THE EFFECT OF INSULIN AND CARDIAZOLE-SHOCK ON PROTEIN-BOUND IODINE IN BLOOD, STUDIED IN SCHIZOPHRENIC PATIENTS

1960 ◽  
Vol XXXIV (I) ◽  
pp. 157-162 ◽  
Author(s):  
V. Štolc ◽  
J. Pogády

ABSTRACT Significant alterations in the PBI levels occur during insulin shock. In acute schizophrenic states the PBI value falls during the first half hour following administration of coma inducing insulin dose (P < 0.001) while it rises (P < 0.05) in chronic states. In both groups PBI values are significantly higher as against initial values (P < 0.001). PBI values persist at raised levels, as compared to the initial levels, even after interruption of insulin coma through glucose administration. During cardiazole-shock PBI values increase within five minutes following the shock dose. Possible mechanisms explaining these observations are discussed.

1955 ◽  
Vol 101 (424) ◽  
pp. 673-682 ◽  
Author(s):  
D. N. Parfitt

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.


1952 ◽  
Vol 98 (412) ◽  
pp. 411-420 ◽  
Author(s):  
John W. Lovett Doust ◽  
Robert A. Schneider

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.


1950 ◽  
Vol 96 (402) ◽  
pp. 285-292 ◽  
Author(s):  
Desmond McGrath

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.


1959 ◽  
Vol 105 (441) ◽  
pp. 1017-1021 ◽  
Author(s):  
J. G. Thorpe

Recent work at this hospital (Thorpe and Baker, 1958) has suggested that schizophrenic patients tested one week after completing a course of twenty E.C.T.s do not show significantly more impairment in some psychological functions than similar patients treated with insulin coma or chlorpromazine therapies. This finding may come as a surprise to many, particularly in view of the fact that disorientation, memory loss, and confusion are frequently seen during the course of electrical treatment.


1937 ◽  
Vol 83 (347) ◽  
pp. 630-635 ◽  
Author(s):  
C. B. Molony ◽  
M. S. Honan

Salm (1) has recently described stuporous conditions which developed in schizophrenic patients undergoing the insulin shock treatment. He concludes that such cases constitute a serious problem, because, if they do not yield to the repeated administration of sugar, one is at a loss in regard to specific treatment.


1952 ◽  
Vol 98 (412) ◽  
pp. 401-403 ◽  
Author(s):  
Linford Rees ◽  
G. M. King

Recent research has given rise to the hope that the secretory products of the adrenal cortex might be useful in the treatment of schizophrenia.Two main lines of research have stimulated renewed interest in the role of the adrenal cortex in the pathophysiology of schizophrenia. A number of investigations have produced evidence that the responsivity of the adrenal cortex of schizophrenic patients to stress is lower than that of normal controls (Freeman et al., 1944; Hoagland et al., 1946; Pincus and Elmadjian, 1946; Pincus et al., 1949).Another series of investigations has shown that adrenocortical activity is stimulated by insulin coma therapy, electronarcosis and electroconvulsive therapy (Hemphill and Reiss, 1942; Mikkelsen and Hutchins, 1948; Rees (1949a); Parson et al., 1949).Cranswick and Hall (1950) reported that desoxycortone acetate and ascorbic acid appeared to be therapeutically valuable in schizophrenia. Rees and King (1951) carried out a controlled investigation on the treatment of schizophrenia with desoxycortone acetate and ascorbic acid, and found no evidence that the method was of any therapeutic value. It was pointed out that the investigation did not preclude the possibility that other products of the adrenal cortex might be therapeutically useful in schizophrenia.The present paper describes a controlled investigation in the therapeutic value of cortisone administration in schizophrenia.We are indebted to Dr. Ernest Evans, Consultant Physician, East Glamorgan Hospital, for making available a supply of cortisone for the investigation.


1941 ◽  
Vol 98 (3) ◽  
pp. 422-429 ◽  
Author(s):  
B. H. MCNEEL ◽  
J. G. DEWAN ◽  
C. R. MYERS ◽  
L. D. PROCTOR ◽  
J. E. GOODWIN

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