Cauda Equina Syndrome

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Chapter 105 Cauda Equina Syndrome

Cauda equina syndrome (CES) is a complex of symptoms and signs, including low back pain, unilateral or bilateral radiculopathy, lower extremity motor weakness, sensory disturbance including saddle anesthesia, and loss of visceral function (i.e., bladder and bowel incompetence ranging from frequency to bladder and anal sphincter paralysis, and erectile dysfunction), that results from either acute or chronic cauda equina compression (Box 105-1). This syndrome is characterized by a variable clinical presentation that depends on the anatomic location (lumbar, sacral, or coccygeal/focal central or complete compression), rapidity, and duration of compression of the cauda equina. Motor weakness involving the lumbar, sacral, and coccygeal roots in isolation or in combination is often present. Hypesthesia or anesthesia is often present in the dermatomal distribution of L3 to Coc1, inclusive. Radicular signs and symptoms may be either unilateral or bilateral. Bowel or bladder dysfunction is common and is the source of the hallmark signs and symptoms of CES. The knee and ankle jerk may be absent. There are typically no upper motor neuron findings, and the Babinski sign is absent. CES, particularly if unrecognized and untreated, often results in paraplegia, severe paraparesis, permanent bladder and bowel incontinence, or sexual dysfunction.

Pathophysiology

Spinal nerve root compression commonly occurs in conditions such as acute herniated disc, spinal stenosis, trauma (e.g., burst fractures), metastatic or primary tumors of the spine, or spinal infections (e.g., epidural abscess) (Box 105-2). Acute CES most commonly presents secondary to lumbosacral intervertebral disc prolapse (Fig. 105-1). However, the pathophysiology of the symptoms and signs related to spinal nerve root compression remains poorly defined.

Several experimental studies have assessed the pathophysiologic mechanism of CES. Delamarter et al.1,2 developed an animal model of CES, subjecting 30 beagle dogs to L6-7 laminectomy and cauda equina compression. Neurologic recovery was assessed in animals undergoing 75% constriction of the cauda equina followed by immediate, early, or delayed decompression. The first group was constricted and immediately decompressed. The remaining groups were constricted for 1 hour, 6 hours, 24 hours, and 1 week, respectively, before being decompressed. Evoked potentials were measured before and after surgery, before and after decompression, and 6 weeks after decompression. Six weeks after decompression, all dogs were killed, and the neural elements were analyzed histologically. After compression, all 30 dogs had significant lower extremity weakness, tail paralysis, and urinary incontinence. All dogs recovered significant motor function by 6 weeks after decompression. The dogs with immediate decompression typically recovered neurologic function within 2 to 5 days. The dogs receiving 1- and 6-hour compression recovered within 5 to 7 days. Dogs receiving 24 hours of compression remained paraparetic for 5 to 7 days, with bladder dysfunction persisting for 7 to 10 days and tail dysfunction for up to 4 weeks. The dogs with compression for 1 week were paraparetic and incontinent during the duration of cauda equina compression. They recovered the ability to walk by 1 week and regained bladder and tail control by the time of euthanasia. Immediately after compression, all five groups demonstrated at least 50% deterioration of the posterior tibial evoked potential amplitudes.2 Delamarter et al.2 demonstrated axoplasmic flow blockade and wallerian degeneration of the motor nerve roots distal to the constriction and of the sensory roots proximal to the site of constriction, as well as dorsal column degeneration. Severe arterial narrowing occurred at the level of the constriction with venous congestion of the roots and dorsal root ganglia of the seventh lumbar and first sacral nerves.1 Evoked potentials were the most sensitive predictor of neural compression, revealing neurologic abnormalities before the appearance of neurologic signs and symptoms.1 Cystometrograms were not sensitive until severe compression was achieved. Bladder dysfunction was correlated with axoplasmic flow blockade and early sensory changes during neurovenous congestion.

