The Iliolumbar Ligament and Chronic Low Back Pain: Anatomy, Causation, Assessment & Treatment
Iliolumbar ligament Anatomy
The location of the iliolumbar ligaments is between the iliac crest to transverse process of L4 and L5. The nerves from the L4 and L5 ventral rami pass around the Iliolumbar ligaments as shown in figure 2. Kim (2017) examined 14 fixed cadavers and found huge variation in the routes of the L4 and L5 lumbosacral trunks relative to the inferior and superior bands of the iliolumbar ligaments. With both passing anteriorly or posteriorly variously in multiple combinations amongst different cadavers.
Figure 2. from Kim et al (2017)
As shown in figure 3 below palpation of the iliolumbar ligament is challenging to bordering on impossible. It sits directly under the longissimus which is innervated in contrast to the iliolumbar ligament and thus it is very hard to differentiate the longissimus from the ligament when trying to palpate the ligament. Then once you get through the longissimus it’s clear the lumbosacral trunks can pass around both bands of the iliolumbar ligament thus sensitivity in this area is surely more likely from pressuring a sensitive nerve trunk. In contrast a more lateral approach to palpation of the longissimus makes it theoretically possible to differentiate longissmus sensitivity from iliolumbar ligament sensitivity.
Kilter et al (2010) reported finding many proprioceptive fibers specifically in the iliac wing attachment site of the iliolumbar ligament. However Wang et al’s (2018) dissection study did not identify nerve fibers within the iliolumbar ligament. However, surrounding tissues were found to have innervation. Nervous tissue has been discovered within the fat anterior and posterior to the iliolumbar ligament. Thus, the fat may be a mechano-sensory organ that conducts neural information. Nerve cells in fat within the iliolumbar ligament may actually transmit nociception (Viehofer et al. 2015). Perhaps this is what Kilter et al (2010) found, or innervated adipose tissue may have infiltrated the iliolumbar ligament. Indeed fat tissue at the enthesis of ligaments and tendons has been included as part of the “enthesis organ” and described as valuable in proprioception at other sites such as the Achilles tendon (Benjamin et al. 2006). Benjamin et al (2006) argued that fat tissue accumulation around the enthesis of tendons and organs was not a sign of degeneration, but rather a functional adaptation. Benjamin et al (2006) lean towards almost suggesting some sort of subconscious decision process in depositing this fat in the way they write about it. In contrast it is probable this fat could be susceptible to overuse/ microtrauma leading to hypertrophy as with fat in other mechanically challenged locations.
The common tender spot 5-7cm lateral to the PSIS has been attributed to the iliac insertion of iliolumbar ligament, however Maigne and Maigne’s (1991) dissection study of 37 cadavers demonstrated that the iliac insertion of the iliolumbar ligament was impalpable because it attaches anteriorly on the iliac crest. Conversely, the dorsal rami of L1 and L2 were superficial and palpable as they crossed the iliac crest 7cm lateral to the spine bilaterally. This supported the claim that the tender point originates from the cutaneous dorsal rami of L1 and L2 (cluneal nerves) rather than the iliac attachment of the iliolumbar ligament.
Biomechanics of the Iliolumbar Ligament
The anterior band restricts lateral tilting of the pelvis while the posterior band assists in restricting flexion and prevents the L5 vertebrae from slipping over the sacrum (Butt et al., 2015). The removal of the ventral band of the ILL in 12 cadavers greatly increased the mobility of the sacroiliac joint and, therefore, increased instability within the joint (Pool-Goudzward et al. 2002). Bilateral transection of the iliolumbar ligaments increased flexion and extension by 1.7 and 1.1 degrees, respectively. This represented 23% and 21% increases in flexion and extension (Yamamoto et al. 1990). In right axial rotation, Yamamoto et al (1990) found increases were statistically significant when both one and two iliolumbar ligaments were transected. They suggested the iliolumbar ligaments restrict contralateral axial rotation. Lateral bending resulted in the most statistically significant findings. When both ligaments were transected, right lateral flexion increased by 1.3 degrees, which represented a 33% increase. In left lateral flexion, bilateral transection of the iliolumbar ligament increases left lateral flexion by 1.0 degree, which represented a 24% increase.
