Researched at http://www.ivis.org. See citations for full text available at IVIS. Cervical and Thoracolumbar Disc Disease: Diagnosis and Treatment. Bjšrn Meij, DVM, PhD, DECVS,WSAVA 2005 Congress. Internet Publisher: International Veterinary Information Service, Ithaca NY (www.ivis.org), Last acessed: 2/27/07. "1. General considerations Intervertebral disc disease (IVDD) is a frequent neurologic problem affecting dogs and occurs rarely in cats. Disc diseases in canines occur in the cervical, thoracic, lumbar and lumbosacral region. The end of the spinal cord in dogs lies inside lumbar vertebra L6. Cervical and thoracolumbar disc disease affect the spinal cord whereas lumbosacral disc disease affects the cauda equina. The intervertebral disc consists of the ring-like, fibrous, collagen-rich annulus fibrosus and the central, gelatinous, water-rich nucleus pulposis. Degeneration of discs is associated with decreased water content and two types are distinguished: 1) Hansen type I degeneration: chondroid degeneration with extrusion of nucleus material through a ruptured dorsal annulus fibrosus and the dorsal longitudinal ligament into the vertebral canal, and 2) Hansen type II degeneration: fibroid degeneration with bulging or protrusion of the partially ruptured and thickened annulus fibrosus. When the intervertebral disc ruptures and herniates, it causes damage to the nervous system which initially results in pain. The pain suffered with disc disease arises from several sources: 1) discogenic pain (stretching or ruptures in the annulus fibrosus), 2) meningeal pain (mechanical contact or mass effect of extruded disc material on the meninges [dura mater] and/or foreign body inflammatory response to nucleus pulposis material in vertebral canal), 3) radicular pain (compression or entrapment of nerve roots, 'root signature'). The spinal cord itself has no sensory nerve fibers. Injury to the spinal cord may ultimately lead to neurological deficits and with increasing pressure and/or longer duration the extent of deficits may be more prominent and less reversible. An extradural mass in the spinal canal will exert its effect on the spinal cord from the periphery to the center. The neuroanatomic background explains the classical stepwise development of deficits: ataxia (loss of coordination, loss of proprioception)>>paresis (muscle weakness)>>paralysis (loss of voluntary motor function)>>loss of deep pain sensation. The proprioceptive (position sense) nerve fibers are the largest, and most susceptible to compressive forces and lie superficially in the dorsal funiculus. In contrast, the small deep pain nerve fibers that are most resistant to pressure lie in deeply positioned spinothalamic tracts. This explains why loss of deep pain perception is such a severe clinical sign. Based on the neuroanatomy a scale of neurological deficits is possible which will be used in the description of patients with cervical and thoracolumbar disc disease. 2. Neurological grading in canine intervertebral disc disease: Grade 0: normal. Grade 1: cervical or thoracolumbar pain, hyperaesthesia. Grade 2: paresis (muscle weakness) with decreased proprioception, ambulatory (able to walk). Grade 3: severe paresis with absent proprioception, not ambulatory (not able to walk). Grade 4: paralysis (not able to stand or walk), decreased or no bladder control, conscious deep pain perception present. Grade 5: paralysis, urinary and fecal incontinence, no deep conscious pain perception. Neurological grading in canine IVDD is valuable to follow the progression of neurological deficits in time (improvement or worsening), to choose the mode of therapy, for prognosis, and for assessment of outcome after medical or surgical treatment. 4. Thoracolumbar disc disease Thoracolumbar disc disease is a common condition that predominantly affects chondrodystrophic breeds (e.g., Dachshund). Peak incidence is around 6-7 years of age. Nonchondrodystrophic breeds (e.g., German shepherd) are less frequently affected. Hansen type I disc disease is seen mainly in chondrodystrophic dogs, whereas Hansen type II is more typical for non-chondrodystrophic breeds. Over 50% of all thoracolumbar disc lesions occur at the T12/T13 and T13/L1 disc and over 75% occur between T11/T12 and L1/L2. Lumbosacral disc disease, a cauda equina disease at L6/L7 or L7/S1, occurs frequently in large breed dogs (e.g., Shepherd dogs) and is associated with Hansen type II disc disease, vertebral instability and spinal stenosis and the complex is called degenerative lumbosacral stenosis but will not be discussed further in this abstract. The pain resulting from thoracolumbar disease is usually less dramatic than that associated with cervical disc disease. The dog may show kyphosis