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FIG. 28-4. Sagittal view discography in a 46-year-old man
with low back pain. Note nor mal cotton ball–type images at
L3-L4 and L4-L5, whereas there is abnormal spread of contrast in the L5-S1 disc. (Cour tesy of Dr. Kaj Tallroth, Orton
Hospital, Helsinki, Finland.)
CHAPTER 28/LUMBAR DISC DISORDERS / 303
TABLE 28-4. Summar y of position statement of Nor th
American Spine Society Diagnostic and Therapeutic
Committee on lumbar discography
Lumbar discography can be used in select cases such as:
• When there is persistent pain with suspicion of disc
abnormality, and noninvasive tests have not provided
sufficient diagnostic information.
•To determine whether discs within a proposed fusion
segment are symptomatic, and whether adjacent discs
are asymptomatic.
• In patients who have undergone previous spine surgery,
but with nonremitting significant pain, to differentiate
between postoperative scar and recurrent disc herniation.
•To investigate the condition of a disc within, or adjacent
to, a fused spinal segment, to better delineate the source
of symptoms.
•To confirm a contained disc herniation, possibly requiring
minimally invasive discectomy.
Modified from Guyer RD, Ohnmeiss DD. Lumbar discography position statement from the North American Spine Society Diagnostic and Therapeutic Committee. Spine 1995;20:
2048–2059, with permission.
Internal disc disruption has been postulated to be an
important cause of low back pain, and a taxonomy has
been established by the International Association for the
Study of Pain (Table 28-5) (34). The clinical usefulness
and interpretation of discography is, however, controversial (33,62–69). In particular, it has been observed that
discographic pain reports are not only related to anatomic
abnormalities within the disc, but also to scores on the
Minnesota Multiphasic Personality Inventory (MMPI)
(70), somatization disorder, compensation issues, and
abnormal results on psychological testing (69). Thus, it
would seem mandatory to perform psychological testing
on any patient undergoing discography with interpretation of pain provocation, particularly if the discography
procedure is used for preoperative evaluation. Even
though discography may be problematic for clinical decision making, studies performed with discography have
considerably widened the horizons for understanding
mechanisms of low back pain and the locations of pain
generators within the spine (62,64), including intricate
mechanisms of pain radiation (65).
FIG. 28-5. Sagittal and anteroposterior discography views in
a 36-year-old woman with low back pain. There is slight
abnormal spread of contrast at the L3-L4 level, with more
severe degeneration in the two lowermost discs, as seen by
the widespread distribution of contrast. (Cour tesy of Dr. Kaj
Tallroth, Orton Hospital, Helsinki, Finland.)
TABLE 28-5. Inter national Association for the Study of
Pain (IASP) taxonomy for internal disc disr uption
The pain should be reproduced on provocation discography
Computed tomography/discography should reveal internal
disc disruption
As a control, stimulation of at least one other disc should
fail to reproduce the pain
From Schwarzer AC, Aprill CN, Derby R, et al. The prevalence and clinical features of internal disc disruption in
patients with chronic low back pain. Spine 1995;20:
1878–1883, with permission.
304 /SECTION V/SPECIFIC CLINICAL ENTITIES
NONOPERA TIVE TREATMENT
Types and Results
For treating lumbar disc disorders, a profusion of alternative therapies are available to the clinician, as is often
the case when there is a lack of more precise knowledge
regarding etiology and pathophysiology. The clinician
may, however, obtain support in the choice of therapies
from several recentl y published guidelines, and the mainstay of any treatment protocol should be to try to adhere
to such guidelines whenever possible (11,28–32,39).
With an increasing shift to self-management strategies
that empower patients to participate in decisions in their
care (27,71,72), all patients should be provided with basic
information regarding course and prognosis (Table 28-6).
