Conus medullaris tumor co-existed with chronic low back pain: a case report and literature review

Introduction

In 2020, low back pain (LBP) affected approximately 619 million people globally, making it the leading cause of years lived with disability worldwide (1). Most cases of LBP are mechanical in nature, with lumbosacral radiculopathy being among the most common diagnoses in outpatient settings (2). Rarely, lower back pain signals more serious causes such as tumors, infections, or inflammatory disorders. Conus medullaris syndrome (CMS) is a rare and often underrecognized cause of chronic lower back pain due to its overlapping features with more common conditions (3). Intradural extramedullary tumors, which account for approximately 65% of primary spinal cord tumors, represent about 1.3% to 2.6% of all central nervous system neoplasms (4). Their annual incidence ranges from 0.74 to 1.11 per 100,000 person-years (5).

Diagnostic delays in CMS lead to permanent neurological deficits, reduced quality of life, and increased healthcare costs. These delays are exacerbated by systemic barriers, such as limited access to advanced imaging and the misattribution of symptoms to more common conditions. Spinal cord injuries, including CMS, contribute significantly to global disability, with projections indicating a continued burden through 2030 (6). Comparing diagnostic delays in CMS to similar challenges in conditions like cauda equina syndrome, spinal arteriovenous malformations, or transverse myelitis highlights systemic disparities in diagnostic efficiency and provides a lens through which to examine broader healthcare inequities. We present this article in accordance with the CARE reporting checklist (available at https://jss.amegroups.com/article/view/10.21037/jss-25-4/rc).

Case presentation

A 48-year-old right-handed Caucasian female presented approximately 18 months prior with progressive worsening neurological symptoms. However, she is known to have chronic lower back pain mechanical in origin for years and has been treated conservatively. The worsening of her symptoms included bilateral progressive leg weakness, numbness, shooting pain down to her feet, difficulty walking, and bowel and bladder dysfunction. This was followed months later by the onset of bilateral leg weakness and numbness. The pain was sharp and stabbing, mainly on the right leg, and she experienced tingling from the knees down, difficulty walking, and loss of control over bowel and bladder function.

Despite these symptoms, clinical suspicion remained anchored on her autoimmune history, which included Hashimoto’s thyroiditis, systemic lupus erythematosus (SLE), sarcoidosis, and osteoporosis with a history of spontaneous fractures. Early evaluations misattributed her neurological decline to sarcoidosis, leading to delays in appropriate imaging. The initial lumbar spine magnetic resonance imaging (MRI) years ago demonstrated only Modic changes and facet arthropathy at L4–5 and L1–2. She was treated with physical therapy and epidural injections. The focus of the medical team was anchored towards autoimmune etiology and was treated accordingly. She also experienced back stiffness, headaches, eye pain, insomnia, and systemic symptoms exacerbated by stress and weather changes.

However, the patient reported no improvement despite the treatment she received and was self-referred to the author for further management. Upon examination revealed thoracolumbar tenderness, spastic paraparesis in the right leg, clonus, muted toe responses, positive Babinski reflexes, a sensory level at T8, and impaired proprioception.

Imaging and diagnosis

The author immediately ordered a thoracic lumbar spine MRI which revealed an intradural extramedullary circumcised oval-shaped mass measuring approximately 1.9 cm × 0.8 cm × 0.5 cm, as shown in Figure 1A,1B at T11-T12 with enhancement. The spinal MR angiography was performed to rule out a variant arterial malformation such as AV fistula. The test was concluded negative.

Figure 1 Preoperative imaging. (A) Sagittal T1-weighted (T1) and T2-weighted (T2) MRI with contrast demonstrating an extramedullary intradural enhancing mass compatible with a schwannoma at T11–T12. (B) Axial view confirming the extramedullary mass causing posterior displacement of the spinal cord. MRI, magnetic resonance imaging.

Surgical intervention

The author performed a bilateral limited laminectomy at T11–T12 with preservation of the bilateral T11–T12 facets. The surgery was conducted under continuous neuromonitoring using somatosensory evoked potentials. A midline durotomy was performed under microscopic magnification. The intradural mass was identified and isolated, as shown in Figure 2A-2C. A stimulation probe was applied over the mass to confirm the absence of viable neurons. The blood supply to the mass was coagulated, and frozen section analysis revealed a schwannoma. Notably, the mass was observed to contact the spinal cord with each pulsation, which correlated with the severity of the patient’s symptoms. The mass was successfully dissected, as seen in Figure 2C. The dura was closed with a watertight seal, and the skin incision was closed, as shown in Figure 2D. Postoperative imaging of the isolated mass is presented in Figure 3. A summary of the patient’s symptom progression and clinical interventions is provided in Table 1.

