Degenerative and Compressive Structural Disorders. Disk Disease.

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Spinal cord compression secondary to intervertebral disk protrusion-extrusion continues to be one of the most common neurological disorders seen in clinical practice [67]. Terms used for this disorder include ruptured disk, prolapsed disk, slipped disk and herniated disk. Disk protrusion-extrusion more accurately describes this process. Protrusion implies that the disk is bulging into the vertebral canal as a result of dorsal shifting of central nuclear material. The outer fibrous envelope of the disk is still intact. Disk extrusion indicates that the outer fibrous layers have ruptured with subsequent extrusion of nuclear material into the vertebral canal. The clinical expression of disk extrusion is referred to as disk disease. The term intervertebral disk displacement is presently in vogue as another descriptor of disk disease.

There are 26 intervertebral disks in the canine and feline spinal column, excluding the coccygeal region, and they form approximately 18% of the length of the spine. Disks are widest in the cervical and lumbar regions, and narrowest in the thoracic spine. Each disk consists of two structurally different regions: (a) a central gelatinous area, the nucleus pulposus (NP), and (b) a surrounding fibrous envelope, the annulus fibrosus (AF), which contains an inner, more fibrocartilaginous matrix termed the “transitional zone” (TZ) [68-71]. The NP is oval-shaped and eccentrically positioned between the middle and dorsal thirds of the disk. It is a highly specialized tissue originating from the embryonic notochord. Throughout fetal life, the NP is the fastest growing region of the disk, and in the neonate, it occupies a considerable area of the disk. The AF is a fibrocartilaginous tissue consisting of bands of parallel fibrous bundles that run obliquely between adjacent vertebrae. The ventral annulus is about twice as wide as the dorsal annulus. Biochemically, the major macromolecular components of the canine disk include collagenous and non-collagenous protein (NCP), proteoglycan (PG) aggregates, and glycoproteins. The PG subunits consist of glycosaminoglycans (GAGs) covalently bound to a central protein core. The main GAGs in canine intervertebral disks are hyaluronic acid, chondroitin sulfate-4, chondroitin sulfate-6, and keratan sulfate. Higher orders of aggregation intimately involve hyaluronic acid. Aggregated PGs are formed by the association of many PG molecules with a single chain of hyaluronic acid, the complex being stabilized by a glycoprotein link. The GAGs are long-chained, sulfated polyanions that attach to the central protein core like the bristles of a brush.The greatest concentration of the GAGs in disk occur in NP and TZ regions of the disk.

Structures that are anatomically and physiologically closely related to disks include cartilaginous end-plates, vertebral end-plates, and conjugal and dorsal longitudinal ligaments. Conjugal ligaments, also known as transverse intercapital ligaments, are present between the second and tenth thoracic vertebral bodies in dogs, and between the second and ninth thoracic vertebral bodies in cats. Conjugal ligaments run over the dorsal part of the disk, ventral to the dorsal longitudinal ligament (a flat structure that lines the floor of the vertebral canal), and connect the heads of each set of ribs. The conjugal ligaments play an important role in the prevention of disk extrusion into the vertebral canal in the thoracic region. Dorsal longitudinal ligaments run the length of the vertebral canal, are attached to the dorsal borders of the vertebral bodies and form fan-like coverings over the dorsal aspects of each disk. Stretch of this ligament is thought to partially account for pain associated with disk protrusion-extrusion. Cartilaginous end-plates are thin layers of hyaline cartilage that cover vertebral body epiphyses and form the rostral and caudal boundaries of each disk. Vertebrae on either side of the disk have a specialized plate of dense, smooth bone termed the vertebral end-plate. These plates are perforated by numerous small canals that are related to the underlying marrow spaces. Each plate consists of an outer peripheral zone and an inner zone that accommodates the NP region of the disk.

