Surgery of the Cauda Equina

General Principles and Techniques

The cauda equina is the leash of nerve roots derived from the terminal spinal cord segments from L7 caudally (Cd1-Cd5) that travels through the vertebral canal in the lumbosacral area. The lumbosacral area, or lumbosacral junction, is the bone (e.g., L7 vertebra, sacrum) and connective tissue (e.g., L7-S1 articular facet joint capsules, interarcuate ligament, disk) enclosing the cauda equina. Dorsal laminectomy is removal of the lamina; this usually entails partial or complete removal of the dorsal spinous process of L7 and cranial parts of the sacral spine. Facetectomy is partial or full removal of the L7/S1 articular processes (facets), and foraminotomy is the removal of specific regions of these processes in order to enlarge the L7/S1 intervertebral foramen. Both facetectomy and foraminotomy are used in this region of the spine to relieve pressure on the L7 nerve root if necessary. Dysesthesia and paresthesia are similar terms that describe abnormal sensations caused by irritation of nerve roots and/or nerves. Descriptions of such abnormal sensations in people include pricking, burning, and tingling. It is believed that dogs with cauda equina lesions have similar sensations because affected patients often stare or bite at areas around the rump and pelvic limbs.

General Considerations

The most common clinical sign associated with lesions of the cauda equina is pain or hyperesthesia. Hyperesthesia (pain) may arise from compression and/or inflammation of meninges and nerve roots of the cauda equina, bony components of the lumbosacral area, L7/S1 disk, or L7/S1 articular process (facet) joint capsules. Hyperesthesia may be manifested in a number of ways. Some patients exhibit obvious discomfort when rising or sitting down. Others may be reluctant to jump or climb stairs. A unilateral or bilateral pelvic limb lameness, which may be exacerbated by increased activity, may also indicate hyperesthesia in the area of the lumbosacral joint and cauda equina. With some conditions, the patient may appear to be in constant pain (e.g., diskospondylitis, vertebral tumor), whereas in others, careful palpation of the lumbosacral area is required to elicit a painful response. Dogs and cats with cauda equina lesions often appear painful upon extension of the coxofemoral joints. This is likely because the extension is pulling on nerve roots that are already irritated by a disease process at the lumbosacral junction. Because clinical signs of cauda equina disease can mimic those of hip dysplasia, it is important not to confuse the two disorders, especially in dogs that are predisposed to both disorders and may have radiologic evidence of hip dysplasia (e.g., German Shepherds).

Proprioceptive deficits are also often evident in patients with cauda equina lesions. Interference with afferent proprioceptive fibers at the level of the cauda equina can produce various degrees of proprioceptive deficits to the pelvic limbs. This can be as mild as delayed proprioceptive positioning reactions or as severe as pelvic limb ataxia with dragging the dorsal aspect of the toes (“knuckling”). Dogs with cauda equina lesions are not typically ataxic in the manner that ataxia is usually described; these dogs do not display truncal ataxia when walking; rather, they misstep occasionally and stumble. Proprioceptive deficits may or may not be symmetric. Voluntary motor deficits to the muscles innervated by the sciatic nerve and caudal (coccygeal—tail innervation) nerves may be clinically detectable, as the cord segments and nerve roots of the cauda equina give rise to these nerves. Pelvic limb weakness may be apparent with damage to sciatic nerve contributions, and decreased to absent tail tone and movement may occur with damage to caudal segments and/or nerve roots.

In some cases, the patient may exhibit an abnormally low tail carriage, which the owner often notices. Abnormal reflex activity such as decreased to absent withdrawal and gastrocnemius reflexes may be seen. In the author’s experience, most dogs with progressive cauda equina compression (e.g., degenerative lumbosacral stenosis) have poor pelvic withdrawal reflexes only at the level of the hock. The patellar reflex is typically normal or may appear hyperreflexive. Caudal thigh muscles normally inhibit the action of the quadriceps muscle group when the patellar reflex is elicited. Removal of this tonic antagonistic influence by disrupting the nerve supply to the caudal thigh muscles may result in an apparently hyperactive patellar reflex (i.e., patellar pseudo-hyperreflexia). A decreased to absent perineal reflex may result from cauda equina lesions. Urinary and fecal abnormalities, with varying degrees of urinary and fecal incontinence, may occur with damage to sacral segments and/or roots. Bladder dysfunction is classically lower motor neuron (LMN) in nature. Nociceptive (pain perception) deficits in areas of the pelvic limbs, perineum, and tail may occur with severe lesions of the cauda equina; these are usually traumatic in nature.

