Lumbar Disc Herniations, Discogenic Back Pain, and Cauda Equina Syndrome

Ovid: Spine

Editors: Bono, Christopher M.; Garfin, Steven R.
Title: Spine, 1st Edition
> Table of Contents > Section V
– Degenerative Disorders > 17 – Lumbar Disc Herniations, Discogenic
Back Pain, and Cauda Equina Syndrome

Lumbar Disc Herniations, Discogenic Back Pain, and Cauda Equina Syndrome
Christopher M. Bono
The disc is the anterior border of the spinal canal at
the facet joint level. It is covered by the thin posterior longitudinal
ligament, which is concentrated centrally and leaves the posterolateral
disc bare. This anatomy is thought to contribute to posterolateral (or
paracentral) herniations being the most common herniations. Nerve roots
branch from the cauda equina one level above their exiting foramen. The
L5 nerve root leaves the cauda equina approximately at the level of the
L4 vertebral body, then descends to pass beneath the L5 pedicle, where
it turns lateral to exit the spinal canal.
The location of the disc herniation determines which root is primarily affected. The central zone is delineated by the lateral borders of the cauda equina. The lateral recess
is between the lateral border of the cauda equina and the medial border
of the pedicle. Within the lateral recess, fragments that migrate
medial to the nerve root are termed axillary herniations. The foraminal zone
is between the medial and lateral borders of the pedicle. Herniations
beyond the lateral border of the pedicle are within the far-lateral or extraforaminal zone.
Herniations in the foraminal or extraforaminal zones usually affect the
exiting nerve, whereas in the other zones the descending (or
traversing) nerve root is affected. Fragments can displace cranially or
The exact inciting event leading to disc herniation is
unknown. Some investigators believe that an acute traumatic episode
leads to displacement of the disc, although this most likely is related
to force imparted onto a previously degenerated disc, which has
developed a focal annular weakness. In support of this idea, acute
sciatica from disc herniation often is predated by a history of
previous back pain. Postural variations can influence intradiscal
pressures. The highest pressures have been recorded in patients with
the torso forward flexed with weight in hand.
The relationship between disc herniation and sciatica is
not completely understood. In animals and humans, pure compression of a
noninflamed nerve produces sensory and motor changes without pain,
whereas pain is elicited with manipulation of inflamed nerves. These
findings suggest that herniated discs large enough to cause mechanical
compression of a nerve root may produce focal deficits, but that
associated sciatic-type pain is produced only if the nerve root is
irritated or inflamed concurrently. Neurochemical factors, such as IgG,
IgM, and tumor necrosis factor-α, also may have a role in the
production of sciatic pain. There is evidence of systemic inflammatory
responses to disc herniations as well.
Classification of Disc Herniations
Disc herniations can be described by their morphology, as follows:
  • Protruded—eccentric bulging through an intact anulus fibrosus
  • Extruded—crosses the anulus but is in continuity with the remaining nucleus
  • P.143
  • Sequestered—not continuous with the disc space (free fragment)
  • Contained—subligamentous (by posterior longitudinal ligament or the outer anulus)
  • Uncontained—cross the posterior longitudinal ligament or outer anulus
History and Symptoms
Pain is the most common complaint. Some patients
describe a specific incident (e.g., fall, twist, heavy lifting).
Radicular pain is more typical and often the more “treatable” of the
complaints. Lower lumbar or lumbosacral disc herniations can lead to
the classic symptoms of pain radiating below the knee, following a
dermatomal distribution. S1 radicular pain may radiate to the back of
the calf or the lateral aspect or sole of the foot. L5 radicular pain
can lead to symptoms on the dorsum of the foot. L2 and L3 radiculopathy
can produce anterior or medial thigh and groin pain. Groin pain also
may indicate L1 pathology. It is important to ask questions pertaining
to bowel and bladder function.
Physical Examination
Gait should be observed. A sciatic list may be present,
usually manifest as the patient leaning away from the side of leg pain.
