Ventral Cervical Epidural Abscess Presenting as a Stroke Mimic With Paradoxical Thoracic Sensory Level: Diagnostic Challenges and Multimodal Management

Introduction

Spinal epidural abscess (SEA) is an uncommon but increasingly recognized infection; its incidence has increased over recent decades, affecting 5/10 000 to 8/10 000 hospital admissions [1]. Lumbar involvement predominates (49%), followed by thoracic involvement (31%); cervical spine involvement occurs in only 24% of cases [2]. The cervical location poses unique diagnostic and therapeutic challenges, particularly when abscesses develop ventrally (occurring in 30% to 45% of cervical cases) compared with the typical posterior predominance observed in thoracolumbar infections [3].

Diagnostic challenges intensify when cervical epidural abscesses present with atypical neurological patterns. Historical data reveal initial misdiagnosis rates of 75% to 89%, with emergency departments missing the diagnosis on the first evaluation in 75% to 84% of cases [4]. The classic triad of back pain, fever, and neurological deficits appears in only 8% to 15% of initial presentations [5]. Cervical lesions can produce paradoxical sensory levels below the actual pathological level due to vascular compromise and inflammation, leading to incorrect anatomical localization.

Cervical epidural abscesses frequently mimic stroke presentations, particularly when involving the anterior structures [6]. The absence of cranial nerve involvement, despite profound motor deficits, should prompt the consideration of spinal pathology. The confined epidural space at the cervical level contributes to uniquely rapid progression patterns, with documented cases showing deterioration from partial weakness to complete quadriplegia within 12 hours [7]. Herein, we report a case that exemplifies these diagnostic challenges while exploring innovative multimodal management approaches.

Case Report

A 51-year-old man with poorly controlled hypertension and 2 months of heroin use presented to the emergency department with 1 week of progressive back soreness that evolved into severe pain radiating bilaterally to the shoulders and neck. Over the preceding 3 days, he had developed a persistent fever and progressive left-sided limb weakness. Initial neurological examination revealed asymmetric weakness favoring the left side, prompting a stroke workup; brain computed tomography (CT) revealed no acute intracranial pathology. Within hours of admission, the motor deficits rapidly progressed to near-complete quadriparesis.

On admission, a neurological examination was performed in a standard sequence. Mental status and cognition were intact. Cranial nerve examination was unremarkable. Motor testing showed strength of 0/5 in the left extremities, 3/5 in the right upper limb, and 1/5 in the right lower limb. Deep tendon reflexes were absent bilaterally in the lower extremities. Sensory examination demonstrated a distinct dermatomal level at T4/T5 (nipple line), more pronounced on the left. Laboratory investigations showed leukocytosis (20 440/μL), elevated C-reactive protein (30.58 mg/dL), and pyuria.

Although acute ischemic stroke was considered at presentation due to the abrupt onset of motor deficits, brain magnetic resonance imaging (MRI) was not obtained because the neurological localization and systemic features favored a spinal etiology rather than an intracranial lesion. Specifically, the patient had preserved consciousness, no cranial nerve involvement, prominent neck/back pain with fever, and a definable sensory level, which collectively suggested cervical spinal cord compression/infection and made an isolated cerebral lesion less likely. Importantly, although the neurological examination showed an apparent dermatomal sensory level at T4/T5, this finding was interpreted cautiously because cervical spinal cord lesions can produce a paradoxical thoracic sensory level [8,9]. Therefore, we prioritized urgent contrast-enhanced MRI of the cervical spine to confirm the suspected diagnosis and avoid delaying time-sensitive decompression and antimicrobial therapy, given that diagnostic delay in spinal epidural abscess is associated with worse neurological outcomes and MRI is the key diagnostic modality [1,4,5]. Contrast-enhanced MRI of the cervical spine demonstrated epidural fluid collection from C2–C7 along both the anterior and posterior longitudinal ligaments with peripheral rim enhancement (Figure 1A–1C). The abscess demonstrated a significant mass effect with severe spinal cord compression at C2–C6, along with cord swelling and edema. Given the rapid neurological deterioration and marked cord compression, emergency surgical decompression and epidural abscess evacuation were performed (C3–C7 laminectomy) without delaying intervention for microbiological confirmation. Postoperatively, the patient received intravenous vancomycin with initial empirical meropenem coverage. Blood cultures subsequently grew methicillin-resistant Staphylococcus aureus (MRSA), supporting hematogenous bacterial infection and guiding antimicrobial management. Intraoperative bone and disc cultures showed no growth, likely related to preoperative antibiotic exposure. Antimicrobial therapy was continued as pathogen-directed treatment.