Interestingly the average length of the male and female African American iliolumbar ligaments was 61.6 mm and 61.3, respectively, while the average length of the male and female Caucasian iliolumbar ligaments was 33.2 mm and 32.2 mm, respectively (Aihara et al., 2005).
Functionally in left side flexion in sitting the L5 vertebra typically rotates right. Dysfunction of this pattern could theoretically be caused by a rupture or strain of the iliolumbar ligament.
Pathomechanics
Cases of inflamed and torn iliolumbar ligaments have been reported (Chantraine et al 2001, El Khoury et al 2016). The presumed mechanism for these injuries is either an acute end range event in rotation, or flexion, or a cumulative microtrauma in side flexion, rotation or flexion. Although the ligament has a role in extension stability so theoretically this is possible direction of injury.
References
Basadonna PT, Gasparini D. 1996. Anatomy of the iliolumbar ligament: a review of its anatomy and a magnetic resonance study. Am J Phys Med Rehabil; 75 (6):451-5.
Benjamin, M., Toumi, H., Ralphs, J.R., Bydder, G., Best, T.M. and Milz, S., 2006. Where tendons and ligaments meet bone: attachment sites (‘entheses’) in relation to exercise and/or mechanical load. Journal of anatomy, 208(4), pp.471-490.
Chantraine, A., Bosson, L., Malaise, M., Onkelinx, A. and de Leval, J., 2001. The occurrence of the ilio-lumbar syndrome in a spinal cord injury patient. Spinal cord, 39(4), p.237.
El Khoury, N., Zebouni, S.H., Revel, M. and Fayad, F., 2016. AB0970 Ultrasonography in Diagnosis and Management of Iliolumbar Syndrome: Case Series.
Harmon, D. and Alexiev, V., 2011. Sonoanatomy and injection technique of the iliolumbar ligament. Pain Physician, 14(5), pp.469-474.
Kim, P.W., 2017. Variations in the L4 and L5 Ventral Rami with Iliolumbar Ligaments in 14 Cadavers. The FASEB Journal, 31(1_supplement), pp.896-13.
Kiter, E., Karaboyun, T., Tufan, A.C. and Acar, K., 2010. Immunohistochemical demonstration of nerve endings in iliolumbar ligament. Spine, 35(4), pp.E101-E104.
Maigne, J.Y. and Maigne, R., 1991. Trigger point of the posterior iliac crest: painful iliolumbar ligament insertion or cutaneous dorsal ramus pain? An anatomic study. Archives of physical medicine and rehabilitation, 72(10), pp.734-737.
Viehöfer, A.F., Shinohara, Y., Sprecher, C.M., Boszczyk, B.M., Buettner, A., Benjamin, M. and Milz, S., 2015. The molecular composition of the extracellular matrix of the human iliolumbar ligament. The Spine Journal, 15(6), pp.1325-1331.
Wang, J.M., Kirkpatrick, C. and Loukas, M., 2018. The Iliolumbar Ligament Does Not Have a Direct Nerve Supply. The Spine Scholar, p.3661.
Iliolumbar Ligament As A Cause of Low Back Pain
Viehofer et al (2015) suggested 50% of non-specific low back pain may be attributable to Iliolumbar syndrome. Iliolumbar syndrome involves a strain, tear, or rupture of one or both iliolumbar ligaments, and may be caused acutely by a heavy-lifting or a fall (Naeim et al., 1982) and chronically by rotation sports and manual work (Harmon and Alexiev, 2011). Patients with Iliolumbar syndrome are thought to present with low back pain and sensitivity around the PSIS and iliolumbar ligament aggravated by standing or sitting for long periods of time (Naeim et al., 1982).
