Abstract
Superior articular process-pedicle impingement may be an underrecognized mechanical pain generator in posture-dependent axial low back pain. We report a case of a 32-year-old male professional football player who presented with low back pain that was provoked by forward flexion and right lateral bending and was refractory to conservative measures. Radiographs and computed tomography scans showed near-elimination of the osseous interval between the right S1 superior articular process and the caudal aspect of the right L5 pedicle, with reactive cortical change. Targeted infiltration of local anesthetic at the suspected impingement interface produced immediate pain relief, and facet-preserving full-endoscopic bony decompression led to sustained improvement at 3 months. We propose that superior articular process-pedicle impingement should be considered in patients presenting with posture-dependent axial low back pain. The following 3 features serve as a practical diagnostic triad: concordant provocation; radiographic or computed tomographic evidence of superior articular process-pedicle contact or near-contact; and an immediate response to targeted local anesthesia. Facet-preserving full-endoscopic decompression is a reasonable option for refractory cases.
Introduction
Low back pain is multifactorial and includes discogenic, facetogenic, neurogenic, myofascial, and sacroiliac etiologies.1-4) Moreover, age-related change and load redistribution within the posterior elements of the spine (facet joints, pedicles, and laminae) can promote hypertrophy of the articular processes and osteophyte formation.5-7) The superior articular process (SAP), an anatomic structure arising from the pedicle-lamina junction, may come into mechanical contact with adjacent bony structures under sagittal malalignment and repetitive extension and rotation loading.8-11)
This report describes an elite athlete with axial low back pain exacerbated by lateral bending in whom there was imaging evidence of impingement between the SAP and the caudal surface of the L5 pedicle. We propose SAP-pedicle impingement as a previously unrecognized cause of posture-dependent osseous impingement. The clinical course in this patient illustrates the key diagnostic points and the rationale for the treatment strategy.
Case Report
The patient was a 32-year-old male professional football player who presented with recurrent low back pain. There were no significant findings in his past medical history or family history. Two months earlier, he had developed sudden-onset left-sided low back pain during hip flexion while performing a high jump. The team physician diagnosed facet joint-mediated pain, and the patient's symptoms were relieved by left L4-5 and L5-S1 facet joint blocks. One month before presentation, he had developed right-sided low back pain when shooting the ball with his left foot. Suspecting concomitant discogenic pain, the team physician administered L4-5 and L5-S1 discoblocks (intradiscal anesthetic injections). The pain resolved transiently and then recurred, at which point he was referred to our hospital for surgical treatment. On physical examination, pain was elicited by forward flexion and right lateral bending, and there was focal tenderness over the right paraspinal region at L5-S1. Neurological examination was unremarkable: the straight leg raise test was negative bilaterally; no sensory disturbance or motor weakness was detected; and deep tendon reflexes, including the patellar and Achilles reflexes, were normal.
Oblique radiographs of the lumbar spine showed abutment of the right S1 SAP against the right L5 pedicle with reactive sclerosis (Figure 1A and B). Plain lumbar computed tomography (CT) scans similarly revealed impingement between the right S1 SAP and the right L5 pedicle (Figure 1C-F). On magnetic resonance imaging (MRI), fat-saturated T2-weighted images showed hyperintensity at the L4-5 and L5-S1 endplates (Figure 2A and B) and at the tip of the right S1 SAP (Figure 2C). Pain during lateral bending to the right, disappeared immediately after fluoroscopic-guided injection of 2 mL of 1% lidocaine into the space between the SAP tip and the pedicle (Figure 3A and B). Injection of 2 mL of 1% lidocaine at L4-5 and L5-S1 reproduced a deep, dull ache in the lower back and immediate attenuation of flexion-provoked pain (Figure 3C). Based on these findings, the preoperative diagnosis was established as a combination of 2 distinct pathologies: (1) right-sided low back pain induced by right lateral bending, attributed to the right S1 SAP-L5 pedicle impingement; and (2) central low back pain induced by forward flexion, attributed to discogenic pain associated with Modic changes at L4-5 and L5-S1.
