Diagnosis and Nonoperative

Management of Lumbar Disk Herniation

Lena Shahbandar, MD,* and Joel Press, MD*,†

Lumbar disk herniation is a common cause of low back pain in the United States. Diagnosis
of lumbar disk herniation in a person complaining of low back pain depends on an
understanding of anatomy and pathophysiology as well as the ability to synthesize various
elements of the history and physical examination. Imaging studies should then be used to
confirm and clarify the diagnosis, but it is important to acknowledge that they cannot
replace the clinical picture because the high rate of asymptomatic disk herniations can be
misleading. The proper nonsurgical treatment of herniated nucleus pulposus revolves
around controlling symptoms to strengthen patients and restore their function, and it may
involve any combination of analgesic medications, physical therapy, therapeutic modali-
ties, and corticosteroid injections. This article aims to clarify current aspects in the
diagnosis and nonoperative management of lumbar disk herniation.
Oper Tech Sports Med 13:114-121 © 2005 Elsevier Inc. All rights reserved.

KEYWORDS low back pain, radiculopathy, sciatica, lumbar disk herniation, epidural steroid
injection, centralization

L ow back pain is one of the leading causes of disability

in the United States, and for people under the age of
45, it is the most common cause of disability. In fact, low
back pain in general is the second most common reason
for physician visits in the United States. The annual inci-
dence of back pain is estimated to be 5%,1 and the lifetime
prevalence is 80%.2
Disk herniation in particular occurs most commonly
between the ages of 40 and 45. Although it is a common
cause of low back pain complaints, lumbar disk herniation
also occurs frequently in asymptomatic patients.3 The
L4-L5 and L5-S1 intervertebral disks are most commonly
affected. It has been shown that approximately 95% of
lumbar disk herniations occur at these 2 sites. Fortunately,
75% of disk herniations resolve spontaneously within 6
months. However, patients with lumbar disk herniation
who undergo surgical intervention are 10 times more
likely than the general population to have a subsequent
operation for herniated disk.4
*Physical Medicine and Rehabilitation, Rehabilitation Institute of Chicago,
Chicago, IL.
†Physical Medicine and Rehabilitation, Northwestern University Medical
School, Chicago, IL.
Address reprint requests to Joel Press, MD, Rehabilitation Institute of
Chicago, 1030 N. Clark St, Suite 500, Chicago, IL 60610. E-mail:
lshahbande@ric.org
Pathophysiology
of Radiculopathy
Various structures in and around the spine have been found
to be responsible for pain. Specifically, pain generators exist
in the outer third of the annulus fibrosis, the facet synovium,
anterior longitudinal ligament, posterior longitudinal ligament,
nerve roots, nerves, and muscles. Disk herniation may cause
pain by mechanical irritation of these structures. Additionally,
pain may be caused by an inflammatory component that occurs
with disk herniation. Disruption of the annulus fibrosis causes
leaking of the nucleus pulposus into the spinal canal, which
contains various irritants to tissue, including glycoproteins,
phospholipase A2, and nitric oxide, which in turn cause an
inflammatory response in and around the pain sensitive nerve
tissues.5-9 The understanding of this process is becoming in-
creasingly important to the nonsurgical treatment of disk herni-
ation.
The level at which a disk herniates does not always corre-
late to the level of the nerve root symptoms. This is better
understood when the anatomy at the level of the disk herni-
ation is considered. When a disk herniates in the posterolat-
eral direction, which is the most common direction of herni-
ation, the nerve root at the level of injury has already exited
the transverse foramen. However, the nerves that exit at the
level below the disk herniation are arranged in an orderly fash-
ion often most proximal to the direction of herniation. Hence, a

114 1060-1872/05/$-see front matter © 2005 Elsevier Inc. All rights reserved.
doi:10.1053/j.otsm.2005.08.002
Lumbar disk herniation
posterolateral L4-5 disk herniation often produces symptoms at
the L5 nerve root, whereas a foraminal L4-5 disk herniation will
more likely produce symptoms at the L4 nerve root. Thus, a
careful history and physical examination, coupled with imaging,
can best distinguish the cause of a patient’s complaints.
Diagnosis
As mentioned earlier, a careful history and systematic phys-
ical examination are essential components of the diagnosis of
lumbar disk herniation. They are critical in the differentiation
of patients with symptomatic herniated disks from those with
asymptomatic herniated disks. Furthermore, the differential
diagnosis of radicular symptoms includes degenerative
changes, spinal stenosis, spondylolisthesis, synovial cysts,
conjoined nerve roots,10 cancer, epidural abscess,11 and vis-
ceral disease such as endometriosis. Given this broad differ-
ential and the possibility of multiple processes existing in the
same patient, a history and physical can be helpful in guiding
the appropriate diagnostic workup and treatment plan.
History
Although it may be difficult to diagnose a herniated disk
based on history alone, certain elements of the history may
help in differentiating herniated nucleus pulposus from other
causes of back pain.
Risk factors for lumbar disk herniation include biome-
chanical stress on the lumbar spine, specifically torsion12 and
hyperflexion13; poor posture; obesity; tobacco14; and occu-
pational hazards including heavy manual labor or prolonged
driving.2 Therefore, a complete social history is essential to an
understanding of the underlying risks that any given patient
may have for disk herniation.
