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Cervical disorders of large breed dogs (Proceedings)
Disease processes of the cervical spinal cord and vertebral column and the pain and paresis produced by these disorders are a common cause of presentation to the veterinarian.
Disease processes of the cervical spinal cord and vertebral column and the pain and paresis produced by these disorders are a common cause of presentation to the veterinarian. Large breed dogs are not immune to cervical disorders and in some instances have conditions that are unique to their size. Other disorders affect both large and small breed dogs but the clinical course, treatment and prognosis may vary between dogs of different sizes. Fortunately, by recognizing the clinical signs of cervical disease and developing a list of differential diagnoses, a diagnostic and treatment plan can often be formed to help relieve a patient of pain and regain the ability to walk.
Clinical signs, neurologic examination and diagnostic procedures
The clinical approach to cervical pain in large breed dogs is similar to that in smaller breeds and is addressed in the section of these proceedings covering cervical pain in small breed dogs.
Intervertebral disc extrusion
One of the most common causes of cervical pain in veterinary patients is caused by extrusion of intervertebral disc material into the spinal canal. Chondroid degeneration of the intervertebral disc resulting in type I (acute) extrusion of the nucleus pulposus or a more chronic type II protrusion of the annulus fibrosus may both occur in large breed dogs. Type I disc extrusions occur more frequently than has been suggested in the past while type II disc protrusions remain a common component of caudal cervical spondylomyelopathy (Wobbler's syndrome). Large breeds with increased incidence of cervical intervertebral disc extrusion include the Doberman Pinscher, Rottweiler, Dalmatian, Weimaraner, German Shepherd and Labrador Retriever, although a disc extrusion may occur in any breed. Symptoms range from cervical pain to non-ambulatory tetraplegia, but paresis is not as common in cervical intervertebral disc disease compared to thoracolumbar disc extrusion. Despite this, a larger percentage of large breed dogs with cervical intervertebral disc extrusion/protrusion do have clinical paresis compared to smaller breeds. In the most severely affected patients cervical pain may be minimal or absent. Intervertebral disc extrusion/protrusion is a very unlikely differential diagnosis for patients less than two years of age.
Diagnosis of cervical disc extrusion may be obtained by survey radiographs if calcified disc material can be seen in the spinal canal but intervertebral disc calcification is not as prevalent in large breeds as in chondrodystophic and smaller breeds. In situ disc calcification does not equal intervertebral disc extrusion and calcification of a disc is not required before extrusion can occur. CT myelography or MRI is recommended to confirm the exact location of extruded disc material prior to surgical intervention. This is especially important in the cervical vertebral column since multiple surgical approaches are available in this area of the spine. In large breed dogs, disc extrusions are more common in the lower cervical vertebral column (C5-C6 and C6-C7).
Both conservative and surgical treatments are available for patients with cervical intervertebral disc extrusion. Conservative treatment, consisting of strict crate confinement and anti-inflammatory agents, may be attempted the first time a patient experiences mild to moderate pain. Corticosteroids generally provide better anti-inflammatory effects and analgesia than non-steroidal anti-inflammatory drugs (NSAIDs) for cervical disc extrusion, but NSAIDs may provide adequate analgesia in many patients with mild to moderate pain. Mixing corticosteroids and NSAIDs is contraindicated as the chance of gastrointestinal side effects is greatly increased without significantly changing the amount of analgesia provided. Use of analgesics and anti-inflammatory drugs without exercise restriction is also contraindicated and may result in significant worsening of clinical signs. For patients with severe cervical pain, any degree of paresis, or patients with repeat or chronic pain, decompressive surgery is usually necessary to provide long term pain relief. When the disc extrusion is centrally located within the spinal canal, decompression can usually be obtained with a ventral slot decompression. When disc material is located lateral to the spinal cord or within the intervertebral foramen, a dorsal laminectomy or hemilaminectomy is necessary to decompress the spinal cord. The prognosis for recovery is often very good but larger dogs may require longer to recover than patients of smaller breeds. The prognosis for recovery is better for patients with acute type I extrusions than for patients with type II protrusions associated with caudal cervical spondylomyelopathy.
Cervical spondylomyelopathy (CSM, wobbler's syndrome)
Caudal cervical spondylomyelopathy occurs in two forms in small animal veterinary patients. The first, and most common, form of this disease occurs in middle aged and older Doberman Pinschers and other large and giant breeds of dogs. In this group of patients spinal cord compression is caused by a type II intervertebral disc protrusion, hypertrophy of the dorsal longitudinal ligament, tipping of the cervical vertebrae and occasionally hypertrophy of the ligamentum flavum. Malformation of the vertebrae and articular facets is also possible in Doberman Pinschers but in general most of the spinal canal stenosis and spinal cord compression is caused by soft tissue structures. The majority of Doberman Pinschers with CSM will have a slowly progressive posterior paresis initially followed by tetraparesis as the disease progresses. Some patients with slowly progressive disease will have an acute worsening of clinical signs while a smaller group of patients will have an acute onset of symptoms with no prior history of neurologic deficits. Neurologic examination early in the course of CSM reveals posterior paresis and ataxia, diminished postural reactions in the pelvic limbs and resistance to flexion and manipulation of the cervical spine. If cervical pain is present at all it is usually mild. As neurologic symptoms progress thoracic limb paresis may also be seen but the thoracic limb weakness is almost always less severe than the pelvic limb weakness. A classic gait of patients with CSM is characterized by a short, stilted, thoracic limb stride with a somewhat wide based pelvic limb ataxia. This gait has been described as a "two engine" gait because the front and rear limbs appear to be moving at different speeds. Muscle atrophy over the spine of the scapulas is also present in many patients with chronic or severe symptoms.
