Coma Therapy Research Articles

Insulin coma and group psychotherapy.

THE MATERIAL reported on in this paper was derived from a private mental hospital in which the emphasis on psychiatric treatment centers about the patient's total hospital experience. Such hospital-treatment experience includes the carefully coordinated services of the psychiatric medical staff, social service case work, nursing care, and various forms of group, physical, occupational, horticultural, and recreational therapies. Electroshock and insulin coma treatments are important forms of adjunctive therapy which are used as indicated. We have realized for some time that both electroshock and insulin coma therapy can be most effective only when they are used as parts of the total psychotherapeutic approach to the patient and his illness. Accordingly, the following treatment program is based on two premises. The first is that in the treatment of schizophrenia, insulin coma is the treatment of choice; the second, that treatment is in no way complete unless it includes the psychotherapeutic program.

Cholesterol changes in schizophrenic patients during insulin therapy.

SEVERAL investigators have reported on blood cholesterol levels in schizophrenic patients receiving insulin coma therapy. Katzenelbogen and associates1reported values on several patients during and after a coma showing that in some subjects there was no change over a period of three hours. Changes in any one coma seemed to be minimal or variable. Randall and associate2reported that the total and free cholesterol increased during therapy and remained high for two weeks after treatment. Gottfried and Willner3tested a few patients before and after a course of insulin therapy and found no significant variation. Recently, Larue and co-workers4sampled patients at more frequent intervals during treatment and demonstrated a greater variability in those patients during the course of therapy than in schizophrenic patients not receiving treatment. Unpublished data on 20 patients obtained by workers in this laboratory before, during, and after a course of insulin

The concentration of adrenaline-like substances in blood during insulin hypoglycaemia.

Since the demonstration of increased sympathetic activities during insulin hypoglycaemia by Cannon, MacIver and Bliss (1924) the assumption has been current that hypoglycaemia also increases the concentration of circulating adrenaline, and repeated attempts have been made to verify this experimentally. Brandt and Katz (1933), using the perfused rabbit ear, the isolated rabbit ileum and the enucleated frog eye as test objects, found that human blood possessed adrenaline-like activities during hypoglycaemia, while control blood was inactive. Meythaler and Wossidlo (1935) reported that the blood of subjects injected with insulin caused an increased vasoconstriction of the perfused rabbit ear and, more recently, Meythaler, Lobenhofer and Haggenmiller (1951) found that the response varied according to the constitutional type of the subject. Heilbrunn and Liebert (1939), however, observed no uniform effects when they tested the blood of patients undergoing insulin shock therapy with the frog perfusion technique; while there was a rise of adrenaline-like activity in some patients, others showed a fall and some failed to show any definite pattern. The results of Tietz, Dornheggen and Goldman (1940) and of Tietz and Birnbaum (1942) who used Shaw's colorimetric method indicated little change in the first two hours after insulin injection, but in the later stages of hypoglycaemia there was a more consistent tendency towards an increase of concentration. The proportion of adrenaline in the chromogenic material estimated by Shaw's method increases during hypoglycaemia, according to Raab (1943). Kalaja (1942), with a fluorimetric method, also found an increase of the blood adrenaline level after insulin injection. On the other hand, Richter (quoted by Jones, 1939) who used the method of Shaw came to the conclusion that adrenaline was not present in significantly increased concentration in arterial blood during those stages of hypoglycaemia when the clinical picture suggested the possibility of adrenalinaemia.

Cortisone in the treatment of schizophrenia.

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.

Studies on the physiology of awareness: an oximetric investigation of the anoxaemia accompanying 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.

Fractures of the spine during insulin shock therapy.