Intervertebral disks function as very effective shock absorbers of the vertebral column, largely due to the gel-like properties of the central NP. Specialized PGs within the nucleus bind many water molecules to form a fluid system that is virtually incompressible. This hydrophilic property allows the nucleus to deform and dissipate forces equally over the AF and cartilaginous end-plates. The transformation of an axial compressive force applied to the spine into tangential stresses on the annulus is the function of the NP, thereby reducing the compressive force on the annulus itself. Disks also provide support for the spinal column, since they represent amphiarthrodial joints in intervertebral articulations.

After birth, the canine disk undergoes structural changes that are most prominent in the NP [71-73]. The gel-like nucleus is eventually replaced by more mature fibrocartilage. This process occurs gradually in most breeds of dogs, so that by 7 to 8 years of age, the entire nucleus has changed, and the distinction between nucleus and annulus is lost. In several other breeds of dogs, however, the aging pattern is quite different. These breeds have been designated chondrodystrophoid due to their characteristic endochondral ossification and intervertebral disk morphology, and include Dachshunds, Beagles, Pekingese, French Bulldogs, Basset Hounds, Welsh Corgis and Cocker Spaniels [70,71]. Such breeds are characterized by varying degrees of short-limbed dwarfism. Other breeds such as Shih-tzus and Lhasa apsos probably should also be included in this group.In chondrodystrophoid breeds, replacement of notochordal cells and the gelatinous NP occurs as early as 4 months of age. This process is generally complete in all disks by 12 to 18 months of age. The central areas of the NP are usually the last to be affected, and extensive degenerative changes frequently precede the final chondrification of this area. With increasing age, degenerative changes observed in the NP include matrix disintegration, peripheral/central calcification, and localized areas of cell death. Radial fissures and clefts may appear in the AF. Commensurate with the morphologic transmutation of the NP, collagen levels approach 30 – 40% dry weight within 6 – 12 months.

Extraordinary changes in all other biochemical parameters occur during the first 2 to 3 years [74-76] . In comparison with disks from non-chondrodystrophoid animals of similar age, PG levels in NP are 40 – 50% lower, glycoprotein and non-collagenous protein values are 30 – 40% lower, and chondroitin sulfate values are 30 – 50% lower. Also, during this period, keratan sulfate replaces chondroitin sulfate(s) as the major GAG. The degree of hydration of disks likely decreases with reduction in GAG content, as has been shown in people. Degenerated disks have a depressed imbibition index, which is a measure of the water-binding capacity of the disk.

The etiology of intervertebral disk protrusion-extrusion remains elusive. It is hypothesized that significant changes in morphology and biochemical parameters of the disk during the first 2 years of life result in a reduction of the disk’s shock absorbing mechanisms [68,69]. While still retaining limited properties of incompressibility, the NP loses its ability to adequately deform and distribute forces in a centrifugal manner. As a result, the AF is subjected to increased loading from axial compression and lower tangential stress, which is disproportionately distributed in the disordered disk. The mechanical failure of the NP ultimately results in disruption of AF fibers and subsequent protrusion-extrusion. Results of biochemical studies suggest that the mechanical efficiency of disks is compromised in chondrodystrophoid dogs by 2 to 3 years of age [74-76]. This time-frame is consistent with the occurrence of clinical disease. Nevertheless, this theory does not explain why clinical disk disease occurs with a relatively high frequency in some non-chondrodystrophoid breeds, such as Miniature Poodles and mixed-breeds; nor does it elucidate why clinical disk disease occurs infrequently in older dogs of any breed. Studies in dogs have shown that disk metabolism in the NP is mainly anaerobic, the main route of nutrient supply into the NP is via the endplate, and that diffusion of nutrients is the main mechanism of metabolite transport [77]. There is probably an optimal, but as yet undefined, range of vertebral stress that is needed to promote and maintain nutritive requirements of disks. Half an hour of moderate exercise per day has been shown to increase nutrient flow into canine disks [78]. In contrast, spinal fusion in the dog results in significant biochemical changes in disks-metabolism is depressed in the immobilized disks but increased in the disks adjacent to the fusion mass [79]. In addition, water content and imbibition of water in NP and AF are significantly depressed in fused disks. That disk displacement occurs with some frequency in disks adjacent to totally calcified disks may also reflect an overstressed disk. Finally, it is conceivable that loss of PGs and mechanical failure of the NP profoundly influence disk nutrition. Whether disk matrix changes are the cause or the effect of nutritional diffusion impairment remains to be determined.

