Clinical Classification of Lumbar Discogenic Pain
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.
A clinical classification of discogenic pain
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.
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