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Spinal Anaesthesia in Electrical Convulsive Therapy

Published online by Cambridge University Press:  08 February 2018

H. J. Shorvon
Affiliation:
E.M.S., Sutton Emergency Hospital
L. M. Shorvon
Affiliation:
E.M.S., Sutton Emergency Hospital

Extract

The value of electrical shock therapy is becoming increasingly recognized and used by psychiatrists in the treatment of depressive states, particularly of the involutional period, states of depersonalization, and to a lesser extent in schizophrenia. One of the major objections to its use, however, has been the complication of fractures, generally crush fractures of the bodies of the mid-dorsal vertebrae (thoracic 4-8), and uncommonly that of limb bones, such as the femur. Another aspect of this problem arises with the occasional case in which the use of shock therapy is desirable, but a previous fracture of the spine or limb bones, or marked bone disease with an increased liability of fracture resulting during treatment, acts as a deterrent to the physician. Even more so is the question of continuing treatment without further damage to the patient, should a fracture have unfortunately resulted before the full course of convulsions is completed. Various methods have been introduced to minimize or abolish the muscular pull producing fractures, including intravenous injections of curare, of concentrated magnesium sulphate solution, or of beta-erythoidin hydrochloride; spinal anaesthesia has been similarly employed.

Type
Part I.—Original Articles
Copyright
Copyright © Royal College of Psychiatrists, 1943 

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References

Androp, S. (1941), J. Nerv. and Ment. Dis., 93, 701.Google Scholar
Bennett, A. E. (1940), J. Amer. Med. Ass., 114, 322.Google Scholar
Cheney, C. C., Hamilton, D., and Heaver, W. (1941), Psychiat. Quart., 15, 214.Google Scholar
Cook, L. C., and Sands, D. E. (1941), J. Ment. Sci., 87, 208.Google Scholar
Easton, N. L., and Sommers, J. (1942), Amer. J. Psychiat., 98, 538.Google Scholar
Hamsa, W. R., and Bennett, A. E. (1939), J. Amer. Med. Ass., 112, 2240.Google Scholar
Hemphill, R. E. (1942), Lancet, 2, No. 6, 152.CrossRefGoogle Scholar
Polatin, P., Friedman, M. M., Harris, M. M., and Horwitz, W. A. (1939), J. Amer. Med. Ass., 112, 1684.Google Scholar
Roberg, O. T. (1939), J. Bone Jt. Surg., 19, 603.Google Scholar
Sommers, J., and Richardson, (1939), Amer. J. Psychiat., 95, 1193.Google Scholar
Stalker, H. (1938), Lancet, 2, 1172.CrossRefGoogle Scholar
Worthing, H. J., and Kalinowsky, L. B. (1942), Amer. J. Psychiat., 98, 533.Google Scholar
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