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Studies on the Physiology of Awareness: An Oximetric Investigation of the Anoxaemia Accompanying Insulin Coma Therapy

Published online by Cambridge University Press:  08 February 2018

John W. Lovett Doust
Affiliation:
University of London; Bethlem Royal and Maudsley Hospitals
Robert A. Schneider
Affiliation:
Institute of Psychiatry

Extract

This investigation deals with the measurement, by a peripheral method of discontinuous spectroscopic oximetry, of the arterial blood oxygen saturation levels in a group of schizophrenic patients undergoing insulin coma therapy.

The association between tissue anoxia and insulin hypoglycaemia was first established by Campbell and Dudley in 1924. Dameshek and Meyerson (1935), using the arterio-venous oxygen difference method with the internal jugular vein as the source of venous blood, showed that the injection of insulin in coma doses was accompanied by an anoxaemia in the schizophrenic patients they studied. This work was confirmed by Himwich, Bowman et al. (1939), and in another paper Himwich (1951, p. 277) and his co-workers found that the correlation of progressively developing clinical symptoms with the decrease of cerebral oxygen uptake was a closer one than the correlation with the more acute fall in the blood-sugar curve. An important symptomatic aspect of insulin hypoglycaemia includes the progressive changes in the levels of consciousness accompanying the approach towards coma. Wilder (1943) has outlined some of these changes, and Frostig (1940) and Himwich (1951, pp. 258-265) have delineated these awareness thresholds and discussed their relationship to the Hughlings Jackson theory of the phyletic organization of the central nervous system. Thus, during the first hour following insulin injection, somnolence and lassitude appear to be associated with suppression of cortical and cerebellar activity; in the second hour further clouding of consciousness, sometimes with excitement, perceptual disturbances, periods of confusion, exacerbations of previously existing hallucinations and latent psychotic syndromes are seen; in the third hour motor restlessness and loss of consciousness suggest the release of basal ganglia and hypothalamus; in the fourth hour deepening stupor and depression of exteroceptive sensitivity indicate a probable release of the midbrain and suppression of pyramidal function; in the fifth hour the deep pre-mortal coma presages medullary release. Similarly, it is with awareness changes that many workers prefer to diagnose the “real coma” level in a patient under treatment. Thus Sakel (1937) held that coma was to be diagnosed when no further personal contact with the patient was possible, and Kalinowsky and Hoch (1946) agree that the real coma level is reached when it is completely impossible to awaken the patient.

Type
Part I.—Original Articles
Copyright
Copyright © Royal College of Psychiatrists, 1952 

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References

Baruk, H., David, , Racine, , Vallanian, and Owsianck, , L'Encèphale, 1945, 8, 88 (1942–1945).Google Scholar
Beiglböck, W., and Dussik, Th., Am. J. Psychiat., 1938, 94 (supp.), 50.Google Scholar
Bellet, S., Am. J. Med. Sci., 1939, 198, 533.Google Scholar
Campbell, J. A., and Dudley, H. W., J. Physiol., 1924, 58, 348.Google Scholar
Dameshek, W., and Myerson, A., Arch. Neurol. Psychiat., 1935, 33, 1.CrossRefGoogle Scholar
Frostig, J. P., Am. J. Psychiat., 1940, 96, 1167.Google Scholar
Gellhorn, E., J. Am. Med. Ass., 1938, 110, 1433.Google Scholar
Georgi, F., Am. J. Psychiat., 1938, 94 (supp.), 67.Google Scholar
Gerard, R. W., Research Publ., A., Nerv. and Ment. Dis., 1938, 18, 316.Google Scholar
Hadorn, W., Arch. f. Kreislaufforsch., 1937. 2, 1.Google Scholar
Hoagland, H., Cameron, D. E., and Rubin, M. A., Am. J. Psychiat., 1937 a, 94, 183.Google Scholar
Idem, Am. J. Physiol., 1937b, 120, 559.Google Scholar
Idem, Elmadjian, F., and Pincus, G., J. Clin. Endocrin., 1946, 6, 301.CrossRefGoogle Scholar
Himwich, H. E., Bowman, K. M., Wortis, J., and Fazekas, J. F., J. Nerv. and Ment. Dis., 1939. 89, 273.CrossRefGoogle Scholar
Idem, Hadidian, Z., Fazekas, J. F., and Hoagland, H., Am. J. Physiol., 1939. 125, 573.Google Scholar
Idem, Brain Metabolism and Cerebral Disorders, 1951. Baltimore.Google Scholar
Hoskins, R. G., The Biology of Schizophrenia, 1946. New York and London.Google Scholar
Kalinowsky, L. B., and Hoch, P. H., Shock Treatment and other Somatic Procedures in Psychiatry, 1946. New York.Google Scholar
Lovett Doust, J. W., Proc. Roy. Soc. Med., 1951 a, 44, 347.Google Scholar
Idem, Ann. Rheum. Dis., 1951 b, 10, 269.Google Scholar
Idem and Schneider, R. A. Brit. Med. J., 1952, i, 449.Google Scholar
Idem, J. Ment. Sci., 1952, 98. 143.CrossRefGoogle Scholar
Messinger, E., Ann. Int. Med., 1938, 12, 853.Google Scholar
Parsons, E. H., Gildea, E. F., Ronzoni, E., and Hulbert, S. Z., Am. J. Psychiat., 1949, 105, 573.Google Scholar
Ray, G. B., Am. J. Physiol., 1946, 147, 622.Google Scholar
Sakel, M., Am. J. Psychiat., 1937, 93, 829.CrossRefGoogle Scholar
Schneider, D. E., The Growth Concept of Nervous Integration, 1949. Nerv. and Ment. Dis. Monogr., New York.Google Scholar
Tietz, E. B., Dornheggen, H., and Goldman, D., Endocrinology, 1940, 26, 641.Google Scholar
Yierordt, K., Z. Biol., 1878, 14, 422.Google Scholar
Wilder, J., Am. J. Digest. Dis., 1943, 10, 428.Google Scholar
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