The supersensitivity of chronically “isolated” cerebral cortex as a mechanism in focal epilepsy

Abstract 1. 1. A technique is described of neuronally isolating an area of cerebral cortex through small stab wounds in the dura mater. This method, a modification of that described by Kristiansen and Courtois 1949, has largely avoided the formation of subdural adhesions and has made it possible to obtain electrocortigrams, in 100 monkeys and 3 humans, at a second operation 2 weeks to 3 1 2 years later, with little injury to the cerebral cortex or pial circulation. 2. 2. “Spontaneous” electrical activity was present in chronic completely neuronally isolated cerebral cortex provided the circulation was adequately maintained (20 monkeys and 2 human preparations) (Echlin et al. 1952; Echlin and McDonald 1954; Grafstein and Sastry 1957). This electrical activity was unstable. abnormal in appearance, often paroxysmal, and bore little resemblance to that recorded from normal cerebral cortex. 3. 3. The resting electrical activity from small blocks of chronically partially isolated cerebral cortex was similar to that usually regarded as characteristic of epileptogenie cortex (Echlin et al. 1952; Echlin 1953; Echlin and McDonald 1954). 4. 4. The nerve cells in areas of chronically “isolated” frontal or parietal cerebral cortex became supersensitive to topically applied acetylcholine (Echlin 1954; Echlin and McDonald 1954; Spiegel and Szekely 1955), eserine and electrical stimulation. The topical application of acetylcholine 0.2 to 0.5 percent widely to the cerebral cortex in such chronic preparations precipitated discharges of rhytmic wave and spike epileptiform electrical activity selectively from the “isolated” area in 90 per cent of the 80 animals and in the 1 human studied. The local use of 1 per cent acetylcholine or of 1 per cent eserine followed by 0.2 to 1 per cent ACH resulted in a spread of the epileptiform rhythmic potentials from the partially isolated zone to the motor cortex and clonic seizures and, less often, generalized electrical and clinical convulsions. 5. 5. In contrast to these findings 0.2 to 0.5 per cent acetylcholine never caused epileptiform electrical discharges when applied topically to the unanesthetized frontal or anterior parietal cortex of normal monkeys (9 preparations) or to the hemisphere homologous to one containing a chronically “isolated” block of grey matter (10 preparations). 6. 6. Evidence is provided that the “isolation factor” rather than injury or ischemia is the important factor in the causation of the supersensitivity of chronically neuronally “isolated” cerebral cortex (Echlin 1956). 7. 7. Characteristics bursting was present in electrocorticograms from the partially isolated cerebral cortex overlying and surfounding brain tumors. The bursts appeared in the EEG as slow waves. It is again suggested that EEG as slow waves. It is again suggested that at least some of the slow waves in the EEG from around brain tumors are the result of the partial isolation of cerebral neurones (Echlin et al. 1952). 8. 8. Acute surgical “isolation” of a temporal lobe spike focus in an epileptic patient caused an activation of the electrical focus. 9. 9. It has been demonstrated that chronic partially isolated human or monkey cerebral cortex has many properties, characteristics and reactions commonly regarded as characteristic of epileptogenic cortex. It therefore seems probable that chronic partial isolation of cerebral neurones by scar tissue, brain tumor, or other pathology, is an important factor — if not the basic factor—in the causation of focal epilepsy.