Lumbar Disc Injury: Mechanisms and Intervention Options

Disc Injury Mechanism

Single plane movements of spinal segments have been studied for disc injury responses. Trunk rotational movements are shown to cause transverse fissures, possibly secondary to shear forces created when torsion continues at bony end-range but rotation has not been shown to cause radial fissures of the disc in isolation with experimentation (Adams & Dolan, 2016). Posterior and posterior-lateral disc herniations occurred in porcine spines with high numbers of cyclic flexion and extension with low-magnitude axial compression loads and more frequent with high loads (Callaghan & McGill, 2001). Cyclic movements with compression also caused inner annular fiber injury, which may be linked to disc annular fatigue and loss of stiffness (Noguchi et al., 2016). Multiplanar movements have also been investigated for disc injury using a computer model (Schmidt et al., 2007). The results suggest the annulus is under highest strain in the posterolateral region, further supporting the most common location of lumbar disc herniations (Schmidt et al., 2007). A disc may herniate under a combination of rotation and lateral bending, rotation and flexion, or lateral bending and flexion movements. The risk of injury is significantly increased when an axial load is also added (Schmidt et al., 2007).

Providing a load on the annular layers of ovine discs were inflicted by increasing intradiscal pressure. A gradual increase in pressure within a neutral positioned segment by injecting a gel into the nucleus caused radial fissures posteriorly through a separation of annular layers (Concentric fissure) and failure to the outer posterior region possibly due to inter-annular cohesion weakness (Veres et al., 2008). A similar study using a gradual increase in pressure in discs of segments flexed 7° created an increase in central-posterior radial fissures and fractures at the mid-annulus or endplate ridge apex along with an increase in herniations compared to a neutral position (Veres et al., 2009). The magnitude of these experimental pressures have been attained with the compression force of football blocking (Gatt et al., 1997). Another study using a gradual increase in pressure and application of rotational forces in flexion was found to reduce the occurrence of radial fissures of the annulus in isolation but facilitated radial fissures that involved an endplate fracture adjacent to the endplate ridge apex (Veres et al., 2010). The annular fibers in the direction of rotation would experience higher axial tensile load (every other layer) creating an uneven load-sharing situation when the nucleus is pressurized increasing stress at the endplate junction and failure at mid-annulus, referred to as the endplate ridge apex (Veres et al., 2010a). Sudden, high-pressure impulse internal loading, similar to a contact or collision load, was applied in a neutral position and caused central-posterior radial fissures and injury of the cartilaginous endplate at the inner-annulus (Veres et al., 2010b). In theory, there was not enough time for inter-annular fluid flow to occur through pores in the annular layers to decrease hydrostatic pressure within the nucleus (Veres et al., 2010b). When segments were positioned in flexion, there was an increase in endplate fractures (Veres et al., 2010b).

Experimental conditions providing axial compression loads on ovine discs were also created. When analyzing injury to ovine discs at varying compression rates (2 and 40mm/min) in neutral and flexion, annular failure and herniation required positioning in flexion and a high compression rate (Wade et al., 2014). Flexion without compression did not provide enough stress to the annulus to cause injury. The annular fissure was initiated adjacent to the endplate ridge apex creating a situation where the inner annular layers are unable to withstand the nuclear pressure and tear allowing the nucleus to lacerate the outer layers and eventually herniate (Wade et al., 2014). The oblique angle of the annular fibers increases from the outer to inner portions making mid to outer layers most stressed with flexion (Wade et al., 2014). With only inner annular layers injured, it is possible that the early phases of disc injury could be asymptomatic if the endplate is not involved. Another study using flexion and high compression rates (40mm/min) found anterior shear and displacement of the superior vertebrae resulting in a load on the oblique annular fibers in the same direction and at the same time relaxing counter-oblique oriented fibers allowing for disruption of lateral fibers with an increase in hydrostatic pressure, forcing nuclear material laterally (van Heeswijk et al., 2017). Once migrated into the outer layers, the weak intra-annular bond between layers allows for a concentric fissure to migrate to the posterior-lateral region of commonly found herniations. When non-degenerated human cadaver discs were placed in either normal lordosis or flexed positions to where the endplates were parallel and compressed to failure, vertebral bodies fractured first with normal lordosis and endplates first in a flexed position with less than half of the axial load (Curry et al., 2016).