There is no evidence that external trauma plays a role in disk degeneration. A force of sufficient magnitude to result in spinal fractures and/or luxations rarely produces traumatic disk protrusion-extrusion. Nevertheless, trauma has been implicated in several large-breed, non-chondrodystrophoid dogs in which tearing of the dural mater secondary to intervertebral disk injury occurred during periods of vigorous running and or struggling [80]. Although trauma does not appear to play a role in the initiation of disk degeneration per se, it may be a factor in the precipitation of protrusion-extrusion once the normal mechanical efficiency of the disk is impaired. It is not unusual for dogs with clinical disk disease to be presented with a history of spinal trauma of variable degree, such as jumping or falling. Perhaps the most logical explanation for the prevalence of disk disease in certain breeds of dogs is a genetic one. Earlier studies suggested that genetic factors are involved in the accelerated aging patterns of disks in Beagles [81]. The heightened susceptibility to disk disease in Dachshunds has been explained by a genetic model that involves the cumulative effect of several genes, with no dominance or sex linkage, subject to environmental modification [82]. In some families of Dachshunds, the prevalence of disk disease was found to be 62%, compared with the estimated breed prevalence of 19%. %. Genetic osteological factors probably play a role as well. For example, midsagittal and interpedicular diameters of the cranial and caudal aspects of cervical vertebral foramina (C3 – C7) are reportedly significantly larger in small breeds than in large breeds and Dachshunds, with seemingly potential predisposition to cervical spinal cord compression [274]. There is no evidence that autoimmune mechanisms are a factor in the pathogenesis of disk degeneration. The roles of inactivity and obesity in disk disease have not been fully evaluated, although in one study, excess body weight did not appear to be a predisposing factor in Cocker Spaniels with disk disease [83].

Neurological signs after extrusion of disk material are caused by impact injury [84], or mechanical compression of the spinal cord [85], or both. While disk protrusion usually precedes extrusion, protrusion or bulging of the disk dorsally into the vertebral canal without rupture of the AF is not usually associated with clinical signs, with the possible exception of pain. This is exemplified in dogs and cats over 7 years of age in which dorsal disk protrusion is relatively common but is subclinical. The velocity with which the disk material extrudes into the canal appears to be more important than the size of the mass. An explosive herniation results in far more severe damage than a slow extrusion. With acute impact injuries, hemorrhage and attendant inflammatory reaction may also contribute to epidural compression. Results of a quantitative radiographic study [86] suggest that the lumbar epidural space in Dachshunds is less than that in German Shepherds (a non-chondrodystrophoid breed) which implies that epidural masses of similar size would cause more spinal cord compression and more severe neurological deficits in Dachshunds. For a review of the pathophysiological events and biochemical cascade occurring with acute trauma to the spinal cord see spinal cord trauma.

Most dogs with disk disease are between 3 and 7 years of age. Eighty-five percent of disk extrusions in dogs occur in the thoracolumbar area and 15% are cervical. Approximately 80% of thoracolumbar extrusions occur between T11 and L3, with less than 2% occurring in the terminal lumbar region (L5 – S1). In one study of large-breed, non-chondrodystrophoid dogs with thoracolumbar disk disease, the mean age was approximately 7 years, and 57 dogs (92%) had Hansen type 1 disk disease, usually at the L1 - L2 site [87]. In this report, 58% of cases were acute in onset. Disk extrusion normally does not occur between T2 and T10, probably because of the presence of the conjugal ligament, although a Hansen type 1 disk extrusion has been reported at the T1 - T2 level in a 7 year old Dachshund with acute neurological deficits to the hind limbs following trauma [88]. Several studies indicate that the most common site in the cervical region is C2 - 3 [89,90]; although results of one study (105 cases) indicated no significant difference in prevalence of disk disease affecting the first four disk spaces (C2 – 3 to C5 - 6) [91] (in this study, prevalence of disk disease at C7 - T1 was significantly less than that involving the first 4 disk spaces)...

