Abstract
Primary
care and emergency care physicians frequently encounter patients with
low back strain and sciatica and must be able to recognize the perilous
signs of cauda equina syndrome (CES), a condition usually caused by
massive disk herniation. Patients with CES may have peripheral neurologic
deficits as well as bowel and bladder dysfunction. Emergent magnetic
resonance imaging is the study of choice to confirm the diagnosis. Surgical
decompression is the only effective treatment for CES. The prognosis
depends on initial signs and symptoms, progression of neurologic deterioration,
and timeliness of surgical decompression. Recovery may occur immediately
after surgery or months or years postoperatively.
Introduction
Low back
pain is a common complaint heard frequently by all physicians who provide
primary care to adult patients. Because this common type of pain is
generally not associated with clinically significant pathology, clinicians
may overlook a rare but potentially disabling neurologic affliction
such as cauda equina syndrome (CES). Most cases of CES result from lumbar
disk herniation with excessive compression on the cauda equina. Clinical
features may include low back pain, sciatica, saddle-area anesthesia,
motor weakness, sensory deficit, and urinary or fecal incontinence.
The condition may progress to permanent incontinence, paraplegia, or
both.1 Therefore, to diagnose and promptly treat CES, clinicians
must be able to recognize the signs and symptoms of this neurologic
syndrome.
Case Report
A 28-year-old
man presented to the emergency department for low back pain and numbness
in both lower extremities. Two days earlier, he had sharp, shooting
pains in the back and buttocks after moving boxes. The pain was relieved
with hydrocodone with acetaminophen. However, on the morning of presentation,
the patient awoke with numbness in both lower extremities and had left
leg weakness so severe that the patient was unable to stand or walk
without support. The patient described the pain as mild while he was
supine and worse when he sat or stood. The patient reported some urinary
hesitancy, dribbling of urine, and constipation. He did have morning
erections. The patient reported that he had had an industrial injury
five years before that resulted in a herniated lumbar disk and subsequent
laminectomy; he had been doing well since then until the time of presentation.
On physical
examination, the patient was alert and oriented and had stable vital
signs. The back was not tender when palpated. The straight-leg-raise
test to 30 did not elicit additional pain in either leg. Motor strength
examination showed some lack of effort on the right side but good motor
function in all muscle groups of the right lower extremity. Motor strength
of the left lower extremity was decreased to 3 out of 5 in the hamstrings,
iliopsoas, and quadriceps muscles; 1 to 2 out of 5 in the ankle and
toe plantar flexor muscles; and 0 out of 5 in the ankle dorsiflexor
muscles and extensor hallicus longus muscle. Tests of the deep tendon
reflexes showed normal right patellar reflex, absent left patellar reflex,
and absent Achilles tendon reflexes bilaterally. Sensory examination
demonstrated hyperalgesia of the left calf and hypesthesia of the scrotum,
perianal area, and left foot. Anal sphincter tone was reduced.
Lumbar
spine radiographs revealed mild narrowing of the intervertebral disk
spaces between L3-4 and L4-5. Emergent magnetic resonance images (MRI)
of the lumbar spine showed herniated disk material located along the
left lateral aspect of the vertebral canal. Disk material extending
from the body of L3 to the body of L4 resulted in moderate central canal
stenosis and compression of the cauda equina.
The radiograph
and MRI both showed evidence of previous L4 laminectomy.
A neurosurgery
consultation was obtained urgently. The patient received an initial
dose of dexamethasone, 10 mg, intravenously, followed by 4-mg intravenous
dose every six hours. The patient was taken to the operating room the
next morning. An L3 laminectomy was done, and herniated disk material
at the level of L3-4 was removed in multiple fragments. Postoperatively,
sensory and motor deficits persisted; the patient had decreased sensation
on the left side of his penis and perineum, left foot drop, hyperalgesia
of the left calf, and decreased anal sphincter tone. He was able to
void without use of a catheter but had some difficulty with initiating
urination. The patient was transferred to the rehabilitation unit for
acute therapy, and the neurologic deficits gradually improved.
One year
after surgery, the patient was able to walk, although the gait was broad
and slow; he was not able to run. He had regained sensation in the left
leg and perineum, although sensation was still mildly decreased. Sexual
function was intact; the patient was able to have erections and had
penile sensation. The patient was able to urinate, but initiating urination
still required effort.
