• Robert@optimalhealthclinic

Why your low back pain may not be where the problem is!

Updated: Sep 26, 2021

Firstly, a definition of low back pain (LBP) is pain perceived in the area arising from the spinous process of the twelfth thoracic vertebra to the sacrococcygeal joint (Bogduk 2012). A common cause of LBP is a functional leg length discrepancy (LLD), an asymmetrical change between the iliac crest (top of the pelvic bone) to the plantar surface of the foot that occurs because of the muscles, ligaments or joints, known as soft tissues, but not the bony structures (Mahmoud et al 2017).

Daveed Magge (2014) recognises that LLD can be a result of a rotational malalignment of the innominate (pelvic bone) on the sacrum. Equally, ankle overpronation, (flat foot) functional spinal scoliosis (curve in the spine) and lateral pelvic tilt can cause compensatory adaptive shorting and lengthening of the various soft tissues, resulting in LLD. For example, if the iliopsoas muscles become hypertonic (abnormally high muscle tone) on one side because of postural adaptations or a hip joint pathology.

The resulting hypertonicity has the effect of reciprocally inhibiting the antagonistic muscle group. (I have a more in depth po on inhabiton).

In this example, the inhibition by the iliopsoas reduces the gluteus maximums (G-Max) function to produce myofascial tensioning of the sacrotuberous ligament (STL). With a lack of tension generated by the inhibited G-Max, the STL becomes lax and can no longer prevent posterior rotation of the innominate, leading to an apparent shorter leg in a supine position (Gibbons 2014).

Additionally, the reciprocal inhibition of the gluteus medius prevents it from stabilizing the innominate, sacrum and their corresponding sacroiliac joint (SIJ) during the gait cycle, causing the compensatory activation of the piriformis on the ipsilateral side and the quadratus lumborum (QL) on the contralateral side (Lavangie & Norkin 2012). When in a supine position, the adaptive shortening of the QL pulls the innominate caudally into a lateral tilt, giving the appearance of a shorter leg. Likewise, the adaptive shortening of the QL can occur on the concave side of a compensatory scoliosis (Magge 2014).

Furthermore, the innominate can become anteriorly rotated through excessive pronation of the subtalar joint, causing the body to try and compensate and lengthen the discrepancy by internally rotating the tibia. The anteriorly rotated innominate will give the appearance of a functionally longer leg when in a supine position due to the acetabulum pulling the head of the femur anteroinferior (Gibbons 2017). Consequently, the vertebral column (VC) and SIJ are maintained in an optimal posture and stabilised by muscles, ligaments and joints. Disruption to these soft tissues, produced by an LLD malalignment, causes the body to compensate, to keep the weight distributed evenly and maintain eye level. If left untreated, this deviation in posture leads to adaptive shorting and lengthening of muscles and ligaments and increases the load on joints that make up the VC (Lavangie & Norkin 2012). The following section will explore how these adaptations could correlate with LBP.

Firstly, muscle hypertonicity can result in ischemic nerve compression, a more common clinical presentation of this being piriformis syndrome, where the sciatic nerve becomes compressed by the tendon in the greater sciatic foramen. The fibular component passes through the muscle in 33.3% of individuals (Barbosa et al 2019), thus causing LBP.

Similarly, ischemic nerve compression occurring due to a hypertonic QL compressing the ilioinguinal and iliohypogastric nerves has been theorised to simulate LBP (Bordoni & Varacallo 2018).

Concerning hypertonicity, Bongaduk (2012) states that LBP “implies a somatic origin” and therefore could be due to muscle fatigue or imbalance produced by hypertonicity in the trunk muscles. For example, as the fibres from the psoas major and Ql effectively anchor the lumbar vertebrae to the ilium, their hypertonicity increases lordosis and lateral side bending, respectively. This has the effect of causing adaptive shorting of the multifidus and lumbar erector spinae (LES), resulting in muscle imbalances by lengthening the muscles the on the contralateral sides (Lavangie & Norkin 2012).

However, when it comes to LLD, Knutson (2005) indicated that increased muscle fatigue due to asymmetry or hypertonicity was not statically significant. Further corroborated by Goubert et al’s (2016) review on if fatigue or inhibition of the lumbar trunk muscles, mentioned above, could be the cause or consequence of LBP, with the literature suggesting only the multifidus undergoes structural changes and are a likely source of LBP. Furthermore, Bongaduk (2012) goes on to conclude that LBP, due to muscular imbalance, is predominantly more likely to be because of increased stress placed upon a joint. This sentiment is also shared when it comes to muscle hypertonicity with Bordoni & Varacallo (2018), stating that “there is no consensus in the literature whether an alteration of the tone of the QL may be the primary cause of back pain.”

