Insulin Coma Therapy and the Construction of Therapeutic Effectiveness in Stalin’s Soviet Union, 1936–1953

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, Bowmanet 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 thefirst hourfollowing insulin injection, somnolence and lassitude appear to be associated with suppression of cortical and cerebellar activity; in thesecond hourfurther clouding of consciousness, sometimes with excitement, perceptual disturbances, periods of confusion, exacerbations of previously existing hallucinations and latent psychotic syndromes are seen; in thethird hourmotor restlessness and loss of consciousness suggest the release of basal ganglia and hypothalamus; in thefourth hourdeepening stupor and depression of exteroceptive sensitivity indicate a probable release of the midbrain and suppression of pyramidal function; in thefifth hourthe 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.

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5. The evolution of treatments

10.1093/actrade/9780199558650.003.0005 ◽

2017 ◽

Author(s):

Mary Jane Tacchi ◽

Jan Scott

Keyword(s):

Electroconvulsive Therapy ◽

Real World ◽

18Th Century ◽

Mood Stabilizer ◽

Psychological Interventions ◽

The Real ◽

Potential Barriers ◽

Insulin Coma ◽

Physical Treatments ◽

Insulin Coma Therapy

For many centuries, the only intervention for melancholia involved admission into an asylum, initially to keep individuals away from society and then, from the 18th century, to provide therapeutic care. ‘The evolution of treatments’ discusses the crude treatments that were first introduced for inpatients such as sedation (barbiturates and insulin coma therapy) and physical treatments (electroconvulsive therapy and psychosurgery). Next, it discusses the development of the medications that are used today for inpatients and outpatients, such as antidepressants and the mood stabilizer lithium. Finally, it looks at the evolution of psychotherapies from early Freudian models through to mindfulness and the potential barriers to providing psychological interventions in the real world.

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Spontaneous Hypoglycaemia and Diabetes Mellitus Associated with the Insulin Coma Therapy of Schizophrenia

Journal of Mental Science ◽

10.1192/bjp.96.402.285 ◽

1950 ◽

Vol 96 (402) ◽

pp. 285-292 ◽

Cited By ~ 3

Author(s):

Desmond McGrath

Keyword(s):

Diabetes Mellitus ◽

The Other ◽

Schizophrenic Patients ◽

Insulin Coma ◽

Short Time ◽

Insulin Coma Therapy

This paper is concerned with two schizophrenic patients showing unusual complications of Sakel's insulin coma therapy. The first had a series of attacks of spontaneous hypoglycaemia apparently uninfluenced by the temporary withholding of insulin; the other developed diabetes mellitus a short time after finishing his treatment.

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