Cerebral Hypothermia by Ventricular Perfusion

Entire cerebral ventricular system was perfused with cold Ringer's solution on dogs from either side of the lateral ventricle to the cisterna magna. Under suitable condition for the perfusion dogs became unresponsive to the external stimuli after ten to thirty seconds of cooling. In the course of perfusion, respiration became slow and deep with a tendensy to slight bradycardia, and blood pressure was lowered, while rectal temperature remained unchanged throughout. With a lapse of ten to thirty seconds after the cessation of perfusion, dogs returned completely to their previous state, and acquired no pathological signs. In the control experiments, dogs perfused with warm as well as hot Ringer under the same conditions did not show such unresponsive state and physiological changes. In the use of saline, however, convulsions and other pathological symptoms were recognized. Measurement of brain temperature during the cooling revealed that the decrease in temperature of the brain matter was remarkable and rapid in the thin layers under internal wall of perfused ventricles, especially in the hypothalamus and circumference of the aqueduct of Sylvius, whereas in the cortical and subcortical tissues the temperature remained almost equal to the body temperature. From the results of the localized cooling per fusion by several routes of flow, the lateral and fourth ventricles might be dismissed from the essential mechanism of unresponsiveness which was elicited only when the third ventricle and the aqueduct was effectively cooled. In the electroencephalographic study, basic patterns of EEG activity were altered neither in the cortical area nor deep in the thalamus even if the responsiveness was lost under ventricular cooling. Intrathalamic responses to the repetitive electrical stimuli to the medial thalamus were not diminished under such condition. However, the responses on the EEG and EMG to the pinching animal's nose were completely abolished during such state of unresponsiveness. Postoperatively dogs survived without any neurological defects or symptoms. Electron microscopical study of the postoperative brain demonstrated merely slight cerebral edema occurred in the periventricular tissue. From these results, it is confirmed that the initiation of experimental unresponsiveness can be produced by the cooling perfusion of cerebral ventricular system under adequate conditions. As for such acquired unresponsiveness, only the hypothermic effect against the ventricular wall is possibly responsible for it. Accordingly, it is surmised that the interception of neuronal transmission on the thin layers under the internal wall of the third ventricle and aqueduct of Sylvius caused by the cooling may play an important role in this unresponsiveness. Cooling ventricular perfusion was carried out on three psychiatric patients with violent behavior under a therapeutic expectation. After the maneuver, all of them became docile and epileptic seizures were subsided effectively. This technique is considered to be feasible and efficacious method as an attempt to treat unmanageable cases in the neurological and psychiatric clinic.