Axillary herniations may cause a list toward the side of herniation. A
footdrop or foot slippage gait may occur with an L4 or L5 paresis. A
Trendelenburg gait suggests hip abductor weakness (L5).
Tenderness to palpation of one or two levels is more
consistent with bone or disc pathology than tenderness at multiple
levels. Paraspinal muscle spasm can be noted in addition to tenderness.
A neurologic exam is requisite in all patients with suspected herniated
discs. Motor, sensory, and reflex examination should be thorough.
Specific Tests
The straight-leg raise test
is performed with the patient in the supine position. The test is
considered positive if sciatic pain is reproduced between 35 and 70
degrees of elevation. More than 70 degrees of elevation causes no
further stretch of the nerve roots. The straight-leg raise test is best
for eliciting L4, L5, or S1 radiculopathy. It is not useful for upper
lumbar roots, for which a femoral stretch test (performed in the prone
position) should be used. If raising the contralateral leg reproduces symptoms in the ipsilateral side, this suggests a herniated disc. Lasègue’s sign is a modification of the straight-leg raise test and involves dorsiflexion of the foot, which aggravates pain.
Diagnostic Imaging
Plain radiographs cannot show a herniated disc. They can
show changes, however, that suggest a herniated disc, such as a
scoliotic list or osseous signs of disc degeneration. These changes
include osteophytes, disc space narrowing, subtle changes in
translation, facet hypertrophy, or changes in sagittal alignment.
Magnetic Resonance Imaging
The disc is readily visualized using magnetic resonance
imaging (MRI). Free fragments can be differentiated from extruded disc
herniations and a symmetric bulge from a contained protrusion. The size
and type of disc herniation can be determined reliably using MRI. In a
postoperative patient with continued or recurrent symptoms, MRI best is
delayed until 6 months after surgery, if symptoms allow. The main
challenge is differentiating scar from new-onset disc. Although
gadolinium-enhanced T1-weighted MRI (which highlights scar but not
disc) is considered the gold standard, more recent evidence suggests
that sophisticated T2-weighted images (obtained with high-powered
magnets) might supplant the need for gadolinium-enhanced MRI.
Computed Tomography
Before the advent of MRI, CT was the imaging modality of
choice for evaluation of herniated discs. CT performed with intrathecal
contrast injection (i.e., CT-myelography) is nearly as sensitive as MRI
in detecting herniated discs.
Nonoperative Treatment
Bed rest should be limited to no more than 2 to 3 days.
Longer periods of inactivity can potentiate prolonged disability and
continued or augmented pain. Exercise therapy and physical
rehabilitation should be included in the nonoperative care of herniated
discs. Treatment goals are to restore strength, flexibility, and
function that were lost secondary to pain, splinting, and spasm.
Nonsteroidal antiinflammatory drugs are first-line agents. In the acute
setting, short-term narcotic use, such as a single dose of a
morphine-derivative analgesic, can be useful for severe pain, but
should not be prescribed in an extended manner. So-called muscle
relaxants frequently are prescribed, but these agents have more
significant sedative effects than production of muscle relaxation.
Selective transforaminal steroid injections can produce symptomatic
short-term relief in many patients. In a restrospective study, 77% of
patients who were considered surgical candidates but were interested in
an injection had clinical resolution and had “avoided” surgery at an
average follow-up of 1.5 years.
Operative Treatment
An absolute indication for lumbar discectomy is a
progressive neurologic deficit. In this circumstance, operative
intervention may be considered conservative care, provided that no
medical contraindications exist. A neurologic deficit most commonly is
associated with a cauda equina syndrome.
The relative requirements for an elective discectomy vary but include the following:
  • Radiologic identification of compressive pathology that is concordant with the patient’s physical signs and symptoms
  • Patient’s strong desire to return to work or activity
  • Failure of at least 6 weeks of nonoperative management,


