Brain surgery . Fig. 39.—Superior Surface of a Brain of a Congenital Imhecile who had Hemi-plegia and Epilepsy. The entire right hemisphere is atrophied. C is the arach-noid, which was thickened and formed the wall of a cystic cavity in the hemi-sphere.—Ferraro. phy involves the anterior portion of the brain, andsometimes the entire hemisphere to a greater or lessextent. In the clinical cases of our third type thesclerotic atrophy involves the posterior and lateralparts of the hemispheres. It is not surprising that TREPHINING FOR IMBECILITY. 127 the variation in the situation should produce va
Brain surgery . Fig. 39.—Superior Surface of a Brain of a Congenital Imhecile who had Hemi-plegia and Epilepsy. The entire right hemisphere is atrophied. C is the arach-noid, which was thickened and formed the wall of a cystic cavity in the hemi-sphere.—Ferraro. phy involves the anterior portion of the brain, andsometimes the entire hemisphere to a greater or lessextent. In the clinical cases of our third type thesclerotic atrophy involves the posterior and lateralparts of the hemispheres. It is not surprising that TREPHINING FOR IMBECILITY. 127 the variation in the situation should produce varyingsymptoms, in view of the facts of the localization ofbrain-functions now known. That there should bea limitation of the sclerotic atrophy to certain lobesor regions—to the frontal, or central, or occipital, or. Fig. 40.—Superior Surface of the Brain of a Congenital Imbecile. The arach-noid being removed the porencephalic cavity is displayed. The cortex is whollydefective over the upper frontal and parietal lobes and the cavity in the hemi-sphere opens into the lateral ventricle at D, in which the choroid plexus, e, isseen. —Ferraro. parietotemporal regions—in various cases has led tothe hypothesis that the origin of the disease lay insome interference with the blood-supply of the part,since it has often been evident that the atrophy waslimited to the region nourished by blood reaching it 128 BRAIN SURGERY. through one arterial trunk. And this hypothesis hasbeen supposed to explain the pathogenesis of thesecases. Yet its weak point is the fact that at theautopsies the vessels usually show no evidences of dis-ease or of plugging, and the infrequency of vascularlesions in infancy cannot be denied. Schultze is doubt-less right in this matter in saying that the pathogene-sis of these defect
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