The Electroencephalographic Observations On Subjects With Marked Propagated Sensation Along Channels

Research Group of Acupuncture Anesthesia, Institute of Medicine and Pharmacology of Fujian Province, etc.

The paper is designed to observe the EEGs on 20 subjects with marked PSC. They were in-patients without any previous history of epileptic attack. The EEGs were recorded respectively according to the 10-20 electrode system and by serial setting of 4-5 electrodes at the cortical somatosensory areas corresponding to contralateral stimulation of acupuncture points. The routine EEG recorded included visual reaction, hyperventilation and flash-evoked test. Hegu, Neiguan, Zusanli, Yanlingquan, etc. were chosen for acupuncture. In some cases, EEG was recorded during the course of advancing and reflux process of PSC in different parts of the body. Data obtained did not show significant differences in the distribution of patterns, rates of alpha rhythm and types of visual reaction between marked PSC cases and normal subjects. All in all, epileptic form discharge, functional spike and other abnormal rhythm were not found, except in one case of cerebral thrombosis, the localized slow waves in EEG were noted. During PSC process, depressive reaction of alpha rhythm, synchronous response and enhanced somato-sensory activity of 18-20 rhythms per second were noted simultaneously. These reactions were normal in response to the external stimulation. During the advancing process or reflux PSC, the EEGs leading from somato-sensory area did not manifest the spreading of abnormal excitation. In accordance to previous reports, about 20% patients with epilepsy showed abnormal electrical activity through hyperventilation in EEGs. When patients were attacked with localized epilepsy, the topical or successive spreading electric activity in EEG was recorded, and the localized sensory  epileptic attack always developed into a motor or major attack when abnormal sensation reached the head. In our observations, none of these changes had been noted. According to the above data, it is impossible to suggest that PSC is a display of the localized sensory epilepsy, but of a normal sensation in some people. By means of EEG recordings, the above data cannot prove that PSC was secondary to the spreading of abnormal excitation in cerebral cortex, but because of the limitations of EEG technique, the above mentioned experiments require further study with improved methods.