Olmarker et al.37 developed an experimental model of acute, graded compression of the cauda equina in pigs that accurately mimics the neural and vascular anatomy of the human cauda equina. There were structural and vascular differences between spinal nerve roots and peripheral nerves that could contribute to differences in compression susceptibility between these two parts of the nervous system. Pressure transmission from the balloon to the nerve roots permitted determination of occlusion pressures for the arterioles, capillaries, and venules of the cauda equina.7 Arteriolar blood flow ceased when the applied pressure approached the mean arterial blood pressure. Capillary blood flow was dependent on flow in connected venules, and the blood flow in some venules ceased at 5 to 10 mm Hg despite venous occlusion pressures ranging from 5 to 60 mm Hg. Compression up to 200 mm Hg for 2 hours did not induce a no-reflow phenomenon upon compression release. However, transient hyperemia was noted at all pressure-time relations studied, indicating nutritional deficit in the compressed segment during compression. Signs of edema were observed in nerve roots exposed to compression for 2 hours at either 50 or 200 mm Hg. The nutritional supply to the cauda equina was impaired at low pressure levels (<10 mm Hg).4,5 Thus diffusion from adjacent tissues with a better nutritional supply, including the cerebrospinal fluid, could not compensate completely for compression-induced effects on the transport of nutrients. However, a certain nutritional supply to the compressed segment was present even at 200 mm Hg compression. A rapid compression rate resulted in more pronounced effects on the nutritional supply than did a slow compression rate. Nutritional impairment was observed both within and outside the compressed nerve segment. An increase in vascular permeability was induced by compression at 50 mm Hg for 2 minutes.6 The magnitude of this permeability increase was dependent on both the magnitude and the duration of compression. The permeability increase was more pronounced for the rapid compression onset rate than for the slow compression onset rate at all pressure-time relations studied. Reduction of muscle action-potential amplitude in tail muscles, after stimulation cranial to the compression zone, was induced by compression at 100 and 200 mm Hg for 2 hours.4,6

Pedowitz et al.8 and Rydevik et al.9,10 presented an experimental model of compression-induced functional changes of the porcine cauda equina that permits electrophysiologic investigation of the neurophysiologic changes induced by nerve root deformation. In several studies, they compared the effects of various pressures and durations of acute compression on spinal nerve root conduction in the pig cauda equina. Changes in both afferent (compound nerve action potentials) and efferent (compound motor action potentials) conduction were induced at an acute pressure threshold of 50 to 75 mm Hg. Higher compression pressures produced a differential recovery in afferent and efferent conduction.9,10 Efferent conduction and afferent conduction were monitored during compression for 2 or 4 hours with compression pressures of 0 (sham treatment), 50, 100, or 200 mm Hg. Recovery was monitored for 1.5 hours. No significant deficits in spinal nerve root conduction were observed with 0 or 50 mm Hg compression, whereas significant deficits were induced by 100 and 200 mm Hg compression. Variance analysis demonstrated significant effects of compression pressure and duration on conduction, with a significant difference between efferent and afferent conduction at the end of the recovery period, suggesting a synergistic interaction between biomechanical and microvascular mechanisms in the production of nerve root conduction deficits.8

Compression of the spinal nerve roots often occurs at multiple levels simultaneously; however, the basic pathophysiology of multilevel compression is poorly defined. Using a thermal diffusion technique, Takahashi et al.11 quantitated intraneural blood flow in the uncompressed segment between two compressive balloons in the porcine cauda equina. At 10 mm Hg compression, there was a 64% reduction of total blood flow in the uncompressed segment compared with precompression values. Total ischemia occurred at pressures 10 to 20 mm Hg less than the mean arterial blood pressure. After two-level compression at 200 mm Hg for 10 minutes, there was a gradual recovery of the intraneural blood flow toward the baseline. Recovery was less rapid and less complete after 2 hours of compression. Double-level compression of the cauda equina induced blood flow impairment, not only at the sites of compression but also in the intermediate nerve segments located between two compression sites, even at very low pressures.

Cauda Equina Syndrome Secondary to Disc Herniation

Epidemiology

CES secondary to a large central disc herniation is a relatively uncommon entity, but its clinical importance far exceeds its rarity (see Fig. 105-1). CES secondary to lumbar disc herniation is an absolute indication for surgical intervention.12

The incidence of CES has been estimated to range from 1.2% to 6%. In 1970, Raaf13 reported an incidence of 2% in 624 patients with protruded discs. In 1972, Spangfort14 reported a 1.2% incidence in 2504 cases, and his review of the literature found a total incidence of approximately 2.4%. In 1986, Kostuik et al.15 reported a 2.2% incidence of CES in patients admitted for lumbar laminectomy. In 1990, Gleave and MacFarlane16 reported cauda equina paralysis secondary to lumbar disc prolapse in 3.2% of cases; this probably overestimated the true incidence because they did not consider nonoperatively treated patients.

