Stef H. Y. Lim1 and Michaela Beasley2 1Bush Veterinary Neurology Service, Leesburg, VA, USA 1Mississippi State University Mississippi State, MS, USA Degenerative lumbosacral stenosis (DLSS), also commonly known as cauda equina syndrome or disease or lumbosacral compression, is commonly seen in canine patients causing pain and neurological dysfunction secondary to the compression of the seventh lumbar (L7) nerve roots, local vasculature, and cauda equina [1–5]. It is prevalent among large male dogs, with German Shepherd, military, and working dogs seemingly predisposed [6, 7]. Manifestation of clinical signs include lumbosacral pain, paresis, lameness, reluctance to jump, and in severe cases neurological deficits including urinary and fecal incontinence and dysesthesias (abnormalities of skin sensation) [1–5, 8, 9]. The anatomy of the connectors and stabilizers of the LS joint consist of the intervertebral disk (IVD), facetal synovial joints, dorsal and ventral longitudinal ligaments, interarcuate ligaments, interspinous ligaments, and perispinal fascia and muscles [1–5,9–11]. Change to the forces of the LS joint can be exacerbated by additional anatomical malformations, such as sacralization of the seventh lumbar vertebrae, malarticulation of the diarthrodial joints at L7–S1 junction, lumborization of the first sacral vertebrae, or other breeds such as Airdale Terriers, Belgian Shepherds (Malinois), German Shepherds, Greyhounds, and Labrador Retrievers that have inherited abnormal motion pattern at L7–S1 [12–14]. The cause of DLSS is multifactorial. The high mobility of the LS joint, especially in a dorsolateral extension, places a high amount of stress on the LS disk space which is responsible for connecting a flexible lumbar spine to the rigid sacrum and pelvis [1–5]. Though the specific progression of events is unknown, DLSS is a combination of LS IVD protrusion, subluxation of the facet joints, thickening of the joint capsule of the articular facets, and hypertrophy of the ligament flavum. However, additional changes – including lumbosacral transitional vertebrae and osteochondrosis of the sacral endplate – may also predispose animals to DLSS [8]. It is speculated that chronic repetitive microtrauma and aging causes the nucleus pulpous to desiccate, thereby leading to changes to the biomechanical ability for the disk to absorb impact. Thus, greater forces are then being absorbed by the annulus fibrosus, which weakens as a sequela, and the dorsal aspect of the annulus develops small tears. This allows the disk to protrude: a Hanson Type II disk. This in turn causes compression along the cauda equina but also subsequent instability, which can result in subluxation between L7 and S1. The body counters the instability by way of the dorsal longitudinal ligament, the interarcuate ligaments, and facetal synovial capsule hypertrophy, and spondylosis deformans forms on the ventral aspect of L7–S1. The combination causes cauda equina compression secondary to the IVD protrusion and dorsal longitudinal ligament ventrally with dorsal compression from interarcuate ligaments with subsequent foraminal stenosis from the facetal joint hypertrophy and spondylosis causing the clinical signs of DLSS [1–5, 9, 11, 13]. In humans, terminology of “entrance,” “middle,” and “exit” zones has been applied to the location of the L5–S1 neurovascular foramen according to their location with relation to the pedicle and articular processes of L5–S1. The entrance zone is located closest to the vertebral canal and is the medial portion of the L5 vertebral pedicle. The middle zone is the center of the pedicle and the exit zone is the intervertebral foramen [15, 16]. Canines differ anatomically with more oblique angles and the lateral recess is longer and narrowing in shape compared to humans [16–18]. With this in mind, unless there is an extremely lateralized protruding disk, the L7 nerve roots will be spared with DLSS with concurrent intervertebral disk herniation (IVDH). As vertebral spacing is lost, the sacral articular process will telescope into the intervertebral neurovascular foramina, which will create dynamic impingement of L7 at the exit zone. Thus, it is important when performing imaging diagnostics to be mindful of which zone(s) L7 nerve root entrapment occurs in to consider appropriate surgical approach and treatment (Figure 14.1) [17]. Diagnosis of DLSS can