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Published Online: September 1939

THE MECHANISM OF THE SYMPTOMS OF INSULIN HYPOGLYCEMIA

Publication: American Journal of Psychiatry

Abstract

1. Simultaneous observations of clinical symptoms, cerebral oxygen utilization, blood sugar level and electrical activity of the brain were made on patients with schizophrenia receiving the insulin treatment.
2. Blood sugar decreases during the first hours after the injection of insulin and then remains at a low level until termination with sugar while the clinical signs continue to develop progressively throughout the entire course of hypoglycemia.
3. The march of the symptoms is correlated with a gradual decrease of cerebral oxygen uptake and the electrical changes.
4. The regression of the symptoms is accompanied by a gradual increase of the oxygen uptake and a reduction of the delta index. The sequence of the symptoms during regression is in an order which is the reverse of their appearance.
5. During hypoglycemia the alpha waves disappear approximately at the time when the functions of the cortex are completely suppressed and reappear with the restoration of cortical functions.
6. It is therefore, concluded that as a result of the hypoglycemia caused by the administration of insulin the metabolism of the brain is diminished. This reducton of cerebral metabolism is the cause of the clinical symptoms as well as the alterations of the cerebral electrical activity of the brain.
7. These conclusions concerning the correlations between the clinical and physiological changes are to be regarded only as a working hypothesis because of the small number of the experiments performed.

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Go to American Journal of Psychiatry
Go to American Journal of Psychiatry
American Journal of Psychiatry
Pages: 371 - 385

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Published in print: September 1939
Published online: 1 April 2006

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H. E. HIMWICH
The Departments of physiology and pharmacology and neurology and psychiatry, Albany Medical College, Union University, Albany, New York, the biological laboratories, Clark University, Worcester, Massachusetts, and Harlem Valley State Hospital, Wingdale, New York.
J. P. FROSTIG
The Departments of physiology and pharmacology and neurology and psychiatry, Albany Medical College, Union University, Albany, New York, the biological laboratories, Clark University, Worcester, Massachusetts, and Harlem Valley State Hospital, Wingdale, New York.
J. F. FAZEKAS
The Departments of physiology and pharmacology and neurology and psychiatry, Albany Medical College, Union University, Albany, New York, the biological laboratories, Clark University, Worcester, Massachusetts, and Harlem Valley State Hospital, Wingdale, New York.
Z. HADIDIAN
The Departments of physiology and pharmacology and neurology and psychiatry, Albany Medical College, Union University, Albany, New York, the biological laboratories, Clark University, Worcester, Massachusetts, and Harlem Valley State Hospital, Wingdale, New York.

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