Radiography

Despite the development of advanced cross‐sectional techniques, radiography remains the most common first‐line imaging test when evaluating patients with pain or neurologic symptoms localized to a spinal segment. Two orthogonal projections are acquired, albeit with caveats. Patients that have undergone trauma should initially have lateral radiographs performed, followed by ventrodorsal projections when there is confirmation that no gross spinal instability or fracture is present. In this situation, when orthogonal projections are required, cross‐table horizontal beam projections are a consideration as the patient does not need to be rolled into dorsal recumbency (as would otherwise be the case for ventrodorsal radiographs). Radiographs also allow careful stress radiography (with the vertebrae in flexion or extension), which is much more challenging with CT or MRI. Positional radiography can evaluate for spinal instability, such as with atlantoaxial instability.

Myelography

Radiographs readily identify the vertebral canal margins but the actual spinal cord is not seen due to effacement with surrounding soft tissues. Myelography involves injection of nonionic iodinated contrast medium into the subarachnoid space around the spinal cord, delineating its margins. Pathology that compresses or expands the spinal cord will be apparent. The subarachnoid space should remain a thin “column” that parallels the margin of the spinal cord. Spinal cord compression is recognized by distortion or narrowing of the subarachnoid space, with different patterns depending on whether the pathology is outside the dura mater (extradural pathology), within the spinal cord (intramedullary pathology), or between the dura mater and spinal cord (intradural‐extramedullary) (Figure 12.1).

Computed Tomography

Computed tomography provides better three‐dimensional anatomy of the spine and better soft tissue contrast than radiography, allowing earlier diagnosis of many spinal diseases compared to radiography. CT has advantages over MRI in that it is more accessible, cheaper, and faster. A typical CT examination of the spine lasts approximately 10 minutes from start to finish whereas an MRI examination is typically a minimum of 30 minutes. Unlike MRI, CT cannot distinguish the spinal cord as separate from the surrounding cerebrospinal fluid (CSF) or meninges. While it does allow visualization of the epidural space and other spinal structures, the soft tissue detail is inferior to MRI. CT may be combined with myelography, allowing better diagnosis by direct visualization of the spinal cord, more similar to MRI, but still provides limited internal detail of the spinal cord.

Magnetic Resonance Imaging

Magnetic resonance imaging is the gold standard for imaging the spinal cord and paraspinal soft tissues. By separating the signal of CSF, spinal tissue, and epidural fat, spinal pathology is directly imaged without the need for intrathecal contrast agent. The downsides of MRI are the longer acquisition time, requirement of anesthesia, and greater expense of an examination.

Typical MRI protocols include T2‐weighted and T1‐weighted images, pre‐ and post‐IV contrast. IV contrast is not necessary for all spinal examinations, particularly those where intervertebral disc extrusion is the most likely clinical diagnosis based on presentation and history. Withholding IV contrast saves time (as postcontrast images are unnecessary) and expense if the diagnosis is made on precontrast images.

Atlantoaxial Subluxation

Atlantoaxial instability is a common disorder in small‐ and toy‐breed dogs. The etiology is complex, but typically involves both soft tissue and orthopedic malformations. Clinical signs are chronic and insidious, affecting all four limbs, though sometimes an acute exacerbation may be present. Though atlantoaxial subluxation may occur due to trauma, it typically is due to incomplete development of the soft tissues and osseous structures in this region. Specifically, ligaments that stabilize this joint are incompletely developed. Moreover, the dens may be shortened and hypoplastic, further leading to instability (Figure 12.2). The result is increased mobility at this joint, resulting in soft tissue inflammation, hypertrophy, and eventual spinal cord compression.

Classically, diagnosis of atlantoaxial instability was achieved through a standard lateral radiograph performed in neutral position compared to a radiograph acquired during gentle neck flexion. Neck flexion results in separation of the lamina of C1 and the spinous process of C2, with dorsal displacement of C2 relative to C1, a motion prevented in normal dogs by the strong, thick atlantoaxial dorsal ligament. On the lateral projection, the normal alignment of C2 relative to C1 is altered, so that the angle of flexion between these vertebrae increases. Risk of spinal flexion in a dog with atlantoaxial instability is obvious, as flexion in a dog with instability can result in significant spinal cord compression as C2 subluxates dorsally and a worsening of clinical signs or even death.

In recent years, other lesions associated with this instability have been recognized with the increased use of CT and MRI imaging. Specifically, atlantoaxial instability may be seen in concert with atlantooccipital overlapping, where the dorsal lamina of C1 protrudes into the caudal fossa of the skull and can result in cerebellar compression (Figure 12.3). This is only possible if there is concurrent malformation and incomplete ossification of the foramen magnum, resulting in a keyhole shape that allows C1 to protrude into the skull (often termed occipital dysplasia). This is difficult to recognize radiographically and requires either CT or MRI to definitively diagnose.

