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Glutamic Acid and its Salts in Petit Mal Epilepsy

Published online by Cambridge University Press:  08 February 2018

D. A. Pond  and
M. H. Pond
D. A. Pond
Affiliation:
Departments of Clinical Neurophysiology and Biochemistry, The Institute of Psychiatry, Maudsley Hospital, London
M. H. Pond
Affiliation:
Departments of Clinical Neurophysiology and Biochemistry, The Institute of Psychiatry, Maudsley Hospital, London
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Extract

The following experiments on glutamic acid were carried out in view of the conflicting reports of Price, Waelsch and Putnam (1943), Waelsch and Price (1944), and Goodman et al. (1948) on its effect in epilepsy. A number of preliminary experiments were made which suggested that there was an apparent difference between the effects of glutamic acid and sodium glutamate. Such a difference does not appear to have been considered by most other investigators. It was decided therefore to try to determine whether a possible reason for the difference was the effect of the sodium ion on water balance, since this is known to be related to the tendency to seizures (McQuarrie et al., 1932, Swinyard et al., 1946, and Weinland, 1949). For comparison potassium glutamate was given in a way to be described below. The experiments will be reported under the following headings:

  1. 1. The acute E.E.G. and clinical effects of intravenous sodium glutamate.

  2. 2. The short term (one week) E.E.G. and clinical effects of glutamic acid, its sodium and potassium salts and a placebo.

  3. 3. Longer term clinical effects in out-patients.

  4. 4. Biochemical studies of the blood and urine levels of glutamic acid by paper chromatography of 7 epileptic patients and 5 non-epileptic control subjects, including salt and water balance studies of patients and controls.

Type
Part I.—Original Articles
Information
Journal of Mental Science , Volume 97 , Issue 409 , October 1951 , pp. 663 - 673
Copyright
Copyright © Royal College of Psychiatrists, 1951 

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