Discussion
Epidemiology
of Low Back Pain, Sciatica, and CES
Seventy
to 85% of adults in the United States report experiencing low back pain
by the age of 50 years;2 national annual incidence of low
back pain is 5%.3 One quarter of patients with back pain
have sciatica,4 a syndrome characterized by pain radiating
from the buttocks down the posterior or lateral aspect of the lower
limb below the knee.5,6 Sciatica may be associated with motor,
reflex, or sensory deficits. The most common cause of sciatica is herniation
of the lower lumbar intervertebral disks, most often involving the disk
between L4-5 and less often the disk between L5-S1 or L3-4; herniation
causes compression or irritation of the lumbar nerve roots.7
Symptomatic disk herniation most commonly occurs in patients who are
30 to 50 years old, although such herniation can occur at any age.8
In contrast to sciatica, cases of CES after disk herniation are relatively
rare; according to Chang et al, the incidence of CES due to lumbar disk
herniation has been reported to range from 1% to 10% of operated disk
cases.9
Etiology
of CES
The adult spinal cord terminates at the level of vertebra L1 to L2 with
the terminal bundle of lumbar and sacral nerve roots within the spinal
canal forming the cauda equina below; the nerve roots then separate
and exit at their specific foramina.10 Compression of the
cauda equina is most commonly caused by herniation of a large quantity
of lumbar disk material, often in association with degenerative or congenital
spinal stenosis, and can result in CES. According to Delamarter et al,
extremely rare causes of CES include compression by tumor, fracture,
penetrating trauma, chiropractic manipulation, chemonucleolysis, postoperative
hematoma, free epidural fat graft, and ankylosing spondylitis.11
Risk factors
for disk herniation include obesity,12 male gender,12
age more than 40 years,12 heavier lifetime loading during
occupational and leisure time activities,13 and history of
back disorders.13 Factors associated with degeneration of
the intervertebral disk include genetic factors and changes in disk
hydration and collagen. 14 These factors reduce effectiveness
of the nucleus pulposus (the inner disk layer) for absorbing shock,
providing resistance to compression, and permitting flexibility of the
vertebral column.10 Instead, the nucleus transmits a greater
portion of applied loads to the surrounding annulus asymmetrically,
an imbalance that may lead to weakness of the annulus and herniation
of the nucleus pulposus material into the spinal canal.14
Clinical
Presentation and Physical Examination for CES
Three
variations of CES have been described: 1) acute CES that occurs suddenly
in patients without previous low back problems; 2) acute neurologic
deficit in patients who have history of back pain and sciatica; and
3) gradual progression to CES in patients who have chronic back pain
and sciatica.15 However, in more than 85% of the cases, the
signs and symptoms of CES develop in less than 24 hours.7
Signs
of CES include severe bilateral sciatica; bilateral foot weakness; saddle-type
hypesthesia or anesthesia in the areas innervated by nerve roots S2
to S5; and retention or incontinence of urine, stool, or both.9
Thus, asking all patients with back pain about the presence of associated
neurologic deficits is imperative and should include questions about
lower extremity and saddle paresthesia, numbness, weakness, gait disturbance,
bowel or bladder dysfunction, and impotence.6 Positive responses
to these symptoms warrant further investigation to rule out the diagnosis
of CES. Coughing, sitting, or bearing down (Valsalva maneuver) may aggravate
sciatic pain, and lying supine may alleviate pain.6 The straight-leg-raise
test, during which the examiner raises the supine patient's fully extended
leg up to 70 degrees, is considered positive for disk herniation and
nerve irritation when it produces a radicular pain radiating down the
lower limb to below the knee in one or both limbs at between 30 and
60 degrees.6,16 A positive straight-leg-raise test result
for the limb on the affected side is 80% sensitive and 40% specific
for disk herniation, a result which suggests involvement of the L5 to
S1 nerve roots or the sciatic nerve. A positive straight-leg-raise test
result for the limb on the contralateral side is 25% sensitive and 90%
specific for disk herniation, a result which suggests involvement of
the L2 to L4 nerve roots.17
Neurologic
examination should evaluate each of the spinal nerve roots. Lumbar disk
herniation typically affects the nerve root inferior to the disk space.