The onset of clinical signs in dogs may be acute (minutes), subacute (hours), or chronic (several days or weeks). These signs may be rapidly progressive, slowly progressive, or may remain static. Clinical signs also may undergo remission, only to recur at a later date. Clinical signs in dogs with recurrent attacks frequently are more severe than those seen at the initial episode. Recurrences have often been considered to be the result of multiple extrusions at the same disk level [97,98]. However, in a recent study, 22 of 25 dogs had a second operation (> 4 weeks after the initial surgery) at a site distinct from the initial lesion [99]. In this study, Dachshunds were at higher risk for recurrences than other breeds.

The two most common neurological syndromes associated with disk disease are thoracolumbar and cervical syndromes. With cervical disk disease, the majority of affected animals will have a history of pain, with or without paresis [90], and frequently, spasms of cervical musculature. Animals may assume a posture with the nose held close to the ground and the back arched. In some dogs, one thoracic limb may be held in partial flexion, with reluctance to support weight or walk on this limb. These animals frequently show considerable pain on manipulation of the head and neck. This combination of signs is termed root signature, since it is believed to be associated with nerve root entrapment near the intervertebral foramen as a result of lateral disk extrusion [100]. A lumbosacral syndrome is uncommonly associated with disk disease. In some animals with lumbosacral disk extrusion, one pelvic limb may be held in partial flexion or a repetitive “stamping” motion may be observed. These animals frequently show considerable pain on manipulation of the limb and lumbosacral spine. This combination of signs has also been termed root signature and is believed to be associated with nerve root compression or entrapment by a fragment of extruded disk material. In a small percentage of dogs, a multifocal syndrome may develop as a result of an acute, explosive extrusion of disk material from a thoracolumbar disk that produces hemorrhagic myelomalacia. With this irreversible disorder, an initial thoracolumbar syndrome may be followed by a lumbosacral syndrome as the lesion descends the cord. As the lesion also frequently ascends the cord, signs of thoracic limb rigidity give way to flaccidity and areflexia followed by death due to respiratory paralysis.