However, the mainstay of any treatment protocol should
be to try to keep the patient active and to try to influence
an often wide array of perceived functional limitations in
daily activities and at work. The principal goal is to continue normal daily activities (27). Table 28-7 presents
some main principles that will guide the clinician in the
treatment of patients with lumbar disc disorders and nonspecific low back pain. Prolonged low back pain and disability will usually require a well-organized multidisciplinary rehabilitation program (82), even if there is
presently a lack of knowledge regarding the optimal content of such programs (83) (e.g., whether any specific
type of exercise has any specif ic physical effect or not)
(84). In one study on multidisciplinary rehabilitation of
patients with chronic low back pain, the most important
variable for determining a successful treatment outcome
was the reduction of subjective feelings of disability,
whereas treatment outcome was not predicted by variables such as medical background, medical diagnosis,
physical impairment, or physical v ariab les such as mobil-
TABLE 28-6. Some clinically relevant facts regarding the
course and prognosis of nonspecific low back pain
It is very common, in fact, it may be considered abnormal
to live a single year without a backache (73).
Recovery from an acute spell of low back pain is generally
rapid (74).
It is not an acute disease that can be cured, but once
established, a chronic problem with intermittent
exacerbations (1).
After 1 year 10%–45% still suffer from low back pain
(75,76). In about one third the pain may still be disabling
at 1 year (77).
Only about 2% remain on sick leave after 1 year (76).
Recurrences are common and have been reported in about
40% within 6 months (78) and about 75% within 1 year
(75).
Even though recurrences are common, both pain and
disability are usually less severe during such recurrences
(75).
Once low back pain has become chronic, pain intensity and
physical functioning improve only little after 1 year (79).
TABLE 28-7. Main principles for managing lumbar disc
disorders
Neither sick leave nor inactivity will benefit recovery from
low back pain (27).
To prevent adverse effects of fear avoidance beliefs, a
principal goal should be the continuation of normal daily
activities (27,80,81). Advice to stay active often leads to
shorter periods of work loss and fewer recurrences, in
comparison with traditional medical treatment (39).
Chronic cases will benefit from multidisciplinary
rehabilitation programs (27).
Traditional biomedical education, based on an injury model,
will not reduce future low back pain, nor work loss (39).
Lumbar belts or supports do not reduce work-related low
back pain, nor work loss (39).
With respect to persistent symptoms and disability, and the
response to treatment and rehabilitation, individual and
work-related psychosocial factors play a key role (39).
Workers’ own beliefs that their low back pain was caused
by work, and their own expectations about inability to
return to work, should be monitored, because they are
important prognostic factors (39).
Most workers will be able to continue working, or can return
to their ordinary work, within a few days or weeks, and do
not need to wait until they are completely pain free (39).
The longer a worker is away from work, the lesser the
chance of returning to work. For example, it has been
shown that if a worker is off work for 4–12 weeks, the
estimated risk of still being off work at 1 year is
10%–40%. With work absence of 1–2 years chances to
return to any type of work are near nil (39).
With protracted work absence, treatments become
ineffective for returning people to work, even though the
treatments may still produce some clinical improvement
(39).
ity, strength, endurance, or physical performance (82).
There are several available validated condition-specific
(19,85–93) and generic (94–97) functional disability
scales that may be used for assessing outcome. It is
important to remember, however, that disability is multifactorial (52,98).
With respect to the choice of treatment program, there
is presently insufficient evidence to justify intensive and
expensive programs, which are likely to be less costeffective (39). In the treatment protocol, the role of the
workplace and work-related factors should not be overlooked, since recent studies suggest that a close association between clinical care and occupational intervention
may produce superior results to other treatment protocols, particularly in patients with subacute work-related
low back pain (99). However, there is a need for more
detailed information on the role of various risk factors for
the various phases of work-related disability (100).
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CHAPTER 29
Facet Joint Denervation: A Minimally Invasive Treatment for Low Back Pain in Selected Patients
David J. Hall
It is accepted that the lumbar zygapophyseal joints (facet
joints) are a potential source of low back and referred leg
pain. However, as a clinical entity, facet syndrome remains ill-defined and hence the extent and signif icance
of its contribution in disabling low back pain is a subject
of ongoing debate. Nevertheless, it is possible to identify,
through diagnostic testing, a very select group of patients
that can be successfully treated by percutaneous radiofrequency facet joint denervation.
BACKGROUND
Although Goldthwait (1), in 1911, is credited as the
first to recognize the lumbar facet joint as a potential
source of back and leg pain, it was Ghormley (2), in
1933, who first coined the term “f acet syndrome.” However, their theories focused more on the facet joint exerting mechanical pressure on nerves as the origin of symptoms.
