Insulin Sub-Coma
Insulin coma therapy (ICT) came to the U.S. from central Europe at the end of the 1930s. It was introduced at the same time as convulsive therapy (ECT, electroshock). These were the first successful treatments for schizophrenia at a time when that diagnosis was associated with persistent psychosis, prolonged asylum incarceration, aggressive outbursts, suicide, and dementia.
The treatments were unpleasant and dangerous. They were given without anesthesia. The ICT mortality rate varied from 1% to 10% of patients treated. Prolonged coma, in which the patient did not respond to the administration of glucose, was a constant threat. ECT was safer, with lower mortality rates, but patients suffered fractures, severe memory loss, and spontaneous seizures.
The hormone insulin was discovered in 1922. It was quickly tested in patients suffering with illnesses for which no treatment was known. In Berlin, between 1928 and 1931, Dr. Manfred Sakel used insulin to reduce the anxiety, nervousness, tremors, vomiting, weight loss, and agitation of patients undergoing opiate withdrawal. With insulin, they became calm, gained weight, and were much more cooperative. At times, when the dose of insulin was high, the patient went into a coma. After such events, the patients were less argumentative, less hostile, and less aggressive.
A standardized treatment protocol was developed. Insulin injections led to two to three hours of low blood sugar levels. Insulin is a hormone that drives sugars from the blood to storage in the liver. When blood sugar levels fall precipitously, the brain cannot sustain consciousness and the patients become stuporous. The sequence of confusion, weakness, awkward walking, slurred speech, and stupor are occasionally seen when diabetic patients have an "insulin reaction," a sharp fall in blood glucose in response to too large a dose of insulin.
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