key: cord-0040535-wtw6jozx
authors: Platt, Simon R.
title: Disorders of the Spinal Cord
date: 2009-05-15
journal: Handbook of Small Animal Practice
DOI: 10.1016/b978-1-4160-3949-5.50028-5
sha: 19656b547071734f152216b2a6ae857810d61185
doc_id: 40535
cord_uid: wtw6jozx

nan

I. Instability or malformation of the atlantoaxial joint allows excessive fl exion of the cervical (C) 1-2 vertebral joint. II. Subsequent ventral cord compression occurs from the cranial aspect of the body of the axis.

I. It most commonly occurs in young, toy, and small-breed dogs (<2 years). II. Subluxation is often associated with failure of normal structural development of the atlas, axis, and their supporting ligaments. III. It can occur following minor trauma in the presence of joint instability. IV. Clinical signs arise from concussion and compression of the spinal cord by the axis.

I. Onset is usually acute; however, signs can be slowly progressive and may wax or wane. II. Neck pain occurs in at least 60% of cases (Beaver et al., 2000) . III. Ataxia, tetraparesis, postural reaction defi cits, with normal to exaggerated spinal refl exes occur in 85% of cases (Beaver et al., 2000) . IV. Animals with tetraplegia are at risk of death from respiratory failure. V. Occasionally, signs of brainstem dysfunction are seen.

I. Confi rm the diagnosis with lateral survey radiographs of the cervical spine. II. Note an increased space between the dorsal lamina of C1 and the spinous process of the C2. III. Use ventrodorsal views to assess most accurately the presence and size of the dens. IV. Flex the neck carefully to confi rm instability, if subluxation is not readily apparent. V. Computed tomography (CT) can provide accurate information about the dens.

VI. Magnetic resonance imaging (MRI) can provide important information about spinal cord compression, parenchymal pathology, and ligamentous involvement.

I. Trauma II. Intervertebral disc disease III. Meningomyelitis: various forms Treatment I. Treat cases with acute onset of severe neurological signs with external head and neck splinting. II. Conservative therapy may be appropriate for some dogs with mild signs. III. Apply external splinting and restrict exercise strictly for 6 to 8 weeks.

A. Long-term effi cacy of this approach is uncertain. B. Dogs are always at risk of repeated injury following splint removal. IV. Surgical management is recommended for dogs with neurological defi cits. A. Dorsal and ventral approaches to the atlanto-axial junction have been described (McCarthy et al., 1995; Platt et al., 2004) . B. Surgery is aimed at realignment of the vertebrae, decompression of the spinal cord, and osseous fusion of the atlantoaxial joint. C. Surgical complications include injury to soft tissues, laryngeal paralysis, implant failure, and death in up to 20% of cases (Beaver et al., 2000) .

I. Nonsurgical approach is most successful in dogs that are affected for ≤30 days (Havig et al., 2005 ). II. Surgical success ranges from 50% to 90% (McCarthy et al., 1995; Beaver et al., 2000) . III. Prognosis is better in young dogs (<24 months) and in those with clinical abnormalities for ≤10 months (Beaver et al., 2000) . IV. Prognosis is fair to good for those with mild to moderate neurological defi cits, and guarded for those with an acute onset of tetraplegia. V. Radiographs repeated 6 to 8 weeks after surgery may help determine the presence of osseous healing.

Disorders of the Spinal Cord | Simon R. Platt CHAPTER 24 | Disorders of the Spinal Cord 257

I. Several distinct types of malformation are recognized. II. Hemivertebrae are wedge-shaped, with the apex directed dorsally, ventrally, or medially across the midline, which often results in angulation of the vertebral column. III. Block vertebrae appear as fusion of adjacent vertebrae, which may involve the vertebral bodies, vertebral arches, dorsal spinous processes, or entire vertebrae at any level of the vertebral column. IV. Butterfl y vertebrae have a sagittal cleft in the vertebral body. V. Transitional vertebrae have the characteristics of, and occur at, two major divisions of the vertebral column. 

I. Myelodysplasia results from incomplete closure or development of the neural tube. II. Anomalies of the central canal include hydromyelia, duplication, or absence of the canal. III. Anomalies of the grey matter involve the ventral median fi ssure or dorsal median septum. IV. Grey matter ectopias, chromatolysis, and loss of nerve cell bodies may also be present. V. Syringomyelia is a fl uid dilatation, usually in the dorsal funiculus of the spinal cord. VI. With the exception of the Weimaraner, the pathogenesis of this condition is unknown.

I. The most common sign is a symmetrical, "bunny hopping" pelvic limb gait. II. A variable transverse thoracolumbar myelopathy usually occurs in young animals (4 to 6 weeks), which is typically nonprogressive.

A. Proprioception defi cits B. Ataxia C. Paresis or paralysis III. A classic fi nding is a bilateral fl exor refl ex in the pelvic limbs (both limbs respond to stimulation of one limb). IV. In Weimaraners, myelodysplasia may be associated with abnormal hair "streams" on the dorsum and koilosternia. 

I. Hydromyelia is a fl uid dilatation of the central canal. II. Syringomyelia is a fl uid dilatation in the spinal cord that may communicate with the central canal. III. It is often diffi cult to distinguish between these two conditions.

I. Both conditions can be a secondary, long-term complication of any spinal cord disease. II. Any condition that causes obstruction of normal CSF fl ow along the spinal cord can cause these abnormalities. III. They are most commonly seen in the cervical region, but lesions can occur in any portion of the spinal cord. IV. Cervical syringohydromyelia occurs as a component of congenital anomalies associated with caudal occipital malformation syndrome, which is most commonly reported in the Cavalier King Charles spaniel, but can be seen in other small breed dogs. V. Occipital bone malformation causes "overcrowding" of the caudal fossa that interferes with the normal fl ow of CSF between the intracranial and spinal compartments.

I. Clinical signs vary with lesion location. II. Signs are often progressive, but can be acute and can occur at any age. III. Clinical signs do not correlate with the severity of the syringohydromyelia or with the concurrent severity of cerebellar herniation and hydrocephalus (Lu et al., 2003) . IV. Typical signs consistent with a transverse myelopathy include the following: A. Proprioception defi cits B. Ataxia C. Paresis or paralysis V. Additional signs include pain, paresthesia, spinal deformity (torticollis, scoliosis), and persistent fl ank scratching (Rusbridge et al., 2000) .