Later, in 1971, Rees (3,4) published his work on multiple bilateral subcutaneous rhizolysis, where he reported
a technique of denervation of the posterior spinal structures, including the facet joints, merely by the sweep of a
Beaver blade and claimed apparently successful treatment in 998 out of 1,000 consecutively treated patients.
Following up on Rees’ work, Sheal y (5) initiall y e xperimented with Rees’ technique but encountered problems
with hematomata in several patients that led him to the
use of a radiofrequency lesioning device under fluoroscopy guidance. Mooney (6) was impressed by his
observations of Shealy’s technique and was stimulated,
along with Robertson (7), to undertake their important
work in an attempt to provide more scientific evidence of
the facet joint as a source of back pain. In their study,
injection of the zygapophyseal joints in normal volun-
teers induced both back and referred leg pain and, moreover, they found that the pain could be obliterated by
injection of local anesthetic into the same joints.
Accordingly, the concept of the facet joint block as a
diagnostic test was born. Since then there have been
numerous studies exploring the utility of facet joint injections as both a diagnostic and therapeutic tool in the treatment of low back pain; it is fair to say that there have
been widely varying results (8–16). Nevertheless, injection of local anesthetic into lumbar facet joints or at their
nerve supply is accepted as a diagnostic test of facet joint
pain and it was a natural progression to explore facet joint
denervation procedures in the hope of providing longerlasting and perhaps permanent relief of facet joint pain
(6,17–26). In order to refine techniques of facet joint
denervation there was a renewed interest in anatomic
studies to improve the understanding of innervation of
lumbar spine structures and, in particular, to precisely
map the afferent nerve supply of the facet joint (18,
26–30).
ANATOMY
The major afferent nerve supply to the facet joint is
provided by the medial branch of the posterior primary
ramus. The medial branch descends from the posterior
primary ramus over the base of the transverse process in
a groove at the root of the superior articular process,
which is bridged by the mamillo-accessory ligament (Fig.
29-1). The mamillo-accessory ligament is formed by a
condensation of the intertransverse ligament f ibers passing from the mamillary body to the transverse process
and occasionally it is ossified. After passing under the
bridge of the mamillo-accessory ligament, the medial
branch courses across the lamina deep to multifidus and
307
308 /SECTION V/SPECIFIC CLINICAL ENTITIES
FIG. 29-1. A sketch of a dorsal view of the branches of the
left lumbar dorsal rami. Mamillo-accessor y ligaments (mal)
have been left in situ covering the L1 and L2 medial
branches. A, articular branches; ib, inter mediate branch; ibp,
intermediate branch plexus; lb, lateral branch; m, medial
branch; is, interspinous branch, zj, zygapophyseal joint.
(From Bogduk N.The innervation of the lumbar spine. Spine
1983;8(3):289.)
finally enters the muscle. Deep to the muscle it sends
fibers innervating the caudal portion of the facet joint
immediately abo ve before sending fibers to the facet joint
below.
Paris (29) proposed a greater multiplicity in afferent
supply to the facet joint. In particular, he described an
ascending facet branch that passed to the posterior aspect
of the facet joint one level above, and throughout its
course was entirely intramuscular and did not lie on any
bony structures. He also suggested a more proximal origin of branches to multifidus and theorized that they
would contain accessory afferent supply to the facet
joints. However, this description of the anatomy, and in
particular the ascending facet branch, could not be verified by Bogduk in his anatomical dissections (18,26–30).
The existence of an intramuscular ascending facet joint
branch infers a “triple innervation” of the facet joints
where a single medial branch supplies the adjacent facet
joint and the joints above and below. However, there is
broader acceptance of the “dual innervation” as proposed
by Bogduk where the medial branch supplies its adjacent
facet joint and the joint immediately below. There is
agreement throughout the literature that the medial
branch of the posterior primary ramus is constant and is
fixed adjacent to the bone in the region of the mamilloaccessory ligament. There is no evidence of nerve fibers
crossing the midline so that facet joints on each side have
a unilateral innervation.
