The Management of Cluneal Nerve Referred Pain with Prolotherapy

James Inklebarger, MD & Nikforos Galanis, MD


Lumbar, upper buttock and leg pain attributed to entrapment of medial branches of the superior cluneal (MBSC) nerve at the region of the posterosuperior iliac crest has been well documented in the literature. As it is with other nerve entrapments, MBSC dysfunctions may be predisposed by abdominal or spinal myofascial weakness post surgery, degenerative disc disease, scar tissue and a variety of endocrine, and metabolic factors, and even be generated by the nerves themselves.

Case series reports have described a plethora of pain management strategies, including bed rest, with or without pain or anti-inflammatory medications, nerve blocks, radio-frequency ablation (RF), manual manipulation therapies, massage and surgical nerve release techniques.

Identifying MCSC nerve entrapments by seeking ‘trigger points’ or localized tender points at the posterior iliac crest raises suspicion that the problem exists. Image-guided (fluoroscopy or ultrasound) or anatomical landmark corticosteroid-anesthetic nerve blocks if successful, help to confirm the diagnosis and cluneal nerve involvement and in some cases provide long-term pain relief and tolerance to rehabilitation. Should cluneal nerve injection provide only temporary pain relief, the next steps might be radiofrequency ablation (RF) and finally arthroscopic release. Taking such as step-wise approach to diagnosis and treatment may offer more effective pain management. This paper proposes that cluneal nerve pain and entrapment may be a manifestation of spinal ligament instability and that prolotherapy, in stabilizing these structures, may afford and alternative approach to RF and surgical management.

Journal of Prolotherapy. 2018;9:e982-e991.


Impingement of the medial branch of the superior cluneal (MBSC) nerves are thought to be an overlooked cause of low back pain, with this impingement occurring where the branches of these nerves pass over the superior rim of the iliac crest in osseofibrous tunnels formed by the thoracolumbar fascia.

Immunohistochemical staining of the iliolumbar ligaments (ILL) have demonstrated a rich supply of nerve tissue. Those results may indicate that the ILL plays an important role in proprioceptive coordination of lumbosacral region, in addition to its known biomechanical supportive functions. Moreover, the presence of type IV nerve endings suggests that the injury of this ligament might contribute to the low back pain.1

Other similar cadaveric studies seem to also support the hypothesis of a morphological and physiological basis for sacral ligaments pain generation, by noting the presence of calcitonin gene-related peptide (CGRP) and substance P, tracing nociceptive fibers and receptors within the anterior capsular and interosseous sacroiliac ligaments, suggesting the need for both extra and intra capsular sacroiliac joint injections for optimal pain relief.2

Cadaveric dissection has even noted cluneal nerve branches embedded within the deep fascial layer of the long posterior sacral ligament’s (LPSL) it. It would therefore appear that this adipose and lose connective tissue deep layer of the LPSL, actually provides a transit pathway for the lateral branches of the dorsal sacral rami between the posterior sacral region and the gluteal region. These histological studies may imply morphological basis that putative sacroiliac joint pain may be due to a chronic LPSL dysfunction and subsequent entrapment neuropathy of the lateral branches of the dorsal sacral rami within the deep layer of long posterior sacroiliac ligament.3

Additionally, the LPSL has close anatomical approximation with the erector spinae muscles, the posterior layer of the thoracolumbar fascia, and parts of the sacrotuberous ligament (tuberoiliac ligament), forming a functional link between legs, spine, and arms. The ligament is tensed when the sacroiliac joints are counternutated and slackened when nutated. The reverse holds for the sacrotuberous ligament. Slackening of the long dorsal sacroiliac ligament can be counterbalanced by both the sacrotuberous ligament and the erector muscle. Pain localized within the boundaries of the long ligament could indicate among other things a spinal condition with sustained counternutation of the sacroiliac joints.4

The superior cluneal nerves innervate the skin of the upper part of the buttocks. They are the terminal ends of lateral rami of the posterior rami of the lumbar spinal nerves (L1, 2, 3).

