Hemorrhagic lumbar synovial cyst mimicking a neoplastic process: illustrative case

Abstract

BACKGROUND

Synovial cysts with extensive hemorrhage, marked mass effect, and tumor-like appearance are rare and may mimic neoplastic processes.

OBSERVATIONS

A 56-year-old man presented with progressive mechanical low back pain, neurogenic claudication, gait instability, and bilateral weakness. MRI revealed a 2.0-cm lesion arising from the right L3 facet joint, causing severe central canal and right foraminal stenosis with displacement of the cauda equina. Imaging features suggested pigmented villonodular synovitis. Intraoperatively, however, the lesion appeared fleshy, partially encapsulated, and dural adherent, resembling a nerve sheath tumor, with necrotic regions suggesting malignancy. Frozen-section analysis demonstrated benign fibroconnective tissue with marked reactive and degenerative changes, including necrosis and hemosiderin deposition, without evidence of neoplasia. Intraoperative confirmation of benign pathology shifted operative priorities toward anatomical preservation rather than extent of resection; gross-total removal was nevertheless achieved and the patient had complete neurological recovery. Permanent pathology was most consistent with a degenerative synovial cyst with hemorrhage.

LESSONS

This case highlights the importance of integrating imaging findings, intraoperative appearance, and histopathological evaluation rather than relying on a single diagnostic modality. The combination of a focused differential and confirmation of benign pathology guided the extent of resection, balancing maximal lesion removal with preservation of adjacent structural elements.

https://thejns.org/doi/10.3171/CASE26317

Spinal lesions can arise from a variety of etiologies,¹ including primary and secondary tumors,^2,3 infections,⁴ inflammation,⁵ vascular abnormalities,⁶ traumatic injuries,⁷ and degenerative conditions.⁸ Spinal lesions warrant prompt evaluation as they can lead to substantial morbidity, including chronic pain and sensorimotor deficits.¹ Assessment of spinal lesions relies on patient history, physical examination, and imaging findings such as location, invasion, metastasis, and enhancement, with CT and MRI playing complementary roles.¹ CT best delineates bony involvement, such as cortical destruction and osseous integrity, whereas MRI excels in evaluating soft tissue extension, including perineural and dural invasion.^1,9 However, radiographic features frequently overlap across spinal pathologies, as diverse disease processes often produce similar imaging manifestations, including mass effect, enhancement, and soft tissue signal changes, complicating definitive diagnosis.^1,10 Similarly, intraoperative characteristics, including gross appearance, degree of encapsulation, tissue consistency, necrosis or hemorrhage, and dural adherence, may be shared across a wide range of neoplastic and nonneoplastic spinal lesions.^1,10 In cases in which a definitive diagnosis cannot be established preoperatively or intraoperatively, surgical management must proceed with careful consideration of the differential diagnosis. Adjunctive tools such as intraoperative ultrasound and frozen-section and stimulated Raman histological analysis can guide operative decision-making by indicating signs of malignancy and evaluating the extent of resection and decompression.

Here, we present a case of a synovial cyst that radiographically mimicked pigmented villonodular synovitis (PVNS) and intraoperatively resembled a peripheral nerve sheath tumor, with histopathology favoring a synovial cyst. This case demonstrates the diagnostic ambiguity of certain spinal masses and offers strategies for surgical decision-making under uncertainty.

Illustrative Case

A 56-year-old man with hypertension, chest palpitations, and class I obesity presented with 1 month of progressive mechanical low back pain and bilateral lower extremity weakness. Symptoms worsened with standing and walking and were relieved by lumbar flexion, consistent with neurogenic claudication. Over the preceding 3 weeks, he developed intermittent bilateral leg buckling that ultimately required crutches for ambulation. He endured periods of severe back pain flares that resulted in him being temporarily bedridden, although he noted improvement with pain medication. He denied radicular pain, sensory loss, or bowel or bladder dysfunction. On examination, asymmetric left distal lower extremity weakness was present, with dorsiflexion 4/5 and toe extension 2/5, and gait was markedly unstable; sensation, reflexes, and rectal tone were normal.

