Update on equine neurologic diseases (Proceedings)

In the field of equine neurology, there has been the discovery of a few new disorders, in addition to some newer diagnostics, and/or therapeutics.

Parelaphostrongylus tenuis infection in young horses is a recently reported neurologic disease of horses. In areas of North America that routinely diagnose P. tenuis in small ruminants and camelids, infection in the horse should be considered and will be seen!. The clinical sign of acute onset scoliosis is nearly diagnostic for the equine disease. Affected horses have been 6 mo-3 years of age. The parasite appears to have a migratory predilection in the horse for the dorsal gray column of the cervical and sometimes thoracic cord. If the lesion extends three or more vertebral segments, acute onset scoliosis with the head deviated away from the lesion side will occur. Hypalgesia to analgesia will be found on the affected (convex) side over the affected segments. There may be very mild ataxia and paresis of the limbs on the affected side. In the few cases we have performed CSF collection and evaluation on, the results were unremarkable, unlike P. tenius in small ruminants and camelids. The signs are characteristic enough in horses in an endemic area to make the diagnosis. Initially, there is no pain in manipulation of the neck, but after several weeks, arthritic changes develop. Treatments have included high doses of ivermectin and steroids, but lesions have been so advanced that successful treatment does not seem possible. Some clients have worked with physical therapists to provide exercises and braces in hopes of a return to normalcy, but this has been uniformly unsuccessful.

Temporohyoid osteoarthropathy is now one of the more common neurologic disorders we see in the horse. Since 2000, we have examined 24 horses with this condition. The etiology of this arthritic disease is unknown, but previous otitis interna/media is generally blamed. A small number of cases have active infection (mostly gram positive cocci and one case aspergillus). The disease is most common in middle age horses, youngest being 3 years of age, and approximately 40% have bilateral disease, although the clinical signs are almost always unilateral. The signs are variable with some horses having behavioral signs associated with being ridden or while eating; these are likely signs of pain. Acute onset of neurologic signs are believed to occur when the fused T-H joint fractures. Fractures may be associated with sudden movements of the head and have been repoted in horses being tubed or after dental procedures. Clinical signs are those associated with cranial nerve VII and/or VIII dysfunction. Diagnosis is by signs, endoscopy of the guttural pouch, radiographs or computed tomography. CSF can be inflammatory in approximately 25% of cases and in a rare case, septic (consider Staph aureus). Treatment goals are directed towards decreasing inflammation and infection, if present, and preventing complications, of which exposure keratitis is perhaps the greatest. Approximately 50% of the horses return to use. Unfortunately, we are not able to predict clinical response at the time of the initial diagnosis! We have routinely recommended a ceratohyoidectomy for both patient comfort and to prevent further fractures at the fused T-H joint(s).

Diagnosis of cervical vertebral compressive myelopathy (CVCM) continues to be an area of investigation. Intra-vertebral ratios on plain cervical films has proven to be the screening test of choice for most clinics, but sensitivity and specificity of the test are variable between clinics/radiologist reading the films, and there is poor correlation between the site of the abnormal ratio and the lesion site. Since the site of cord compression is often inter-vertebral rather than intra-vertebral in horses, an additional inter-vertebral measurement has been recommended. The inter-vertebral measurements more accurately reflect specific site(s) of compression and location and number may affect decisions to proceed with a myelogram and possibly surgery. Recently, we have even questioned the accuracy of the 50% reduction in the dorsal myelographic column for diagnosis of CVCM. Accuracy of this criteria seems to vary with vertebral site, C5-C7 being most accurate. Measurement of the reduction in dural diameter at the inter-vertebral sites in comparison to adjacent mid-vertebral body dural diameter might be more accurate for compression in the mid-cervical region.

Additional diagnostics for EPM have been recently published. If veterinarians are only testing serum as a screening test for EPM, the IFA test may be the preferred test. Titers > 160, with compatible history and clinical signs indicate a moderate or higher probability of EPM. Racing and western performance horses have been found to be at increased risk of EPM. Intermittent treatment of at risk horses has been evaluated as a means of preventing CNS infection with S. neurona. Administration of ponazuril every 7 days has some efficacy. This time frame corresponds with recent research that investigate the kinetics of S. neurona invasion in the horse.

Recently, we have described a syndrome of symmetrical tetraparesis and ataxia and cervical pain associated with epidural hematoma (no known trauma) at C5-C6. The onset is acute and severity of signs are often 3 to 4/5 ataxia. Cause of the hematoma is unproven, but should be included in the differential diagnosis of horses with these signs. Pathophysiology, diagnosis, treatment, and prognosis will be discussed. Additional equine neurologic diseases that appear on PubMed since 2006 and will be discussed include ivermectin toxicity, hyperammoniaemia, equine motor neuron disease, fluphenazine adverse effects, and traumatic brain injury.

References

Cohen N.D. et al. A multicenter case-control study of risk factors for equine protozoal myeloencephalitis. J Am Vet Med Assoc 2007;231(12):1857-1863.

Duarte, P.C., Ebel E.D., Traub-Dargatz, J., Wilson, W.D., Conrad, P.A., and Gardner, I.A. Indirect fluorescent antibody testing of cerebrospinal fluid for diagnosis of equine protozoal myeloencephalitis. Am J Vet Res 2006;67(5):869-876.

Elitsur, E., Marsh, A.E., Reed, S.M., et. al. Early migration of Sarcocystis neurona in ponies fed sporocysts. J Parasitol 2007;93(5):1222-1225.

Feary, D.J., Magdesian, K.G., Aleman, M.A., and Rhodes, D.M. Traumatic brain injury in horses: 34 cases (1994-2004). J Am Vet Med Assoc 2007;231(2):259-266.

Hahn, C.N., Handel, I., et.al. Assessment of the utility of using intra- and intervertebral minimum sagittal diameter ratios in the diagnosis of cervical vertebral malformation in the horse. Vet Radiol Ultrasound 2008;49(1):1-6.

Levine, J.M., Adam, E., MacKay, R.J., Walker, M.A., Frederick, J.D., and Cohen, N.D. Confirmed and presumptive cervical vertebral compressive myelopathy in older horses: a retrospective study (1992-2004). J Vet Intern Med 2007;21(4):812-819.

Mackay, R.J., Tanhauser, S.T., Gillis, K.D., Mayhew, I.G., Kennedy, T.J. Effect of intermittent oral administration of ponazuril on experimental Sarcocystis neurona infection in horses. Am J Vet Res 2008;69(3):396-402.

Orsini, J.A. (ed). Clinical Techniques in Equine Practice: Neurology. 2006;5(1).

Mohammed, H.O., Divers, T.J., Summers, B.A., and de Lahunta, A. Vitamin E deficiency and risk of equine motor neuron disease. Acta Vet Scand 2007;49(1):17.

Tanabe, M., Kelly, R., de Lahunta, A., Duffy, M.S., Wade, S.E., and Divers, T.J. Verminous encephalitis in a horse produced by nematodes in the family protostrongylidae. Vet Pathol 2007;44(1):119-122.