Sims and Moorman (1996) hypothesised that micro-trauma to the iliolumbar ligament is the primary cause of many cases of chronic low back pain because (1) it is the weakest component of the multifidus triangle; (2) there is increased susceptibility to injury due to its angulated attachment; (3) it is a primary inhibitor of excess sacral flexion; (4) it plays an increased role with progressive disc degeneration and (5) it is a highly innervated nociceptive tissue.
Kilter et al (2010) reported finding many proprioceptive fibers specifically in the iliac wing attachment site of the iliolumbar ligament. However Wang et al’s (2018) dissection study did not identify nerve fibers within the iliolumbar ligament. However, surrounding tissues were found to have innervation. Nervous tissue has been discovered within the fat anterior and posterior to the iliolumbar ligament. Thus, the fat may be a mechano-sensory organ that conducts neural information. Nerve cells in fat within the iliolumbar ligament may actually transmit nociception (Viehofer et al. 2015). Perhaps this is what Kilter et al (2010) found, or innervated adipose tissue may have infiltrated the iliolumbar ligament. Indeed fat tissue at the enthesis of ligaments and tendons has been included as part of the “enthesis organ” and described as valuable in proprioception at other sites such as the Achilles tendon (Benjamin et al. 2006). Benjamin et al (2006) argued that fat tissue accumulation around the enthesis of tendons and organs was not a sign of degeneration, but rather a functional adaptation. Benjamin et al (2006) lean towards almost suggesting some sort of subconscious decision process in depositing this fat in the way they write about it. In contrast it is probable this fat could be susceptible to overuse/ microtrauma leading to hypertrophy as with fat in other mechanically challenged locations.
The common tender spot 5-7cm lateral to the PSIS has been attributed to the iliac insertion of iliolumbar ligament, however Maigne and Maigne’s (1991) dissection study of 37 cadavers demonstrated that the iliac insertion of the iliolumbar ligament was impalpable because it attaches anteriorly on the iliac crest. Conversely, the dorsal rami of L1 and L2 were superficial and palpable as they crossed the iliac crest 7cm lateral to the spine bilaterally. This supported the claim that the tender point originates from the cutaneous dorsal rami of L1 and L2 (cluneal nerves) rather than the iliac attachment of the iliolumbar ligament.
Based on these potential causes it is fun to make some wild speculations.
A patient moving repeatedly in to end range at the lumbosacral joint could strain the ligament either acutely as in golf, or under high load e.g. with deadlifting or chronically as in sitting with a flexed lumbosacral junction or in sleeping with hip flexed fully and the spine flexed. Acutely this could lead to a strain and the inflammatory process may sensitise the nearby L4 and L5 trunks or the nociceptors in the fat at the enthesis. Whilst chronically placing the iliolumbar ligament under repeated load could lead to a similar inflammatory situation or even lead to a “Hoffa’s fat pad like” hypertrophy of the enthesis fat both of which could lead to sensitivity in the region.
There are other possibilities for how the iliolumbar ligament could contribute to low back pain where it is not the/a source of nociception. For example a lax or torn iliolumbar ligament would lead to an increase in side flexion, rotation, flexion and extension at the lumbosacral junction. Hypothetically this could lead to increased load on other ligaments, muscles and fascia involved in controlling these movements. For example the thoracolumbar fascia may take more load during contralateral side flexion on the affected side. Such an increase in mechanotransduction could lead to thickening and possibly increased tone in the thoracolumbar fascia increasing pressure on the cluneal nerves as they cross over the iliac crest as seen in Maigne’s syndrome. Similarly a torn right iliolumbar ligament without sufficient compensation in the frontal plane to control side flexion could lead to increased left side flexion of L5 and thus a left sided facet joint problem, or promote an increase in posterolateral right disc pressure.
This chain of events is at best highly speculative and included purely for consideration of the potential importance of the ligament. As humans we are highly adaptive and multiple systems such as the nervous system and immune system as well as the musculoskeletal system will be compensating for a lax or torn iliolumbar ligament.
References
Basadonna PT, Gasparini D. 1996. Anatomy of the iliolumbar ligament: a review of its anatomy and a magnetic resonance study. Am J Phys Med Rehabil; 75 (6):451-5.