Figure 2 Intraoperative visualization. (A) Microsurgical exposure of the intradural extramedullary tumor following midline durotomy. (B) Identification and dissection of the tumor capsule from adjacent nerve roots. (C) Tumor mobilization and confirmation of absence of neural elements with stimulation probe. (D) Watertight dural closure and final layered wound closure.

Figure 3 Gross pathology. Excised tumor specimen photographed on surgical gauze with measurement scales. The mass was well-circumscribed, consistent with a benign schwannoma.

Postoperative course and outcome

Postoperatively, the patient demonstrated immediate improvement in neurological function, including restoration of balance, proprioception, and strength. She regained sensation in her legs and was able to ambulate again. Postoperative MRI demonstrated no residual tumor and restoration of spinal cord contour, consistent with Figure 4A,4B. While chronic LBP and manifestations of SLE persisted, the neurological deficits caused by the tumor resolved completely. By 8 months, she had returned to full function, and at a 3-year follow-up, she remained pain-free and neurologically intact.

Figure 4 Postoperative imaging. (A) Sagittal T1-weighted MRI with contrast showing postoperative changes, limited laminectomy defect, and preservation of facets. (B) Axial T1-weighted MRI with contrast demonstrating total resection of the tumor, restoration of spinal cord contour, and normalization of CSF flow. CSF, cerebrospinal fluid; MRI, magnetic resonance imaging.

The patient’s recovery trajectory compared to reported literature is summarized in Table 2.

Ethical statement

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

The present case presents the classic features of conus medullaris, including bilateral lower limb weakness, sensory changes, and sphincter dysfunction, were initially present but misattributed to sarcoidosis (3). Failure to realize this contributed to a substantial delay in identifying the intradural tumor compressing the conus. This case highlights a diagnostically challenging presentation of a thoracic intradural extramedullary tumor manifesting as chronic lower back pain with progressive neurological deficits. The treatment of choice, which was performed by the author, resulted in a remarkable recovery for the patient.

To our knowledge, few cases have reported thoracic spinal tumors masquerading as chronic mechanical lumbar pathology for over a year, particularly in the setting of misleading autoimmune comorbidities. Pain in spinal tumors may mimic radiculopathy or mechanical back pain, complicating early diagnosis (8). This case underscores the importance of revisiting the differential diagnosis when progressive neurological signs—such as spastic paraparesis, saddle anesthesia, or urinary incontinence—emerge despite inconclusive lumbar imaging (8).

Neurological findings such as bladder incontinence and diminished anal sphincter tone, as observed here, are well-established negative prognostic indicators (3). These symptoms are associated with a higher likelihood of persistent dysfunction, even following complete surgical resection. While specific postoperative data for CMS remain limited, a study in patients with cauda equina syndrome, which shares overlapping sacral dysfunction, reports persistent urinary, bowel, and sexual dysfunction in approximately 41.8% to 53.3% of cases at 63 days postoperatively (3).

In this case, the thoracic lesion was initially misdiagnosed as a spinal arteriovenous malformation, highlighting how imaging characteristics can overlap with other non-compressive spinal pathologies such as transverse myelitis or syringomyelia (9). This diagnostic pitfall further delayed surgical intervention, reinforcing the importance of correlating evolving clinical symptoms with detailed MRI signatures that distinguish intramedullary from extramedullary lesions (9).

Unlike mechanical LBP—which generally lacks progressive neurological deficits—conus medullaris tumors may clinically resemble foraminal stenosis due to overlapping lower limb symptoms. However, they often present with distinct features such as sphincter involvement and spasticity, which are frequently missed without advanced imaging (9,10). In this case, these overlapping features, coupled with an autoimmune background, contributed to diagnostic uncertainty. Benign intradural tumors such as schwannomas may initially remain asymptomatic but can trigger neuropathic pain and spinal cord edema through mechanisms such as venous hypertension or ischemic injury, resulting in progressive neurological decline (8,11). Such decline may arise not only from direct compressive effects, but also from impaired venous drainage or cord ischemia, mechanisms increasingly recognized in spinal cord pathology (7,8).

Surgical decompression remains the mainstay of treatment. Evidence suggests that earlier intervention yields better neurological outcomes, with recent guidelines supporting prompt surgery within 48 hours of symptom onset (11). Further delay may compromise recovery due to irreversible neuronal damage. This reinforces the critical need for early and accurate recognition of spinal cord-level pathology, particularly when symptoms deviate from typical mechanical back pain patterns.

