eMedicine Specialties > Orthopedic Surgery > Spine

Cauda Equina Syndrome

Author: Jason C Eck, DO, MS, Assistant Professor, Department of Orthopedics and Physical Rehabilitation, UMass Memorial Medical Center
Coauthor(s): Scott D Hodges, DO, Consulting Surgeon, Department of Orthopedic Surgery, Center for Sports Medicine and Orthopedics; S Craig Humphreys, MD, Orthopedic Spine Surgeon, Department of Orthopedic Surgery, Center for Sports Medicine and Orthopedics
Contributor Information and Disclosures

Updated: Mar 3, 2009

Introduction

During development, the spinal cord and vertebral column grow at disproportionate rates, with the vertebral column growing more rapidly than the spinal cord. Spinal nerves exit the vertebral column at progressively more oblique angles because of the increasing distance between the spinal cord segments and the corresponding vertebrae. Lumbar and sacral nerves travel nearly vertically down the spinal canal to reach their exiting foramen.

The spinal cord tapers to an end near the first lumbar vertebra, forming the conus medullaris. The fibrous extension of the cord is the filum terminale. The bundle of nerve roots in the subarachnoid space distal to the conus medullaris is the cauda equina (see Image 1).

Pathophysiology

Cauda equina syndrome is caused by any narrowing of the spinal canal that compresses the nerve roots below the level of the spinal cord. Numerous causes of cauda equina syndrome have been reported, including traumatic injury, disk herniation, spinal stenosis, spinal neoplasm, schwannomas, ependymomas, inflammatory conditions, infectious conditions, and iatrogenic causes.

Trauma

• Traumatic events leading to fracture or subluxation can lead to compression of the cauda equina.¹
• Penetrating trauma can cause damage or compression of the cauda equina.
• Spinal manipulation resulting in subluxation has caused cauda equina syndrome.²
• Rare cases of sacral insufficiency fractures have been reported to cause cauda equina syndrome.³

Herniated disk

• The reported incidence of cauda equina syndrome resulting from herniated lumbar disk varies from 1-15%.⁴
• Ninety percent of lumbar disk herniations occur either at L4-L5 or L5-S1 (see Image 3).^5,6

• Seventy percent of cases of herniated disks leading to cauda equina syndrome occur in patients with a history of chronic low back pain (LBP), and 30% develop cauda equina syndrome as the first symptom of lumbar disk herniation.⁷
• Males in the fourth and fifth decades of life are most prone to cauda equina syndrome secondary to disk herniation.⁸
• Most cases of cauda equina syndrome secondary to disk herniation involve large particles of extruded disk material, compromising at least one third of the canal diameter.
• Patients with congenital stenosis that sustain a disk herniation are more likely to develop cauda equina syndrome because even a small disk herniation can drastically limit the space available for the nerve roots.
• Rare cases of transdural disk herniations have been reported to cause cauda equina syndrome.

Spinal stenosis

• Narrowing of the spinal canal can be due to a developmental abnormality or degenerative process.
• Severe cases of spondylolisthesis and Paget disease can lead to cauda equina syndrome.

Neoplasms

• Cauda equina syndrome can be caused by primary or metastatic spinal neoplasms, usually originating from the prostate in males.⁹
• Ninety-six percent of patients with cauda equina syndrome secondary to spinal neoplasm develop early severe pain.
• Later findings include lower extremity weakness due to involvement of the ventral roots.
• Patients generally develop hypotonia and hyporeflexia.
• Sensory loss and sphincter dysfunction are also common.

Schwannomas

• Schwannomas are benign encapsulated neoplasms that are structurally identical to a syncytium of Schwann cells.¹⁰
• These growths may arise from peripheral or sympathetic nerves.
• Schwannomas are visible using myelography, but MRI is the criterion standard. Schwannomas are isointense on T1 images, hyperintense on T2 images, and enhanced with gadolinium contrast.

Ependymomas

• Ependymomas are gliomas derived from relatively undifferentiated ependymal cells.
• They often originate from the central canal of the spinal cord and tend to be arranged radially around blood vessels.
• Ependymomas are found most commonly in patients aged approximately 35 years.
• They can lead to increased intracranial pressure (ICP), and cerebrospinal fluid (CSF) has an increased protein level.
• MRI findings can be used to help the physician in the diagnosis of cauda equina syndrome. Lesions appear isointense on T1-weighted images, hypointense on T2-weighted images, and enhanced with gadolinium contrast.

Inflammatory conditions

• Long-lasting inflammatory conditions of the spine, including Paget disease and ankylosing spondylitis, can lead to cauda equina syndrome secondary to spinal stenosis or fracture.

Infectious conditions

• Infectious conditions, including epidural abscess, can lead to deformity of the nerve roots and spinal cord.¹¹
• MRI can display the abnormal appearance of the nerve roots being forced to one side of the dural sac.
• Symptoms generally include severe back pain and a rapidly progressing motor weakness.

Iatrogenic causes

• Complications of spinal instrumentation have been reported to cause cases of cauda equina syndrome, including misplaced pedicle screws¹² and laminar hooks.^13,14
• Continuous spinal anesthesia also has been linked to cases of cauda equina syndrome.¹⁵
• Rare cases of cauda equina syndrome caused by epidural steroid injections, fibrin glue injection,¹⁶ and placement of a free fat graft have been reported.¹⁷
• Several cases involved the use of hyperbaric 5% lidocaine. Recommendations are that hyperbaric lidocaine not be administered in concentrations greater than 2%, with a total dose not to exceed 60 mg.^18,19

Symptoms

Symptoms of cauda equina syndrome include the following:

• Low back pain
• Unilateral or bilateral sciatica
• Saddle and perineal hypoesthesia or anesthesia
• Bowel and bladder disturbances
• Lower extremity motor weakness and sensory deficits
• Reduced or absent lower extremity reflexes

Low back pain can be divided into local and radicular pain.