The medial branch of the superior cluneal nerve passes over the iliac crest through a tunnel formed by the thoracolumbar fascia and the superior rim of the iliac crest. This branch of the superior cluneal nerve may become restricted in its osseofibrous tunnel against the iliac crest, just as osteofibrous tunnels affect other nerves, such as in carpal tunnel syndrome.

Lu et al 1998, described for the first time the anatomic relationship of the superior cluneal nerve to the posterior iliac crest and thoracolumbar fascia. They dissected 15 cadavers and found that the medial branch of the superior cluneal nerve is confined within a tunnel consisting of the thoracolumbar fascia and the superior rim of the iliac crest as the nerve passes over the iliac crest. (See Figure 1.) The location is 7-8 cm lateral to the midline (sacral spinouses) on the iliac crest just lateral and superior to the posterior superior iliac spine (PSIS). These investigations noted that the medial branch of the superior cluneal nerve passes superficially over the iliac crest, and is covered by two layers of dense fibrous fascia. It had also been noted that these nerves might also be damaged in during spinal surgery.6

Challenges in Management: Maigne’s Syndrome and the Double Crush Phenomenon

In some surgical case reports, no true cluneal nerve entrapment has been noted on operative exploration, and persistent post-operative pain has been described in case reports. One such case described residual pain in the region of the long posterior sacral ligament on both sides, with palpation on the LPSL consistently reproducing LBP and leg tingling radiating from the buttocks to the calves on both sides. It was also reported that 6 post operative nerve blocks attempts over 6 months were non-productive and yielded no substantial permanent change in low back pain.7

Maigne in performing cadaver studies, noted that the MBSC nerves arise from cutaneous branches of the T11-L4 dorsal rami.8 He went on to propose that cluneal nerve entrapments may not only arise from impingements at the posterior iliac crest, but the associated of low back pain may also be related to patho-mechanical changes in the unilateral thoracic lumbar junction facet joints impinging on these nerves. (See Figure 1.)

Figure 1. Illustration of the Superior Cluneal nerves crossing the posterior iliac crest.

Though no pain was produced upon direct palpation of the thoracolumbar primary nerve impingement source, thoracolumbar junction facet joint dysfunction did in his opinion, affect the proximal part of the nerves, contributing to symptoms lower down where the nerves crossed the posterior superior margin of the iliac crest. Here the nerves are more superficially vulnerable and prone to entrapment. It was speculated that this observed variance in the thoracolumbar origin of cutaneous nerve sensory branches contributed to iliac pain in a similar fashion, as cervicogenic nerve root entrapment may cause carpal tunnel syndrome.9

This ‘double crush’ phenomenon was first described by Upton and colleagues in 1973. In reference to the cluneal nerves it became known as ‘Syndrome Des Les Maigne.’10,11

Several authors have also described nerve entrapment within the osseofibrous tunnels where the MBSC nerves pass over or near the iliac crest. Maigne in later papers confirmed this, describing consistent cadaver dissection findings of MBSC nerve transit within osteofibrous tunnels, which proposed a pain generation mechanism of nerve entrapment at the superficially vulnerable position of the iliac crest.5,8,12,13

Cadaveric dissection studies have also sought to define the anatomical relation of the superior cluneal nerve to the posterior iliac crest and thoracolumbar fascia. Proximal dissection above the perforating point of the nerve showed that the medial branch of the superior cluneal nerve is confined within a tunnel consisting of the thoracolumbar fascia and the superior rim of the iliac crest as it passes over the iliac crest. The intermediate and lateral branches of the superior cluneal nerve either pierce the thoracolumbar fascia or pass through an orifice or fissure in the thoracolumbar fascia. In 2 of 15 specimens, the medial branches of the superior cluneal nerve were constricted within the osteofibrous tunnel. The nerve was entrapped between the rigid fibers of the thoracolumbar fascia and the iliac crest.5

However, more recent work have noted that though 39% of the MBSC nerves do transit within these anatomically described osseofibrous tunnels, only 5% actually display macroscopic signs of entrapment.14