INTRODUCTION IN A PREVIOUS communication, 1 an analysis of electric-shock fractures was presented in which correlations with possible predisposing factors were discussed. It was the purpose of the present, similar invesigation to study insulin-shock fractures of the thoracic portion of the spine in an effort to correlate such fractures with any determinable theoretical predisposing or etiologic factors and to determine the incidence of such fractures with insulin shock treatment. A review of the literature did not reveal any information along these lines. General Comment Regarding Insulin Shock.— Insulin shock is defined as a circulatory insufficiency resulting from overdosage with insulin which causes the sudden reduction of blood sugar. It is marked by tremor, sweating, vertigo, diplopia, convulsions, and collapse. 2 Insulin shock therapy for certain psychoses was developed in 1928 by Manfred Sakel, 3 and the fact that it is still being used despite the difficulty of its administration is

Ineffectiveness of desoxycorticosterone acetate in inhibiting the depression of blood eosinophils in patients receiving insulin-shock therapy

Ineffectiveness of desoxycorticosterone acetate in inhibiting the depression of blood eosinophils in patients receiving insulin-shock therapy

HYALURONIDASE AS AN ADJUNCT IN INSULIN COMA THERAPY

Back to table of contents Previous article Next article ArticleNo AccessHYALURONIDASE AS AN ADJUNCT IN INSULIN COMA THERAPYFRANK A. STRACCIA, and ALBERT E. SCHEFLENFRANK A. STRACCIASearch for more papers by this author, and ALBERT E. SCHEFLENSearch for more papers by this authorPublished Online:1 Apr 2006https://doi.org/10.1176/ajp.108.9.702AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail "HYALURONIDASE AS AN ADJUNCT IN INSULIN COMA THERAPY." American Journal of Psychiatry, 108(9), pp. 702–703 Access content To read the fulltext, please use one of the options below to sign in or purchase access. Personal login Institutional Login Sign in via OpenAthens Purchase Save for later Item saved, go to cart PPV Articles - American Journal of Psychiatry $35.00 Add to cart PPV Articles - American Journal of Psychiatry Checkout Please login/register if you wish to pair your device and check access availability. Not a subscriber? Subscribe Now / Learn More PsychiatryOnline subscription options offer access to the DSM-5 library, books, journals, CME, and patient resources. This all-in-one virtual library provides psychiatrists and mental health professionals with key resources for diagnosis, treatment, research, and professional development. Need more help? PsychiatryOnline Customer Service may be reached by emailing [email protected] or by calling 800-368-5777 (in the U.S.) or 703-907-7322 (outside the U.S.). FiguresReferencesCited byDetailsCited byInsulin Therapy with Hyaluronidase in Multiple Injections: (Method of Sacerdoti-Yagdjoglou)3 May 2017 | Canadian Psychiatric Association Journal, Vol. 4, No. 3The Psychiatric Quarterly, Vol. 30, No. 1-4Oral Surgery, Oral Medicine, Oral Pathology, Vol. 9, No. 5Journal of Mental Science, Vol. 102, No. 428 Volume 108Issue 9 March 1952Pages 702-703 Metrics PDF download History Published online 1 April 2006 Published in print 1 March 1952

Narcosynthesis immediately following insulin shock; five-year follow up and supplementary report.

The same favorable results as reported for the original group of 11 patients were obtained in the second larger group justifying the conclusion that narcosynthesis immediately following insulin coma appears to deserve its place in the treatment of mental disease, and especially seems worth while in patients who have previously not responded either to insulin coma therapy alone, or to the prognostic pre-insulin sodium amytal interview. This type of treatment on the basis of this study not only seems to hasten considerably the recovery of the patients and lessen appreciably their hospital stay, but also seems to produce a more prolonged and well-sustained recovery. In fact, 10 out of 11 patients of the preliminary group have adjusted satisfactorily outside the hospital for periods of over 5 years, and 26 of the 30 patients of the second group have also made satisfactory extra-institutional adjustment for periods of 3 to 5 years without recurrence of symptoms of mental illness.

Fatalities in insulin therapy of the psychoses; analysis of eight cases.

ASSOCIATED with the Massachusetts Department of Mental Health is an ' agency designated to investigate certain deaths occurring in psychiatric hospitals. In the last 11 years eight deaths incident to insulin coma or subcoma therapy have been reviewed: four in state hospitals, two in private institutions, one in a veterans hospital, and one following treatment in a patient's home. Numerous fatal insulin reactions have been reported. 1 Most of the clinical papers have been concerned with the events of the final coma. Little attention has been paid to factors, other than overt organic diseases, which give warning of an untoward reaction. Certain clinical features and aberrant physiological responses occurring prior to the fatal reaction, and of possible value in prognosticating it, are presented in this report. Case 1. —A white man aged 47, with a diagnosis of schizophrenia, paranoid type, was treated with insulin coma. On the 63d treatment, 28th coma,

Test evidence of personality change and prognosis by means of the Rorschach and Wechsler-Bellevue tests on 17 insulin-treated paranoid schizophrenics.