I. MRI is essential to document parenchymal changes and associated lesions, such as occipital malformation. II. Survey radiographs are usually normal unless concurrent scoliosis is present. III. Myelography may show obstruction of the fl ow of CSF at the foramen, but is often normal.

IV. Cisterna magna puncture is contraindicated given the likelihood of inadvertent puncture of the spinal cord. V. Lumbar CSF analysis may show chronic infl ammation, but is frequently normal.

I. Other developmental disorders II. Intervertebral disc disease III. Meningomyelitis IV. Neoplasia Treatment I. Medical therapy involves antiinfl ammatories (prednisone 0.5 to 1.0 mg/kg PO SID and carprofen 2.0 mg/kg PO BID). II. A diuretic, such as acetazolamide (10 mg/kg PO TID to QID), may be used concurrently on a short-term basis to reduce CSF production. III. Gabapentin (10 mg/kg PO BID) can be used for neuropathic pain and paraesthesia. IV. Physical therapy (e.g., massage, passive range-of-motion exercises) may be helpful. V. Surgical therapy can be performed in cases of caudal occipital malformation syndrome. A. Foramen magnum decompression with dura and arachnoid excision is preferred for syringohydromyelia associated with occipital malformation syndrome (Vermeersch et al., 2004) . B. Myelotomy with syrinx decompression and marsupialization of the dura can be used for treatment when the condition is related to other causes.

I. Medical therapy may be effective in mildly affected animals. II. Surgical therapy aims to stabilize the condition rather than improve it. III. Surgical therapy often alleviates neck pain. IV. Recurrence of signs from reformation of the syrinx requires repeated surgery. V. Overall prognosis depends on the severity of signs.

I. These lesions are CSF-fi lled diverticuli of the arachnoid membrane rather than true cysts. II. Synonyms include subarachnoid cyst, meningeal cyst, and leptomeningeal cyst.

I. Most commonly a congenital malformation, these lesions may be secondary to trauma, infl ammation, subarachnoid hemorrhage, and neoplasia. II. The intraarachnoid accumulation of CSF in the diverticulum results in compression of the spinal cord. III. Typically solitary lesions occur commonly at the C2 to C3 and C5 to C6 intervertebral sites or in the caudal thoracic region; however, they can occur at any site (Jurina et al., 2004) . IV. The diverticuli are usually located dorsally over the spinal cord.

I. They can occur as an incidental fi nding. II. They are most commonly seen in the cranial cervical cord of young adult, large-breed dogs, particularly rottweilers, or in the thoracolumbar spinal cord of older, smaller breeds (e.g., pug) (Rylander et al., 2002; Skeen et al., 2003) . III. Signs usually consist of a chronic and progressive transverse myelopathy.

A. Proprioception defi cits B. Ataxia C. Paresis or paralysis IV. Neurological defi cits may be asymmetrical and pain is a variable feature. V. Dogs may have early onset of fecal or urinary incontinence (Skeen et al., 2003) .

I. Survey radiographs are unremarkable. II. Myelography reveals a focal "tear-drop" accumulation of contrast medium in the subarachnoid space or an intradural fi lling defect. III. Contrast-enhanced CT or MRI demonstrates the CSF-fi lled diverticulum within the arachnoid membrane and spinal cord compression. IV. MRI can also identify associated parenchymal abnormalities, especially in rottweilers. V. Surgical fi ndings and histopathology of excised tissues confi rm the diagnosis.

I. Cystic neoplasms II. Meningomyelitis III. Other developmental disorders IV. Intervertebral disc disease Treatment I. Medical therapy may improve a small proportion of dogs and is only recommended in cases with mild neurological defi cits. II. Medical therapy involves antiinfl ammatory drugs and exercise restriction.

A. Prednisone 0.5 to 1.0 mg/kg PO SID B. Carprofen 2.0 mg/kg PO BID III. Surgical exploration is used to confi rm the diagnosis and decompress the spinal cord. IV. Complete surgical excision is usually not possible. V. Partial excision (fenestration) and marsupialization of the dura is recommended.

I. Depending of the degree of signs, the overall prognosis is good following surgery.

II. Factors associated with a good outcome include an age <3 years and duration of clinical signs <4 months (Skeen et al., 2003) . III. Recurrence of signs from reformation of the diverticulum is possible. IV. Lifelong antiinfl ammatory therapy has been advised in some cases.

Defi nition I. A dermoid or pilonidal sinus is an invagination of the skin, dorsal to the spine, that extends below the skin to variable depths. II. It can extend to the dura mater and may communicate with the subarachnoid space. 

I. Intervertebral disc disease (IVDD) implies degeneration of the intervertebral disc structures and subsequent herniation of disc material into the vertebral canal. II. Extrusion of the nucleus pulposus through the annulus fi brosis is a Hansen type I lesion. III. Protrusion of the annulus caused by shifting of nucleus pulposus is a Hansen type II lesion. IV. Explosive disc disease that occurs peracutely, without compression, is a type III or high-velocity low-volume disc herniation.

I. Type I disc disease commonly affects chondrodysplastic breeds (e.g., dachshund, beagle, Pekingese, Lhasa apso, shih tzu) and chondrodystrophic-like breeds (e.g., American and English cocker spaniel, miniature poodle) (Cherrone et al., 2004) . A. Type I disc disease is most commonly associated with chondroid disc degeneration. B. Disc degeneration occurs in 75% to 100% of all discs by 1 year of age in chondrodystrophoid breeds (Morgan and Miyabayashi, 1988) . C. Type I disc disease is associated with an acute onset of signs. D. Often there is mineralization of the nucleus pulposus. II. Type II disc disease commonly affects older, large-breed, achondrodystrophic dogs. A. Type II disc disease is associated with degeneration characterized by fi brous metaplasia of the nucleus pulposus. B. Type II disc disease causes slow, progressive spinal cord compression. III. Although uncommon in cats, type I disc disease occurs most frequently (Munana et al., 2001) .