Benjamin, M., Toumi, H., Ralphs, J.R., Bydder, G., Best, T.M. and Milz, S., 2006. Where tendons and ligaments meet bone: attachment sites (‘entheses’) in relation to exercise and/or mechanical load. Journal of anatomy, 208(4), pp.471-490.
Harmon, D. and Alexiev, V., 2011. Sonoanatomy and injection technique of the iliolumbar ligament. Pain Physician, 14(5), pp.469-474.
Kiter, E., Karaboyun, T., Tufan, A.C. and Acar, K., 2010. Immunohistochemical demonstration of nerve endings in iliolumbar ligament. Spine, 35(4), pp.E101-E104.
Maigne, J.Y. and Maigne, R., 1991. Trigger point of the posterior iliac crest: painful iliolumbar ligament insertion or cutaneous dorsal ramus pain? An anatomic study. Archives of physical medicine and rehabilitation, 72(10), pp.734-737.
Naeim, F., Froetscher, L. and Hirschberg, G.G., 1982. Treatment of the chronic iliolumbar syndrome by infiltration of the iliolumbar ligament. Western Journal of Medicine, 136(4), p.372.
Sims, J.A. and Moorman, S.J., 1996. The role of the iliolumbar ligament in low back pain. Medical hypotheses, 46(6), pp.511-515.
Viehöfer, A.F., Shinohara, Y., Sprecher, C.M., Boszczyk, B.M., Buettner, A., Benjamin, M. and Milz, S., 2015. The molecular composition of the extracellular matrix of the human iliolumbar ligament. The Spine Journal, 15(6), pp.1325-1331.Wang, J.M., Kirkpatrick, C. and Loukas, M., 2018. The Iliolumbar Ligament Does Not Have a Direct Nerve Supply. The Spine Scholar, p.3661.
Assessing The Iliolumbar Ligament
There is no gold standard for diagnosing an iliolumbar ligament sprain. This represents my best efforts based on the available literature.
Diagnosis
Exclude red flags
Patient complaining of pain over iliolumbar ligament, around and medial to PSIS.
Patient complaining of pain with sitting/ standing for long periods, pain at end range extension, flexion, contralateral side flexion, unilateral hip flexion to end range
Acute cause, such as heavy lifting or rotating to end range
Chronic cause, sitting with flexed lumbosacral junction, potentially sleeping postures
Theoretically could be involved in Anylosing Spondylitis.
Exclude red flags, neurologenic, discogenic, facetogenic, longissimus and sacroliliac joints.
Then refer for ultrasound investigation if a secialist available or MRI if not.
Rationale for Assessment
Pain in the region of the iliolumbar ligament is most likely from facet or disc lesion at the L4/5 or L5/S1 level. Thus a disc lesion should be excluded as per Peterson et al (2017) by the patient being unable to centralise symptoms, I personally like to add long sitting trunk flexion base purely on experience. Facet symptoms cannot be fully excluded if pain is “typically” worse with the legs straight in supine and eased with the legs bent and spine flexed, again the patient will be unable to centralise their symptoms. Longisimmus diagnosis hasn’t been discussed and I use pain on resisted posterior pelvic tilt in prone from a neutral pelvis coupled with pain on palpation with a lateral approach to the muscle. SIJ symptoms can be ruled out with the Laslett rule (Laslett et al 2003) coupled with no provocation on sacroiliac shear test (Kurosawa et al 2017). Of course there is a possibility the sacroiliac test may provoke symptoms in an iliolumbar ligament strain. If the pain is over the iliolumbar ligament and this pain is provoke on SIJ tests then the iliolumbar ligament should be excluded by referral for ultrasound investigation.