and reluctance to run or jump, and discomfort when picked up or when palpated in the thoracolumbar region. Pain alone may be misinterpreted as being of abdominal origin. Neurological deficits are more prominent in thoracolumbar disc disease than in cervical disc disease and may range from mild posterior ataxia and paresis to complete posterior paralysis and paraplegia (Figure 4), bladder and fecal incontinence, and depressed or absent deep pain sensation in the pelvic limbs. The withdrawal reflex (spinal reflex) should not be mistakenly interpreted as conscious (cerebral) sensation of deep pain applied to the toes. Spinal hyperreflexia in the pelvic limbs is common due to loss of central inhibition on spinal reflexes. The forelimbs are not affected by thoracolumbar disc disease and should be neurologically intact. The neurological deficits are caused by extradural compression and spinal cord injury and the deficits become more severe with greater and longer spinal cord compression. In addition to the actual mass effect, the rate at which spinal cord injury occurs is also important. If it is rapid, like in a explosive rupture of the disc, the spinal cord cannot compensate and more severe neurological deficits occur. In these cases, progressive ischemic myelomalacia (rather than the mass of extradural disc material found during surgery) may be the main cause of the severe neurological deficits. Most of these dogs show grade 4 or 5 deficits. The clinician should be suspicious when this problem arises; in these cases there is progressive loss of pelvic limb reflexes, the level of panniculus cut-off moves cranially and paralyzed dogs become depressed. The prognosis of these dogs is poor. Treatment Treatment options may be nonsurgical or surgical. Nonsurgical treatment. Strict cage rest is the most important consideration in nonsurgical treatment of thoracolumbar disc disease. Judicious use of anti-inflammatory medication (NSAIDs or corticosteroids) may be helpful. The animal should rest in a confined space (bench) for 2-4 weeks and is only allowed outside the cage for urination and defecation. Animals that do not rest, especially during treatment with NSAIDs, have a great risk of (sudden) deterioration of neurological status with worsening of the prognosis. Overall recovery in dogs with grade 1-3 deficits is 80% to 90%. For paraplegic dogs with grade 4 or 5 deficits non-surgical treatment is rarely the treatment of choice because of the low response rate, high rate of recurrence, neurological worsening during treatment, and development of complications. In dogs with grade 5 neurological deficits the duration of absence of conscious deep pain sensation is an important prognostic parameter. Dogs with grade 5 neurological deficits should be regarded as emergencies and require surgery within 24-48 hours. When grade 5 neurological deficits persist beyond 3 days the result of any treatment (surgical or nonsurgical) becomes minimal. Surgical treatment. Dorsal right-sided or left-sided hemilaminectomy is the most common surgical treatment for thoracolumbar disc disease (Figure 6). Dorsal laminectomy is not recommended in the thoracolumbar area because it causes considerable biomechanical instability and may lead to neurological worsening. Indications for hemilaminectomy are grade 2 or 3 lesions unresponsive to medical therapy, grade 4 and 5 lesions less than 48 hours duration and myelographic evidence of significant spinal cord compression. The dog is positioned in a ventral recumbent position and supported with bags. Accurate identification of the affected disc is by palpation of the last rib-vertebral body joint and the transverse process of L1. There are frequent anatomical variations in the T13/L1 junction and therefore the survey radiographs (besides the CT or MR images) are required in the operating room to relate anatomic findings during the approach with radiographic findings. Hemilaminectomy is performed using powered instruments and rongeurs. It is performed on the side of the disc herniation which is determined by the myelogram. Fenestration of the affected disc and prophylactic fenestration may be performed of the disc on either side. Fenestration of all high risk discs (T11/T12-L2/L3) requires extensive dissection and is not advised. Burring is progressed until the inner cortical lamina is thinned out. Rongeurs are used to enlarge the opening. Extruded disc material is usually situated lateral and ventral of the spinal cord and frequently entraps the exiting nerve root at the intervertebral foramen. The disc material is removed by the combination of gentle suction, flushing with saline solution and the use of a thin ball-tipped probe to scoop out material from beneath the spinal