By some unaccountable oversight (not smart maybe) stringhalt was not included in our text, Equine Pathology. I should like to make up that deficit here with such thoughts as I have on this sometimes perplexing condition.
There appear to be four forms of stringhalt. The clinical signs are apparent to all and shall not be belabored here.
1. Australian stringhalt: A number of horses of any age are afflicted in a given pasture. The stringy gait is almost invariably bilateral and disappears if the animals are removed from pasture. The cause, still incompletely defined, seems to be a type of dandelion. I have had no experience of this condition and have not reviewed the more recent literature which I shall leave to the interested reader.
2. Pseudostringhalt: Actually there is nothing pseudo about this. It is quite genuine, unilateral, and caused by painful lesions anywhere in the affected hindleg but usually the more distal part of the leg. It seems evident that the pain as the leg comes into support causes a sudden, reflex withdrawal of the foot from the surface. With removal or melioration of the cause, the stringhalt disappears.
3. Unilateral stringhalt: This affliction of one hindleg is not associated with 2. There is no clinical explanation for the cause, and it is often though not invariably relieved by section of the lateral extensor tendon. I have seen perhaps a dozen horses at postmortem with this condition and have had reports from other pathologists of a number of other cases. Most, but not all, cases are in older horses.
In all of these cases there has been a compressing or entrapping lesion of the obturator nerve on the affected side. In some cases that lesion has been an osteophytosis in and around the acetabular notch (with no explanation of the cause of that lesion in some cases but healed acetabular fracture in others). In other cases there has been infiltration and/or compression of the obturator nerve by melanoma.
The following hypothesis is taken from my Biomechanics of Lameness in Horses published in 1969. That book is no longer in print. Since the hypothesis developed there still seems valid, I repeat it here.
A hypothesis is suggested together with the observation of Vaughn in cattle (quoted by Palmer 1965). It is interesting to note that at the time of experimental neurectomy of the obturator nerve, pinching the intact nerve caused flexion, with the limb held quivering in mid-air, a phenomenon also seen by the author in some post-parturient cattle during progression.
Let us assume a lowered threshold of excitability (increased excitability) of the obturator nerve because of the damage to the nerve by osteophytes or tumor. Proprioceptive impulses from the stifle joint may well be among those which inform the central nervous system that the support phase of the stride has been completed and protraction should begin. Stringhalt is basically a spastic, exaggerated protraction movement.
Many proprioceptive impulses probably arise from the collateral ligaments of the stifle joint. The lateral extensor muscle is the only muscle of the gaskin which is attached to the lateral collateral ligament. Hoffman 1953 demonstrated branches of the obturator nerve to the medial collateral ligament of the stifle.
If we take it, then, that there is a lowered threshold for firing of proprioceptive impulses from the ligaments of the stifle because of damage to the obturator nerve, we can assume that the central nervous system receives information that the leg should be protracted before that is in fact the case. The result is the sudden jerking of the leg into protraction. The surgical severing of the lateral extensor tendon could have its salutary effect by reducing tension in the collateral ligament and so reducing the overall rate of proprioceptive signals from the stifle. Failure of that surgery might be attributable to such a low threshold for the obturator that the total signal load cannot be reduced sufficiently.
4. Bilateral stringhalt: In theory the cause for unilateral stringhalt could be operating bilaterally in any given case. In practice, however, I have never encountered not heard of such a case. Indeed I have only seen, at postmortem, two cases of bilateral stringhalt both in aged horses. Postmortem examination did not reveal gross or microscopic lesions of the obturator nerve. The significant postmortem findings in both cases were in the thalamus.
In one case the thalamic lesion was a large area of hemorrhage and necrosis caused by the migration of Strongylus vulgaris larvae. The onset of clinical signs was abrupt and lasted only for several days when the animal had to be put down.
In the second case the thalamus on section was a dirty, translucent yellowish-amber color. Histologically, there was the typical siderofibrosis of multiple blood vessels frequently seen in the thalamus of older horses. In this case the siderofibrosis was more severe than any I had seen or have seen since. It was accompanied by diffuse demyelination and gliosis.
The hypothesis, or at least the suggestion, can be made that since the thalamus is the central receiving area for sensory information from the periphery, damage to the thalamus could provide a central lowered threshold for proprioceptive signals as the damaged obturator nerve provided a peripheral lowered threshold.
Clearly, there is a great deal of speculation here and a shortage of cases and facts. I trust that this narrative can be justified, however, by encouraging others to look for the changes described. Despite a long career in the postmortem room, I saw all too few (for my taste!) cases of stringhalt, particularly bilateral stringhalt. Perhaps with a number of eyes looking, more could be learned and these hypotheses confirmed, rejected, or modified.
 Palmer A C Introduction to Animal Neurology. F A Davis, Philadelphia. 1965.
 Hoffman G. Beitrag zur Innervation des Kniegelenkes des Pferdes. Monatschrift Veterinärmedicin. 8:569. 1953.