Aggressive lumbar vertebral hemangioma presenting with foot drop mimicking spinal tuberculosis: A case report

Abstract

Background:

Aggressive vertebral hemangiomas are uncommon vascular lesions that may present with epidural extension and neurological deficit. In tuberculosis-endemic regions, atypical vertebral hemangiomas may mimic spinal tuberculosis, resulting in diagnostic confusion and delay in definitive management.

Case Description:

A 20-year-old male presented with a 1-year history of left lower-limb radiculopathy followed by progressive left foot drop for 1 month. The patient had previously received empirical antitubercular therapy without clinical improvement. Magnetic resonance imaging demonstrated an expansile lesion involving the L1 vertebral body and posterior elements with epidural extension causing severe canal stenosis and compression at the conus medullaris and cauda equina junction. Preserved intervertebral discs and characteristic imaging findings suggested an aggressive vertebral hemangioma. The patient underwent posterior stabilization with D12 and L2 pedicle screw fixation along with L1 laminectomy and decompression. Intralesional chemical cauterization using absolute alcohol was performed intraoperatively. Histopathological examination confirmed vertebral hemangioma. Significant postoperative neurological improvement was observed with recovery of foot dorsiflexion.

Conclusion:

Aggressive lumbar vertebral hemangiomas may rarely present with foot drop and mimic spinal tuberculosis. Careful radiological evaluation and individualized surgical management with timely decompression and stabilization are essential for favorable neurological outcomes.

INTRODUCTION

Vertebral hemangiomas are common benign vascular lesions of the spine; however, aggressive variants causing osseous expansion, epidural extension, and neurological deficits are rare.[2,5] These lesions may mimic infectious or neoplastic disorders, particularly spinal tuberculosis in endemic regions, leading to diagnostic confusion and delayed treatment.[4] Symptomatic lumbar vertebral hemangiomas are uncommon, and presentation with foot drop is exceptionally rare.[5,6] We report a case of aggressive L1 vertebral hemangioma presenting with radiculopathy and progressive foot drop that was initially misdiagnosed and treated as spinal tuberculosis, highlighting the importance of characteristic radiological findings and timely surgical intervention.

CASE REPORT

A 20-year-old male presented with low back pain radiating to the left lower limb for 1 year and progressive left foot drop for 1 month. He had previously received empirical antitubercular therapy for suspected spinal tuberculosis without improvement. Clinical examination revealed weakness of left ankle dorsiflexion and impaired gait, with no bowel or bladder involvement.

Computed tomography (CT) demonstrated coarse vertical trabeculations within the vertebral body with a classical “polka-dot” appearance on axial sections, suggestive of vertebral hemangioma [Figure 1]. Magnetic resonance imaging (MRI) demonstrated an expansile lesion involving the L1 vertebral body and adjacent posterior elements. The lesion appeared hyperintense on both T1- and T2-weighted images. Cortical thinning and posterior epidural extension were noted at the D12–L1 level, producing severe canal stenosis with compression at the conus–cauda transition zone. Paravertebral extension was present; however, intervertebral discs were preserved [Figure 2].

Figure 1:

Preoperative computed tomography scan. (A) Sagittal reconstruction showing an expansile lesion involving the L1 vertebral body with coarse vertical trabeculations and thinning of the posterior cortex. (B and C) Axial images demonstrating the characteristic “polka-dot” appearance with thickened vertical trabeculae, suggestive of vertebral haemangioma.

Figure 2:

Preoperative magnetic resonance imaging of the dorsolumbar spine. (A) Sagittal T2-weighted images showing an expansile, hyperintense lesion involving the L1 vertebral body with posterior cortical thinning and epidural extension. There is severe canal stenosis with compression of the conus-cauda transition zone at the D12-L1 level. (B-E) Axial T2-weighted images at the level of L1 vertebra demonstrating posterior epidural soft tissue component causing marked compression of the thecal sac and cauda equine.

The patient underwent D12–L2 fixation, L1 laminectomy, decompression, and intralesional alcohol cauterization [Figure 3].

Figure 3:

Intraoperative photograph demonstrating posterior decompression after L1 laminectomy with pedicle screw stabilization. Intralesional absolute ethanol was administered following decompression to achieve tumor devascularization before completion of stabilization.

At 3-month follow-up, the patient showed significant improvement in foot dorsiflexion and gait, and MRI demonstrated adequate neural decompression [Figure 4]. Histopathological examination demonstrated numerous thin-walled vascular channels lined by flattened endothelial cells interspersed with bony trabeculae, confirming the diagnosis of vertebral hemangioma.

