Congenital Spinal Malformations

DISEASES OF THE SPINE

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CONGENITAL SPINAL MALFORMATIONS Cleta Sue Bailey, DVM, PhD, and Joe P. Morgan, DVM, Vet Med Dr

Congenital malformations of the spinal column occur frequently in the dog and cat, and in dealing with them, a clinician should consider the following four issues: 1. Clinical significance. Many spinal anomalies do not produce neurologic disease and are detected only as incidental findings on radiographs of neurologically intact animals. In animals with myelopathies, cauda equina syndromes, or radiculopathies, any spinal malformation that is discovered must be investigated thoroughly to establish its clinical significance. 2. Other malformations. The embryologic formation and development of the spinal column is closely interrelated to that of other tissues and organs. Therefore additional malformations, spinal and nonspinal, may be present and may affect the viability of the animal. 3. Heritability. Strong evidence exists suggesting the heritability of some spinal anomalies. Many anomalies seem to be sporadic occurrences, however. Still the potential for heritability must be considered carefully in potential breeding animals. 4. Treatment. Most animals with clinically significant spinal malformations are left untreated or euthanatized. Pets are assuming an increasingly important role in the lives and well-being of people, however, and enduring emotional attachments are made to even very young animals. As a result, veterinarians are more From the Department of Surgery (CSB), and the Department of Radiological Sciences OPM), University of California, Davis, School of Veterinary Medicine, Davis, California

VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE VOLUME 22 • NUMBER 4 • JULY 1992

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often being asked to treat these animals and should be willing to develop and attempt various treatment options. HEMIVERTEBRA AND BLOCK VERTEBRA

Hemivertebra and block vertebra are congenital anomalies that are usually encountered in dogs and cats as incidental radiographic findings. If present, neurologic disease caused by these malformations is usually spinal cord trauma/compression secondary to (1) stenosis of the vertebral canal, (2) progressive deformity or spinal angulation with growth or aging, or (3) instability, perhaps exacerbated by trauma or degenerative disc disease. Rarely myelopathies in animals with vertebral malformations may be due to concurrent neural malformations, such as spinal dysraphism. Hemivertebra

Hemivertebra is the result of failure (defect or error) of formation of part of a vertebra, usually part of the vertebral body.64 The failure has been attributed to persistence of the notochord or lack of ossification. 56 Tanaka and Uthoff,64 however, studied 266 human embryos and fetuses and concluded that congenital vertebral malformations are likely to occur during the stage of resegmentation and to be related to the abnormal distribution of the intersegmental arteries. Depending on the portion of the vertebra that fails to form, a hemivertebra may be a wedge-shaped vertebra with the base oriented dorsally (Fig. 1), ventrally, or medially. Failure of formation of the central portion of the vertebra may yield two hemivertebrae, right and left, within the same segment. This malformation is more correctly termed butterfly vertebra (Fig. 2) rather than hemivertebra. 56 Hemivertebrae may be single or multiple and may be associated with other vertebral malformations producing complex spinal malformations. Although apparently rare, hemivertebrae may also be associated with malformations of neural tissue, for example, spinal dysraphism58 and spinal arachnoid cyst. 44 Drew15 postulated an association between hemivertebrae and neonatal mortality in English Bulldogs. Although not described in his report, early mortality could be due to associated malformations in other organ systems. In dogs, hemivertebra is seen most frequently in the screw-tailed breeds (Bulldog, French Bulldog, Pug, Boston Terrier); the kinked tail is due to caudal hemivertebrae. Hemivertebra occurs in the German Short-haired Pointer as an autosomal recessive disorder3 1 and also occurs sporadically in other breeds. 14, 35 Diagnosis

If present, neurologic signs of myelopathy usually (not always) appear in immature animals and may be acute, chronic, progressive,

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Figure 1. Hemivertebrae. Lateral (A) and ventrodorsal (B) radiographs of the thoracic spine (pathology specimen) of a 6-month-old Pug with two dorsal hemivertebrae (arrows) creating kyphosis of the spine. The adjacent cranial and caudal vertebrae have a compensatory shape. The details of the malformation are more easily seen on this bone specimen than on whole body radiographs, but the malformation is still difficult to see on the ventrodorsal view.

or intermittent. The conformation of the animal may be visibly or palpably abnormal. Radiographically the hemivertebra and adjacent vertebrae appear to be formed of normal bone tissue with smooth cortical shadows. Adjacent disc spaces are usually well-formed but may be wider or narrower than normal. Vertebral end plates are smooth and may have normal thickness or be sclerotic. Adjacent vertebrae may have a compensatory shape (Figs. 1 and 3). Vertebral osteophytes may be present owing to abnormal distribution of mechanical forces in the malformed area of the spine (Fig. 3). The differential diagnosis of hemivertebra includes traumatic or pathologic fracture. Myelography of the entire spine should be performed to ascertain the clinical significance of a hemivertebra and to look for other congenital or concurrent lesions that may be significant. The diagnosis of hemivertebra as the cause of neurologic deficits must be supported by neuroanatomic correlation between the clinical and radiographic lesion, radiographic demonstration of cord compression at the site of the

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Figure 2. Butterfly vertebra. Ventrodorsal radiograph of a 2-year-old Bulldog with failure of formation of the central portion of the T6 (arrow) yielding a butterfly vertebra.

Figure 3. Hemivertebrae. Lateral radiograph of the thoracic vertebrae of a 2-year-old French Bulldog with hemivertebrae of T4-T6 and T9 (solid arrows). The T3 and T7 vertebral bodies and the T7 spinous process have developed a compensatory shape, and spondylosis is also present (open arrow) indicating some instability. The dog had progressive paraparesis with upper motor neuron signs in the pelvic limbs. Pathologic examination revealed spinal cord compression at the site of the hemivertebrae.

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hemivertebra (Fig. 4), and elimination of other lesions as causes of the myelopathy. Treatment

Spinal cord compression by a hemivertebra may be treated by surgical decompression and stabilization if necessary. In uncomplicated cases, particularly in young animals with mild neurologic deficits, clinical signs may resolve satisfactorily following surgery. Thepossibility of associated neural malformation must be kept in mind, however, and a cautious prognosis should be given.

Figure 4. Hemivertebrae. Lateral radiograph (A) and lateral myelogram (B) of the cranial thoracic spine of 4-month-old Bulldog with hemivertebrae and kyphosis at T3 and T4 (open arrow). The myelogram shows elevation of the ventral contrast column (solid arrows) and thinning of both contrast columns indicating spinal cord compression. Neurologically, the dog had an upper motor neuron paraparesis.