The diagnosis of CSM requires imaging that allows for visualization of the spinal cord, such as myelography, CT myelography or MRI. In addition to the routine lateral and ventral/dorsal myelographic projections, a lateral projection with linear traction is also usually performed to demonstrate whether the spinal cord compression is static or dynamic. Dynamic compression is often identified in Doberman Pinschers, and can be demonstrated with decreased spinal cord compression in the linear traction views. The most common site of compression in Doberman Pinschers is C4-C5, C5-C6 and C6-C7. Computed tomography and MRI can also be performed to obtain additional information regarding the severity of the compression. Recent information also suggests that CT and MRI may be able to identify spinal cord atrophy associated with chronic compression and provide additional prognostic information. Treatment of CSM can be conservative (crate confinement and corticosteroids) or surgical, however, in most patients clinical signs will progress with only conservative treatment. Numerous surgical techniques have been described to provide cervical stability and decompress the spinal cord, but no single surgical technique has consistently proven to be superior to others. The choice of surgical technique is based on the type of lesion present, severity of neurologic symptoms, available equipment and the surgeon's preferences. Regardless of the surgical technique chosen, early surgical intervention is important for optimal results, as patients that are non-ambulatory prior to surgery have a lower prognosis. Although intervertebral disc protrusion is an important feature of CSM in Doberman Pinschers, the dynamic and chronic nature of the disease makes surgical complications and the overall success rate of surgery lower than correction of type I cervical intervertebral disc extrusions.
The second form of CSM occurs in young (≤ 2 years) large and giant breeds, especially Great Danes and Mastiffs. Clinical signs in the young giant breeds are also slowly progressive and non-painful, although pet owners often initially mistake the paresis and ataxia for puppy clumsiness. Myelography, CT and MRI are also used to demonstrate the extent and location of the spinal cord compression and to plan surgery. In this form of CSM vertebral malformation, especially enlargement of the articular facets, spinal canal stenosis and hypertrophy of the ligamentum flavum are the predominant findings (Figure 2). Unlike CSM as seen in Doberman Pinschers, the form of CSM seen in young dogs is usually predominantly a static disease process. Surgical treatment is usually necessary as conservative treatment often results in progression of clinical symptoms.
Diskospondylitis occurs at all levels of the vertebral column including the cervical spine. In the cervical vertebral column diskospondylitis occurs most frequently at C5-C6, C6-C7 and C7-T1, with more cranial involvement much less common. Bacterial infection, often associated with bacteremia and cystitis, is the most common cause of diskospondylitis, but fungal agents, post-operative infection and foreign bodies may also result in disc infection. In canine patients Staphylococcus intermedius is the most frequent cause of diskospondylitis. Brucella canis also deserves mention because of the zoonotic potential of this pathogen.
In addition to pain, clinical signs of diskospondylitis include systemic signs (inappetence, lethargy, fever), vertebral pain, weight loss and occasionally paresis and ataxia. Diskospondylitis can usually be demonstrated with well positioned survey radiographs. Radiographic findings may include collapse of the intervertebral disc space, lysis of the adjacent vertebral endplates, shortening of the vertebral body, vertebral body lysis and ventral bone production. When neurologic deficits are present myelography, CT or MRI should be performed to evaluate the degree of spinal cord compression. An etiologic diagnosis should be attempted by performing a series of blood cultures, culture of the urine and possibly direct culture of the intervertebral disc space by fluoroscopy or curettage if decompressive surgery is being performed. Antimicrobial sensitivity testing is recommended if a pathogen is cultured. Initial treatment in patients with no or mild neurologic deficits is directed at treating Staphylococcus intermedius while awaiting culture results. A change in antibiotic may be necessary based on culture and antimicrobial sensitivity results. In patients with severe neurologic symptoms, surgical decompression of the spinal cord and stabilization of the vertebral column may be necessary.
Fungal diskospondylitis also occurs and is usually caused by opportunistic pathogens such as Aspergillus tereus. Diskospondylitis caused by disseminated Aspergillosis most frequently occurs in young, female German Shepherds. Diagnosis of disseminated Aspergillosis can be challenging, and while serologic titers can be performed false negative results are common. One of the most reliable methods of diagnosing disseminated Aspergillosis is examination of the urine sediment for fungal hyphae and urine fungal culture. The prognosis for complete resolution of fungal diskospondylitis is guarded to poor, even with long term anti-fungal treatment.
