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Presented at the McKenzie Conference, Ottawa,
Canada, August 2001
A
Clinical Classification of Lumbar Discogenic Pain
Its Relationship to the McKenzie Classification
Jean-Yves Maigne, MD, Physical Medicine, Hotel-Dieu Hospital, 75181
Paris Cedex 04, France |
The intervertebral disc appears to be the most frequent
source for low back pain. But as the disc is a complex structure, different
type of pain syndromes should arise from this structure, all labelled
“discogenic pain”. This paper is aimed to try to differentiate these pain
syndromes and to classify them on a clinical basis. Sciatic (or radicular)
pain, which is a well known and documented topic will not be discussed here,
this paper dealing only with pain in the lumbar area.
The background data are both anatomical and clinical.
From an anatomic point of view, the disc is not only a shock absorber, as it
is often written down. Bogduk considers that structurally and mechanically,
the anulus resembles a ligament. This dual function open the way to a new
reflection on discogenic pain (see below).
Clinically, certain signs or symptoms are regarded as
evoking disc pathology: mechanical pain provoked by a heavy lift or any
unusual physical activity, guarded lumbar movements or pain worsened by
coughing.
It should also be reminded that there is no gold standard
for discogenic pain. Plain X-ray films only show non specific aspects of the
degenerating (or aging) process, which is almost as frequent in patients as
in asymptomatic persons. Provocation discography is controversial. Some
claim that it is the only way to identify a symptomatic disc. Schwartzer et
al have studied 92 patients with low back pain. Among them, 39% had a
particular entity called “internal disc disruption”, consisting in the
association of low back pain and a radial fissure within the anulus becoming
painful at injection. These authors were unable to find a specific
examination sign among these patients. On the other hand, other researchers
point out that discography can be positive even in patients with pain
obviously not discal in origin or psychologically distressed (see Carragee
et al). Furthermore, this is an invasive procedure with a septic risk. MRI
could be more specific, when exhibiting subchondral changes around the disc,
evoking an inflammatory process (as described by Modic), but this is a rare
situation.
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A clinical classification of
discogenic pain
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Identifying all the patients whose pain arises from the
disc appears to be an impossible task. But some clinical syndromes are
frequent and could be linked with experimental observations. These syndromes
could also interestingly be compared with the McKenzie classification in its
three syndromes, the postural, derangement and dysfunction syndromes.
1)
Dehydration of the nucleus
If a slow (within years) dehydration process appears as a
normal feature of the aging disc, dehydration appearing after a loading in
certain position could be not so well tolerated. Adams et al demonstrated
that after a creep loading of 3 hours in the sitting posture, peaks of
stress concentration appeared within the anulus, which were potentially
aggressive for the free nerve endings of the anulus and endplates, therefore
a source for pain. Adams suggested the term “flat tyre syndrome”.This is a
frequent situation, where patients experience low back pain following
remaining static for a long time in an end position, such as sitting on a
bad seat or, for example, vacuuming (excessive lumbar flexion) or standing
up and marking time (excessive lumbar extension). This situation was
described by Troisier, under the name of “lombalgie de la position extreme”
(low back pain related to an end position) and matches perfectly with the
postural syndrome described by McKenzie, where pain is produced by position,
not by movements, where activity relieves the pain and where clinical
examination is normal.
2)
Mechanical lesions of the anulus
If, according to Bogduk, one consider the anulus as a
ligament, a traumatic rupture of some of its collagen fibres could be
likened to a “discal sprain” (Maigne, 1992). Pathologic studies have
identified three different type of annular fissures. Rim lesions, or
transversal fissures, are a post-traumatic rupture of the fibres attaching
on the vertebral rim. Radial fissures are most often located in the postero-lateral
region of the disc. They also appear as the result of a traumatic lesion
(bending and axial torsion). Circumferential tears can result from torsion
or enzymatic (i.e. degenerative) process. It is also frequent to examine
patients whose low back pain appeared immediately (within 24 hours) after an
abnormal physical task: heavy lift, false movement or any demanding physical
activity. At examination, the pain is reproduced by forward bending, a
feature which may indicate that ruptured annular collagen fibres are
stretched. In the majority of cases, the pain resolves within two months,
indicating a healing process.In case of a radial tear, the fissure provides
a track for nuclear material. If that material enter the fissure (a
condition depending upon its size, location and mechanism), it may reach the
peripheral layers of the disc (disc hernia causing sciatica) or remain
entrapped into the anulus (lumbago, characterised by a list without
radicular pain or disc herniation). In both cases, the pressure applied on
the walls of the fissure could account for the deformity or deviation in
flexion which is frequently observed. This condition could correspond to the
derangement syndrome described by McKenzie. According to this author, the
derangement syndrome occurs more frequently in men between 20 to 55 yrs of
age and is elicited by a single severe strain, or a less severe strain
applied more frequently, or a sustained flexion strain (the most common).