Preoperative Management

Specifics of preoperative management depend largely on the disease process. In cases of degenerative lumbosacral stenosis, most patients will benefit from analgesic drugs prior to scheduling for surgery. There are multiple options for oral analgesic drug therapy for these patients, including nonsteroidal anti-inflammatory drugs (NSAIDs), tramadol, and either gabapentin or pregabalin (see p. 1440). Pregabalin appears to be effective in relieving pain associated with nerve root compression in dogs with degenerative lumbosacral stenosis. In the author’s opinion, there is no advantage of corticosteroids over NSAIDs in patients with cauda equina lesions, and there are potential disadvantages of corticosteroid use. Patients with radiographic evidence of diskospondylitis (see p. 1558) should be treated with appropriate antibiotic regimens (e.g., oral cefadroxil, 22 mg/kg every 8 hours or clindamycin, 11 mg/kg every 8 hours). The L7/S1 disk space is the most common site for diskospondylitis, and some dogs will have this infectious process as well as degenerative lumbosacral stenosis. It is prudent to control the infection before considering surgical decompression; in some cases, treatment of the infectious disease resolves clinical signs of disease and surgery is not needed. In traumatic fractures/luxations of the lumbosacral area, treatment is similar to that described for trauma to other regions of the spine (see pp. 1505 and 1525). These patients need to be stabilized from a cardiovascular standpoint and evaluated for injury to other organ systems. Additionally, these patients need to be kept as immobile as possible to avoid further damage to the nerve roots of the cauda equina.

Anesthesia

Anesthetic management of the patient with a cauda equina lesion is similar to that described for patients with other spinal surgical disorders (see pp. 1468 to 1508).

Antibiotics

Intravenous antibiotics (e.g., cefazolin, 22 mg/kg IV) should be administered perioperatively (30 minutes prior to the initiation of surgery and every 90 to 120 minutes thereafter during surgery) and either discontinued after surgery or within 24 hours. Some neurosurgeons (including the author) prefer to continue them orally (e.g., cefadroxil, 22 mg/kg PO every 8 hours) for 10 to 14 days postoperatively. In cases of suspected bacterial diskospondylitis, oral antibiotics are administered long term (months).

The lumbosacral junction has many features in common with other regions of the lumbar spine (see p. 1509), but there are several unique features (Fig. 42-1). The dorsal spinous process of L7 is considerably shorter than that of L6 and the intervertebral foramen of the lumbosacral junction is dorsoventrally flattened in comparison with cranial lumbar vertebrae. The lateral aspects of this foramen have been referred to as the lateral recesses and contain the L7 nerve root as it runs caudally toward the L7/S1 intervertebral foramen. The sacrum is composed of three fused vertebrae, and the fused dorsal spinous processes form a median sacral crest. The dorsal lamina of the sacrum is considerably thinner than the L7 dorsal lamina, and in small dogs and cats it may not have a visually distinguishable inner medullary cancellous bone layer. The prominent ilial wings of the pelvis project dorsally over the dorsal aspect of the sacrum and cranially to the level of the L6/L7 disk space.

FIG 42-1 Anatomy of the lumbosacral junction. A, Lateral view. B, Dorsal view.