MRI of the lumbar spine demonstrated a 2.0-cm contrast-enhancing mass arising from the right L3 facet joint with associated severe synovitis (Fig. 1A and B). The synovial proliferation extended along the adjacent paravertebral soft tissues, into the right posterolateral spinal canal, and into the right neural foramen, producing severe right and moderate left foraminal stenosis. The mass caused severe canal stenosis with displacement of the thecal sac and cauda equina into the left anterolateral recess. Areas of intrinsic T1 hyperintensity and a T2-hypointense lining along the thecal sac suggested blood products and hemosiderin deposition, raising concern for PVNS (Fig. 1C and D). CT imaging demonstrated degenerative facet arthropathy without evidence of osseous destruction.

FIG. 1.

Preoperative MR images demonstrating a synovial proliferative mass arising from the right L3–4 facet joint. A: Sagittal T2-weighted MR image showing a 2.0-cm lesion originating from the right L3 facet joint with associated severe synovitis. The synovial proliferation extends along the paravertebral soft tissues and into the spinal canal. B: Axial T2-weighted MR image obtained at L3–4 demonstrating extension of the mass into the right posterolateral canal and right neural foramen, resulting in severe right and moderate left foraminal stenosis. The lesion causes severe central canal stenosis with displacement of the thecal sac and cauda equina into the left anterolateral recess. C: Sagittal MR image showing areas of intrinsic T1 hyperintensity within the right L3–4 facet-associated lesion (arrows), consistent with subacute blood products. D: Axial MR image demonstrating a thin T2-hypointense lining along the thecal sac adjacent to the lesion (arrow), compatible with hemosiderin deposition. Together, these findings raised concern for PVNS.

Given the patient’s rapid neurological decline over 3 weeks, with progressive bilateral weakness culminating in crutch dependence, urgent surgical intervention was deemed necessary to prevent permanent neurological injury and he was scheduled for a L3–4 laminectomy with resection of the lesion.

The patient was positioned prone on a Jackson frame, with all pressure points carefully padded. Intraoperative neuromonitoring, including somatosensory and motor evoked potentials with sphincter monitoring, was established and baseline recordings obtained. The L3–4 level was localized on the skin surface using intraoperative fluoroscopy, and a standard posterior midline approach was performed via a midline incision, with subperiosteal dissection exposing the spinous processes, lamina, facet joints, and transverse processes from L3 to L5; the level was reconfirmed fluoroscopically prior to decompression. Under the operating microscope, a laminectomy of L3–4 was performed, and intraoperative ultrasound was used to localize the epidural lesion prior to dural exposure.

On exposing the lesion, a smooth fleshy, pink extradural mass was encountered spanning the midline and the right posterolateral canal from L3 to L4. The lesion appeared partially encapsulated with a soft core and was tightly adherent to the underlying dura, closely mimicking the intraoperative appearance of a peripheral nerve sheath tumor (Fig. 2A), with necrotic regions similar to a malignant peripheral nerve sheath tumor (MPNST) (Fig. 2B). The mass appeared to originate from the right L3 foramen and extended deeply into the posterolateral soft tissues. On incising the capsule, extensive necrosis was noted. Frozen-section analysis was negative for signs of malignancy, and the focus shifted to decompression with preservation of normal anatomical structures. Further dissection revealed a focal capsular defect containing hemosiderin-rich necrotic material (Fig. 2B). After debulking the necrotic cavity, the lesion was mobilized from its ligamentous attachments. The foraminal component required a right L3 foraminotomy and medial facetectomy to achieve complete resection. Intraoperative ultrasound confirmed adequate decompression and gross-total resection (Fig. 3).

FIG. 2.

