Cauda equina compression caused by lumbosacral stenosis is a well known clinical entity. Large breed dogs are more often affected than small breed dogs or cats, and acquired conditions are by far more common than congenital diseases. In middle aged non-chondrodystrophic large breed dogs, degenerative lumbosacral stenosis is the single most important cause of cauda equina syndrome. The clinical signs are caused by neural compression of the cauda equina and nerve roots in the vertebral canal or the neural foramina. Animals of both sexes at any age may be affected by cauda equina compression and it has been reported in one year old dogs with congenital vertebral canal stenosis and in dogs with large osteochondrotic fragments. The typical dog with cauda equina compression is a male large breed working dog (probably a German Shepherd Dog), six years of age and suffers from degenerative lumbosacral stenosis (DLSS).
Recommended imaging protocol
The problems in imaging the cauda equina arise from the specific anatomy of the region with superimposition of the pelvis and the iliosacral joints, the often short dural end sac, and the pathology often affecting neural structures outside the vertebral canal.
Lateral and ventrodorsal survey radiographs in neutral position
MRI with the dog in dorsal recumbency and the legs slightly extended. The minimal protocol for suspected DLSS includes a sagital T2-w, a transverse T1-w and T2-w sequence and a dorsal high resolution sequence (e.g., gradient echo with T1 characteristics or a fluid sensitive true FISP, CBASS or BASG) for reconstruction.
A fat suppressed sequence (e.g., STIR) is indicated if an inflammatory or neoplastic process has to be ruled out. After a trauma or in cases with a suspected neoplastic or inflammatory lesion post contrast T1-w sequences in the transverse and dorsal planes are also performed.
If MRI is not available, or not suitable (metallic implants near the junction), CT becomes the method of choice. High resolution axial scans, suitable for reconstruction of the L5-sacrum region is done. Some authors recommend dynamic flexion-extension CT-studies. The benefit of such a procedure may be the better appreciation of the dynamic nature of a compression either by reactive tissue, vd motion of the sacrum or exaggerating the compressing effect of a herniated disc and hypertrophied ligaments. Intravenous CM is indicated when a neoplastic or inflammatory lesion is suspected. A myelo-CT can be helpful as well.
If neither MRI nor CT is available, the lateral and vd survey radiographs in neutral position are followed by dynamic cisternal myelography. After injection of the contrast medium into the cisterna magna (0.3ml/kgBW) the table is tilted and the lumbosacral spine will be kept in flexion until the dural sac is filled with CM. The lateral projection with the spine in flexion is then followed by extensional and vd views.
In cases with equivocal result, due to a short or thin dural sac, a combined disco- epidurogram can be performed. The combined procedure will give information on the integrity of the lumbosacral disc and space occupying lesions in the vertebral canal. Epidurography is an easy technique, but it may be difficult to be interpreted because of artifacts (e.g., the epidural fat).
A number of clinical entities may affect the cauda equina: trauma, congenital and developmental conditions, degenerative disorders, tumour, inflammation/infection, or vascular diseases.
A variety of congenital anomalies involving the lumbosacral region have been described. Lumbosacral transitional vertebrae (TV) are described in many breeds: German Shepherd Dog, Labrador Retriever, Rhodesian Ridgeback, Malinois, Brittany Spaniels, Doberman Pinschers and many more. In some breeds it may be inherited. Incompletely fused or a sacrum consisting of only two vertebrae are signs of lumbarisation of S1. Partial or complete fusion of L7 with the sacrum are signs of sacralisation of L7. TV may also occur as fusion of the first caudal vertebra with the sacrum and other combinations. Complete TV are symmetric with either both transverse processes of L7 in contact with the ileum (sacralisation), or the wings of S1 are seen as transverse processes. Asymmetrical TV is seen as a unilateral fusion or detachment and may lead to rotation of the pelvis with the side of fusion rotated dorsally. Dorsal rotation of the pelvis in the long axis of the body favours ipsilateral hip dysplasia. TV do not cause stenosis of the vertebral canal and neural compression, but predispose to DLSS. They are associated with disc degeneration and spondylotic changes. In the German Shepherd dog there also may be an association of TV and congenital stenosis of the vertebral canal.
Spina bifida, blockvertebrae, hemivertebrae, dysgenesis or agenesis of sacral and/or caudal vertebrae usually are not associated with neurologic deficits. Spina bifida may be associated with spinal dysraphism and is most often seen in brachycephalic dogs with screwed tail and Manx cats. In these animals agenesis of part or all caudal vertebrae, the sacrum, hemivertebrae, and blockvertebrae are very common. If vertebral anomalies are associated with spinal dysraphism neural deficits are usually present. The radiologic diagnosis of meningocele, myelomeningocele, or dermoid sinus requires myelography, CT or MRI.