    including observation and therapy with or without selective injections

There are many techniques of surgical discectomy.
Standard open discectomy is the most common surgical approach. It
involves careful incision planning, laminotomy or partial laminectomy
to provide adequate visualization of the pathologic condition, gentle
retraction of the neural elements, and direct excision of the
herniation. As an adjunct to open discectomy, some investigators
advocate the use of a microscope for better visualization and
minimizing incision size. Alternatives to interlaminar techniques have
been developed for excision of foraminal and extraforaminal lateral
disc herniations (more common in elderly patients), which involve
exposures between the transverse processes and lateral to the pars
Various percutaneous methods of treatment have been
developed. Some methods entail placement of the cutting device
intradiscally to decompress the disc space to retract the herniated
fragment. Other methods involve directly visualizing the neural
elements and disc using an endoscope. Chemical digestion of the disc
(i.e., chemonucleolysis) previously was popular, but enzyme-related
complications and results inferior to open discectomy have limited its
continued popularity in the United States.
Postoperative Care.
After an uncomplicated, simple open discectomy, the
patient usually is discharged on postoperative day 1 or 2. The activity
level recommended varies among surgeons. Concerns are that aggressive
movements and load can predispose to reherniation or excessive
scarring. This concern has led many surgeons to limit lifting and
bending after discectomy for about 3 to 4 weeks. Although this is
probably the predominant practice, there is little literature to
support such extended periods of protected activity. Unrestricted
activity protocols have shown comparable success and reherniation rates.
Surgical Outcomes.
The outcomes of surgical discectomy are reliable when
one adheres to strict preoperative selection criteria. In a careful
review of the literature, many factors were shown to affect surgical
outcome. In one study, patients with larger herniations had a better
outcome after discectomy than patients with small (<6 mm) fragments.
Patients with highly positive straight-leg raise test results and
younger patients with large disc herniations also tend to have better
results. Good or excellent clinical results of open discectomy for
paracentral and intraforaminal disc herniations are reportedly about
80%. Patients should be advised that the operation is intended
primarily to relieve leg pain, not back pain. Central discs are
associated with poorer outcomes (50% good or excellent). In experienced
hands, endoscopic discectomy can yield results as satisfying as open
discectomy. There is insufficient evidence to conclude that using a
microscope leads to superior clinical results.
Psychological and social factors have been shown by many
authors to influence surgical results of lumbar discectomy profoundly.
Patients who are self-confident, only mildly depressed, and generally
optimistic are more likely to do well. Other predictors of good results
are a high preoperative pain index, a higher education level, an
overall satisfaction with life, and the perception that the patient’s
job was of light or suitable duty. In one study, the best predictor of
outcome was the psychological score as measured by the Minnesota
Multiphasic Personality Inventory.
Complications of discectomy are summarized as follows:
  • Recurrent herniation
    can occur in 0% to 12% of cases. Some investigators have recommended
    aggressive disc curettage to decrease reherniation rates; however, this
    can lead to a higher rate of postoperative back pain. The results of
    surgical discectomy for a recurrent disc are comparable to primary
  • Wound infections have been reported in 0% to 3% of cases.
  • Epidural abscess is rare, with reported rates of 0.3%, and should be managed with surgical evacuation.
  • Pyogenic discitis may occur after discectomy 2.3% of the time.
  • Vascular injuries are exceedingly rare.
  • Incidental dural tears occur in 0% to 4% cases.
  • Instability is rare after discectomy. Preservation of the facet joints is helpful in avoiding this complication.
Diagnosis and treatment of discogenic low back pain are
difficult and controversial. The difficulty stems primarily from the
facts that (1) there is no objective test to determine origin of low
back pain, and (2) radiologic abnormalities, such as disc degeneration
and lumbar spondylosis, are common in asymptomatic patients. An
explosion of interest has occurred in the basic scientific
understanding of the biochemical and biomechanical changes associated
with disc degeneration.
The term internal disc derangement
has been introduced more recently. This term refers to a pathologic
mechanical or chemical condition of the disc that leads to low back
pain. The exact mechanism is elusive; however, innervation of the
posterior anulus by branches of the sinuvertebral nerve has been well
documented. This is the suggested pathway of nociceptive pain
transmission from the disc.
Clinical Presentation
The diagnosis of internal disc derangement is difficult.
Clinical presentation is that of low back pain with or without leg pain
that often is present for years but highlighted by increasingly more
frequent acute episodes of pain. Back symptoms are predominant. Leg
pain infrequently extends below the knee. Flexion usually aggravates
pain more than extension.
Imaging Findings
Plain radiographs often are negative but may show disc space collapse, end plate sclerosis, or osteophytes. MRI is


