by R.M. Clemmons, DVM, PhD
Associate Professor of Neurology & Neurosurgery


Parapareis (weakness in the rear limbs) and paraplegia (paralysis of the rear limbs) unaccompanied by signs of additional CNS disturbance suggests that the disease is located caudal to T2. If the rear limb reflexes are intact, the lesion is between T2 and L3. If the rear leg reflexes are diminished to absent, the lesion is between L4 and S2. This can be refined further in that lesions between L4 and L5 result in loss of femoral nerve function, manifested as a decrease in the patellar tendon reflex and inability to support weight in the rear legs. Lesions between L6 and S2 result in sciatic nerve dysfunction, reducing rear leg withdrawal, cranial tibialis muscle, gastrocnemius muscle and sciatic nerve reflexes.

The differential diagnosis of paraparesis and paraplegia include a number of congenital diseases, including vertebral malformations, various spinal cord malformations, multiple cartilaginous exostoses, lysosomal storage diseases, and breed-specific disorders. Other disorders are similar to those which affect the cervical spinal cord including meningomyelitis (from various causes), degenerative disc disease, spinal cord trauma, fibrocartilaginous infarction, and neoplasia. In some breeds, the differential also includes degenerative myelopathy.

Diagnostic Approach:

The neurologic assessment of patients with rear leg problems helps to confirm that the disease is neurologic in nature and its location. Weakness can indicate neurologic disease, muscle disease or systemic illness. On the other hand, reproducible deficits in proprioception usually is indicative of neurologic disease, whether knuckling, stumbling or falling or conscious proprioceptive deficits or dysmetria of unconscious proprioceptive dysfunction. When deciding whether a rear leg lameness is secondary to orthopedic or neurologic disease, examination of proprioceptive function can help make the differentiation.

Unlike cervical disease, there are several neurologic tests which can assist in lesion localization with TL disease. If the lesion is between T2 and L3, Schiff-Sherrington syndrome may be seen. Also, between T2 and L4 is the panniculus response, where superficial stimulation of the skin over the back results in stimulation of intraspinal pain pathways with the resultant contraction of the latisimus dorsi muscle. Due to the overlap of sensory dermatomes, the panniculus response will be absent 1-2 segments caudal to the lesion. Hyperpathia on deep palpation will be present at the cranial edge of the lesion and hyperesthesia will be evident on pin prick of the skin at the cranial and caudal edges of the lesion. By locating hyperpathia and hyperesthesia and demonstrating the loss of the panniculus response 1-2 segments caudally, the lesion is found.

The ancillary diagnostic tests for TL spinal disease are identical to those for cervical disease with the exception that lumbar CSF should be obtained in most instances. Since the flow of CSF is from cranial to caudal, lumbar CSF more accurately represents changes within the TL spinal column. This is usually obtained by carefully passing a needle into the subarachnoid space between L5-L6 or L4-L5.

Specific Conditions:

Intervertebral Disc Disease:

Intervertebral disc (IVD) disease is a surgical disease. Now, that has been said I will attempt to explain the disease and why surgery is the treatment of choice. Not only is IVD disease a common problem, it is one which I personally like, since it is one neurologic disease which can be cured. IVD disease can occur as a protrusion of the IVD (Hansen's Type 2 IVD) with the dorsal annulus still covering the disc material or as a herniation of the nucleus pulposus into the neural canal (Hansen's Type 1 IVD). The former is most common in non-chondrodystrophic animals (straight-legged dogs) and occurs as a result of age-related changes in the IVD. As animals age, the water content of the IVD diminishes and the collagen content increases (similar to nuclear sclerosis of the eye). This results in a decrease in the IVD elasticity, leading to degeneration of the annulus fibrosis and protrusion of the IVD. Depending upon the location, this can result in spinal cord or nerve root compression and development of neurologic signs. The onset of signs increases with age, peaking around 8-10 years of age. This type of IVD protrusion is uncommon before 5-6 years of age.

On the other hand, chondrodystrophic breeds of dogs are prone to the development of IVD herniation early in life. In these breeds (including dachshunds, beagles, pekinese, miniature poodles, cocker spaniels, pomeranians and basset hounds), there is a metaplasia of the nucleus pulposus whereby the normal collagen fibers of the nucleus are replaced by hyaline fibers. The hyaline fibers are less elastic than collagen fibers leading to degeneration of the annulus fibrosis. The hyaline fibers during this degenerative process calcify, creating further inelasticity. Due to the fact that the annulus fibrosis is thinnest dorsally toward the spinal cord, the least line of resistance for the degeneration and breakdown of the annulus is toward the spinal cord. Ultimately, the annulus ruptures allowing the herniation of the degenerative nucleus into the neural canal, compressing the spinal cord. Not only does the IVD material compress the spinal cord, but the degenerative material is irritative in nature. The presence of the herniated material in the epidural space causes inflammation, furthering the swelling associated with the herniation.