I. Type I disc disease typically occurs in dogs between 3 and 5 years of age.

II. Type II disc disease typically occurs in dogs between 6 and 9 years of age. III. On average, affected cats are 10 years of age (Munana et al., 2001) . IV. Signs refl ect the region of the affected spinal cord. V. Cervical disc disease accounts for 15% of cases (Coates, 2000) . VI. Thoracolumbar (T-L) disc disease accounts for 85% of cases (Coates, 2000) . VII. Thoracolumbar disc disease typically occurs between T11 to L3 vertebrae. VIII. Severity of signs ranges from pain, paresis and ataxia, loss of motor abilities, or loss of nociception (deep pain perception). IX. IVDD most commonly causes a transverse myelopathy.

A. Proprioception defi cits B. Ataxia C. Paresis and paralysis X. Asymmetrical clinical signs are often seen. XI. Cervical disease usually results in less-severe clinical signs than thoracolumbar disease. A. Apparent neck pain is the most common clinical sign with cervical disc disease. B. Nonambulatory tetraparesis is more common in large-breed dogs with cervical disease than smallbreed dogs (Cherrone et al., 2004) . C. Lower motor neuron (LMN) defi cits or monoparesis can be seen with caudal cervical disc disease. XII. LMN defi cits may be seen in the pelvic limbs with herniations caudal to L3 that cause compression of the lumbosacral spinal cord or cauda equina. XIII. Progressive hemorrhagic myelomalacia occurs in up to 11% of dogs that have lost nociception . A. The lesion may ascend, resulting in cranial progression of analgesia, and ultimately cause tetraplegia and respiratory failure. B. The lesion may descend, resulting in LMN signs in the pelvic limbs, as well as urinary and fecal incontinence.

I. Spinal radiographs may be suggestive of disc herniation or be normal. A. Characteristic fi ndings include a narrowed or wedged intervertebral disc space, small intervertebral foramen with narrowed articular processes, or mineralized disc material in the vertebral canal. B. Type I disease is not associated with spondylosis, although spondylosis may be associated with type II disease (Levine et al., 2006) . II. Myelography is important for determining the site (or sites) of disc herniation before surgery. A. Characteristic fi ndings include extradural spinal cord compression or diffuse spinal cord swelling. B. Myelography may be normal when there is lateral or intraforaminal extrusion. III. CSF analysis is needed before myelography.

IV. CT can accurately identify the site and lateralization of type I disc herniation, without the need for concurrent myelography (Olby et al., 2000) . V. MRI is extremely sensitive in localizing disc disease, extradural compressions, and associated parenchymal disease (Ito et al., 2005; Besalti et al., 2006; Chang et al., 2006) B. Contradictory data exist on its effi cacy when administered within 8 hours of the onset of the disc extrusion (Olby et al., 1999) . C. The recommended dose is 30 mg/kg IV followed 2 and 6 hours later by 15 mg/kg IV and continued QID for a maximum of 48 hours. D. Potential side effects include pancreatitis, gastrointestinal hemorrhage, diarrhea, and colonic perforation.

I. Recovery of nonambulatory dogs varies according to the time interval from onset of signs to surgery, initial severity of neurological dysfunction, and speed of onset of signs. II. The prognosis is good for dogs with mild to moderate sensory and/or motor defi cits. III. Success rates following cervical disc surgery range from 87% to 100%, whereas success following thoracolumbar disc surgery range from 58% to 95% (Coates, 2000) . IV. Recovery rates with medical therapy in nonambulatory dogs with thoracolumbar disc disease range from 43% to 51% (Coates, 2000) . V. Paraplegic dogs with loss of nociception have a 69% chance of recovering the ability to walk and a 58% chance of recovering nociception, if treated within 48 hours of onset of signs . VI. The return of nociception within 2 weeks of surgery is a good prognostic indicator for recovery Laitinen and Puerto, 2005 ) VII. Recurrence rates after surgery range from 2.7% to 41.7% with thoracolumbar IVDD (Coates, 2000) . VIII. Recurrence rates after surgery range from 10% to 33% with cervical IVDD (Cherrone et al., 2004) . IX. Recurrences usually (96%) develop within 3 years of the initial event (Mayhew et al., 2004) . X. Recurrence rates of 34% to 40% have been reported following conservative therapy, with an average interval to recurrence of 1.7 years (Coates, 2000) .

I. Cervical vertebral malformation or malarticulation results in compression of the cervical spinal cord segments. II. Synonyms include wobbler syndrome, caudal cervical malformation-malarticulation, cervical spondylopathy, cervical vertebral instability, and cervical vertebral stenosis. 

I. Clinical signs refl ect chronic compression of the cervical spinal cord. II. Onset of clinical signs is gradually progressive over several months or years; however, acute onset is occasionally seen. III. Initial signs usually begin in the pelvic limbs and progress to tetraparesis. IV. Signs usually refl ect a C1-C5 or C6-T2 myelopathy. V. Neck pain is uncommon, although the dogs may resist movement of the neck.

I. Survey radiography may be normal or show a variety of pathologic changes. II. Radiographic changes include malalignment remodeling and sclerosis of the vertebrae, narrowing of the intervertebral disc (IVD) space, degenerative changes of the articular facets, and spondylosis. III. Myelography is essential to determine neural involvement, and to identify static and dynamic lesions. IV. CT or MRI can identify spinal cord compression and atrophy, as well as parenchymal pathology secondary to chronic compression. V. The high potential for morbidity and postoperative complications must be considered and discussed with the owner.

I. Most affected dogs require surgical therapy for long-term relief. II. The prognosis with surgery depends on the number of sites affected, chronicity, and neurological status of the dog; it can vary from 20% to 80%. III. Recurrence can occur from implant failure or adjacent disc disease (domino effect).

I. Spondylosis deformans is a chronic, degenerative, noninfl ammatory disease characterized by the production of osteophytes on the spine that result in the formation of spurs or complete bony ridges across the intervertebral disc space. II. Ankylosing spondylosis and ankylosing spondylitis are sometimes used synonymously; however, ankylosis is uncommon and the condition is not infl ammatory.

I. Osteophyte production occurs in response to degenerative changes in the intervertebral discs. II. The changes may be secondary to aging and trauma. III. The disease has been reported in dogs >2 years of age, with 75% of dogs affected to some extent by 9 years of age (Levine et al., 2006) . IV. Because of the high prevalence in female boxers, it is possibly an inherited disease; however, all dog breeds can be affected. V. The caudal thoracic, lumbar, and lumbosacral spinal segments are most frequently affected in dogs, and the highest incidence occurs at the level of T7-T8 in cats. VI. An association may exist between radiographically apparent spondylosis and type II disc disease (Levine et al., 2006) .

