Cervical spondylomyelopathy (wobbler syndrome)

What it is

Cervical spondylomyelopathy (CSM) groups the disorders of the caudal cervical spine that narrow the vertebral canal and compress the spinal cord, often in a dynamic way that changes with the position of the neck. Two main forms are recognised:

• Disc-associated CSM: protrusion of the dorsal anulus of one or more caudal cervical discs, sometimes with hypertrophy of the ligamentum flavum. Compression may worsen with extension of the neck.
• Osseous-associated CSM: malformation and proliferation of the articular processes, pedicles or vertebral arch, which narrow the canal from the sides and from above.

After surgery at one site, the adjacent disc may develop a new compression (the "domino lesion").

Who it affects

• Disc-associated form: middle-aged to older large-breed dogs, classically the Dobermann.
• Osseous-associated form: young adult giant breeds, such as the Great Dane, mastiff, Bernese mountain dog and Rottweiler.

Anatomy involved

The lesions sit mostly between C5 and C7, at the C5–C6 and C6–C7 discs in the Dobermann; in giant breeds several sites between C4 and T1 are often affected. In this region the cervical intumescence gives rise to the nerves of the thoracic limb, so compression can affect both the long tracts to the pelvic limbs and the lower motor neurons of the thoracic limbs. The articular processes of the caudal cervical vertebrae and C7, a transitional vertebra without a transverse foramen, are frequent sites of osseous malformation.

Clinical signs

Slowly progressive, symmetrical ataxia that starts in the pelvic limbs: a wide-based, swaying gait with scuffing of the nails. In many dogs the thoracic limbs take short, stiff steps while the pelvic limbs are ataxic ("two-engine gait"). Neck pain is variable; some dogs show root signature or low head carriage. Signs may worsen suddenly after minor trauma. Advanced cases are tetraparetic.

Diagnosis

• Neurological examination localising the lesion to C6–T2 or C1–C5.
• Survey radiographs show the shape of the vertebrae but correlate poorly with the site of compression; they help to rule out discospondylitis or tumours.
• MRI is the method of choice; CT myelography with traction or flexion-extension views shows the dynamic component.
• Dobermanns should be checked for von Willebrand disease before surgery.

Treatment

Medical: restricted activity, a harness instead of a collar, corticosteroids or NSAIDs and analgesics; it may stabilise or improve some dogs, but the disease often progresses. Surgical: ventral slot for a single disc protrusion, distraction-stabilisation techniques for dynamic lesions, and dorsal laminectomy for dorsal or multiple compressions. Prognosis is guarded and depends on the severity and duration of signs.

In the horse

In the horse the disease is called cervical vertebral compressive myelopathy or cervical vertebral malformation-malarticulation, and it is one of the most common causes of ataxia. Unlike in the dog, the intervertebral discs are not involved: compression is caused by malformation of the vertebrae and their articular processes, stenosis of the vertebral canal and osteoarthritis of the articular process joints. Two types are described, which often overlap:

• Type 1, dynamic instability: young horses, from a few months to about 2 years of age, with malformed, unstable vertebrae that compress the cord when the neck is flexed, mainly between C3 and C5. It is linked to rapid growth, high-energy diets, osteochondrosis of the articular processes and a genetic predisposition.
• Type 2, static stenosis: somewhat older or adult horses, in which osteoarthritis of the articular processes, hypertrophy of the ligamentum flavum and synovial cysts narrow the canal permanently, mainly between C5 and C7.

It affects males and Thoroughbreds, warmbloods and Tennessee Walking Horses more often. The horse has seven cervical vertebrae and a long neck; almost all compressions lie in the cervical vertebrae C3–C7. C6 has a ventral lamina on its transverse process that may be absent on one or both sides, a common anatomical variation whose link with the disease is unproven.

Signs are a symmetrical ataxia with paresis and spasticity (hypermetric steps, toe dragging, circumduction of the pelvic limbs), usually at least one grade worse in the pelvic than in the thoracic limbs, which worsens on tight circles, when backing, on slopes or with the head raised. Severity is graded on a 0 to 5 scale. Adult horses with osteoarthritis may show neck stiffness or pain and thoracic limb lameness. An ataxic horse is dangerous to ride and handle.

Diagnosis combines the neurological examination with lateral radiographs of the neck, on which the ratio between the minimum sagittal diameter of the canal and the height of the vertebral body (intra- and intervertebral) is measured; a low ratio indicates stenosis. Myelography and CT myelography localise the compression, although their agreement with necropsy is imperfect. Equine protozoal myeloencephalitis, equine herpesvirus-1 myeloencephalopathy, equine degenerative myeloencephalopathy (associated with vitamin E deficiency) and trauma must be ruled out.

Conservative treatment of foals with type 1 is based on restricting dietary energy and protein and exercise to slow growth, with anti-inflammatory drugs; in adults with osteoarthritis, corticosteroids are injected into the articular process joints. Ventral interbody fusion of the affected vertebrae is the most widely used surgical technique, but its evidence comes from retrospective case series. Many affected horses are euthanised, and drug use is subject to national regulations and withdrawal periods, because the horse is a food-producing animal in many countries.

Key studies

• Levine et al. (2008), case-control study of 811 horses with cervical vertebral compressive myelopathy and 805 controls from the North American veterinary hospital database (1974–2007). Geldings (OR 2.0; 95% CI 1.5–2.6) and entire males (OR 2.4; 95% CI 1.8–3.2) were at higher risk than females; Thoroughbreds, Tennessee Walking Horses and warmbloods were overrepresented compared with Quarter Horses, and horses under 7 years had higher odds than those aged 10 or more. It is based on hospital discharge diagnoses without uniform confirmation.
• Levine et al. (2010), multicentre case-control study of 270 horses with cervical vertebral malformation-malarticulation and 608 controls from 6 hospitals (1992–2007). Cases were younger (median 2 versus 7 years) and more often Thoroughbreds, warmbloods or Tennessee Walking Horses. Agreement with necropsy was 65–71% for radiography and 67–78% for myelography. Of 263 horses with a known outcome, 65.4% were euthanised. It is retrospective and the population comes from referral hospitals.
• Hoffman and Clark (2013), retrospective study of 103 Thoroughbreds with a presumptive diagnosis of cervical malformation managed conservatively. Of the 70 discharged for treatment, 30% went on to race; those that raced had a lower neurological grade, and kyphosis or cranial stenosis on radiographs were associated with not racing. Diagnosis was presumptive, without myelographic or necropsy confirmation in every horse.
• Saville et al. (2017), prospective study of 97 horses examined by two board-certified internists, the second unaware of the history. They agreed that 60 were abnormal and 21 normal, and disagreed on 16. Agreement was good or excellent for the presence of ataxia or lameness in 80% of horses, but only in 20% for spasticity, muscle atrophy and overall severity. It shows how subjective the neurological examination on which diagnosis rests is; the data were collected in 1997–1998.
• Strootmann et al. (2026), retrospective study of pre-purchase radiographs of 200 sound warmbloods. Absence of the ventral lamina of C6 was found in 30% and remodelling of the C6–C7 joints in 32.5%, with no association with competition results. It indicates that this variation is common in sound horses and should not be read as disease on its own. It is retrospective, from a single clinic, and performance was measured only by competition results.