So rather than a single entity of posterior iliac crest area nerve entrapment, there may be an combined interplay between thoracolumbar facet joint instability above and lumbopelvic ligamentous laxity below, with the ‘double crush’ phenomenon predisposing the MBSC nerves to aberrant stretching and traction forces at the point of vulnerability where they cross over the rim of the iliac crest within osseofibrous tunnels. Over time, chronic lumbopelvic ligamentous instability may predispose a reactive hypertrophy of the thoracolumbar fascia, which would eventually produce a true MBSC nerve entrapment in the osseofibrous tunnels, or as branches pass under the long posterior sacroiliac ligament.7

However, there are several published cases series and case reports describing surgical release of severe MBSC iliac region nerve entrapment, providing dramatic relief of unilateral buttock pain.15-18

Diagnoses and Methods of Examination

The diagnosis of cluneal nerve entrapment may be challenging. Pain over the medial portion of the iliac crest and in the gluteal or lumbosacral area are often attributed to a facet syndrome, lower lumbar disc problem or an iliolumbar syndrome (involvement of the iliolumbar ligament).7 Clinical symptoms of cluneal nerve entrapment have been described as low back pain, which may radiate to the ipsilateral leg. Clinical signs include tenderness at iliac crest rim just above the dimple at the buttock and decreased touch sensation of the buttock just below the iliac crest. A diagnosis of medial cluneal nerve entrapment is made by palpation of the iliac crest or LPSL resulting in marked local tenderness and pain relief after local anesthetic injection.7

Certainly, this contentious area is adequately innervated by branches from the cluneal nerve and from the terminal innervation of the ligamentous construction of the posterior sacroiliac joint. However, there are other pain generators to consider. The buttock is composed of diverse, interacting and interdependent anatomical structures of which striated muscle is in abundance. Any of these structures may selfishly precipitate buttock discomfort or outright pain. However, intrinsic direct localized trauma apart, not all of these structures are capable of producing a pattern of localized, upper buttock pain of an acute, subacute or chronic in quality, and the pain may also be referred.

Authors have reported that the diagnosis of Maigne’s syndrome can only be made clinically. Classic signs are: a positive iliac-crest point test, a positive pinch-roll test, localized facet joint area tenderness at the thoracolumbar junction, and deep tenderness are located at the level of the iliac crest at a point, which is consistently located circa seven centimeters from the midline. For the posterior iliac crest point sign; pressure at this point causes a sharp pain similar to the patient’s complaint. This sign requires careful and precise localization. Once the irritated nerve is located, deep pressure and gentle movement produce marked tenderness. The opposite iliac crest is examined in a similar manner and is commonly unaffected. The skin and subcutaneous tissues of the lower lumbar and upper gluteal region are examined.19

Spinal Stability Tests

Unfortunately research on defining symptoms and signs of spinal instability is sparse. Furthermore, the diagnosis of clinical spine instability is controversial for a number of reasons, including poor reliability-validity of special tests, and poor correlation between spinal motion and symptom severity.20 However, It is has been generally defined spinal segmental hypermobility or motor unit laxity beyond normal physiologic limits.21 However, tests such as the prone stability test below (See Figures 2 & 3.) has better (0.87) inter-rater reliability22, than some other tests, and this test may be useful in helping to identify patients who may be suffering from cluneal nerve-related pain secondary to spinal instability.

Figures 2 & 3. Prone spinal instability tests.

The Prone Stability Test has 2 Parts. The patient is first asked to lie prone with his legs hanging of the bench but with contact to the ground. Posterior to anterior downward pressure (springing) is then applied by the examiner with his hypothenar eminence, starting at the lumbosacral joint and advancing cephalad to the joints above up to the lower thoracic spine in an attempt to provoke pain. (It is the author’s opinion that this test may also be used for sacroliac joints too by applying direct posterior to anterior springing pressure over each joint) If pain is SIJ, lumbar or lower thoracic segmental discomfort or pain is provoked, the patient is asked to lift his legs off of the floor. For the 2nd part of the test, the examiner re-applies pressure to the spine. If the area which was painful with the legs on the floor is now pain-free or the pain is reduced, this is considered to be a positive test. This finding may imply the presence of segmental hypermobility, and that the patient paraspinal muscles are actively capable of stabilizing his spine, which would imply that a spinal stabilization exercise program may be an appropriate first step. The test may also imply however, that the patient is a candidate for spinal ligament stabilization prolotherapy.