Fibrocartilagenous embolus (FCE)
Fibrocartilagenous embolus may occur at any level of the spinal cord including the cervical spine. The exact pathogenesis of FCE is still unclear but fibrocartilage identical to that found in the intervertebral disc causes occlusion of spinal cord arteries and veins resulting in ischemic myelopathy. Characteristics of this disease include peracute onset of paresis or plegia, often after mild trauma or exercise. Any breed of dog may experience an FCE, but this disorder is more common in young to middle aged large and giant breeds. Miniature schnauzers, miniature Pinschers and Shetland sheepdogs are small breeds that are frequently affected. A very important aspect of patients with FCE is that clinical signs do not progress and pain is not present beyond the first 12-24 hours. Clinical signs of a cervical FCE are almost always asymmetric because of the asymmetry of the blood supply to the cervical spinal cord.
Clinical signs include hemiparesis or asymmetric tetraparesis, upper motor pelvic limb signs (extensor rigidity, hyperreflexia), and upper or lower motor neuron thoracic limb signs (depending on the location of the infarction). If the ischemia damages the tectotegmental spinal cord tract or involves spinal cord segments T1-T3 an ipsilateral Horner's syndrome may be seen. Ipsilateral loss of the panniculus reflex may also be seen when spinal cord segments C8 and T1 are damaged. When patients are examined soon after the FCE has occurred they often are very anxious. If pain is present early in the course of this disorder it is usually mild to moderate, and should subside without treatment within 24 hours.
Diagnosis of an FCE is often highly suggested by the signalment, history and clinical examination. No definitive antemortem diagnostic test is available to consistently confirm the presence of an FCE, although an area of intraparenchymal hemorrhage or edema can sometimes be demonstrated with CT or MRI. If there are questions regarding the diagnosis a myelogram and CSF analysis are often performed to rule out extradural compression (especially intervertebral disc extrusion) and meningomyelitis.
Treatment of an FCE consists of supportive care and physical therapy. Most patients with FCE begin showing clinical improvement within a week of developing paresis and many will make a complete recovery, although the prognosis is not as good for patients with severe lower motor neuron symptoms.
Primary or metastatic neoplasia of the spinal cord, vertebrae and surrounding tissues often results in cervical pain and paresis. Vertebral tumors (primary and metastatic), nerve sheath tumors and cervical meningiomas are among the most common tumors identified. Most tumors in the cervical area occur in middle aged to older dogs, although some forms of cervical neoplasia such as feline lymphoma and certain forms of canine osteosarcoma are more common in younger patients. Clinical signs depend on the location and extent of the tumor. An acute onset of clinical signs is possible when vertebral collapse (pathologic fracture) or vascular changes (either infarction or hemorrhage) occur within a tumor. Veterinary patients may hide symptoms of neoplasia so that a tumor is very advanced prior to the onset of clinical signs. Diagnosis of cervical neoplasia may be obtained with a variety of diagnostic techniques, including survey radiography, myelography, CT, MRI, CSF analysis and electromyography. CT and MRI are especially helpful in finding nerve sheath tumors in the brachial plexus. Histologic examination of a mass is required for definitive diagnosis of a tumor and will also provide important prognostic information. Treatment of cervical neoplasia often involves a combination of surgical debulking, chemotherapy and radiation therapy.
Subarachnoid cysts are not true cysts (there is no epithelial lining) but rather a cerebrospinal fluid filled dilation of the subarachnoid space and cavitation of the surrounding spinal cord. Both congenital and acquired etiologies may occur but both result in thickening and adhesions of the dura to the spinal cord. In the cervical area subarachnoid cysts have been most often identified in large breed dogs, especially in Rottweilers.
Clinical signs include a slowly progressive, non-painful or intermittently painful tetra or posterior paresis. Diagnosis is often possible with myelography when a "tear drop" dilation is seen within the dorsal subarachnoid space. Computed tomography and MRI are also valuable for identifying subarachnoid cysts and are especially useful for identifying asymmetry in the cysts that sometimes occurs. Temporary improvement of the clinical signs associated with subarachnoid cysts may be seen following administration of corticosteroids, but more definitive and long term treatment usually requires dorsal laminectomy and durectomy to decompress the spinal cord and remove the accumulation of spinal fluid and adhesions of the dura to the spinal cord. Recovery and prognosis in most patients following surgery is good if the entire dural lesion can be removed.
Corticosteroid responsive meningitis is suspected to be an immune mediated cause of meningitis that primarily affects young (4-16 months), medium to large breeds. The predominant symptom is severe, sometimes waxing and waning, cervical pain and reluctance to move. Diagnosis is based on demonstration of elevated cerebrospinal fluid protein, non-degenerative neutrophilic or eosinophilic pleocytosis and failure to find other causes of meningitis/myelitis. Treatment involves long term treatment with corticosteroids. Immunosuppressive dosages are used initially and then tapered over several months. Prognosis for recovery is good, but relapse of symptoms is common, especially if corticosteroids are discontinued early or only lower dosages are given.