DISEASES OF THE SPINE 0195-5616/92 $0.00 + .

20

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 develop-
ment 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 mal-
formations 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, Cali-
fornia

VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE

VOLUME 22 • NUMBER 4 • JULY 1992 985

986 BAILEY & MORGAN

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 find-
ings. 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 ossifica-
tion. 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), ven-
trally, 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 malfor-
mations. Although apparently rare, hemivertebrae may also be associ-
ated with malformations of neural tissue, for example, spinal
dysraphism58 and spinal arachnoid cyst. 44 Drew15 postulated an associ-
ation between hemivertebrae and neonatal mortality in English Bull-
dogs. 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,
 CONGENITAL SPINAL MALFORMATIONS 987

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 hemiver-
tebra as the cause of neurologic deficits must be supported by neuroan-
atomic correlation between the clinical and radiographic lesion, radio-
graphic demonstration of cord compression at the site of the
988 BAILEY & MORGAN

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 parapa-
resis with upper motor neuron signs in the pelvic limbs. Pathologic examination revealed
spinal cord compression at the site of the hemivertebrae.
 CONGENITAL SPINAL MALFORMATIONS 989

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. Thepossibil-
ity 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.
990 BAILEY & MORGAN

Block Vertebra

A block vertebra is the result of failure of segmentation, attributed

to abnormalities of the intersegmental arteries in the developing em-
bryo.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 radio-
graphic 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/luxa-
tion, 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.
 CONGENITAL SPINAL MALFORMATIONS 991

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 lumbo-
sacral pain.
992 BAILEY & MORGAN

(2) occipitoatlantoaxial malformations, and (3) occipital dysplasia. At-

lantoaxial subluxation and spinal cord trauma/compression are the
significant clinical sequelae to the first two conditions. Occipital dyspla-
sia, 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 predomi-

nantly 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 devel-
opment 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.
 CONGENITAL SPINAL MALFORMATIONS 993

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 quadra-
paresis. 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 expres-
sion 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. Clin-
ical 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
994 BAILEY & MORGAN

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 approx-
imately 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 atlan-
toaxial 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
 CONGENITAL SPINAL MALFORMATIONS 995

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 myelo-
pathies, 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 occipitoatlan-
toaxial 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 atlantali-
zation 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 concur-
rent atlantoaxial subluxation, which is a frequent finding. History and
996 BAILEY & MORGAN

clinical signs are therefore similar to those already described for atlan-
toaxial subluxation associated with odontoid process malformations.
The treatment of the atlantoaxial subluxation is also similar. Surgical
stabilization, however, may be complicated by abnormal stress distri-
bution produced by occipitoatlantal fusion, and the stabilization tech-
nique must be carefully planned. 53

Dorsal Notch of the Foramen Magnum

(Occipital Dysplasia46)

An unusually large foramen magnum with a dorsal midline exten-

sion 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 neuro-
logically 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 thor-
oughly 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 exos-
toses 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.
 CONGENITAL SPINAL MALFORMATIONS 997

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 osteocarti-
laginous 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 discov-
ered. 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
998 BAILEY & MORGAN

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 trans-

verse 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).
 CONGENITAL SPINAL MALFORMATIONS 999

Exostoses contained within the vertebral canal are difficult to identify

on non-contrast enhanced films. Myelography or other imaging tech-
nique 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 exam-
ination 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 devel-
opment (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, myelo-
dysplasia) 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 hu-
mans 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 devel-
opmental arrest theory attributed to von Recklinghausen, (2) Patten's
neural overgrowth hypothesis, (3) the hydrodynamic theory of Gardner,
1000 BAILEY & MORGAN

Figure 12. Spina bifida. Ventrodorsal radiograph of a pathology specimen from a 6-month-
old Pug, in which the laminae and spinous process of T1 have failed to fuse (arrow). This
is the same dog shown in Figure 1.
 CONGENITAL SPINAL MALFORMATIONS 1001

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.
1004 BAILEY & MORGAN

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.
 CONGENITAL SPINAL MALFORMATIONS 1003

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 en-
vironmental 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 malfor-
mation. 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).
1004 BAILEY & MORGAN

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, contrast-
enhanced 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-
 CONGENITAL SPINAL MALFORMATIONS 1005

Figure 17. Spina bifida. Lateral (A) and ventrodorsal (B) radiographs of 4-year-old mixed-
breed 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 classi-
fications 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
1006 BAILEY & MORGAN

A. Hypertrophy of the posterior (dorsal) longitudinal ligament-or

ligamentum flava
B. Massive central disc herniation or massive subligamentous extru-
sion of sequestered disc material
Some elements of Verbiest's classification seem applicable to ani-
mals 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 malfor-
mation) 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.
6).23,34 Transitional vertebrae in dogs may also be stenotic or predispose
40

an animal to acquired stenosis. A strong association between lumbo-

sacral 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 protru-
sion, 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
 CONGENITAL SPINAL MALFORMATIONS 1007

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.
1008 BAILEY & MORGAN

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 ky-
phosis 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-
 CONGENITAL SPINAL MALFORMATIONS 1009

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.
1010 BAILEY & MORGAN

Figure 21. Thoracic spinal stenosis of a Doberman Pinscher. Lateral myelogram of a 7-

year-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 non-
chondrodystrophic dogs. In humans, stenosis of the bony chondro-
dysplastic 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
 CONGENITAL SPINAL MALFORMATIONS 1011

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 degen-
eration, although contrast-enhanced radiography was done on only
one dog. No mention was made of the presence of vertebral malfor-
mations. 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 Le-
Couteur/ 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 mononeurop-
athy 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 inter-
mittent 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 subluxa-
tion, 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-
1012 BAILEY & MORGAN

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 non-
contrast 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 abnor-
malities difficult. Contrast-enhanced radiography, such as epidurogra-
phy, 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. Decom-
pressive 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 inter-
vention. 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.

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Address reprint requests to

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