Why does acute back pain become chronic?BMJ 1997; 314 doi: https://doi.org/10.1136/bmj.314.7095.1639 (Published 07 June 1997) Cite this as: BMJ 1997;314:1639
Chronic back pain is not the same as acute back pain lasting longer
- Malcolm I V Jayson, Professora
- a Rheumatic Diseases Centre and Manchester and Salford Back Pain Centre, University of Manchester, Hope Hospital, Salford M6 8HD
Acute episodes of back pain are remarkably common. There is a high natural remission rate, with about 90% of cases resolving within six weeks.1 For patients with simple backache–acute onset of pain in the back without nerve root symptoms or signs of serious spinal pathology–bed rest is indicated only if the patient is in great pain and unable to stand or walk, and should be only for a short period. Analgesia and early physical activation improve the rate of recovery and allow early return to work.2
Despite these optimistic findings the prevalence of chronic or recurrent back problems is high–present in up to 39% of adults.3 Much effort is expended searching for a specific organic diagnosis such as a herniated lumbar spine, annular tears, spinal stenosis, or spondylolisthesis. But in the vast majority of cases it is impossible to identify the source of the pain. Patients may show limitation of spine movements, radiological spondylosis, facet joint osteoarthritis, or signs of disc degeneration and protrusion on magnetic resonance imaging. However, these commonly identified features have only weak correlations with the presence of back pain.
Extensive epidemiological studies have demonstrated little or no correlation between back problems and inherited factors, height, weight, deformity (unless gross), spinal movements, muscle strength, or radiological signs of disc degeneration. Much more important are cardiorespiratory disease, smoking, psychological morbidity, poor work conditions, social class, education, and income.4 In particular, studies in people not suffering from back pain show that potent predictors of future episodes of back pain include previous back pain, neck pain and other musculoskeletal pain, numbers of children (in men as well as women), work dissatisfaction, and psychiatric morbidity.5
There is increasing evidence that vascular damage plays a fundamental role in the pathogenesis of mechanical back pain. Degenerative disc disease is associated with atherosclerosis and spinal artery stenosis, and the degrees of disc degeneration and obliteration of the anastomotic arteries surrounding the disc are associated with increased vascularity in the annulus fibrosus.6 The correlations between back pain and cardiovascular disease and smoking support a possible role for arterial disease. Disc degeneration and protrusion are associated with pressure on the epidural venous plexus, leading to venous dilatation, oedema of the nerve root, perineural and intraneural fibrosis, and neuronal atrophy.7 Venous compression can occur at two or more levels in the spine, leading to isolated segments of poor perfusion.8 An inflammatory response is often observed in relation to mechanical spine damage.9 Pathological studies show that the local tissue reaction to herniated nuclear material seems to be due to endothelial proliferation, vascular dilatation and activation, and collagen proliferation,10 with pain fibres within this proliferating vascular tissue. These changes are not readily identifiable in life but, nevertheless, clearly offer the potential for pain production and also relate to the epidemiological associations with vascular disorders.
Some patients develop back and lower limb pain associated with hyperaesthesia, hyperpathia (excessive pain experienced from a minor noxious stimulus), allodynia (pain generated by minor stimulation of the skin), and vasomotor changes in the lower limbs with sensitivity to cold. The clinical features suggest sympathetically maintained pain, otherwise known as reflex sympathetic dystrophy. The sympathetic chains run down the sides of the vertebral columns, anastomosing with sympathetic fibres around and within the spine and intervertebral disc.
Involvement of the sympathetic system has long been recognised in patients with back problems and particularly in patients who have undergone failed spinal surgery. Altered vascular perfusion in the lower limbs, thought to be due to sympathetic dysfunction, is found in 80% of patients with sciatica and 69% of patients with low back pain.11 Sympathetic blocks with local anaesthetic may provide temporary relief of symptoms, and this technique is often used as a diagnostic test for sympathetically maintained pain. Unfortunately, surgical sympathectomy seems to provide only short term relief. Recent work suggests that sympathetically maintained pain may arise from altered central neuromodulation within the spinal cord, and sympathetic syndromes of this sort form part of the complex regional pain syndrome.
Peripheral injury increases excitability of the central nervous system. Within the dorsal horn, stimulation of peripheral pain fibres causes increased activity with prolonged periods of discharge, so that patients continue to feel pain long after the physical cause of the pain has healed. The dorsal horn cells develop increased sensitivity to afferent impulses. As a result, the patient experiences pain and tenderness that is disproportionate to the evidence of peripheral tissue damage, giving rise to the phenomena of hyperpathia and allodynia. The dorsal horn receptor fields may expand so that pain is felt over a much wider area than the damage to pain fibres would predict.12
This mechanism within the dorsal horn helps to explain why many people experience increased sensitivity to minor stimulation and pain that is persistent, disproportionate to the degree of tissue damage, and widespread. This type of pain is usually identified by comparison with the normal contralateral limb. However, if the syndrome affects both lower limbs, the diagnosis is difficult and clinical acumen is paramount.
We are now beginning to study central perception of back pain within the brain itself. Studies of patients with atypical facial pain in whom no specific cause or abnormality can be identified have shown abnormal activation of the cingulate region of the brain,13 and similar studies are currently ongoing in patients with chronic back problems. Altered central neuromodulation within the brain and spinal cord provide a mechanism for integrating physical and psychological influences and are likely to be directly relevant to the altered prognosis associated with psychological disorders.
The assessment of chronic back problems is changing rapidly. Patients should have a careful assessment for specific lesions causing pain. In some this may include intravenous enhanced computerised tomography or magnetic resonance imaging to identify vascular problems. A careful clinical history and examination, supplemented by psychological screens for depression and abnormal somatic perception as well as a pain drawing, will identify the patients in whom psychological influences and central neuromodulation should be considered. We now realise that, for many patients, chronic back pain is not the same as acute back pain lasting longer.