Literature Review for Rehabilitation of Chronic Low Back Pain:

Knowledge of yoga has traditionally passed directly from teacher to student without documentation. ‘Light On Yoga’ by BKS Iyengar (1966) is the definitive text for Iyengar Yoga providing basic illustrations and lay instructions. Further details are contained in the publications of respective Iyengar Yoga associations throughout the world. Instructions illustrating use of props for remedial work is in Mehta and Mehta SM&S with whom the author studied for several years. Extensive subjective and anecdotal claims are made for the rehabilitative qualities of Iyengar yoga but with scant scientific validation. Nevertheless, yoga stretching and strengthening practices are used in back rehabilitation.

The biomechanics of the lumbar spine is covered extensively in Kapandji and Hartley. Pathology related to the biomechanics is provided by Corrigan and Maitland (1998) and Maitland (2002). Prentice places more emphasis on acute rather than chronic injury but offers a useful range of rehabilitation exercises. Laughlin (1998), Schatz and Key are aimed at the lay reader providing accessible illustrated accounts of biomechanics and pathology whilst referring to yoga in the process of rehabilitation of chronic low back pain.

Prentice argues that back pain from an acute injury usually lasts less than three weeks. Pain that lasts longer than six weeks is usually due to re-injury or continued stresses causing the original injury (Prentice p277). Long-term chronic back pain is usually out of proportion to a related injury is probably largely psychological becoming dissociated from any physical cause and associated with emotional distress or depression (Prentice, p278). Maitland decrees a clear aetiology for low back-pain is rare and there is no identifiable pathology for many patients (Maitland 2002). Treatment in these cases needs to be related to symptoms rather than diagnosis (Maitland et al 2002). McKenzie places more importance on the ability to diagnose the importance of the condition.

Chronic low back pain can originate from visceral, vascular and psychological disorders but sports therapists are limited in their ability to reduce low back pain in these cases. This paper and the training package is therefore concerned primarily with chronic back pain originating from mechanical sources that may be influenced by postural, strength and flexibility training. All texts reviewed referred to the importance of the condition of the intervertebral discs, facet joints and surrounding muscle and soft tissue in the health and mobility of the lumbar spine although there is conjecture concerning relative importance of these respective structures. Chronic low back pain in most cases is thought to be mechanical with the intervertebral disc as the most likely cause of pain (Schwarzer) although most minor back pain is mostly caused by muscle and ligament strains that diminish without treatment (Murtagh 1983, p. 322). The outer region of the annulus fibrosis is innervated (Coppes et al). Discs are mobile and resilient in early life losing their mobility in later life when they have little recuperative powers when damaged (Maitland p190). Paradoxically most people over thirty years old have degeneration in their vertebral structures but few have chronic back pain (Laughlin, 1989). Pathology may be benign but it serves as a causal explanation if back problems subsequently occur (Laughlin 1989). In a study reported by Vernon, the correlation between spinal joint dysfunction and pain was ‘mild to moderate’. Loeser notes the observation of nerves, muscles or joints cannot prove or disproving the presence of pain.

The space between adjoining vertebrae is narrowed as disc height is lost resulting in the surrounding structures pressing on spinal nerves as they exit the spinal cord. Disc degeneration is associated with sciatica, spondylosis, vertebral instability, isolated disc resorption, acute cauda equina syndrome and juvenile disorder (Corrigan & Maitland p47). Material from a prolapsed disc often projects through the posterior wall of the annulus to be restrained by the posterior longitudinal ligament. If the ligament ruptures the disc material may compress the nerve root. This can produce back pain and leg pain although it can remain asymptomatic (Corrigan and Maitland p 47). The appearance of the degenerated disc remains normal so early detection is difficult (Corrigan and Maitland). Pain occurs when the annulus containing neural fibres begin to tear and is perceived as a deep, dull ache, (Coppes et al, 1990; Bogdtik and Tworney, 1991). Pain is initially local but refers more widely particularly to the buttocks. It is relieved by rest and irritated by forward flexion.