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Block Vertebra

A block vertebra is the result of failure of segmentation, attributed to abnormalities of the intersegmental arteries in the developing embryo.64 The malformation may occur at any point along the spine and may involve part or all of a vertebra (Fig. 5). Often the block vertebra is shorter in length than the equivalent number of normal segments, and abnormal angulation of the spine or stenosis of the vertebral canal may be present (Fig. 6). Block vertebra is usually an incidental radiographic finding. Pain and neurologic deficits secondary to neural compression may be produced, however, by a stenotic block vertebra (Fig. 6), spinal angulation, or instability (Fig. 7) associated with the malformation. 23 The differential diagnosis for block vertebra includes vertebral fusion secondary to discospondylitis, vertebral fracture/luxation, or disc surgery, but the reactive bone associated with these lesions is not present with a block vertebra. The diagnostic and therapeutic approach to block vertebra is similar to that of hemivertebra already described. MALFORMATIONS OF THE OCCIPITAL BONES, ATLAS, AND AXIS

Three major types of spinal column malformations occur at the craniovertebral junction of dogs and cats: (1) malformations of the dens,

Figure 5. Block vertebra. Lateral (A) and ventrodorsal (B) radiographs of a 4-year-old Dachshund. The fifth and sixth lumbar vertebral bodies form a partial block vertebra, with a remnant of the intervertebral disc evident (arrows). The dog had no neurologic deficits referable to this malformation.

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Figure 6. Focal spinal stenosis and block vertebra. This block vertebra, composed of the T13 and L1 segments (arrows), produced spinal stenosis and upper motor neuron paraparesis in this puppy.

Figure 7. Block vertebra. Lateral radiograph of a 5-year-old mixed-breed cat with a block vertebra composed of the fifth, sixth, and seventh lumbar segments (straight arrow) and associated kyphosis. Note the laminae also are involved in the block formation. The malformation resulted in lumbosacral instability, spondylosis (curved arrow), and lumbosacral pain.

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(2) occipitoatlantoaxial malformations, and (3) occipital dysplasia. Atlantoaxial subluxation and spinal cord trauma/compression are the significant clinical sequelae to the first two conditions. Occipital dysplasia, producing the keyhole shape, or dorsal notch, of the foramen magnum, has doubtful clinical significance. Malformations of the Dens

Malformations of the odontoid process of the axis are predominantly seen in miniature and toy breeds of dogs but also occur sporadically in other dogs. The dens is abnormally short or may even be absent (Figs. 8 and 9). In some dogs, a separate ossicle may be present between the tip of the short dens and the foramen magnum. These abnormalities have been attributed to the congenital absence of an ossification center for the dens 19, 32 or to the development of the dens as a separate ossification center. 41 ,45 Observations on the development of ossification centers in miniature and nonminiature breeds, however, are not compatible with these hypotheses. 74, 77 Instead Watson and Stewart77 propose a trauma-induced ischemic necrosis of the mid portion of the dens as the cause of the abnormality. The breed predilection has not yet been explained, and further work on the pathogenesis of this condition needs to be done. Other malformations associated with the dens are abnormal angulation of the dens reported in two dogs 47, 63 and absence of the transverse ligament of the atlas in a dog. 71

Figure 8. Malformation of the axis and atlas and occipital bones. Lateral (A) and ventrodorsal (B) radiographs of a 7-year-old Toy Poodle with an history of intermittent, upper motor neuron quadraparesis that was worse in the thoracic limbs. The body of the axis is abnormally shaped, the dens is hypoplastic (arrow), and the atlas is hypoRlastic with an abnormally thin lamina. The occipital bone also is thin, and the occipital condyles are not well-formed.

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Figure 9. Malformation of the dens and atlas. Lateral (A) and ventrodorsal (B) radiographs of a 10-month-old Pomeranian with a history of progressive upper motor neuron quadraparesis. The absence of the dens is apparent on both views (single arrows). Atlanta-axial luxation is demonstrated by an increased distance between the C1 lamina and the C2 spinous process (A, double arrow) and malalignment of C1 and C2 (B). The atlas also is hypoplastic with an abnormally short cranial-caudal dimension and thin lamina.

A number of dogs with odontoid process malformations also have a malformed atlas or occipital dysplasia (see Figs. 8 and 9). The craniocaudal dimension of the atlas is shorter than normal,12 and the lamina is abnormally thin. This malformation of the atlas is not reported to be the cause of neurologic disease. The presence of a thin lamina is important, however, because wire placed around the lamina in the dorsal stabilization procedure may cut through the lamina causing failure of the stabilization. Occipital dysplasia is discussed later. Clinical Signs

Except for the cases of abnormal dens angulation, which produced direct spinal cord compression, the common clinical sequela to odontoid process malformations is atlantoaxial instability and subluxation (see Fig. 9), resulting in trauma and compression of the spinal cord (Fig. 10). Affected dogs are usually less than 1 year of age, although occasionally adults are affected. In these older dogs, the clinical expression of the malformation may be due to progressive weakening and ultimate failure of the ligaments supporting the abnormal atlantoaxial articulation or to trauma superimposed on the weak articulation. Clinical signs vary from cervical pain to complete, transverse, cranial cervical myelopathy and may be acute, chronic, or episodic. Often the thoracic limb neurologic deficit is more severe than the pelvic limb deficit. The

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Figure 10. Spinal cord trauma due to atlanto-axial luxation. This 1-year-old Maltese ran into a door and was acutely quadraplegic. Necropsy revealed absence of the dens and severe spinal cord hemorrhage and malacia (arrows) secondary to atlanto-axial luxation. (Courtesy of Robert J. Higgins, BVSc, PhD, Davis, CA.)

trauma to the spinal cord may be so severe that hemorrhage and edema extend into the brain stem, producing caudal brain stem and cranial nerve deficits. The authors have seen several dogs with a history of acute opisthotonic episodes, which lasted for a few minutes to approximately an hour. These episodes were thought to be seizures, and the dogs were referred for determination of the cause of the seizures. Further questioning of the owners revealed that the dogs were not unconscious during these episodes and that the episodes were related to exercise or falling rather than sleep or drowsiness. These facts suggested that, at least, the dogs were not having generalized seizures. Radiographs demonstrated odontoid malformations and atlantoaxial subluxation, and the episodes ceased with stabilization of the atlantoaxial joint. A similar clinical syndrome may have been seen by Watson and deLahunta 71 and Denny et al. 12 Diagnosis

The diagnosis of dens malformation is made by radiographic demonstration of the anomaly. The abnormally shaped dens (or absence of the dens) may be seen on ventrodorsal views (see Figs. 8 and 9) or

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on oblique lateral views, which rotate the transverse processes of C-l so they are not superimposed on the dens. Open-mouth views may also show the abnormality but may be dangerous because of flexion of the atlantoaxial joint. Straight lateral views may show the subluxation as a greater than normal distance and angulation between the vertebral arches of C-l and C-2 (see Fig. 9). A flexed lateral view may demonstrate the subluxation even more dramatically, but again this positioning is dangerous. Treatment