Aiming for an early return to professional sports activity, the patient elected to undergo full-endoscopic spine surgery (FESS) under local anesthesia. We planned partial resection of the right S1 SAP via a transforaminal approach, together with disc cleaning surgery at L4-5 and L5-S1. Local anesthesia consisted of targeted subcutaneous infiltration with 0.5% lidocaine for a total of 10 mL under endoscopic visualization. Using the walking technique, an additional 10 mL of 0.5% lidocaine was sequentially infiltrated into the right L5-S1 facet joint, the right S1 SAP (tip, mid-portion, and base), the cranial S1 endplate, and the annulus fibrosus. Before insertion of the endoscope, discography was performed using a 1:1 mixture of indigo carmine and iohexol (Omnipaque 240; GE Healthcare, Chicago, IL, USA); 2 mL of the mixture was injected into the L5-S1 disc for blue staining. After placement of the endoscope, burring was initiated at the base of the SAP. As burring progressed toward the SAP tip, synovium-like inflamed soft tissue was encountered (Figure 4A) and cauterized as thoroughly as possible. Further burring at the tip exposed the L5 pedicle, the surface of which was eroded at the contact site (Figure 4B). Upon completion of SAP tip burring, adequate space between the SAP and the pedicle was confirmed (Figure 4C). Attention was then turned to the disc procedures. The vessels on the disc surface were coagulated by bipolar cautery, the disc surface was exposed and perforated, the nucleus pulposus was removed for reduction of intradiscal pressure and debridement, and the endoscope was inserted into the disc cavity. Focal bleeding was noted on the caudal endplate at L5-S1, and bipolar coagulation reproduced the concordant low back pain. The disc was cleaned as extensively as feasible, concluding the L5-S1 procedure. The right L4-5 level was then addressed in the same fashion under local anesthesia. After insertion of the endoscope into the disc, focal bleeding was observed at the cranial endplate, and bipolar coagulation again reproduced the concordant low back pain. The disc was cleaned thoroughly, completing the L4-5 procedure. The procedure was performed under local anesthesia and was completed uneventfully, with no intraoperative complaints of pain or signs of exiting nerve root irritation. The total operation time was 127 minutes, and blood loss was minimal.
The patient's pain during lateral bending to the right resolved immediately postoperatively, with a decrease in pain during forward flexion. Postoperative CT confirmed complete resection of the S1 SAP tip (Figure 5A-F). Sprint training resumed at 1.5 months, and the patient returned to full participation in sport within 3 months. He reported no further concerns related to low back pain at 6 months after surgery, and the outcome was excellent according to the Macnab criteria.
Discussion
The pain mechanism in this case was thought to be repetitive, posture-dependent contact between the SAP and the caudal surface of the cranial pedicle, which provoked mechanical pain originating from the periosteum and subcortical bone. Mechanical pain originating from these areas is biologically plausible, given that periosteal afferents are richly nociceptive and respond to noxious mechanical stimulation, and bone pain can arise from periosteal activation.12) Age-related changes in the posterior elements (facet arthropathy, osteophyte formation, and capsular thickening), sagittal malalignment, and, particularly in professional athletes or others engaged in high-intensity activity, repeated extension, rotation, and side-bending loads may accelerate morphological remodeling of the SAP.8,13-15) Moreover, facet tropism has been shown to increase contact forces at the facet joint and intradiscal pressure under flexion-extension, axial rotation (torsion), and anterior shear, which may promote morphological remodeling (e.g., osteoarthritis-like hypertrophy and osteophyte formation) over time.16) Furthermore, loss of disc height narrows the bony clearance between the SAP and the lateral and inferior cortices of the cranial pedicle. When this proximity becomes critical, posture-specific bony impingement, such as during lateral bending or extension, can occur, reproducing localized tenderness and axial low back pain. In our patient, L5 facet tropism and right-dominant disc height loss (Figure 1) likely contributed to the reduced space between the S1 SAP and the L5 pedicle.
Baastrup's disease ( "kissing spines" ) and Bertolotti's syndrome are 2 disorders that produce similar bony impingement. Baastrup's disease is characterized by close approximation or contact of adjacent lumbar spinous processes with degeneration of interspinous soft tissue and bursitis and typically produces extension-provoked positional pain. In symptomatic cases, MRI often shows a fluid-like signal or bursal change in the interspinous region and is associated with older age and coexisting degenerative stenosis. These features have been documented in imaging-pathology series and pictorial reviews.17-19) Lin et al.20) found that full-endoscopic interspinous plasty under local anesthesia in patients with Baastrup's disease-related chronic low back pain enlarged the interspinous space on postoperative CT and yielded improvements in visual analog scale and Oswestry disability index scores at the 12-month follow-up. Bertolotti's syndrome denotes low back pain associated with a lumbosacral transitional vertebra, in which an enlarged L5 transverse process forms a pseudoarticulation (or fusion) with the sacrum or ilium; arthritic change and abnormal load transfer at this pseudoarthrosis are proposed sources of pain and may coexist with degeneration of adjacent segments.21,22) Of note, percutaneous FESS has been used in Bertolotti's syndrome with encouraging results. Paudel et al.23) reported 3 symptomatic cases treated by full-endoscopic resection of the pseudoarticulation, concluding that the technique was feasible and safe, with good outcomes and the advantage of minimal invasiveness.