Osteochondrosis and intravertebral disc herniation are two developmental disease processes described in the lumbosacral area, both may have the same pathogenesis and are associated with disc pathology.
Osteochondrosis most often is observed at the dorsal aspect of the endplate of the sacrum. The aetiology is unclear, but a hereditary background seems possible in the German Shepherd Dog. Obviously, important regional differences exist for the prevalence of this condition. Reports from the United States of America are sparse, whereas the condition has been described on the European Continent as well as in Great Britain in various large breeds with a highest risk for the German Shepherd Dog. Males are more often affected than females. Radiologic diagnosis requires precise lateral (superimposed iliac wings) and dorsal positioning (frog leg position) or linear tomography. The radiographic signs of sacral osteochondrosis are as follows:
Deformation of the sacral endplate with the dorsal part angled caudally
Deformation of the intervertebral disc space which becomes butterfly like
Lipping of the dorsal border of the sacrum leading to a narrowed vd diameter of the vertebral canal
Sclerosis of the dorsal part of the endplates which can be severe
Isolated fragment in the vertebral canal, or a radiolucent line at the base of the elongated sacral endplate
On projection the cranial border of the sacrum becomes irregular, sometimes one or more isolated fragments can be seen
Discography usually shows leaking of the contrast medium through the gap between the fragment and the endplate. CT and MRI are the most sensitive imaging modalities for the condition. The free fragment and the secondary degenerative lesions of the discovertebral apparatus are easily identified.
Intravertebral disc herniation (Schmorl's node) at the lumbosacral level is rare. It can be located anywhere in the endplate of either L7 or the sacrum. It is a sign of disturbance (developmental or degenerative) in the vertebral endplate and may be associated with pain. The features are sharply defined lucent defects with sclerotic margins in a vertebral endplate (?). The aetiology and pathogenesis is unclear.
Osteochondrosis of an endplate always leads to disruption of the intervertebral disc, disc degeneration, and carries a very high risk for development of DLSS. Dogs suffering from osteochondrosis usually manifest clinical signs of cauda equina compression at a relatively young age (4.8 years).
Degenerative disorders are the most commonly seen pathologic conditions of the lumbosacral segments. They may affect the discovertebral apparatus and/or the facet joints. Either condition can lead to hypertrophic changes of the dorsal longitudinal and flaval ligaments, to apposition of bone within the vertebral canal and/or the neuroforamina, and finally to compression or encroachment of the cauda equina. Therefore, the term degenerative lumbosacral stenosis (DLSS) is used for both conditions. Transitional vertebrae, sacral osteochondrosis, the anatomic conformation of the lumbosacral junction such as the orientation of the joint facets, the dimension of the disc and high mechanical load(?) play an important role in the pathogenesis of DLSS.
Intervertebral disc degeneration with disc herniation is the most important cause of DLSS. Dogs with TV or osteochondrosis are predisposed. Any medium to large breed dog can be affected, but there is a breed predisposition for the German Shepherd Dog which makes up for >50% of dogs affected with DLSS. In this breed, the lumbosacral disc at a young age already shows more often and more severe disc degeneration compared to other breed dogs. Depending on the underlying cause and breed, dogs at almost any age may be affected. The mean age of the clinical onset or diagnosis varies between 4.7 years in dogs with osteochondrosis and 8 years.
The diagnosis of degenerative disease affecting the lumbosacral discovertebral and facet joints often can be made radiographically. However, the diagnosis of cauda equina and nerve root compression requires myelography, epidurography, CT or MRI with MRI currently being the most sensitive diagnostic imaging modality. However, it has to be stressed that the correlation of the abnormalities found with CT or MRI and the clinical signs are poor: care has to be taken not to over interpret these findings.
Lumbosacral disc degeneration: disc mineralization, vacuum phenomenon, narrowed disc space, sclerotic endplates
Disc herniation (protrusions more common than extrusions): narrowed intervertebral disc space, thickened and sclerotic endplates
Ventral displacement of sacrum ("instability")
Hypertrophy of the ventral and dorsal longitudinal and flaval ligaments
Hypertrophic degenerative disease of the facet joints
Stenosis (decreased vd-diameter) of vertebral canal or neural foramina
Disc herniations may be centrally into the direction of the vertebral canal usually causing bilateral signs, paresis of the tail, and with pronounced compression also signs of pudendal nerve compression. Dorsolateral herniation into the lateral aspects of the vertebral canal or neural foramen will lead to unilateral signs. Remember, degenerative changes with vertebral canal stenosis and signs of cauda equina compression are not restricted to the lumbosacral junction. Lesions anywhere between L5 and the sacrum will present with similar neurological signs.