Treatment includes therapy of spinal cord trauma and compression, if present, and stabilization of the atlantoaxial joint. For the principles of therapy of spinal cord trauma and compression, the reader is referred to current textbooks on veterinary neurology. Stabilization of the joint may be achieved by surgical stabilization; a number of techniques have been described. 12, 28, 60, 70 In some dogs, particularly small, young dogs, external support may suffice. Surgical stabilization is more secure, but the morbidity/mortality rate is high in dogs with acute, severe myelopathies, particularly with the dorsal wiring technique. 12 In these cases, aggressive medical therapy and external support may be preferable until the dog is more stable, at which time surgical stabilization can be done. Dogs with cervical pain or mild neurologic deficit may be managed with only medical therapy and external support. The authors have treated several young dogs in this fashion using human cervical collars. Gilmore22 also reported success with this treatment regimen. Occipitoatlantoaxial Malformation

Occipitoatlantoaxial malformation is a collective name given to the group of congenital malformations that affect the occipital bones, the atlas, and the axis. The malformation is characterized by fusion of the atlas to the occipital bones; a hypoplastic atlas, often with rudimentary transverse processes; and an axis with enlarged transverse processes and hypoplastic spinous process and dens. Congenital occipitoatlantoaxial malformations are rare in domestic animals but have been reported in dogs and a cat. 53, 72, 75 The malformation may be an example of transitional vertebrae with occipitalization of the atlas and atlantalization of the axis (particularly as occurs in the familial malformation of Arabian horses 76 ). In contrast, the asymmetrical malformations reported in the dog and cat may result from faulty joint development. 72 Although a developmental relationship exists between malformations of the axial mesenchyma-derived tissue and neural tube malformations, cases of occipitoatlantoaxial malformation associated with cranial cervical spinal cord anomaly have not been reported in the dog or cat. (One case has been reported in a calf. 33 ) Thus neurologic signs of cranial cervical myelopathy associated with this malformation are the result of concurrent atlantoaxial subluxation, which is a frequent finding. History and

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clinical signs are therefore similar to those already described for atlantoaxial subluxation associated with odontoid process malformations. The treatment of the atlantoaxial subluxation is also similar. Surgical stabilization, however, may be complicated by abnormal stress distribution produced by occipitoatlantal fusion, and the stabilization technique must be carefully planned. 53 Dorsal Notch of the Foramen Magnum (Occipital Dysplasia46)

An unusually large foramen magnum with a dorsal midline extension or keyhole shape has been associated with a variety of clinical signs in the dog, including ataxia, seizures, personality changes, dysphagia, and paresis. 4, 27 This malformation, however, is found in many neurologically normal miniature and toy breed dogs as well as sporadically in other dogs, and the clinical significance has therefore been questioned. 46, 81 A recent study of the shape and ossification pattern of the supraoccipital bone found marked variation in shape and a dorsal notch in 33 of 36 skulls examined. None of the dogs had neurologic deficits referable to the brain or spinal cord. The authors concluded that the dorsal notch should be regarded as a variation in the normal morphologic pattern and not an anomaly.73 Dogs with caudal brain stem, cerebellar, or cranial cervical spinal cord signs should be thoroughly investigated with appropriate diagnostic procedures, including cerebrospinal fluid analysis and preferably computed tomography or magnetic resonance imaging, before occipital dysplasia is implicated as the cause of the clinical problems. OSTEOCARTILAGINOUS EXOSTOSES (OSTEOCHONDROMATOSIS)

Osteocartilaginous exostoses are cartilage-capped bony projections that arise from the epiphyseal-metaphyseal regions of bones that develop by enchondral ossification. The vertebrae, ribs, and long bones are most frequently affected. The exostoses are theorized to be the result of displacement of a group of chondrocytes from the periphery of a growth plate (physis). The chondrocytes move shaftward as the bone grows, and subsequently "new" growth plates develop producing bony projections at right angles to the bone shaft. The exostoses are formed and enlarge by endochondral ossification. Histologically exostoses resemble the physis and metaphysis of growing bone, with normal cortical and cancellous bone and a cap of hyaline cartilage. Growth of the exostoses generally ceases when skeletal maturity is reached. Radiographically exostoses appear as well-marginated bony projections of variable size and shape protruding from any bone except the flat bones of membranous origins (Fig. 11). Radiolucent areas of cartilage may be present within the exostoses.

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Figure 11. Multiple osteocartilaginous exostoses. This 2-year-old Malamute had a 4-week history of paraparesis with upper motor neuron signs in the pelvic limbs. Several exostoses are visible on the lateral (A, B) and ventrodorsal (C) spinal radiographs (arrows). At necropsy, an exostosis at T10 was found compressing the spinal cord. This exostoses was difficult to see on the noncontrast radiographs. Myelography would be necessary to better demonstrate this lesion.

Solitary Exostoses

Solitary exostoses have been infrequently reported in the veterinary literature and appear to be of two different forms, solitary osteocartilaginous exostoses and solitary cartilaginous exostoses. Solitary Osteocartilaginous Exostoses

These exostoses occur, as described previously, as outgrowths from endochondral bones and containing elements of normal bone and cartilage and are rare in the dog and cat. 1, 50, 51, 54, 55, 67 Solitary lesions may in fact be a variant of multiple cartilaginous exostosis (see next) or simply represent situations in which other exostoses were not discovered. If an exostosis is solitary, complete excision should be curative. Solitary Cartilaginous Exostoses

The solitary cartilaginous exostoses reported by Bichsel et aP all occurred as masses between the dorsal vertebral laminae of the first two cervical vertebrae. The masses appeared to arise from the dorsal lamina of C-l or from the dorsal atlantoaxial ligaments and produced

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spinal cord compression either directly or by displacement of the vertebrae. The masses contained fibrous and cartilaginous tissue with areas of dystrophic calcification. The lack of bone formation in the lesions differentiated them from osteocartilaginous exostoses and prompted the authors to apply the term cartilaginous exostoses. A family history of the affected dogs could not be established. Multiple Cartilaginous Exostoses (Osteochondromatosis)

Multiple cartilaginous exostoses (MCE) occur in the dog and cat, but the canine and feline disease have important differences from each other. Canine Multiple Cartilaginous Exostoses

Canine MCE is a disease of immature dogs, with the lesions appearing and enlarging during endochondral bone formation (see Fig. 11). No breed or sex predisposition is apparent, although a hereditary basis is suspected. 9, 21 Malignant transformation of the exostoses may occur, yielding osteosarcoma or chondrosarcoma. 3, 13,43 Thus the disease resembles the disorder of hereditary multiple exostoses of people. 20 Because of the existence or future development of multiple lesions and the possibility of malignant transformation before surgical removal, the prognosis for cure by surgical removal is guarded. Feline Multiple Cartilaginous Exostoses