The disc is able to absorb and dissipate compressive forces because of its gel like nucleus and the containment of nutritious fluid absorbed from surrounding structures facilitated by spinal movements. The load on areas in the spine varies with posture, structure and musculature and affects the health of the discs. Pressure within the discs is less when standing than in sitting and less with normal lordosis than with a straight or kyphotic back. Pressure on the discs when standing is 30% lower than when sitting favouring yoga posture performed standing. Lying down puts least pressure on the discs that is half of that when sitting (Nacheinson and Morris1964; Corrigan & Maitland p 15). The greatest risk to injury to the discs is compression especially with rotation with added risk when lifting heavy objects (Bogduk and Tworney, 1991).

The synovial facet joints are reinforced by a fibrous capsule and ligaments. They stabilise the spine protecting the intervertebral discs from shear forces caused by excessive flexion, extension and rotation (Hartley p3). Injury to the facet joints will affect the function of intervertebral discs. Conversely, injury to the discs will lead to dysfunction of the facet joints. Facet joints can degenerate independently of the disc and be a source of chronic low back pain often precipitated by minor trauma. However, most facet joint problems are associated with disc degeneration where loss of disc space causes joint impingement. The facet joints normally protect the disc from rotational stress but cannot do so when impacted with loss of disc height. This in turn causes compression and facet joint degeneration (Corrigan and Maitland).

Muscle tension may contribute to back pain especially when tension is held in muscle tissue around a previous injury. Back pain associated with the facet joints is irritated by back extension, lateral flexion with extension and hyperextension, prolonged sitting, standing or rest. Flexion may offer relief (Corrigan & Maitland p72). Mobilisation, postural and back exercises are indicated (Corrigan Maitland p73). Muscle tension increases as a protective mechanism around the site of a trauma to limit movement so avoiding further injury. Tension may persist long after the injury has otherwise healed becoming chronic and habitual. Pain occurs when movement goes beyond the limited range of motion. Pain, in turn, stimulates muscle tension resulting in the establishment of a vicious circle with increased muscle tension and limited range of movement installed as the new norm. Stretching and strengthening movements to align collagen fibres is essential in rehabilitation otherwise limited range of movement can lead to postural habits persisting after the injury has otherwise healed. Poor posture affecting the health of the back can also be established through mimicry of peers or parents or adopted in response to emotional factors Postural training or re-education is then required (Laughlin 1998).

Rehabilitation of patients with chronic low back pain is not an exact science and the efficacy of muscle reconditioning functional restoration is not fully document and is subject to conjecture (Quebec Task Force, 1987). There is little evidence to lend support any particular rehabilitation programme. Elnagger reported on studies claiming both flexion and extension exercises (similar to those in the accompanying package) improved range of movement and reduced pain but neither exercise was more advantageous than the other. Koes reviewed studies claiming little differentiation of exercise type in promoting rehabilitation but concluded the studies were of poor quality. Patients may therefore be best advised to do a variety of back strengthening, flexibility, endurance and aerobic exercises with pain tolerance as the guiding factor and resume normal daily activities as soon as possible with the aim of improving spinal mobility and disc nutrition. Disc nutrition depends on fluid exchange for which motion of the surrounding muscles and the intervertebral joints is vital. Ghosh claims disc degeneration results from inadequate nutrition resulting from bad posture and inactivity.

Rehabilitation of the lower back needs to take account of the interrelationship between the lumbar vertebrae, sacrum, ilium and legs as they are integrated to the extent that any alteration of musculature in one affects the others (Hartley p1). The pelvis generally compensates for asymmetry or unbalanced forces in the legs but the resulting uneven stresses can cause pain in the ligaments or muscle imbalance in the pelvic region. Reduced flexibility in the hips will result in increased forces being transmitted through the pelvis and lumbar spine. Alignment in muscular skeletal structures is generally desirable but asymmetry is common and does no necessarily indicate pathology. Problems are evident when asymmetry is accompanied with pain and mechanical dysfunction (Hartley p1). Asymmetry and a healthy lordosis require a suitable balance of strength and flexibility in the hip and back flexor and extensor muscles. The synergy between muscles is affected if any of the muscles suffers fatigue, injury or overuse. (Hartley p1). The curves in the spine provide longitudinal shock‑absorption and resistance to axial compression loads (Kapandji, vol. 3 p. 20 ff).