be difficult, but should always begin like any other examination: thorough history; physical, neurologic, and orthopedic examinations. One of the most common complaints for patients with DLSS is pain and weakness. Once neurological abnormalities are noted, clinical signs include mild paresis, decreased to loss of tail function, proprioceptive ataxia, and incontinence (urinary, fecal, or both) [1–5, 8, 9]. These deficits are secondary to the sciatic nerve involvement (caudal thigh and muscles distal to the stifle) and pelvic and pudendal nerves causing lower motor neuron urinary incontinence and fecal incontinence secondary to poor anal sphincter tone [1–5, 9]. Physical examination should include a thorough neurological and orthopedic examination on top of the baseline physical examination. Common findings on physical exams include atrophy of gluteal or stifle flexor muscles, pain when pressure is applied over the lumbosacral space – which can be elicited with a lordosis test, and “tail jack” (Figure 14.2) [1, 9]. Direct palpation of the sciatic nerve at its exit zone can be accomplished with what we have described as the “sciatic nerve entrapment test”; however, concurrent iliopsoas pain can also be triggered with this movement (Figure 14.3). Orthopedic examination is crucial as hip dysplasia and cranial cruciate ligament ruptures can complicate DLSS or appear similar without a thorough exam. Pain elicited on extension of the hip is not specific enough to distinguish between DLSS from primary orthopedic disease [5]. Figure 14.1 Illustration of the foraminal zones for the L7 nerve roots (entry, middle, exit). When performing imaging diagnostics, evaluation of the zones of L7 nerve root entrapment may aid in the surgical planning. Figure 14.2 Both the lordosis test and tail jack have been described as methods to elicit pain associated with the lumbosacral joint. In this photo, the lordosis test is being performed. Thumb pressure is placed over the lumbosacral joint as the joint is being extended. A painful response is considered positive. Figure 14.3 We routinely use what we describe as a “sciatic entrapment test” to evaluate patients for lumbosacral pain and discomfort. To perform the test, both hands are used with the thumbs placing pressure over the lumbosacral joint. Then the hands are rotated outward causing the thumbs to roll across the paraspinal muscles. Patients with lumbosacral pain and discomfort will almost immediately flex the stifles and go into a sitting position. Photo (a) shows the position of the hands and (b) shows a patient with a positive response. This can also be seen in some dogs with iliopsoas pain. Common neurological abnormalities include ataxia, depressed cranial tibial, gastric, and withdrawal reflexes. Pseudo‐hyperreflexia of the patellar reflex can also be appreciated from the secondary lack of contralateral muscle tone of the flexor muscles of the stifles [5, 19]. Neurologic diseases that can mimic DLSS include degenerative myelopathy (DM); however, pain is typically not concurrent with degenerative myelopathy and early DM cases usually present with a thoracolumbar localization. It is advised that prior to performing any surgery or invasive procedures, genetic testing be performed for degenerative myelopathy to ensure that it will not compound your attempts to improving DLSS [19]. As DLSS is multifactorial with involvement of soft tissues including IVD and multiple ligaments, plain radiography and contrast studies are not ideal. Radiographs can provide quick investigation of the lumbosacral joint and rule out boney neoplasias, trauma, diskospondylitis, and possible vertebral abnormalities [20–24]. Radiographs are not accurate as they can produce false‐positive (presence of degenerative changes without clinical signs) and false‐negative (inability to show soft tissue changes) results [19, 25]. Positional radiography has revealed that L7–S1 is the most mobile of all the vertebral segments in dogs with DLSS [15]. As DLSS includes instability as part of the contributing factors to the disease process, it was once thought that extension and flexion of the pelvic limbs were important; however, because radiographs are two‐dimensional imaging, instability is difficult to assess [25]. Dogs with LS disease have an increased LS angle when positioned in neutral position, increased angle in flexion, and decreased angle in