Feline MCE is a different disease entity than MCE in the dog, with a probable relationship to feline leukemia virus. 49, 67 The disease occurs primarily in young adult cats, and the lesions usually originate from the perichondrium of flat or irregular bones such as the skull, scapula, pelvis, rib, and vertebrae. Two cats with unusual foci, lesions of the elbow and stifle joints, were reported by Hubler et al. 24 Unlike the disease in the dog, the bone masses first appear after skeletal maturity and rapidly enlarge resulting in unsightliness or potentially fatal organ dysfunction. Clinical Signs, Diagnosis, and Treatment

The most common neurologic manifestation of exostoses is transverse myelopathy caused by spinal cord compression, although cauda equina syndrome or even mononeuropathy is possible depending on the site of the exostosis. Radiographically spinal exostoses are seen most clearly if they are part of one of the projecting processes or have a component on the outside of the vertebral lamina (see Fig. 11).

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Exostoses contained within the vertebral canal are difficult to identify on non-contrast enhanced films. Myelography or other imaging technique is necessary to confirm spinal cord or cauda equina compression. Diagnosis of exostosis as the cause of neurologic dysfunction is made by a positive correlation between the location of an exostosis and the neuroanatomic location of the lesion as indicated by the neurologic examination. Differential diagnosis of the radiographic osseous density potentially includes other bone tumors, fracture callus, and fungal bone infection. Definitive diagnosis of exostosis is made by histologic examination of a biopsy specimen. Treatment of the neurologic dysfunction involves surgical removal of the exostosis and decompression of affected neurologic structures. Prognosis for recovery of neurologic function depends on the severity of the deficit and completeness of removal of the exostotic lesion. If removal is complete and the animal has reached skeletal maturity, regrowth of the lesion is not likely. A cautious prognosis should be given because of the possibility of additional, undetected exostoses and the potential for malignant transformation. SPINA BIFIDA

Spina bifida and associated abnormalities have been reported in the dog and cat as well as other vertebrate species; for recent veterinary reviews, see Child and LeCouteur,lO Wilson,8o and Braund. 6 This defect is part of the complex of spinal dysraphism and is the most common dysraphic defect. Dysraphism (raphe [Greek], seam) means defective fusion of parts that normally unite. 61 Spina bifida is the absence of a portion of the dorsal elements of the vertebra owing to failure of formation during embryologic development (Figs. 12 and 13). The defect may occur with no clinically obvious neural or orthopedic malformation or dysfunction and in this situation is termed spina bifida occulta. In humans, however, spina bifida is often associated with intraspinal or intracranial dysraphic defects (e.g., occult spinal dysraphism and Arnold-Chiari malformation), other vertebral malformations (e.g., hemivertebra and block vertebra), and genitourinary malformations. Such association has also been reported in animals, particularly Bulldogs (Fig. 14) and Manx cats. u , 80 The term spina bifida aperta (spina bifida manifesta, spina bifida cystica, myelodysplasia) applies to the open dysraphic disorders, that is, lesions that are open or threatening to be open to the environment. Thus spina bifida aperta encompasses the cystic forms (protruding cyst containing meningeal or neural tissue-meningocele, myelomeningocele [Fig. 15]) as well as myeloschisis (a flat plaque of neural tissue open to the body surface). Other neural malformations are particularly frequent in humans with spina bifida aperta; virtually all infants with spina bifida aperta also have Arnold-Chiari malformation. 18, 48 The embryogenetic theories of spina bifida fall into four general categories: (1) the developmental arrest theory attributed to von Recklinghausen, (2) Patten's neural overgrowth hypothesis, (3) the hydrodynamic theory of Gardner,

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Figure 12. Spina bifida. Ventrodorsal radiograph of a pathology specimen from a 6-monthold Pug, in which the laminae and spinous process of T1 have failed to fuse (arrow). This is the same dog shown in Figure 1.

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Figure 13. Spina bifida. Radiograph of a transverse section of a thoracic vertebra with a bifid spinous process (arrow). This lesion was an incidental finding.

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Figure 14. Spina bifida. Lateral survey radiograph (A) and myelogram (B) of a 1-year-old Bulldog with lower motor neuron fecal and urinary incontinence. The noncontrast radiograph shows an increase in the ventrodorsal diameter of the caudal lumbar vertebral canal (solid arrows). The myelogram shows divergence of the contrast columns, suggesting widening of the spinal cord. Pathologic examination detected syringomyelia and hydromyelia. Sacral spina bifida (open arrows) in particular can be associated with congenital spinal cord malformations.

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Figure 15. Myelomeningocele. Malformed caudal lumbosacral spinal cord (straight arrow) and meninges (curved arrow) of a myelomeningocele in a dog with lumbosacral spina bifida. The dog had lower motor neurons signs of the pelvic limbs, bladder, and anus. (Courtesy of Robert J. Higgins, BVSc, PhD, Davis, CA.)

and (4) the theory of neuroschisis proposed by Padget. The pathology of spina bifida is so diverse, however, that no single theory is likely to explain all forms of this disorder or of spinal dysraphism in general. 18 The relatively high incidence of spina bifida in some breeds of animals (e.g., Bulldogs, Manx cats) suggests a heritable basis to the disorder. I?, 29 Teratogenic compounds, nutritional deficiencies, and environmental changes during pregnancy are also known to induce this defect. 8, 26 A combination of several genes and several environmental factors may interact to produce the malformation. 66 Clinical Findings

Clinical findings vary with the severity and location of the malformation. The severe deformities of spina bifida aperta are evident at birth as dorsal midline, open regions of the spinal canal, or protruding cysts often draining cerebrospinal fluid. Less severe lesions may have abnormal directions of hair growth, a skin dimple at the site 'of the malformation, or an open tract draining cerebrospinal fluid (Fig. 16).

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Figure 16. Spina bifida with myelomeningocele. The lateral (A) and ventrodorsal (B) radiographs of this 5-month-old Bulldog show sacrocaudal dysgenesis and spina bifida of L6, L7, and the sacrum. The survey radiographs show the defect most clearly in the lamina of L7 (white arrows). The myelogram (C) demonstrates the dorsal deviation of terminal spinal cord (black arrows) into the myelomeningocele, as well as a tract to the skin (open arrow) that was draining cerebrospinal fluid.

