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Cauda Equina Syndrome
Article Last Updated: Jan 10, 2007
AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: Michael S Beeson, MD, MBA, FACEP, Professor of Emergency Medicine, Northeastern Ohio Universities College of Medicine; Program Director, Emergency Medicine Residency, Summa Health System
Michael S Beeson is a member of the following medical societies: American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Editors: Kirsten A Bechtel, MD, Associate Professor of Pediatrics, Department of Pediatrics, Yale University School of Medicine; Consulting Staff, Department of Pediatric Emergency Medicine, Yale-New Haven Children's Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; J Stephen Huff, MD, Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center; John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center; Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Author and Editor Disclosure
Synonyms and related keywords:
CE syndrome, CES, lumbosacral nerve root compression, neuromuscular disorders, urogenital disorders, sciatica, saddle sensory disturbances, bladder dysfunction, bowel dysfunction, variable lower extremity motor loss, variable lower extremity sensory loss, low back pain, radiating pain, perineal anesthesia, incontinence, pain radiating to legs, poor anal sphincter tone, lumbar disc disease, spinal anesthesia, late-stage ankylosing spondylitis
Background
The cauda equina (CE) is formed by nerve roots caudal to the level of spinal cord termination. Cauda equina syndrome (CES) has been defined as low back pain, unilateral or usually bilateral sciatica, saddle sensory disturbances, bladder and bowel dysfunction, and variable lower extremity motor and sensory loss.
Lesions involving the termination of the spinal cord (conus medullaris) are not discussed in this article. Please refer to Spinal Cord Injuries.
Pathophysiology
CES may result from any lesion that compresses CE nerve roots. These nerve roots are particularly susceptible to injury, since they have a poorly developed epineurium. When well developed, as in peripheral nerves, they protect against compressive and tensile stresses. The microvascular systems of nerve roots have a region of relative hypovascularity in their proximal third. Increased vascular permeability and subsequent diffusion from the surrounding cerebral spinal fluid supplement the nutritional supply. This property of increased permeability may be related to the tendency toward edema formation of the nerve roots, which may result in edema compounding initial and sometimes seemingly slight injury.
Frequency
United States
CES is uncommon, both atraumatically as well as traumatically. It is often reported as a case report due to its rare presentation.
Mortality/Morbidity
CES is not fatal. Morbidity is variable, depending on the etiology of the syndrome. Morbidity is associated with the long-term sequelae of the effects of CES, such as bladder infection, decubitus ulcers, or venous thromboemboli.
Race
No predilection exists on the basis of race.
Sex
No predilection exists on the basis of sex.
Age
Traumatic CES is not age specific. Atraumatic CES occurs primarily in adults as a result of surgical morbidity, spinal disc disease, metastatic cancer, or epidural abscess.
History
A patient with cauda equina syndrome (CES) often presents with nonspecific symptoms, with back pain the most significant and dramatic. Occasionally, history of incontinence of urine or stool, or occasionally saddle paresthesias, is volunteered. If not volunteered, this history should be elicited from anyone complaining of low back pain.
- Low back pain
- Acute or chronic radiating pain
- Unilateral or bilateral lower extremity motor and/or sensory abnormality
- Bowel and/or bladder dysfunction
- Usually with associated saddle (perineal) anesthesia (Examiner can inquire if toilet paper feels different when wiping.)
- Bladder dysfunction may present as incontinence but often presents earlier as difficulty starting or stopping a stream of urine. Urinary incontinence is on the basis of overflow.
Physical
- Pain often is localized to the low back; local tenderness to palpation or percussion may be present.
- Reflex abnormalities may be present; they typically include loss or diminution of reflexes. Hyperactive reflexes may signal spinal cord involvement and exclude the diagnosis of CES.
- Pain in the legs (or radiating to the legs) is characteristic of CES.
- Sensory abnormality may be present in the perineal area or lower extremities. Light touch in the perineal area should be tested.
- Muscle weakness may be present in muscles supplied by affected roots. Muscle wasting may occur if CES is chronic.
- Poor anal sphincter tone is characteristic of CES.
- Babinski sign or other signs of upper motor neuron involvement suggest a diagnosis other than CES, possibly a diagnosis of spinal cord compression.
- Anesthetic areas may show skin breakdown.
- Alteration in bladder function may be assessed empirically by obtaining urine via catheterization. A significant volume with little or no urge to void, or as a postvoid residual, may indicate bladder dysfunction.
Causes
- Trauma
- Lumbar disk disease
- Abscess
- Spinal anesthesia
- Tumor, metastatic, or CNS elements
- Late-stage ankylosing spondylitis
- Idiopathic
- Inferior vena cava thrombosis
- Lymphoma
- Sarcoidosis
Back Pain, Mechanical
Guillain-Barré Syndrome
Lumbar (Intervertebral) Disk Disorders
Neoplasms, Spinal Cord
Spinal Cord Infections
Spinal Cord Injuries
Other Problems to be Considered
Conus medullaris syndrome
Spinal cord compression
Lumbosacral plexopathy
Peripheral nerve disorder
Imaging Studies
- Plain radiography - Unlikely to be helpful but perform in search of destructive changes, disk-space narrowing, or spondylolysis
- CT with and/or without contrast - Lumbar myelogram followed by CT
- MRI - Superiority of MRI over CT only suggested by case reports (Early consultation with the appropriate subspecialty is encouraged to guide imaging studies.)
Other Tests
- Catheterization for residual urine volume may reveal urinary retention suggesting a neurogenic bladder.