Almost all chondrodystrophic dogs will show some degree of IVD degeneration within a year of age. The earliest I have seen clinical IVD herniation is these dogs is at 7 months. Usually the onset is between 2-3 years of age with the peak incidence being between 4-6 years of age. There are 26 IVD in dogs, any one of which can herniate. However, IVD herniation is less common in the upper thoracic region due to the conjugal ligament which connects the rib heads and reinforces the dorsal annulus in that area. Of the remaining spinal column regions, 20% of IVD herniations occur in the cervical region (C2-C7) with 80% of these at C2-3. In the thoracolumbar spinal column, 80% of the IVD herniations occur with 67-75% of these occurring at T12-13 or T13-L1. The incidence rapidly dissipates cranially and caudally from the TL junction. The incidence between T1 and T9 is less than 0.5%. From L4 caudally, each disc has an incidence of around 2.5%. Cervical IVD herniation will cause quadriparesis (or quadriplegia) while TL IVD herniations result in paraparesis to paraplegia.

In addition to location, the dynamic factor dictates the severity of clinical signs. The amount of traumatic force imparted by a small amount of material traveling rapidly is greater than a larger amount going slow. In the worst case, this means the time for intervention is also quiet short. In most cases of IVD disease, definitive treatment must be started before 24 hours in order to achieve the greatest success. In some cases, this time is shorter. Unfortunately, delaying treatment to see the outcome may preclude success. We treat severe IVD disease as a medical and surgical emergency. In patients with complete motor and sensory paralysis, the patient should be treated for acute spinal injury and be immediately referred to a center who can diagnose and definitively treat the problem. In patients who are paralyzed but retain deep pain, then it is possible to treat them for acute spinal injury and observe them for signs of improvement. If they are worse or no better within 24 hours, they then constitute and emergency referral. On the other hand, it is best to refer these patients at the outset. In patients with mild paresis or mere back pain, they can be worked-up for the rule/out and referred if they do not make improvements in 5-7 days. These later patients may benefit from surgical intervention, but might also recover from the current IVD herniation with medical management. They are still surgical candidates upon recovery, to prevent future IVD disease.

Medical management of IVD disease consists of absolute rest for a minimum of 30 days or 3 weeks beyond return to clinical normalcy. This confinement must be in a cage no more than 2.5 x 1.5 times the animal's body length. An airline carrier is ideal. Many patients will benefit from corticosteroid management during the initiation of treatment. I think this should only be done under direct veterinary supervision. If the patient feels better and then becomes active before healing has occurred, they are at great risk to get worse. We see this outcome commonly. It could be prevented in many cases, with absolute confinement of the patient. Owners do not always comply, allowing their pet to worsen. For that reason, I prefer to treat these patients in the hospital for the first 5-7 days, going home without medication, only confinement. I would give 30 mg/kg of methylprednisolone (Solu Medral or Solu Delta Cortef) IV, initially; followed by 15 mg/kg every 8 hours for the first 24 hours. Then, I give oral prednisolone at 1 mg/kg/day in 2 divided doses for 5 days. If more steroids are needed, I give 0.5 mg/kg every other day in the morning. During steroid medication, it is necessary to protect against steroid-gastritis. I use misoprostil (50-100 µg) every 12 hours until using alternate day steroids. Many patients feel better with muscle relaxants. I prefer diazepam at 0.25-0.5 mg/kg every 8 hours. Once the animal has recovered and has been normal without medication for 3 weeks, prophylactic IVD fenestration can be performed. It is felt that 60% of patients with moderate to mild IVD disease will recover with medical management. On the other hand, 50-80% of these patients will experience additional IVD disease at the same or other site during their lives. Clinically, I usually see recurrence of IVD disease in patients without prophylactic fenestration every 6 months to a year.

As such, I prefer the surgical approach, decompression to treat the acute disease combined with fenestration to prevent future problems. Fenestration is a statistical game, removing the nuclear material (and creating fibrosis within the disc for additional support) so that the chance of IVD herniation at the fenestrated site is lessened. Fenestration does not remove material from the neural canal, laminectomy is needed for that. In the neck, fenestration of C2-C6 reduces the likelihood of future herniation by 99% in that region (.99 x .2, overall). In the TL region, fenestration of T11-L3 reduces the chances by 95% in that region (.92 x .8, overall). By combining cervical and TL fenestration, the overall chances of recurrent IVD disease is reduced by 93%. While not all patients read the same statistical books, generally this will eliminate future IVD disease. If decompression is needed for the patient to recover, fenestration can be performed to prevent recurrence. In cases where fenestration has not been done, the patient remains at risk for recurrent IVD disease.