The spinal defect may be palpable. Physical examination may be normal, but neurologic deficits may be present and reflect the site of the malformation, which is usually in the lower lumbar or sacral spine in minimally affected animals. The neurologic deficits may also reflect malformations elsewhere in the central nervous system. Animals with simple spina bifida occulta have no neurologic deficits related to the malformation, which is usually discovered as an incidental radiographic finding (Fig. 17). Diagnosis and Treatment

The vertebral arch defect is evident on non-contrast enhanced radiography (see Figs. 16 and 17). If treatment is contemplated, contrastenhanced radiography or imaging techniques will yield additional information about the morphology of the malformation and will aid in the planning of surgical intervention. Treatment of spina bifida in animals is rarely attempted. Severe lesions are incompatible with life or an acceptable quality of life as well as being unsightly, and animals so affected are usually euthanatized. Animals with less severe forms of spina bifida aperta and mild neuro-

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Figure 17. Spina bifida. Lateral (A) and ventrodorsal (B) radiographs of 4-year-old mixedbreed cat with no neurologic deficits. Spina bifida of L6, with absence of the spinous process (arrows), was an incidental finding.

logic deficits may respond to reconstructive surgical procedures, as long as primary spinal cord anomalies are not present. In planning therapy, the clinician must remember the potential for additional malformations to be present. SPINAL STENOSIS

Spinal stenosis is a generic term indicating a narrowed vertebral canal that may produce a variety of neurologic syndromes owing to compression of the spinal cord, cauda equina, nerve roots or spinal nerves. The stenosis can be focal, segmental (affecting a few vertebrae), or generalized throughout the spine. The existence of different classifications of human spinal stenosis 2, 36, 69 reflects the lack of understanding regarding the pathogenesis of some categories of this disorder, and the situation is no clearer in veterinary medicine. Verbiest69 proposed the following simplified classification of human stenosis: I. Stenosis produced by the bony walls A. Congenital stenosis B. Developmental stenosis owing to inborn errors of skeletal growth C. Idiopathic developmental stenosis D. Acquired stenosis E. Recurrent stenosis II. Stenosis produced by the nonosseous components of the walls of the vertebral canal

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A. Hypertrophy of the posterior (dorsal) longitudinal ligament-or ligamentum flava B. Massive central disc herniation or massive subligamentous extrusion of sequestered disc material Some elements of Verbiest's classification seem applicable to animals and are utilized in this discussion of congenital and genetically associated stenoses. Congenital Spinal Stenosis

The word congenital is used to indicate that the stenosis is a specific malformation of the spine (or part of a more extensive spinal malformation) that is present at birth; however, the causative agents are no longer active, as such, during postnatal life. 69 The stenosis may occur alone as a primary lesion (Fig. 18)30, 40, 62, 79 or in association with other congenital anomalies of the spinal cord or spine. 30, 58 In humans, focal or segmental congenital stenosis may occur with spinal dysraphism or as a result of block or transitional vertebrae. 69 Pain and neurologic deficits have also been reported in dogs with block vertebrae (see Fig. 40 6).23,34 Transitional vertebrae in dogs may also be stenotic or predispose an animal to acquired stenosis. A strong association between lumbosacral transitional vertebra and cauda equina syndrome has been shown for the German Shepherd (Fig. 19).39 The transitional segment may not be stenotic but may predispose adjacent intervertebral discs to early degeneration and potential disc protrusion, vertebral instability or malalignment, and neural compression by hypertrophy of adjacent soft tissue. 4o The initial manifestation of clinical signs in middle age does not preclude the congenital origin of stenosis. Congenital stenosis may also occur in association with hemivertebrae. This condition is discussed under "Hemivertebra and Block Vertebra." The concept of absolute versus relative stenosis is important. Absolute stenosis indicates a midsagittal vertebral diameter that is small enough to result in direct neural compression. Relative stenosis implies a diameter that is less than "normal" but asymptomatic. Relative stenosis carries a risk of becoming symptomatic on the development of space-occupying conditions of the vertebral canal, such as disc protrusion, that would otherwise be clinically insignificant. 16, 68 Most dogs, and humans, develop clinical signs associated with stenosis in adult life. The existence of a relative stenosis, rather than an absolute stenosis, may playa role in this delayed onset. Thoracic Vertebral Stenosis in Doberman Pinschers

The authors have frequently noted the presence of segmental vertebral stenosis in the cranial thoracic spine of Doberman Pinschers

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Figure 18. Segmental spinal stenosis. Lateral (A) and oblique (B, C) myelographic views of the cranial thoracic vertebrae of an 8-month-old Bullmastiff. The dog had a 2-month history of upper motor neuron paraparesis. The T3 and T4 vertebrae are stenotic. The contrast columns are thinned (arrows) and the spinal cord is narrowed on all views, indicating spinal cord compression in this area.

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Figure 19. Transitional vertebra. Lateral and ventrodorsal radiographs of a 7-year-old German Shepherd with a lumbosacral transitional vertebra. The lateral view (A) shows the failure of fusion of the first sacral segment (straight arrow), and the ventrodorsal view (8) shows the asymmetry of the transverse processes of that segment (curved arrows). This dog had difficulty rising and jumping and hindquarter muscle atrophy, but also had severe hip dyspasia. Notice the prosthetic implant in the left coxafemoral joint.

(Fig. 20). The malformation is seen on non-contrast enhanced spinal radiographs of these dogs, most of which are radiographed for the diagnosis of a cervical myelopathy and subsequently diagnosed as having caudal cervical spondylopathy or disc protrusion. Vertebrae T-3-T-6 are most commonly affected and show a decrease in the dorsoventral diameter of the vertebral canal as compared with adjacent vertebrae. A mild curvature of the spine, a combination of lordosis and kyphosis, is also present. Spinal cord compression is usually not present, as determined by myelography. The contrast columns may be attenuated, however, and the potential for cord compression certainly exists (Fig. 21). Interestingly Hoerlein23 illustrated cranial thoracic kyphosis in a 10-month-old Doberman Pinscher, and Leyland35 reported a hemivertebra and stenosis at T-5 producing spinal cord compression in a Doberman Pinscher puppy. Developmental Stenosis Owing to Inborn Errors of Skeletal Growth

The term inborn errors indicates incoordination of ossification and bone growth as a consequence of hereditary transmission or fresh mutation of a normal gene. The errors are based on metabolic or other disturbances of cells involved in skeletal development. The dispropor-

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Figure 20. Thoracic spinal stenosis of a Doberman Pinscher. Lateral noncontrast radiograph (A) and lateral myelogram (B) of a 10-year-old Doberman Pinscher showing segmental stenosis of T3 and T4. On the myelogram, the ventral contrast column is thinned (arrows) and the spinal cord is displaced dorsally. The dog's neurologic signs were not localizable to this lesion.

