Associate Professor of Neurology & Neurosurgery
In developing the differential diagnosis for quadriparesis, the basic
mechanisms of disease must be considered along with the signalment and
history. Congenital diseases are not uncommon in the cervical spinal column
of dogs. These include agenesis of the dens (with resultant atlantoaxial
subluxation), blocked vertebra, multiple cartilaginous exostoses, leukoencephalomyelopathy
of Rottweilers, and hereditary ataxia of Jack Russell and Smooth-haired
Fox terriers. In older animals, degenerative intervertebral disc (IVD)
disease, inflammatory meningomyelitis and neoplasia are not uncommon. If
the signs are symmetrical, then nutritional, metabolic and toxic diseases
must be considered. On the other hand, most asymmetrical diseases can be
separated into their most likely causes, which must be included in the
differential. These causes are discospondylitis, meningomyelitis, IVD disease
The ancillary diagnostic tests for spinal cord disease are similar regardless
of the cause and include the minimum data base, spinal radiographs, EMG,
CSF tap and analysis, myelography and MRI. The minimum data base will often
be normal or may need to be expanded based upon the physical and neurologic
examinations. In older patients, routine chest and abdominal radiographs
and abdominal ultrasound may help make a diagnosis of the cervical disease
or assist in making the prognosis. Spinal radiographs may show signs of
degenerative disc disease, congenital malformation, spinal arthritis or
discospondylitis. The later disease being the only disease diagnosis which
can be made on plain spinal radiographs. The other diseases will need additional
imaging techniques to confirm that they are the source of the problem.
In acute diseases, the EMG may not help identify denervation until 5-7
days have past; however, nerve conduction velocity studies may help identify
damaged nerves or diffuse LMN disorders. On the other hand, in chronic
diseases, the EMG may help to localize the disease process, so that radiographs
can concentrate on the lesion. The CSF tap can help determine the presence
of inflammation or infection in cervical diseases. The problem of inflammatory
myelitis is increasing, making CSF tap and analysis critical in assessing
cervical neurologic disease. Even when other neurologic conditions are
identified, myelitis may be present. Unfortunately, many patients are treated
with corticosteroids before being adequately worked-up for cervical disease.
The work-up performed in the face of the steroids may be erroneous. As
such, surgical intervention may be performed, only later to discover the
cause of neck pain was inflammatory meningomyelitis. Spinal myelography
helps to contrast the spinal cord when looking for mass lesions. It can
be an extremely valuable diagnostic aid in determining the need for surgical
intervention and what surgical approach is best. In cervical vertebral
malformation complex, the lesion is dynamic. The only imaging technique
which can provide dynamic views is the myelogram. Myelography, therefore,
remains the single most important imaging technique for assessing surgical
diseases in the cervical spine. When the myelographic data is lacking or
when it is not clear what the lesion represents, MRI can add diagnostic
detail. MRI may be important in assessing neoplastic disease processes,
including nerve root tumors. The sequence of diagnostic tests logically
follows the pattern of minimum data base, EMG, spinal radiographs, CSF
tap, myelography and, finally, MRI. If an accurate diagnosis is made along
the way, the remaining test may not be needed.
The clinical signs of meningomyelitis are, generally, neck pain and asymmetrical neurologic deficits. The deficits depend upon which pathways are involved in the disease process. The signs are usually progressive, but may develop acutely. In dogs and cats, the causes of meningomyelitis are, in order of likelihood, viral, inflammatory, protozoal, fungal, rickettsial and bacterial diseases. The viral disease most commonly seen in dogs is canine distemper (even in vaccinated dogs). In cats, feline leukemia virus (FeLV), feline infectious peritonitis (FIP) and feline immunodeficiency virus (FIV) are the most common viral infections. Toxoplasmosis can occur in both dogs and cats, while dog also may develop Neospora caninum infections. Aspergillosis is not uncommon in dogs, while cryptococcosis is more common in cats. Cats do not appear to have rickettsial diseases, but dogs have been shown to develop meningomyelitis from both ehrlichiosis and Rocky Mountain spotted fever. Titers for these agents should be performed on the serum and/or CSF when presented with meningomyelitis.