Intraoperative appearance of the lesion during L3–4 decompression. A: Intraoperative view following L3–4 laminectomy showing a smooth, fleshy, pink extradural lesion with a partially defined capsule and broad-based adherence to the underlying dura. This tumor-like configuration closely simulated a peripheral nerve sheath tumor, illustrating how nonneoplastic lesions may resemble nerve sheath tumors intraoperatively. B: Intraoperative photograph demonstrating the focal capsular defect containing hemosiderin-rich necrotic material encountered during exposure. Debulking of this necrotic cavity permitted mobilization of the lesion from its ligamentous attachments, enabling complete removal.

FIG. 3.

Intraoperative photograph of a substantial portion of the resected mass, consisting of dark, friable, hemosiderin-rich necrotic tissue. This material was removed from the lesion cavity, and intraoperative ultrasound subsequently confirmed adequate decompression and gross-total resection.

Postoperatively, the patient recovered without complications. By postoperative day 3, lower extremity strength had returned to 5/5 bilaterally, he was ambulating independently, and neurogenic claudication had fully resolved. There was no evidence of CSF leakage, and he was discharged home on postoperative day 4. At follow-up 3 weeks later, the patient had returned to his neurological baseline, with complete resolution of preoperative symptoms and no functional limitations. Postoperative imaging was not obtained, as the patient did not return for follow-up beyond the 3-week visit, at which he had returned to his neurological baseline. Subsequent permanent histopathological evaluation by a bone and soft tissue pathology specialist demonstrated fibroadipose and fibroconnective tissue with reactive and degenerative changes, hemorrhage with hemosiderin deposition, and nontumoral necrosis (Fig. 4), without an identifiable synovial lining, most consistent with a degenerative synovial cyst with hemorrhage. Immunohistochemical staining was not performed, as no unclassifiable cell population was identified on routine H&E staining.

FIG. 4.

Pathology. A: Dense connective tissue with new bone formation. B: Granulation tissue. C: A collection of hemosiderin-laden macrophages in dense connective tissue. D: Focal fat necrosis. Scale bar in each image = 100 μm. All slides are stained with hematoxylin and eosin.

Informed Consent

The necessary informed consent was obtained in this study.

Discussion

Observations

The principal observation in this case was the discordance between imaging, surgical appearance, and histopathology in a lumbar facet joint mass; while MRI suggested PVNS, and intraoperative appearance initially raised concern for a nerve sheath tumor, permanent histological analysis ultimately confirmed a synovial cyst.

Initial MRI findings had raised concern for PVNS. PVNS is a benign neoplastic proliferation of synovial tissue,¹¹ most commonly involving the knee¹² and only rarely affecting the spine;¹³ among spinal cases, PVNS is more often found in the cervical portion.¹³ Despite this, there have been cases of PVNS in the lumbar spine with a similar presentation to this case, causing mass effect on the thecal sac or cauda equina.^14–16 Radiographically, PVNS classically demonstrates low signal intensity on both T1- and T2-weighted MRI and blooms due to hemosiderin deposition,¹¹ although hemorrhagic components may result in hyperintense T1 signal.¹⁷ Intraoperatively, PVNS typically appears as a brown-tinted friable villous or nodular synovial proliferation.¹¹ Histologically, PVNS is characterized by synovial hyperplasia with villous and nodular architecture, lipid- and hemosiderin-laden macrophages,¹⁸ and multinucleated osteoclast-type giant cells.¹⁸ In the present case, several features supported PVNS in the differential diagnosis, including a synovial proliferation with lumbar facet joint origin, contrast enhancement, hemorrhagic signal characteristics, dark friable intraoperative appearance, and histopathological evidence of hemosiderin. This lesion’s intrinsic T1 hyperintensity and T2-hypointense thecal lining further supported PVNS on preoperative imaging, more closely resembling the classic PVNS signal pattern than the typical T1-hypointense, T2-hyperintense appearance of synovial cysts. However, histopathological analysis ultimately did not show any evidence of PVNS, and thus we concluded the lesion was a synovial cyst.

