Low back pain
Summary of a research paper Michael Kosasih
Allegri, M., Montella, S., Salici, F., Valente, A., Marchesini, M., Compagnone, C., ... & Fanelli, G. (2016). Mechanisms of low back pain: a guide for diagnosis and therapy. F1000Research, 5.
Background
Low back pain (LBP) is the most common musculoskeletal condition seen amongst adults (up to 84% prevalence). The authors state that chronic low back pain (CLBP) has well-defined underlying pathological causes and that it is a disease, not a symptom. Diagnosing patients with LBP can be challenging, requiring complex clinical reasoning and decision-making. The authors argue that finding the pain generator involves careful examination of several structures and that a diagnosis not based on a specific pain generator can lead to therapeutic mistakes.
Aim
To provide a clinical guide to help identify pain generators based on anatomical understandings, which will direct therapists towards correct diagnoses and treatment approaches.
LBP epidemiology
CLBP prevalence:
15-45% in French healthcare workers
13.1% in US for people aged 20-69 y/o
5.91% in Italy
The prevalence of acute & CLBP in adults doubled in the last decade and continues to increase dramatically in the aging population among all ethnic groups and genders
Based on a 2006 review, total costs associated with LBP in the US exceeded $100 billion/year with two-thirds attributed to lost wages and reduced productivity
Looking for the pain generator
Identifying the source of pain is essential in selecting appropriate treatment
LBP symptoms can originate from many different sources including nerve roots, muscle, fascial structures, bones, joints, discs and abdominal organs
Important to consider the influence of psychological factors on LBP
According to the authors, scans are only necessary if there is an unclear aetiology, neurological deficits or other medical conditions
American College of Radiology recommends no imaging for LBP within the first 6 months unless red flags are present
Imaging findings are poorly related to symptoms – i.e. pathology often does not always equal pain!
Recent guidelines state that clinicians should carefully determine the mechanisms that sustain acute/chronic pain. Treatment must then be tailored to these specific mechanisms
Anatomy of the low back
The spine is designed to be strong in order to protect the spinal cord and nerve roots. However, it is also highly flexible to permit mobility in many different planes. The authors go on to describe basic anatomy of the vertebral column and spinal cord.
Pathophysiology of spinal pain
Central sensitisation occurs in several chronic pain disorders, including LBP, temporomandibular disorders, OA, fibromyalgia, headaches and lateral epicondylalgia. It is characterised as an increase in excitability of neurons within the CNS, resulting in normal inputs producing abnormal responses. Tactile allodynia and spreading of pain hypersensitivity are attributed to central sensitisation.
Type of spinal pain according to pain generator
The authors argue that most LBP is incorrectly considered to be non-specific and of an unknown cause. They say that muscle tension and spasm are the most common causes of LBP. Other causes are outlined below.
Pain generator
Description
Radicular pain
Radicular pain = pain travels along the nerve root without neurological deficits. This pain is caused by ectopic discharges originating from an inflamed or lesioned dorsal root or its ganglion. Pain typically radiates from the back and buttock into the leg along a dermatomal distribution. The most common cause is disc herniation, with inflammation of the affected nerve (instead of compression) is the most common pathophysiological process.
It is different to radiculopathy. Radiculopathy is not necessarily associated with pain & impairs conduction along a spinal nerve or nerve root, resulting in either dermatomal or myotomal deficits – both can lead to impaired reflexes. These disorders can occur simultaneously or independently of each other.
Facet joint (FJ) syndrome
FJs have many free & encapsulated nerve endings which activate nociceptive afferents and are also modulated by sympathetic efferent fibres. FJ pain accounts for up to 30% of CLBP with nociception originating in the synovial membrane, hyaline cartilage, bone or fibrous capsule. Patients usually present with or without pain referred to legs (terminating above the knee), often radiating to the thigh/groin, and without radicular patterns. Pain is off-centre and pain is worse in the back than the leg. Back stiffness primarily present in the morning. Aggs – hyperextension, rotation, lateral flexion & uphill walking; standing up after waking or prolonged rest.
7 features of FJ pain:
Older age
Hx of LBP
Normal gait
Maximal pain with Lx extension
Pain not aggravated with Valsalva manoeuvre
Lack of leg pain
Lack of muscle spasm
Sacroiliac joint (SIJ) pain
The SIJ is a common source of pain amongst CLBP patients. Pain may arise from ligamentous or capsular tension, extraneous compression or shear forces, hypermobility, altered joint mechanics or kinetic chain dysfunction causing inflammation. Intra-articular sources – OA; extra-articular sources – ligament sprain or primary enthesopathy. During the physical exam, it is important to assess the movement of the joint (e.g. with a stress test consisting of pressing down on the iliac crest) which may reproduce the pain. SIJ pain must be considered in cases where patients complain of postural LBP aggravated with sitting & postural changes. It’s also possible that SIJ pain is often associated with FJ pain as both are related to postural issues.
Lumbar spinal stenosis (LSS)
Can develop due to scar tissue after spinal surgery, disc herniation, ligament hypertrophy or hypertrophy of articular processes. Most cases are degenerative, associated with age-related changes. It involves gradual narrowing of the spinal canal resulting in compression of neurovascular structures. Normal spinal canal diameter = 15-27mm; diameter in LSS = <10mm. Common symptoms – midline back pain, radiculopathy with neurologic claudication, motor weakness, paraesthesia & sensory impairments. Eases – trunk flexion, sitting, stooping or lying; but these eases can become less effective as condition progresses. Aggs – prolonged standing, lumbar extension & walking downhill. Most useful findings are age, radiating leg pain exacerbated by standing/walking & pain cessation when seated, positive stoop test.
Discogenic pain
Symptoms of disc degeneration (DD) are aspecific, axial & without radicular radiation. They occur in the absence of spinal deformity or instability. The pathology involves degradation of the nucleus pulposus with fissures in the annulus fibrosis. DD is often a diagnosis of exclusion among other types of CLBP.