Rationale For Ultrasound Investigation
El Khoury et al (2016) reported on 30 patients that underwent ultrasound assessment for iliolumbar syndrome on the basis of clinical findings. LBP with presence of tenderness on palpation of the posterior/ medial aspect of the iliac crest. Patients were evaluated by ultrasound. Patients included in this study were relatively young with a mean age 38.87 years (22–65 years). The sex ratio is 5/1 (female/male). The patient is in the prone position and the probe is positioned almost horizontally for L5 and in slightly oblique direction for L4. To confirm the diagnosis, we should have a swollen hypoechoic iliolumbar ligament with reproduction of the usual back pain during the passage of the probe above the ligament. Also, the thickness of the inflamed ligament should be higher than 1mm. Ultrasound was always performed bilaterally to compare both sides. Patients who failed standard treatment were injected under ultrasound guidance or in clinic with 80mg of methyl-Prednisolone and 5cc of local xylocaïne. The patient’s assessment of usual LBP was recorded 20mn after the injection of xylocaïne. Ultrasound showed, in all patients, an inflammation of the iliolumbar ligament. In four patients, the iliolumbar ligament was inflamed at both sides. The mean thickness of the ligament was 2.64 mm (1.5–6mm). There was an associated tendonitis of the gluteus medius muscle in 5 patients, diagnosed also on US. All patients noted the disappearance of the usual LBP 20 minutes after the injection.
Harmon and Alexiev (2011) reported complete resolution of symptoms in a 46-year-old male patient (BMI 28) with a 7-2/10 reduction in pain following local anastheitc along the iliolumbar ligament and then complete resolution following prolotherapy. He presented with persistent, debilitating right-sided lower back pain following lifting a heavy weight 12 months previously. The pain was centered on the right iliac crest, and was associated with tenderness to palpation in this region. There was pain also in the right lateral hip region and the medial aspect of the right groin. Lumbar lateral flexion to the left exacerbated the pain. Neurological exam was normal. X-ray and magnetic resonance imaging (MRI) of the lumbar spine were normal.
Other Discussed Tests
Lumbosacral Movement Assessment
This could perhaps be justified in a patient with easily palable transverse processes at L5 and a high suspicion of an iliolumbar ligament tear, e.g. an acute episode leading to pain in the region of ligament, where discogenic, facetogenic, SIJ, lognissimus and cluneal nerves have been excluded.
Sitting
Assess transverse process movement pattern with movement
Trunk flexion – theoretically symmetrical
Side flexion
Theoretically should see right rotation of L5 on left side flexion.
In theory these movements could help indicate a tear of the iliolumbar ligament although the reliability of such an assessment is highly dubious due to the difficulty in palpating the transverse processes, anatomical variation, handiness paterns and movement variability.
Palpation
As shown in the image below palpation of the iliolumbar ligament is challenging to bordering on impossible. It sits directly under the longissimus which is innervated in contrast to the iliolumbar ligament and thus it is very hard to differentiate the longissimus from the ligament when trying to palpate the ligament. In contrast a more lateral approach to palaption of the longissimus makes it theoretically possible to differentiate longissimus sensitivity from iliolumbar ligament sensitivity. Thus if the longissmus can be excluded with no pain on a lateral approach to palaption, and no positive on resited testing of the longissimus, a case can be made to image the iliolumbar ligament.
It’s quite possible therapists may in fact be producing sensitivity from the L4 or L5 lumbosacral trunks when palpating for iliolumbar ligament as can be seen with the proximity in Kim’s (2017) dissection study.
Figure 2. from Kim et al (2017)
References
El Khoury, N., Zebouni, S.H., Revel, M. and Fayad, F., 2016. AB0970 Ultrasonography in Diagnosis and Management of Iliolumbar Syndrome: Case Series.
Harmon, D. and Alexiev, V., 2011. Sonoanatomy and injection technique of the iliolumbar ligament. Pain Physician, 14(5), pp.469-474.
Kim, P.W., 2017. Variations in the L4 and L5 Ventral Rami with Iliolumbar Ligaments in 14 Cadavers. The FASEB Journal, 31(1_supplement), pp.896-13.
Kurosawa, D., Murakami, E., Ozawa, H., Koga, H., Isu, T., Chiba, Y., Abe, E., Unoki, E., Musha, Y., Ito, K. and Katoh, S., 2017. A diagnostic scoring system for sacroiliac joint pain originating from the posterior ligament. Pain medicine, 18(2), pp.228-238.