extension comparatively to dogs who do not have DLSS [26, 27]. In another paper by Suwankong et al. [28], step lesions between L7 and S1 have been reported in 69% of dogs with DLSS, and can be appreciated in normal dogs free of clinical signs associated with DLSS [25, 28, 29]. For correct positioning for a lateral radiograph of the lumbosacral joint of the dog, a small foam pad is placed under the lumbar spine and a foam block between the hindlimbs to prevent oblique views of the LS joint (Figure 14.4). Both extended lateral and flexed radiographs should be performed. However, note that lumbosacral articular facets positioned dorsolateral to the vertebral canal at the lumbosacral intervertebral space summate dorsally over the vertebral canal, and should not be mistaken for a compressive boney lesion [25, 30]. It is important to note that the presence of radiographic changes suggestive of DLSS does not always correlate with clinical signs [25, 26, 31]. It is also true that the absence of abnormalities on radiographs does not preclude the diagnosis of DLSS. Radiographs may be more useful for diagnosing other orthopedic diseases, such as canine hip dysplasia and changes secondary to cranial cruciate ligament ruptures. If MRI and CT are unavailable, myelograms can be utilized; however, these have fallen out of favor in comparison to the previously mentioned advanced imaging modalities. The contrast agent should be given via cisternal puncture only to prevent inadvertent epidural injection of contrast. Myelograms should be performed in neutral, flexion, and extension. Flexion is recommended to precede extension to allow for the flow of contrast to disperse [32]. Dogs that have DLSS show dorsally displaced and compressed contrast columns [25]. Limitations are similar to radiographs, which include the inability to reveal compression of the L7 nerve root within the foramen, that stenosis may be present despite a lack of abnormalities seen on myelogram, and that artifacts can be caused secondary to the dural sac extending over the LS joint appreciated in most large breed dogs [25]. CT allows for cross‐sectional evaluation of the vertebral canal and for the ability to 3D reconstruct and evaluate the LS joint. Transverse views can help identify thickened or entrapped nerve roots [5]. Dynamic CT (extension and flexion) should be performed as disk protrusion and telescoping of S1 can be overlooked without extension views [15]. There is a negative linear relationship between the angle of the LS junction and intervertebral foraminal area whereby the intervertebral foramen and lumbosacral interarcuate space appear wider on flexion than extension (Figure 14.5) [15, 25]. Figure 14.4 Positioning for lateral radiographs of the lumbosacral joint of the dog. These two views show the foam block is placed between the pelvic limbs, and a small foam pad is placed under the lumbar spine to prevent obliquity. Figure 14.5 (a) Bone window showing image of L7–S1 in flexion vs (b) bone window showing image of L7–S1 in extension. The interarcuate space appears wider in flexion than extension. Source: Jones JC et al. [2008] / American Veterinary Medical Association. CT images also allow for the evaluation of the entrance, middle, and exit zones of the intervertebral foramina, and the width of the intervertebral foraminal area [15, 16]. With this knowledge, the appropriate surgical approach can be considered for the particular area of stenosis causing impingement of the L7 nerve root [15]. Other changes indicating DLSS on CT include the increased opacity of soft tissue within the intervertebral foramina, narrowing of vertebral canal and loss of epidural fat, IVD protrusion, diskospondylitis/diskospondylosis, thickened or osteophytosis or articular processes, and subluxations [25, 33]. Soft tissue is most accurately assessed by MRI [27]. Similar to CT, MRI allows for the collection of images that can be assessed on multiple planes. However, the one significant advantage is the ease of visualizing the L7 nerve root as it can be followed throughout its journey through from the entrance zone to the exit zone and its course visualized as it travels from the foraminal exit ventral to the SI joint [16]. As DLSS has a dynamic component on the size of the lumbosacral foramina, utilizing MRI’s imaging sensitivity for soft tissue and adjusting the body’s position during the scan is key