PATHOLOGY
In the majority of cases the cause of lumbar facet joint
pain is not known. Although facet joint osteoarthritis is a
relativel y common occurrence, it is rare to find other definite recognizable pathology affecting the zygapophyseal
joint such as systemic inflammatory arthropathy, facet
joint fracture, or infection (6,7,15,31–34). Exclusion of
such disorders is important, leaving osteoarthritis, which
has been proposed as a cause of facet joint pain. Interestingly, it has been demonstrated that facet joint degeneration almost invariably follows disc degeneration at the
same level and, accordingly, degenerative changes within
the facet joint rarely, if ever, exist in isolation (32–34). In
spite of this, a study by Schwarzer (12), evaluating
patients by provocative discography and facet joint
blocks, concluded that it was rare to suffer symptomatic
disc degeneration in combination with symptomatic facet
joints.
DIAGNOSIS
Although most clinicians recognize a clinical presentation, which is presumed attributable to facet joint pain,
there is no literature to support any pathognomonic historical, physical examination or imaging findings associated with lumbar facet joint syndrome (6,9,11,14,15,16,
19,31). Typically, it is thought that facet joint pain is
aggravated b y rest in any posture and is relie v ed by movement. The pain may be unilateral or bilateral in the lower
back, with or without radiation to the lower limbs.
Radiculopathy is absent and the pain should not radiate
below the knee. Morning stiffness ma y be associated with
a stooped posture on rising; lumbar extension is the
movement most likely to aggravate symptoms. Despite
the consistency of this description throughout the literature, clinical features have not proved to be predictive of
the response to diagnostic facet joint blockade (13–16).
Facet joint injections form part of the investigative
armamentarium when evaluating patients with nonradicular low back pain who have failed to respond to appropriate nonoperative management, including an exercise
program, and in whom there are no sinister features
of alternative underlying pathology. Lumbar facet joint
injections, combined with the use of intra-articular corticosteroids, have been used as both a diagnostic and therapeutic modality. However, their use remains controversial (7,8,10,11,15). As a therapeutic option, some authors
have found facet joint injections to be of no use, whereas
at best the injections may pro vide temporary relief of sufficient duration to allow resolution of symptoms by natural processes or through an appropriate rehabilitation
program.
A series of studies undertaken by Bogduk and associates have shown that targeted medial branch blockade is
a valid diagnostic test in the evaluation of facet joint pain
(12,13,16). Indeed, from a technical viewpoint, medial
branch block is more easily performed than facet joint
injections and there is less prospect of diffusion of the
local anesthetic to involve surrounding str uctures, which
may confound the response.
In addition, differential blocks undertaken on separate
occasions using local anesthetic agents with different
pharmacologic properties and durations of action have
been able to exclude false-positive results (13). Based on
these studies and others where the placebo response is
controlled, facet joint pain is thought to ha v e a pre v alence
of up to 40% in chronic nonradicular low back pain
(14,15).
If facet joint pain is accepted as a significant contributor in disabling low back pain, then it follows that facet
joint denervation may provide long-term or even permanent relief of symptoms attributable to the facet joints.
Facet joint denervation is appealing given the accessibility of the facet joint and, more particularly, the medial
branch of the posterior primary ramus, which has a constant course adjacent to an easily identifiable bony landmark.
Bearing this in mind, when investigating a patient for
consideration of radiofrequency denervation, it is logical
that a medial branch block is a more appropriate diagnostic tool than facet joint block because it directly evaluates the structure scheduled for ablation.
TECHNIQUE
The original technique described by Shealy (5) targeted the electrode lateral to the midpoint of the facet
joint and then swept the electrode in a cephalad and caudad direction so that there were three electrode positions
for each joint covering the lateral aspect of the facet joint.
The following modified technique is recommended in
view of improved anatomic knowledge.