Thus, herniation of the L4-5 intervertebral disc would typically impinge
on the L5 nerve root.6 Sensory examination should be conducted
using both light touch and pinprick;6 cold temperature sensation
can be easily tested using the cold metal end of a tuning fork. Sensory,
motor, and reflex innervation by nerve roots L1 through S5 are summarized
in Table 1. Because the L4 nerve root controls ankle dorsiflexion, the
L4 nerve root can be tested by heel walking.6,14 The L5 nerve
root can be evaluated by using the Trendelenburg test.6,14
The Trendelenburg test requires the patient to stand on one leg and
the physician to stand behind the patient with hands on the patient's
hips; a drop in the pelvis on the side opposite the raised leg implies
presence of either L5 nerve root or hip joint pathology.14
The S1 and S2 nerve roots together are responsible for plantarflexion
of the ankle and can be tested by asking the patient to stand and to
walk on the toes.6
CES or
spinal cord compression should be considered until proven otherwise
in all patients who have low back pain with bowel or bladder incontinence.6
Bladder dysfunction usually is secondary to detrusor muscle weakness
and an areflexic bladder; this dysfunction initially causes urinary
retention followed by overflow incontinence in later stages.18
Patients who have back pain with urinary incontinence but who have normal
neurologic examination results should have a urinary postvoid residual
volume measured.6 A postvoid residual volume greater than
100 mL indicates overflow incontinence and mandates further evaluation;6
a volume less than 100 mL rules out diagnosis of CES.6 The
anal wink reflex, elicited by gently stroking the skin lateral to the
anus, normally causes reflexive contraction of the external anal sphincter.6
Rectal examination should be done to assess anal sphincter tone and
sensation if any of the characteristic signs or symptoms of CES are
present.6
Diagnosis,
Treatment, and Prognosis of CES
Although
plain radiographs are of limited value for diagnosing lumbar disk herniation,
they can be used to rule out other pathology.14 Plain lumbar
spinal radiographs should be obtained if neurologic dysfunction is discovered
on physical examination or if patient history suggests the presence
of tumor, infection, or fracture.6 Although radiograph findings
are often unremarkable, the presence of decreased disk height may be
suggestive of disk herniation.14
Computed
tomography (CT) or magnetic resonance imaging (MRI) may be considered
for evaluation of a patient with signs of disk herniation.19,20
MRI is the widely accepted standard for the rapid and complete evaluation
of a patient with clinically significant spinal pathology and should
be obtained emergently when the diagnosis of CES is suspected.19
Abnormalities on MRI are commonly found in asymptomatic patients;20
MRI should therefore be used as a means of confirming a diagnosis in
the presence of neurologic signs rather than as a screening tool.20
In the series of CES cases reported by Shapiro, 75% of CT or MR images
of CES cases showed large quantities of disk material occupying more
than one third of the spinal canal diameter.7
Treatment
with high doses of steroids may provide rapid relief of pain as well
as improve function while appropriate diagnostic studies and consultations
are being obtained.6 Dexamethasone is commonly given intravenously
at doses of 4 to 100 mg.6
CES is
an absolute indication for emergent surgical decompression;11
laminectomy followed by gentle retraction of the cauda equina (to avoid
complications of increased neurologic compromise) and diskectomy is
the technique of choice.7 Timing of the decompression has
not been unanimously agreed upon. Traditionally, patients with CES who
have surgery within 24 hours of initial symptoms are believed to have
clinically significantly better neurologic recovery.7 However,
some studies1,7,21 found no statistically significant improvement
in outcome between patients surgically treated within 24 hours compared
with those surgically treated within 24 to 48 hours. Other studies9,11
suggest that surgery performed on an expedient rather than emergent
basis did not compromise neurologic recovery.
Outcome
for patients with CES can be predicted primarily by their symptoms at
presentation.6 Patients who are ambulatory at initial evaluation
generally remain ambulatory;6 those who are paretic but can
walk with assistance have a 50% chance of walking unassisted after recovery;
those who are paralyzed when seen initially rarely will walk again.6
About 79% of patients who require urinary catheterization at initial
evaluation will continue to use a catheter after recovery.6
Patients with a history of chronic low back pain have an increased risk
of urinary and rectal dysfunction after surgery.1 Postoperative
recovery time can range from months to years. Most patients improve
within the first two years after surgical decompression, although some
continue to clinically improve for up to five years after surgery.1
Conclusion
Acute
compression of the cauda equina is a neurologically compromising and
potentially debilitating syndrome. Physicians who evaluate low back
pain must be able to recognize the signs and symptoms of this relatively
rare but critical spinal syndrome and must expedite emergent evaluation
with appropriate history and physical examination, imaging studies,
and consultations. Patients with neurologic deficits of the lower extremities,
perianal region, scrotum, penis, bowel or bladder (or both) need further
evaluation. Patients with bowel or bladder incontinence should be considered
to have neurologic spinal compromise until proven otherwise and need
emergent imaging studies, preferably MRI. If the diagnosis of CES is
confirmed, surgical intervention should be done as soon as possible
to prevent progression of neurologic symptoms and to allow maximum neurologic
recovery.