In the present case, our joint-preserving full-endoscopic targeted bony decompression of the culprit SAP interface produced similar relief of a mechanical pain generator. This finding is consistent with the broader concept that precise endoscopic removal of the osseous point of contact can be an effective, stability-sparing strategy when conservative measures fail.
A practical diagnosis relies on concordance between posture-dependent clinical features and morphological evidence centered on CT. Clinically, emphasis is placed on axial low back pain reproduced by ipsilateral lateral bending and/or extension, with focal paraspinal tenderness at the implicated level and an absence of radicular symptoms or objective neurological deficits. On imaging, multiplanar (coronal, axial, sagittal) reconstructions are used to measure the SAP-pedicle (SP) distance between the SAP tip and the cortical surface of the cranial pedicle (lateral and predominantly inferior cortices). The primary findings are direct contact or conspicuous shortening of the SP distance, including side-to-side and interlevel comparisons. Supportive signs include cortical sclerosis or small osteophytes at the presumed contact site and focal bone marrow edema on fat-suppressed MRI. Three-dimensional CT is useful for depicting and communicating the spatial relationship, allowing instant visualization of the narrowest region. The differential diagnosis includes facet joint pain, Baastrup's disease, juxtafacet cysts, lumbar spondylolysis (pars interarticularis defect), and sacroiliac joint disorders. Diagnostic narrowing is achieved when the provoking posture and localization of shortening or obliteration of the SP distance are congruent. When appropriate, targeted local anesthetic injection adjacent to the SAP tip under fluoroscopic or CT guidance may be performed, and immediate short-lived pain relief strengthens the inference of causality. In contrast, a medial branch block alone, though useful for differentiating facetogenic pain, may have limited specificity when bone-to-bone contact is the principal pain generator.
In addition to partial resection of the S1 SAP, we performed full-endoscopic disc cleaning (FEDC) at L4-5 and L5-S1 to address the Modic changes. Sairyo et al.24) first described transforaminal FEDC, an intradiscal debridement and drainage procedure performed under local anesthesia, for intractable chronic low back pain attributable to type 1 Modic change, demonstrating symptomatic improvement in the index case. Since then, early series from the same group have suggested favorable pain and disability outcomes after FEDC in carefully selected patients with Modic changes.25,26) However, higher-quality comparative studies are still needed.
In summary, when posture-dependent axial low back pain with site-specific paraspinal tenderness aligns with shortening or obliteration of the SP distance on CT, and when immediate, reversible analgesia after targeted injection of local anesthetic is present despite failure of conservative therapy, minimal bony decompression to eliminate the impingement while preserving stability is recommended.
Several limitations should be acknowledged. This is an observational report of a single case; therefore, the generalizability of the proposed concept has yet to be confirmed. The pathophysiological inference rests on clinical and imaging concordance and the response to targeted anesthetic, none of which definitively proves causality. In particular, placebo effects or nonspecific analgesia owing to spread of the injectate (e.g., to the dorsal ramus or nerve root, given the 2 mL volume used) cannot be fully excluded. Imaging assessment relied primarily on static modalities; dynamic assessment might have demonstrated posture-related changes more directly. Furthermore, thresholds for an abnormal SP distance have not been established. Future efforts should include larger case series incorporating dynamic imaging and objective metrics to validate this concept.
In conclusion, this report identifies SP impingement as a potential novel generator of low back pain and proposes a practical algorithm spanning diagnosis through treatment. A pragmatic diagnosis can be achieved by aligning posture-reproducible pain, radiographic and CT evidence of shortening or obliteration of SP distance, and an immediate response to targeted local anesthetic injection. In cases refractory to conservative therapy, facet-sparing, minimal bony decompression via FESS is a reasonable and effective treatment option. Postoperatively, restoration of the SP distance on CT paralleled symptomatic improvement in our patient, supporting the mechanical nature of pain generation.
Acknowledgments
The authors thank ThinkSCIENCE (Tokyo, Japan) for English-language editing of this manuscript. The editors had no role in the study design, data collection, analysis, interpretation, or the decision to submit the manuscript.
Conflicts of Interest Disclosure
All authors have no conflict of interest.
Ethics Approval
This report was performed in accordance with the Declaration of Helsinki and approved by the ethics committee of Tokushima University Hospital (approval number 3642).
Informed Consent
Written informed consent was obtained from the patient for the publication of this case report and accompanying images.
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