The diagnosis is made on CSF tap and analysis. Generally, we approach animals with neck pain and quadriparesis by performing a minimum data base including a CBC, chemistry profile, urinalysis and appropriate radiographs. With the CBC, we run plasma fibrinogen levels. This is a crude estimate of systemic inflammation, but a valuable tool in assessing the potential for meningomyelitis. It may be the only abnormality noted in the CBC. Once the minimal data base is evaluated, we proceed with anesthesia and CSF tap. While this is being processed, spinal radiographs are taken. If the CSF indicates inflammation by increase in cells and protein and the survey radiographs do not demonstrate significant findings, we then treat the inflammation rather than proceed with myelography. Based upon the response to therapy, we reassess the need for further tests. CSF titers are submitted for the relevant infectious agents providing confirmation of the specific disease causing organism. In those cases where a specific disease causing organism can be found, the treatment is adjusted appropriately. When no organism is found, the tentative diagnosis of inflammatory meningomyelitis is made. Many newer forms of meningomyelitis are now recognized including steroid-responsive meningomyelitis. This is usually associated with an increase in blood vessel fragility and may lead to an apparently blood-contaminated CSF tap. On examination, however, there is a marked increase in non-degenerative neutrophils in the CSF.
As in beagles
with necrotizing vasculitis (beagle neck pain syndrome), many patients
with steroid-responsive meningomyelitis have elevations in alpha 2 globulins
on serum electrophoresis. Steroid-responsive meningomyelitis probably represents
a form of vasculitis which results in inflammation in the CNS. Conventional
therapy with corticosteroids will not always resolve this condition, since
steroids only suppress the symptoms of the disease. Although some dogs
recover from this disease following corticosteroid management, many would
probably benefit from alternative therapy. Conventional therapy involves
giving prednisolone at 1 mg/kg/day in three divided doses. Once the signs
resolve (usually within 72 hours), the dosage is reduced to twice a day.
This is further reduced to daily medication in the morning and, finally,
to alternate day therapy. We find that many patients will benefit from
anti-oxidant therapy, including vitamin E, vitamin C and selenium. Additional
medications of benefit include omega-3-fatty acids, ginkgo biloba extract
and green tea. When pain is present, garlic, ginger and feverfew may help
reduce the inflammation without causing additional gastrointestinal signs.
Some patients will be relieved by the alternative medication, reducing
or replacing the corticosteroid.
The primary complaint in discospondylitis is pain at the site of infection. In severe cases, quadriparesis and anorexia may be present with cervical discospondylitis. The diagnosis is confirmed by routine spinal radiographs showing characteristic lysis and sclerosis of the adjacent endplates of the vertebrae. This is one of the few neurologic conditions where the diagnosis can be made on routine radiographic examination. The minimum data base includes a CBC (with a marker of inflammation such as the plasma fibrinogen level), urinalysis (with culture), fecal examination, Brucella canis titer, and spinal radiographs. Chest radiographs and echocardiography may be indicated if there is a heart murmur. Since the radiography changes may not occur until 2-3 weeks from the start of clinical signs, repeat radiographic examination is indicated when discospondylitis is high on the differential list. The CBC may reflect changes consistent with infection (including neutrophilia) or be normal. On of the important monitors is the marker of inflammation. We use fibrinogen, since it is easy and inexpensive to run. When the fibrinogen levels are elevated, this is a good indicator of a disease with much tissue reaction. On the other hand, when the fibrinogen is low, I am particularly concerned about the possibility of fungal disease. In the later case, I usually perform a routine chest radiograph looking for discospondylitic-like lesions between the sternebrae. When lesions are also present between the sternebrae, most often fungal infection is the cause of the discospondylitis lesions.
The causative agents are bacteria (Staphylococcus, Streptococcus and Corynebacterium are the most common, although Brucella can occasionally be seen as a cause), parasitic (Spirocerca lupi in thoracic discospondylitis), and fungal (Aspergillus and Nocardia). As such, the treatment and prognosis vary depending upon the organism causing the infection. Parasitic infections are rare except in the Southwestern US and usually represent advanced cases of parasitism. Brucella canis infection is not uncommon, but much less so than the other bacterial causes. When Brucella appears to be the cause, antibiotic therapy must take this into account (usually, I use doxycycline). Fungal infections with Aspergillus do not respond well to antifungal drugs. Recently, there have been reports of controlling the infection for extended period using itraconazole. I use raw garlic in hopes that it will help control the problem.