1. Carp's finding that there is no significant increase in I. Q. scores as a result of insulin treatment is confirmed. Since Carp's data was unavailable to the author except in abstract form, it is impossible to comment on Carp's finding that there was no change in Rorschach protocols pre- and post-treatment. 2. There are suggestions of improvement in the reality level of perception and affective control as a result, presumably, of insulin shock treatment but the change is not statistically significant. 3. Clinical ratings of improvement between the pre- and post-Rorschach records, as a result of insulin shock therapy, are most closely related to the loss in total number of responses. 4. The relationship between loss in ability to respond and improvement suggests that insulin possibly effects improvement by means of impairment. It is suggested that impairment might serve to desensitize the organism and to preclude complex reactions. The organism is thought of as returning to a more primitive level of adjustment. 5. A series of signs culled from the literature and applieda priori to the Rorschach records of 15 paranoid schizophrenic patients without knowledge of psychiatrists' ratings proved to be of value in making prognostic estimates of improvement under insulin shock therapy.

The emotional reactions of a schizophrenic patient to shock therapy

A young woman who now appears to be recovering from schizophrenia with psychological treatment, after failing to respond to organic therapies, was able to verbalize a rather full description of emotional and physical reactions to both insulin and electric shock therapy. Outstanding, were her erotization of the shock experience and her longings to find a good mother figure. The patient's statements are presented, as nearly as possible, in the form of a verbatim transcription; and it is hoped that her impressions may prove to be of value as an addition to scientific thought concerning the therapeutic action of the shock therapies.

An evaluation of the Rorschach test as a prognostic aid in the treatment of schizophrenia by insulin coma therapy, electronarcosis, electroconvulsive therapy and leucotomy.

The possibility of using the Rorschach test to predict outcome of insulin coma treatment of schizophrenia has been investigated by Piotrowski (1938, 1939 and 1941).

Effect of potassium on electrocardiographic abnormalities produced during insulin shock.

DEVIATIONS from the normal electrocardiogram have been reported in schizophrenic patients in the course of insulin-shock therapy.1Thiamine deficiency2; hypoglycemia3; anoxia, with decreased blood flow through the coronary arteries,4and epinephrine release5have been implicated in these changes. Other investigators have demonstrated the occurrence of hypopotassemia in diabetic acidosis and in other clinical disorders and have described characteristic cardiovascular and electrocardiographic changes associated with decreased serum-potassium concentration.6Messinger4and Hadorn1bobserved that the most frequent electrocardiographic abnormalities associated with hypoglycemia was a flattening or inversion of the T wave and sinus arrhythmia; other findings were a pathological Q wave in lead III, changes in R and S voltage, slight widening of the QRS complex, and appearance of U waves or auricular and ventricular extrasystoles. Bellet and his co-workers,6hfound similar changes in pattern associated with hypopotassemia and classified these as follows:

Analysis of prognostic factors in insulin therapy.

DEEP insulin-shock therapy has been established as an accepted treatment for schizophrenia and certain allied disorders for over a decade. Many publications indicate that higher ratios of satisfactory results are obtained from insulin-treated patients than from controls, particularly if the treatment is administered early in the course of the disease. 1 The purpose of this investigation is to determine what factors, if any, are of prognostic significance with reference to this form of therapy. MATERIAL One thousand patients, all males, were treated with deep insulin-shock therapy over a three-year period. The selection of these patients was not on the basis of probable prognosis but entirely on the presentation of a diagnosis of schizophrenia or an allied functional psychosis. Of these, 1,000 patients the data on 639 were subjected to final analysis. Excluded were 52 patients who did not complete the course of treatment because of complications, 1 who died of

Neurological complications of insulin shock therapy with electroencephalographic studies; case studies.