I. Compression of the cord or spinal nerves from osteophytic projections into the spinal canal is rare. II. Rarely, compression of neural tissue may result in a transverse myelopathy or neuropathy.

I. Diagnosis is based on radiographic identifi cation of osteophyte formation on the ventral surface (in the region of the metaphysis) of the vertebral body or bodies. II. Osteophytes may occur at either normal or narrowed disc spaces. III. Myelography can detect associated spinal cord compression and its cause. IV. CT or MRI helps identify spinal cord compression or foraminal stenosis.

I. Diskospondylitis II. Trauma III. Intervertebral disc disease

I. Treatment is usually not necessary. II. Analgesia and exercise restriction may help dogs that exhibit only discomfort. III. Surgical decompression may be necessary in cases with clinical signs. IV. If clinical, the prognosis is guarded owing to the high risk of recurrence.

Spinal extradural synovial cysts arise from the articular facets and surrounding connective tissues of the cervical and thoracolumbar vertebrae of dogs.

I. The cysts commonly occur in the cervical spine of young, large-breed dogs and in the thoracolumbar spine of older, large-breed dogs (Dickinson et al., 2001b) . II. Occurrence has been associated with degenerative disc disease and trauma. III. Increased mechanical stress and joint motion may predispose the thoracolumbar junction to osteoarthritis and synovial cyst formation. IV. Histopathology of the cyst reveals fi brous connective tissue with a synovial cell lining.

I. Clinical signs are consistent with a transverse myelopathy at the site of the lesion. II. Signs include proprioception defi cits, ataxia, paresis or paralysis, often accompanied by paraspinal hyperesthesia.

I. Degeneration and remodeling of the articular processes are seen at the site of the lesion. II. Myelography demonstrates spinal cord compression. III. CT and MRI better defi ne the lesion.

I. Spinal stenosis II. Intervertebral disc disease III. Cervical spondylomyelopathy IV. Neoplasia

I. Surgical decompression of the spinal cord with cyst removal is indicated in dogs with neurological defi cits or refractory pain. II. Recurrence rates are unknown, but surgery usually provides long-term resolution of signs (Dickinson et al., 2001b) .

I. Spinal stenosis indicates a narrowing of the vertebral canal that may be focal, segmental (affecting several adjacent vertebrae), or generalized (present throughout the vertebral column). II. Bony impingement on neural elements may be congenital, developmental, acquired, or idiopathic. III. Compression of neural tissue occurs by nonosseous components of the vertebral canal. IV. Hypertrophy of the dorsal, longitudinal ligament and the ligamentum fl avum may be involved. V. Disc extrusion or protrusion may occur.

I. Congenital stenosis may occur as a primary lesion or may be seen in association with other congenital vertebral anomalies. II. Segmental vertebral stenosis occurs in the cranial thoracic spine of several dog breeds (e.g., Doberman pinscher). III. Developmental stenosis may result from inborn errors of skeletal growth in dogs. IV. Hypertrophy of the nonosseous components of the vertebral canal has been reported in rottweilers secondary to ligamentous proliferation at C2-C3.

I. Clinical signs refl ect the location of the lesion, regardless of the precise cause. II. Onset of signs is usually insidious and progressive.

I. Diagnosis can be made by survey radiography. II. Myelography is essential for precise localization of the spinal stenosis. III. CT or MRI may aid in identifi cation of the location and the extent of soft tissue and parenchymal involvement (Abramson et al., 2003) . 

I. For dogs, prognosis varies with severity of signs. II. The prognosis for dogs having reached skeletal maturity is better than for immature dogs.

III. The prognosis for cats concurrently infected with FeLV is guarded because of increased risk of recurrence.

I. It is a slowly progressive noninfl ammatory disease of the spinal cord consisting of axonal degeneration and demyelination. II. It is synonymous with chronic degenerative radicular myelopathy.

I. The etiology remains unknown. II. Immune-related degeneration has been proposed. III. German shepherd dogs may have a genetic predisposition. IV. Pathologic changes have been identifi ed throughout the spinal cord, as well as in the red, lateral vestibular, and dentate nuclei (Johnston et al., 2000) . V. Lesions are most prominent in thoracic segments of the spinal cord.

I. Signs are usually nonpainful, insidious, progressive ataxia and paraparesis of the pelvic limbs that ultimately leads to bladder incontinence and paraplegia over 6 to 12 months. II. It occasionally (10% to 20%) causes reduced patella refl exes from dorsal nerve root involvement (Averill, 1973) . III. Nociception (deep pain perception) is usually unaffected. IV. It occurs most frequently in the German shepherd dog, and is also recognized in the Pembroke Welsh corgi, boxer, and other breeds. V. It is rare in cats. VI. Average age of affected dogs is 9 years old; dogs younger than 5 years are rarely affected (Longhofer et al., 1990) .

I. Tentative antemortem diagnosis is based on classic clinical signs and the exclusion of other diseases. II. An increased protein level may be found in lumbar CSF. III. CT and myelography reveal spinal cord atrophy (Jones et al., 2005) .

I. Intervertebral disc disease II. Neoplasia III. Myelitis IV. Orthopedic disease

I. Effective treatment has not been reported. II. Medical treatments that have been advised but not proven include the following: A. Aminocaproic acid 500 mg PO TID B. N-acetylcysteine 70 mg/kg PO TID for 2 weeks then TID every other day III. Long-term prognosis is uniformly poor.

I. It is a demyelinating disorder of the brain and spinal cord. II. It is reported in rottweilers in United States and Europe.

I. Bilateral symmetrical demyelination occurs in the white matter of the spinal cord, brainstem, and cerebellum. II. Lateral and dorsal funiculi are commonly affected in the cervical and thoracic spinal cord. III. The precise etiology is unknown, but the condition may be heritable.

I. Onset is at 18 to 42 months of age. II. Slow progressive clinical signs develop over a 6-to 12month period. III. Clinical signs are consistent with a C1-C5 myelopathy and include tetraparesis, hypermetria, and exaggerated segmental refl exes.

I. Tentative diagnosis is based on signalment, clinical signs, and exclusion of other diseases. II. Defi nitive diagnosis is made with histopathology. 

I. Diskospondylitis is infection of the intervertebral disc and adjacent vertebrae. II. Vertebral osteomyelitis is infection of only the vertebra. III. Vertebral physitis is infection restricted to the physis.