By highlighting this atypical trajectory—where a thoracic lesion masqueraded as lumbar radiculopathy over a prolonged period—this case contributes to the growing body of literature emphasizing the importance of broad differential consideration and early thoracic imaging when conus involvement is suspected.

To aid in distinguishing CMS from other spinal pathologies presenting with back pain and neurological deficits, a comparative table of key clinical features and imaging strategies is provided below (Table 3).

Conclusions

This case highlights the diagnostic complexity of CMS, particularly when overlapping symptoms are misattributed to autoimmune conditions or attributed solely to chronic lower back pain. Despite hallmark features such as progressive bilateral lower extremity weakness and sphincter dysfunction, the diagnosis was delayed due to premature anchoring on non-compressive etiologies. Use of thoracic imaging and neurosurgical consultation ultimately led to complete neurological recovery following tumor resection. This underscores the need for heightened clinical vigilance, multidisciplinary collaboration, and consideration of spinal cord-level pathology when patients present with progressive deficits and inconclusive lumbar imaging. Broader efforts to establish diagnostic guidelines and improve provider awareness for rare spinal tumors like CMS may reduce morbidity and support timely intervention in future cases.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://jss.amegroups.com/article/view/10.21037/jss-25-4/rc

Peer Review File: Available at https://jss.amegroups.com/article/view/10.21037/jss-25-4/prf

Funding: None.

Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://jss.amegroups.com/article/view/10.21037/jss-25-4/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. GBD 2021 Low Back Pain Collaborators. Global, regional, and national burden of low back pain, 1990-2020, its attributable risk factors, and projections to 2050: a systematic analysis of the Global Burden of Disease Study 2021. Lancet Rheumatol 2023;5:e316-e329. [Crossref] [PubMed]
2. Alexander CE, Weisbrod LJ, Varacallo MA. Lumbosacral Radiculopathy. In: StatPearls. Treasure Island (FL): StatPearls Publishing; February 27, 2024.
3. Rider LS, Marra EM. Cauda Equina and Conus Medullaris Syndromes. In: StatPearls. Treasure Island (FL): StatPearls Publishing; August 7, 2023.
4. Patel P, Mehendiratta D, Bhambhu V, et al. Clinical outcome of intradural extramedullary spinal cord tumors: A single-center retrospective analytical study. Surg Neurol Int 2021;12:145. [Crossref] [PubMed]
5. Phankhongsab A, Sopchokchai I, Piromchai P. Epidemiology study on the prognostic factors of intradural extramedullary spinal tumors. J Craniovertebr Junction Spine 2024;15:361-6. [Crossref] [PubMed]
6. Liu Y, Yang X, He Z, et al. Spinal cord injury: global burden from 1990 to 2019 and projections up to 2030 using Bayesian age-period-cohort analysis. Front Neurol 2023;14:1304153. [Crossref] [PubMed]
7. Khan ESKBM, Thean CAP, Zakaria ZB, et al. A Rare Presentation of Spinal Schwannoma Causing Conus Medullaris Syndrome: A Case Series on Surgical Outcome. J Orthop Case Rep 2020;10:101-5. [Crossref] [PubMed]
8. Ottenhausen M, Ntoulias G, Bodhinayake I, et al. Intradural spinal tumors in adults-update on management and outcome. Neurosurg Rev 2019;42:371-88. [Crossref] [PubMed]
9. de Paiva JLR, Sabino JV, Pereira FV, et al. The Role of MRI in the Diagnosis of Spinal Cord Tumors. Semin Ultrasound CT MR 2023;44:436-51. [Crossref] [PubMed]
10. Kane SF, Abadie KV, Willson A. Degenerative Cervical Myelopathy: Recognition and Management. Am Fam Physician 2020;102:740-50.
11. Kwon BK, Tetreault LA, Evaniew N, et al. AO Spine/Praxis Clinical Practice Guidelines for the Management of Acute Spinal Cord Injury: An Introduction to a Focus Issue. Global Spine J 2024;14:5S-9S. [Crossref] [PubMed]
12. Lam J, deSouza RM, Laycock J, et al. Patient-reported bladder, bowel, and sexual function after cauda equina syndrome secondary to a herniated lumbar intervertebral disc. Top Spinal Cord Inj Rehabil 2020;26:290-303. [Crossref] [PubMed]
13. Allegri M, Montella S, Salici F, et al. Mechanisms of low back pain: a guide for diagnosis and therapy. F1000Res 2016;5 F1000 Faculty Rev 1530;