Excessive lordosis occurs if the hamstrings and abdominal muscles are weak and the hip and back extensors are tight. Excessive lumbar lordosis puts more pressure on the disc at the lumbar-sacral junction (Corrigan & Maitland, p14) at it causes a downward and forward shearing force that exerts an uneven pressure on the disc (Hartley p3) This can lead to lumbar strain, disc degeneration and herniation and a potential for developing spondylolysis or spondylolisthesis, facet joint degeneration and nerve root impingement. Excessive lordosis and anterior pelvic tilt is often associated with hyper- extending knees (genu recurvatum) (Hartly). Excessive lordosis when standing compresses the posterior lumbar spine.

Controlled spinal flexion can help correct excessive lordosis. The normal lumbar lordosis should be flattened but not reversed with full forward bending (Hartley). Spinal flexion exercises can increase abdominal flexor muscle strength, improve trunk stability, open the intervertebral foraman and stretch some posterior structures, including hamstrings (Corrigan & Maitland p56). ). Flexion occurs at all lumbar vertebrae but L5-S1 has proportionally the greatest range. Facet joint capsular ligaments provide most of the resistance to lumbar flexion and forward rotation although the disc provides some resistance to flexion (Adams, Hutton, and Stott). Forced forward bending can strain the erector spinae muscles, latissimus dorsi and the lumbodorsal fascia especially if the hamstrings are tight. Forward flexion increases pressure within the disc that presses out substantial amounts of fluid that, if habitual, can lead to low back pain (Twomey and Taylor, 1995). Injury caused by excessive flexion is more likely to occur at the supraspinous, interspinous and facet capsular ligaments before there is any injury to the disc (Adams and Hutton) but the nucleus will move posteriorly if there is damage to the annulus firbrosus (Hartley, p43). Intra abdominal pressure protects the discs when the trunk is flexed (Corrigan & Maitland p15).

A flat lumbar with a posterior pelvic tilt occurs if the hamstring muscles are tight and the back extensors are weak and is associated with tight hamstrings that increase stress on the lower back in flexion (Hartley p1). Extension exercises are advocated by McKenzie to reduce disc pressure and re-establish lumbar lordosis, reduce stress on the posterior disc and ligaments and move the nucleus anteriorly to a central position within the disc (Corrigan & Maitland p 56).

In lumbar extension, most movement takes place at L4 and S1 with a smaller range of movement between LI and L4 (Yamamoto et al). Excessive back extension puts tensile forces on the anterior disc that can weaken the anterior of the annulus fibrosis, push the nucleus forwards and stretch the anterior fibers of the annulus fibrosis and the anterior longitudinal ligament. There is also compression on the posterior of the intervertebral disc that can strain the facet joints. Compressive forces act more on the facet joints in back bending if the intervertebral disc height is decreased by injury (Hartley). In lumbar extension, the articular processes are compressed and the spineous processes touch (Kapandji). The inferior articular processes impact on the superior articular processes and lamina of the vertebra below (Bogduk & Twomey). Compression induced by excessive back hyperextension can injure the intervertebral disc and facet joints impinging the synovial membrane and damaging the articular cartilage. It can also injure the periosteum of the vertebrae lamina and the anterior longitudinal ligament and fracture the vertebral arch and spinous process (Hartley).

Excessive rotation at the lumbar can split the annulus fibrosis of the disc with most risk to the posterior aspect. The articular facets restrict rotation at the upper lumbar joints to about one degree per vertebrae. Three degrees of rotation is available at the lumbosacral junction so the lower lumbar joints are subject to the most stress. This may account for more occurrence of disc degeneration at L4-L5 or L5-SI. In lateral flexion, shearing forces through the discs and facet joints will increase if the lordotic curve is increased (Hartley).

References to follow (also available on request).