I. Infection of the intervertebral disc is most commonly associated with Staphylococcus intermedius. II. Other less commonly identifi ed organisms include Streptococcus spp., Escherichia coli, Actinomyces spp., Brucella canis, and Aspergillus spp. III. Young German shepherd dogs are predisposed to aspergillosis.

IV. Young basset hounds may be predisposed to diskospondylitis associated with systemic tuberculosis. V. Infection may arise from hematogenous spread from distant foci of infection, extension of a paravertebral infection, penetrating wounds, surgery, or plant material (grass awn) migration. VI. Infection causes extradural spinal cord or cauda equina compression. VII. It is infrequently seen in cats.

I. It occurs most commonly in intact male, middle-aged, large-and giant-breed dogs. II. Single or multiple sites can be infected. III. The L7-S1 IVD space is most commonly affected. IV. The thoracolumbar spine is more commonly affected than the cervical spine. V. Clinical signs refl ect the location of the lesion. VI. Spinal pain is the most frequent initial clinical sign. VII. Approximately 30% of dogs have signs of systemic illness (e.g., fever, weight loss) (Thomas, 2000) . VIII. Clinical signs may be present for several weeks or months before diagnosis.

I. Diskospondylitis should be considered in animals with spinal pain or pyrexia. II. Imaging of the entire spine is done to look for foci of infection. III. Hematological changes are not usually present unless there is concurrent, systemic infection. IV. Urinalysis may reveal bacterial or fungal agents. V. Aerobic, anaerobic, and fungal cultures of blood and urine are positive in up to 75% and 50% of cases, respectively (Thomas, 2000) . VI. Serology for brucellosis is positive in 10% of cases and is performed in all dogs suspected of having diskospondylitis, because of its zoonotic potential (Thomas, 2000) . VII. Defi nitive diagnosis is usually made with spinal radiography.

A. Radiographic changes include narrowing of the IVD space and lysis of the vertebral endplates, which are surrounded by sclerosis. B. The entire spine must be evaluated. C. Radiographs also are used to monitor response to therapy (Shamir et al., 2001) . D. Radiographic changes often lag behind clinical improvement. VIII. Myelography is indicated in animals with substantial neurological defi cits. IX. CSF analysis may be normal or may have an increased white blood cell (WBC) count and/or protein content. X. CT can identify subtle endplate erosion and paravertebral soft-tissue swelling. XI. MRI can identify infl ammatory lesions within the disc space and adjacent soft tissues (Gonzalo-Orden et al., 2000; Cherubini et al., 2004) .

XII. Percutaneous, fl uoroscopic-guided needle aspiration and culture of the disc space may confi rm the etiology in up to 75% of cases (Thomas, 2000) . XIII. Surgical biopsy of the lesion may be warranted in refractory cases.

I. Spondylosis deformans II. Vertebral neoplasia III. Intervertebral disc disease IV. Meningomyelitis V. Myositis VI. Polyarthritis

I. Treatment consists of long-term use of an antimicrobial that is effective against the causative organism, as determined by culture and sensitivity testing. II. If an organism is not cultured, direct empirical therapy against Staphylococcus spp. is started.

A. Cephalexin 20 to 30 mg/kg PO TID B. Cefazolin 20 mg/kg IV, IM, SC QID C. Amoxicillin 20 mg/kg PO BID III. Intravenous antimicrobials are given to animals with severe neurological defi cits. IV. Antimicrobials are provided for a minimum of 6 to 8 weeks. V. Resolution of signs usually occurs within 2 weeks of instituting therapy; however, neurological defi cits can persist. VI. Continued pain is indicative of active disease. VII. Failure to respond to fi rst-line antimicrobials requires the addition of a second antimicrobial. A. Enrofl oxacin 5 to 11 mg/kg PO BID (dogs) B. Doxycycline 25 mg/kg PO SID (dogs); may cause vomiting C. Trimethoprim-sulfadiazine 15 mg/kg PO BID VIII. Surgical exploration for internal decompression and possible stabilization may be necessary in refractory cases (Auger et al., 2000; Kinzel et al., 2005) . IX. Fluconazole 2.5 to 5 mg/kg PO BID is recommended for Aspergillus spp. infections. X. Ideally, fungal infections are treated based on sensitivity testing. XI. Nonsteroidal antiinfl ammatory drugs can be used to alleviate pain. A. Carprofen 2 mg/kg PO BID B. Ketoprofen 1 mg/kg PO SID for 5 days XII. The prognosis is very good unless there is an associated endocarditis or a fungal etiology.

I. It is a noninfectious, infl ammatory disease affecting the meninges and associated vasculature. II. Synonyms include necrotizing vasculitis, juvenile polyarteritis syndrome, corticosteroid-responsive meningitis/ meningomyelitis, aseptic suppurative meningitis, and pain syndrome.

I. The etiology and pathogenesis of this condition are not well understood. II. The disease may be triggered by an environmental factor that leads to dysregulation of the immune system (Tipold et al., 1999) . III. Immunoglobulin (Ig) A may play a role in the pathogenesis (Tipold et al., 1995) .

I. It is reported in the beagle, Bernese mountain dog, boxer, German short-haired pointers; it may occur in other breeds. II. Affected dogs are often young, large-breed dogs between 7 and 18 months old. III. Signs occur acutely or may follow a waxing and waning course over weeks to months. IV. Dogs are usually febrile, anorexic, and hyperesthetic, with cervical rigidity. V. Concurrent immune-mediated polyarthritis or glomerulonephritis may be present. VI. Neurological defi cits, weakness, and ataxia can be seen in the chronic cases. A. Acute polioencephalomyelopathy with glial and neuronal necrosis occurs in immature or immunodefi cient dogs. B. Chronic leukoencephalomyelopathy with demyelination occurs in older or immunosuppressed dogs. C. Demyelination is more frequent in the chronic stages of the disease. D. The mechanism by which demyelination occurs may be a primary effect of the virus on glial cells or may occur secondary to immunological mechanisms (Vandevelde and Zurbriggen, 2005 ). E. The white matter of cerebellum, cerebellar peduncles, optic nerves, optic tracts, and spinal cord are most frequently affected.

