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Idiopathic Cluneal Neuralgia Successfully Treated With Radiofrequency Nerve Ablation: A Case Report

Zheng, Danielle MD, PhD; Lamer, Tim J. MD

doi: 10.1213/XAA.0000000000000922
Case Reports
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Middle cluneal nerve entrapment neuropathy/neuralgia (MCN-EN) is a rare and potentially underdiagnosed etiology for chronic low back pain. Symptoms include pain in the buttock and posterior superior iliac spine area that is increased by activity and direct pressure over the area, and is “neuropathic” in nature. Previous case reports describe successful treatment of MCN-EN with nerve block and/or surgical decompression of the MCN. We present a case report detailing the first successful use of radiofrequency nerve ablation in treating MCN-EN.

From the Department of Anesthesiology and Perioperative Medicine, Division of Pain Medicine, Mayo Clinic, Rochester, Minnesota.

Accepted for publication September 25, 2018.

Funding: None.

The authors declare no conflicts of interest.

Address correspondence to Danielle Zheng, MD, PhD, Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, 200 1st St SW, Rochester, MN 55905. Address e-mail to zheng.danielle@mayo.edu.

Low back pain has a complex etiology. Recently, the middle cluneal nerve (MCN) has been identified as an underdiagnosed pain generator in chronic low back pain.1–3 Based on anatomical studies, it is hypothesized that the MCN can be compressed at the interface between the iliac bone and long posterior sacroiliac ligament (LPSL).2,4,5 Previous case reports have documented successful treatment and pain relief with surgical sectioning6 and surgical decompression of the MCN.1,3 A PubMed and Ovid search revealed no previous treatment with radiofrequency (RF) ablation. We present the first case report of middle cluneal neuralgia treated with cooled RF ablation. A written Health Insurance Portability and Accountability Act authorization to use/disclose existing protected health information was obtained.

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CASE DESCRIPTION

We secured written patient consent before submission of this case report. A 72-year-old woman presented with a 3-year history of insidious onset right low back and upper buttock pain, with no inciting event. She described severe paroxysmal lancinating pain around the lumbosacral junction and posterior superior iliac spine (PSIS) with radiation caudally to the sciatic notch. Functionally, the pain prevented her from golfing and yard work, and she could only sit on her left buttock; even car rides were difficult due to bumps causing her pain. Over the past several years, she had tried ice packs, heat packs, topical spray, lidocaine patches, acupuncture, tramadol, and hydrocodone, with limited benefit. Gabapentin was not trialed because the patient had mild cognitive impairment. Physical examination maneuvers for sacroiliac (SI) joint pain, facet joint pain, and hip pain did not reproduce her symptoms (negative straight leg raise, Stinchfield, Patrick’s test, distraction, hip range of motion, lumbar extension; equivocal posterior thigh thrust, Gaenslen; increased symptoms with forward flexion). She had localized tenderness and pain to light palpation (allodynia) and firm palpation (hyperalgesia) at the lumbosacral junction above the PSIS, suggesting a possible neuropathic pain condition. Neurological examination was otherwise normal. Previous diagnostic right SI joint injection (2 years before), right lumbar and sacral vertebrae (L4–L5 and L5–S1) facet joint injections (1 year before), and ultrasound-guided intraarticular hip injection (2 months before) did not relieve her pain, thus ruling out these structures as pain generators (Figure 1). Magnetic resonance imaging of the lumbar spine down to SI joints revealed no major bony abnormalities to account for her symptoms and no obvious compression of lumbosacral nerve roots to suggest a radiculopathy. Based on the neuropathic features of her pain, location of her pain around the PSIS, and lack of relief with SI joint and facet joint injections, a presumptive diagnosis of middle cluneal neuralgia was made.

Figure 1.

Figure 1.

The patient’s preprocedure pain rating was 7 of 10. She underwent a diagnostic fluoroscopically guided right dorsal ramus/lateral branch nerve block at S1–3, as well as L5 dorsal ramus and L4 medial branch local anesthetic (bupivacaine) nerve block, with 100% relief for 24 hours. She then underwent cooled RF ablation of the same nerves 1 week later. The skin and subcutaneous tissues were anesthetized with lidocaine. Using anteroposterior and lateral fluoroscopy, a 17-gauge cooled RF cannula was then advanced to a line approximately 8 mm lateral to the right S1, S2, and S3 posterior neural foramina. Measured tissue impedances were satisfactory. At each sacral foraminal level, motor testing was performed up to 2.5 V and was negative for any sacral root stimulation. Before lesioning, each foraminal location was injected with 1 mL of 2% lidocaine. RF lesioning was performed at 60°C for 150 seconds at each site. Multiple lesions were created by moving each of the cannula approximately 8–10 mm to create hemicircumferential lesions around each foramen. After the RF treatment, each site received bupivacaine, and the needles were withdrawn from the skin.

