Why the cluneal nerves matter

Low back pain work-ups focus, rightly, on the disc, the facet joints and the sacroiliac joint. Peripheral nerve entrapment has been overshadowed by these spinal causes, even though the cluneal nerve syndrome was first described in 1957, when pressure on the superior or middle cluneal nerves under local anaesthesia reproduced pain in the back, groin, leg and foot [1].

Estimates of SCN entrapment range from 1.6% to 14% of patients with low back pain [1,3]. In a prospective series of patients presenting with low back and/or leg symptoms, 12% had an SCN disorder, and about half of these had leg pain or tingling [9]. MCN entrapment was found in 13% of low back pain patients in another series [3]. Bilateral SCN entrapment is not unusual [1].

The clinical relevance is simple: these nerves are superficial, easy to examine and easy to block, and a correct diagnosis opens up treatments that are low in morbidity.

Anatomy

The cluneal nerves are three groups of purely sensory nerves supplying the skin of the buttock. The superior and middle groups arise from the lateral branches of the dorsal rami (roughly T11–S4). The inferior group arises from the ventral sacral plexus via the posterior femoral cutaneous nerve [1,2]. Because each group shows extensive and variable branching, it is more accurate to speak of the cluneal nerves in the plural [1].

Superior cluneal nerves (SCN)

Origin. Classically L1–L3, but cadaver work shows contributions from T11/T12 down to L5. L4 contributed in 45% and L5 in 10% of specimens, and most SCN branches draw on three or four levels [6,13]. Lower lumbar contributions help explain why SCN entrapment can produce leg pain [1,14].

Course. The nerves run through the paraspinal muscles (within or between iliocostalis and longissimus), behind quadratus lumborum, then pierce the thoracolumbar fascia and cross the posterior iliac crest [1,4].

Branches and landmarks. Usually medial, intermediate and lateral branches, although more than three branches cross the crest in about a third of specimens [6]. Where they cross the crest they lie, on average, 5, 6.5 and 7.3 cm lateral to the PSIS [4]. The most medial branch lies about 7–8 cm from the midline (range 5–9 cm with body size) [1]. Mean diameter is about 1.1 mm [4]. The “middle branch of the SCN” is not the same as the MCN [2].

Entrapment site. Where the nerves pass through the thoracolumbar fascia over the crest. Branches that pierce the fascia below the crest pass through an osteofibrous tunnel formed by the fascia and the bone. The medial branch is involved most often (about 40% of specimens), and roughly half of dissections show at least one branch in a tunnel [1].

Territory. Skin over the posterior iliac crest and the upper two-thirds of the buttock, as far laterally as the greater trochanter [1].

Middle cluneal nerves (MCN)

Origin and course. Lateral branches of the S1–S3 dorsal rami (L5–S4 in some descriptions) leave the dorsal sacral foramina and form loops on the back of the sacrum, the posterior sacral network. They then run horizontally or inferolaterally below the PSIS, cross the long posterior sacroiliac ligament (LPSL) and pierce gluteus maximus [1,2]. Whether they run over, through or under the LPSL varies between studies [2].

Landmarks. At their origin they lie about 2 cm above, level with, and 1.5 cm below the PSIS; mean diameter about 0.8 mm [4]. The network is centred on S2 [1].

Entrapment site. Where the nerves pass under or through the LPSL. Repeated stretch of gluteus maximus and the skin with hip flexion adds a further mechanism [1].

Territory. Skin over the posteromedial buttock. Branches may communicate with the medial SCN [1,2].

Inferior cluneal nerves (ICN)

Branches of the posterior femoral cutaneous nerve (S1–S3) wrap around the lower border of gluteus maximus and run upwards to supply the lower buttock, the skin beside the anus and beside the labia majora or scrotum [2]. ICN entrapment causes pain on sitting rather than back pain [1], and belongs with the deep gluteal and pelvic differentials.

Pathophysiology and risk factors

Entrapment usually results from a combination of traction, friction and repetitive compression. These lead to perineural oedema, inflammation and scarring that stop the nerve gliding normally [1,3]. Contraction of latissimus dorsi and gluteus maximus tightens the thoracolumbar fascia, adding a dynamic component [1].

• Iatrogenic injury: posterior iliac crest bone graft harvest, spinal fusion, sacroiliac screw placement, decubitus ulcer surgery and muscle flaps [2,3]. Staying within about 5 cm of the PSIS on the crest reduces the risk to the SCN [4]. With wider use of allograft, entrapment is now a more common cause than injury [1].
• Vertebral compression fracture: SCN disorders were more than twice as common in patients with vertebral fractures (27% versus 12%) [3,9]. Plain films are worth reviewing.
• Altered tone and posture: Parkinson’s disease, kyphosis and quadratus lumborum spasm [1,2].
• Demographics: more common in older patients and women, but also seen in young, physically active groups such as soldiers and athletes [2,3].
• Double crush: foraminal stenosis or disc disease at T12–L2 may make a distally compressed SCN more symptomatic [1].