Clinical Syndrome

CES can mimic the typical presentation of a lumbar intervertebral disc herniation with low back pain and unilateral radiculopathy. However, back and perianal pain often predominates, and radicular symptoms may be minimal. Severe back pain, often out of proportion with the radicular pain, should alert the physician to a possible CES lesion and mandates periodic evaluation to exclude a progressive neurologic deficit. Accurate diagnosis may be delayed if the lesion is incomplete or evolving. CES often presents with abnormal radicular signs and normal or upper motor neuron lesion activity, but it can present as a lower motor neuron lesion.

Clinical presentation varies depending on the level and location of the disc herniation. For example, a large central disc herniation can compress several or all of the traversing cauda equina roots. A disc at L2-3 with complete compression may present with motor-sensory disturbance from L3 (+L2) to S5. An L5-S1 disc may cause CES without motor or sensory loss in the lower extremities. This scenario happens when the herniation is focally central and compresses the lower centrally located sacral nerve roots, serving bowel and bladder function, but leaves the S1 roots unaffected. If slowly progressive, large central disc herniations can also mimic the presentation of an intraspinal tumor.

When compromised, the centrally placed sacral fibers to the lower abdominal/pelvic viscera produce the symptoms characterizing cauda equina compression. Initial leg pain may be followed by foot numbness and difficulty with ambulation. Sensory deficits are common and often involve the lower sacral roots. Perianal numbness, saddle dysesthesia or anesthesia, and a loss of the anal reflex or diminished rectal tone characterize the syndrome. Difficulty with urination, including either frequency or retention with overflow incontinence, can develop relatively early in the clinical course. The onset of bladder and rectal paralysis with saddle anesthesia should be viewed with a high index of suspicion in any patient with backache and sciatica. In men, a recent history of impotence can often be elicited. This should be clarified as to whether the impotence is pain mediated or neurologically (unable to obtain an erection) mediated.

Some reports contend that bilateral sciatica is a necessary component of CES, but a number of large series refute this notion. In a review of 31 patients by Kostuik et al.15 in 1986, sciatica was bilateral in 14 patients and unilateral in 17. Severe saddle anesthesia was indicative of a poor prognosis, particularly for return of bladder and bowel function.15 However, any correlation of factors such as severity of somatic signs and symptoms, symptom duration before surgical decompression, and the size and location of disc protrusion with recovery of bowel and bladder function was unclear. In a review of 58 patients by Doman et al. in 2009, urinary retention of more than 500 mL alone or in combination with two or more of the following symptoms—bilateral sciatica, urinary retention, or rectal incontinence—were the most important predictors of MRI-confirmed cauda compressions.17

Clinical Course

Tay and Chacha18 reported eight cases observed over a 5-year period that fell into three clinical groups. The first group of patients noted sudden onset of symptoms without previous back problems. The second group noted recurrent episodes of backache and sciatica, with the most recent episode resulting in cauda equina involvement. The final group of patients had slowly evolving backache and sciatica that progressed to cauda equina paralysis. Disc prolapse occurred between the L5 and S1 vertebrae in 50% of the patients, most of whom had no limitation in straight-leg raising. Urgent myelography and disc removal within 2 weeks of symptom onset resulted in substantial recovery of motor and bladder function within 5 months after surgery. Sensory and sexual function recovery was incomplete for as long as 4 years postoperatively.18 Patients at the preclinical and early stages have better functional recovery than patients in later stages after surgical decompression.19

Choudhury and Taylor20 reported on 42 patients with lumbar disc disease and herniation who presented with CES. Simple disc herniation accounted for the syndrome in only five cases. Associated structural lesions were noted in the remaining 37 cases, and operative manipulation and trauma during disc removal through an interlaminar approach was reported in two patients.20

