Margaret A. Lennox

Cingulate-cerebellar mechanisms in the physiological pathogenesis of epilepsy☆

Abstract 1. 1. The effects of electrical stimulation of the anterior cingulate gyrus are described. 2. 2. Respiratory, motor and electroencephalographic effects are observed and include suppression and facilitation in each category. Respiratory effects consist of arrest and hyperpnoea. Motor effects consist of arrest of spontaneous motor movement and facilitation in the form of a jerk of the muscles of the face. With increasing intensity of stimulation, the jerking involves progressively the muscles of the neck, forelimbs, trunk and hindlimbs, in that order. 3. 3. Electroencephalographic suppression has been reported in detail previously. An after-discharge may also be produced by stimulation of the anterior cingulate gyrus but not of the pre- or sub-callosal areas nor of the posterior cingulate gyrus. Optimum parameters of stimulation are: frequency — 30 per sec., pulse duration — 11 to 16 msec. and intensity — 2 to 3 volts. The stimulus is applied for 10 sec. and the after-discharge persists 5 to 30 sec. after cessation of stimulation. It usually shows a characteristic 3 per sec. spike and wave configuration, although the rate may be 12 to 18 per sec. It is transmitted preferentially to the cerebellum where it may be amplified and at a faster rate. It is seen less often in the lateral cerebral hemispheres, has been recorded from the hippocampal formation, or may remain localized. 4. 4. Electrical stimulation of the uncus elicits local after-discharge which spreads preferentially to the temporal tip and posterior orbito-frontal areas, but may involve the anterior cingulate gyrus and cerebellum as well. 5. 5. Electrical stimulation of the cerebellum does not elicit local or transmitted after-discharge. 6. 6. Dilantin elevates the threshold of motor cortex to the point of unresponsiveness at maximal stimulation but does not alter the threshold of the anterior cingulate gyrus. Tridione elevates the treshold of the motor cortex and of anterior cingulate gyrus slightly. 7. 7. The similarities are reviewed between the effects of stimulation of the anterior cingulate gyrus and the clinical seizures of the petit mal triad. It is suggested that petit mal triad seizures are attributable to discharge in a system which includes the anterior cingulate gyrus and cerebellum as well as the anterior and mid-line thalamic nuclei. 8. 8. A functional integration in this system of the hippocampal formation and entorhinal areas afferent to it is suggested.

Electroencephalographic study of experimental cerebro-vascular occlusion

It was possible to follow the changes in the electroencephalogram during a protracted period in a group of 29 dogs in whom the middle cerebral artery had been clipped to its origin. A slight variation in the location of the clip was unavoidable but useful in that the size of the resulting infarcts differed. Massive lesions included the cortex in the fronto-temporo-parietal region, the striatum, the internal capsule and the anterior portions of the thalamus and, rarely, the hypothalamus. The majority of lesions were confined to the internal capsule and to the caudate nucleus. The clinical syndrome consisted of a contralateral spastic hemiparesis with the loss of the placing reaction and of position sense. Forced circling movements occurred towards the side fo the lesion, persisting even after blindfolding the animal. The changes in the electroencephalogram varied with the size of the lesion. In the scalp to ear records, slow frequencies were most conspicuous over the involved hemisphere in all types of recordings and were most prominent in recording to the contralateral ear. In the scalp to scalp records, flattening was evident over the frontal and temporal regions and slow frequencies were conspicuous posteriorly. Flattening was found over the entire hemisphere only in the most massive lesions and then in both types of recordings. The scalp to scalp records tended to become more symmetrical after two to three weeks, the flat tracings being replaced at times by high voltage slow frequencies. The abnormalities in the scalp to ear records tended to persist for the duration of the experiment. Flat records were obtained in the electrocorticogram overlying the area of infarction, and high voltage slow waves were found in the peripheral zone. Using the multipolar needle electrodes, an unusually low voltage to flat records was obtained from the depths of the lesion. A fairly constant change was the loss of the high voltage 10-12 per sec. spindles from the fronto-central scalp electrodes and from electrodes placed on the sigmoid gyri. The sleep records were far superior to the waking records as a diagnostic aid, the latter being of value only during the first post-operative week.