Clinical presentation

The typical picture is deep, aching, poorly localised and usually one-sided low back or buttock pain. Referral into the thigh or leg is common [1,2]. Symptoms are aggravated by lumbar flexion, extension and rotation, changes in posture, standing, walking and rolling in bed [2]. Dysaesthesia is occasionally the dominant complaint [2]. In a 2026 systematic review of 236 surgical cases, every patient had low back pain, most had buttock or thigh symptoms, and about a third had leg symptoms [7].

Clinical examination

The most important part of the diagnosis is thinking of it [1]. The examination is quick, needs no equipment and should be part of every assessment of low back and buttock pain.

Step 1: Ask the patient to point

Ask the patient to indicate the site of pain with one finger. A finger placed on the iliac crest a hand’s breadth from the spine, or just below the PSIS dimple, should prompt a focused cluneal examination [1].

Step 2: Find the landmarks and the tender points

With the patient prone or standing slightly flexed, mark the midline, the PSIS dimples and the iliac crests (Figure 4). Then look for the point of maximum tenderness that reproduces the patient’s own pain.

Step 3: Provocation and supporting signs

• Lumbar hyperextension, lateral bending away from the painful side and rotation may reproduce SCN pain [1].
• Combined full flexion of the ipsilateral hip and knee has been proposed as a provocative test, although it is not specific [1].
• Skin rolling over the buttock and crest, compared with the other side, may reveal tender, thickened skin in the territory of an irritated dorsal ramus branch (Maigne’s sign) [1].
• Palpate gluteus medius along the crest and towards the greater trochanter to identify coexisting myofascial pain [1].

Step 4: Confirm a normal neurological examination

The cluneal nerves are purely sensory. Strength, reflexes and dermatomal sensation should be normal. A motor or reflex deficit points to radiculopathy, either alone or alongside cluneal entrapment [1,2].

Diagnosis and differential

Cluneal neuralgia is a clinical diagnosis confirmed by a diagnostic local anaesthetic block, which is regarded as the reference standard [2,7]. Imaging is used mainly to exclude other causes.

Interpreting the diagnostic block

• Threshold: 50% or more relief is the usual standard [7]. Some surgical series required more than 75% for the SCN [8].
• Volume: keep it small. The published techniques use about 1–2 mL at the target [1,8]. Larger volumes (the RFA series used 8 mL of 0.25% bupivacaine for landmark-guided diagnostic blocks [6]) are more likely to spread to neighbouring structures and reduce specificity.
• Steroid: leave it out of a purely diagnostic block, so that a short-acting anaesthetic response can be read cleanly.
• Record the response with a pain diary over the hours after the block, and repeat the block before ablation or surgery. The RFA protocol below requires two positive blocks [6].
• Caution: the sensitivity and specificity of single peripheral nerve blocks have not been studied, and the MCN point lies next to the sacroiliac joint region, so a positive MCN block does not exclude SI joint pain [1].

Differential diagnosis

Image-guided cluneal nerve blocks

There are no major arteries or nerves next to the SCN or MCN, so landmark injections are feasible [2]. However, the nerves are tiny, their branching is highly variable, and the precision of the block determines its diagnostic value. Ultrasound and fluoroscopy each help in different ways: ultrasound shows the soft tissues and the nerve itself, while fluoroscopy shows the bony targets and is the platform for radiofrequency work [1,6].

General principles

• Patient prone, with a pillow under the lower abdomen to reduce lumbar lordosis [6]. Full aseptic technique.
• Mark the point of maximum tenderness before imaging, and correlate it with the image.
• Diagnostic block: about 1–2 mL of local anaesthetic after negative aspiration. Therapeutic block: local anaesthetic with or without steroid [1,2].
• A peripheral nerve stimulator can confirm proximity to the nerve by reproducing concordant paraesthesia [1].
• Usual precautions for anticoagulation, infection and steroid use apply [1].

Ultrasound-guided SCN block

1. Probe: high-frequency linear probe. Probes of 18 MHz or more resolve structures of about 250–500 µm and allow the SCN to be identified [2,16].
2. Position: palpate and mark the posterior iliac crest about 6–7 cm from the midline. Place the probe transversely over the crest at this point [1,5].
3. Find the crest: it appears as a bright bony line with a dark acoustic shadow beneath it. Slide the probe superiorly and posteriorly along the crest [1].
4. Identify the tunnel: the components of the osteofibrous tunnel can be seen. These are the thoracolumbar fascia over the crest, the small notch in the posterior crest, the perineural fat pad, and the nerve itself as a small hypoechoic (sometimes honeycomb) structure just at or below the border of the crest. Power Doppler often shows a small vessel in the perineural fat alongside the nerve [1,5].
5. Compare sides: scanning the asymptomatic side helps identify swelling or changes in the perineural tissue [5].
6. Needle: in-plane or out-of-plane approach into the perineural fat beneath the fascia, avoiding the vessel. Inject 1–2 mL and watch it spread around the nerve [1].

Cadaver work confirms that the medial SCN branch can be identified reliably with high-resolution ultrasound [16], and a randomised trial showed that the SCN can be blocked successfully with an ultrasound-guided technique [10].