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Figure 21. Thoracic spinal stenosis of a Doberman Pinscher. Lateral myelogram of a 7year-old Doberman Pinscher. The T4 vertebra is stenotic, the ventral contrast column is thinned (arrows), and the spinal cord appears narrowed. The myelogram also showed cord compression due to a C5-C6 Type II disc protrusion. Neurologically, the dog had a caudal cervical myelopathy with more pronounced deficits in the pelvic limbs than the thoracic limbs. The contribution of the stenotic lesion to the dog's clinical syndrome is unknown but interesting to consider.

tionate bone growth is already present at birth, but the causative agents remain active during maturation; therefore the term developmental is used to distinguish this group from the congenital stenoses. 69 Stenoses associated with achondroplasia and hypochondroplasia in humans are examples of conditions included in this category. These conditions result in generalized spinal stenosis, which is usually more pronounced in the lumbar spinal column. The vertebrae have concentrically narrow vertebral canals, scalloped vertebral bodies, and short pedicles. The spinal cord and cauda equina are normal size, however, resulting in a disproportion between the dimensions of the vertebral canal and the volume of its contents. This condition is also seen in dogs. 38 The relative stenosis in chondrodystrophic dogs may be part of the reason that -clinical disc protrusion is more common in these dogs than in nonchondrodystrophic dogs. In humans, stenosis of the bony chondrodysplastic vertebral canal frequently increases during postnatal growth because ,of excessive periosteal bone formation, resulting in thickening of the pedicles, laminae, and articular processes. 69 As with congenital stenosis, clinical signs may not develop until later in life and may be related to only one level of the stenotic spine. 36, 37 Idiopathic Developmental Stenosis

The word developmental indicates a genetic disturbance in which pathologic effects are apparent in their entirety only when growth is complete and the vertebrae have attained full size. 69 In humans, clinical signs develop in adult life, and symptoms may not occur unless an

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additional factor compromises the available space. About 50% of the human cases are complicated by disc herniation. The pathomorphology of human idiopathic developmental stenosis shows some similarities to that of achondroplasia, such as scalloping of the lumbar vertebral bodies, a high incidence of disc herniations above the L-4 level, and thickening of the bone of the vertebral arches. The hypertrophy of bone is limited to structures of the vertebral arch, that is, the pedicles, laminae, and articular processes; the ligamenta flava may also be hypertrophied. 36 These similarities may be a reason for considering that developmental stenosis is the result of another type of inborn error of growth. 16,69, 78 Inappropriate nutrition has also been proposed as a factor in humans. 36 The 15 cases of canine lumbosacral stenosis reported by Tarvin and Prata65 may belong in this category. These dogs had no radiographic evidence of spondylosis, instability, neoplasia, infection, or disc degeneration, although contrast-enhanced radiography was done on only one dog. No mention was made of the presence of vertebral malformations. Thickened vertebral laminae, pedicles, and ligamenta flava were noted at surgeries performed on the dogs. The fact that three of the dogs in this study were chondrodystrophic (Beagle,7 Lhasa Apso) is interesting. Clinical Signs of Spinal Stenosis

Regardless of cause, the clinical signs of spinal stenosis reflect the site of the lesion. The signs of lumbar spinal stenosis, the most commonly reported stenotic condition in dogs, have been reported and reviewed in numerous articles, including those by Child and LeCouteur/ o Indrieri,25 Morgan and Bailey,40 Schulman and Lippincott,57 Lenehan,34 and Braund. 6 The clinical signs usually constitute a cauda equina syndrome, although lumbar myelopathy or even mononeuropathy from compression of nerve roots or a spinal nerve within a stenotic intervertebral foramen is possible. Abnormalities may be unilateral or symmetrically or asymmetrically bilateral. The onset may be acute or insidious, with a progressive or intermittent course. Neurogenic intermittent claudication (exercise-induced lameness caused by compression or ischemia of neural structures that have been clinically or subclinically damaged by stenosis16, 69) is a common symptom in humans and seems to occur in dogs as well.57, 65 As a breed, the German Shepherd is overrepresented in reports of dogs with cauda equina syndrome owing to lumbar spinal stenosis/ compression (not including trauma, infection, or neoplasia). Some of these dogs have vertebral malformations such as transitional vertebrae (see Fig. 19); others apparently have stenosis of the sacral vertebral canal. Most are reported as having L-7-S-1 spondylosis and subluxation, some of these with L-7-S-1 disc protrusions, and no malformations or bony stenosis. 40, 42, 57 These latter cases may simply represent degen-

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erative conditions of the spine, resulting in or from disc protrusion. Clearly this syndrome, or syndromes, in the German Shepherd requires careful characterization.

Diagnosis The diagnosis of congenital or developmental stenosis is made primarily by radiography. Because these categories of stenosis have bony changes, theoretically the disorder should be visible on noncontrast enhanced radiographs (see Figs. 6 and 20). Unfortunately overlying structures such as the vertebral bodies and pelvis and the common occurrence of degenerative changes such as disc degeneration and spondylosis can make the accurate visualization of stenotic abnormalities difficult. Contrast-enhanced radiography, such as epidurography, discography, or myelography, is usually necessary to demonstrate compression of neural structures and eliminate other potential causes of the clinical signs (see Figs. 18, 20, and 21).40 The imaging techniques of planar tomography, computed tomography, and magnetic resonance imaging allow more accurate characterization of the bony abnormalities. Electrodiagnostic tests such as electromyography, nerve conduction velocity determination, evoked potential studies, urethral pressure profile, and cystometry may be necessary to verify and localize the lesion in animals with subtle clinical signs and radiographic signs.

Treatment Treatment of spinal stenosis may be either medical, primarily directed at pain relief, or surgical. Management with analgesic and anti-inflammatory drugs and rest may be adequate in animals with mild symptoms. In many instances, however, the animal becomes refractory to such therapy as the stenotic condition worsens. Decompressive surgery is indicated in these cases and may actually be more beneficial if performed early in the course of the disease. Dorsal laminectomy and deep dorsal laminectomy, combined with facetectomy and foraminotomy as necessary, are the surgical procedures of choice. 52, 57, 65 Internal stabilization or fusion may be indicated in animals with gross instability evident on stress radiography. 42, 59 Pain relief following surgery is often dramatic, and in general the clinical signs in most animals abate satisfactorily, if not completely, following surgical intervention. Disappointing results are often seen in animals with urinary and fecal incontinence, but this may be due in large part to owner intolerance of any subnormal excretory function.

