Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology), DECVN
Lumbosacral pain in dogs has multiple aetiologies. Pathological abnormalities of the lumbosacral region have been termed cauda equina syndrome, lumbosacral stenosis, degenerative lumbosacral stenosis, lumbosacral spondylopathy, spondylolisthesis, lumbosacral malformation-malarticulation, and lumbosacral disease. Lumbosacral disease is a collective term for a variety of pathological conditions that may include malformation, growth abnormalities, degeneration, compression, inflammation, infection, displacement and reduced vascular circulation. These conditions may involve the last lumbar vertebra, the sacrum, the lumbosacral disc, the soft tissue structures around the lumbosacral joint or the cauda equina and associated nerve roots. The most common cause of lumbosacral disease is degenerative lumbosacral stenosis. Lumbosacral instability, including dorsal dislocation of L7, has also been reported. Morphometric studies suggest that multilevel congenital or developmental stenosis of the lumbosacral canal may contribute to acquired lumbosacral stenosis in large-breed dogs. Other causes of acquired stenosis include discospondylitis, neoplasia, and traumatic fracture/luxation of L7-S1, sacrum, or the sacrococcygeal junction. Also, lumbosacral osteochondrosis, a developmental disturbance of the end plate of either the sacrum or L7 vertebra, with subsequent separation of an osteochondral flap, has been reported as a cause of lumbosacral stenosis in mature dogs
Diagnosis of this condition can be difficult especially when considering there may be a need to identify a surgically correctable lesion with a high degree of confidence.
Clinical Signs of Lumbosacral Disease
Lesions involving spinal cord segments L4-5 through S1-3 (+ coccygeal segments) or lumbosacral nerve roots that form the cauda equina (including femoral, obturator, sciatic, pudendal, pelvic, and coccygeal nerves) will result in a lumbosacral syndrome. The lumbosacral syndrome reflects various degrees of involvement of the pelvic limbs, bladder, anal sphincter, and tail. Clinical signs will range from flaccid weakness to paralysis of pelvic limbs and tail. Owners often note that affected dogs have difficulty rising or climbing stairs, and show signs of pain or stiffness during extensive physical activity. Clinical signs may include pain (the most commonly reported sign) during direct palpation (especially downward pressure) of the lumbosacral area or during lumbosacral hyperextension, unilateral or bilateral pelvic limb paresis or lameness, proprioceptive deficits, tail paresis, hypotonia of anal sphincter with faecal incontinence, and urinary incontinence. Patellar and withdrawal reflexes (as well as gastrocnemius and cranial tibial reflexes) may be depressed or absent in pelvic limbs, as may be perineal (anal) and bulbocavernosus (in male dogs) reflexes. Tone in pelvic limb muscles may be reduced or absent. After 1 to 2 weeks of clinical signs, segmental muscle atrophy due to denervation will be observed. "Segmental" refers to the particular spinal cord segment involved in the lesion (e.g., segmental atrophy may develop in the iliopsoas, quadriceps, and sartorius muscles following an injury to the L4-6 spinal cord segments). Pain perception in pelvic limbs, tail, and perineum may be reduced or absent. Pelvic limb postural reactions such as hopping and placing may be depressed. Thoracic limb function is unaffected. Normal micturition requires synchronized contraction of the urethral smooth muscle and relaxation of the urethral skeletal muscle. Urethral smooth muscle is supplied by pelvic (parasympathetic) and hypogastric (sympathetic) nerves; pelvic and hypogastric nerves form the pelvic plexus. The pudendal nerve innervates the urethral skeletal muscle. Lesions involving the pelvic nerves, sacral cord segments, or pathways to and from the brainstem will abolish the micturition reflex. Consequently, the bladder will distend with urine and eventually overflow. Lesions of the sacral segments will also result in loss of innervation to the skeletal muscle of the urethra. As a result of minimal urethral resistance, manual expression of the bladder is easy in such cases. Thus, animals with sacral cord lesions may suffer from continual overflow incontinence. The anal sphincter may be flaccid and dilated, resulting in faecal incontinence. Since the external anal sphincter is innervated by the pudendal nerve, which also originates in the sacral segments, the perineal (anal) reflex provides a good assessment of sacral spinal cord function.
In some animals with lumbosacral disc 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 is termed "root signature" and is believed to be associated with nerve root compression or entrapment by a fragment of extruded disk material. The occurrence of exercise-induced pain in some affected dogs, termed neurogenic intermittent claudication, may be related to dilatation of radicular vessels and subsequent compression of adjacent nerve roots in a stenotic region, e.g., intervertebral foramen or lateral recess of the caudal L7 vertebral foramen narrowed by a degenerative process.
On plain films, indirect evidence of degenerative lumbosacral stenosis includes spondylosis deformans, disk space narrowing, and end-plate sclerosis. None of these abnormalities are specific however, and they occur in clinically normal dogs. There may be evidence of lumbosacral fracture/luxation, osseous neoplasia, intradiscal osteomyelitis associated with discospondylitis, or congenital lumbosacral stenosis. However, the greatest limitation of survey radiography is the inability to assess compression of neural tissue. Survey radiographs need to be performed with the animal deeply sedated or under general anaesthesia, properly positioned and preferably with an empty colon.