Next, using fluoroscopic guidance, a 100-mm, 18-gauge RFK (Racz-Finch Kit) RF cannula with a 10-mm active tip was advanced to the junction of the transverse process and superior articulating process at the right L5 and sacral ala levels to lesion the L4 medial branch nerve and the L5 dorsal ramus. This was confirmed using posterior-anterior (PA), lateral, and oblique fluoroscopic views. Motor testing was performed at 2 Hz up to 3 V, and the measured tissue impedances were satisfactory. With final needle positioning, there was no evidence of radicular stimulation. Before lesioning, 1 mL of 2% lidocaine was injected. Lesioning was performed at 80°C for 75 seconds times 2 (total 150 seconds).

Figure 2.

Figure 2.

Figure 3.

Figure 3.

This lesion technique is as described in previous reports7,8 (Figures 2 and 3). At 2-week and 3-month follow-up, she endorsed 65%–90% reduction in pain, resulting in improvement in quality of life (able to garden and ride in car) and ability to wean off oral opiates.

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DISCUSSION

The MCN composed of sensory branches from the dorsal rami of S1–S3 (Figure 4). It may pass through the LPSL between the PSIS and posterior inferior iliac spine before innervating the skin overlying the posteromedial area of the buttock.2,4 While the etiology of medial cluneal neuralgia is unclear, anatomical studies have provided evidence that the MCN may become compressed as it passes through the LPSL, and thus may be a pain generator.4,9 In particular, Konno et al9 found that among 30 hemipelves, 16% had MCN branches that penetrated the LPSL, of which 40% had obvious constriction under the ligament; in addition, there was some anastomosis between the MCN and superior cluneal nerve (SCN) in the subcutaneous tissues of the buttock. These findings suggest that MCN neuralgia may not be rare and is potentially underdiagnosed.

Figure 4.

Figure 4.

Diagnosis of MCN entrapment neuralgia requires a high degree of suspicion. Aota1 and Kim et al3 both describe greatly limited lumbar motion, leg symptoms, palpation of an MCN tender point on the LPSL (35–40 mm caudal to the PSIS) resulting in marked tenderness and provocation of symptoms, and relief of pain with local anesthetic injection. In our patient, diagnosis was made on the basis of the location of pain in the low back/PSIS area, the neuropathic nature of the pain, and ruling out SI joint pain (negative SI-provocative maneuvers, negative imaging, and no relief from image-guided intraarticular SI joint injection). In patients with persistent low back and buttock pain, who have been ruled out for lumbosacral facet and SI joint as pain generators, MCN entrapment should be on the differential diagnosis.

Previous literature has focused on SCN entrapment neuropathy/neuralgia (EN), which is a known cause of low back pain and often occurs in the setting of iliac crest bone harvesting.10 While SCN-EN also presents with pain with lumbar motion and leg symptoms, it is often associated with a tender site 70 mm lateral to the midline on the iliac crest, where the SCN passes through fascia over the iliac crest.5 Treatment has involved deafferentation of the SCN6 and surgical decompression.5 Similarly, in previous case reports, MCN neuralgia that improved with local anesthetic block was then treated successfully with surgical decompression of the MCN.1,3,6

In our case, the patient presented with neuropathic pain symptoms suggestive of MCN-EN with alleviation of pain after local block, and was treated definitively with cooled radiofrequency ablation (RFA). Cooled RFA of the sacral lateral branch/dorsal rami nerves has been demonstrated to relieve chronic SI joint pain.7,11–13 Because there is a complex network of small nerve fibers anastomosing, the cooled RFA approach was chosen because it can produce a larger lesion.8 The MCNs share the same origin from the sacral dorsal rami; therefore, we were able to use an approach similar to that of RFA for SI joint pain (Figures 2–4). We chose to include L4–5 because, although most anatomic studies have demonstrated S1–3 involvement of the MCN, all reports demonstrate considerable variation, including occasional contribution from L5. Given that the patient had undergone many previous injections, we did not want to risk partially blocking the MCN. Advantages of RFA compared to surgical release include being a minimally invasive, outpatient procedure, little to no recovery time, fewer side effects, and quicker return to work and other activities. Disadvantages include the potential for pain to return after some time, and the potential for a high false-positive rate during initial diagnostic injection. In conclusion, this case report demonstrates a promising novel treatment for MCN-EN.

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DISCLOSURES

Name: Danielle Zheng, MD, PhD.

Contribution: This author helped draft the manuscript.

Name: Tim J. Lamer, MD.

Contribution: This author helped care for the patient and draft the manuscript.

This manuscript was handled by: Mark C. Phillips, MD.

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REFERENCES

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