Laslett M, Young S, Aprill C, McDonald B. 2003. Diagnosing painful sacroiliac joints. A validity study of a McKenzie evaluation and sacroiliac provocation tests. Aust J Physiother. 49:89–97.
Petersen, T., Laslett, M. and Juhl, C., 2017. Clinical classification in low back pain: best-evidence diagnostic rules based on systematic reviews. BMC musculoskeletal disorders, 18(1), p.188.
Iliolumbar Ligament Treatment
Education
Anatomy
From the assessment it looks like the source of your pain is the iliolumbar ligament inflammatory event from tear/ or nociception from the enthesis fat.
Pain
DEPENDS ON WHETHER ENTHESIS OR INFLAMMATORY EVENT.
The nerves from the region send signals back to the spinal cord. If this is strong enough it goes to the brain and your brain “decides” where and how much pain to feel based on all the inputs and all your previous experiences. Our pain is a protective best guess of the brain.
Context Sensitivity
Prolonged sitting is likely irritating and sitting more “upright” can help sometimes, as can taking regular breaks to stand and walk. For the time being heavy lifting, anything you couldn’t lift 20 times normally should be avoided.
Otherwise move as normally as you can as we know this helps.
Understanding The Immune System
Our danger detectors (nociceptors) are sensitive to the immune system, and when ill or injured we are more sensitive. This makes perfect sense from an evolutionary point of view as when ill or injured this led us to protect ourselves. Thus eating poorly, a lack of sleep, increased psychological stress and other impacts on us can make us more sensitive and thus may increase your symptoms.
The immune system also interacts with our nerves to get us to withdraw from activity and socialise less. So don’t be surprised if you feel a bit down or feel less like socialising.
Travelling
When driving or flying try and take regular breaks to stand up and stretch.
Prognosis
Everybody is
different so it is hard to be specific, but our aim is to avoid excessive
strain on the ligament and promote an environment that encourages repair of the
ligament.
Home Exercise Programme
General Exercise
Walking is usually very helpful with these symptoms. Walking has a low level anti-inflammatory effect, puts gentle pain free movement through the lumbar spine which can help calm things down.
Often it might be sensitive to start but should ease off as you do more. If it starts getting sensitive as you walk longer take a rest and gradually try to build up day by day.
Stretching Programme
To address deficits in range of motion found on assessment, which may lead to strain on the ligament.
| No. | Stretch | ||
| 1. | Adductors | ||
| 2. | Abductors | ||
| 3. | Global flexion range of motion Calves Hamstrings Glutes Errector spinae | ||
| 4. | Global extension range of motion Psoas Abdominals |
Exercise Programme
To address deficits in control through range, which may lead to strain on the ligament, based on movement assessment.
| No. | Exercise | ||
| 1. | Supine Lateral Ball Roll | ||
| 2. | Frontal plane hip hinges | ||
| 3. | Frontal plane lean/ dynamic on Swiss ball | ||
| 4. | Horse stance series | ||
| 5. | Reverse hyper extension | ||
| 6. | Lower abdominal series |
Manual Treatment
Could be used to help address range of motion deficits that could be contributing to strain on the ligament.
Direct treatment of the ligament bordering on impossible.
Referral
Diagnostic anaesthetic and possibly steroid can be considered.
Prolotherapy can be considered if not resolving after 6 weeks.
PRP and Stem cells may be worth discussing at the same time as prolotherapy is considered.
Rational for Manual Therapy
It is hard to justify deep transverse frictions or any approach targeted at “touching” the ligament due to its depth. Manual therapy techniques to put the ligament under tension to induce creep are feasible.
Rationale for Posture and Seating Advice
The iliolumbar ligaments resist posterior rotation of the ilia, thus it is theorised that prolonged sitting with the ilia posteriorly rotated could chronically strain the ligaments and thus immobilization of the lumbosacral and sacroiliac joints could decrease iliolumbar pain (Snijders et al., 2004).