The classic symptoms of a herniated nucleus pulposus are
described as back pain followed by pain and paresthesias
radiating to the leg. Often, the leg pain is more pronounced
than the back pain. It is often seen in a patient with a history
of low back pain who complains of acute injury with flexion
and rotation of the lumbar spine.
In a study by Young et al,15 various clinical examination
and history elements were compared in lumbar disk pain,
sacroiliac joint pain, and zygoepophysial joint pain. In 80%
of people with diskogenic pain, the back pain was midline.
The pain tends to be exacerbated by flexion and alleviated by
extension, although this is not always the case. Transitional
movements (such as standing from a seated position) also
tend to make the pain worse in both diskogenic and sacroiliac
joint pain.15
Description of the back and leg pain in sciatica are also
critical to the diagnosis of lumbar disk herniation. Sciatica is
defined as a sharp pain, often with paresthesias, radiating in
a dermatomal distribution. This must be differentiated from
referred pain, which is described as aching and burning pain,
often in the buttock. The symptoms of sciatica have a 95%
specificity for lumbar disk herniation when defined as such.16
Moreover, this pain does not have to radiate below the knee
to be considered the pain of disk herniation.17
115
Finally, it is important to note that history is critical in
ruling out cauda equina syndrome. Symptoms of cauda
equina syndrome include bilateral lower limb pain or weak-
ness accompanied by saddle anesthesia and/or bowel or
bladder dysfunction, which is usually described as urinary
retention. This, of course, is a surgical emergency, and inter-
vention can be curative if done in a timely manner.18
Physical Examination
Physical examination of a person with low back pain is per-
formed in a systematic manner. First, inspection of posture is
noted followed by examination of lumbar range of motion.
Neural tension tests should also be performed. Finally,
strength and sensation of the lower extremities should be
tested as well as the reflexes of the L4, L5, and S1 myotomes.
On inspection of standing posture, lumbar shift can be
seen. This is a lateral pelvic shift in relation to the lumbar
spine and is highly suggestive of lumbar disk herniation.18
While the patient is still standing, a thorough examination of
lumbar range of motion should be performed, with special
attention paid to the reproduction of symptoms. In most
patients with lumbar disk herniation, symptoms migrate to-
ward the spine, or “centralize,” on extension, and they mi-
grate toward the extremity, or “peripheralize,” on flexion.
Centralization of symptoms is not only helpful in diagnosing
lumbar disk herniation, but it also has prognostic signifi-
cance because patients who centralize tend to respond to
conservative therapy. The specificity of the centralization
phenomenon is very high, but it has poor sensitivity.15,19,20
Finally, on range of motion, inflexibility secondary to muscle
spasm and segmental muscle atrophy may be seen.
Neural tension tests can also be useful indicators of lumbar
disk herniation. The straight leg raise test is done with the
patient supine and is considered positive if symptoms are
reproduced on the ipsilateral side at less than 70° of passive
hip flexion. Dorsiflexion and hip internal rotation can be
used to add further stress to the nerves. The crossed straight
leg raise test is positive if the maneuver above reproduces
contralateral symptoms. This test has a higher specificity than
the straight leg raise, although the degree of specificity and
sensitivity of these tests varies widely in the literature. Fi-
nally, the slump sit test is the seated version of the straight leg
raise. The patient is asked to slouch forward in the seated
position, and the leg is then extended. This test can be useful
in differentiating true positive straight leg raises from psycho-
somatic low back pain18,21,22 (Fig. 1).
Lastly, strength, sensation, and reflexes help localize the
myotome of injury. On strength testing, it is important that
the physical examiner obtains a mechanical advantage and
that the muscles tested are stressed sufficiently to detect
weakness. It is often necessary to repeatedly stress the muscle
to find subtle weakness. For instance, the ankle plantar flex-
ors cannot be considered 5/5 in strength unless the patient is
able to do repeated single-leg plantar flexion in a standing
position. Sensation testing is a subjective element of the
physical examination, but it can be helpful if sensory deficits
clearly follow a dermatomal distribution. The pinprick exam-
116
Figure 1 Slump-sit test. The patient is asked to slump forward, flex-
ing the cervical spine; then the knee is extended. Reproduction of
radicular symptoms indicates irritation of the nerve and a positive
test.
ination is a useful screen for sensory deficits. Finally, reflexes
must be done carefully because they are the most objective
finding of the physical examination. Specifically, reflex asym-
metry should be noted. The patellar reflex is a screen for the
L3-L4 distribution, the medial hamstring reflex delineates
the L5 distribution, and the Achilles tendon reflex represents
the S1 distribution. It is notable that the medial hamstring
reflex is most difficult to attain, but again asymmetry of the
reflex is the key element of this component of the physical
examination22 (Table 1).
Imaging
An extensive discussion of imaging studies is beyond the
scope of this section, but it is important to note that there is a
high rate of abnormal imaging in asymptomatic patients.
Early postmortum studies revealed extrusion of disks into the
spinal canal in 39% of asymptomatic individuals.23 More
recent studies have reinforced this concept and shed clinical
significance on this matter. Thirty-six percent of computed
tomography scans and 24% of myelograms have been shown
to be abnormal in asymptomatic people.24,25 Furthermore, in
a study by Boden et al3 in 1990, 24% of asymptomatic indi-
viduals were found to have lumbar disk herniations on mag-
netic resonance imaging (MRI). These findings reinforce the
importance of clinical correlation of radiographic findings.
