Clinical Signs

The clinical signs of spinal cord compression are usually insidious in onset, although owners sometimes report a traumatic incident before recognizing any ataxia. Such traumatic incidents may occur because of mild or previously unrecognized neurological deficits (e.g., occasional tripping) that result in a fall.

Horses with CSM generally have neurological deficits that are recognizable in all limbs, characterized by symmetrical weakness, ataxia, and spasticity.⁴ In most instances the hindlimbs are more severely affected than the forelimbs, probably because of the more superficial location of hindlimb tracts in the white matter of the spinal cord. At rest, severely affected horses may have a base-wide stance and delayed responses to proprioceptive positioning, whereas at the walk, weakness may be manifest by stumbling and toe dragging. Horses with prolonged clinical signs of CSM may therefore have hooves or shoes that are chipped, worn, or squared at the toe. Ataxia (a sign associated with defective proprioception) is evident as truncal sway at a walk, inconsistent and erratic foot placement, and circumduction and posting (pivoting on the inside limb) of the hindlimbs during circling. Moderately to severely affected horses sometimes have lacerations on the heel bulbs and medial aspects of the forelimbs from overreaching and interference. Spasticity, characterized by a stiff-legged gait and exaggerated movements, may be observed in moderately affected horses, especially in the forelimbs or in the hindlimbs when stepping over curbs or poles. When prompted to back, horses may stand base-wide, lean backward, and drag the forelimbs. Occasionally, signs associated with the forelimbs may be more severe than those in the hindlimbs, particularly in horses with caudal cervical lesions, probably because of involvement of local spinal cord grey matter.

A grading scale (0 to 5) is often used to score horses with signs of spinal ataxia and weakness: 0, normal; 1, very mild deficits detectable only with complex movements (e.g., walking with head elevated, on an incline or when circling); 2, mild-moderate deficits that are detectable at the walk; 3, marked deficits obvious at the walk; 4, severe deficits that result in difficulty remaining standing; 5, recumbent. Some clinicians favor an approach in which individual limbs are scored separately for signs of ataxia and weakness, with a global score being used to summarize the total neurological deficit. Such an approach is helpful when evaluating disease progression and response to treatments.⁵

Asymmetrical ataxia and paresis are observed occasionally in horses with dorsolateral compression of the spinal cord caused by proliferative, degenerative articular processes and periarticular soft tissues.⁶ Infrequently, signs of compressive radiculopathy, such as cervical pain, atrophy of the cervical musculature, cutaneous hypalgesia, and hyporeflexia of cervical reflexes adjacent to the site of spinal cord compression may be evident. These signs are more commonly observed in horses older than 4 years of age with moderate-to-severe arthropathy of the fifth to seventh cervical vertebrae (C5 to C7) and usually result from peripheral nerve compression by proliferative articular processes as the nerve root exits the vertebral canal through the intervertebral foramen.⁷

In some instances arthropathy of the caudal cervical vertebral articular processes may produce forelimb lameness, caused by spinal nerve root compression, without producing clinical signs of spinal cord compression.⁸ Affected horses typically have a short cranial phase of the stride and a low forelimb foot arc and may stand or walk with the head and neck extended (see Chapter 53). Rarely, diskospondylosis of the cervical vertebrae produces a short-strided gait and cervical pain, with or without spinal ataxia (Figure 60-1). Horses with diskospondylosis or arthropathy of the caudal vertebrae may exhibit signs of lameness, pain, or stiffness with the neck in only certain positions or when the head and neck are manipulated or the horse is turned. For example, some affected horses may be unwilling to turn the neck laterally when offered food.

Figure 60-1 Lateral-lateral radiographic image of the caudal aspect of the neck of a 4-year-old Paint gelding with cervical pain and spinal ataxia. Cranial is to the left. Note the abnormal intercentral articulation between the sixth and seventh cervical vertebrae (arrows). This represents end-stage diskospondylosis.

Dynamic spinal cord compression usually occurs in younger horses (<2 years of age) and is associated with instability of the cervical vertebrae, particularly between C3 and C6. Dorsal laminar extension, caudal epiphyseal flare, or abnormal ossification patterns may contribute to the problem. Static vertebral canal stenosis (type II) is characterized by constant spinal cord compression, regardless of neck position (Figure 60-2), and is seen usually in older horses.⁹ It generally results from osteoarthritis (OA) of the articular processes and proliferation of periarticular soft tissue structures. Synovial cysts, which are often associated with OA of the articular processes, may produce waxing and waning, or acute-onset asymmetrical neurological signs. In some horses with static compression, flexion of the neck stretches the ligamentum flavum and relieves spinal cord compression, whereas extension exacerbates the problem.

Figure 60-2 Lateral-lateral radiographic image during myelographic examination of the fifth to seventh (C7) cervical vertebrae of a 3-year-old Thoroughbred colt with static spinal cord compression. The dorsal and ventral contrast columns are attenuated by more than 50% at the fifth and sixth (C6) and sixth and seventh cervical vertebral articulations.

Diagnosis

The following neurological disorders should be considered potential differential diagnoses and may produce signs similar to or indistinguishable from CSM: equine protozoal myeloencephalitis (EPM), equine degenerative myeloencephalopathy (EDM), equine herpesvirus–1 (EHV-1) myelitis, occipitoatlantoaxial malformation, spinal cord trauma, vertebral fracture, vertebral abscess or neoplasia, and verminous myelitis (see Chapter 11).

Horses with traumatic cervical vertebral disorders usually exhibit pain during manipulation or palpation of the neck, and the disorder may sometimes be differentiated from CSM by standing radiographic examination. Occipitoatlantoaxial malformation (see Chapter 53) occurs primarily in Arabian horses and is diagnosed definitively by radiological evaluation (see Figure 53-4, B). EDM is diagnosed by exclusion (unremarkable cerebrospinal fluid [CSF] cytological examination findings, negative immunoblot analysis for Sarcocystis neurona, and negative radiological findings and myelographic examination findings). A veterinarian may suspect EDM based on the age (usually less than 18 months) and during neurological examination (hyporeflexia, and similar degrees of ataxia in the forelimbs and hindlimbs), but definitive diagnosis is achieved only by postmortem examination. Although several breeds have been reported with the disease, EDM appears to have a familial predisposition in Standardbred horses.¹⁰ Horses with EHV-1 myelitis may have urinary incontinence, poor tail tone, and hindlimb lower motor neuron weakness. Signs associated with cranial nerve involvement may occasionally be observed. In EHV-1 myelitis, CSF evaluation typically reveals xanthochromia and albuminocytological dissociation (high protein concentration, normal cell count); a rising EHV-1 serum antibody titer, virus isolation, and polymerase chain reaction (PCR) diagnosis all may be used to provide supportive evidence of EHV-1 myelitis. In areas where EPM is endemic (such as North and South America) or in horses exported from these regions, distinguishing between EPM and CSM can be difficult. Asymmetrical ataxia, focal sweating, and focal muscle atrophy should direct diagnostic efforts toward EPM; however, symmetrical spinal ataxia does not preclude a diagnosis of EPM. EPM-affected horses with symmetrical ataxia are differentiated from those with CSM on the basis of standing radiographic examination, CSF immunoblot analysis for S. neurona,

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