Figure 4:

Postoperative magnetic resonance imaging (MRI). Postoperative (A and B) axial and ( C and D )sagittal MRI images (T2-weighted) showing adequate decompression of the spinal canal at the D12–L1 level with reduction of the epidural component and restoration of thecal sac.

Preoperative foot drop and postoperative neurological improvement are demonstrated in Supplementary Videos 1 and 2, respectively.

DISCUSSION

Aggressive vertebral hemangiomas account for <1% of vertebral hemangiomas and may cause neurological deficits due to epidural extension and neural compression.[5,6] Although thoracic involvement is more common, symptomatic lumbar lesions are uncommon, and presentation with foot drop is particularly rare.[5] Selected published cases and the present case are summarized in Table 1. Characteristic imaging findings, including the corduroy and polka-dot signs demonstrated in the present case [Figures 1 and 2], are important diagnostic clues that help distinguish vertebral hemangioma from other spinal pathologies.[6]

Table 1:

Summary of selected published cases of symptomatic vertebral hemangioma and the present case

Vertebral hemangiomas are generally benign, slow-growing vascular lesions that remain asymptomatic throughout life. Only a small proportion demonstrates aggressive behavior characterized by osseous expansion, cortical erosion, epidural extension, and neural compression. Progressive neurological deterioration usually results from epidural extension rather than malignant transformation or rapid tumor growth. Recognition of this natural history is important because symptomatic lesions require early intervention before irreversible neurological injury develops.[2,5]

In tuberculosis-endemic regions, aggressive vertebral hemangiomas may mimic Pott’s disease, resulting in delayed diagnosis and inappropriate treatment.[4] Preservation of intervertebral disc spaces and characteristic trabecular architecture favor vertebral hemangioma over spinal tuberculosis.[4] Surgical decompression remains the preferred treatment in patients with progressive neurological deficits, while adjunctive modalities such as embolization and ethanol ablation may be used in selected cases.[1,3,5] In the present case, posterior decompression was selected because neurological compression resulted predominantly from epidural extension of the lesion rather than complete destruction of the vertebral body. Preoperative imaging demonstrated preservation of vertebral body height without pathological collapse or significant anterior instability. Therefore, posterior decompression combined with pedicle screw fixation was considered sufficient to achieve neural decompression while maintaining spinal stability. Vertebral body resection or corpectomy is generally reserved for patients with extensive vertebral body destruction, pathological fracture, marked mechanical instability, or persistent anterior compression that cannot be adequately addressed through a posterior approach. In our patient, preservation of vertebral body height and structural integrity on preoperative imaging supported a posterior-only strategy.[1,5]

Absolute ethanol was used intraoperatively as an adjunctive devascularizing agent because it causes endothelial destruction, thrombosis, and fibrosis of abnormal vascular channels, thereby reducing tumor vascularity and intraoperative bleeding. Heiss et al. demonstrated that intralesional ethanol produces thrombosis and fibrosis of abnormal vascular channels, resulting in durable devascularization of vertebral hemangiomas; however, careful administration is necessary to avoid neurological complications associated with extravasation.[3]

Posterior pedicle screw fixation was performed to maintain spinal stability following decompression and to reduce the risk of postoperative instability associated with laminectomy and posterior element involvement. Instrumented stabilization also facilitates early rehabilitation while providing long-term biomechanical support.

Our patient demonstrated excellent neurological recovery following posterior decompression, pedicle screw stabilization, and adjunctive intralesional ethanol ablation. This case highlights the importance of individualized surgical planning based on the extent of neural compression and spinal stability rather than routine vertebral body resection.

CONCLUSION

Aggressive vertebral hemangioma should be considered in the differential diagnosis of atypical spinal lesions presenting with neurological deficits, particularly in tuberculosis-endemic regions. Recognition of characteristic CT and MRI findings allows timely diagnosis and appropriate surgical planning. Individualized treatment with posterior decompression, stabilization, and adjunctive intralesional ethanol ablation can achieve excellent neurological recovery while avoiding unnecessary radical vertebral body resection.

Ethical approval:

Institutional Review Board approval is not required.

Declaration of patient consent:

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given consent for their images and other clinical information to be reported in the journal. The patient understands that the patient’s names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship:

Nil.

Conflicts of interest:

There are no conflicts of interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation:

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

Supplementary Video available on:

https://doi.org/10.25259/SNI_677_2026

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