for successful diagnosis. It is recommended that the LS joint be imaged in extension, as this allowed for improved diagnosis of subclinical compressive lesions and IVD protrusion. Patients placed in neutral and hyperextended positions during MRI exhibit exaggerated differences with the neuroforaminal dimension. The exit zones are larger than the entrance zones in neutral position and smaller than the entrance zone in hyperextension. It is suspected that hyperextension position is more dynamic for the compression of the exit zone secondary to ligaments and IVD protrusions [16]. Traditional diagnosis of DLSS on MRI involves looking at the spine from parasagittal, transverse, and dorsal planes. MRI images in oblique planar images show smaller neuroforamina than in standard parasagittal planar images [16]. In those images, the middle zone was noted to be the narrowest zone. This has been supported by past studies utilizing CT scans that measured the middle and exit zones as being the narrowest on cross‐sectional images compared to that of the entrance zone [33]. Thus, oblique planes may provide increased sensitivity for the diagnosis of lumbosacral stenosis and nerve root compression [16]. It has also been suggested that a 1–2 mm slice protocol should be avoided due to partial‐volume artifacts and false‐positive findings [25, 33]. Force plate analysis (FPA) can detect changes in the propulsive forces of the pelvic limbs in dogs that are affected with DLSS. It is a noninvasive measurement of canine locomotion. In dogs with DLSS, the propulsive forces are significantly lower than that of healthy dogs. However, this can be a difficult diagnostic modality to interperate in dogs with DLSS, as it is typically utilized for patients with a mono‐limb lameness vs a bilateral pelvic limb ataxia [36–38]. Electromyography (EMG) can be used to support the diagnosis of DLSS, but it is not specific for the source of the abnormality or lesion. Thus, somatosensory evoked potentials (SEPs) are more sensitive toward the detection of L7 nerve compression associated with DLSS – as is an increase in F‐wave onset latency and the F‐ratio. However, these tests are extremely time consuming and demanding, and are not utilized often as they do not assist in evaluating potential surgical planning [39–40]. Medical treatment can be useful for some patients with a mild manifestation of DLSS; however, 32% may still require surgery. A more aggressive conservative therapy involves epidurals utilizing methylprednisolone acetate, which is a slow‐release depot corticosteroid with an elimination half‐life of 139 hours [41]. This allows for local delivery of steroids while minimizing the systemic side‐effects of corticosteroids. Signs of systemic absorption of corticosteroids include polyphagia, polydipsia, and polyurea; however, these clinical signs tend to be transient in nature [41, 42]. Epidural injection would be an appropriate treatment option for patients who do not show proprioceptive deficits and have appropriate urinary and fecal continence. The recommended dose of methylprednisolone acetate (40 mg/ml concentration) is 1 mg/kg, with a minimum volume of 0.5 ml and a maximum volume of 1 ml over three injections suggested at day 1, 14, and 41 [41] or as needed [39, 40]. Once the medication has been given, the author prefers to flex and extend the LS region with the most affected side ventral to aid in the flow of the corticosteroid into the middle and exit zones of the affected L7 nerve roots; the patient can then be flipped if necessary for bilateral lesions. Studies have shown that with a 0.2 ml/kg injection of iodinated radiographic contrast medium, LS epidurals can travel as far as the TL junction, so an epidural injecton can also be used to treat higher disk protrusions in dogs with multifocal lesions [43]. Guidance of the spinal needle can be performed with fluoroscopy, CT, or ultrasound if needed [40–46].
14
Lumbosacral Decompression and Foraminotomy Techniques
Pathophysiology and Anatomy
L7–S1 Foramina Anatomy
Diagnosis
History and Clinical Signs
Physical Examination Findings
Orthopedic Examination Findings
Neurologic Examination Findings
Radiography
Myelography (Contrast Study)
Computed Tomography (CT)
Magnetic Resonance Imaging (MRI)
Force Plate Analysis
Electrodiagnostics
Treatment: Conservative and Medical Therapy
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