Ultrasound-guided MCN block

1. Find the PSIS: it can be hard to palpate accurately, especially in larger patients. Identify its most posterior and inferior point on ultrasound and use this as the reference [1].
2. Find S2: the second dorsal sacral foramen lies about 2–3 cm medial to this point, along a line about 45° below the horizontal. S1 is 1–1.5 cm above S2, and S3 is 1–1.5 cm below [1].
3. Target: in a transverse view, the foramen appears as a gap in the bright dorsal sacral surface. Place the needle tip at the lateral border of the S2 foramen, where the posterior sacral network converges [1]. Alternatively, target the tender point over the LPSL, about 3.5 cm caudal to the PSIS [8].
4. Inject about 1–2 mL of local anaesthetic [1,8].

There is no established landmark-only technique for the MCN. It is likely that some “blind sacroiliac joint injections” are in fact MCN injections, which is one reason why image guidance matters here [1].

Fluoroscopy-guided SCN block

1. View: anteroposterior, patient prone [1,6].
2. Target: the point of maximum tenderness is usually at the medial iliac crest. Look for the osseoaponeurotic orifice, which shows on fluoroscopy as a small cephalad bony protrusion on the posterior crest, about 7–8 cm from the midline [6]. A traction spur at the iliolumbar ligament attachment is occasionally seen [1].
3. Palpate over the image to confirm that the target matches the tender point [1].
4. Needle: advance to bony contact on the superior border of the crest, keeping a slight medial angle along the expected path of the nerve and advancing only to periosteal contact. Inject about 1 mL on top of the crest [1,6].
5. Nerve stimulation can confirm placement before injection [1].

Fluoroscopy-guided MCN block

The MCN can receive contributions from several sacral levels, but the network is centred on S2. About 1 mL of local anaesthetic at the lateral border of the S2 foramen is usually sufficient [1].

Landmark technique

With the patient prone or standing flexed at the hips, mark the posterior iliac crest 6–7 cm from the midline at the point of maximum tenderness. Advance a 25–22 gauge, 1.5–2 inch needle perpendicular to the skin until it contacts bone, keeping the needle on the crest. After negative aspiration, inject about 1 mL [1]. This is reasonable for the SCN, but the variable anatomy makes image guidance preferable when the block is being used to decide on ablation or surgery.

Complications and precautions

Complications are uncommon and relate to needle position, nerve trauma, bleeding and infection. With landmark technique, keep the needle on the iliac crest. Prolonged pain at the injection site may indicate neuritis. Standard precautions for local anaesthetics and steroids apply [1,2].

When blocks are not enough

Conservative care comes first: analgesics, topical agents, neuropathic medication, physiotherapy and modification of aggravating postures and loading [1,2]. Therapeutic blocks with local anaesthetic, with or without steroid, give some patients long-term relief, but recurrence after injections is reported in 23–41% [7]. When a block gives clear but short-lived relief, longer-lasting options can be considered.

Radiofrequency ablation of the SCN

SCN radiofrequency ablation was first described in 2022 [15]. A 2026 technical report from Abd-Elsayed and colleagues sets out a reproducible, fluoroscopy-guided method [6]:

• Selection: at least 3 months of pain despite conservative care, a positive iliac crest sign about 7 cm from the midline, and two diagnostic blocks each giving 50% or more relief.
• Placement: AP fluoroscopy; 18–22 gauge RF cannula (100–150 mm, 5 or 10 mm active tip) to the superior border of the crest at the osseoaponeurotic orifice, then rotated 3–5 mm off the border, usually superomedially. Ultrasound is added selectively to show fascial planes and nerve piercing sites.
• Testing: sensory stimulation at 50 Hz must reproduce the patient’s own pain; motor stimulation at 2 Hz up to 2 V must produce no distal motor response.
• Lesion: local anaesthetic, then 80 °C for 90 seconds. If pain persists, reposition a few millimetres medially or superolaterally, retest, and lesion again to capture additional branches.
• Cooled RF: a 17 gauge, 100 mm cooled probe with a 4 mm active tip at 80 °C for 2 minutes 30 seconds creates a larger lesion to accommodate variable branching.
• Aftercare: expected effects are local bruising, soreness and transient quadratus lumborum spasm. No serious complications have been reported in published SCN RFA studies. Follow-up is at 6–8 weeks.

Outcome data are observational. Small case series report an average pain reduction of about 50% lasting 6–12 months [6], and one treatment pathway reported good to excellent benefit in over 90% of patients at 12–24 months [2].

Other options

A practical treatment pathway

The PainSpa approach

At PainSpa, Dr Murli Krishna (Consultant in Pain Medicine, FFPMRCA) assesses low back and buttock pain with the cluneal nerves firmly on the differential list. Every assessment includes a focused landmark examination, and diagnostic and therapeutic blocks are performed under ultrasound or fluoroscopic guidance, drawing on his extensive experience of image-guided injections across a wide range of pain conditions. Where blocks confirm the diagnosis but relief is short-lived, patients are counselled on the full range of longer-lasting options, and coexisting spinal and sacroiliac pain generators are addressed at the same time.

Information for patients

References

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This article is intended for healthcare professionals and is not a substitute for individual clinical assessment.