Hostname: page-component-586b7cd67f-g8jcs Total loading time: 0 Render date: 2024-11-22T06:29:25.058Z Has data issue: false hasContentIssue false

Fluid Distribution and the Response of Depression to E.C.T. and Imipramine

Published online by Cambridge University Press:  29 January 2018

D. G. Brown
Affiliation:
University Department of Psychiatry, 15 Hyde Terrace, Leeds 2
R. P. Hullin
Affiliation:
University Department of Biochemistry, 9 Hyde Terrace, Leeds 2
J. M. Roberts
Affiliation:
St. James's Hospital, Leeds 9

Extract

Interest has been directed lately to the changes in sodium metabolism in depressive disorders, revealing a complex picture. Gibbons' finding (1960) that recovery with electroconvulsive therapy (E.C.T.) was associated with an apparent drop in total exchangeable sodium, was attributed by Coppen et al. (1962) to failure of his technique to allow for redistribution of sodium between body compartments. Their own work, allowing for different equilibration rates with isotopic sodium, showed no change in total exchangeable sodium during successful treatment with E.C.T., but did not exclude intercompartmental shifts. Coppen had in fact previously shown (1960) that the transfer of sodium from blood to cerebrospinal fluid is abnormally slow in depression, and is corrected during effective electroconvulsive therapy. Demonstration of significant shifts of electrolytes and fluid between, e.g., extracellular and intracellular spaces might thus cast light on important physiological factors in depressive illnesses.

Type
Research Article
Copyright
Copyright © Royal College of Psychiatrists, 1963

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Altschule, M. D., Ascoli, I., and Tillotson, K. J., Arch. Neurol. Psychiat., 1949, 62, 619.Google Scholar
Anderson, W. McC., and Dawson, J., J. Ment. Sci., 1962, 108, 80.CrossRefGoogle Scholar
Bowler, R. G., Biochem. J., 1944, 38, 385.CrossRefGoogle Scholar
Coppen, A. J., J. Neurol. Neurosurg. Psychiat., 1960, 23, 156.CrossRefGoogle Scholar
Coppen, A. J. Shaw, D. M., and Mangoni, A., Brit. Med. J., 1962, ii, 295.CrossRefGoogle Scholar
Crammer, J. L., ibid., 1959, i, 545.Google Scholar
Gibbons, J. L., Clin. Sci., 1960, 19, 133.Google Scholar
Hamilton, M., J. Neurol. Neurosurg. Psychiat., 1960, 23, 56.CrossRefGoogle Scholar
Lavietes, P. H., Bourdillon, J., and Klinghoffer, K. A., J. Clin. Invest., 1936, 15, 261.CrossRefGoogle Scholar
McCance, R. A., and Widdowson, E. M., Proc. Roy. Soc. London, 1951, B138, 115.Google Scholar
Roberts, J. M., J. Ment. Sci., 1959, 105, 693.CrossRefGoogle Scholar
Russell, G. R. M., Clin. Sci., 1960, 19, 327.Google Scholar
Schottstaedt, W. W., Grace, W. J., and Wolff, H. R., J. Psychosom. Res., 1956, 1, 287.Google Scholar
Trolle, C., Acta Psychiat. Kbh., 1945, 20, 235.CrossRefGoogle Scholar
Submit a response

eLetters

No eLetters have been published for this article.