Case Studies
Chantraine et al. (2001) described a case study of a 70 year old patient who began to get low back pain after a recent wheelchair change, the patient began to experience low back pain, alleviated only by lying in a kyphotic position or standing in a forward position. Various treatments for pain relief including physical therapy, stretching, mobilization, and acupuncture were unsuccessful. They found a “trigger point” in the left iliac crest when the patient contracted the surrounding muscles. Using echotomography they found a torn left iliolumbar ligament. However there are many issues with attributing the patient’s symptoms to the iliolumbar ligament. The iliolumbar ligament is not innervated (Wang et al 2018), and there was no follow up with steroid or anaesthetic to confirm this as the site of the patient’s pain. Furthermore the history makes little sense, a wheelchair bound patient with no acute injury. Perhaps it could have occurred chronically due to prolonged load in an abnormal position? However, if the ligament was torn and is not innervated it’s unlikely the innervated fat at the enthesis would give rise to nociception, more likely another tissue may be placed under higher levels of mechanical load perhaps the thoracolumbar fascia or the lower fibers of quadratus lumborum for example. Given the history it is surely as likely the tear was chronic and possibly contributing to abnormal mechanics but to attribute the patient’s symptoms to the iliolumbar ligament tear without alleviation of symptoms without a diagnostic injection is sloppy at best.
Harmon and Alexiev (2011) injected a local anaesthic along the course of the iliolumbar ligament in a patient suspected of iliolumbar syndrome and the patient’s pain decreased from 7/10 pre-injection to 2/10 post-injection. Range of motion was also improved. Subsequently the patient underwent prolotherapy and achieved a total resolution of symptoms. Although previously prolotherapy involving the iliolumbar ligament as part of a general prolotherapy approach to the ligaments of 4-5 and 5-1 motion segments in chronic low back pain patients has been largely unsuccessful (Dechow et al 1999).
El Khoury et al (2016) reported on 30 patients with iliolumbar inflammation based on ultrasound findings. The patients received a treatment with NSAIDs and a 12-session course of physical therapy, but this standard therapy was insufficient in 67% of cases.
Pain relief from a presumed iliolumbar ligament syndrome has been demonstrated with an infiltration of the iliolumbar ligament when treated with lidocaine and dextrose (Naeim et al 1982). Subjects who were treated with the lidocaine-dextrose mixture reported more pain relief than those who were treated with lidocaine alone.
References
Chantraine, A., Bosson, L., Malaise, M., Onkelinx, A. and de Leval, J., 2001. The occurrence of the ilio-lumbar syndrome in a spinal cord injury patient. Spinal cord, 39(4), p.237.
Dechow, E., Davies, R.K., Carr, A.J. and Thompson, P.W., 1999. A randomized, double-blind, placebo-controlled trial of sclerosing injections in patients with chronic low back pain. Rheumatology, 38(12), pp.1255-1259.
El Khoury, N., Zebouni, S.H., Revel, M. and Fayad, F., 2016. AB0970 Ultrasonography in Diagnosis and Management of Iliolumbar Syndrome: Case Series.
Harmon, D. and Alexiev, V., 2011. Sonoanatomy and injection technique of the iliolumbar ligament. Pain Physician, 14(5), pp.469-474.
Naeim, F., Froetscher, L. and Hirschberg, G.G., 1982. Treatment of the chronic iliolumbar syndrome by infiltration of the iliolumbar ligament. Western Journal of Medicine, 136(4), p.372.
Snijders, C.J., Hermans, P.F., Niesing, R., Spoor, C.W. and Stoeckart, R., 2004. The influence of slouching and lumbar support on iliolumbar ligaments, intervertebral discs and sacroiliac joints. Clinical Biomechanics, 19(4), pp.323-329.
Wang, J.M., Kirkpatrick, C. and Loukas, M., 2018. The Iliolumbar Ligament Does Not Have a Direct Nerve Supply. The Spine Scholar, p.3661.