A definitive diagnosis of disk disease requires radiographic confirmation of presence of a mass lesion or, in absence of a mass lesion, evidence of characteristic changes in the disk-vertebral articulations. Typical radiographic features of disk disease include narrowing of the disk space, intervertebral foramen and articular facet at the site of the herniated disk, wedging of contiguous vertebral bodies so that the dorsal part of the disk space appears narrower than the ventral part, and presence of an opacified mass in the vertebral canal. In situ calcified disks, in the absence of any other abnormality, are a common finding in chondrodystrophoid breeds of dogs and are of little significance -it has been estimated that dystrophic calcification occurs in 20 to 77% of disks in some chondrodystrophoid breeds within the first year or two of life [71,101-103], especially in Dachshunds in whom calcification appears to be inherited [104,272]. Recent studies suggest that exercise has a modulating effect on rate of occurrence of disk calcification in Dachshunds (moderate exercise reduced the rate of occurrence of disk calcification) [105]. In some cases, particularly in acute extrusions, plain radiographic findings may be minimal or equivocal and myelographic studies will be necessary to define the extent and location of spinal cord compression. In one study, accuracy for determining sites of intervertebral disk protrusion using survey radiography was only in the 51 – 61% range [280]. The importance of accurate localization of lesions is demonstrated by the presence of asymmetrical neurological signs contralateral to the myelographic and surgical lesion in some dogs, especially those with Hansen type 1 extrusion [106]. Contrast studies also are indicated when there is evidence of more than one disk lesion. The most common myelographic change is narrowing and dorsal deviation of the ventral contrast column at the level of disk protrusion/extrusion. If the disk extrusion is acute, spinal cord swelling may result in complete blockage of contrast material at, or immediately rostral to the level of the disk extrusion. Note that dogs with thoracolumbar or cervical disk disease that have clinical signs of back or neck pain alone, without neurologic deficits, may have substantial compression of the spinal cord [90,107]. Results of experimental studies suggest that high-dose contrast enhancement (e.g., 0.3 mmol/kg of gadoteridol) might facilitate the detection of recurrent herniated disk fragments [108]. While plain radiography and myelography have long been the methods of choice for the diagnosis of disk disease, other non-invasive neuroimaging procedures such as magnetic resonance imaging (MRI) [109] and computed tomography (CT) [110-112] may be more accurate, technically easier, and safer (myelography may exacerbate clinical signs and induce seizures). In one report, preoperative CT confirmation of the relationship between the spinal cord and the protruded disk was used in planning the surgical approach in dogs with cervical disk disease [113]. MRI is considered to give better information about the condition of the intervertebral disk (e.g., the hydration status of the nucleus pulposus) than radiography [114]. In fact, classification of degenerating intervertebral disks and identification of MR imaging characteristics of each type have been reported in experimental studies in dogs [115]. Hemorrhage may also be identified using MRI [278]. Analysis of CSF, especially if sampled from the lumbar subarachnoid space, may reveal markedly elevated protein levels and increased numbers of mononuclear white blood cells [116]. These changes are more likely to be found in dogs with severe and acute neurological signs. Recent studies have shown a significant increase in lumbar CSF glutamate concentrations in both acute and chronic cord compression injuries secondary to disk herniation in dogs [117].

Gross pathological findings occurring subsequent to disk disease usually depend on whether disk protrusion-extrusion is partial or complete and whether it occurs acutely or gradually. While many disks in older animals of any breed may protrude, it is uncommon to find more than one extruded disk, even in animals that have had a history of multiple episodes. This suggests that many recurrences are due to multiple extrusions from single disks (see below). In disk protrusion, the AF may bulge dorsally into the vertebral canal, without rupturing. This is known as a Hansen type 2 disk [71], and it appears as a small, round to dome-shaped bulging of the dorsal surface of the disk. A Hansen type 1 disk [71] is characterized by rupture of the dorsal annulus, with extrusion of degenerate NP into the vertebral canal around the spinal cord. In some instances, the extruded nuclear material will be contained by the dorsal longitudinal ligament. Typically, disks extrude in a dorsomedian, paramedian, or dorsolateral plane. In the cervical region, where the vertebral canal/spinal cord ratio is larger than that of the thoracolumbar region, lateral and intraforaminal extrusions may be more common than in other spinal regions, producing spinal root rather than spinal cord compression. Rarely, disk material may herniate through the cartilaginous end-plate into the vertebral body (resulting in an intravertebral herniation or Schmorl’s node) [118], or into the spinal cord itself (intramedullary extrusion) [279].
The spinal cord may be swollen, indented, flattened, or atrophic. In chronic cases, a fibrous adhesion may be evident between the extruded mass and the dura mater. In many instances of Hansen type 1 disk extrusion, hemorrhage will be associated with the extruded disk material, producing a soft, granular, salt and pepper consistency. In some cases, the volume of epidural hemorrhage may exceed that of the extruded disk material. The extruded material may form a circumscribed mass or may lie flattened around the sides of the dura mater. The extruded material may have migrated one or two vertebral levels away from the site of the affected disk. This form of extrusion is usually present in dogs with thoracolumbar disk disease. Since extruded disks are not completely absorbed, single disks that may have had multiple extrusions are recognized by their stratified appearance. The oldest component may be dark gray, hard, and adherent to the dura. Subsequent laminations are lighter in color and more friable [97]. In chronic disk disease with slow, progressive extrusion, the degenerate material frequently has a gritty consistency and an opaque and cheesy appearance. This type of extrusion is more often observed in dogs with cervical disk disease.

