Abstract
Both the immediate cause and seat of tetany are still obscure. It has been suggested, though never proven, that a poison must circulate in the blood to cause the tetanic twitchings. It has also been suggested that these twitchings may result from a lack of calcium in the circulating fluids. It has been shown that tetany does not appear in a limb to which the nerves have been cut. It is conceivable that this is due to the fact that no impulses reach that limb from the spinal cord. The present experiments show that if the nerves be cut during tetany, their electrical excitability remains the same as that of the intact nerves on the opposite side. Further, it is shown that if the nerves be cut before the development of tetany, they become hyperexcitable to an extent which equals that of the intact nerve on the opposite side, although they are quite separate from the spinal cord. Since degeneration occurs within two or three days, such observations must be made with due regard to this fact. The peculiar character of this rise in the excitability is seen in the figures obtained for the cathode and anode opening shocks to which the nerves become especially excitable. In complete anemia or after the death of the animal there is a period of about one half hour during which this characteristic rise in the excitability of the nerve to the cathode and anode opening shocks appears. Nevertheless, the excitability of the nerves is, throughout this period, very much lowered and the curve is in no way comparable, therefore, to that in tetany.
Transfusion of the blood of an animal in tetany into the vessels of a normal animal has not succeeded in producing a characteristic tetany nor even a marked change in the excitability of the nerve.
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