Imaging studies are very helpful in supporting the clinical
diagnosis but cannot supplant history and physical examina-
tion because lumbar disk herniation may be incorrectly de-
scribed as the cause of nonradicular low back pain symp-
toms.
Furthermore, abnormal MRIs should not be used to pre-
dict future back pain in patients. In a 7-year follow-up study
by Borenstein et al26 in 2001, MRIs were performed on
asymptomatic individuals. Seven years later, no significant
relationship was found between the MRIs with asymptomatic
disk abnormalities and the patients who later developed back
pain.
L. Shahbandar and J. Press
Natural History
The natural history of lumbar disk herniation is generally
very favorable. Study of pathophysiology reveals that disk
herniation is caused by repetitive injury to the annulus fibro-
sis with gradual prolapse of the intervertebral disk.27 After
disk herniation, the disk size often regresses. Multiple studies
have shown that patients with lumbar disk herniation who
do not undergo surgical intervention routinely have signifi-
cant reduction in disk size. In fact, more than half of these
patients show 70% or greater reduction in disk size. Specifi-
cally, larger disk herniations result in greater regression.28-30
Management
The approach to nonoperative management of lumbar disk
herniation is often multifaceted and may include medica-
tions, physical therapy, and corticosteroid injections.
Bedrest
Although current medical knowledge discourages strict bed-
rest because of the harmful effects of immobility on the body,
older recommendations of bedrest for acute pain were not
without reason. A study by Pearce and Moll31 in 1967 re-
vealed that 70% of patients treated with strict bedrest im-
proved, whereas 30% had a poor response. This largely pos-
itive response helped to support the principle of bedrest, and
this method of treatment most likely was successful because
it stopped the inciting biomechanical stressors that resulted
in disk herniation. However, studies of patients with acute
back pain revealed that bedrest resulted in increased likeli-
hood of developing chronic pain and more days of work
missed.32,33 Therefore, in making recommendations in the
acute period after disk herniation, physicians need to weigh
the potential advantages against the disadvantages of inactiv-
ity.
Oral Medications
The basic principle in using oral medications in the acute
period is to control the pain so that the patient is able to
remain active. In general, medications work less effectively if
prescribed as needed because they result in broad swings in
serum drug levels, requiring larger doses. Therefore, medica-
tions should be prescribed around the clock, with as-needed
medications reserved for breakthrough pain. Various classes
Table 1 Classic Findings in Common Nerve Root Injuries
Nerve Deficiencies
Root Sensation Strength Reflexes
L4 Medial lower leg Knee extension Patellar
Medial malleolus Ankle
dorsiflexion
L5 First web space Great toe Medial
extension hamstrings
Hip abduction
S1 Lateral foot/heel Plantarflexion Achilles
Lumbar disk herniation
of oral medications commonly used generally for low back
pain can also be used for acute lumbar disk herniation. These
classes include acetaminophen, nonsteroidal antiinflamma-
tory medications, opioids, and muscle relaxants.34
Acetaminophen is an analgesic, antipyretic medication
with no significant antiinflammatory properties, and it is ef-
fective for mild to moderate pain. In normal healthy individ-
uals, liver failure is rare as long as the total daily dose does not
exceed 5 g.
Nonsteroidal anti-inflammatory medications (NSAIDs) are
analgesic, anti-inflammatory, and antipyretic, and they have
been shown to be of benefit in the acute pain common in
lumbar disk herniation but are less effective for chronic
pain.35,36 The choice of NSAID is based on toxicity because
there is no significant difference among the various NSAIDs
in efficacy, but the toxicity profile is variable. It is important
to note that NSAIDs have a ceiling effect; therefore, increased
doses beyond the maximum recommended do not provide
more relief.37
Opioid analgesic medications act by binding with opiate
receptors in the central nervous system, which modulate the
pain response, and they are to be used for moderate to severe
acute pain. Because of the high risk of dependence and abuse,
there is very little indication for long-term use in low back
pain. Opioid analgesics do not have a ceiling effect, but tol-
erance occurs in patients, thereby necessitating progressively
larger doses in many patients who chronically use opi-
oids.34,37
Muscle relaxants have also been used in treating the pain of
lumbar radiculopathy. Although the mechanism of action is
uncertain, these medications act centrally either by altering
the polysynaptic spinal and supraspinal pathways to inhibit
muscle contraction or by causing nonspecific sedation. Mus-
cle relaxants reduce pain when compared with placebo, or
they can be used in combination with analgesics for no longer
than 1 week.38,39
Therapy
In patients with lumbar disk herniation, the goal of therapy is
to reduce pain and restore function. Modalities have a limited
role in this regard, and the primary focus of therapy should
be on aerobic exercise, core muscle strengthening, and flex-
ibility training.
Modalities
Although therapeutic modalities can help to promote heal-
ing, many modalities are often applied without an under-
standing of the rationale of use or the indications and contra-
indications. In the treatment of lumbar disk herniation,
various modalities may be beneficial, whereas others are con-
traindicated.
