Diabetic and Insulin Coma

BMJ ◽  
1955 ◽  
Vol 1 (4921) ◽  
pp. 1091-1092
Author(s):  
H. Josephs
Keyword(s):  
Insulin Coma

Irreversible Hypoglycaemic Coma in Islet-Cell Adenoma and in Schizophrenia

1955 ◽  
Vol 101 (424) ◽  
pp. 673-682 ◽  
Author(s):  
D. N. Parfitt
Keyword(s):  
Personal Experience ◽  
Islet Cell ◽  
Severe Hypoglycaemia ◽  
Insulin Dosage ◽  
Cell Adenoma ◽  
After Effects ◽  
Schizophrenic Patients ◽  
Insulin Coma ◽  
Trained Staff ◽  
Hypoglycaemic Coma

As an approach to the problem of schizophrenia it is proposed to compare the effects and after-effects of severe hypoglycaemia due mainly to islet-cell adenoma of the pancreas in otherwise healthy people with the effects and after-effects of severe hypoglycaemia therapeutically induced in schizophrenics.The difficulties are plain. Personal experience of patients with functioning islet-cell adenoma is limited almost always to a few cases, whereas average experience of insulin coma treatment covers some hundreds of cases; moreover, there is little overlap of experience except in the post-mortem room or in the laboratory for morbid histology. During insulin treatment there is constant supervision by a trained staff, medical and nursing, so that serious developments can be met by immediate intravenous sugar and investigations are continual; with adenomata there is no observation until, perhaps, a general practitioner is called in about alarming symptoms of one kind or another and sometimes months or even years elapse before a patient gets into hospital, where the intensity of observation and even more so of investigation may exceed that available in mental hospitals. Insulin coma treatment has a more or less standard aim, to produce coma of increasing duration up to a maximum of something like an hour which is then repeated thirty times or more; dosage is built up with the greatest care. Adenomata produce conditions varying from the hardly serious to the fatal under the influence of an insulin dosage which is quite unknown.This comparison is based chiefly on an analysis of 290 serial courses of insulin coma treatment given to schizophrenic patients at Holloway Sanatorium during the four years 1950 to 1953 inclusive, and on the 258 cases of islet-cell adenoma reported by Crain and Thorn (1949) and the 398 cases, all that could be traced up to that date and including the Crain and Thorn cases, analysed by Howard, Moss and Rhoads (1950). Many separate papers have been consulted for more detailed approaches and for extra information, although of course those published before 1950 were included in the reviews already mentioned. Despite the difficulties of this comparison, it can be shown that the similarities between the two groups follow expectation and are very strong indeed, so that the differences which emerge have at least possible significance.

scholarly journals Insulin coma therapy: let's be factual

2014 ◽  
Vol 38 (6) ◽  
pp. 308-308
Author(s):  
Harold Bourne
Keyword(s):  
Insulin Coma ◽  
Insulin Coma Therapy

Insulin Coma

BMJ ◽  
1962 ◽  
Vol 2 (5304) ◽  
pp. 608-608
Author(s):  
W. Brand
Keyword(s):  
Insulin Coma

Modification of Insulin Resistance

1956 ◽  
Vol 102 (428) ◽  
pp. 576-588 ◽  
Author(s):  
Edward Marley
Keyword(s):  
Deep Coma ◽  
Insulin Dosage ◽  
Insulin Resistant ◽  
Significant Difference ◽  
High Insulin ◽  
Insulin Coma ◽  
The Central Nervous System ◽  
Resistance To Insulin ◽  
High Doses ◽  
Special Instance

Sakel (1938a) drew attention to the difficulty of establishing satisfactory comas in a minority of patients attending for Deep Insulin therapy. This phenomenon has since been confirmed by other workers including Tillim (1938) whose patient received 500 units of insulin without the production of deep coma, by Hall (1940) who reported an instance in which 1,000 units of insulin was equally unsuccessful, by Reznikoff and Scott (1942) who described how neither 120 nor 1,000 units of insulin when injected intravenously produced any significant difference in hypoglycaemia in insulin resistant patients, and more recently by Fogarty (1953) whose case required 5,000 units of insulin for the production even of sopor. Other recorded examples of resistance to massive doses of insulin include those of Bantinget al.(1938) and Tennent (1944).Various explanations of this perverse response to insulin have been formulated, including that of Jones (1939) who proposed that resistance to insulin was both a problem of true insulin insensitivity and also of an anomalous response of the central nervous system to hypoglycaemia. Medunaet al.(1942) preferred to ascribe it to anti-insulin factors in the blood, but a more interesting interpretation derived from Freudenberg (1952) who suggested that if the effects of high insulin dosage employed in insulin coma treatment were regarded as a special instance of a stress response, then the fluctuations and differences in response could be equated in terms of the General Adaptation Syndrome of Selye. High doses were thus an index of an effective “alarm stage” characterized by a discharge from plentiful adrenocortical reserves.

THE MENSTRUAL CYCLE AND INSULIN COMA TREATMENT IN SCHIZOPHRENIA

1954 ◽  
Vol 119 (6) ◽  
pp. 512-516 ◽  
Author(s):  
SIDNEY MERLIS ◽  
STANLEY T. MICHAEL
Keyword(s):  
Menstrual Cycle ◽  
Insulin Coma

The Treatment of Prolonged Insulin Coma

1961 ◽  
Vol 107 (447) ◽  
pp. 194-238 ◽  
Author(s):  
William Whittle Kay
Keyword(s):  
Adrenocorticotrophic Hormone ◽  
Insulin Coma ◽  
Prolonged Coma

This thesis gives an account of the use of cortisone and adrenocorticotrophic hormone (ACTH) in the treatment of prolonged comas occurring in the course of deep insulin coma treatment. Cases in which neither hormone was used are also included. The pathology and aetiology of this type of prolonged coma are discussed and a classification of the cases seen is made.

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

1952 ◽  
Vol 98 (412) ◽  
pp. 411-420 ◽  
Author(s):  
John W. Lovett Doust ◽  
Robert A. Schneider
Keyword(s):  
Clinical Symptoms ◽  
Venous Blood ◽  
Insulin Injection ◽  
Personal Contact ◽  
Blood Oxygen Saturation ◽  
The Real ◽  
Arterial Blood ◽  
Schizophrenic Patients ◽  
Insulin Coma ◽  
Insulin Coma Therapy

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.

Sign in / Sign up

Export Citation Format

Share Document