References 1. Ackerman N, Halliwell WH, Renze IG, et al: Solitary osteochondroma in a dog. J Am Vet Rad Soc 14 (2):13-15, 1973 2. Arnoldi CC, Brodsky AE, Cauchoix J, et al: Lumbar spinal stenosis and nerve root entrapment syndromes. Clin Orthop 115:4-5, 1976

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3. Banks WC, Bridges CH: Multiple cartilaginous exostosis in a dog. J Am Vet Med Assoc 129:131-135, 1956 4. Bardens JW: Congenital malformation of the foramen magnum in dogs. Southwest Vet 18:295-298, 1965 5. Bichsel P, Lang J, Vandevelde M, et al: Solitary cartilaginous exostoses associated with spinal cord compression in three large-breed dogs. J Am Anim Hosp Assoc 21:619-622, 1985 6. Braund KG: Degenerative and developmental diseases. In Oliver JE, Hoerlein BF, Mayhew IG, eds: Veterinary Neurology. Philadelphia, WB Saunders, 1987, p 199 7. Braund KG, Ghosh P, Taylor TKF, et al: Morphological studies of the canine intervertebral disc. The assignment of the beagle to the achondroplastic classification. Res Vet Science 19:167-172, 1975 8. Campbell LR, Dayton OJ, Sohal GS: Neural tube defects: A review of human and animal studies on the etiology of neural tube defects. Teratology 34:171-187, 1986 9. Chester OK: Multiple cartilaginous exostoses in two generations of dogs. J Am Vet Med Assoc 159:895-897, 1971 10. Child G, LeCouteur RA: Diseases of the spinal cord. In Ettinger SJ, ed: Textbook of Veterinary Internal Medicine, ed 3. Philadelphia, WB Saunders, 1989, pp 685-686 11. DeForest ME, Basrur PK: Malformations and the Manx syndrome in cats. Can Vet J 20:304-314, 1979 12. Denny HR, Gibbs C, Waterman A: Atlanto-axial subluxation in the dog: A review of thirty cases and an evaluation of treatment by lag screw fixation. J Sm Anim Pract 29:37-47, 1988 13. Doige CE, Pharr JW, Withrow SJ: Chondrosarcoma arising in multiple cartilaginous exostoses in a dog. J Am Anim Hosp Assoc 14:605-611, 1978 14. Done SH, Drew RA, Robins GM, Lane JG: Hemivertebra in the dog: Clinical and pathological observations. Vet Rec 96:313-317, 1975 15. Drew RA: Possible association between abnormal vertebral development and neonatal mortality in bulldogs. Vet Rec 94:480-481, 1974 16. Epstein JA, Epstein BS: Stenosis of the lumbar and cervical spinal canal. In Vinken PJ, Bruyn GW, eds: Handbook of Clinical Neurology. Vol 32, Congenital Malformations of the Spine and Spinal Cord. New York, North-Holland, 1978, pp 329-346 17. Fingeroth JM, Johnson GC, Burt ]K, et al: Neuroradiographic diagnosis and surgical repair of tethered cord syndrome in an English Bulldog with spina bifida and myeloschisis. J Am Vet Med Assoc 194:1300-1302, 1989 18. French BN: Midline fusion defect and defects of formation. In Youmans JR, ed: Neurological Surgery, Vol 4, ed 3. Philadelphia, WB Saunders, 1990, pp 1081-1235 19. Gage ED, Smallwood JE: Surgical repair of atlanto-axial subluxation in a dog. Vet Med Small Anim Clin 65:583-592, 1970 20. Gambardell PC, Osborne CA, Stevens JB: Multiple cartilaginous exostoses in the dog. J Am Vet Med Assoc 166:761-768, 1975 21. Gee BR, Doige CE: Multiple cartilaginous exostoses in a litter of dogs. J Am Vet Med Assoc 156:53-59, 1970 22. Gilmore DR: Nonsurgical management of four cases of atlantoaxial subluxation in the dog. J Am Anim Hosp Assoc 20:93-96, 1984 23. Hoerlein BF: General spinal disorders. In Hoerlein BF, ed: Canine Neurology: Diagnosis and Treatment, ed 3. Philadelphia, WB Saunders, 1978, pp 447-448 24. Hubler M, Johnson KA, Burling RT, et al: Lesions resembling osteochondromatosis in two cats. J Sm Anim Pract 27:181-187, 1986 25. Indrieri RJ: Lumbosacral stenosis and injury of the cauda equina. Vet Clin North Am Small Anim Pract 18:697-710, 1988 26. Kalter H: Teratology of the Central Nervous System: Induced and Spontaneous Malformations of Laboratory, Agricultural and Domestic Animals. Chicago, University of Chicago Press, 1968 27. Kelly JH: Occipital dysplasia and hydrocephalus in a toy poodle. Vet Med Small Anim Clin 70:940-941, 1975 28. Kishigami M: Application of an atlantoaxial retractor for atlantoaxial subluxation in the cat and dog. J Am Hosp Assoc 20:413-419, 1984 29. Kitchen H, Murray RE, Cockrell BY: Animal models for human disease: Spina bifida, sacral dysgenesis and myelocele (in) Manx cats. Am J Pathol 66:203-206, 1972