more useful. On T2-weighted images, the disc appears dark, an
indication that it has lost its normal water content. The predictive
value of the so-called high-intensity zone within the posterior anulus
(which represents a peripheral annular tear) for low back pain is
questionable. Bone edema can be noted around the end plate (Modic
changes). The role of discography is controversial (see Chapter 3).

Nonoperative Modalities
Nonoperative treatment modalities include the following:
  • Activity modification
  • Medications, including nonsteroidal antiinflammatory drugs
  • Epidural steroid injections
  • Physical therapy, with a focus on lumbar
    extension exercises, paraspinal muscle strengthening, stretching, and
    generalized conditioning
Invasive Modalities
Intradiscal electrothermal therapy has been introduced
more recently. This modality involves percutaneous insertion of a
heating coil into the disc to coagulate collagenous tissue and
nociceptive nerve endings within the posterior anulus. Clinical results
have varied, with one report showing about 50% pain reduction in about
50% of patients treated. Two more recently presented randomized
prospective studies comparing intradiscal electrothermal therapy with
nonoperative care showed modest (1 to 2 points on visual analogue
scale) benefits.
Fusion is the most common method of surgical treatment
of chronic discogenic low back pain. Results have varied widely in the
reported literature. Even in carefully selected patients,
posterolateral fusion is successful in only about 50% of cases.
Interbody fusion techniques, such as posterior lumbar interbody fusion
and anterior lumbar interbody fusion, have produced better clinical
results, with reported success rates of 75% to 90%.
On the forefront of technology are motion-sparing
procedures, such as total disc arthroplasty and nuclear replacement.
From preliminary data, it seems that total disc arthroplasty can be as
successful as interbody fusion. The long-term benefits of preserving
motion on decreasing the incidence of adjacent segment degeneration
remain to be seen.
Cauda equina syndrome most commonly occurs from a
herniated lumbar disc, but it also can develop secondary to tumor,
abscess, or hematoma. It is more common with central herniation (27% of
central herniations), although it can occur with paracentral or lateral
herniations as well. It is more frequent in men in their 30s. An L4-5
disc is the usual culprit. Cauda equina syndrome should be considered a
true surgical urgency because the neurologic results are affected by
the time to decompression. The clinical diagnosis of cauda equina
syndrome relies on many components, including perineal sensory deficit
(so-called saddle anesthesia), bowel or bladder incontinence, new-onset
lower extremity sensory deficit, and a new or progressive motor
deficit. In addition to a meticulous physical examination, evaluation
of cauda equina syndrome should include measurement of a bladder
postvoid residual. Normally, postvoid residual should be less than 50
to 100 mL. The postvoid residual is often abnormal preoperatively and
can be an important parameter to follow postoperatively.
Decompression and discectomy can be via a laminotomy or
through a formal laminectomy. Proponents of laminectomy believe this
provides superior visualization of the dura and avoids excessive
traction. Adequate exposure is particularly relevant for removal of
central disc herniations. Discectomy is performed best within 48 to 72
hours of the onset of symptoms; this leads to better sensory, motor,
urinary, and rectal function recovery. Motor strength may continue to
improve for 1 year after surgery. Although the postvoid residual
usually decreases to less than 110 mL by 6 weeks, bladder function may
continue to improve for 16 months. Early surgery does not seem to
affect substantially the resolution of postoperative pain compared with
delayed intervention. Preoperative neurologic status seems to be the
greatest predictor of recovery.
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