Microscopic changes in the spinal cord are dependent on the rate of disk extrusion and duration of cord compression. Gradual or mild compression produces varying degrees of demyelination and axonal degeneration. Sudden, massive extrusions often result in focal or multifocal hemorrhage and necrosis in gray and white matter. Localized edema may result in pronounced cord swelling and collapse of the subarachnoid space. Rarely, disk material will be present within the cord parenchyma. In necrotic areas of the spinal cord, vessels and mesenchymal (connective tissue) elements are usually preserved. Lipid macrophages are observed in those cases of a few days duration. In more chronic cases, marked proliferation of astrocytes and microglial cells may be a feature, especially in areas that border the necrotic zone, together with trabeculae of blood vessels and connective tissue that cross the necrotic areas [84]. In longer standing lesions, the gray matter often has a fenestrated appearance due to loss of neurons and fibers. Astrocytic gliosis may result in marked sclerosis of the gray matter. An epidural inflammatory reaction composed of neutrophils, red blood cells, fibroblasts, large mononuclear cells, occasional multinucleate giant cells, chondrocytic-like cells, and fibrocartilaginous debris may be present.

Medical management usually is directed at animals with their first signs of disk disease. Mild clinical signs often resolve after at least three weeks of confinement with outside activity limited to leash exercise. Recurrences of clinical signs are common in this group of animals. Severe, unremitting pain may be managed with prednisolone, 0.5 mg/kg, PO, bid, for 72 hours. Muscle spasms may respond to muscle relaxants, e.g., methocarbamol (Robaxin), 20 mg/kg, PO, tid, for 7 to 10 days, or diazepam, 2 – 5 mg, PO, tid, for several days. High dose methylprednisolone succinate should be considered in paraplegic/tetraplegic animals with acute spinal cord injury (see spinal trauma). Acupuncture is considered another form of conservative treatment [119-122]. The analgesic response to acupuncture is reportedly most effective in dogs showing pain with or without mild paresis. Animals receiving this treatment should have restricted activity.

Surgical treatment is indicated in animal with clinical signs unresponsive to medical management, recurrent and/or progressive clinical signs, or in animals that are paralyzed. The approaches most widely used are dorsolateral hemilaminectomy / pediculectomy or dorsal laminectomy for thoracolumbar diskdisease and ventral slot-decompression for cervical disk extrusions, although a thoracolumbar lateral approach has its proponents [89,123-128]. In a recent study, significant improvement in clinical results was seen in caudal cervical disk protrusions when additional surgical distraction and stabilization were provided following ventral slot decompression [129]. Dorsal laminectomy has also been successfully performed in dogs (especially those < 15 kg) with cervical disk disease [130].While some studies of thoracolumbar disk disease indicate that removal of disk material using these techniques significantly improves the degree of completeness of recovery [131], successful results have been reported using fenestration alone [98,132-134]. Prophylactic fenestration [89] in addition to decompression remains somewhat controversial [135] but is still performed by many surgeons in order to reduce the chance of subsequent herniation involving other disks [136-138]. A variety of other surgical procedures have been described, including percutaneous diskectomy [139], but their effectiveness await large clinical trials. Although still not commonly employed for the treatment of disk disease, chemonucleolysis (e.g., using collagenase or chymopapain injected directly into the disk) has its exponents [140-143] and may be more effective than fenestration at removing nuclear material from the disk [144]. Experimental autographic disk transplantation for potential use in humans with chronic disk disease is in its infancy but initial surgical studies in dogs showed promise [145]. Potential treatment complications include cardiac dysfunction from manipulation of the vagosympathetic trunk during cervical surgery, and vertebral luxation as a complication of the ventral slot procedure, especially in mid to lower cervical vertebrae [146]. Furthermore, cervical vertebral fusion may predispose adjacent disks to herniation [147]. Corticosteroid therapy (usually associated with use of dexamethasone) may lead to gastrointestinal hemorrhage, ulceration, colonic perforation and pancreatitis [148-150].
Complications may be kept to a minimum by administering corticosteroids for as short a time as possible. Prophylactic use of intestinal protectants, e.g., bismuth subsalicylate (Pepto-Bismol®) in conjunction with frequent administration (at least four times daily) of antacids, e.g., magnesium or aluminum hydroxide, or H2 antagonists such as cimetidine (Tagamet®, at 20 mg/kg, PO, tid) also may reduce the prevalence of gastrointestinal hemorrhage.

