17-year-old, neutered male, quarterhorse, (Equus caballus).Horse developed severe atrophy of facial muscles on the left side of the face 2 months prior to presentation to the teaching hospital. The weekend prior to submission the patient developed rear limb ataxia. Probing palpation of the cervical region revealed hyperesthesia and hyper-responsiveness. Probing around the mid cervical region did not elicit a response. Treatment with dexamethasone yielded some improvement in clinical signs. The horse was euthanized at the owner elected request.

Gross Description:  

The muscles on the left side of the face were diffusely atrophied and hemorrhage was present in the anterior compartment of the right eye.  There was narrowing of the spinal canal between C2 and C3. The dura mater at the C2-C3 articulation was focally reddened. The third cervical vertebral body (C3) contained a 2.5 x 1.5 cm region of red and depressed tissue (bony sequestration) rimmed by thick white tissue (fibrosis) at its ventral border. The dorsal vertebral body of C2 also had a 1.5 cm linear band of firm white tissue (fibrosis) that traversed the bone in a dorsal-ventral direction.

Histopathologic Description:

Extending from just caudal of C1 to C5, there is a locally extensive area of rarefaction and multifocal to coalescing accumulations of glial cells and gitter cells, unilaterally involving the dorsal funiculus at the level of the gracile and cuneate fasciculi.  Spinal cord inflammation is most concentrated at C3 and includes significant perivascular cuffing, few to moderate lymphocytes and plasma cells and scattered eosinophils. The associated spinal gray column is unilaterally affected with similar inflammation in these sections. Numerous swollen axons (spheroids) are present at C2 and C3 spinal cord sections. At the level of C2, there are occasional glial nodules in the contralateral dorsal funiculus as well. Small numbers of lymphocytes and plasma cells are diffusely present in the meninges and are more concentrated over the dorsolateral funiculus. The dorsal spinal nerve root ganglia are infiltrated with small numbers of lympho-cytes and plasma cells at the level of C2 and C3. 

Cervical spinal cord (C1-C5): Meningo-myelitis, nonsuppurative and eosinophilic, unilateral, focally extensive, severe with spheroid formation, cervical spinal cord, dorsal funiculus.



Contributor Comment:  

The gross and histopathologic findings in this case are highly suggestive of cervical stenotic myelopathy. The unilateral distribution of the lesions coincides with the focus of stenosis observed in the spinal canal. Microscopic changes in the spinal cord include rarefaction, accumulations of glial and gitter cells, and lymphocytes, plasma cells, and scattered eosinophils.  The horse, in this case, was 17 years old, considerably older than the typical case of cervical vertebral stenotic myelopathy (8-18 months and 1-4 years of age). However, several retrospective studies have documented this condition in horses up to 22 years of age.3,4

Cervical vertebral stenotic myelopathy, commonly referred to as “Wobbler’s syndrome”, is characterized by lesions in the spinal cord caused by narrowing of the spinal canal or compression by the vertebral articular processes.6,7 There are two pathological syndromes: cervical vertebral instability (CVI) and cervical static stenosis (CSS). Clinical signs for both pathological syndromes include ataxia with the hindlimbs more commonly and more severely affected than the forelimbs.7 Cervical vertebral instability is characterized by the narrowing of the spinal cord when the neck is ventroflexed. The cranial articular process of the vertebral bodies project in a ventro-medial direction and impinge on the spinal cord.  C-3 to C-5 of the spinal cord is the most affected area.6 Young, rapidly growing horses between the ages of 8-18 months are predisposed to this condition. Breed dispositions include Thoroughbreds and Quarter horses, and males are affected more often than females. Contributing factors may be ad libitum feeding of high-energy and high-protein diet as well as copper deficiency.6,7

Cervical static stenosis is the less common syndrome. It is characterized by the compression of the spinal cord at the level of C-5 to C-7 due to the thickening of the ligamentum flavum and the dorsal laminae of the vertebral arches.6 Predispositions are similar to those seen in CVI except horses aged one to four years are commonly affected.3 The position of the neck does not determine whether or not the chord is compressed.

