The question now arises as to whether we can conceive the communication of such traumatic and therefore acquired epilepsy to the germ-cells. This is obviously impossible under the epigenetic theory of development described above. In what way can the germ-cells be affected by molecular or histological changes in the pons varolii and medulla oblongata? Even if we assume, for the sake of argument, that the central nervous system exercises trophic influences upon the germ-cells, and that such influences may consist of something more than variations in nutritive conditions, and may even include the power of altering the molecular constitution of the germ-plasm in spite of its usual stability; even if we concede these suppositions, how is it conceivable that the changes produced would be of the exact nature and in the exact direction necessary in order to confer upon the germ-plasm the molecular structure of the first ontogenetic stage of an epileptic individual? How can the last ontogenetic stage of the ganglion cells in the pons and medulla of such an individual, stamp upon the germ-plasm in the germ-cells of the same animal—not indeed the peculiar structure of the stage itself—but such a molecular constitution as will ensure the ultimate appearance of epilepsy in the offspring? The theory of epigenesis does not admit that the parts of the full-grown individual are contained in the germ as preformed material particles, and therefore this theory cannot allow that anything is added to the germ-plasm; but in accepting the above-made supposition, we are compelled to assume that the molecular structure of the whole of the germ-plasm is changed to a slight extent. Nägeli is quite right in maintaining that the solid protoplasm alone, as opposed to the fluid part, i.e. that part of the protoplasm which has passed into solution, can act as the bearer of hereditary tendencies. This appears to be undoubtedly proved by the fact that the amount of material provided by the male parent for the development of an embryo is in almost all animals far smaller than the amount provided by the female parent. In Mammalia the share contributed by the father probably only forms about one hundred-billionth part of that contributed by the mother, and yet nevertheless the influence of the former in heredity is on an average equal to that exerted by the latter[225]. Now, from the point of view of epigenesis, no molecule of the brain of an epileptic animal can reach the germ-cell except in a state of solution, and therefore no direct increase in the germ-plasm can be referred to such molecules, quite apart from the fact that such addition, even if possible, could not be of any value, because the last stage of the epileptic tendency must be represented in the nerve-cells and nerve-fibres of the diseased brain, while the first stage ought to be represented in the germ-cell.