A sudden, ultra-high rate of compression loading (400mm/min), as encountered in a contact or collision sport, in flexion found 83% of the segments suffered herniations and 70% a rupture at the annulus-endplate junction (Wade et al., 2015) which is comparable to the 65% endplate junction failure found clinically with disc patients (Rajasekaran et al., 2013). The annular layers will experience the highest strain at the endplate ridge apex and tear, further compression leads to herniation (Wade et al., 2015). With the segment in a flexed position, the oblique annular fibers in the direction of flexion are stretched and the counter-oblique fibers are relaxed creating weak points in the layers presenting a pathway for posterior-lateral nuclear migration and herniation (Wade et al., 2015).

When compression is applied to discs in complex positions, such as a postural combination of 0-13° flexion, 0-10° lateral flexion, 0-4° rotation and 0-800N compression with a 2Hz cycle, 76% endplate junction fractures and 24% outer-posterior annulus injury occurred (Berger-Roscher et al., 2017). It appears flexion and lateral flexion are factors for endplate fractures and rotation increases the risk. It was suggested the “crackling” sound often reported from the low back by patients may be caused by an endplate junction fracture (Berger-Roscher et al., 2017). Prepositioned segments in 7° of flexion, 20° of laterally flexion, and 5° of rotation and submitted to high compression rates (40mm/min.) demonstrated most discs suffered from mid-annular alternate layer damage and nuclear material extruded into the area via annular rupture and circumferential tracking posterior-laterally (Wade et al., 2017). A disc in a complex posture significantly reduces its ability to withstand compressive loading without failure (Wade et al., 2017).

Sudden compression in complex postures such as a segment prepositioned in 7° of flexion, 20° of laterally flexion, and 5° of rotation and subjected to ultra-high compression rates (400mm/min.) on the disc resulted in an anterior shear of the superior vertebrae and inability for nuclear material to infiltrate through the annulus (Shan et al., 2017). Ultra-high compression rates produced more direct annular fissures with circumferential tracking to the posterior-lateral region along with endplate fractures than lower compression rates (Shan et al., 2017). With sudden compression there is less time for nuclear fluid to equalize within the disc. The high incidence of endplate fractures is caused by increased hydrostatic pressure in the nucleus and an increase in tensile load on the annular fibers with disc sudden forceful distraction. An increase in endplate-annulus junction tears suggests complex postures play a significant role in herniations.

Disc Injury Intervention

Athletes with disc injuries from 1990-2009 either discontinued sporting activity or received a discectomy (Iwamoto et al., 2010). Both approaches seemed satisfactory in returning athletes to their original levels of sports activities (Iwamoto et al., 2010). Professional athletes with disc herniation had no significant difference in outcomes between surgery or no surgery (Hsu et al., 2011). These outcome studies suggest conservative care is as effective as surgical procedures even without providing specific treatment strategies.

A recommended progression (4 Phase) for the treatment of lumbar disc injuries in athletes is provided a based-on literature inquiring disc healing, nutrient transfer and load adaptation. Disc healing is restricted due to a low cell density and extensive mechanical loading (Adams & Dolan, 2016). With a limited blood supply, the cells of the disc can survive at very low levels of oxygen but need significant levels of glucose (Hughes et al., 2012). Nutrition to the cells of the disc is dependent on the transfer of nutrients from blood vessels located at the outer annulus and through the endplates by diffusion (Hughes et al., 2012).