Interestingly, McKenzie notes that reduction of derangement often provide
immediate and lasting relief from pain, indicating that there is no
inflammatory component (i.e. it is a purely mechanical problem) and, a
personal view, that there is a spontaneous healing of the lesion.
3) Inflammatory
lesion of the disc
It is now well admitted that the so-called “mechanical”
back pain have an inflammatory component. Inflammatory cells and
pro-inflammatory enzymes or breakdown products have been found in the disc.
Some inflammatory changes in the vertebral end-plates can be showed by MRI
in certain cases and NSAIDs can improve the patients. Inflammation is more
or less present in many cases of painful degenerated disc. Efficacy of
NSAIDs could be a convenient criteria for inflammation. There is a condition
described by Revel, and called “discopathie destructrice rapide” (rapid
degrading discopathy). It is defined by low back pain related to a rapid
narrowing of the disc space (more than 50% in less than 2 years, a
degradation not seen in controls). Revel noticed that NSAIDs were more
efficient in this condition than in other forms of low back pain (even if
this efficacy was partial and if NSAIDS were unable to stop the process).
More recently, we have described a subgroup of low back pain patients where
a 10 day course of oral steroids was able to make signs and symptoms
disappear as soon as the 3rd day of treatment in 70% of the
cases, thus confirming that inflammation here play the primary role. It
should be underlined that oral steroids are deemed inefficient in low back
pain and thus contra-indicated by the guidelines. The features of this
syndrome are: 1- pain occurring spontaneously (without any traumatism),
worse in the second half of the night (the patient being often woken up at
4-5 in the night by the pain), with stiffness in the morning, and 2- pain
worsened by lumbar extension (at the end range), the flexion being quite
free. Some minor criteria may also be commonly found: partial efficacy of
NSAIDs (followed by a relapse after the treatment) and failure or
impossibility of a manipulative therapy (because the lumbar spine is locked
and no cracking sound can be heard). Surprisingly, 90% of the patients are
females between 30 and 60 years of age. We have some arguments to
incriminate the disc, that will not be developed here.
These conditions should be paralleled with the McKenzie
dysfunction syndrome. In this syndrome, pain often commence without any
apparent reason (which is a characteristic of inflammation). McKenzie says
that the pain is felt at the end range of certain ordinary movements. He
notes that there is stiffness in the morning, loosening as the day
progresses. As time passes, flexion and extension become reduced and the
morning stiffness does not pass. Often the patient states that he feels
better when he is active and moving about than when at rest. All these
features are typical of inflammation and resemble our own description.
McKenzie does not speak of inflammation, but of an adaptive shortening and
resultant loss of mobility causing pain prematurely (before achievement of
full normal end range movement). We think that in some cases, it could be
another way of description of an identical phenomenon, the patient
restricting his/her motion by fear of pain. Here, a confirmation could be
brought by a better issue of physical therapy with a concomitant treatment
of NSAIDs.
References
Adams M, McMillan DW, Green TP, Dolan P. Sustained
loading generates stress concentration in lumbar intervertebral discs. Spine
1996;21:434-8
Bogduk N, Twomey LT. Clinical anatomy of the lumbar
spine. Churchill Livingstone, ed 2, Melbourne, 1991
Maigne JY.
Classification des lesions discales lombaires. Rev Med
Orthop 1992;30:5-8
McKenzie R. The lumbar spine. Mechanical diagnosis and
therapy. Spinal publication. 1998
Troisier
O.Sémiologie et traitement des lesions discales et ligamentaires du rachis.
Ed Masson 1973
Revel M. La
discopathie destructrice rapide. Rev Med Orthop
1990 ;20 :19-22
Schwarzer A,
Aprill C, Derby R Fortin J, Kine G, Bogduk N. The prevalence and clinical
features of internal disc disruption in patients with chronic low back pain.
Spine, 1995:1878-83.
