Updates & Features
Chronic Low Back Pain (cLBP): What are we Talking About?
May 2019
Dr Emilio Quetglas, The PainSolve Team
Chronic low back pain (cLBP) symptoms can derive from many potential anatomic sources, such as nerve roots, muscle, fascial structures, bones, joints, intervertebral discs, and even organs within the abdominal cavity. Furthermore, symptoms can also spawn from aberrant neurological pain processing causing neuropathic LBP.1,2 Additionally, LBP can also be influenced by psychological factors.3
It is now becoming clearer that the cause of cLBP is a combination of genetically-based susceptibility factors in the nervous and immune systems, as well as local pathological risk factors. Due to its heterogeneity, cLBP may not just be one, but several distinct conditions – a conclusion that one can easily reach if the approach to cLBP is mechanistically driven and considered before initiating a symptom-oriented treatment.4
LBP (acute or recurrent, predominantly) is generally still considered to be non-specific, as seen in around 70% of cases.5 Of course, it is true that the spine is composed of structures such as muscles, tendons, ligaments, and fascias, which are all able to generate pain, although in these cases a myofascial trigger component can be found in the absence of any other finding. Among others, discogenic pain (or pain due to disc degeneration), which has traditionally been considered as non-specific cLBP due to misdiagnosis, reaches a prevalence between 26–42% (Table 1), and is due to the degradation of the nucleus pulposus matrix with accompanying radial and/or concentric fissures in the anulus fibrosus.6 The typical patient history is of pain in the centre of the lower back with minimal radiation, usually to one or both buttocks. Pain may be reduced with extension and is better with standing and lying flat. The pain is often described as a deep, dull ache. There is often tightness in the paraspinal and gluteal muscles. Pain is often worsened with sitting/driving, lumbar flexion, bending, twisting, Valsalva manoeuvre, and coughing. Increased intrathecal and intradiscal pressures are believed to play a role.7 Smokers, the obese, those with jobs requiring prolonged sitting, and those with physical jobs, especially with repetitive lifting and vibration exposure, are at increased risk of discogenic LBP and lumbar disc disease.8–10 Pain being nociceptive in its origin can lead to internal disc disruption and the appearance of radicular pain.
Table 1: Estimated prevalence of cLBP conditions
| cLBP entity | Prevalence (%) |
| Non-specific LBP | 70 |
| Specific cLBP | 30 |
| Discogenic pain | 26–42* |
| Radicular pain | 4 |
| Radiculopathy | 1.8 |
| Facet joint syndrome | 15–45 |
| Spinal stenosis | 3 |
| Spondylodiscitis | 0.003 |
| Ankylosing spondylitis | 2 |
| Cancer pain | 0.9 |
| Others (congenital, trauma, etc.) | 7.5 |
*Actually diagnosed as non-specific LBP
Facet joint syndrome can also be confounded as a non-specific cLBP, but finds its mechanism in the lumbar zygapophyseal joints, the posterior articular process of the lumbar column. They are supplied by the medial branches of the dorsal rami. These joints have a large amount of free and encapsulated nerve endings that activate nociceptive afferents and that are also modulated by sympathetic efferent fibres.11,12 Lumbar zygapophyseal or ‘facet’ joint pain has been estimated to account for up to 30% of cLBP cases.13 Diagnosis of facet joint syndrome is often difficult and requires a careful clinical assessment and an accurate analysis of radiological exams. Patients usually complain of LBP with or without somatic referral to the legs terminating above the knee, often radiating to the thigh or to the groin. There is no radicular pattern. Back pain tends to be off-centre and the pain intensity is worse than the leg pain; pain increases with hyperextension, rotation, lateral bending, and walking uphill. It is exacerbated when waking up from bed or trying to stand after prolonged sitting. Finally, patients often complain of back stiffness, which is typically more evident in the morning.14,15
Last but not least, another erroneous diagnostic of non-specific cLBP is the sacroiliac joint (SIJ) syndrome. The SIJ syndrome is well recognised as a source of pain in many patients who present with cLBP.16,17 It is thought that pain could be generated by ligamentous or capsular tension, extraneous compression or shear forces, hypermobility or hypomobility, altered joint mechanics, and myofascial or kinetic chain dysfunction causing inflammation.18 It can also be a source of somatic referred pain, due to the noxious stimulation of nerve endings within the SIJs. SIJ syndrome can mimic sciatica from nerve root compression, and it is known as sciatica-like syndrome.19 Patients are more often female, have shorter stature, a shorter duration of symptoms, and more commonly have pain radiating to the groin and a history of a fall on the buttocks.18
Having clarified these confusing concepts, it can be assumed that the prevalence of non-specific cLBP can be reduced dramatically through the application of a detailed examination and an accurate diagnosis. In between other etiologies of specific cLBP, other than those discussed later in more detail, trauma can be seen, which can include: nociceptive, inflammatory and neuropathic components; skeletal irregularities and congenital anomalies of the spine; inflammatory diseases or infections (including osteoarthritis and rheumatoid arthritis as well as spondylitis, obviously with a main inflammatory component); cancer with an important inflammatory or neuropathic component, depending on allocation; osteoporosis fragility fractures, in which the nociceptive component plays a major role; Paget’s disease of bone and others.
Radicular pain evoked by ectopic discharges emanating from an inflamed or lesioned dorsal root or its ganglion; generally, the pain radiates from the back and buttock into the leg in a band only 2–3 cm wide (only following a dermatomal distribution for C4 and S1).20, 21 Disc herniation is the most common cause, and inflammation of the affected nerve rather than its compression is the most common pathophysiological process. It is not only a discharge in nociceptive afferents, it is due to a heterospecific discharge in the nerve.
Radiculopathy is yet another, distinct entity.22 It is a neurological state in which conduction is blocked along a spinal nerve or its roots. When sensory fibres are blocked, numbness is the symptom and sign. When motor fibres are blocked weakness ensues. Diminished reflexes occur as a result of either sensory or motor block. The numbness is dermatomal in distribution and the weakness is myotomal. However, radiculopathy is not defined by pain; it is defined by objective neurological signs.
Lumbar spinal stenosis (LSS) can be congenital or acquired (or both).23 It can be determined by inflammatory/scar tissue after spine surgery, or even in absence of previous surgery by disc herniation, thickening of the ligaments, or hypertrophy of the articular processes.24 The majority of cases of LSS are degenerative, related to changes in the spine with aging.25 LSS is determined by a progressive narrowing of the central spinal canal and the lateral recesses and consequent compression of neurovascular structures.26 The most frequent symptoms of LSS are midline back pain, radiculopathy with neurologic claudication, motor weakness, paresthesia, and impairment of sensory nerves.27 Symptoms may have a different distribution depending on the type of LSS. Trunk flexion, sitting, stooping, or lying can all ease the discomfort, while prolonged standing or lumbar extension can aggravate the pain. Sitting or lying down become less effective in alleviating pain as the condition progresses, and rest pain or a neurogenic bladder can develop in severe cases.28,29 Neurogenic claudication pain is the classical symptom of LSS, caused by venous congestion and hypertension around nerve roots. Pain is exacerbated by standing erect and by downhill ambulation but alleviated with lying supine more than prone, sitting, squatting, and lumbar flexion.30,31
Conclusion
In conclusion, cLBP still triggers a certain amount of confusion, probably contained in the term itself because tries to compile several heterogeneous conditions, different in their pathophysiology, clinically and, in terms of management, under the same entity. Perhaps this is too simplistic an approach, only justified by the common location of all these conditions in the spine.
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