Clinically relevant soft tissue structures in the lumbosacral junction include the termination of the spinal cord and the cauda equina nerve roots as well as supportive joint and ligamentous tissues and blood vessels. In medium to large-breed dogs, the spinal cord ends (conus medullaris) at the L6 or L7 vertebral level (Fig. 42-2). In small dogs and cats, the spinal cord terminates more caudally, around the S1 vertebral level. The filium terminale is a meningeal extension beyond the conus medullaris that attaches to the caudal (coccygeal vertebrae). As in the rest of the vertebral canal, paired venous sinuses (internal vertebral venous plexuses) are located on the floor of the canal. Radicular vessels (artery and vein) travel through the L7/S1 intervertebral foramina along with the L7 nerve root. Small blood vessels also exit the dorsal sacral foramina-these are usually cauterized at surgery or occluded with bone wax. Supportive connective tissues at the lumbosacral junction include the intervertebral disk and dorsal longitudinal ligaments ventrally, the articular process (facet) joint capsules laterally, and the ligamentum flavum (interarcuate ligament) and interspinous ligaments dorsally.

FIG 42-2 Anatomic relationship of vertebral bodies to spinal cord termination and cauda equina in a medium to large-breed dog.

Surgical Technique

Dorsal laminectomy is used to access the cauda equina, with or without removal of articular process tissue (foraminotomy or facetectomy). Crucial to the performance of a dorsal laminectomy in this region of the spine is proper positioning. The patient should be positioned in a manner that opens the L7/S1 space. The pelvic limbs are flexed, and positioned along the patient’s abdomen (Fig. 42-3).

FIG 42-3 Positioning patients with the pelvic limbs tucked under the abdomen helps accentuate the L7-S1 interarcuate space.

Dorsal Laminectomy

Position the patient in sternal recumbency with the pelvic limbs pulled cranially as shown in Fig. 42-3. Maintain this position with sandbags, towels, a deflated air cushion, or a V-trough. Using the iliac crests and L6 dorsal spinous process as landmarks, create a midline incision from the dorsal spinous process of L5 to the end of the sacral crest (base of the tail). Sharply incise through subcutaneous tissue and fat to reach the thick lumbodorsal fascia. Incise this fascial layer on midline and around the dorsal spinous processes of interest with a No. 11 blade, Mayo scissors, or a combination of the two. Elevate the multifidus lumborum (cranially) and sacrocaudalis dorsalis medialis (caudally) muscles from the dorsal spinous processes and median sacral crest using either Freer periosteal elevators (small dogs and cats) or Army-Navy osteotomes (large dogs). Continue this periosteal elevation to expose the dorsal lamina of L7 and the sacrum. Exposure of the L7/S1 junction is facilitated by also exposing L6/L7. Fully expose the articular processes of L7/S1 laterally to the level of the medial aspect of the ilium on each side. Place Gelpi retractors cranially and caudally. Sharply excise the interarcuate ligament between L7 and S1. Identify the interarcuate space of L7/S1 and carefully excise ligamentum flavum tissue with a No. 11 blade and a nontoothed Bishop Harmon forceps so that the bone edges of caudal L7 and cranial S1 are visualized. Remove the dorsal spinous process of L7 and the cranial half of the median sacral crest with a bone cutter and/or rongeur. Use a high-speed air drill to create the dorsal laminectomy defect, drilling through outer cortical and inner cancellous bone to reach the inner cortical layer. The lateral aspects of the L7 dorsal lamina are thickest, and the dorsal lamina of the sacrum is considerably thinner than that of L7.

Once the inner cortical bone is soft enough, remove it with fine-tipped Lempert rongeurs and/or flake it off with the spatula end of a Gross ear hook and spoon. Remove any remaining periosteum and/or interarcuate ligament (ligamentum flavum) and overlying epidural fat to expose the cauda equina (Fig. 42-4). In some chronic cases of degenerative lumbosacral stenosis, the ligamentum flavum and/or endosteum may be adhered to the nerve roots; in this case, carefully dissect the connective tissue off the nerve roots with a No. 11 blade. Using a probe (e.g., Gross ear hook and spoon), feel under the edges of the laminectomy defect, especially laterally and in the region of each intervertebral foramen. If compression of the L7 nerve root is still apparent after dorsal laminectomy and removal of compressive annulus tissue, perform a facetectomy or foraminotomy.

