PUTTING SCHIZOPHRENIA'S DEMONS TO SLEEP | Behavioral Healthcare Executive Skip to content Skip to navigation


February 1, 2006
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The use of insulin coma therapy led to a greater understanding of schizophrenia's biologic origin

Throughout history, patients with schizophrenia wrestled with internal “demons” while being demonized by society. One doctor sought to quiet the demons through insulin coma therapy. To appreciate the significance of insulin coma therapy is to understand how schizophrenia was viewed in the first half of the 20th century. Hospitals were filled with people with schizophrenia, and insulin coma therapy represented hope. This article looks at the discovery of insulin coma therapy, describes its administration, chronicles its rise and fall, and takes note of its contributions to psychiatric care.

An Accidental Discovery

The search for a cure for schizophrenia became the Holy Grail of world psychiatric research in the early 20th century. Worcester State Hospital (Massachusetts) statistics for 1929-1930 reflect the immense therapeutic challenge of patients with schizophrenia. Eighty-three of 414 first-time admissions (20%) had the diagnosis of dementia praecox schizophrenia). Of readmissions, 36 of 86 (42%) were people with schizophrenia. Of those who died in the hospital, 42 of 202 (21%) carried a diagnosis of schizophrenia. And of those patients with schizophrenia who died, 50% had been in the hospital 20 or more years!1 Even accepting the tendency at the time to make the diagnosis of schizophrenia, a significant number of psychiatric institutionalized patients were people with schizophrenia.

To a world crying out for a treatment for schizophrenia came Manfred Joshua Sakel, MD, from Vienna. Dr. Sakel, described as “a strange, withdrawn, and sometimes difficult man,” was working at a Berlin addiction sanatorium catering to artists, actors, and physicians.2 In the course of treating a well-known diabetic actress in 1927, he accidentally put her into a mild insulin coma. This produced in her a remarkable diminution in her opiate craving. He reasoned that an insulin coma could reduce the excitement during morphine withdrawal.

Dr. Sakel published his research on curing morphine addiction with insulin coma in 1930. By then he had been putting patients with addiction and psychosis into deep hypoglycemic coma and having them reemerge into consciousness, as this treatment resulted in marked improvement of their psychotic symptoms. Following initial animal experiments, Dr. Sakel started treating psychotic patients with deep insulin coma, with good results. By 1933 he had moved to the Neuropsychiatric University Clinic in Vienna, and in 1934 and 1935 published 13 reports indicating an 88% improvement rate for patients with schizophrenia treated with insulin coma. This was an outstanding result and was eagerly received by both the psychiatric community and the general public.

How It Worked

A patient was started on a small dose of insulin, such as 20 units, and this dose was increased for each session until a full coma for at least one hour was achieved. Although insulin was administered subcutaneously in the early years, it later became the practice to administer insulin and glucose (which ended the coma session) intravenously for more accurate control over the coma state.

Insulin coma therapy was felt to be most effective when the patient went into a stage three coma, i.e., loss of corneal and deep tendon reflexes. The patient was allowed to remain at this level for one to five hours before being given carbohydrates slowly via a stomach tube or intravenously to be gradually aroused.

Although the minority, some patients experienced seizures while in a hypoglycemic state. Some therapists felt that this was desirable, causing marked improvement. Others were wary of the possibility of neuronal damage and felt that seizures should be avoided. Interestingly, a survey of geriatric patients with schizophrenia who had been institutionalized for a long time, published in 2000, found no difference in cognitive decline between patients who had received insulin coma therapy in earlier years and those who had not.3 In fact, a study in 2004 demonstrated it would take a flat EEG, caused by prolonged hypoglycemia (fewer than 18 ml/dl of glucose), to result in neural injury, and this was below the level used in insulin coma therapy.4

Patients received insulin coma therapy three to five times a week and received around 50 treatments in a series. Upon awakening from a coma, a typical patient felt hungry, asked for food, and was no longer aware of delusions. The fatality rate varied from 1 to 10%. A typical patient might experience complete relief of symptoms during and after a course of treatment, only to relapse gradually over the subsequent months, perhaps requiring retreatment.

Waxing and Waning Interest

The publication of Dr. Sakel's work and visiting psychiatrists’ direct observations led to the widespread adoption of insulin coma therapy. By May 1936 the successful use of insulin coma therapy in 22 countries was reported to the Swiss Psychiatric Society.5 In the United States by the early 1940s there were three major treatments for patients with schizophrenia: insulin coma therapy, Metrazol, and electroshock therapy. Between 1935 and 1941, in 305 psychiatric hospitals, at least one of the three therapies had been administered to 75,000 patients; 54% of all American mental institutions offered insulin coma therapy during these years.6