Dens hypoplasia is commonly present in dogs with atlantoaxial instability (Figures 12.2 and 12.4). This is difficult to identify on a straight lateral projection of the spine as the large superimposed wings of C1 overlap the dens of C2, making identification of the dens difficult in all dogs. Slight, intentional obliquity of the head rotates the wings of C1 in a way that the dens may be appreciated (see Chapter 6). The ventrodorsal projection also highlights the dens and is another way to assess potential hypoplasia, though the risks of positioning a dog with suspected subluxation should be weighed against the information provided by a VD projection. Moreover, some dogs that are clinically normal may have undeveloped dens, so identification of this anomaly alone cannot diagnose instability without the dynamic positioning.

Both MRI and CT are able to recognize morphologic abnormalities of C2 and C1, and can help confirm spinal cord compression, but dynamic imaging of the spine to confirm atlantoaxial subluxation is typically still reserved to radiography given the dangers with prolonged flexion required by MRI and CT to diagnose this instability.

Transitional Vertebrae

Transitional vertebrae have characteristics of two different vertebral types, and may be symmetric or asymmetric between their left and right halves. These anomalies typically are of the vertebral arch rather than the vertebral body. For instance, a thoracolumbar vertebral segment will have one lateral half that appears to be a thoracic vertebral body with a small adjacent rib, whereas the other lateral half will appear similar to a lumbar segment and have a broad transverse process (Figure 12.5). The most caudal ribs may be hypoplastic or aplastic bilaterally. Similarly, a lumbosacral transitional segment may have one lumbarized half and one sacralized half or both may be lumbarized. This may be seen involving only one vertebral segment (Figure 12.6) or multiple segments (Figure 12.7).

Transitional segments are most common at the thoracolumbar and lumbosacral junctions, but cervicothoracic transitional segments do occur, most commonly characterized by small vestigial ribs on C7. Those at the cervicothoracic and thoracolumbar junctions are typically incidental and do not result in clinical signs, though thoracolumbar transitional segments may complicate vertebral counting prior to spinal surgery and cause crowding of regional anatomy (Figure 12.8). Transitional segments at the lumbosacral junction increase the risk of intervertebral disc degeneration and instability, which can result in nerve impingement and cauda equina syndrome (Figure 12.9). Lumbosacral transitional segments may also affect normal hip development [1, 2]. Sacral congenital abnormalities are expected in some breeds (such as English bulldogs) and typically do not result in clinical signs (Figure 12.10).

Hemivertebrae

Hemivertebrae are congenital vertebral body malformations that represent a defect that occurred during vertebral body formation [3]. They are the most common malformation seen in the spine, and are most common in brachycephalic breeds such as the pug and English bulldog. They are most common in the midthoracic region, but occur as far caudal as the thoracolumbar junction, and are rare in the cervical or lumbar area (Figure 12.5). They may result in deviation of the long axis of the spine, directing it dorsally (kyphosis), ventrally (lordosis), or to the side (scoliosis). This degree of deviation is typically mild, but hemivertebrae result in vertebral canal stenosis and spinal cord compression if severe (Figure 12.11).

Though most dogs with hemivertebrae are neurologically normal, kyphosis in particular is a risk factor for development of clinical signs from spinal cord compression [3, 4].

Classification schemes for the different shapes of hemivertebrae are based on which portions of the vertebral body are incompletely formed and to what degree [3, 5]. In general, hemivertebrae have a wedge type of shape, with some degree of ventral and/or lateral vertebral body hypoplasia or aplasia [3, 5]. Hemivertebrae are not always wedge shaped, however, and median aplasia, where there is incomplete or absence of the central region of the vertebrae, results in a “butterfly vertebrae” recognized by the resemblance to a butterfly when evaluated on the ventrodorsal projection (Figure 12.5). In some dogs, there may be symmetric and incomplete development of a vertebral body (termed symmetric hypoplasia), resulting in a diffusely shortened vertebral body but this does not cause any spinal malalignment.

Block Vertebra

Block vertebrae are congenital defects in segmentation, where adjacent vertebral developmental bodies do not separate into two different vertebrae. The result is one long vertebral segment with adjacent fusion of the vertebral bodies and possibly the vertebral arches (Figure 12.12). These are usually not clinically relevant and do not cause symptoms, but can predispose to intervertebral disc degeneration (Figure 12.13) and herniation (Figure 12.14) in the adjacent discs due to increased loading from a fulcrum effect [6].