First, cryotherapy may be applied in the acute phase of
lumbar disk herniation for improving pain control and de-
creasing muscle spasticity. Cold treatments result in vasocon-
striction and reflexic vasodilation, decreased local metabo-
lism and oxygen demand, and decreased inflammation.
Second, traction may be considered in patients with disk
herniation without segmental instability, spinal infection,
117
acute ligamentous injury, osteoporosis, or local neoplasm.
Appropriate traction, although difficult to obtain in normal
clinical practice settings, can result in reduced disk pressure
and stretching of soft tissues.40 The main problem with ap-
plication of traction in the lumbar spine is that the force
necessary to generate appropriate traction is quite large, and
patients often experience discomfort in the traction ma-
chines. Inversion traction may be an alternative, if not con-
traindicated. Finally, contraindicated modalities in lumbar
disk herniation with radicular findings include ultrasound
and other deep-heating therapies because these therapies in-
crease the inflammatory reaction.41
Therapeutic Exercise
In 1983, the first randomized controlled trial showing the
benefit of therapy in herniated nucleus pulposus was per-
formed. This study randomized 126 patients into nonopera-
tive and operative groups. The nonoperative group was given
nonspecific exercises, and of these patients 25% were “cured”
and 36% had “satisfactory improvement” in symptoms. Fur-
thermore, although the surgical group did better at 1 year
postoperatively, the 2 groups showed no significant differ-
ence in outcomes at 4 years after intervention.42
Since this time, other studies on patients with lumbar disk
herniation have further delineated the benefits of therapeutic
exercise. Saal and Saal,43 in 1989, showed the benefit of spe-
cific exercise in patients with lumbar disk herniation. The
patients in this group received aggressive therapy including
back school and spine stabilization. Of this group of patients,
90% reported good or excellent outcomes, and 92% returned
to work.43
One main principle that has recently been used in therapy
for low back pain is that of preferential direction of exercise.
This term uses the concept of centralization of symptoms.
Patients with low back pain tend to “prefer” certain directions
of lumbar motion. The direction of preference is the direction
in which centralization occurs. Patients are then treated with
progressive exercises in the direction of the preference to
restore strength and range of motion. In a study by Donelson
et al20 in 1990, centralization occurred in 87% of patients
with low back pain and radiating leg pain. Of those who
centralized, 98% of the patients with acute symptoms had
good or excellent outcomes, whereas 77% of patients with
subacute symptoms and 81% of patients with chronic symp-
toms had good or excellent outcomes. Only 4 patients in the
study needed surgery, and all 4 of these patients did not
centralize on examination. Interestingly, preferential direc-
tion exercises are successful for patients who centralize re-
gardless of chronicity of the pain. Similar studies have shown
that most people centralize on lumbar extension and periph-
eralize on lumbar flexion, so most patients receive a regimen
that includes progressive lumbar extension exercises.44
This concept of preferential direction has also been shown
to be a good predictor of patients who do not need surgery. In
1992, Alexander et al45 showed that patients with herniated
nucleus pulposus who were selected for nonsurgical inter-
vention based on lumbar extension testing were able to
achieve full lumbar extension within 5 days of therapy and
118
none required surgery. Furthermore, it has been shown that
repeat end-range exercising in patients who centralize results
in good outcomes without surgery even in the presence of
neurologic deficits. On the other hand, lack of centralization
on exercise predicts the need for surgery.46-50
Another component of therapy for patients with lumbar
disk herniation is equipping patients with skills to manage
their pain long after the acute episode of back pain has re-
solved. One such example is the control of early morning
flexion. In a study by Snook et al51 in 1998, patients with
chronic pain were taught to limit early morning flexion, and
these patients were found to have significant improvements
in pain and impairment ratings as well as reduced medication
usage. In a follow-up evaluation 3 years later, most patients
continued to limit their morning flexion and most of these
patients benefited from further reductions in pain.52 Addi-
tionally, proper posture can help reduce pain. Specifically,
lordotic posture generally centralizes and diminishes pain,
whereas kyphotic posture exacerbates pain symptoms. Lum-
bar back rolls help reinforce proper lordotic posture.53
Given this information about centralization and preferen-
tial direction as well as the preponderance of an extension
bias among patients with lumbar disk herniation, there is a
tendency for people to generically recommend extension ex-
ercises for all patients without special regard to each individ-
ual’s examination. This shotgun approach can be harmful
and counterproductive. It is important to remember that not
all patients prefer extension, and therapy needs to be catered
to the individual patient’s preferential direction to maximize
the benefit of centralization method.
Corticosteroids
Because inflammation around the spine contributes to the
pathology of lumbar disk herniation, corticosteroids are of-
ten used to reverse this inflammatory process and relieve
symptoms of pain. Corticosteroids can be administered
orally, intramuscularly, and epidurally.
Oral Corticosteroids
A short course of oral corticosteroids can be used in the
treatment of lumbar disk herniation. The advantage of using
oral corticosteroids is the avoidance of complications that are
possible in more invasive methods of delivery of steroids.
Although the concern with oral steroids is the long list of
adverse effects common to systemic steroids, the short course
minimizes this risk. Hence, in patients for whom injected
steroids is an unfavorable choice, oral corticosteroids may be
a viable option.