Prehospital Care
Prehospital care should focus on associated symptoms related to the pain (ie, what besides the pain is different).
- Stabilize acute life-threatening conditions.
- Immobilize the spine if traumatic.
Emergency Department Care
No proven medical treatment exists, and therapy generally is directed at the underlying cause of CES.
- Some may suggest methylprednisolone in a regimen similar to that for traumatic spinal cord injury or another regimen of steroid for the acute syndrome.
- For penetrating trauma, steroids have not shown significant benefit. Surgery is controversial. The timing of decompression is controversial, with immediate, early, and late surgical decompression showing varying results.
Consultations
- Early neurosurgical, neurologic, or orthopedic consultations are recommended, depending on the suspected etiology of CES.
Steroids may be recommended in acute or traumatic CES. Early consultation regarding the use of steroids and any specific regimen is encouraged.
Steroids have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli. They may decrease edema around nerve root segments.
A regimen of methylprednisolone (Solu-Medrol, Depo-Medrol) may be used. One possible regimen may be the dose used in traumatic spinal cord injuries, but no studies exist to support this over any other regimen.
Further Inpatient Care
- Admit patients to appropriate service (usually neurology, neurosurgery, or orthopedic surgery) with frequent neurologic checks. Ideally, the admitting physician or service should examine the patient at the time of admission.
Further Outpatient Care
- Patients in whom acute cauda equina syndrome (CES) is being considered should not be treated or investigated on an outpatient basis without evaluation by a consultant and/or appropriate imaging.
Transfer
- Consider patients with CES for transfer if appropriate subspecialty care is not available.
Complications
- Residual weakness, incontinence, impotence, and/or sensory abnormalities are potential problems if therapy is delayed.
Prognosis
- The prognosis for CES improves if a definitive cause is identified and appropriate treatment occurs early in the course. Surgical decompression may be performed emergently, or, in some patients, delayed, depending on the etiology.
Patient Education
Medical/Legal Pitfalls
- Failure to consider the diagnosis of CES in patients presenting with back pain and with bowel and/or bladder dysfunction
- Failure to document history, neurologic examination, or comment on sphincter function in patients with back pain and possible CES
- Failure to consider possible spinal cord involvement with resulting disability
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Epidural abscess with effacement of thecal sac in a 56-year-old man. |
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Media type: MRI
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- Ahn UM, Ahn NU, Buchowski JM, et al. Cauda equina syndrome secondary to lumbar disc herniation: a meta-analysis of surgical outcomes. Spine. Jun 15 2000;25(12):1515-22. [Medline].
- Boukobza M, Guichard JP, Boissonet M, et al. Spinal epidural haematoma: report of 11 cases and review of the literature. Neuroradiology. Aug 1994;36(6):456-9. [Medline].
- Busse JW, Hsu WS. Rapid progression of acute sciatica to cauda equina syndrome. J Manipulative Physiol Ther. Jun 2001;24(5):350-5. [Medline].
- Choudhury AR, Taylor JC. Cauda equina syndrome in lumbar disc disease. Acta Orthop Scand. Jun 1980;51(3):493-9. [Medline].
- Cohen MS, Wall EJ, Kerber CW, et al. The anatomy of the cauda equina on CT scans and MRI. J Bone Joint Surg Br. May 1991;73(3):381-4. [Medline].
- Davis DP, Bruffey JD, Rosen P. Coccygeal fracture and Paget's disease presenting as acute cauda equina syndrome. J Emerg Med. Mar-Apr 1999;17(2):251-4. [Medline].
- Delamarter RB, Sherman JE, Carr JB. 1991 Volvo Award in experimental studies. Cauda equina syndrome: neurologic recovery following immediate, early, or late decompression. Spine. Sep 1991;16(9):1022-9. [Medline].
- Gleave JR, Macfarlane R. Cauda equina syndrome: what is the relationship between timing of surgery and outcome?. Br J Neurosurg. Aug 2002;16(4):325-8. [Medline].
- Hall ED. The neuroprotective pharmacology of methylprednisolone. J Neurosurg. Jan 1992;76(1):13-22. [Medline].
- Hussain SA, Gullan RW, Chitnavis BP. Cauda equina syndrome: outcome and implications for management. Br J Neurosurg. Apr 2003;17(2):164-7. [Medline].
- Kaiboriboon K, Olsen TJ, Hayat GR. Cauda equina and conus medullaris syndrome in sarcoidosis. Neurologist. May 2005;11(3):179-83. [Medline].
- Mohit AA, Fisher DJ, Matthews DC, et al. Inferior vena cava thrombosis causing acute cauda equina syndrome. Case report. J Neurosurg. Jan 2006;104(1 Suppl):46-9. [Medline].
- Rigler ML, Drasner K, Krejcie TC, et al. Cauda equina syndrome after continuous spinal anesthesia. Anesth Analg. Mar 1991;72(3):275-81. [Medline].
- Rydevik B. Neurophysiology of cauda equina compression. Acta Orthop Scand Suppl. 1993;251:52-5. [Medline].
- Rydevik B, Brown MD, Lundborg G. Pathoanatomy and pathophysiology of nerve root compression. Spine. Jan-Feb 1984;9(1):7-15. [Medline].
- Small SA, Perron AD, Brady WJ. Orthopedic pitfalls: cauda equina syndrome. Am J Emerg Med. Mar 2005;23(2):159-63. [Medline].
Cauda Equina Syndrome excerpt Article Last Updated: Jan 10, 2007
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