I. Distemper myelitis can occur in any age or breed of dog and vaccination does not always confer protection. II. The CNS may be the only system affected. III. Spinal cord signs depend on the location of the lesion, with T3-L3 segments frequently involved. IV. Signs may be acute or chronic, progressive or relapsing, and occur bilaterally, with occasional asymmetry (Vandevelde and Zurbriggen, 2005 

I. Specifi c antiviral therapy is not available. II. Administration of modifi ed-live virus vaccines is only effective if given before clinical signs appear. III. Short-duration prednisone therapy (0.5 to 1.0 mg/kg PO SID to BID for 1 to 3 days) may provide some relief. IV. The prognosis for recovery is poor.

I. Meningitis is infl ammation of the meninges. II. Myelitis is infl ammation of the parenchyma of the spinal cord. 

I. Ischemic myelopathy involves vascular compromise of the spinal cord that often progresses to local infarction. II. The term is often used synonymously with fi brocartilaginous embolic myelopathy (FCEM), which denotes a specifi c cause of the ischemia.

I. Acute spinal cord infarction can be secondary to FCEM, neoplastic emboli, and intravascular coagulation. II. FCEM is characterized by acute spinal cord infarction from embolization of fi brocartilage identical to that of the nucleus pulposus.

A. Many theories exist as to the pathophysiology of the embolization, but none are proven. B. Fibrocartilaginous emboli occlude arteries and/or veins of the leptomeninges and spinal cord parenchyma. C. Achondrodystrophic, medium-to large-breed dogs are predisposed. D. There is an increased incidence in miniature schnauzers. E. It is infrequently reported in cats (Mikszewski et al., 2006) .

I. Classically, clinical signs are peracute in onset, nonprogressive, nonpainful, and often asymmetrical. II. Transverse myelopathy occurs, with signs compatible with the location of the infarction. A. Proprioception defi cits B. Ataxia C. Paresis or paralysis III. Thoracolumbar signs are more common than cervicothoracic, but signs can occur in any region and often involve the intumescence. IV. Clinical onset is frequently associated with trauma or exercise. V. Maximal neurological defi cits develop within 12 hours and are then nonprogressive. VI. Severe signs are accompanied by loss of nociception (deeppain perception).

I. Tentative diagnosis is based upon history, signalment, and compatible clinical signs. II. Myelography may demonstrate intramedullary spinal cord swelling in the early stages (Gandini et al., 2003) . III. MRI documents parenchymal pathology (Abramson et al., 2005; Mikszewski et al., 2006) . IV. CSF may reveal mild pleocytosis or a normal cell count with an elevated protein level (albumino-cytological dissociation).

I. Trauma of the spinal cord II. Intervertebral disc disease III. Myelitis IV. Neoplasia affecting the spinal cord V. Hemorrhage of vessels in or around the spinal cord

I. There is no specifi c medical therapy for FCEM; however, the use of high-dose corticosteroid therapy has been considered.

A. The dose of methylprednisolone recommended is 30 mg/kg IV followed 2 and 6 hours later by 15 mg/kg IV and continued QID for a maximum of 48 hours. B. Potential side-effects include pancreatitis, gastrointestinal hemorrhage, diarrhea, and colonic perforation. II. Clinical improvement depends on the severity of sensorimotor dysfunction. III. A poor prognosis has been correlated with lack of improvement within 14 days, involvement of the intumescences, and a lack of deep pain perception. IV. Supportive care, physiotherapy, and hydrotherapy may aid in recovery.

I. Primary and secondary tumors can affect the vertebrae, meninges, and spinal cord. II. Feline lymphoma may be associated with FeLV infection. III. Neoplasia can be classifi ed as extradural, intraduralextramedullary, or intramedullary. A. Extradural tumors can be primary or secondary. 1. Primary vertebral tumors: fi brosarcoma, osteosarcoma, chondrosarcoma, hemangiosarcoma, myeloma 2. Secondary vertebral tumors: mammary, prostatic, thyroid carcinomas, malignant melanoma, metastatic osteosarcoma 3. Epidural tumors: lymphoma, metastatic tumors B. Intradural extramedullary tumors include meningioma, peripheral nerve sheath tumor, lymphoma, and nephroblastoma. C. Intramedullary tumors include astrocytoma, oligodendroglioma, ependymoma, and metastases. IV. Primary and secondary extradural tumors are more common than intradural extramedullary tumors; intramedullary tumors are rare. V. Spinal neoplasia accounts for 27% of all spinal disease in cats (Marioni-Henry et al., 2004) . A. Epidural lymphoma is the most common spinal tumor of cats. B. Meningioma is the most common benign, nonlymphoid tumor of cats (Rossmeisl et al., 2006) . C. Osteosarcoma is the most common malignant, nonlymphoid tumor of cats.

I. Spinal tumors occur most commonly in animals >5 years old (Dernell et al., 2000) .

II. Direct trauma to the spinal cord results in primary and secondary injuries. III. Direct trauma to the spinal cord (concussion) may be followed by sustained compression, distraction, or both.

I. Type I intervertebral disease II. Vertebral fractures and luxations III. Fibrocartilaginous embolism IV. Spinal instability: atlantoaxial subluxation Pathophysiology I. Acute spinal cord injury is often caused by a combination of events that can include concussion, compression, ischemia, and laceration (primary injuries). II. Each of these primary injuries can lead to secondary injury, which is a series of biochemical and metabolic events that expand the primary zone of tissue necrosis. III. Most secondary injuries occur within 24 hours and contribute to clinical deterioration.

I. Neurological examination is performed (carefully) to localize the site of the trauma before any sedation or analgesia is done. II. Concurrent trauma involving other organ systems is frequently present and must also be assessed. III. Neurological signs refl ect the site of injury. IV. Progressive hemorrhagic myelomalacia is suspected with continued deterioration.

I. The diagnosis is made based on history and supportive clinical signs. II. Thorough evaluation of the entire animal is essential to identify concurrent abnormalities. III. Survey spinal radiography commonly delineates traumatic luxation and/or subluxation and fractures of the vertebral column.

A. Lateral survey radiographs are taken of the whole spine before manipulation of the animal. B. General anesthesia maybe necessary for accurate positioning, but is delayed until the animal is stabilized. C. Sedation or analgesia may assist with positioning, but in creases the risk of neurological deterioration secondary to paravertebral muscle relaxation. IV. Advanced imaging is required to assess nervous tissue. V. Myelography assists in assessing the degree of associated spinal cord compression. VI. CT is invaluable in identifying bony defects that may not be apparent on survey radiography. VII. MRI provides information about spinal cord compression, extradural hemorrhage, and parenchymal structure, but may not provide much detail about fractures and luxations.