Corticosteroids should be stopped immediately, when gastrointestinal complications are noted. In a recent study in dogs with acute degenerative disk disease treated by surgery and corticosteroid administration, both omeprazole (a gastric acid pump inhibitor) and misoprostol (a synthetic prostaglandin E1 analog) were ineffective in treating or preventing the further development of gastric mucosal lesions [150].

Paralyzed patients need to be maintained in a sanitary environment, with twice daily bladder catheterization, frequent removal of soiled bedding, and use of foam rubber pads or water beds to prevent development of decubital ulcers. In addition , active physiotherapy (see also spinal trauma and chapter on rehabilitation) that includes assisted standing and walking exercises, and supervised swimming for 15 minutes twice daily, is an integral part of the nursing care since it will delay disuse muscle atrophy.
The following statements may be used as a general guide to assess prognosis:

Animals that are paretic or paralyzed but have normal pain sensation have a good prognosis following medical and/or surgical management. Results of a recent surgical study (using hemilaminectomy and fenestration) with an 86% success rate indicated that the rate of onset of clinical signs significantly influenced the clinical outcome but not the length of recovery time, while the duration of clinical signs did not seem to significantly affect the outcome, but did affect the length of recovery time [281]. The presence of postoperative voluntary motor function is also reported to be a favorable prognostic indicator for early return to ambulation [282].

Animals that are paralyzed with loss of bladder control and with reduced pain sensation have a guarded-to-favorable prognosis following surgical intervention (decompression and/or fenestration).

Animals that are paralyzed with loss of bladder control and loss of pain sensation have a guarded-to-unfavorable prognosis.

Dogs with absent deep pain perception that undergo surgery within 12 to 36 hours have a better chance of recovery (more complete and over a shorter time-period) than those in which surgery is delayed [100]. Evaluation of the degree of myelographic spinal cord swelling might also assist in establishing a prognosis in severely affected animals [151]. As a caveat to prognostication, several studies have shown that severity of spinal cord dysfunction, based on clinical signs, does not necessarily predict outcome. In one recent report, 50% of dogs with loss of bladder control and loss of deep pain sensation recovered completely or partially [152].
A functional scoring system for pelvic limb gait of dogs with acute thoracolumbar spinal cord trauma (from spontaneously-occurring disk disease) has been developed to allow quantification of recovery to be assessed and potentially facilitate evaluation of pharmacotherapeutic clinical trials [153]. Spinal cord evoked potentials and somatosensory potentials may be useful in localizing spinal cord lesions and assessing lesion severity [154,155]. Other evoked potentials such as magnetically elicited transcranial motor evoked potentials may be sensitive indices of severity of spinal cord lesions in dogs with disk disease but do not appear to be reliable predictors of neurologic recovery [156]. In one report involving 10 cats with disk disease, prognosis was adjudged to be most favorable in cats following surgical decompression [96].

Source
Braund’s Clinical Neurology in Small Animals: Localization, Diagnosis and Treatment, Vite C.H. (Ed.)
International Veterinary Information Service, Ithaca NY (www.ivis.org), 2003; A3218.0103 http://www.ivis.org/advances/Vite/braund17/chapter_frm.asp?LA=1#Disk_disease last accessed 10/9/07