The peripheral action of tetanus toxin

IT was noted very early in the experimental work on tetanus toxin that when one of the extremities of an animal received an injection of the toxin subcutaneously, intramuscularly or intraneurally, the limb became rigidly extended after an interval of 1-4 days. This rigidity was found to occur in the absence of other manifestations, and, if the dose injected was not too large, the muscles eventually regained their normal state. This interesting phenomenon has been called local tetanus, and it can hardly be distinguished from the unremitting closure of the jaws which is so characteristic of the generalized disease in man. Meyer and his co-workers [1903, 1916] believed that this state of continuous, but strictly localized, rigidity was brought about by the action of the toxin on central neurons, just as are the tactile reflex spasms and convulsions of the more generalized form of the disease. They supposed that the toxin was carried in the motor axis cylinders to the motor neurons of the central nervous system after its absorption by the motor nerve terminals of the skeletal muscles. These conceptions were quite generally accepted until the recent series of experiments carried out by Abel and his colleagues [cf. Abel, Firor & Chalian, 1938], which show quite clearly that there is no evidence that tetanus toxin reaches the central nervous system by any way other than the blood stream. In their view, the symptoms produced by tetanus toxin are due to a twofold action: (1) a peripheral action, in the region of the motor end-plates of the muscles, which the injected toxin reaches directly, resulting in an enduring, local muscular rigidity; and (2) a fixation to the anterior horn cells of toxin, reaching them through the circulation, resulting in the appearance of reflex motor tetanus without any constant rigidity. A full account of this controversy and the experimental facts relating to it may be found in the many papers from Abel's laboratory.