This retrospective study included 13 patients with persistent (n=2) or recurrent (n=11) LBP and/or leg pain, whose LDH had been treated by primary discectomy between April 2013 and May 2015. They included eight men and five women, with a mean age of 58.2 years (range, 33–78 years). All had undergone primary lumbar discectomy for LDH, five at our institution and eight elsewhere. None presented with trauma around the knee, malignancy, active infection, Parkinson’s disease, dementia, or psychological issues. The LDH level was L4/5 in 11 patients and L5/S1 in the other two. The mean interval between symptom exacerbation and presentation at our department was 12 months (range, 1–60 months); the mean postoperative follow-up period was 26.4 months (range, 9–39 months) (Table 1). Acetaminophen, non-steroidal anti-inflammatory drugs, and/or tramadol failed to control their pain; none were given codeine or morphine.

We carefully assessed the patients to confirm that SCN entrapment played a role in their LBP using established diagnostic criteria [11,12,17]. LBP was considered to be the result of SCN-EN if there was unilateral pain involving the iliac crest and buttocks, there was a trigger point over the posterior iliac crest located 7 cm from the midline (corresponding to the nerve compression zone), and the patient experienced numbness and radiating pain in the SCN area when the trigger point was compressed. Most patients experienced symptom relief within 2 hours of the administration of a local nerve block (2 mL of 1% lidocaine injected at the trigger point in the buttock); however, some reported the recurrence of pain after the analgesic effect of the injection wore off. SCN was blocked with a minimal amount of local analgesic to avoid misdiagnosis of the origin of the patient’s pain.

The diagnosis of CPN-EN was based on symptoms including numbness and/or pain from the lower leg to the dorsum of the foot, which appeared when the patient walked or stood and resulted in intermittent claudication [13,15,16]. All patients were positive for Tinel’s sign at the CPN around the neck of the fibula.

Tarsal tunnel syndrome (TTS) results from entrapment of the posterior tibial nerve in the tarsal tunnel on the medial malleolus. Its diagnosis is based on symptoms such as numbness and/or pain in the sole of the foot, without heel involvement, which appear when the patient walks or stands for a prolonged time [7,18,19]. All the patients with TTS were positive for Tinel’s sign at the tarsal tunnel.

The treatment outcomes were assessed on a numeric rating scale (NRS) and with the Roland-Morris Disability Questionnaire (RDQ). The scores were recorded before treatment and at the latest follow-up. The data were assessed with paired t-tests using StatMate III software (ATMS Co. Ltd., Tokyo, Japan). Differences of p<0.05 were considered statistically significant.

Although surgical treatment for LDH can deliver good results, 5%–40% of operated patients manifest FBSS [1-6]. Of these, 3%–18% suffer recurrence of the LDH [4,5,20]. Patients with FBSS but no recurrence of the LDH have been observed to exhibit epidural fibrosis, epidural hematoma, inadequate decompression of coexisting segmental stenosis, segmental instability, dural tear, and/or arachnoiditis [1-6]. Long-lasting back pain has been reported by 10%–30% of patients after primary discectomy for radiculopathy [21-23]. Consequently, the potential causes of postoperative pain must be considered in patients with FBSS manifesting as LBP after LDH surgery.

We evaluated and treated 13 patients with persistent or recurrent symptoms after LDH surgery. Radiological studies confirmed LDH recurrence in three of the patients and lateral recess stenosis in one patient; they underwent additional lumbar decompression surgery. The other nine patients manifested no radiological abnormalities that explained their persistent or recurrent symptoms. However, treatment for PN neuropathy resulted in symptom abatement in these patients, suggesting that factors other than lumbar disease were involved. We believe that the persistent postoperative symptoms of two patients with LDH (cases 10, 13) were due to coexisting PN neuropathy, which had not been addressed during the LDH surgery. Our findings indicate that concomitant PN disease should be considered in patients with persistent or recurrent symptoms after LDH surgery.

Previously, we have documented the usefulness of less invasive treatments for PN neuropathy in patients with LBP and leg pain [8-13,16,18]. These symptoms are similar to those elicited by lumbar disease. The presence of SCN-EN in 1.4%–14% of patients is higher than is commonly expected [8-12,17]. Of our 13 patients with FBSS manifesting as persistent LBP, 12 required treatment for SCN-EN, with SCN block and SCN neurolysis proving beneficial. According to earlier reports, SCN block successfully addressed SCN-EN in 28%–100% of patients, even in those with severe LBP [12,17,24]. In the present study, eight of the 12 patients with FBSS reported abatement or disappearance of their pain after SCN blockage, suggesting that this procedure should be considered for patients with LBP after LDH surgery.

In nine of the 10 patients with unilateral symptoms due to SCN-EN, the symptoms were on the same side as the lumbar lesion. The sinuvertebral nerves around vertebral structures such as the outer annulus fibrosus of the intervertebral discs contribute to the elicitation of pain around the spine, including discogenic or vertebral joint pain [25]. Although the pathogenesis of SCN-EN remains unknown, stimulation of the sinuvertebral nerve by LDH and/or unilateral nerve root irritation caused by radiculopathy may play a role, and SCN-EN may be misdiagnosed as lumbar herniation in patients with LBP.

Out of the 13 patients, six underwent neurolysis for CPN-EN. This is the most common PN neuropathy of the lower limb and the most frequent cause of leg numbness and pain involving the affected area without severe paresis or intermittent claudication [13-16,26]. Because PN neuropathy can manifest symptoms similar to those of L5 radiculopathy due to lumbar lesions, a differential diagnosis is important, even after LDH surgery. CPN-EN can be treated by less invasive neurolysis under local anesthesia. However, the diagnosis of CPN-EN can be difficult because it cannot always be detected electrophysiologically; careful symptom assessment may yield a correct diagnosis. Previously, we have reported that the repetitive plantar flexion test is a useful provocation test for diagnosing CPN-EN [13,14,16].

TTS is an EN of the posterior tibial nerve within the tarsal tunnel. The symptoms are sensory disturbance in the sole of the foot without heel involvement, paresthesia, and a sensation of coldness or the presence of a foreign body [7,18,19]. The symptoms are exacerbated by prolonged standing or walking and the condition may be misdiagnosed as spinal disease. TTS has been observed in 4.8% of patients with lumbosacral radiculopathy [27], suggesting it may underlie the residual symptoms in patients with FBSS.

GMM is located in the buttock, partially beneath the gluteus maximus muscle. It can be the origin of buttock pain with lateral and/or posterior femoral pain [28,29]. The diagnosis of GMM pain is based on clinical symptoms. Treatment consists of GMM block and decompression surgery under local anesthesia [28,29]. As with lumbar disease, the pain is exacerbated by sitting, standing, and walking; a differential diagnosis in patients reporting LBP requires the identification of the underlying cause. Of our patients, two required treatment for GMM pain. Although GMM pain is not reflective of PN neuropathy, the latter should be considered for patients with residual symptoms due to FBSS.

This study had some limitations. The study population was small, the follow-up period was short (mean, 26.7 months), and the interval between surgery and symptom recurrence varied among the patients. The symptoms were persistent in some and recurrent in others, and they manifested immediately after, soon after, or a long time after surgery. In addition, this was a retrospective study and not all patients underwent their first operation at our institution. Consequently, our findings may not accurately reflect the incidence of true PN neuropathy in patients with FBSS after LDH surgery. We do not know what proportion of the total number of patients operated during our study period manifested FBSS, and we cannot comment on the overall effectiveness of surgical PN treatment. Nonetheless, we recommend that spinal surgeons consider PN disease for patients with FBSS.