Peripheral nerve sheath tumors became a prominent consideration intraoperatively. These tumors arise from peripheral nerve sheaths and include predominantly benign entities such as schwannomas and neurofibromas, with rare malignant variants such as MPNSTs.¹⁹ On MRI, nerve sheath tumors typically appear as well-circumscribed,¹⁹ fusiform²⁰ lesions with low to intermediate T1 signal, high T2 signal, and contrast enhancement.²¹ Intraoperatively, nerve sheath tumors commonly present as encapsulated,²² fleshy masses,¹⁹ with MPNSTs particularly having large areas of necrosis and hemorrhage.¹⁹ Histologically, nerve sheath tumors are characterized by spindle cell proliferation, while malignant variants demonstrate increased cellularity and infiltrative growth.²³ The lesion’s foraminal extension, partial encapsulation, and broad dural adherence closely resembled the typical intraoperative appearance of a peripheral nerve sheath tumor, with necrosis matching that of MPNST.²⁴ However, the high T2 signaling or histology indicators for any nerve sheath tumors were not present, and frozen-section and permanent histopathological analysis was able to rule out a malignant process such as MPNST.

Histopathological analysis ultimately confirmed a synovial cyst. Synovial cysts are benign, degenerative lesions that arise from synovial joints. In the spine, they most frequently originate from the lumbar facet joints, most commonly at the L4–5 level,²⁵ and only approximately 3% demonstrate hemorrhagic transformation.²⁶ When synovial cysts undergo acute hemorrhage, they typically cause a sudden expansion in size, compressing neural elements and resulting in severe, sudden-onset symptoms. On MRI, cysts appear as well-circumscribed, epidural mass lesions that are generally T1-hypointense and T2-hyperintense, but signals can vary based on protein content, hemorrhage, and calcification.²⁷ Intraoperatively, hemorrhagic synovial cysts have been reported to appear xanthochromic²⁸ or brown²⁹ and fluid filled,³⁰ can be attached to the dura,³¹ and may cause spinal compression.³² Histologically, hemorrhagic synovial cysts typically show a fibroconnective tissue wall lined by synovial cells, disrupted by blood and hemosiderin.³³ While this case did not match the classically described radiographic or intraoperative presentation of a synovial cyst, the diagnosis was confirmed histopathologically.

There are many cases of synovial cysts mimicking other types of lesions,^34–36 and hemorrhagic cysts are often misdiagnosed due to their rarity.³⁷ To our knowledge, only one case of a hemorrhagic facet joint cyst mimicking a nerve sheath tumor has been described. Robins et al. reported an L4–5 lesion with MR images obtained 14 months apart, demonstrating rapid interval growth, raising concern for an aggressive metastatic process or nerve sheath tumor; however, histopathological analysis revealed collagenous and fibrotic tissue consistent with a facet joint cyst.³⁸ Similar to our case, the lesion was dural adherent, compressive, and appeared dark red intraoperatively.³⁸ While serial imaging was not available in our case to confirm rapid growth, the patient’s symptoms progressed rapidly. The main difference was the scalloped texture described by Robins et al.,³⁸ while the lesion in this case demonstrated a smooth surface, more consistent with nerve sheath tumors. While there were no cases found that explicitly mention mimicking PVNS, one review found that among 23 cases, 30.4% had a hypointense T2 signal, and among 28 cases, 21.4% displayed contrast enhancement, both of which are more commonly associated with PVNS.³³ This case adds to the literature by illustrating that hemorrhagic synovial cysts may present atypically and closely mimic both nerve sheath tumors and PVNS across imaging, intraoperative, and histopathological domains, highlighting the potential for discordant findings and the importance of cautious intraoperative decision-making.