FIG 42-4 L7-S1, S2 dorsal laminectomy provides exposure of the filum terminale and cauda equina.

Facetectomy and Foraminotomy

Perform a facetectomy by sharply incising and removing the articular process joint capsule tissue of L7/S1, then drilling off the facets from dorsal to ventral using a high-speed air drill. Remove the most ventral aspect of the facets with a fine-tipped Lempert rongeur to avoid ensnaring the L7 nerve root with the burr. To perform a foraminotomy, visually bisect the dorsoventral length of the L7/S1 articular facets. Using a small (1- to 2-mm) burr, drill a longitudinal trough through the facet tissue at this bisection and then snip off the ventral layer of bone (dorsal limit of the intervertebral foramen) with a fine-tipped Lempert rongeur. An angled burr guard is recommended for this procedure. Attempting a foraminotomy by drilling within the intervertebral foramen is not recommended for fear of damaging the L7 nerve root. Close the site routinely. To help prevent seroma formation, use an interrupted subcuticular pattern for closure.

Healing of the Cauda Equina

The nerve roots of the cauda equina are more resistant to injury compared with spinal cord parenchyma and respond to injury similar to the response of peripheral nerves. Nerve injury is typically classified according to severity. From least severe to most severe, nerve injury is classified as class I (neurapraxia), class II (axonotmesis), and class III (neurotmesis) (Table 42-1). Class I injury or neuropraxia refers to a transient lack of nerve function, with little or no structural damage to the axons or their supportive connective tissue structures. This temporary dysfunction may be due to ischemia (no structural damage) and/or mild paranodal demyelination. The degree of motor and proprioceptive dysfunction is variable, but nociceptive function is preserved for the most part (large-diameter axons are preferentially affected). Spontaneous recovery is expected within days to a month, depending on the degree of demyelination. Neurogenic muscle atrophy is unlikely, as the axons are structurally intact. With class II injury (axonotmesis), some or all of the axons of the nerve are disrupted structurally, but the connective tissue support (e.g., Schwann cell basal lamina, endoneurium) remains intact. These axons can regrow along the connective tissue scaffold. Substantial motor, proprioceptive, and nociceptive dysfunction is expected, the extent of which depends on the number of axons damaged. Neurogenic muscle atrophy is likely with this class of injury. Class III injury or neurotmesis denotes complete severance of the axons of the nerve, as well as the connective tissue support. These axons will not regrow (no guiding scaffold) without surgical intervention. Complete motor, proprioceptive, and nociceptive (i.e., no pain perception) dysfunction occurs with this class of injury. Neurogenic muscle atrophy is to be expected. A severe class II injury may be clinically indistinguishable from a class III injury. In addition to the extent of nerve injury, the length of nerve required to regenerate affects prognosis. Axons grow at a rate of 1 to 4 mm per day. In people with nerve injuries, muscle motor end-plate degeneration tends to occur if the damaged nerve does not reestablish contact with the target muscle within 18 months. Therefore, proximal nerve injuries have more guarded prognoses than distal injuries, even if axonal regeneration occurs.

Table 42-1

Causes and Characteristics of Nerve Injuries

Nerve Injury Classification	Causes	Characteristics
Class I (Neurapraxia)	Ischemia (no structural damage) and/or mild paranodal demyelination	Transient lack of nerve function Little to no structural damage to axons Variable motor and proprioceptive dysfunction Nociceptive function is generally preserved Spontaneous recovery within days to a month
Class II (Axonotmesis)	Mainly seen in crush injury	Structural disruption of axons Connective tissue support remains intact Axons may regrow along connective tissue scaffold Substantial motor, proprioceptive, and nociceptive dysfunction Neurogenic muscle atrophy
Class III (Neurotmesis)	Occurs with severe contusion, stretch, or laceration	Complete severance of axons of the nerve and connective tissue Axons will not regrow without surgical intervention Complete motor, proprioceptive, and nociceptive dysfunction Neurogenic muscle atrophy