies in the deficiency of magnesium have been made since that time by many investigators.

My original work was directed toward the role of magnesium in bone apatite; while I was investigating that field, it became obvious that magnesium might play a vital role in the physiology of the central nervous system.

Beck observed in 1952 that a deficiency of magnesium might well produce effects similar to hypophysectomy. Martin, Meke, and Wertman did a very comprehensive study on the clinical influence of magnesium metabolism and again noted that in the state of epilepsy there is a deficiency of serum magnesium. Numerous investigators have noted a form of tetany and occasional petit mal in this syndrome where a low magnesium intake was noted.

After I reviewed most of the literature, which is not very extensive according to references, it became very obvious to me that very little work had been done regarding this most important  and extremely active mineral.

Until the work of Martin, Meke, and Wertman, normal serum levels [of magnesium] had not been accurately determined. In approximately 500 cases, our normal for this area was 1.60 mEq*. All of these determinations were done by means of a flame spectrophotometer. We, too, have observed deficiency signs in other diseases, such as renal pathology, diabetic states, congestive heart failure, [problems in] postoperative patients, intestinal obstruction, toxemia of pregnancy, asthma, starvation, and depressed metabolic states.

In order to arrive at some basis for this study, we recalled for review all of the previously diagnosed children [suffering either] petit mal or grand mal type of seizures. In presenting these facts, I would like to point out that I feel additional studies are indicated—to follow the magnesium levels and the clinical response of these patients and to determine the renal threshold of the mineral magnesium. In future studies it is my plan to do both urinary and fecal excretions in order to determine the threshold of each individual case.

The basic studies included PBI [protein-bound iodine], serum magnesium, serum calcium, serum sodium, potassium, and, in most cases, the total 17-ketosteroids [urine] excretion and bone age.

Of thirty children studied, all of them showed a serum magnesium level of 1.5 mEq and below. After clinical studies on other types of disturbance, we have arrived at 1.5 mEq as the lower limit of normal for people residing in this area. The chemistry of the mineral magnesium is to find an intracellular element classed as an anesthetic [sic].

It was my intention in these cases to uncover a deficiency in magnesium, if such existed, and to correct that deficiency by means of an oral preparation. It was hoped the magnesium supplement would control the children’s petit mal and grand mal seizures. The results obtained in this series have been encouraging. For your consideration I list some cases of previously diagnosed epilepsy in children.

Case No. 1. Four-year-old boy with history of petit mal seizures, particularly during stress periods, with onset at the age of eighteen months. Laboratory findings were as follows: PBI 2.8, serum magnesium 1.1 mEq, serum calcium 4.5 mEq, serum sodium 138 mEq, serum potassium 4.2 mEq, total 17-ketosteroids 2.5, bone age retarded. Therapy consisted of 450 mg magnesium, by mouth, in addition to his diet, together with thyroid extract. Within two weeks the serum magnesium level had risen to 1.6 mEq, and his clinical signs were greatly improved. This child has been maintained on this regimen for a period of three years without remission.

Case No. 2. S.M., age thirteen, history of grand mal seizures since the age of three. These seizures were under fair control using anticonvulsant drugs. However, the individual had marked depression and signs of mental retardation. Initial laboratory findings were as follows: PBI 1.2, serum magnesium 1 mEq, serum calcium 4.6 mEq, serum sodium 142 mEq, serum potassium 4.8 mEq, 17-ketosteroids 4.5. Again, high oral intake of magnesium was instituted, along with correction of the metabolic state. Within a period of three months, all anticonvulsant drugs had been withdrawn, and the patient was maintained at a level of 1.6 mEq normal serum magnesium. Clinically, he was much improved mentally and neurologically.

Twenty-eight other cases, with approximately the same studies and treatment, have been observed. In all cases except one, clinical improvement has been obtained by correcting the magnesium deficiency. Serum calcium levels were within normal limits in all cases. Approximately half of these children had a low PBI and a low steroid level. Since most of the children had not reached puberty, the steroid level was not given much consideration. All anticoagulant [sic, anticonvulsant] drugs were removed over a period of time.

In presenting these findings, I would like to point out the following:

  1. The possible role of magnesium therapy in the control of petit and grand mal epileptic seizures in children.
  2. The need for further studies to determine the effect of the mineral magnesium on the vasomotor center.
  3. The desirability of studies to determine the serum magnesium levels in the hyperirritable child who does not present clinical findings of petit or grand mal seizures.
  4. The need for clinical studies to determine secondary conditions, such as metabolic derangement, where a deficiency of serum magnesium might be present.
  5. The presence of some evidence that damage to the hypothalamus and adjacent areas may well result in a clinical deficiency of magnesium, resulting in a hyperirritability of the central nervous system, which in turn might manifest itself either as petit or grand mal seizures.


This is a presentation of laboratory and case findings in epileptic children presenting deficient magnesium levels. These studies have been done to ascertain, if possible, the role of serum magnesium in the central nervous system, especially the hypothalamus. There is clinical evidence to support the possibility that it has a very vital role. There is also clinical evidence to suppose that deficient serum magnesium levels may be raised by the adequate intake of some suitable magnesium compound.

In all cases serum calcium levels were within normal range. By using this approach to epilepsy—in addition to the complete neurological examination, which should always be done—it may be possible to control many cases without using depressant drugs. By balancing the physiological state, with special emphasis on intracellular chemistry, an easier and finer control of these unfortunate individuals may be possible.

Additional correlative studies are now in progress, and it is hoped that within the near future these will provide further clinical and laboratory data of use to the clinician.

*Note: “mEq” is the concentration in terms of reactive particles per liter and is a term used where injectibles are employed; mg is the concentration in terms of weight per volume. To convert from mEq to mg, divide the mEq by the following conversion factors:

Sodium 0.435
Potassium 0.256
Calcium (both total and ionizable) 0.500
Magnesium 0.833
Magnesium 0.580
Chloride 0.282
NaCl 0.171

By Lewis B. Barnett, MD, FACS, the Hereford Clinic and Deaf Smith Research Foundation, Hereford, Texas. Reprinted from Clinical Physiology, Vol. 1, No. 2, Fall 1959 (Atlanta, Texas) by the Lee Foundation for Nutritional Research. 

Reprint No. 114
Lee Foundation for Nutritional Research
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Note: Lee Foundation for Nutritional Research is a nonprofit, public-service institution, chartered to investigate and disseminate nutritional information. The attached publication is not literature or labeling for any product, nor shall it be employed as such by anyone. In accordance with the right of freedom of the press guaranteed to the Foundation by the First Amendment of the U.S. Constitution, the attached publication is issued and distributed for informational purposes.


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