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30. Knecht CD, Blevins WE, Raffe MR: Stenosis of the thoracic spinal canal in English Bulldogs. J Am Anim Hosp Assoc 15:181-183, 1979 31. Kramer JW, Schiffer WP, Sande RD, et al: Characterization of heritable thoracic hemivertebra of the German Shorthaired Pointer. J Am Vet Med Assoc 15:814-815, 1982 32. Ladds P, Guffy M, Blauch B, et al: Congenital odontoid proce~s separation in two dogs. J Sm Anim Pract 12:463-471, 1970 33. Leipold H, Brandt G, Strafuss A, et al: Congenital defect of the atlantooccipital joint in a holstein-Friesian calf. Cornell Vet 62:646-653, 1972 34. Lenehan TM: Canine cauda equina syndrome. Comp Cont Educ Pract Vet 5:941-950, 1983 35. Leyland A: Ataxia in a doberman pinscher. Vet Rec 116:414-415, 1985 36. Moreland LW, Lopez-Mendez A, Alarcon GS: Spinal stenosis: A comprehensive review of the literature. Semin Arthritis Rheum 19:127-149, 1989 37. Morgan DF, Young RF: Spinal neurological complications of achondroplasia. Results of surgical treatment. J Neurosurg 52:463-472, 1980 38. Morgan JP, Atilola M, Bailey CS: Vertebral canal and spinal cord mensuration: A comparative study of its effect on lumbosacral myelography in the Dachshund and German Shepherd Dog. J Am Vet Med Assoc 191:951-957, 1987 39. Morgan JP, Bahr A, Franti CE, Bailey CS: Lumbosacral transitional vertebrae as a predisposing cause of cauda equina syndrome in the German Shepherd Dog. J Am Vet Med Assoc; submitted for publication 40. Morgan JP, Bailey, CS: Cauda equina syndrome in the dog: Radiographic evaluation. J Sm Anim Pract 31:69-77, 1990 41. Oliver JE, Lewis RE: Lesions of the atlas and axis in dogs. J Am Anim Hosp Assoc 9:304-313, 1973 42. Oliver JE, Selcer RR, Simpson S: Cauda equina compression from lumbosacral malarticulation and malformation in the dog. J Am Vet Med Assoc 173:207-214, 1978 43. Owen LN, Bostock DE: Multiple cartilaginous exostoses with development of a metastasizing osteosarcoma in a Shetland Sheepdog. J Sm Anim Pract 12:507-512, 1971 44. Parker AJ, Adams WM, Zachary JF: Spinal arachnoid cysts in the dog. J Am Anim Hosp Assoc 19:1001-1008, 1983 45. Parker AJ, Park RD: Atlanto-axial subluxation in small breeds of dogs: Diagnosis and pathogenesis. Vet Med Sm Anim Clin 68:1133-1137, 1973 46. Parker AJ, Park RD: Occipital dysplasia in the dog. J Am Anim Hosp Assoc 10:520525, 1974 47. Parker AJ, Park RD, Cusick PK: Abnormal odontoid process angulation in a dog. Vet Rec 93:559, 1973 48. Pollay M: Spinal dysraphism: Aperta and occulta. In Rosenberg RN, Grossman RG, eds: The Clinical Neurosciences. Vol 2, Neurosurgery/Neurosurgery. New York, Churchill Livingstone, 1983, pp 1419-1433 49. Pool RR: Osteochondromatosis. In Bojrab MJ, ed: Pathophysiology in Small Animal Surgery. Philadelphia, Lea & Febiger, 1981, pp 641-649 50. Power JW: Osteochondromatosis in the racing Greyhound. J Sm Anim Pract 16:803807, 1975 51. Prata RG, Stoll SS, Zaki FA: Spinal cord compression caused by osteocartilaginous exostoses of the spine in two dogs. J Am Vet Med Assoc 166:371-375, 1975 52. Raffe MR, Knecht CD: Disorders of the lumbosacral plexus. In Newton CD, Nunamaker OM, eds: Textbook of Small Animal Orthopaedics. Philadelphia, JB Lippincott, 1985, pp 825-832 53. Read R, Brett S, Cahill J: Surgical treatment of occipito-atlanto-axial malformation in the dog. Aust Vet Pract 17:184-189, 1987 54. Rubin LF: What is your diagnosis? J Am Vet Med Assoc 138 (4):27-30, 1961 55. Schmidt RE, Langham RF: A survery of feline neoplasms. J Am Vet Med Assoc 151:1325-1328, 1967 56. Schmorl G, Junghanns H: The Human Spine in Health and Disease, ed 2 (American ed). New York, Grune & Stratton, 1971 57. Schulman AJ, Lippincott CL: Canine cauda equina syndrome. Comp Cont Educ Pract Vet 10:835-844, 1988 58. Shell LG, Carrig CB, Sponenberg DP, et al: Spinal dysraphism, hemivertebra, and

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stenosis of the spinal canal in a Rottweiler puppy. J Am Anim Hosp Assoc 24:341344, 1988 Slocum B, Devine T: L7-S1 fixation-fusion for treatment of cauda equina compression in the dog. J Am Vet Med Assoc 188:31-35, 1986 Smith GK, Walter MC: Fractures and luxation of the spine. In Newton CD, Nunamaker DM, eds: Textbook of Small Animal Orthopaedics. Philadelphia, JB Lippincott, 1985, pp 314-317 Stedman's Medical Dictionary, ed 24. Baltimore, William & Wilkins, 1982 Stigen 0, Hagen G, Kolbjornsen 0: Stenosis of the thoraco-Iumbar vertebral canal in a Basset Hound. J Sm Anim Pract 31:621-623, 1990 Swaim SF, Greene CE: Odontoidectomy in a dog. J Am Anim Hosp Assoc 11:663667, 1975 Tanaka T, Uthoff HK: The pathogenesis of congenital vertebral malformations. Acta Orthop Scand 52:413-425, 1981 Tarvin G, Prata RG: Lumbosacral stenosis in dogs. J Am Vet Med Assoc 177:154159, 1980 Thompson MW, Rudd NL: The genetics of spinal dysraphism. In Morley TP, ed: Current Controversies in Neurosurgery. Philadelphia, WB Saunders, 1976, pp 126146 Turrel JM, Pool RR: Primary bone tumors in the cat: A retrospective study of 15 cats and a literature review. Vet Radiol 23:152-166, 1982 Verbiest H: Neurogenic intermittent claudication in cases with absolute and relative stenosis of the lumbar vertebral canal (ASLC and RSLC), in cases with narrow lumbar intervertebral foramina, and in cases with both entities. Clin Neurosurg 20:204-214, 1972 Verbiest H: Lumbar spinal stenosis. In Youmans JR, ed: Neurological Surgery, Vol 4, ed 3. Philadelphia, WB Saunders, 1990, pp 2805-2855 Walker TL, Tomlinson J, Sorjonen DC, et al: Diseases of the spinal column. In Slatter DH, ed: Textbook of Small Animal Surgery. Philadelphia, WB Saunders, 1985, pp 1373-1379 Watson AG, deLahunta A: Atlantoaxial subluxation and absence of transverse ligament of the atlas in a dog. J Am Vet Med Assoc 15:235-237, 1989 Watson AG, deLahunta A, Evans HE: Morphology and embryological interpretation of a congenital occipito-atlanto-axial malformation in a dog. Teratology 38:451-459, 1988 Watson AG, deLahunta A, Evans HE: Dorsal notch of foramen magnum due to incomplete ossification of supraoccipital bone in dogs. J Sm Anim Pract 30:666-673, 1989 Watson AG, Evans HE, deLahunta A: Ossification of the atlas-axis complex in the dog. Anat Histol Embryol 15:122-183, 1986 Watson AG, Hall MA, deLahunta A: Congenital occipitoatlantoaxial malformation in a cat. Comp Cont Educ Pract Vet 7:245-252, 1985 Watson AG, Mayhew IG: Familial congenital occipitoatlantoaxial malformation (OAAM) in the Arabian horse. Spine 11:334-339, 1986 Watson AG, Stewart JS: Postnatal ossification centers of the atlas and axis in miniature schnauzers. Am J Vet Res 51:264-268, 1990 Watts C: Spinal stenosis. In Rosenberg RN, Grossman RG, eds: The Clinical Neurosciences. Vol 2, Neurology/Neurosurgery, New York, Churchill Livingstone, 1983, pp 1459-1465 Wheeler SJ: Vertebral abnormalities in dogs. J Sm Anim Pract 32:149-150, 1991 Wilson JW: Spina bifida in the dog and cat. Comp Cont Educ Pract Vet 8:626-635, 1982 Wright JA: A study of the radiographic anatomy of the foramen magnum in dogs. J Sm Anim Pract 20:501-508, 1979

Address reprint requests to Cleta Sue Bailey, DVM, PhD Department of Surgery University of California, Davis School of Veterinary Medicine Davis, CA 95616