• Local pain is generally a deep aching pain resulting from soft-tissue and vertebral body irritation.
• Radicular pain is generally a sharp, stabbing pain resulting from compression of the dorsal nerve roots. Radicular pain projects in dermatomal distributions.

Urinary manifestations of cauda equina syndrome include the following:

• Retention
• Difficulty initiating micturition
• Decreased urethral sensation
• Typically, urinary manifestations begin with urinary retention and are later followed by an overflow urinary incontinence.

Bowel disturbances may include the following:

• Incontinence
• Constipation
• Loss of anal tone and sensation

Pain and deficits associated with nerve root involvement are shown in the table below.

Open table in new window

Radiographic and Laboratory Findings

The diagnosis of cauda equina syndrome generally is possible on the basis of medical history and physical examination findings. Radiologic and laboratory studies are used to confirm the diagnosis and for localizing the site of the pathology and the underlying cause.

Due to its ability to depict the soft tissues, MRI generally has been the favored test for assisting the physician in the diagnosis of cauda equina syndrome.^20,21,22  Urgent MRI is recommended for all patients who have new-onset urinary symptoms with associated back pain or sciatica.

Myelography,²³ CT, and MRI are each used in specific cases with good degrees of accuracy. Each test can be used to determine the level of pathology and aid in the determination of the cause of the syndrome.

Depending on the findings from the history and physical examination, laboratory studies can include basic blood tests, chemistries, fasting blood sugar, sedimentation rate, and syphilis and lyme serologies. CSF examination should also be included if signs of meningitis are present.²⁴

Urodynamic studies are useful to evaluate the degree and cause of sphincter dysfunction, as well as to monitor recovery of bladder function following decompression surgery. Intraoperative monitoring of somatosensory and motor evoked potentials allows for evaluation of radiculopathy and neuropathy.

Medical Management

Nerve root ischemia is partially responsible for the pain and decreased motor strength associated with cauda equina syndrome. As a result, vasodilatory treatment can be useful in some patients. Mean arterial blood pressure should be maintained above 90 mm Hg to maximize blood flow to the spinal cord and nerve roots.

Treatment with lipoprostaglandin E1 and its derivatives has been reported to be effective in increasing blood flow to the cauda equina region and reducing symptoms of pain and motor weakness. This treatment option should be reserved for patients with modest spinal stenosis with neurogenic claudication. No benefit has been reported in patients with more severe symptoms or patients with radicular symptoms.

Other medical treatment options are useful in certain patients, depending on the underlying cause of the cauda equina syndrome. Anti-inflammatory agents and steroids can be effective in patients with inflammatory processes, including ankylosing spondylitis.

Patients with cauda equina syndrome secondary to infectious causes should receive appropriate antibiotic therapy. Patients with spinal neoplasms should be evaluated for the suitability of chemotherapy and radiation therapy.

Caution should be used in all forms of medical management for cauda equina syndrome. Any patient with true cauda equina syndrome with symptoms of saddle anesthesia and/or bilateral lower extremity weakness or loss of bowel or bladder control should undergo no more than 24 hours of initial medical management. If no relief of symptoms is achieved during this period, immediate surgical decompression is necessary to minimize the chances of permanent neurologic injury.

Surgical Treatment

In many cases of cauda equina syndrome, emergency decompression of the spinal canal is the appropriate treatment option. The goal is to relieve the pressure on the nerves of the cauda equina by removing the compressing agent and increasing the space in the spinal canal. Traditionally, cauda equina syndrome has been considered a surgical emergency, with surgical decompression considered necessary within 48 hours after the onset of symptoms.^12,25,26,27

For patients in whom a herniated disk is the cause of cauda equina syndrome, a laminotomy or laminectomy to allow for decompression of the canal is recommended, followed by gentle retraction and discectomy.

Many clinical and experimental reports have presented data on the functional outcome based on the timing of surgical decompression.²⁸ Several investigators have reported no significant differences in the degree of functional recovery as a function of the timing of surgical decompression.^25,26,29 Even with these findings, however, most investigators recommend surgical decompression as soon as possible after the onset of symptoms to offer the greatest chance of complete neurologic recovery.

Investigators have attempted to identify specific criteria that can aid in predicting the prognosis of patients with cauda equina syndrome.

• Patients with bilateral sciatica have been reported to have a less favorable prognosis than patients with unilateral pain.
• Patients with complete perineal anesthesia are more likely to have permanent paralysis of the bladder.³⁰
• The extent of perineal or saddle sensory deficit has been reported to be the most important predictor of recovery.³¹ Patients with unilateral deficits have a better prognosis than patients with bilateral deficits.
• Females and patients with bowel dysfunction have been reported to have worse outcomes postoperatively.³²

Multimedia

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Media file 1: Illustration demonstrating the relevant anatomy of the cauda equina region

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Media file 2: Illustration demonstrating an example of cauda equina syndrome secondary to a spinal neoplasm

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Media file 3: Sagittal MRI of a patient with cauda equina syndrome secondary to a large lumbar disk herniation

Keywords

cauda equina syndrome, CES, lumbosacral nerve root compression, neuromuscular disorders, urogenital disorders, lumbar stenosis, lumbar disc herniation, spinal stenosis, incontinence

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