By in large, the most common causes of discospondylitis are secondary
to bacteria which can be treated using a combination of sulfa drugs (sulfadimethozine,
15 mg/kg every 12 hours) and either cephalosporins (22 mg/kg every 8-12
hours) or enrofloxacin (5-7.5 mg/kg every 12 hours). I prefer the former
combination and treat the infection for a minimum of 6-8 weeks. Radiographic
repair usually lags behind remission of the infection; however, following
the response to therapy and continuing therapy beyond the time of radiographic
quiescence seem the best policy. In cases which do not respond, the urine
should be reexamined and abdominal ultrasound of the kidneys performed,
looking for evidence that fungal disease was the real cause. Rarely, the
infection will result in bony compression or instability requiring surgical
intervention. Most often, spinal cord compression is the result of soft
tissue inflammation which subsides quickly with appropriate antibiotic
The onset of clinical signs can be acute or slow and insidious. There is evidence of ataxia in all four limbs with the pelvic limbs being more affected. There will be both conscious and unconscious proprioceptive dysfunction with a wide-based stance in the rear legs. The forelegs may show a stiff and stilted gait with atrophy or fasciculations of the deltoideus, biceps and infra- and supraspinatus muscles. There is usually some degree of neck pain on palpation and neck manipulations. One sign of this is a reluctance to hop medially with the forelegs.
can be suspicioned on survey radiographs of the neck, looking for narrowed
IVD spaces and sclerosis of the demi-facets. CSF analysis is usually within
normal limits, although a small number of cases will show a mild increase
in cells (4-10 cells/µl) and protein (25-35 mg/ml). EMG can help
confirm the location and the denervation of the muscles with fasciculations.
The diagnosis in confirmed on myelography, which shows evidence of IVD
protrusion and the presence of ligamentous or bony intrusion into the neural
canal. Since CVM represents a dynamic lesion, myelography with mildly flexed
and extended views is the diagnostic technique of choice. It is also important
to take a "lazy" lateral view, since stretching the neck can reduce the
lesion so as to overlook it. If the lesion is alleviated with flexion and
accentuated on extension, the problem is partially due to ligamentous hypertrophy.
On the other hand, if flexion and extension do not affect the lesion, it
is probably secondary to IVD protrusion. I feel that a single lesion is
better than multiple ones. Further, an IVD protrusion is less problematic
than one with ligamentous hypertrophy.
The treatment of CVM is surgery. In cases where surgery is not possible (patient has complications or is elderly), medical management with prednisolone and diazepam may provide temporary relief. However, in the absence of compelling reasons not to perform surgery, surgical decompression is needed. There are several surgical techniques available to treat Wobbler's disease including dorsal laminectomy, ventral slot and ventral slot with distraction (by various means). In cases of multiple lesions, dorsal laminectomy was the method of choice, in the past. Dorsal laminectomy has risks and the success rate is the lowest of methods for correcting CVM. In qualified hands, it is still a good technique. The overall success is around 75% with a 20-25% morbidity and a 5-10% mortality. Large breeds do not tolerate dorsal laminectomy well. Ventral slot is excellent for IVD protrusion, but increases compression from ligamentous hypertrophy. In simple IVD protrusion, ventral slot has a 90-95% success rate with a 5% morbidity and <1% mortality. The morbidity and mortality increase for ventral slots when ligamentous hypertrophy is present. When ligamentous hypertrophy is present, ventral slot alone is generally inadequate to correct the problem. A number of techniques have been described to perform a ventral slot and maintain distraction across the IVD space. These methods include various implants from Harrington rods to screws (or pins) and methylmethacrylate. The method we use is a modified "screw and washer" technique. The washer we use is a polypropylene ring made from the end of an endotracheal tube. This is packed with bone graft and the screw stabilizes the implant while fusion takes place. In this method, the "slot" is performed by discectomy without removing the endplates. It is my belief that fusion is the goal of CVM surgery and this is best done in distraction. Another popular method (which I do not believe provides adequate fusion) is to inject methylmethacrylate between the vertebrae at the ventral slot site. This can be used as a salvage procedure.
Following surgery, the patient should be kept quite for 30 days and
supported with a neck brace and bandage. After the first month, the activity
level is gradually returned to normal. Depending upon the severity of the
initial damage, most patients will improve, reaching 80% of their recovery
in the first 3 months. There is a potential for the "domino" effect, whereby
the IVD on either
side of the surgery site will develop problems in 6 months to 2 years following
the initial correction. I find that this is more often when the beginnings
of CVM were present in the beginning. We now are much more aggressive than
in the past, fixing multiple lesions from the start.
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Last updated 27 August 2002