The term “wobbler” disease is a rather casual, lay-type description of signs associated with mid-to-caudal cervical spinal cord disease seen in large and giant-breed dogs. There are classically two major forms of the syndrome, one most commonly seen in young giant-breed dogs (great Danes being the most representative breed) and the other more common in older large-breed dogs (Doberman pinschers, most typically). Whether these are part of a spectrum of a single disease entity or whether they are completely different diseases that share a common location and resultant neurologic signs remains controversial. When considered as a single syndrome, the term “wobbler” disease is the most commonly used synonym for what is more properly termed cervical spondylomyelopathy (CSM) [1]. CSM is a multifactorial neurological disorder characterized by abnormal development of the cervical spinal column. Typical lesions include vertebral canal stenosis, disc protrusion, ligamentous hypertrophy, vertebral column subluxation, and articular process hypertrophy leading to varying degrees of neurologic deficits and neck pain [1–4]. Clinical signs are associated with spinal cord and nerve root compression in addition to facet inflammation and paraspinal muscle spasm. Compressive lesions may be dynamic (improving with flexion or extension) or traction responsive (improving after application of linear distractive force), or they may be static (remaining unchanged by positional alteration) [5, 6]. Figure 7.1 depicts three different types of static compression in Doberman dogs attributable to disc protrusion and/or vertebral malformation/subluxation/“tipping” in disc-associated wobbler syndrome (DAWS). Figures 7.2 and 7.3 depict static compression in a great Dane and a basset hound affected by osseous proliferation narrowing the spinal canal and producing stenotic myelopathy or osseous-associated wobbler syndrome (OAWS). Figure 7.4 depicts the effect of flexion and extension on a Doberman affected by DAWS showing how the compressive lesion is dynamically compressing the spinal cord.

CSM is likely the most common disease of the cervical spine of large- and giant-breed dogs. Doberman pinschers are at increased risk (incidence rate approximately 60%) and are usually presented when middle aged [7]. Other breeds, including great danes, are also commonly affected, and this breed most commonly presents when young [2, 6, 8–10]. The C5–C6 and C6–C7 vertebral levels are most frequently affected, hence the common autonym of caudal cervical spondylomyelopathy (CCSM). Lesions affecting both of these levels simultaneously have been recognized in approximately 20% of affected dogs [11].

The question whether wobbler disease is or is not related to disc disease is probably patient dependent. Disc disease when present, often occurs concomitant with multiple other manifestations of osseous and positional anomalies of vertebrae in affected dogs, but cause or effect has been difficult to establish. This is a complex disease syndrome where different morphologic changes can cause various clinical signs. There is poor correlation between either the type or severity of the disease as diagnosed on imaging modalities and the magnitude or duration of clinical signs [12]. The disease may progress for prolonged periods and clinical debilitation can be triggered by relatively minor trauma. This is particularly true of disc-associated CSM or DAWS, since motion can exacerbate disc protrusion resulting in acute deterioration [4, 13, 14] (Figure 7.3). Moreover, such deterioration may be difficult to address because of the chronicity of preexisting spinal cord abnormalities [4] (Figure 7.1).

Whether wobbler disease is related to disc disease has practical and prognostic relevance for a particular patient and for a population of affected dogs. When a dog is classified as being affected by DAWS based on appropriate imaging, there are significant implications regarding treatment. The fact that more than 20 different surgical techniques have been reported for treatment of CSM implies that no single technique is able to completely address all of the variable manifestations of this complex disease. With appropriate classification however, more refined protocols for intervention are possible, which might in turn improve surgical outcomes.

Etiology

The etiology of CSM is unknown. Genetic, congenital, conformational, and nutritional causes have been proposed [4]. Though canine CSM shares similarities with cervical spondylotic myelopathy of humans, etiology in human patients is likely different from dogs [15]. It has been suggested that vertebral instability may predispose to chronic degenerative disc disease in dogs, or that disc disease may itself be a primary entity and may distort the dorsal longitudinal ligament, exacerbating cord compression [1, 13, 16]. However, as discussed in the following, the whole issue of “cervical vertebral instability” (CVI) remains very controversial and undetermined. The first description of the syndrome in basset hounds suggested that the disease was likely to be sex-linked inherited [17]. A study in Borzois suggested that CSM was inherited with an autosomal recessive pattern, but no explanation was given why only females were affected [9]. In spite of the frequency of the disease in Dobermans, previous studies have failed to demonstrate the mode of inheritance implied by the high prevalence in the breed [18–21].

Computed tomography of the cervical spine of neonatal Dobermans revealed stenosis of the cranial vertebral canal and asymmetry of the vertebral bodies of the fifth, sixth, and seventh cervical vertebrae, with the seventh most affected, intimating that Dobermans may be born with congenital vertebral canal stenosis [21]. Regarding body conformation, it had been proposed that abnormal forces exerted by a large head on a long neck along with a rapid growth rate may lead to abnormal stresses between vertebral bodies, inciting vertebral changes and spinal cord compression [22]. However, no correlation was found between radiographic changes associated with CSM in 138 Dobermans aged 1–13 years and head size, neck length, body length, or height at the withers [21]. Overfeeding and excessive dietary calcium were shown to increase the incidence of CSM in great danes [23, 24], but CSM prevalence has not decreased in spite of abandonment of such feeding regimes. In a study of Dobermans affected by CSM, no association was found with dietary factors [21].