Treatment Methods

Initial management of spinal instability associated cluneal nerve pain, relies on an elimination of potential flaring activities. As the aim is healing in the presence of full range of motion, Mayo belts and other back braces that limit full flexion of the lower are not recommended.

High BMI patients may benefit from weight loss and as it is with Meralgia Paresthetica, the wearing of constrictive clothing and belts, which may but pressure on these subcutaneous nerves should be avoided.23

There may also be recreational, sport or occupational risk factors. Weight lifters, builder or other tradesman may strap heavy tools to their waists for prolonged periods, or police officers who must continually wear utility belts laden with hand-cuffs, radios, pistols, ammunition clips while sitting or repetitively getting in and out of vehicles may be also be vulnerable. A course of non-steroidal anti-inflammatories (NSAIDs) may be trialed. For thoracolumbar junction involvement, a course of modified pelvic tilt exercises has also been recommended.24 Regional massage, spinal manipulation and soft tissue mobilization techniques may also be trialed. A combined approach of progressive spine strengthening rehabilitation and postural exercises along with spinal manipulation and targeted thoracolumbar corticosteroid injections achieves a more favorable outcome.25,26

Should these measures only provide temporary relief, then cluneal nerve blocks via anatomical landmarks or ultrasound guidance may be all that is required. However, if the pain returns a series of neural prolotherapy (superficial 12.5-25% dextrose sterile water subcutaneous regional injections, neuroprolotherapy) may be trialed and then spinal ligament targeted prolotherapy with continued rehabilitation exercises to more comprehensively address any underlying instability issues.

Subcutaneous neural prolotherapy injections may facilitate cluneal nerve regeneration while injections targeting relaxed spinal ligaments aim to improve lumbopelvic stability.

Case One

A 58 year old female house-wife presented to the an emergency department complaining of progressively worsening right unilateral non-radicular low back & posterolateral upper buttock pain, progressively worsening over time, with night pain and sleep disturbance. The pain was worsened by turning in bed, and she had noticed a focally tender area on self-palpation of the right posterior iliac crest as the sight of her pain. She reported that a prior course of physiotherapy with spinal manipulation had not eased the symptoms, but she did experience some temporary respite from pain with ibuprofen and paracetamol. The pain was interfering with her ability to clean house. X-rays obtained of the lumbo-sacral spine reported some mild lower lumbar segment facet joint arthrosis but were otherwise unremarkable.

On examination lumbar range of motion was symmetrical without any end of range discomfort. Gait and posture were generally unremarkable. Leg length was equal bilaterally and neural tension tests negative. Deep tendon reflexes and Babinski tests were also unremarkable, as was strength testing of the lower limbs. Hip and knee range of motion were full and pain free. The lower limbs were neurovascularly intact. Focal tender points were noted at the anatomical location of the right superior cluneal nerves at the posterior iliac crest, and prone spinal stability tests reproduced pain in the right sacroiliac joints and lower lumbar segments. However, prone thoracolumbar junction springing was unremarkable.

Anatomical landmark injections were performed with 20 mg of Kenalog in 5 ml of 1% lidocaine, in the palpably painful area, which corresponding to the anatomical location of the right superior cluneal nerve producing immediate relief. The benefits of injection lasted for circa 3 weeks but the pain then returned. One off bilateral lumbar side posture osteopathic manipulations were performed on the lumbar spine. The patient then underwent a series of 8 lumbar prolotherapy injections. The solution used was 50/50 concentration of P2G (phenol-glycerin-glucose) mixed with an equal amount of 1% lidocaine for a total volume of 20 ml. This solution was injected into the lower lumbar segment supraspinus and interspinus ligaments and their corresponding facet joints, and transverse process tips bilaterally. Solution was also injected into the attachments posterior iliac crests iliolumbar ligaments, sacro-iliac joints and the enthesis of the gluteus medius. She was advised to take only paracetamol analgesia if the need arose. Aside from transient localized soreness and some bruising following the first injections there were no other side effects reported. She was also advised to perform gentle seated trunk forward flexion exercises and simple standing leg swing 20 repetitions both morning and evening. She was also advised to self-massage (knead) the sore area at the posterior iliac crest. The pain abated and she returned to her habitual housework without symptoms. The patient remained pain free on one year follow-up.