Facet Dysplasia

Incomplete development of the caudal articular processes of the vertebrae at the thoracolumbar junction has been described in brachycephalic dogs. These articular processes may be either hypoplastic or completely aplastic, resulting in decreased vertebral column stability (Figure 12.15). Pugs are particularly affected. This malformation is associated with progressive neurologic symptoms from chronic cord disease from chronic instability. This may be recognized on survey radiographs by incompletely formed or absent articular processes, but is most easily recognized when cross‐sectional imaging is performed in these patients (Figure 12.16) [7].

Spina Bifida

Spina bifida is a defect in the normal embryologic development of the neural tube, characterized by failure of the vertebral arches/lamina to close over the spinal cord [8]. This is recognized by a duplication of the spinous process to the left/right sides of the midline on the ventrodorsal radiograph or absence of normally formed spinous processes (Figure 12.17). Typically, this malformation is not associated with neurologic defects and the underlying meninges and spinal cord are presumed normal. If instead, the meninges protrude through the open vertebral arch, the defect is referred to as meningocele, and if the meninges and neural tissue extend into the opening, it is referred to as meningomyelocele [8]. Radiographs cannot determine the degree of meningeal/neural involvement, which usually relies on MRI, though CT with a myelogram would accurately assess the degree of neural involvement (Figure 12.18).

Osteosclerosis

Osteosclerosis is defined by a diffuse increase in opacity of long bone and vertebral medullary cavities (Figure 12.19). This radiographic appearance is occasionally seen in young or older patients, and may be attributed to multiple disease processes, though the cause is not always identified. Osteopetrosis is a rarely reported inherited bone disease caused by abnormal osteoclast function, resulting in osteosclerosis in young patients. Osteosclerosis has been described in cats infected by feline leukemia virus and also described as a paraneoplastic change [9].

Congenital Hypothyroidism

This rare congenital disorder in dogs and cats is caused by an abnormality somewhere along the hypothalamic‐pituitary‐thyroid axis, resulting in decreased production of thyroid hormones. Most commonly, it is due to dysgenesis of the thyroid gland [10, 11]. As thyroid hormone is necessary for normal bone development, all bones are equally affected, with animals displaying disproportionate dwarfism with delayed epiphyseal maturation and epiphyseal dysgenesis [11]. In the spine, the vertebrae will have a shortened appearance and are often decreased in opacity (Figure 12.20). There may be secondary degenerative changes to the spinal articular joints.

Osteogenesis Imperfecta

Osteogenesis imperfecta is a well‐documented but rare heritable bone disease that results in diffuse skeletal maldevelopment, sometimes referred to as “brittle bone disease” [12, 13]. The cause is a defect in the genes that encode the precursor molecules to collagen type 1, which makes up 90% of the organic substance of bone. Defects in this matrix reduce overall bone mineralization. These weakened bones are predisposed to folding fractures and are frequently malformed. Patients will commonly appear stunted. Radiographically, there is diffuse decrease in opacity of the vertebrae, and endplates and cortical bone will appear thin (Figure 12.21). Fractures and malformation of the spine are typical. Because this is a diffuse disease, similar changes are expected in the long bones.

Nutritional Secondary Hyperparathyroidism

Patients fed a diet with inappropriate levels of calcium and vitamin D are at risk of nutritional hyperparathyroidism. The resultant mobilization of calcium from osseous structures results in vertebrae which are more lucent than expected (Figure 12.22). The overall appearance is similar to osteogenesis imperfecta, but the conditions are readily differentiated when a complete diet history is collected.

Discospondylitis

Discospondylitis is infection (usually bacterial) of the intervertebral disc. The infection typically spreads to the disc through a hematogenous route, though rarely infections may be fungal in etiology and caused by local infections (such as those caused by epidural infections or migrating grass awns; Figure 12.23) [14]. The infection starts in the cartilaginous endplate of the vertebral body, and is recognized radiographically when lysis of the osseous endplate develops [14]. The bacterial source is most commonly in the urinary tract or prostrate, as bacterial infections in this area may enter the bloodstream and lodge in the vertebrae via venous drainage of the caudal abdomen that flows through the venous sinuses.

Radiography is the most common screening method for discospondylitis. The osseous endplates demonstrate permeative or moth‐eaten lysis causing an irregular margin (Figure 12.24). The adjacent vertebral body responds by bony deposition and a region of increased opacity. With time, the intervertebral disc space will collapse (Figure 12.25). Bony proliferation occurs at the margin of the vertebral bodies, with an appearance similar to spondylosis deformans. In juvenile dogs less than 6 months of age, intervertebral disc narrowing may occur before endplate lysis [15].

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