Facts are wanting with regard to these lesions in the domestic animals, but anatomical, physiological and pathological consideration are strongly suggestive of their occurrence. The vascular network of the spinal cord favors a tardy circulation, and this in turn is favorable to the arrest of solid bodies and the delay, proliferation and colonization of microbes. The median spinal artery receives a supply of blood by two trunks, right and left, entering by the intervertebral foramina at each intervertebral articulation. It has not, therefore, one continuous, equable, onward flow, but rather numerous independent currents corresponding to the entering vessels, and with intervening eddies or areas of comparative stagnation. The nervous material of the cord admits no large arteries but only capillary trunks which anastomose freely in its substance. This would seem to entail a sluggish flow, which would favor microbian arrest and colonization, even if the small size of the vessels serves to shut out clots of any material size. Finally the abundant venous plexus, and especially the two lateral venous sinuses, communicating freely with each other and, through each intervertebral foramen, with the extra spinal veins determine a similar tardy flow that should be favorable to morbid processes. If we pass back of these vessels, we find the posterior aorta to be at once the largest and the most direct channel for the entrance of emboli coming from the left heart or lungs. This danger is counteracted in greater part by the fact that the greater part of this blood passes into the large vessels which supply the liver, spleen, kidneys, stomach, bowels, and hind limbs, and while embolism is well known in these parts it has not been demonstrated as yet in the spinal cord. The toxins produced in infectious diseases and circulated in the blood can often lead to destruction of the endothelium, and inflammation of the deeper structures. In this way any circulating microbes find a ready infection atrium. Hektoen seems to have demonstrated this in the case of tubercular meningitis. By pressure of the neoplasm on the vessel or by fibroid thickening and contraction of the walls of the vessel, the subsidiary cord is denied its full supply, and degeneration of the nervous substance is invited. In the human subject degeneration of the cord has been shown to follow the line of such diseased arteries. Thrombosis follows in every case in which the serous coat is involved, and embolism can easily occur from clots small enough to enter the capillary vessels. Lamy’s experiment of blocking the small arteries with inert powder, shows that this will give rise to foci of hemorrhagic softening, which commence in the gray substance. The blocking, however, must be multiple to produce any material effect, as the free anastomosis of the spinal capillaries otherwise secures an abundant blood supply to adjacent parts. In case of an infective