In cases in which a definitive diagnosis at the time of operation is not possible, it is important to weigh the relative likelihoods and risks of competing diagnoses. Among these entities, benign nerve sheath tumors are the most common, accounting for approximately 24%–31% of spinal tumors.³⁹ Synovial cysts are relatively common degenerative lesions, occurring in 0.65%–2.6% of the general population, although hemorrhagic variants comprise only 3%–10% of intraspinal synovial cysts. In contrast, spinal MPNSTs are rare, with an annual incidence of 0.3–0.4 per 100,000 persons,⁴⁰ while spinal PVNS is exceedingly rare, with fewer than 100 cases reported to date.⁴¹ From a risk standpoint, both PVNS and benign nerve sheath tumors are associated primarily with local progression rather than systemic spread. Lesion enlargement or recurrence may result in progressive neural compression or osseous erosion,⁴¹ but these entities carry minimal risk of metastasis or mortality. However, in both conditions, subtotal resection is associated with substantially higher rates of recurrence.⁴² In contrast, MPNSTs carry a substantially poorer prognosis, with reported 5-year survival rates ranging from 21% to 69%.⁴³ However, complete gross-total resection increases the 5-year survival rate to greater than 90%.⁴⁴

Regardless of the underlying diagnosis, the lesion in this case had progressed to cause significant compression of the cauda equina with resulting neurogenic claudication. Without intervention, ongoing compression posed a risk of irreversible neurological sequelae, including sexual dysfunction, bowel or bladder incontinence, and lower extremity paralysis.⁴⁵ Thus, decompression of the cauda equina was paramount. While MPNST remained within the differential diagnosis, achieving maximal resection was prioritized, given its prognostic implications. Once malignancy was excluded through frozen-section analysis, however, the surgical objective shifted toward adequate decompression and maximal lesion removal while preserving anatomical structure. Although this approach carries a higher risk of recurrence, it would provide symptom relief without introducing new neurological deficits and preserve the option for future intervention if required. In this case, however, gross-total resection with adequate decompression was still achievable while leaving the facets and other local structures intact, resulting in complete neurological recovery.

This case illustrates the substantial diagnostic overlap among spinal lesions and highlights how different diagnostic modalities may yield discordant findings. Accordingly, operative planning should be guided by integration of all available data, balancing the relative likelihoods and risks of competing diagnoses, rather than reliance on any single modality.

Lessons

Lesions of the lumbar facet joint may be difficult to diagnose and closely mimic neoplastic masses both radiographically and intraoperatively. Frozen-section histopathological evaluation is essential for intraoperative decision-making, even if the results are nondefinitive. Early surgical decompression remains the primary treatment for patients with severe lumbar canal stenosis. Complete neurological recovery is achievable when intervention is timely, and risks are weighed in accordance with a multidisciplinary differential diagnosis informed by imaging, experience, and histopathology. This case highlights the importance of structured decision-making in the setting of diagnostic uncertainty, demonstrating that excellent outcomes can be attained through careful integration of imaging findings, intraoperative assessment, and frozen-section analysis, even in the absence of a definitive diagnosis.

Acknowledgments

ChatGPT (GPT-5.2, OpenAI) was used for language editing and clarity. We generated all scientific content, analysis, and conclusions.

Disclosures

The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.

Author Contributions

Conception and design: Oermann, Kapoor, Weiss, Hoda, Littig. Acquisition of data: Kapoor, William, Littig, Wang, Garrison. Analysis and interpretation of data: Kapoor, Alyakin, William, Hoda, Littig, Wang. Drafting the article: Oermann, Kapoor, Weiss, William, Hoda. Critically revising the article: Oermann, Kapoor, Alyakin, Weiss. Reviewed submitted version of manuscript: Oermann, Kapoor, Alyakin. Approved the final version of the manuscript on behalf of all authors: Oermann. Administrative/technical/material support: Oermann, Littig, Wang. Study supervision: Oermann, Littig. Radiology: Littig.

Correspondence

Eric K. Oermann: NYU Langone Medical Center, New York University, New York, NY. eric.oermann@nyulangone.org.