Intramuscular Corticosteroids
Intramuscular injection of corticosteroids can be an effective
method of treatment in patients with lumbar disk herniation.
In 1975, a study showed that intramuscular dexamethasone
was effective in improving symptoms in patients with back
pain. One hundred patients were treated with a 7-day course
of intramuscular dexamethasone, and significant symptom
L. Shahbandar and J. Press
improvement was found within 24 to 48 hours of the onset of
treatment. Not only did this study show that steroids can be
helpful in disk herniation, but it also brought more credence
to the belief that inflammation is partly responsible for
pain.54
Epidural Corticosteroid Injections
Peridural and epidural injections of steroids with or without
anesthetic agents have been used in the treatment of low back
pain and sciatica for greater than 40 years, yet the efficacy of
such therapy continues to be contested. Many early studies
used anesthetic alone and demonstrated efficacy,55,56
whereas others have argued the benefits of corticosteroids.57
Many articles have been published both in favor and against
epidural steroid injections, and the range of success is any-
where from 33% to 77%.58-60 Part of the problem with the
analysis of epidural injections is that sample size is often
small, technique often varies from study to study, and studies
are not always done on discreet diagnostic entities of low
back pain.61 Understanding the mechanism of action, com-
plications, and risks, as well as surveying the progress in the
administration of epidural steroid injections may further elu-
cidate this issue.
Local corticosteroids suppress the immune response by
anti-inflammatory and antinociceptive mechanisms as well
as mechanical debridement, and they help to arrest the “pain-
spasm” cycle. Specifically, corticosteroids stabilize nerve root
membranes by suppressing ectopic discharges, diminishing
the migration and accumulation of lymphocytes, and block-
ing phospholipase A2 activity.7 Additionally, corticosteroids
block C fiber transmission, thus altering the pain signal.62
However, there is no evidence to suggest that corticosteroids
affect the natural history of disk regression.
On the other hand, anesthetic agents act by blocking so-
dium channels, which then inhibit firing of neurons. Like
corticosteroids, they generally block small-diameter C fibers
more readily than A fibers.58 Additionally, lidocaine im-
proves blood flow and reduces endoneurial pressure in the
dorsal root ganglion, thus reducing what is thought to be part
of the pathogenic changes in herniated nucleus pulposus.63
The contraindications to epidural steroid injections in-
clude known hypersensitivity to the drugs, local or systemic
infection, local malignancy, or bleeding disorders. The ad-
verse effects of the drugs themselves are broad, but, in gen-
eral, short-term use poses far fewer complications than does
long-term use. However, corticosteroids may mask signs of
infection by causing immunosuppression; alter electrolyte
levels, blood pressure or fluid balance; aggravate peptic ulcer
disease; suppress the adrenal axis; precipitate avascular ne-
crosis or osteoporosis; and induce psychosis. Local anesthet-
ics may cause cardiac depression, malignant hyperthermia,
and hypersensitivity. If the anesthetic agent is unintention-
ally injected into the intravascular space, severe mental status
changes, seizures, respiratory arrest, and even death may
occur.58,64
The complications of the procedure depend on the ap-
proach to the injection. Generally, serious risks are the fol-
Lumbar disk herniation
lowing: dural puncture or subarachnoid injection, which
may cause spinal leak and a postural headache, or serious
toxicity from the medications as noted earlier; infection in-
cluding epidural abscess;65 bleeding with resultant hema-
toma; bladder dysfunction from prolonged local anesthetic
blockade; and neurologic complications of direct injury to
spinal nerves. More common side effects include vasovagal
reaction, minor bleeding, and local tissue damage.58
Because the range of success of epidural steroid injections
is very broad, efforts have been made to identify cases that are
more likely to respond to these injections. Patients with sub-
acute radicular leg pain or chronic pain with no prior surgery
are more likely to respond to steroid injections than patients
with chronic pain and prior lumbar spine surgery.66
Another factor that seems to lend toward success with
epidural steroid injections is the use of fluoroscopy and se-
lective procedures. Studies have shown that only 60% of
injections done without fluoroscopy by experienced physi-
cians are placed correctly.67 On the other hand, studies done
with fluoroscopy show high rates of accuracy, lower rates of
failure, and lower risks of complications.68 Specifically, trans-
foraminal epidural steroid injections seem to be meeting with
greater levels of success. Reported positive outcomes with
this method range in the 70% to 85% success rates.69,70
Not surprisingly, complications of the transforaminal flu-
oroscopically guided approach are fewer. In a study by
Botwin et al71 in 2000, 322 such injections were performed.
The complications included nonpositional headaches, in-
creased back pain, leg pain, facial flushing, vasovagal reac-
tion, and increased blood sugar. No dural punctures oc-
curred. The overall incidence of minor complications was
9.6%, and all complications resolved without morbidity.
