Comparison of the clinical and radiographic appearance of the cervical vertebrae with histological and anatomical findings in an eight-month old warmblood stallion suffering from cervical vertebral stenotic myelopathy (CVSM)

Abstract

Background Cervical vertebral stenotic myelopathy (CVSM) remains one of the most important abnormalities of the cervical spine resulting in neurological deficits in horses. The aim of the following study was to compare the results of the clinical and neurological examination, the results of myelography and the post mortem anatomical and histological appearance of the spinal cord and cervical vertebrae in a horse with CVSM. Case presentation The following study describes a clinical case of an eight-month-old stallion with ataxia. Plain cervical radiographs indicated narrowing of the spinal canal. Conservative therapy using NSAIDs did not result in any improvement in the gait of the horse. Due to economic constraints, surgical intervention was excluded. The owner chose to humanely euthanise the horse. Immediately after euthanasia, post mortem myelography was performed, and measurements of the myelographic dye column were taken. They revealed a 67% DMC reduction and a 64% DD reduction at the C3/C4 level. Afterwards, an anatomical dissection was performed. The cervical vertebrae and vertebral canal were macroscopically inspected and measured and indicated a 44% narrowing of the canal at the C3/C4 level. The spinal cord was removed and underwent histological evaluation after staining. Microscopic lesions were visible at the level of the compression and included axonal degeneration with partial or complete loss of myelin in the white matter of the lateral and dorsal funiculi as well as the formation of dysfunctional so-called “spongy structures”. An increase in the number of microglial cells and collagen was also observed. The formation of glial scars was excluded. Immunohistochemical studies revealed a negative transmembrane glycoprotein CD68(−) – monocyte response and a negative tumor necrosis alpha TNFα (−) reaction. Conclusions CVSM may be difficult to diagnose, even for experienced veterinary surgeons. Currently, an ex vivo histopathologic examination of the spinal cord is thought to be the gold standard in the diagnosis of CVSM. Our histological examination revealed no CVSM-specific glial scar formation and a CD68(−) negative and TNF-α negative reaction, which have not been previously reported. Histological lesions in CVSM may vary depending show inter-individual variability and on the treatment, which further hinders ex-vivo diagnostics.

Multiple cervical spondylolisthesis and thoracic vertebral malformation in an 11 month-old Chilean Caballo Raza Chilena colt

“…Cervical vertebral malformation (CVM) (also known as cervical vertebral compressive myelopathy, wobbler syndrome and cervical stenotic myelopathy) (Reed et al 2007, Cardona et al 2013, Kühnle et al 2018, Szklarz et al 2019 is a common and widely described cause of ataxia and paresis affecting many different breeds of horses (Levine et al 2010). Ataxia and weakness commonly seen in horses with CVM are caused by narrowing of the cervical vertebral canal and compression of the spinal cord, often combined with malalignment and malformation of the cervical vertebrae.…”

Characteristic computed tomographic myelography findings in 23 Thoroughbred horses

“…A limitation of radiographic assessment is the use of intra- and intervertebral ratio, as this measurement has been reported to be unreliable with a variation of 5–10% [ 19 ]. Although, radiographic myelography may reveal the site and degree of dorsal and ventral compression, determining lateral compression remains challenging [ 20 ].…”

Investigation of a contributing factor for cervical vertebral stenotic myelopathy using computed tomography for measuring the cervical vertebral volume

“…The primary clinical signs of CVSM include general proprioceptive ataxia and weakness [ 5 , 8 ]. Some factors in predisposed horses, including nutrition, rapid growth, and exercise, are considered as factors contributing to the development of CVSM [ 4 , 6 , 10 , 11 ].…”