To summarise, changes in lumbar muscle tone have been theorised to produce LBP, however, other than piriformis syndrome, the evidence suggests that altered tone leads to altered function in surrounding soft tissues, as the muscles in this section are connected with ligaments and joints that serve to stabilise the lumbar spine and SIJ by the thoracolumbar fascia (Bordoni & Varacallo 2018). Therefore, it is meaningful to explore how their changes due to LLD can affect the SIJ, intervertebral discs, zygapophyseal joints and ligamentous tissue.

Firstly, loads placed upon the SIJ can increase with an LLD and are influenced by the muscles mentioned in the preceding paragraphs. Kiapour et al’s (2020) systematic review on the biomechanics of the SIJ purports it to be responsible for 15% of low back pain. Although there are many conflicting studies on the SIJ being a source of pain, it is a synovial joint innervated by the L-4 to S-2 nerve roots, with both fibro and hyaline cartilage that is subject to early degenerative changes (Poilliot et al 2019).

For instance, the SIJ is stabilised by secure ligamentous attachments that during gait increase in tension, which serves to unite the sacrum and innominate.

Tension is accomplished by the myofascial tensioning of the sacrotuberous ligament (STL) generated through the thoracolumbar fascia by G-Max muscle, which attaches it and the iliolumbar ligament formed by the LES and Ql (Lavangie & Norkin 2012). Additionally, the multifidus and LES work together within the thoracolumbar fascia, which creates an extension force that compresses the SIJ and stabiles the lumbar spine. However, these muscles are impaired in their function as a result of LLD, as explored previously, and results in the ligaments becoming lax, preventing stabilisation (Gibbons 2014).

Additionally, stabilisation of the SIJ also occurs by the nutation of the sacrum, an anterior movement of the base of the sacrum. However, during anterior innominate rotation, the sacral-base moves into the opposing motion of counternutation. The counter-nutated position decreases the stability of the SIJ by again causing laxity in the ligaments mentioned above and straining the sacroiliac ligament (Gibbons 2017).

The inability to stabilize the SIJ and disruption to the surrounding ligamentous tissue is significant as abnormal biomechanics can initiate structural changes to the accessory soft tissues of the SIJ which can result in sacroiliac pain (Poilliot et al 2019). Hammer et al (2019) suggested that postural adaptations could lead to “pathological changes occur in the SIJ ligaments,” resulting in pain of noninflammatory causes.

Moreover, Kim et al (2020) note that if the pelvis is out of normal range or the muscles and ligamentous tissues are lax, the spine will try and compensate, potentially predisposing the disk to degeneration and placing abnormal load upon the zygapophyseal joints (Facet joint).

For example, a counter-nutated sacrum produces an oblique sacral rotation, which means the lumbar spine will have to compensate by rotating in the opposing direction (Bongaduk 2012). The sustained rotation motion generated can place excessive torsion upon the intervertebral disk, effectively unwinding the annulus fibrosis, making the annuls subject to what amounts to a ligament sprain. As the sinuvertebral nerves innervate the outer two-thirds of the annulus, it is cable of generating LBP (Kim et al 2020).

Additionally, the hypertonic iliopsoas, multifidus or LES can create an excessive lumbar lordosis, resulting from the body's attempt to keep the head over the sacrum as previously stated (Lavangie & Norkin 2012). The impact of this excessive lordosis is substantial compressive loads being placed upon the intervertebral discs, which increases pressure on the annulus, also resulting in strain. The increased pressure also forces the nucleus pulposus (NP), the gel-like fluid within the disc, into the weakened annulus, with the NP proteins capable of stimulating the sinuvertebral nerves. The migrated NP is also capable of causing the disc to bulge outward, compressing the lumbar spines root nerves in a comparable way to the piriformis impinging the sciatic nerve (Kim et al 2020).

Furthermore, increased lumbar lordosis or rotation can cause an impacted zygapophyseal joint. The impacted zygapophyseal joint can cause the fibro adipose meniscalcord within the joint to become trapped. Additionally, rotation then occurs around the restricted joint, causing the contralateral joint capsule to become strained (Bongaduk 2012). Subsequently, entrapment and capsular strain can result in LBP. Perolat et al’s (2019) review suggests the prevalence of zygapophyseal joints are implicated in 15-45% of LBP.

In conclusion, this essay has shown that muscle hypertonicity and subsequent inhibition can disrupt other soft tissues, leading to the inability to stabilise the innominate and withstand rotational malalignments, which can produce the appearance of LLD in the supine position. Disruptions caused and the body’s ability to compensate leads to further disruption to the soft tissues, which leads to a breakdown in the body’s ability to resist load across the corresponding joints. This breakdown in compensation leads to the potential of nerve entrapment, ligamentous strains and disc degeneration all of whom can produce lower back pain.

Reference list

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