Even in patients who are surgical candidates, treatment
with corticosteroid injections can be a successful alterna-
tive. In 2000, a study by Riew et al72 showed that among
patients with lumbar radicular pain and radiographic ev-
idence of nerve root compression who were ready to go to
surgery, epidural injection of steroid and anesthetic was
very successful. In fact, 20 of 28 patients who received this
treatment chose not to continue on to surgery. On the
other hand, only 9 of 27 patients who received epidural
injection of anesthetic alone chose to cancel surgery.72
Another study in 2004 compared epidural steroid injec-
tions to diskectomy in patients with large lumbar disk
herniations. Although diskectomy resulted in more defin-
itive relief, epidural steroid injections were effective for 3
years in nearly one half of patients who had not had prior
improvement with conservative care.73
Overall, although still a controversial topic, epidural ste-
roid injections may be of benefit to patients with radicular
pain whose symptoms do not improve with more conserva-
tive management. Although not as definitive a treatment as
diskectomy, they may serve as a low-risk alternative to sur-
gery in patients with lumbar disk herniation. However, the
role of steroid injections is not to replace physical activity and
therapy; rather, steroids serve to control pain so that patients
can work with therapists on their biomechanics and improve
their functional outcomes.
119
Conclusions
In summary, various elements of the history and physical
examination are essential in establishing the diagnosis of a
symptomatic lumbar disk herniation. Although imaging
studies are useful, it is important to acknowledge that they
cannot replace the clinical picture because the high rate of
asymptomatic disk herniations can be misleading. The
proper nonsurgical treatment of herniated nucleus pulposus
revolves around controlling symptoms to strengthen patients
and restore their function, and it may involve any combina-
tion of oral medications, physical therapy, therapeutic mo-
dalities, and corticosteroid injections. However, it is essential
that the treatment be catered to the individual patient be-
cause nonspecific treatments are unlikely to result in positive
outcomes and may only serve to the detriment of our pa-
tients.
References
1. Herring SA, Weinstein SM: Assessment and nonsurgical management
of athletic low back injury, in Nicholas JA, Hershman EB (eds): The
Lower Extremity and Spine in Sports Medicine. St. Louis, Mosby, 1995,
pp 1171-1197
2. Kaul M, Herring SA: Rehabilitation of lumbar spine injuries, in Kibler
WB, Herring SA, Press JM, et al (eds): Functional Rehabilitation of
Sports and Musculoskeletal Injuries (ed 1). Gaithersburg, MD, Aspen
Publishers, 1998, pp 188-215
3. Boden SD, Davis DO, Dina TS, et al: Abnormal magnetic-resonance
scans of the lumbar spine in asymptomatic subjects. J Bone Joint Surg
Am 72:403-408, 1990
4. Bruske-Hohlfeld I, Merritt JL, Onofrio BM, et al: Incidence of lumbar
disc surgery. A population-based study in Olmsted County, Minnesota.
Spine 15:31-35, 1990
5. Marshall LL, Trethewie ER, Curtain CC: Chemical radiculitis. Clin Or-
thop Relat Res 129:61-67, 1977
6. Kawakami M, Weinstein JN, Spratt KF, et al: Experimental lumbar
radiculopathy. Immunohistochemical and quantitative demonstrations
of pain induced by lumbar nerve root irritation of the rat. Spine 19:
1780-1794, 1994
7. Franson RC, Saal JS, Saal JA: Human disc phospholipase A2 is inflam-
matory. Spine 17:S129-S132, 1992(suppl)
