Thoracic spinal subdural hematoma after spinal cord stimulation trial: a case report

Introduction

Background

The incidence and mechanisms underlying intracranial hematomas-including epidural hematomas and subdural hematomas (SDH), are well described. Intracranial epidural hematomas are typically caused by rupture of the middle meningeal artery following fracture of the overlying temporoparietal bone, while intracranial SDH commonly arises from rupture of bridging veins in the subdural space.

Rationale and knowledge gap

Comparatively, there is limited understanding of spinal hematomas, especially those occurring in the absence of a clear etiology. Classically, spinal hematomas occur in the presence of known risk factors, including trauma, spinal surgery, or vascular abnormalities, often accompanied by a history of coagulopathy and/or anticoagulant use (1,2).

Objective

We present the case of spinal subdural hematoma (SSDH) that developed after an uncomplicated spinal cord stimulation (SCS) in a patient without any known risk factors in accordance with the CARE reporting checklist (available at https://jss.amegroups.com/article/view/10.21037/jss-25-137/rc).

Case presentation

A 78-year-old man with a history of shingles presented to Stony Brook University Hospital with complaints of generalized weakness and multiple ground-level falls. The patient reported days of dizziness, trouble walking, and generalized weakness that resulted in three ground-level falls onto his lower back. He also had left gluteal pain, but denied numbness, tingling, or bowel or bladder incontinence.

About 9 months before his presentation, the patient developed a shingles infection in his left thoracic region that left him with residual, chronic pain in the T4–T7 distribution. After failing a course of neuropathic pain medications, the patient received an uncomplicated interlaminar epidural steroid injection in the T4–T5 space. He experienced minor relief with the steroid injection and opted for an SCS trial. A pre-SCS, non-contrast magnetic resonance imaging (MRI) scan of the thoracic spine revealed no significant abnormalities. One month before presentation, the patient was fully consented for SCS and subsequently underwent an uneventful trial of percutaneous dorsal column stimulation. Under fluoroscopic guidance, entry was made at the T11–T12 space, and leads were placed at the T3 (right) and T6 (left) spinal level. Fluoroscopy confirmed proper placement of the SCS leads in the epidural space without signs of dural puncture or cerebrospinal fluid leak. At a mid-trial check 2 days later, the patient reported mild improvement in pain with no complications. At follow-up 6 days after the SCS trial, he requested postponing permanent implantation, though he reported no new symptoms.

Other significant past medical history includes hypertension, hyperlipidemia, diabetes mellitus type 2, coronary artery disease, chronic obstructive pulmonary disease, and transcatheter aortic valve replacement about 2 years before his presentation, but he discontinued aspirin use for over 6 months before the SCS trial. He denied any personal and family history of coagulopathy or recent anticoagulant use.

On examination, the patient showed signs of left leg weakness, gait instability, and urinary retention. Preoperative labs were notable for a low serum sodium level of 128 mEq/L and a normal platelet count, prothrombin time, and activated partial thromboplastin time. He underwent an MRI scan of the lumbar spine (Figure 1), which showed intrathecal lower lumbar T1/short tau inversion recovery (STIR) signal, a fluid-fluid level, and cauda equina enhancement suggestive of subarachnoid hemorrhage. A reflex MRI scan of the thoracic spine showed a well-circumscribed, compressive T2–T3 subdural collection (Figure 2).

Figure 1 Preoperative MRI of the lumbar spine showing a fluid-fluid level with cauda equina enhancement in the L4–L5 region, suggestive of a subarachnoid hemorrhage. (A) T1-weighted sagittal view with gadolinium. (B) T2-weighted sagittal view. MRI, magnetic resonance imaging.

Figure 2 Preoperative MRI of the thoracic spine showing a well-circumscribed lesion (2.08 cm × 0.94 cm) occupying the T2–T3 subdural space. (A) T2-weighted sagittal view. (B) T2-weighted axial view. (C) T1-post gadolinium weighted sagittal view. (D) T1-post gadolinium weighted axial view. MRI, magnetic resonance imaging.

The patient underwent emergent laminectomy and intradural decompression. The patient’s dura was notably slightly hardened and yellowish, akin to the appearance of the outer dural membrane in a non-acute intracranial SDH. A sample of the excised lesion sent for pathology showed blood, with necrosis of many white blood cells, and fibrovascular tissue, with mild chronic inflammation, all consistent with a hematoma. Further workup with spinal angiogram revealed no vascular abnormalities. Postoperative MRI scans (Figure 3) confirmed complete excision of the hematoma and relief of the thoracic compression, and lumbar imaging showed decreased T1/STIR signal in the lumbar spine, consistent with resolving subarachnoid hemorrhage. The patient developed intermittent urge incontinence but gradually recovered function. He was discharged for 6 weeks of spinal rehabilitation.

Figure 3 Postoperative MRI of the thoracic spine confirming hematoma evacuation. (A) T2-weighted sagittal view. (B) T1-post gadolinium weighted sagittal view. MRI, magnetic resonance imaging.

