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The syndrome of prolonged coma is a phenomenon occasionally encountered during the course of insulin therapy as used in selected cases of schizophrenia. It is a complication which becomes obvious when the induced hypoglycemia is terminated by the administration of dextrose in quantities sufficient to bring about hyperglycemia. The picture differs from that of the usual uncomplicated recovery which follows the hypoglycemic state in that its criteria are:(1) normal blood sugar or induced hyperglycemia; (2) a shifting neurologic picture; (3) peripheral manifestation of fluctuant control of the autonomic nervous system, such as alterations in regulation of heat, disturbances in cardioregulatory function, sudomotor hyperactivity and hyperpnea, with consequent tetany; (4) convulsive phenomena or their equivalents; (5) prolonged coma, and (6) associated with recovery of consciousness, disturbances in the sensorium, alterations in memory function and a quantitative reduction in all higher cortical functions. The last-mentioned psychopathologic residua reflect the widespread cytologic changes which are demonstrable histologically in the brain tissue.We have correlated certain observations in an attempt to explain the occurrence of prolonged coma on a physicochemical basis.We suggest a mechanism for insulin shock which is based on the assumption that the demonstrable histopathologic and physiologic changes which accompany hypoglycemia induced by large doses of insulin may be explained on a basis of physical, biochemical and colloidal changes. We believe that, as a result of certain physicochemical processes, there is progressive cellular hydration. We conceive this process to be a reversible one, dependent on certain vari¬ ables and accomplished by the restoration of the normal dextrose substrate. However, if this point of simple reversibility is passed, additional agents must be employed to restore the cellular balance, and in cases in which the progressive hydratien has been excessive all efforts at resto¬ ration of normal cellular function fail and death of the cell follows. The location, the size and the From the Markle Unit of the Pennsylvania Hospital. phase of the lesion, we believe, determine the variable and shifting neurologic picture, as well as the morbidity and the mortality rate.CLINICAL CONSIDERATIONS < In this presentation of 51 periods of prolonged coma occurring in 38 patients, it must be emphasized that all patients received a solution of dextrose intravenously in sufficient amounts to raise the blood sugar to a normal level or above ; with the majority of the patients this was con¬ firmed by determination of the level of the * blood sugar. If the patient failed to respond, pro¬ vided his blood sugar was normal or above, and a sufficient period of time (fifteen to twenty minutes) had been allowed for the cellular utili¬ zation of the dextrose, the condition was judged to be prolonged coma. Excellent clinical descriptions of this complication have been given Goldman,5 in a series of 108 patients, reported...

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