8. McCarron RF, Wimpee MW, Hudkins PG, et al: The inflammatory
effect of nucleus pulposus. A possible element in the pathogenesis of
low-back pain. Spine 12:760-774, 1987
9. Kawakami M, Tamaki T, Hayashi N, et al: Mechanical compression of
the lumbar nerve root alters pain-related behaviors induced by the
nucleus pulposus in the rat. J Orthop Res 18:257-264, 2000
10. Bottcher J, Petrovitch A, Soros P, et al: Conjoined lumbosacral nerve
roots: Current aspects of diagnosis. Eur Spine J 13:147-151, 2004
11. Deyo RA, Loeser JD, Bigos SJ: Herniated lumbar intervertebral disk.
Ann Intern Med 112:598-603, 1990
12. Farfan FH, Cossette JW, Rebertson GH, et al: The effects of torsion in
the lumbar intervertebral joints: The role of torsion in the production of
disc degeneration. J Bone Joint Surg Am 52:468-497, 1970
13. Adams MA, Hutton WC: Prolapsed intervertebral disc: A hyperflexion
injury. Spine 7:184-191, 1982
14. Akmal M, Kesani A, Anand B, et al: Effect of nicotine on spinal disc
cells: A cellular mechanism for disc degeneration. Spine 29:568-575,
2004
15. Young S, Aprill C, Laslett M: Correlation of clinical examination char-
acteristics with three sources of chronic low back pain. Spine J 3:460-
465, 2003
16. Deyo RA, Rainville J, Kent DL: What can the history and physical
examination tell us about low back pain? JAMA 268:760-766, 1992
120
17. O’Neill CW, Kurgansky ME, Derby R, et al: Disc stimulation and pat-
terns of referred pain. Spine 27:2776 –1781, 2002
18. Akuthota V, Willick SE, Harden RN: The adult spine: A practical ap-
proach to low back pain, in Rucker KS, Cole AJ, Weinstein SM (eds):
Low Back Pain, A Symptom-Based Approach to Diagnosis and Treat-
ment (ed 1). Boston, MA, Butterworth-Heinemann, 2000, pp 15-39
19. Donelson R, Silva G, Murphy K: Centralization phenomenon. Its use-
fulness in evaluating and treating referred pain. Spine 15:211-213,
1990
20. Donelson R, Aprill C, Medcalf R, et al: A prospective study of central-
ization of lumbar and referred pain. A predictor of symptomatic discs
and annular competence. Spine 22:1115-1122, 1997
21. Vroomen PC, de Krom MC, Knottnerus JA: Diagnostic value of history
and physical examination in patients suspected of sciatica due to disc
herniation: A systematic review. J Neurol 246:899-906, 1999
22. Geraci MC, Alleva JT, McAdam FB: Physical examination of the spine
and its functional kinetic chain, in Cole AJ, Herring SA (eds): Low Back
Pain Handbook (ed 2). Philadelphia, PA, Hanley and Belfus, 2003, pp
69-93
23. McRae DL: Asymptomatic intervertebral disc protrusions. Acta Radiol
46:9-27, 1956
24. Wiesel SW, Tsourmas N, Feffer HL, et al: A study of computer-assisted
tomography. I. The incidence of positive CAT scans in an asymptom-
atic group of patients. Spine 9:549-551, 1984
25. Hitselberger WE, Witten RM: Abnormal myelograms in asymptomatic
patients. J Neurosurg 28:204-206, 1968
26. Borenstein DG, O’Mara JW, Boden SD, et al: Value of magnetic reso-
nance imaging of the lumbar spine to predict low-back pain in asymp-
tomatic subjects. J Bone Joint Surg Am 83:1306-1322, 2001
27. Adams MA, Hutton WC: Gradual disc prolapse. Spine 10:524, 1985
28. Maigne JY, Rime B, Deligne B: Computed tomographic follow-up study
of forty-eight cases of nonoperatively treated lumbar intervertebral disc
herniation. Spine 17:1071-1074, 1992
29. Bozzao A, Gallucci M, Masciocchi C, et al: Lumbar disc herniation: MR
imaging assessment of natural history in patients treated without sur-
gery. Radiology 185:135-141, 1992
30. Teplick JG, Haskin ME: Spontaneous regression of herniated nucleus
pulposus. AJR Am J Roentgenol 145:371-375, 1985
31. Pearce J, Moll JMH: Conservative treatment and natural history of acute
lumbar disc lesions. J Neurol Neurosurg Psychiatry 30:13-17, 1967
32. Rozenberg S, Allaert FA, Savarieau B, et al: Compliance among general
practitioners in France with recommendations not to prescribe bed rest
for acute low back pain. Joint Bone Spine 71:56-59, 2004
33. Deyo RA: Early diagnostic evaluation of low back pain. J Gen Int Med
1:328-338, 1986
34. Schofferman J: The use of medications for low back pain, in Cole AJ,
Herring SA (eds): Low Back Pain Handbook (ed 2). Philadelphia, PA,
Hanley and Belfus, 2003, pp 133-150
35. Piperno M, Hellio le Graverand MP, Reboul P, et al: Phospholipase A2
activity in herniated lumbar discs. Clinical correlations and inhibition
by piroxicam. Spine 22:2061-2065, 1997
36. Van Tulder MW, Scholten RJ, Koes BW, et al: Non-steroidal anti-
inflammatory drugs for low back pain. Cochrane Database Syst Rev
2:CD000396, 2000
37. Mazanec D: Medication use in sports rehabilitation, in Kibler WB,
Herring SA, Press JM, et al (eds): Functional Rehabilitation of Sports
and Musculoskeletal Injuries (ed 1). Gaithersburg, MD, Aspen Publish-
ers, 1998, pp 71-78
38. Borenstein DG, Korn S: Efficacy of a low-dose regimen of cyclobenza-
prine hydrochloride in acute skeletal muscle spasm: results of two
placebo-controlled trials. Clin Ther 25:1056-1073, 2003
39. Basmajian JV: Acute back pain and spasm. A controlled multicenter
trial of combined analgesic and antispasm agents. Spine 14:438-439,
1989
40. Press JM, Livingston BP: The effective use of rehabilitation modalities,
in Kibler WB, Herring SA, Press JM, et al (eds): Functional Rehabilita-
tion of Sports and Musculoskeletal Injuries (ed 1)., Gaithersburg, MD,
Aspen Publishers, 1998, pp 79-84
L. Shahbandar and J. Press
41. Gnatz SM: Increased radicular pain due to therapeutic ultrasound ap-
plied to the back. Arch Phys Med Rehabil 70:493-494, 1989
42. Weber H: Lumbar disc herniation—A controlled, prospective study
with ten years of observation. Spine 8:131-140, 1983
43. Saal JA, Saal JS: Nonoperative treatment of herniated lumbar interver-
tebral disc with radiculopathy. An outcome study. Spine 14:431-437,
1989
44. Donelson R, Grant W, Kamps C, et al: Pain response to sagittal end-
range spinal motion. A prospective, randomized, multicentered trial.