JPC Diagnosis:  

Spinal cord, dorsal medial fasciculi: Necrosis, focally extensive, asymmetric with lymphohistiocytic and eosinophilic perivasculitis and lepto-meningitis, quarterhorse, Equus caballus.

Conference Comment:  

This interesting case generated spirited discussion amongst conference participants. While attendees essentially agreed with the contributor’s histopathologic description and morphologic diagnosis, there was no consensus for the histogenesis of the necrotizing lesion in the spinal cord of this horse. The conference moderator offered an alternative inter-pretation of an infectious cause, with Sarcocystis neurona causing acute onset weakness, ataxia, and a focally extensive area of necrosis in the dorsal medial spinal cord with corresponding lymphohistiocytic and eosinophilic leptomeningitis. The conspicuous eosinophilic component of the perivasculitis and leptomeningitis in this case, may suggest a parasitic etiology. S. neurona is an apicomplexan protozoan parasite which causes equine protozoal myeloencephalitis (EPM), a relatively common and severe neurologic disease in horses. Opossums are the definitive host for the parasite and spread the disease by fecal shedding of sporocysts into the environment.1 Unfortunately, no api-complexan schizonts or merozoites were observed in any examined tissue sections. Other potential etiologies offered by conference participants included acute intervertebral disc rupture and fibro-cartilaginous embolism, although disk material was not visualized within the section.

As noted by the contributor, the age of the horse (17-years-old) is a highly atypical presentation for both cervical stenotic myelopathy and cervical static stenosis.2,3,5 While most cases of cervical stenotic myelopathy involve ventral compression of the spinal cord and spinal nerves with Wallerian-type degeneration of the white matter of the dorsal and ventrolateral spinal cord affecting the descending spino-cerebellar tracts of both the pelvic and thoracic limbs,2,5 in this section,  the ventral and lateral spinal cord is relatively unaffected.  The lesions seen in the submitted section of spinal cord are primarily located in the dorsomedial spinal cord at the level of the fasciculus gracilus  and fasciculus cuneatus.

Some conference participants noted occasional scattered 2x5 um filamentous bacilli multifocally throughout the neuro-parenchyma. The brain and spinal cord are exquisitely susceptible to post-mortem autolysis and putrefaction. As a result, the conference moderator cautioned attendees against overinterpreting artifactual bacterial overgrowth within post-mortem tissue samples of the central nervous system, especially when they are not associated with inflammation, as in this case.


1. Bowman DD. Protozoans. In: Georgis Parasitology for Veterinarians. 9th ed. St. Louis, MO: Saunders Elsevier; 2009:104-105.
2. Janes JG, Garrett KS, McQuerry KJ, et al. Cervical vertebral lesions in equine stenotic myelopathy. Vet Pathol. 2015; 52:919-927.
3. Levine JM, Adam E, MacKay RJ, et al. Confirmed and presumptive cervical compression myelopathy in older horses: A retrospective study (1992-2004). J Vet Intern Med. 2007; 21:812-819.
4. Levine JM, Scrivani PV, Divers TJ, et al. Multicenter case-control study of signalment, diagnostic features, and outcome associated with cervical vertebral malformation-malarticulation in horses.  J Am Vet Med Assoc. 2010; 237(7):812-822.
5. Reed SM. Cervical vertebral stenotic myelopathy: Pathogenesis. Proceedings of the International Equine Neurology conference. College of Veterinary Medicine, Cornell University, New York. 1997:45-49.
6. Thompson K.  Bones and joints. In: Pathology of Domestic Animals,  5th Edition. Edinburgh : Saunders; 2007: 44-46.
7. Zachary JF, McGavin DM. Nervous system. In: Pathologic Basis of Veterinary Disease. 5th ed. St. Louis, MO: Mosby; 2012:816, 833-835.

Click the slide to view.

2-1. Cervical spinal cord, horse.

2-2. Cervical spinal cord, horse.

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