Case Two

A 42 year old female presented to a musculoskeletal medicine out patient department complaining of 5 years of chronic and worsening right unilateral upper buttock pain which had not responded to courses of paracetamol, codeine, tramadol, or gabapentin. The pain was disturbing her sleep and interfering with her activities of daily living. Several courses of physiotherapy, exercise programs, acupuncture, and spinal manipulation had failed to alleviate her pain, and her symptoms had progressively worsened over the past year or so and she became intolerant to rehabilitation exercises and was having activities of daily living difficulties. She had become more sedentary and was upset at her subsequent weight gain. She was tearful on initial consultation, reporting that she had recently been reviewed by a pain management team and was informed that aside from the medications, there was nothing more that could be offered in the way of pain relief.

Exquisitely tender points were noted in the region of the right posterior iliac crest around 7 centimeters from the midline, with further tender points in the right lumbodorsal fascia. Prone segmental springing tests were positive on the bilateral sacro-iliac joints, and lower lumbar segments. There was no pain on springing of the thoracolumbar junction. Lumbar spine range of motion was symmetrical but forward bending was limited to 80 degrees, with the patient reporting that end of range forward bending and left lateral flexion reproduced a generalized pain in the right lower back region. The lower limbs were otherwise neurovascularly intact.

Initially, the tender points, corresponding to the anatomical location of the right MBCS branches were infiltrated with 40 mg of Kenalog in 10 ml of lidocaine. Post injection, the palpable tenderness at the posterior iliac crest was relieved and she was able to achieve a few more degrees of forward and left lateral bending. The following week and course of 8 weekly lumbosacral prolotherapy injections was commenced, comprehensively treating the lumbosacral spine in the method described in case one. The patient continued to perform gentle spine range exercises throughout the treatment period to tolerance. On one-year telephone follow up she reported that aside from a few ‘niggles’ she was essentially pain free. She had carried on with her exercises and made it a part of her daily routine. She had also resumed household and shopping activities, had become more active, was sleeping better, had lost weight, and was able to bend forward to pick up objects off the floor.


In both of the above cases, patients presented with unilateral upper buttock tender points in the anatomical region of the MBCS branches at the posterior iliac crest, along with positive prone lumbar instability tests. Their primary pain was also abated by anesthetic blocks administered at the anatomical sites of the cluneal nerves. (See Figure 1.)

The diagnosis and management of lower lumbar, upper buttock pain is challenging. It has been speculated the MBCS nerves may be responsible for so-called pseudo-sciatica, when they become entrapped in transit of the thoracolumbar fascia over the iliac crest. It is also been proposed that cluneal nerve entrapment may mimic sciatic symptoms of low back pain with referred pain into the posterior thigh, hamstrings, calf and on occasion the ankle and foot.27

However, if the Sacrospinous ligament is strained these same types of pain patterns from the lower inner portion of the buttock, posterior thigh and posterior calf, may also terminate as far down as the plantar portion of the heel of the foot. If present for several days a degree of atrophy of the hamstrings and calves may occur, along with a decreased Achilles reflex, coupled with the limitation of straight leg raise. Identifying the primary pain generator in these scenarios can be quite challenging and imaging may not be very helpful, particularly in subjects over the age of 40, who may also present with x-ray or MRI imaging of degenerate lumbar discs or facet joint arthrosis.

The current prod and inject physical examination diagnoses of cluneal nerve entrapment may miss other pain generators. Nuances and meanings of terms such as trigger points (TPs) and tender points are inconsistently defined, with diagnosis confined exclusively to history and physical examination.28

Recent Delphi panel consensus of 2 of 3 diagnostic TPs criteria (taut band, hypersensitive spot, referred pain), and delineation between active and latent trigger TPs, will be useful in establishing evidence-based definitions.29

Hallmark physical features of tender points, taut muscle bands, and characteristic pain reproduction and referral have poor inter-rater reliability.30

Exhaustive literature reviews have also concluded that trigger point diagnosis has poor physical examination reliability.28,30,31