THERE are numerous reports of neurological and psychiatric changes occurring as result of hypoglycemia. Many of these are described as complications of insulin overdosage in diabetic patients1or of hyperinsulinism in patients with pancreatic adenoma.2 In the literature on insulin coma treatment of schizophrenia there are also many such reports. These have been collected and summarized by Spencer.3In his thorough collation he includes reports of confused, stuporous states; motor and sensory aphasias; various paralyses, such as monoplegias, facial pareses and hemiplegias, and dysarthrias and rotary movements. There is no general agreement on the incidence of such complications. Fleeting sensory disturbances, such as numbness and tingling of extremities and impairment of taste, have also been reported as occurring as a possible transient change in the central nervous system of patients receiving insulin or as result of vitamin B deficiency. These complications may occur as sequelae to a

MMPI performance and insulin shock therapy.

MMPI performance and insulin shock therapy.

Insulin shock therapy, a statistical survey of 393 cases.

1. Insulin shock therapy was found to be effective in the treatment of 182 cases of schizophrenia in the following terms : discharged from the hospital, 34.1% ; remained discharged after a period of 21 to 75. months, 19.8% ; and full social recovery (after that period of time) estimated at about 6%. These figures indicate that insulin shock therapy is certainly not sufficient as a sole form of treatment in schizophrenia. It may have more value when used as a preliminary approach to psychotherapy or milieu therapy. On the other hand the low social recovery rate, after 40 months (average) of evaluation, is discouraging. 2. Race was not a significant factor in this form of therapy. 3. The older the patient the better the remission status following therapy, i. e., fewer relapses occurred. 4. There was no indication that insulin shock therapy is especially effective in any particular type of schizophrenic reaction. 5. The effectiveness was found to decrease as the length of illness prior to therapy was increased. 6. Of 182 schizophrenic patients showing remission after a course of insulin shock therapy as the first form of shock treatment, 41.9% later suffered relapses, within a time evaluation period averaging 3⅓ years. 7. Insulin shock therapy was effective in some patients (17.0% of cases) who had failed to respond with electroshock treatment. 8. Electroshock therapy was effective in some patients (15.0% of cases) who had failed to respond with insulin treatment. 9. A second course of insulin treatment was found to be of very little value if the patient had failed to respond with the first course. 10. The level of the fasting blood sugar prior to insulin shock therapy had no effect on the outcome of the treatment. 11. Almost invariably a substantial gain in weight was produced during the course of insulin shock therapy. This had little bearing on the ultimate improvement of the patient. 12. The length of treatment was of no value in estimating the prognosis. 13. Convulsive attacks during insulin coma seemed to have a favorable therapeutic effect. 14. There was no marked change in blood pressure following insulin shock therapy. 15. Paranoid schizophrenics required a smaller dosage of insulin to produce symptoms of hypoglycemia than did the other types of schizophrenia. 16. Insulin shock therapy can be expected to produce certain complications and a mortality rate of about 0.5%.

The influence of insulin shock therapy on the electrocardiogram

A study before and after a series of insulin shock treatments in 259 patients with schizophrenia was undertaken to determine the incidence of significant electrocardiographic alterations. It was concluded that this form of therapy is not associated with any cumulative injury to the myocardium which could be detected in the electrocardiogram.

The Concentration of Adenosinetriphosphate (ATP) Citrate and Calcium in Blood During Insulin Shock Therapy

Concentration changes of blood constituents other than glucose occurring during hypoglycaemia, and particularly during insulin shock therapy, have been studied by several authors (e.g., Harris, Blalock and Horwitz, 1938; Katzenelbogen et al., 1939) though not always with concordant results. One of the most constant features of insulin hypoglycaemia is a decrease in the level of inorganic phosphate during the phase of blood-sugar fall and a gradual return to normal after the blood-sugar curve has reached its lowest value. This fact which was described soon after the discovery of insulin (see Cori (1931) for a review of the older literature) is generally attributed to the increased phosphate esterification consequent upon the enhancement of glucose utilisation and is in harmony with the current concept that the function of insulin is primarily that of a promotor of glucose phosphorylation.