At a 6-week clinic follow-up visit, the patient reported an improvement in his left leg weakness, gait imbalance, and mobility. He complained of persistent postherpetic thoracic pain and bladder and bowel incontinence but denied saddle anesthesia. Follow-up X-ray showed no change in the thoracic spine alignment.

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 the 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

Key findings

Hematomas are solid, extravascular collections of blood within a body space. Central nervous system hematomas are notoriously concealed within the compact, inflexible neuraxial space as they compress vital structures, potentially causing life-threatening and irreversible neurological deficits (3).

This study is the first to report an SSDH following an uncomplicated SCS. Given the absence of classic risk factors and the 1-month delay in presentation, a distinct model for the pathophysiology underlying chronic SSDH should be sought.

Strengths and limitations

This is a single case report. While the unconventional case presentation offers a unique insight into SSDH, the following limitations should be considered when interpreting the pathological mechanism in this patient. Firstly, we cannot rule out spontaneous SSDH as a possible etiology. Secondly, dural anatomy varies slightly between the cranial and spinal compartments—one notable difference is the number of distinct dural layers. Unfortunately, SSDH lacks an extensive pathophysiological characterization in the literature compared to its intracranial counterpart, prompting our extrapolation from intracranial chronic subdural hematoma (CSDH) based on shared pathologic qualities.

Comparison with similar research

SSDHs are rare accumulations of blood within the thecal sac. Known risk factors for SSDH include trauma, spinal surgery, or vascular abnormalities (such as arteriovenous malformations), often in the context of coagulopathy or anticoagulant use (2,4-8). However, an estimated one-third of cases are reportedly idiopathic (6).

One potential source of trauma resulting in spinal hematoma is SCS, where electrodes are implanted in the epidural space to relieve nerve pain from a myriad of causes (9). A 2022 meta-analysis reported a pooled incidence of 0.81% for all hematomas in patients with SCS, with the incidence of neuraxial hematomas specifically estimated to be 0.32% (10). Unsurprisingly, most neuraxial hematomas reported were primarily located in the spinal epidural space (6,11-13), consistent with the typical location of lead placement. There has also been a case of intracranial SDH following SCS, which was managed via an emergent craniotomy (4). Notably, many of these complications occurred acutely following dural puncture and in patients receiving anticoagulant medications.

Explanations of findings

Edlmann et al. describe a pathologic process of sustained inflammatory response, seen in intracranial CSDH, that results in new membrane growth and fluid accumulation in the subdural space (14). Building on the work of Inglis (15), Edlmann et al. suggest that proliferation of dural border cells—specialized fibro-cellular connective tissue cells—intended for inflammation, angiogenesis, and repair will instead promote the formation of a new membrane that houses fragile, highly permeable capillaries. These vessels undergo blood leakage and fluid exudation restricted to the neomembrane-bound subdural space, and the resulting hemorrhage triggers further dural border cell proliferation, potentiating an intracranial CSDH positive-feedback cycle. Clinical evidence for the intracranial CSDH cycle is demonstrated in the utility of anti-inflammatory agents and middle meningeal artery embolization as treatment options for intracranial CSDH (16,17).

Given the subdural location, delayed timing, and intracranial CSDH-like appearance of the hematoma in our patient, we suspect that the mechanisms underlying this SSDH case are similar to those underlying intracranial CSDH pathophysiology. Specifically, we posit that epidural trauma from SCS lead placement caused shear stress, leading to an angiogenic and inflammatory response with an eventual neomembrane formation and a space-occupying hematoma responsible for the subacute myelopathic presentation. The slow course of hematoma development likely delayed presentation and intervention in this case, increasing the risk of residual sequelae postoperatively in our patient. We chose to intervene with surgical decompression for our patient because of the acuity and severity of his presentation. However, alternative approaches such as conservative management and percutaneous drainage have been documented for SSDH (18,19). Our patient did not qualify for conservative management, given his significant neurologic decline (18). Percutaneous drainage has shown beneficial outcomes for patients with extensive hematomas presenting as rachialgia without any neurologic deficit (19). However, our patient presented with lower extremity weakness, and MRI revealed a moderate-sized, localized nidus in the thoracic region.

Implications and actions needed

We urge clinicians to maintain a high index of suspicion for SSDH in patients presenting with subacute neurologic decline following a recent epidural SCS trial, as this rare but serious complication is often under-recognized, and early identification is critical to prevent permanent neurologic injury from spinal cord compression.

Conclusions

SSDHs are rare but can result in irreversible sequelae from spinal compression. Physicians caring for patients post-SCS trial or placement should be vigilant for atypical mechanisms underlying this pathology to anticipate disease presentation and ensure prompt diagnosis and treatment.

Acknowledgments

We would like to thank the Department of Neurological Surgery at the Renaissance School of Medicine at Stony Brook University for their care of our patients. Our abstract was presented at the 42nd National Neurotrauma Society Symposium, Philadelphia, Pennsylvania held between the 15th and 18th of June, 2025.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://jss.amegroups.com/article/view/10.21037/jss-25-137/rc

Peer Review File: Available at https://jss.amegroups.com/article/view/10.21037/jss-25-137/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jss.amegroups.com/article/view/10.21037/jss-25-137/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 the 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/.

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