In one study, over 30% of German Shepherds with clinical signs of cauda equina compression had radiographic abnormalities compatible with osteochondrosis of the sacral end plate. In another study, transitional vertebrae were found in nearly 40% of German Shepherds with degenerative lumbosacral stenosis and in 11% without.
In dogs with lumbosacral osteochondrosis, a radiolucent defect occurs in the dorsal aspect of the affected end-plate along with one or more bone fragments in the vertebral canal and lipping, angling, and sclerosis of the dorsal part of the end-plates. Stress radiography, such as dynamic flexion/extension studies, may accentuate the lumbosacral instability. One study evaluated the LS angle and degree of subluxation of the sacrum in relation to L7 as seen on survey radiographs in 52 normal dogs and 32 normal dogs with LS spondylosis (of which 24 had neurological deficits). The conclusion was that such measurements were not helpful in the diagnosis of this disease.
Epidurography and discography may provide useful information. In one study, combined survey radiography and discography-epidurography were correctly positive in 16 of 18 dogs (89%). Alone, epidurography has been reported to be diagnostic in 78%-93% of dogs confirmed surgically. It is easier to perform than myelography and has less morbidity. The disadvantage is that filling of the epidural space may be incomplete because this space is poorly defined, contains fat and has multiple lateral openings. Flexed and extended views of the LS joint during epidurography may accentuate a compressive lesion. Concomitant filling of the vertebral venous sinuses or the paravertebral venous system may occur in normal dogs but is more common in those with LS disease.
Myelography has limited value in the evaluation of the cauda equina because the dural sac is elevated from the vertebral canal floor and often ends before the lumbosacral junction; It has been reported that 85% of normal dogs and 80% of dogs with degenerative lumbosacral stenosis had a dural sac that ended at the level of the sacrum and that myelography with the LS joint in neutral, flexed and extended positions was successful in the diagnosis of LS disease. In another study, 77% of 30 dogs had a dural sac that ended within the sacrum. Myelography allows evaluation of the spinal cord cranial to the LS region and thus may help to rule out other diseases.
Myelography performed at the cerebellomedullary cistern produces less local artifact than does lumbar injection; lumbar myelography can be non-diagnostic when there is epidural leakage.
Computed tomography and MRI are probably the diagnostic procedures of choice although findings of similar CT changes (but not vertebral subluxation) in the lumbosacral spine of older dogs without clinical disease may complicate diagnosis. Dorsal and sagittal images can be reformatted from the transverse ones. CT is accurate and allows evaluation of structures that cannot be visualised completely with conventional radiography such as the lateral recesses, intervertebral foramen and articular processes. It provides bone detail superior to that seen with MRI and soft tissue contrast superior to that of conventional radiography. It allows visualisation of individual nerve roots because of the contrast provided by the epidural fat. Disadvantages of CT are the use of ionising radiation and the cost and limited availability of this procedure.
In a study evaluating canine lumbosacral stenosis using intravenous contrast- enhanced CT, the positive predictive values for compressive soft tissues involving the dorsal canal, ventral canal and lateral recesses were 83%, 100%, and 81% respectively. A gas-filled lumbosacral disk space (vacuum disk phenomenon) along with smaller gas bubbles in between the degenerated L5-L6 dorsal articular facets (vacuum facet phenomenon) has also been revealed by CT in a 7 year old Rottweiler with cauda equina syndrome. A diagnostic role for CT densitometry awaits further studies.
MRI can clearly reveal soft tissue, such as cauda equina, epidural fat, and intervertebral disk, at the lumbosacral region without use of contrast medium. MRI is also considered to give better information about the condition of the intervertebral disc (e.g., the hydration status of the nucleus pulposus) in dogs with degenerative lumbar spine diseases, than radiography OR CT. However, no correlation was found between severity of the clinical signs and the severity of cauda equina compression as assessed by MRI in one study. In humans, it has been proposed that MR imaging can lead to overdiagnosis of disc disease because many people without back pain have disc bulges or protrusions on MR imaging. As MR imaging is used more frequently now in veterinary medicine, inconsistency between disc abnormalities and clinical signs must be considered, and the diagnosis should always be based upon clinical acumen in addition to the imaging.
Electromyographic (EMG) studies can demonstrate fibrillation potentials in lumbosacral paraspinal muscles, pelvic limbs, coccygeal muscles, and anal sphincter; as such this procedure can help confirm neurological disease as well as mapping out denervation. One study found that EMG was accurate in predicting the presence or absence of cauda equina compression in all cases. Another study found that some dogs with LS disease (particularly those presented with only pain) had normal findings on EMG, however. Dogs with mild disease can have a largely neurapraxic lesion that does not produce denervation.
In those cases where results of ancillary aids are equivocal, exploratory surgery may be the only means available for definitive diagnosis and treatment. Grossly, marked compression and indentation of nerve roots may be seen, associated with stenotic lesions, bone fragments, disc material, inflammatory lesions, neoplasia, etc.
References are available upon request.