Beverly K. Sturges,     Davis, California

General Considerations: Anatomy and Physiology

The atlas (C1) and axis (C2) form a pivotal joint that allows free movement of the head about the longitudinal axis of the spine. Most rotational head movement centers around the dens, a bony process projecting rostrally from the body of the axis. The dens is held in place on the ventral aspect of C1, within the vertebral canal, by several ligaments (Figures 235-1 and 235-2):

The atlas articulates rostrally with the occipital condyles of the skull and forms a joint of which the main movements are flexion and extension of the head, the “yes” joint. Caudally, the atlas articulates with the axis allowing lateral and rotational movement of the head, the “no” joint. Working together, these two joints allow free motion of the head in all directions. The large nuchal ligament that attaches the spinous process of C2 to those of T1 and T2 functions in suspension of the head, forming a fulcrum at the AA joint (see Figures 235-1 and 235-2).

Pathophysiology

Instability of the AA region allows excessive flexion of the C1-2 joint that may result in subluxation of C2 relative to C1 and injury to the spinal cord (Figure 235-3). This usually occurs secondary to congenital or developmental abnormalities of the bones or ligaments of the AA joint, traumatic injury to the joint, or a combination of both (Figure 235-4). In many instances the abnormalities present are associated with the dens and include agenesis or hypoplasia of the dens, dorsal angulation of the dens, and fracture or avulsion of the dens from the axis. Absence or rupture of associated AA ligaments often contributes to the instability caused by congenital anomalies in the region. All of these findings are common in toy and miniature breeds of dogs. Traumatic rupture of the AA ligaments without associated anomalies of the AA joint is possible but usually occurs as a result of major traumatic injury to the cervical vertebral column. This is the most common cause of AA instability in large-breed dogs. Recently there have been reports (Owen et al, 2008; Warren-Smith et al, 2009) of larger-breed dogs with absence or incomplete ossification of the atlas (Figure 235-5). Associated AA subluxation in most of these dogs suggests another predisposing factor to AA instability. This was further investigated in another study characterizing the morphology of the atlas on computed tomography (CT) in various classes of dog breed (Parry et al, 2010). Dogs with ossification abnormalities involving the atlas were significantly more likely to have associated AA subluxation, although the underlying pathophysiology behind these findings is not known. AA subluxation rarely is seen in cats. Only a handful of cases have been reported, and all of them have been associated with congenital occipitoatlantoaxial malformations or malformations of the dens (C2).

Regardless of the underlying cause, dorsal displacement of the cranial portion of the body of the axis into the vertebral canal causes compression, edema, and inflammation of the spinal cord that may extend cranially into the caudal brainstem. In addition, intraaxial hemorrhage into the central nervous system parenchyma also may contribute to the clinical signs (Kent et al, 2010). Cervical pain, myelopathy of varying degrees, and possible caudal brainstem signs may occur.

Diagnosis