Acknowledgment
Robert
Sallis, MD, Advisor, Family Medicine Residency Program, reviewed the
manuscript.
References
1. Ahn
UM, Ahn NU, Buchowski JM, Garrett ES, Sieber AN, Kostuik JP. Cauda equina
syndrome secondary to lumbar disc herniation: a meta-analysis of surgical
outcomes. Spine 2000 Jun 15;25(12):1515-22.
2. Research
on low back pain and common spinal disorders. NIH Guide 1997 May 16;26(16).
Available from: http://grants.nih.gov/grants/guide/pa-files/PA-97-058.html
(accessed June 2, 2003).
3. Carey
TS, Evans AT, Hadler NM, et al. Acute severe low back pain: a population-based
study of prevalence and care-seeking. Spine 1996 Feb 1;21(3):339-44.
4. Borenstein
DG, Wiesel SW, Boden SD. Low back pain: medical diagnosis and comprehensive
management. 2nd ed. Philadelphia: Saunders; 1995.
5. Kahanovitz
N. Sciatica: verifying the diagnosis, offering relief. J Musculoskeletal
Med 1998 Jan;15(1):51-9.
6. Della-Giustina
DA. Emergency department evaluation and treatment of back pain. Emerg
Med Clin North Am 1999 Nov;17(4):877-93, vi-vii.
7. Shapiro
S. Medical realities of cauda equina syndrome secondary to lumbar disc
herniation. Spine 2000 Feb 1;25(3):348-51; discussion 352.
8. Murrey
DB, Hanley EN Jr. Surgery for lumbar disc herniation: what are the choices?
J Musculoskeletal Med 1999 Jan;16(1):39-45.
9. Chang
HS, Nakagawa H, Mizuno J. Lumbar herniated disc presenting with cauda
equina syndrome. Long-term follow-up of four cases. Surg Neurol 2000
Feb;53(2):100-4;discussion 105.
10. Arce
D, Sass P, Abul-Khoudoud H. Recognizing spinal cord emergencies [published
erratum appears in Am Fam Physician 2002 May 1;65(9):1751]. Am Fam Physician
2001 Aug 15;64(4):631-8.
11. Delamarter
RB, Sherman JE, Carr JB. 1991 Volvo Award in experimental studies. Cauda
equina syndrome: neurologic recovery following immediate, early, or
late decompression. Spine 1992 Sep;16(9):1022-9.
12. Kostova
V, Koleva M. Back disorders (low back pain, cervicobrachial and lumbosacral
radicular syndromes) and some related risk factors. J Neurol Sci 2001
Nov 15;192(1-2):17-25.
13. Borenstein
DG. Epidemiology, etiology, diagnostic evaluation, and treatment of
low back pain. Curr Opin Rheumatol 1997 Mar;9(2):144-50.
14. Humphreys
SC, Eck JC. Clinical evaluation and treatment options for herniated
lumbar disc. Am Fam Physician 1999 Feb 1;59(3):575-82, 587-8.
15. Tandon
PN, Sankaran B. Cauda equina syndrome due to lumbar disc prolapse. Indian
J Orthop 1967;1:112-9.
16. Bratton
RL. Assessment and management of acute low back pain. Am Fam Physician
1999 Nov 15;60(8):2299-308.
17. Rose-Innes
AP, Engstrom JW. Low back pain: an algorithmic approach to diagnosis
and management. Geriatrics 1998 Oct;53(10):26-8, 33-6, 39-40 passim.
18. Comarr
AE. Neurourology of spinal cord-injured patients. Semin Urol 1992 May;10(2):74-82.
19. Coscia
M, Leipzig T, Cooper D. Acute cauda equina syndrome. Diagnostic advantage
of MRI. Spine 1994 Feb 15;19(4):475-8.
20. Boden
SD, Davis DO, Dina TS, Patronas NJ, Wiesel SW. Abnormal magnetic-resonance
scans of the lumbar spine in asymptomatic subjects. A prospective investigation.
J Bone Joint Surg Am 1990 Mar;72(3):403-8.
21. Shapiro
S. Cauda equina syndrome secondary to lumbar disc herniation. Neurosurgery
1993 May;32(5):743-6; discussion 746-7.
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