Hypertrophic degenerative changes of the facet joints are common and may cause stenosis of the neuroforamina. Radiological diagnosis of degenerative joint disease of the facet joints are made using the standard projections, sometimes oblique views may be helpful. CT and MRI are the imaging modalities of choice. The facet joints present with hypertrophic changes with sometimes severe osteophytosis which may impinge upon the nerve roots and cause radiculitis or root compression.
Juxtaarticular (facetal) synovial or ganglion cysts may be considered as a specific sign of degenerative joint disease of the facet joints. Synovial cysts are lined by an epithelium and filled with synovial fluid, whereas ganglion cysts are not. They are located at the ventral margins of the facet joints and grow into the lateral aspects of the vertebral canal at the level where the nerve roots leave the vertebral canal. Large cysts may contribute to or cause nerve root compression. MRI is the diagnostic modality of choice, since fluid sensitive sequences clearly can distinguish between soft tissue and cystic structures. On T1-w images they have a low signal intensity, in T2-w and fat suppression sequences (distinguishes between fat and fluid) they are round to ovoid structures with high signal intensity. Rim enhancement may be observed in T1-w sequences after administration of paramagnetic contrast medium.
Spondylosis deformans is a very common finding at the lumbosacral junction in middle aged to older dogs. Spondylotic changes may be located anywhere at the level of the neural foramina, at the lateral or ventral aspect of the vertebral endplate where it meets the cortex of the vertebral body. However, spondylosis usually is not associated with clinical signs. Occasionally, if located near the neural foramina they may impinge on the nerve roots and cause signs of radiculitis. As in other locations, spondylosis may be a sign of intervertebral disc degeneration or chronic inflammation, but is very often idiopathic.
Lumbosacral instability can be seen in many dogs, clinically affected and normal. It is characterized as a step in the dorsal border of the bodies of L7 and the sacrum, with the sacrum usually displaced ventrally. Ventral displacement of the sacrum can be exaggerated or induced by flexion--extension. This condition has been named lumbosacral instability and is discussed as a specific entity and possible cause of DLSS. Biomechanically, gliding of two vertebral bodies against each other is termed translation and is normal to a certain degree: normal flexion-extension is composed of both rotation and translation. Whether instability as a primary disease really exists is an open question. In the authors opinion translation to a noticeable degree does not occur in dogs with a normal lumbosacral disc. Lumbosacral "instability" very likely occurs secondary to a loss of intradiscal pressure allowing disc gliding and thus may be a sign of intervertebral disc degeneration.
The correlation between "instability" and cauda equina compression is poor. Non-contrast flexion-extension radiographs are of little diagnostic importance. In dogs with this condition and DLSS, extension will exaggerate compression which can be shown using dynamic contrast media procedures or dynamic CT.
Fractures or surgical excision of the articular processes will always result in true lumbosacral instability. In these cases the sacrum will move in a dorsal direction resulting in an abnormal alignment of L7 and the sacrum. In chronic cases the disc will be destructed and the sacrum will be almost fixed in this abnormal location with reduced flexion-extension.
The lumbosacral junction is a common location for discospondylitis. Primary bone or soft tissue tumours are rare in this region. Nerve root tumours and tumours of the lumbosacral plexus do occur and have similar features as tumours of the brachial plexus. The proximity of the lumbosacral junction to the sublumbar lymphatic centres, responsible for the drainage of the perineal area, prostate, uterus and bladder, but also the hind limbs, make this area to a preferred location for metastasis. Sublumbar lymphadenopathy and irregular, palisade like periosteal reactions along the ventral borders of the caudal lumbar vertebrae, the pelvis and transverse processes, are suggestive of metastatic neoplasia.
Differential diagnosis of cauda equina compression include bilateral orthopaedic disease (bilateral cruciate or patellar ligament rupture), osteoarthritis of the hip or stifle joints. Thromboembolism of the caudal aorta and iliac arteries are rare. The presenting signs usually can be distinguished easily from neurologic disease. Masses in the pelvic canal (e.g., paraprostatic cysts, tumours or abscesses, tumours arising from the sacrum, or metastases from perineal tumours), may also cause neural disease due to compression of the sciatic nerve.
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