Recent Delphi categories for myofascial pain syndrome due not seem to have addressed, underlying ligament laxity, referred nerve pain, or physiological-embryologically normally tender points as other potential causes of palpable pain generation. Nevertheless, adjacent spinal ligaments in proximity to cluneal nerves branches must not be overlooked, as these ligaments to be pain generators in themselves. Even in cases of true cluneal nerve entrapment confirmed upon surgical exploration, lumbopelvic ligamentous relaxation may be an underlying, as relaxation of these ligaments may lead to chronic lumbo-pelvic instability. This may in turn may predispose overstretch and irritation of cluneal nerve branches crossing the posterior iliac crest within or external to the osseofibrous tunnels. The continued presence of chronic spinal ligament instability may indeed eventually evolve into reactive soft tissue hypertrophy and in rarer cases, true nerve entrapment. So rather than being an isolated phenomenon, nerve entrapment may originate in continued instability stress forces on the nerves and nerve-adjacent tissues with cluneal nerve pain a symptom, rather than cause.

Coupling palpation examination with spine stability tests may help to better identify candidates of spinal prolotherapy. There are many spine instability tests. The prone spine instability tests was chosen here, as it has fairly good inter-examiner reliability. However, more research is needed to evaluate the clinical value of these tests.

Pain management and surgical approaches seeking to ablate or free nerves from this soft tissue entrapment down in isolation would fail to address or treat any underlying instability. Therefore rehabilitative strengthening and range of motion exercises (to tolerance) are recommended in tandem with any injection therapy.

Caution is advised to avoid too overzealous amounts of pressure in the upper gluteal region on palpatory examination. Some Martial Art systems have pressure point techniques mapped as being vulnerable to pain generation, which coincide were nerves closely underlie to skin. The clan samurai Minamoto no Yoshimitsu (1045-1127), was the first to dissect battle field corpses for vulnerable anatomy, and introduce the pressure point concept into martial arts fighting.32

So firstly, and in order to avoid over diagnosis, clinicians should therefore be aware that physiological tender points may exist in the posterior iliac crest under normal circumstances. Refinements of Minamoto’s original conclusions have been further summarized in the 19th century premise of Hilton’s law which was based upon the pre-migration pre-differentiation ectodermal neural crest common embryological origins of human neural and connective tissues.33

Hilton’s law states that a nerve supplying a joint, also sends innervating branches not only to the muscles and enthesial attachments that move that joint, but into the skin overlying the joint as well.34 This law also may be used to explain the mechanism by which neuroprolotherapy helps to relieve cluneal nerve pain.

Joints, ligaments, and tendons all share TRPV-1 nociceptor C fibre innervation, and even mild C-fibre nerve degeneration and damage has also been implicated in the transmission of deep pain in rheumatoid as osteoarthritis of the knee.35

Chronic constriction injuries of the MBSC nerve at the thoracolumbar junction or as it passes through the deep ligaments and fascial planes, have been supported my animal model experiments which inhibit anterograde and retrograde axoplasmic flow distribution of nerve growth factor.36

Maintenance and restoration of unencumbered axoplasmic flow with free migration of neurotrophic factors, have also been experimentally demonstrated to be important for peripheral nerve homeostasis and regeneration.37,38

Further studies have provided supportive data of a pro-inflammatory the role of 35 in the regulation of somatic and cutaneous pain transmission.39

The MBSC nerves themselves are also innervated nerve by the Nervi Nervorum. Impingement of the Nervi Nervorum may reactively release both substance P and CGRP), thereby amplifying C nerve fibers nociception.40

Not ignoring the cadaver dissection and conclusions of Maigne et al, thoracolumbar junction area dysfunction may also predispose to cluneal nerve entrapment at the iliac crest just as cervical nerve root dysfunction may predisposes to carpal tunnel syndrome, by way of a ‘Double Crush phenomenon.10

Managing thoracolumbar instability may therefore be and important factor for addressing cluneal nerve entrapment at the iliac crest.
There is scan literature regarding the accuracy and/or reliability of either the Prone Instability Test (PIT), or the Passive Lumbar Extension Test (PLE).41 This tests though general may however offer some examiner insight into potential instability contribution to cluneal nerve pain, but further validation will be required.