Spine 16:S206-S212, 1991(suppl)
45. Alexander AH, Jones AM, Rosenbaum DH Jr: Nonoperative manage-
ment of herniated nucleus pulposus: Patient selection by the exten-
sion sign. Long-term follow-up. Orthop Rev 21:1136-1140, 1992
46. Sufka A, Hauger B, Trenary M, et al: Centralization of low back pain and
perceived functional outcome. J Orthop Sports Phys Ther 27:205-212,
1998
47. Werneke M, Hart DL: Centralization phenomenon as a prognostic fac-
tor for chronic low back pain and disability. Spine 26:758-764, 2001
48. Werneke M, Hart DL: A descriptive study of the centralization phe-
nomenon. A prospective analysis. Spine 24:676-683, 1999
49. Wetzel FT, Donelson R: The role of repeated end-range/pain response
assessment in the management of symptomatic lumbar discs. Spine
3:146-154, 2003
50. Kopp J, Alexander AH, Turocy RH, et al: The use of lumbar extension
in the evaluation and treatment of patients with acute herniated nu-
cleus pulposus. A preliminary report. Clin Orthop Relat Res 202:211-
218, 1986
51. Snook S, Webster B, McGorry RW, et al: The reduction of chronic
nonspecific low back pain through the control of early morning
lumbar flexion. A randomized controlled trial. Spine 23:2601-2607,
1998
52. Snook S, Webster B, McGorry RW: The reduction of chronic nonspe-
cific low back pain through the control of early morning lumbar flex-
ion: 3-year follow-up. J Occup Rehabil 12:13-19, 2002
53. Williams MM, Hawley JA, McKenzie RA, et al: A comparison of the
effects of two sitting postures on back and referred pain. Spine 16:
1185-1191, 1991
54. Green LN: Dexamethasone in the management of symptoms due to
herniated lumbar disc. J Neurol Neurosurg Psychiatry 38:1211-1217,
1975
55. Coomes EN: A comparison between epidural anaesthesia and bed rest
in sciatica. BMJ 5218:20-24, 1961
56. Knutsen O, Ygge H: Prolonged extradural anaesthesia with bupivacaine
at lumbago and sciatica. Acta Orthop Scand 42:338-352, 1971
57. Dilke TF, Burry HC, Grahame R: Extradural corticosteroid injection in
management of lumbar nerve root compression. BMJ 2:635-637, 1973
58. Dreyer SJ, Dreyfuss P, Cole A, et al: Injection procedures, in Cole AJ,
Herring SA (eds): The Low Back Pain Handbook (ed 2). Philadelphia,
PA, Hanley and Belfus, 2003, pp 277-295
59. Bush K, Cowan N, Katz DE, et al: The natural history of sciatica asso-
ciated with disc pathology. A prospective study with clinical and inde-
pendent radiologic follow-up. Spine 17:1205-1212, 1992
60. Bush K, Hillier S: A controlled study of caudal epidural injections of
triamcinolone plus procaine for the management of intractable sciatica.
Spine 16:572-575, 1991
61. Samanta A, Samanta J: Is epidural injection of steroids effective for low
back pain? BMJ 328:1509-1510, 2004
62. Johansson A, Hao J, Sjolund B: Local corticosteroid application blocks
transmission in normal nociceptive C-fibres. Acta Anaesthesiol Scand
35:335-338, 1990
63. Onda A, Yabuki S, Kikuchi S, et al: Effects of lidocaine on blood flow
and endoneurial fluid pressure in a rat model of herniated nucleus
pulposus. Spine 26:2186-2191, 2001
64. Knight CL, Burnell JC: Systemic side-effects of extradural steroids.
Anaesthesia 35:593-594, 1980
65. Chan ST, Leung S: Spinal epidural abscess following steroid injection
for sciatica. Case report. Spine 14:106-108, 1989
66. Berman AT, Garbarino JL, Fisher SM, et al: The effects of epidural
Lumbar disk herniation
injection of local anesthetics and corticosteroids on patients with
lumbosciatic pain. Clin Orthop Relat Res 188:144-151, 1984
67. Renfrew DL, Moore TE, Kathol MH, et al: Correct placement of epi-
dural steroid injections: Fluoroscopic guidance and contrast adminis-
tration. Am J Neuroradiol 12:1003-1007, 1991
68. El-Khoury GY, Ehara S, Weinstein JN, et al: Epidural steroid injection:
A procedure ideally performed with fluoroscopic control. Radiology
168:554-557, 1988
69. Lutz GE, Vad VB, Wisneski RJ: Fluoroscopic transforaminal lumbar
epidural steroids: An outcome study. Arch Phys Med Rehabil 79:1262-
1366, 1998
70. Vad VB, Bhat AL, Lutz GE, et al: Transforaminal epidural steroid injec-
121
tions in lumbosacral radiculopathy: A prospective randomized study.
Spine 27:11-16, 2002
71. Botwin KP, Gruber RD, Bouchlas CG, et al: Complications of fluoro-
scopically guided transforaminal lumbar epidural injections. Arch Phys
Med Rehabil 81:1045-1050, 2000
72. Riew KD, Yin Y, Gilula L, et al: The effect of nerve-root injections on the
need for operative treatment of lumbar radicular pain. A prospective,
randomized, controlled, double-blind study. J Bone Joint Surg Am
82:1589-1593, 2000
73. Butterman GR: Treatment of lumbar disc herniation: Epidural steroid
injection compared with discectomy. A prospective, randomized
study. J Bone Joint Surg Am 86:670-679, 2004