The diagnosis of IVD disease is made with radiographs and myelography. Since many cases present with acute signs, EMG does not offer assistance. In some cases, CSF analysis helps rule/out meningomyelitis, but myelography is what determines the extent and surgical approach of choice. In most cases, this will be hemilaminectomy. Myelography helps to confirm the side upon which to perform the laminectomy. Scout radiographs may demonstrate the presence of degenerative disc disease by revealing calcified nuclear material. The site of herniation may show collapse of the IVD space, wedging of the IVD space, collapse of the demi-facets and the presence of calcified material in the neural canal. Coupled with the neurologic examination, this may be enough to determine the need for surgical intervention. When there is doubt about the location or the radiographic changes do not fit the neurologic findings, myelography is needed. Myelography will also help rule/out other diseases which might cause spinal cord compression, such as neoplasia.

Beyond treatment and surgical fenestration, it is possible that certain dietary supplements would benefit chondrodystrophic patients to prevent IVD disease or to facilitate their recovery upon IVD herniation. Tofu (rich in soy lecithin) may aid in spinal cord myelination. Antioxidants like vitamin E, vitamin C and ginkgo biloba may help prevent degeneration and, certainly, appear to help protect the spinal cord from the results of spinal cord injury. Vitamin E and C must be given prior to the damage, while ginkgo biloba may be as effective as methylprednisolone in treating the injury once it has happened. Our current understanding of spinal cord damage suggests that antioxidants may work by sparing spinal cord function, while the steroid receptor may help protect spinal cord architecture. As such, methylprednisolone, which contains both the antioxidant effect and steroid receptor effect, is currently the best medication for the treatment of brain and spinal cord injury.

Fibrocartilaginous Infarction:

Even though animals do not suffer from the same degree of vascular disease as human beings, infarction of the spinal cord with fibrocartilaginous material is not uncommon. It occurs in any breed of dogs, but is most common in large breeds, such as Great Danes, Labrador retrievers and German Shepherds. Although both arteries and veins can be affected, most commonly it is the venous system of the spinal cord which is obstructed, leading to a hemorrhagic infarction. It is believed that herniation of the nucleus pulposus takes place either into the vertebral body or the venous sinuses within the spinal column. Since the vertebral body represents a vascular space communicating with the spinal venous system, the material gains access to the spinal veins. These veins do not have valves, allowing the fibrocartilaginous material to flow up and down the spinal column. When intra-thoracic pressure increases, this material can be back-flushed into small penetrating spinal cord veins. When the intra-thoracic pressure returns to normal, the veins collapse trapping the material and leading to excessive venous pressure upstream to the occlusion. The venules rupture leading to a hemorrhagic infarction. The pattern of infarction usually affects a quadrant of the spinal cord, although initial signs may affect more of the spinal pathways due to inflammation and spinal cord swelling. The infarction can occur anywhere along the spinal cord, but the causal cervical and mid- to lower lumbar spinal cord segments appear to be most frequently involved.

The presence of spinal cord infarction should be suspected whenever a patient presents with acute onset of paresis or paralysis which is markedly asymmetrical and there is no evidence of hyperpathia. Vascular disease is generally acute and non-progressive. In addition, the spinal cord contains pain pathways, but no pain receptors. As such, strict diseases within the spinal cord without meningeal involvement are usually not painful. Most of the other diagnostic tests will be within normal limits. Occasionally, there will be evidence of hemorrhage on CSF analysis. Spinal radiographs, do not demonstrate the disease, but may reveal other evidence of spinal column degeneration. Myelography will be normal or demonstrate mild intramedullary swelling. In a small number of cases (where the vascular occlusion is secondary to a systemic disease), the minimum data base will show evidence of the systemic disease.

The treatment of spinal cord infarction is that for acute spinal cord injury, using methylprednisolone at 30 mg/kg initially. This is followed by 15 mg/kg every 8 hours for the first 24-48 hours. Then, oral prednisolone is begun at 0.5 mg /kg every 12 hours for 5 days. I continue prednisolone at 0.5 mg/kg every other day, in the morning, for up to another 2 weeks. Many cases will improve dramatically within the first week, although they will still improve over several months. If there has been no improvement in the first week, re-examination and additional tests may be indicated. Since usually only a quadrant of the spinal cord is affected, the patient will improve most on the unaffected side. Reorganization will usually allow these patients to function adequately. Spinal cord infarction from fibrocartilaginous material is a sporadic problem and, usually, does not reoccur.

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Last updated 27 August 2002