Under sterile conditions with the patient lying prone
over a pillow to reduce the lumbar lordosis, on a radiolucent operating table, the levels to be denervated are
located by antero-posterior (AP) fluoroscopy. The target
point (i.e., the base of the transverse process where it
meets the root of the superior articular process) is marked
on the skin (Fig. 29-2). A puncture site is marked a cen-
CHAPTER 29/FACET JOINT DENERVATION / 309
FIG. 29-2. Antero-poster ior radiograph of lumbar spine illustrating target points for medial branch neurotomy. The target
points lie exactly at the tip of either the arrows at L1, L2, and
L5, or the guide needles at L3 and L4. Note, at the L3 and L4
levels, how the silhouette of the superior ar ticular process
overlaps the target point, demonstrating why electrodes
should be introduced obliquely. The overhanging superior
articular process protects the target point in a dorsoventral
approach.The guide needles are indicating the target points;
however, a more caudal entry point is now recommended in
order to allow introduction of the electrode more or less parallel to the respective medial branches at L4 and above. On
the right side of the figure the courses of the medial
branches of the dorsal rami have been superimposed.(From
Bogduk N, Long DM. Percutaneous lumbar medial branch
neurotomy: a modification of facet denervation. Spine 1980;
5:196.)
timeter or two lateral and caudal to the target point for the
L1 to L4 levels. (The L5 le v el is treated differently owing
to the different anatomy, and is described in the following.) The lateral and caudal entry point is chosen to prevent deflection of the probe from the target at the base of
the transverse process by the overhanging superior articular process and the bulging mamillary process. Because
it has been shown that the uninsulated portion of the
probe produces a radial spread of the lesion that does not
extend beyond the tip of the electrode, a more caudal
approach is chosen to allow the introduced probe to lie
nearly parallel to the target nerve so that the nerve is more
likely to be encompassed by the radial spread of the
lesion (35). The L5 dorsal ramus courses in the groove
between the ala and the superior articular facet of S1 and
can be approached in a more sagittal direction with the
probe laying parallel to the dorsal primary ramus proper
as it hooks over the sacrum. The intended puncture sites
310 /SECTION V/SPECIFIC CLINICAL ENTITIES
are anesthetized using Lignocaine 1% down to the level
of the deep fascia, being careful not to anesthetize deep
around the facet joint, which may interfere with nerve
conduction and patient response.
An 11 blade is used to puncture the skin before inser-
1
tion of 3
⁄2-inch, 14-gauge Shiley needles with trocars
under AP fluoroscopy. The Shiley needle is advanced
until it is blocked by the base of the transverse process,
which obviates the need for lateral fluoroscopy to check
the depth of placement. The trocar is removed and the
blunt-tipped electrode is introduced via the Shiley needle,
which can be used to steer the electrode. The transverse
process is palpated easily and the electrode is then
directed in a cephalad and medial direction so that it slips
off the transverse process into the intertransverse space.
The probe is then gradually withdrawn so that the uninsulated portion lies at the root of the superior articular
process, more or less parallel to the course of the medial
branch. At L5, as mentioned, the probe comes to lie in a
more sagittal direction in the groove on the superior
aspect of the ala, adjacent to the superior articular facet
and is parallel to the posterior primary ramus proper.
Antero-posterior fluoroscopy is used to confirm the position of the tip of the electrode.
A stimulation mode can be used to confir m that the
electrode tip is properly positioned adjacent to the medial
branch of the posterior primary ramus and away from the
anterior primary ramus. At 2 Hz, motor stimulation may
occur and if twitching of the lower limb muscles is
observed, the probe should be withdrawn to a more posterior position. At 100 Hz, a sensory response is elicited
in the posterior primary ramus, which may produce pain
or tingling similar to the presenting symptoms. However,
the sensory response is not diagnostic and this step
should not be necessary because the symptomatic levels
should have been identified by prior medial branch
blockade.
After satisfactory placement of the electrodes, lesions
are made with a radiofrequency generator; the electrode
tip temperature is raised to 80°C for 90 seconds. During
the production of the lesion, the patient should be awake
and cooperative in order to alert the surgeon as to the
development of an y radicular symptoms that w ould necessitate repositioning the lesioning electrode. Usually the
patient experiences an exacerbation of back pain that
reaches a crescendo and then settles as the lesion is completed. The neurolo gic status is checked immediatel y postoperatively. The procedure is undertaken on an outpatient
basis with minimal or no sedation and the patient is
allowed to return to nor mal activity as symptoms permit.