cord. For closure of the laminar defect an autogenous fat transplant is used to prevent dural adhesions. The most important consideration in the postoperative care after hemilaminectomy is to ensure that the bladder is regularly emptied. Urinary retention is the most common postoperative problem in thoracolumbar disc disease. Great care should be given to bedding and hygiene and paraplegic dogs should be bathed at least once a day to prevent decubitus which complicates the recovery. The dogs should be daily examined for pressure points (ischiadic tuberosities) and the perineum should kept clean at any time. The prognosis for functional recovery is good for dogs with grade 1, 2, and 3 lesions irrespective of the treatment choice. Dogs with grade 4 lesions have better prognosis after surgical treatment than after nonsurgical treatment. In dogs with grade 5 lesions that are treated within 24-48 hours of onset the animal has a chance of making a functional recovery." --- Textbook of Small Animal Orthopaedics, Newton C.D. and Nunamaker D.M. (Eds.) Ithaca: International Veterinary Information Service, 1985; Internet Publisher: International Veterinary Information Service, Ithaca NY (www.ivis.org), Last acessed: 2/27/07 MEDICAL MANAGEMENT "Indications for medical management of the thoracolumbar IVD syndrome are clinical signs of ataxia, paresis with pain, or pain only and no previous history of disk disease. Recurrent episodes of thoracolumbar disk disease may warrant strong consideration of surgical therapy. (28,54) Radiographic confirmation of a disk protrusion should be made whenever possible. When surgery is prohibited by financial considerations or severe systemic disease (e.g., congestive heart failure), medical management is indicated. (54) Medical management has been shown to be as ineffective as surgical therapy in the majority of patients with sensorimotor paralysis for more than 24 hours with signs of hematomyelia. (28) However, some clients do not consider euthanasia as an immediate alternative in these cases and may request some form of therapy. Proper medical therapy for the thoracolumbar IVD patient includes cage rest, corticosteroid therapy, muscle relaxants if indicated, and frequent observation for deterioration of neurologic signs. (28,54,55) Hospitalization for 1 to 2 weeks is often required and is mandatory if corticosteroid therapy is used. The bladder is expressed two or three times daily in the incontinent patient. Frequent evaluation for cystitis is made. (54) Clean soft padding (fleece pads or foam rubber) is maintained in the cage to minimize the potential for decubital ulcer formation. (28,54) Client education is an important component of the medical management regime. The client should be informed of the severity of the disease and of the fact that the signs may suddenly become progressively worse in which case surgical therapy is indicated. (54) Recurrent episodes are frequent and are commonly more severe than the previous one (28,54) SURGICAL MANAGEMENT Indications for surgical management are pain or paresis unresponsive to medical therapy, recurrent or progressive signs of thoracolumbar IVD disease, paraplegia without sensory paralysis, and sensory and motor paralysis for less than 24 hours. (54) Every surgical candidate must have radiographic evidence of an IVD protrusion that coincides with the neurologic findings. (28,54) The surgical procedure of choice in thoracolumbar IVD disease is based on the condition of the patient and the surgeon's experience, ability, and preference. (49,54) Surgical procedures described for thoracolumbar IVD disease are the lateral, (13,53) dorsolateral, (28) and ventral fenestrations; (4) the dorsal laminectomy, (15,21,63) and the hemilaminectomy. (18,28,51) Fenestration is performed as a prophylaxis in combination with a decompressive procedure or following successful medical management of an IVD protrusion. Therapeutically, fenestrating is performed on dogs exhibiting only back pain or mild paresis associated with a Hansen type II IVD protrusion. Decompression of the thoracolumbar spine is indicated when extrusion of IVD material into the spinal canal produces severe ataxia, paresis, or paralysis. The severely paretic or paralyzed dog must be properly managed medically and surgically within the first 24 hours to afford optimal results. Delay in proper management may result in a prolonged recovery period or permanent sensorimotor paralysis. The hemilaminectomy procedure provides good decompression, allows access to the ventral spinal canal for removal of the extruded IVD material, and is easily combined with prophylactic fenestration. The dorsal laminectomy provides no additional advantages and requires more muscle dissection."