The cells of the outer annular layers are similar to tendon and ligament and appear to have a similar healing process (Ahlgren et al., 2000). Consequently, during the acute stage of healing limited motion may be effective, as with the annular healing of sheep disc (Latham et al., 1994). Pressure is placed on the annular layers from the nucleus at its greatest in the morning, which should be addressed though dehydration strategies (Adams et al., 1987). During the initial phase of lumbar disc injury recovery for an athlete, emphasis should be placed on restricted movement, maintaining lumbar lordosis and disc dehydration. Early phase interventions include dehydrating the disc in the morning with shallow lumbar extensions. Ergonomic positions such as a pillow in the low back to emphasize extension and raising the seat to lesson hip flexion and lumbar flexion. Taping the lumbar region using a technique to restrict lumbar flexion as a feedback mechanism to provide lumbar flexion restraint can also be employed.

During the second phase, a repeated tensile load may increase fibroblast proliferation and stimulate collagen synthesis (Lee et al., 2004). Cyclic, gentle flexion of the spine performed in side-lying to minimize compressive loading could stimulate repair of the outer posterior annulus (Tampier et al., 2007). Rotation of the spine applies tension to alternating annular layers (Krismer et al., 1996), consequently, intersegmental mobilization may facilitate inter-laminae movement and minimize adhesion formation and discogenic pain while facilitating nutrient transfer. A single session of joint mobilization significantly increased fluid diffusion with degenerated nucleus pulposus discs (Beattie et al., 2009). With a radial fissure, begin mobilization techniques in the direction that decreases pain to facilitate inter-annular movement (Adams et al., 2010). After a few days, scar formation develops annular mobilization techniques could begin in the direction causing pain to promote remodeling of the fibrous tissue (Adams et al., 2010). Alternating full lumbar extension and flexion static positions may facilitate fluid diffusion by fluctuating hydrostatic pressures (Adams & Hutton, 1983). Either mechanical or manual intermittent traction could also be performed at this stage to provide cyclic loading to facilitate disc metabolism. After pain free movement is experienced, the third phase may begin with motor control training for segmental stability can begin. This is meant to target deep abdominal muscle activation to assist in uni-segmental stability of the lumbar region and shear force restraint. After motor control training is established, McKenzie exercises for repeated lumbar extension and disc nutrition followed by trunk stability training to improve external load restraint may begin. Additional considerations are facilitating rotational movement in the thoracic region and internal rotation of the lead hip to minimize rotational torque forces in the lumbar region.

Discs rely on diffusion to transfer nutrients, so fluctuating changes in intradiscal pressure are important to disc health (Kingsley et al., 2012). A study assessing disc pressures found overnight, disc volume increased 10.6% in volume and walking 8 hours did not decrease disc volume 10.6% (Malko et al., 2002). Running at 70% heart rate maximum for 30 minutes, decreased lumbar disc volume 6.9%, due to an increase in hydrostatic pressure in the disc (Kingsley et al., 2012). Running increased extracellular matrix production and cell proliferation in lumbar discs of rats (Brisby et al., 2010). Walking and low intensity running provide moderate mechanical loading that strengthens tissues by adaptive remodelling (Videman et al., 2010). A systematic review suggested running may have a protective effect on disc (Trompeter et al., 2017). When comparing the effects of dynamic and static compression on the transport and metabolism of oxygen and lactate in and out of the disc, dynamic compression increased oxygen concentration along with decreasing lactate while static compression produced an inverse effect (Huang & Gu, 2008).

Consistent with these findings of metabolic transfer in discs, the last phase suggests interventions that provide a graded increase in repetition and compression loading may facilitate disc metabolism safely and effectively and the combination compression-decompression mechanism in the disc allows for annular adaptation to hydrostatic pressures within the disc. Examples would include beginning with walking progressing to jogging and finally running, all with graded durations.

When to allow a disc injured athlete to return to sport is a difficult decision as evidence to support specific measures to accurately determine a safe return without reoccurring symptoms are lacking. Six weeks of healing was enough time for sheep discs to withstand a high hydrostatic pressure (Ahlgren, 2000) may be a timeline to consider.

Discs that encounter endplate fractures may need treatment like other fracture sites. An endplate fracture could be treated with initial unloading followed by gradual reloading of the disc to give the endplate enough healing time to withstand minimal compression forces (Adams et al., 2010).