Lafuente et al.21 noted sacral sparing and preservation of sphincter control in 8 of 14 cases of cauda equina compression from central lumbar disc herniation and postulated that the triangular shape of the lumbar spinal canal may be one factor for this constellation of findings, because the increase in linear strain on the stretched roots of the cauda equina is least in the more centrally placed lower sacral roots. Kostuik et al.15 identified two distinct modes of presentation. The first was an acute mode (in 10 patients) in which there was an abrupt onset of severe symptoms and signs and a slightly poorer prognosis after decompression, especially for the return of bladder function. The second mode of presentation (in 21 patients) had a more protracted onset, characterized by prior symptoms for varying time intervals before the gradual onset of CES. All patients reported preoperative urinary retention. Bladder function was the most seriously affected function preoperatively and remained so postoperatively. The prognosis for return of motor function was good. Of 30 patients receiving surgery, 27 regained normal motor function.15

Surgical Therapy

Urgent surgical intervention should commence after diagnosis. Choudhury and Taylor20 advocated wide laminectomy with excision of the overhanging facet joints and adequate visualization of the lumbar nerve roots. This yielded good or excellent results in 95% of patients and fair results in the remainder. No postoperative spinal instability or significant morbidity was reported.20

A routine microdiscectomy interlaminar approach necessitates retraction on already severely compromised nerve roots. Furthermore, because of the extent of compression, these roots often have no available canal space; thus, retraction not only increases traction but also may cause direct compression (against the disc or the overlying lamina). For the same reason, the use of large punches with a thick foot plate is also not recommended (compresses underlying roots against the herniated disc) (Fig. 105-3). Consequently, the authors advocate a wide bilateral decompression (laminectomy and medial third facetectomy). To avoid iatrogenic compression of the cauda equina, the surgeon can perform the laminectomy using a high-speed bur to thin out the lamina and then curettes and small punches lateral to the area of maximal compression to release the medial portion of the lamina (see Fig. 105-3). Once the lamina is released, it can be safely lifted away from the cauda equina. The decompression should be adequate enough to allow access lateral to the thecal sac and traversing roots at the level of the affected disc space and/or the sequestered fragment. The surgeon should carefully perform retrieval of the herniated fragment to avoid creating a further mass effect and therefore increased traction on the less mobile central sacral roots. This can be accomplished by performing a lateral anulotomy and discectomy and then pushing the central fragment back into the disc space with a reverse-angle curette. If the fragment is sequestered, it should be manipulated in a lateral direction using a nerve hook or angled curette and then retrieved. Before closure, the surgeon should confirm adequate decompression.

Timing of Surgical Intervention

Controversy persists regarding the definition, cause, diagnosis, and timing of surgical intervention for CES resulting from lumbar disc herniation. Conventional wisdom has been that early detection of CES is essential to maximize the probability of neurologic recovery after decompressive laminectomy and discectomy.22 Some investigators have gone so far as to advocate the necessity for decompression within 6 hours of presentation.23 However, data supporting immediate intervention are far from clear.

Kostuik et al.15 reported 31 patients with CES secondary to a central disc lesion. The average time to surgical decompression after initial presentation ranged from 1.1 days for the group with more acute lesions to 3.3 days for the second group. There was no correlation between these times and return of function. The authors recommended early surgery but noted that decompression did not have to be immediate.15

Shapiro24 studied 14 patients with acute CES from herniated lumbar discs who all presented with bilateral sciatica and leg weakness; 93% had bladder or bowel dysfunction. All patients were emergently studied with CT, myelography, or MRI. Nine patients had large or massive herniations, and five had smaller herniations superimposed on preexisting stenoses. The time to surgery ranged from less than 24 hours to more than 30 days. Postoperatively, six patients (43%) were normal, four patients (28.5%) had chronic pain and numbness, and four patients (28.5%) had persistent incontinence and weakness. Of the 10 patients without postoperative incontinence, 7 underwent surgery within 48 hours of onset. Of the four patients with persistent incontinence, all underwent surgery 48 hours or more after presentation.24

The onset of bladder paralysis is an important indicator for urgent surgery. Dinning and Schaeffer25

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