To date only three randomized controlled trials
(20,22,24) have been published evaluating the effect of
radiofrequency lumbar facet joint denervation in chronic
low back pain. However, the studies are not directly comparable because they each used either different diagnostic
criteria or different surgical technique.
In 1994, Gallagher (20) included 60 patients who were
judged on clinical grounds to have symptoms of lo w back
pain suggestive of facet joint origin. Forty-one patients
reported improvement or w ere equi vocal in their response
following injection of local anesthetic into and around the
facet joints that were thought to be appropriate. Those
patients were randomized to undergo either radiofrequency facet joint denervation or a sham procedure using
the invalidated technique of Shealy. Nevertheless, relief
of symptoms was noted in patients who had a clear
improvement following facet joint injections compared to
patients who were equivocal in their response to the
injections. The results were evaluated at 1 and 6 months
and were statistically significant.
Van Kleef (22), in 1999, reported results in 31 patients
with chronic low back pain selected on the basis of pain
relief following diagnostic blockade of the medial branch
of the posterior primary rami. The technique of lesion
production was similar to the modified technique as
described in the preceding text, although the approach
was more from a posterolateral oblique direction than the
more caudal oblique approach, as promoted by Bogduk
(35). At least 50% pain relief following medial branch
blockade was required to be eligible to enter the study
and then patients were randomized to undergo radiofrequency lesioning or a sham procedure. Interestingly, in
the final analysis, the results were superior in patients
who reported complete relief of pain with diagnostic
nerve blocks compared to those with only partial relief of
pain. Statistical analysis at 3, 6, and 12 months following
treatment showed significant improvement in pain and
functional disability in the treatment group.
In 2001, Leclaire (24) published results examining a
larger sample size of 70 patients but a shorter follow-up of
only 3 months and reported no significant improvement in
the treatment group compared to the sham group. Howev er,
it is noteworthy that patients were included in the study
based on their response to intra-articular facet joint injections rather than diagnostic medial branch blockade.
COMPLICATIONS
There have been no serious complications associated
with the procedure apart from transient radiculopathy and
the report of a skin burn through poor earthing (5,19–25).
RESULTS
Since the introduction of radiofrequency denervation
of the facet joint by Shealy (5), the technique has been
modified and used with varying results (6,17,18–26).
CONCLUSION
It is apparent that there exists a very select group of
patients with disabling low back pain that can be attrib-
CHAPTER 29/FACET JOINT DENERVATION / 311
uted to the facet joints and may be successfully treated b y
facet joint denervation.
The careful use of diagnostic medial branch blockade
is the critical factor in patient selection for facet joint
denervation. Meticulous attention to detail through the
use of differential medial branch blockade is required to
accurately identify a highly selected group of patients
who may respond to radiofrequenc y denerv ation. Following recommended protocols is a tedious process that may
test the patience of the clinician (not to mention the
patient) and may explain the paucity of high-quality studies and the widely varying results published in the literature. Despite a plethora of literature dealing with anatomy
and experimental studies, evaluating the facet joints as a
potential source of pain, there is an extremely narrow e vidence base of high-quality clinical studies examining the
utility of radiofrequency denervation of the facet joints.
In particular, there is a single study (22) that employed
the theoretical best practice methods of patient selection,
accurate lesioning technique, and rigorous scientific
methodology that showed signif icant alleviation of pain
and functional disability in a select group of patients both
on a short- and long-term basis following radiofrequency
denervation.
There are many factors that may lead to failure of the
technique, including the technical adequacy of diagnosis
by medial branch block and the adequacy of subsequent
radiofrequency medial branch neurotomy. Additionally,
there is always the question of alternate symptomatic
pathology and, in particular, symptomatic disc degeneration because disc degeneration has been shown to always
coexist with facet joint degeneration. It has been postulated that late resurgence of symptoms may be associated
with nerve regeneration, in which case repeat procedures
may be indicated after re-evaluation. Nevertheless, the
minimally invasive technique of radiofrequency facet
joint denervation is appealing given the accessibility of
the medial branch of the posterior primary ramus and the
reassurance that the reporting of complications from the
procedure is virtually nonexistent.
