In the later stages the coronary enlargement is plainly seen to be due to an extensive formation of bone. It is, in fact, a reparative callus, and the reason it reaches so large a size is probably to be accounted for by the pull of the extensor pedis upon the detached pyramidal process. As might be expected, this displacement of the fractured portion, with its effect of giving greater length to the extensor pedis, leads to a backward displacement of the os coronæ upon the pedal bone. As a result there is a marked depression at the coronet, the depression being heightened in effect by the exostosis in front. Pyramidal disease is, as a rule, met with in the hind-feet, but occurs also in the fore.
Pathological Anatomy.—When occurring without fracture, the first observable change is a thinning of the articular cartilage of the pyramidal process, through which the bone beneath appears abnormally white. Later the thinning of the cartilage progresses until at last it becomes entirely obliterated. This destruction of the cartilage commences first at the highest point of the articular surface of the pyramid, and gradually reaches further backward into the joint. While this is taking place the new bone is being formed on the front of the os pedis, below and around the process, until, as we have already seen, an exostosis is formed, large enough to be noticeable at the coronet. This, of course, partly implicates the joint and the points of the insertion of the extensor tendon.
Finally, fracture may, or may not, take place. When it does, the exostosis is larger, and the general deformity of the hoof greater.
Treatment.—Ordinary treatment, such as point or line firing, repeated blisters, or hoof section, each of which we have tried, appears to be utterly useless. So far as we have been able to gather from the writings of other practitioners, however, neurectomy returns the animal for a time to usefulness. If the fore-limb is the seat of trouble, either plantar or median neurectomy may be practised; if the hind, then the best results are obtained by section of the posterior tibial.
Reported Cases.—1. This animal, a mare, had been rested for lameness behind for two or three weeks, and then sent out to work, going sound. This was repeated several times, and each time the coachman reported, "Goes very lame behind after she has been at work about fifteen to twenty minutes." She always pulled out sound when I saw her in a halter on the following day, so I had her ridden, and after about seven or eight minutes she began to go lame in a hind-limb. Her lameness got rapidly worse as she was being ridden, and within a quarter of mile of her first showing lameness, she dropped and carried the lame foot in a way that suggested a badly fractured pastern. There was no recognisable disease in the limb to account for this lameness.
'I divided the posterior tibial nerve, and she went back to work moving sound, and continued to work sound up to her death from one of the regularly fatal bowel lesions twist or rupture.
'She worked nearly two years after unnerving, and developed the usual thickening at the coronet.'[A]
[Footnote A: W. Willis, M.K.C.V.S., Journal of Comparative Pathology and Therapeutics, vol. xv., p. 366.]
2. 'The subject of this note was a chestnut mare, nine years old, and used for omnibus work.
'History.—For about two months the mare was lame on the off fore-leg, and in spite of treatment the condition became steadily worse. The off fore-foot was rather long and narrow, and the fetlock-joint was inclined to be bowed outwards, but the degree of lameness was out of proportion to these defects, and the diagnosis was obscure.