I. Type I intervertebral disc disease II. Pathologic fracture secondary to neoplasia III. Fibrocartilaginous embolic myelopathy IV. Ischemic neuromyopathy

I. Initiate stabilization of the cardiovascular and respiratory systems before assessing and treating the spinal injury. II. Immobilize the spine to prevent further vertebral displacement. III. Delay administration of analgesia or sedation until the initial assessments, neurological examination, and diagnostics have been performed. IV. Medical treatment is indicated for animals with mild clinical signs and no evidence of vertebral instability. A. Methylprednisolone sodium succinate

Potential side effects include pancreatitis, gastrointestinal hemorrhage, diarrhea, and colonic perforation

Cage rest for 6 weeks

If spinal instability is detected but the owner declines surgery, an external splint is required to immobilize the area for 6 to 8 weeks

Surgical treatment is indicated in cases with instability, vertebral malalignment, or spinal cord compression. A. Laminectomy ± durotomy are necessary for decompression

Realignment and fi xation can be achieved using Steinmann pins, screws, and polymethylmethacrylate, or vertebral body plates

Postoperative care involves exercise restriction, analgesia, soft bedding, and management of bladder evacuation

Physiotherapy and hydrotherapy may also help recovery

Prognosis depends on the degree of sensorimotor loss and chronicity of lesion at time of surgery, in addition to severity of any systemic disorders

Radiographic diagnosislateralized vertebral osseous compression causing cervical spondylomyelopathy in a Great Dane

Magnetic resonance imaging appearance of suspected ischemic myelopathy in dogs

Cerebrospinal fl uid from a 7-month-old dog with seizure-like episodes

Surgical treatment of lumbosacral instability caused by diskospondylitis in four dogs

Degenerative myelopathy in the aging German shepherd dog: clinical and pathologic fi ndings

Risk factors affecting the outcome of surgery for atlantoaxial subluxation in dogs: 46 cases (1978-1998)

Magnetic resonance imaging fi ndings in dogs with thoracolumbar intervertebral disk disease: 69 cases (1997-2005)

Feline leukemia virusassociated myelopathy in cats

Magnetic resonance imaging features of traumatic intervertebral disc extrusion in dogs

A retrospective comparison of cervical intervertebral disc disease in achondrodystrophic large dogs versus small dogs

MRI fi ndings in a dog with diskospondylitis caused by Bordetella species

Intervertebral disk disease

Dorsal laminectomy for caudal cervical spondylomyelopathy: postoperative recovery and long-term follow-up in 20 dogs

Outcome following treatment of vertebral tumors in 20 dogs (1986-1995)

Radiation induced vertebral osteosarcoma following treatment of an intradural extramedullary spinal cord tumor in a dog

Extradural spinal synovial cysts in nine dogs

Clinical Sarcocystis neurona, Sarcocystis canis, Toxoplasma gondii, and Neospora caninum infections in dogs

Fibrocartilaginous embolism in 75 dogs: clinical fi ndings and factors infl uencing the recovery rate

Magnetic resonance, computed tomography and radiologic fi ndings in a dog with diskospondylitis

Evaluation of nonsurgical treatment of atlantoaxial subluxation in dogs: 19 cases

Prognostic value of magnetic resonance imaging in dogs with paraplegia caused by thoracolumbar intervertebral disk extrusion: 77 cases

Central nervous system pathology in 25 dogs with chronic degenerative radiculomyelopathy

CT myelography of the thoraco-lumbar spine in 8 dogs with degenerative myelopathy

Spinal arachnoid pseudocysts in 10 rottweilers

Treatment of 10 dogs with diskospondylitis by fl uoroscopy-guided percutaneous discectomy

Surgical decompression in dogs with thoracolumbar intervertebral disc disease and loss of deep pain perception: a retrospective study of 46 cases

Evaluation of the association between spondylosis deformans and clinical signs of intervertebral disc disease in dogs: 172 cases

Spinal tumors in 37 dogs: clinical outcome and long-term survival

Messing A: A degenerative myelopathy in young German shepherd dogs

Neurological signs and results of magnetic resonance imaging in 40 Cavalier King Charles spaniels with Chiari type 1-like malformations

Prevalence of diseases of the spinal cord in cats

Risk factors for recurrence of clinical signs associated with thoracolumbar intervertebral disc herniation in dogs: 229 cases

Atlantoaxial subluxation in dogs

Imaging of a spinal nephroblastoma in a dog

Magnetic resonance imaging features of cervical spinal cord meningiomas

Investigating demyelination in the brain in a canine model of globoid cell leukodystrophy (Krabbe disease) using magnetization transfer contrast: preliminary results

Molecular basis of globoid cell leukodystrophy in Irish setters

Fibrocartilaginous embolic myelopathy in fi ve cats

Degenerative changes in the vertebral column of the dog: a review of radiographic fi ndings

Intervertebral disc disease in 10 cats

Current concepts in the management of acute spinal cord injury

The computed tomographic appearance of acute thoracolumbar intervertebral disc herniations in dogs

Long-term functional outcome of dogs with severe injuries of the thoracolumbar spinal cord: 87 cases

A modifi ed ventral fi xation for surgical management of atlantoaxial subluxation in 19 dogs

A modifi ed lateral approach to the canine cervical spine: procedural description and clinical application in 16 dogs with lateralized compressive myelopathy or radiculopathy

Surgical cytoreduction for the treatment of non-lymphoid vertebral and spinal cord neoplasms in cats: retrospective evaluation of 26 cases

Syringohydromyelia in Cavalier King Charles spaniels

Vertebral plasma cell tumors in 8 dogs

Retrospective analysis of spinal arachnoid cysts in 14 dogs

Detection of canine distemper virus by reverse transcriptase-polymerase chain reaction in the urine of dogs with clinical signs of distemper encephalitis

Surgical treatment of an intramedullary spinal cord hamartoma in a dog

Use of a multiplex polymerase chain reaction assay in the antemortem diagnosis of toxoplasmosis and neosporosis in the central nervous system of cats and dogs