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13. Schwarzer AC, Aprill CN, Derby R, et al. The false-positive rate of
uncontrolled diagnostic blocks of the lumbar zygapophyseal joints.
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14. Schwarzer A, Wang S, Bogduk N, et al. Pre v alence and clinical features
of lumbar zygapophyseal joint pain: a study in an Australian population with chronic low back pain. Ann Rheum Dis 1995;54:100–106.
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branch blocks to anesthetize the zygapophysial joint: a physiologic
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CHAPTER 30
Intradiscal Electrothermal Therapy
Jeffrey A. Saal and Joel S. Saal
The treatment of chronic discogenic low back pain presents one of the most difficult challenges to the spine specialist. Nonoperative measures are frequently unable to
reduce pain and improve function in this patient subgroup
(1, 2). Interbody fusion for these patients has yielded
mixed and often poor results (3–5). An alternative therapy to address this problem is therefore desirable. The
SpineCATH system (Smith & Nephew, Inc., Largo, FL)
to perform intradiscal electrothermal therapy (IDET) was
developed to address this difficult clinical dilemma.
Patients with chronic lumbar pain fall into two clinical
categories: chronic recurrent and chronic persistent.
Chronic recurrent patients have multiple pain flares with
varying durations of 2 weeks to 3 months. Many patients
within this group will begin to have more frequent recurrences with fewer pain-free intervals as time passes.
Chronic persistent patients have persisting symptoms that
do not abate and last longer than 3 months. The disc has
been shown to be the pain source in the majority of
patients with chronic symptoms (6). Carey et al. recently
reported that patients who do not experience a resolution
of their back pain within 3 months of onset had a poor
prognosis for further recovery. When the patients were
assessed at 22 months they continued to have persisting
complaints of low back pain and were dissatisf ied with
their outcomes (1). Von Korff reported that although 80%
of patients had resolution of their acute low back pain in
12 weeks, 60% of the patients experienced recurrent
symptoms (2). These recent studies underline the fact that
chronic low back pain does not necessarily have a favorable prognosis and that the long held truth that 90% of
patients will experience resolution of their back pain
within 6 to 12 weeks is incorrect and misleading.
PATHOPHYSIOLOGY OF INTERNAL DISC
DERANGEMENT
The natural history of the degenerating disc includes
loss of nuclear hydrostatic pressure, which leads to buck-
ling of the annular lamellae. This phenomenon leads to
increased focal segment mobility and increased shear
stress to the annular wall. The process progresses to
delamination and fissuring of the annular wall. Annular
delamination has been shown to occur as a separate and
distinct event from annular fissures (7). Fissures can be
radial or concentric. In addition, electron microscopy has
demonstrated micro “fractures” of collagen fibrils with
disc degeneration. The progressive degeneration of the
disc, manifested by any of these morphologic changes,
has been shown to alter disc mechanics (8).
Tearing and delamination of the annulus can cause
chronic pain. Mechanoreceptors in the disc have been
shown to discharge with disc mobilization (9). Nociceptive tissue has been shown to be sensitized resulting in a
decrease in their firing threshold after treatment with
inflammatory enzymes and mediators (10–12).
A scenario for chronic discogenic pain is created when
any combination of annular fissures, delamination, or
microfractures of collagen fibrils leads to mechanical
distortion of annular lamellae and subsequent sensitization of nociceptors that may have also been presensitized
by PLA2 (13), nitrous oxide (14, 15), interleukin 1 (15),
and metalloproteinase enzyme activity (15), or other
chemical mediators. Af ferent stimuli produce substance P
release and nociception. Repetitive stimulation of the
dorsal root ganglion (DRG) has been shown to create
prolonged neural activity from the dorsal horn receptor
fields (10,16,17). As the patient continues to load the
disc, the neuronal activity continues. Clinically, the disrupted disc will often cause referral pain into the buttocks
and leg due to DRG stimulation or from direct chemical
irritation of the nerve roots.
A combination of mechanical and neural properties
creates an interplay that leads to chronic discogenic pain.
A high-intensity zone (HIZ) on the T2 of the magnetic
resonance (MR) image has been shown to correlate with
a pain-producing fissured disc 65% to 95% of the time
(18–20). However, MRI predicts the presence of annular
312