Buttock pain rather than being generated by nerve entrapment, is more likely due to chronic soft tissue strain of the Glutues medius either directly, or indirectly from sacro-iliac joint and/or thoracolumbar (Maigne’s syndrome) instability, which may refer also refer pain to the posterior iliac crest, lateral thigh or groin. However, the iliolumbar ligament itself may also refer pain to the groin as well.

MBCS nerve entrapment may therefore not be an isolated condition, but rather a symptom of multi-dimensional causation, such as the double-crush interplay between lumbo-pelvic ligamentous instability, thoracolumbar junctional dysfunction, gluteus medius strain, SIJ dysfunction and reactive compensatory soft tissue hypertrophy. This may down the line predispose to MBSC nociception, nerve inflammation, and in sometimes even true nerve entrapment, but this may be a sequella rather than underlying cause.

Alleged MBSC nociception if it actually exists, may be achieved by first proficiently treating underlying conditions. Prolotherapy injections offer such a solution, as these injectants, utilizing substances such as dextrose, dextrose-glycerol-phenol (Ongley’s Solution or P2G), or other substances such as sodium morrhuate. Targeting the gluteus medius enthesis, facet joints space, and lumbosacral ligaments, may stimulate natural healing processes through inflammation. Thereby, optimal thoracolumbar and pelvic motor unit stability is achieved which in turn may relieve secondary nerve pain, and prevent further reactive nerve-entraping soft tissue hypertrophy. Solution is also injected around the nerves (neuroprolotherapy). However, accurate spino-pelvic ligament injection delivery to deeper structures requires a in depth practical knowledge of anatomical landmarks and palpation skills. Some may also be perform these techniques under ultrasound or fluoroscopic guidance.

A classical prolotherapy approach may facilitate direct MBSC nerve regeneration, (dextrose saline neuralprolotherapy), while stabilizing the deeper ligamentous thoracolumbar and lumbopelvic joint complexes. Prolotherapy treatment of spinal pain became organized the 1960’s. An English formulated combined dextrose-glycerine-phenol sclerosant solutions proposed a chemically synergistic effect of these substances. In those early days. However, a 50% concentration of dextrose was only a 10% concentration in the Sclerosant was difficult to obtain. Be reformulating, and adding 50% dextrose to the solution a highly effective regenerative solution was achieved. Dr. Ongley noted that this concentration worked very well, with the phenol quelling the cluneal nerves in an almost pain free treatment. Other solutions, such as those used by George Hackett such as the psysillium seed oil-Sylnasol) produced very painful side effects which limited patient compliance and thus fell out of favor.

The hierarchal flow chart, (See Figure 4.), describes a proposed pathway of cluneal nerve pain diagnosis and management.

Figure 4. A proposed pathway for cluneal nerve pain diagnosis and management.

If chronic unilateral low back and upper buttock pain are unresponsive to rehabilitation and other pain generators (disc herniation, facet joint arthropathy, sacroilliitis), have been excluded and active trigger or tender points are identified in the upper buttock region, cluneal nerve blocks may be attempted. Relief of pain with these injections serves to confirm the diagnosis of cluneal nerve involvement. If the results are long lasting then Mackenzie-like stabilization rehabilitation of the thoracolumbar and lumbopelvic spine is recommended. If the pain relief achieved from cluneal nerve injection is temporary, then radiofrequency ablation and consideration of arthroscopic cluneal nerve release followed by rehabilitation may be the next logical steps. Alternatively, lumbopelvic ligamentous prolotherapy and if required thoraco lumbar prolotherapy may be considered in conjunction with rehabilitation. Those who practice neural prolotherapy may also trial this as an intermediate step prior to spinal ligament prolotherapy. However, if spinal ligament instability tests are positive spinal ligament prolotherapy will likely be required to afford optimum pain management and functional outcome. (See Figures 2 & 3.)


Tender or trigger point palpation coupled with spine instability tests may help to confirm a potential diagnosis of underlying spine instability as contributory to cluneal nerve pain. Before considering RF or cluneal nerve release surgery spinal prolotherapy may offer an alternative management to MBSC nerve pain.


I would like to thank Dr. Milne Ongley and Dr. Kulvinder Sigh for their assistance in the preparation of this manuscript.


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