Radiographic fi ndings during recovery from diskospondylitis

Spinal arachnoid cysts in 17 dogs

Spinal lymphoma in cats: 21 cases

A novel intradural extramedullary spinal cord tumor in young dogs

Usefulness of myelography with multiple views in diagnosis of circumferential location of disc material in dogs with thoracolumbar intervertebral disc herniation

Diskospondylitis and other vertebral infections

Neuroimmunological studies in steroid-responsive meningitis-arteritis in dogs

Lymphocyte subset distribution in steroid responsive meningitis-arteritis in comparison to different canine encephalitides

Demyelination in canine distemper virus infection: a review

Suboccipital craniectomy, dorsal laminectomy of C1, durotomy and dural graft placement as a treatment for syringohydromyelia and cerebellar tonsil herniation in Cavalier King Charles spaniels

Steroid-responsive meningitis-arteritis in dogs with non-infectious, nonerosive, idiopathic, immunemediated polyarthritis

I. The hallmark of infectious diseases is multifocal clinical signs. II. Neurological signs refl ect the region of the spinal cord affected. III. Signs include paresis and ataxia. IV. Often there are concurrent, systemic signs of infl ammation. V. Viral diseases may produce the following:A. FIP 1. Cats can be affected at any age but are often between 6 months and 5 years of age. 2. Signs are insidious and may refl ect multiorgan involvement. 3. The CNS signs may be focal, diffuse, or multifocal. 4. Intracranial signs are more common than spinal signs. 5. Clinical signs refl ect the location of the pathology. B. FeLV causes hyperesthesia and progressive paraparesis to paralysis. VI. Bacterial and fungal diseases A. Signs refl ect the location and severity of the pathology. B. Neurological signs are often acute and rapidly progressive, but occasionally fungal infections can be slowly progressive. C. Fever occurs intermittently and is more likely with concurrent bacteremia or disseminated fungal infection. VII. Protozoal diseases are characterized by the following:A. 1. Classically bacterial diseases produce marked neutrophilic pleocytosis, and fungal diseases are associated with a mixed mononuclear and polymorphonuclear pleocytosis frequently with eosinophils. 2. Aerobic, anaerobic, and fungal cultures are performed in suspected cases. C. Serology may be useful for diagnosis of fungal infections.

A. Tentative antemortem diagnosis is based upon serological evidence, compatible clinical signs, and positive response to treatment. B. CSF analysis shows a mixed-cell or mononuclear pleocytosis, and elevated protein levels. C. PCR of the CSF may confi rm the diagnosis (Schatzberg et al., 2003) .

A. CSF analysis may be normal or show mild increases in protein and pleocytosis (predominantly lymphocytes). B. Serology can confi rm the diagnosis. 

I. Clinical fi ndings depend on the location of the tumor. II. Pain is the most common initial clinical signs. III. The most common sign is a transverse myelopathy that is often bilateral, but can be asymmetrical.A. Proprioception defi cits B. Ataxia C. Paresis and paralysis IV. Signs may progress over 1 week to 1 year.V. An acute onset may occur from pathologic fractures, hemorrhage, or ischemia.

I. Tentative diagnosis is based on clinical, radiographic, and CSF analysis, and on advanced imaging fi ndings. II. Thoracic radiography (three views) and abdominal ultrasonography are performed to identify primary or secondary neoplastic lesions. III. Radiography can identify bony lesions of the vertebrae.A. Bone lysis is most common fi nding associated with a vertebral tumor. B. Punched-out lytic lesions in multiple vertebrae commonly occur with multiple myeloma. C. Usually only one vertebra is involved (unless secondary). IV. CSF analysis often reveals nonspecifi c changes.A. The CSF may be normal or may have elevated protein levels. B. Mild to moderate neutrophilic pleocytosis may occur with tumors affecting the leptomeninges. C. Tumor cells are rarely identifi ed, except with lymphoma. V. Advanced imaging may be useful.A. Myelography helps to differentiate intramedullary, intradural-extramedullary, and extradural lesions. B. CT is used to identify bony lesions. C. MRI is the best imaging modality for spinal neoplasia.1. MRI allows specifi c determination of extramedullary or intramedullary lesions (McConnell et al., 2003 ). 2. Intravenous contrast administration helps determine the soft-tissue and osseous extent of the tumor.3. MRI determines extent of disease and assists with surgical planning (McDonnell et al., 2005) . VI. Defi nitive diagnosis requires histopathologic interpretation of biopsy specimens.

I. Intervertebral disc disease II. Diskospondylitis, osteomyelitis III. Meningomyelitis IV. Degenerative myelopathy V. Spinal trauma

I. Long-term prognosis is poor, with survival time often inverse to the severity of neurological defi cits (Dernell et al., 2000) . II. Medical therapy consists of the following:A. Prednisone 0.5 to 1.0 mg/kg PO SID can be used palliatively. B. Chemotherapy may be tried for certain tumors.1. Tumors amenable to chemotherapy include lymphoma and multiple myeloma. 2. In cats with spinal lymphoma, remission rate is 50%, with complete remission duration of 14 weeks, and partial remission duration of 6 weeks (Spodnick et al., 1992) . 3. Long-term control of solitary plasmacytomas can be achieved with chemotherapy and radiation (Rusbridge et al., 1999) . C. Radiation therapy may be tried as primary, adjunctive, or palliative therapy (Dickinson et al., 2001a) . III. Surgical therapy involves surgical decompression of the spinal cord and debulking of the tumor. A. Most vertebral tumors are not surgically respectable. B. The median survival time of dogs with vertebral tumors was 135 days following multimodality therapy that included surgical resection (Dernell et al., 2000) . C. Surgical resection of meningiomas in dogs may lead to remissions of >6 months, and adjunctive radiotherapy may increase remission time to approximately 15 months (Levy et al., 1997) . D. Cytoreductive surgery of malignant, nonlymphoid spinal tumors in cats provides a median survival time of 110.5 days (Rossmeisl et al., 2006) . E. Cytoreductive surgery of benign, nonlymphoid spinal tumors in cats provides a median survival time of 518 days (Rossmeisl et al., 2006) . F. Intramedullary tumors are often diffi cult to excise without damage to the surrounding parenchyma (Sanders et al., 2002) .

I. Injury to the spinal cord may be caused by endogenous (intervertebral disc disease) or exogenous (vehicular trauma) factors.