Serial blood cultures were obtained until clearance, and the first negative set was documented on postoperative day 9. A 6-week course of targeted intravenous antibiotic therapy was initiated on the date of culture clearance. The patient was successfully extubated on postoperative day 7 and transferred to the general ward the next day. Beginning on postoperative day 12, the patient received adjunctive hyperbaric oxygen therapy (HBOT) consisting of 10 sessions at 2.0 to 2.5 atm of absolute pressure. Intravenous laser irradiation of blood (ILIB) was initiated as an investigational anti-inflammatory adjunct. Comprehensive rehabilitation was instituted using repetitive transcranial magnetic stimulation (rTMS) to enhance motor recovery. At the 6-week follow-up, inflammatory markers had normalized (Figure 2). Follow-up cervical spine MRI demonstrated interval reduction of the epidural abscess and residual inflammatory changes consistent with spondylodiscitis and vertebral osteomyelitis (Figure 3A, 3B). Flaccid quadriplegia improved to partial antigravity strength in selected proximal muscle groups, but he remained wheelchair-dependent at discharge with plans for intensive outpatient neurorehabilitation.

Discussion

This case illustrates several critical aspects of cervical epidural abscess management and highlights emerging therapeutic approaches. The diagnostic challenge posed by a stroke-mimicking presentation with paradoxical sensory-level localization is a well-documented but under-recognized phenomenon in cervical SEA [6].

The neurological presentation deserves particular attention. On initial neurological examination, the patient demonstrated a T4/T5 sensory level, which could mislead clinicians toward thoracic localization; however, spinal MRI subsequently revealed extensive cervical pathology spanning C2–C7. A paradoxical thoracic sensory level is a recognized phenomenon in cervical cord lesions. This is primarily attributed to the somatotopic (laminar) organization of the spinothalamic tract, where fibers from sacral and lumbar segments are situated more peripherally than cervical fibers. Consequently, extrinsic compression from an epidural abscess, combined with inflammatory edema, can preferentially disrupt these outer laminae, producing a sensory level far below the anatomical pathology [8,9]. In addition, microcirculatory disturbances such as anterior spinal artery territory compromise and venous congestion unique to cervical anatomy can further contribute to this disproportionate tract dysfunction. A recent series by Papadakis et al analyzed 209 patients and found that 9% presented with quadriparesis on admission, whereas 11.9% had no initial neurological deficits, emphasizing the unpredictable progression patterns [10]. Beyond mimicking stroke, the clinical spectrum of cervical SEA is broad, with presentations sometimes mimicking crowned dens syndrome [11].

The ventral location of an abscess adds to this complexity. Turner et al systematically reviewed 173 patients with cervical epidural abscesses and found 37.2% ventral, 32.6% dorsal, and 30.2% circumferential positioning [12]. Ventral abscesses often require modified surgical approaches, with recent innovations, including anterior transcorporeal endoscopic drainage and linear transvertebral midline decompression, to avoid extensive instrumentation [13]. The anterior and posterior involvement in our case necessitated a traditional posterior laminectomy, given its extensive longitudinal spread and emergent presentation. Furthermore, as highlighted by Epstein, the coexistence of vertebral osteomyelitis and retropharyngeal abscess can further complicate the management of cervical infections [14].

Injection drug use predisposes to bacteremia and hematogenous seeding of the vertebral endplates, promoting spondylodiscitis with secondary epidural abscess, and ventral SEA commonly reflects contiguous subligamentous extension from disc-space infection. Spondylodiscitis refers to infection of the intervertebral disc with adjacent endplate involvement, whereas vertebral osteomyelitis primarily involves the vertebral body; in practice, these entities frequently overlap and are often discussed together as vertebral osteomyelitis and discitis [15,16]. Epidemiologically, MRSA constitutes 34.7% of S. aureus cervical infections, and intravenous drug use is the most frequent risk factor (36.7%) [1,10,17]. Pralea et al showed higher MRSA rates (36% vs 13%, P=0.002) and discharge against medical advice (34% vs 4.7%, P<0.001) among patients with active substance use disorder [17], supporting the plausibility of this mechanism in our patient with recent heroin use. Beyond substance use–associated bacteremia, cervical SEA has also been reported after acupuncture, underscoring that direct inoculation from percutaneous procedures can serve as a precipitating source of infection in the cervical epidural space [18]. In addition, diabetes mellitus is one of the most frequently reported host risk factors for SEA, and recent upper-cervical SEA reports emphasizes diabetes-related susceptibility even in the absence of other clear predisposing conditions [19].

IDSA guidelines for vertebral osteomyelitis emphasize timely diagnosis (MRI), pathogen-directed antimicrobial therapy, and surgical intervention when indicated; they do not provide recommendations for adjunctive modalities such as HBOT, ILIB, or rTMS, and they explicitly do not address epidural abscess without associated native vertebral osteomyelitis [15]. Therefore, these modalities should be interpreted as adjunctive and investigational rather than standard-of-care in SEA. HBOT enhances oxygen delivery to infected tissues and improves leukocyte function and antibiotic penetration. A retrospective series of spinal osteomyelitis patients with epidural involvement showed infection cure in 5/6 patients who had failed standard therapy when HBOT was added [20]. The mechanisms involved include enhanced neutrophil bactericidal activity, improved antibiotic efficacy in oxygenated environments, and promoted tissue healing through angiogenesis.

ILIB is an investigational approach. A recent review synthesizing randomized controlled trials suggests that ILIB is generally safe and can reduce inflammatory and oxidative-stress biomarkers [21]; however, disease-specific evidence for SEA is lacking and causality cannot be inferred from this single case. Given these properties, ILIB was included as an investigational adjunct targeting inflammatory and secondary injury pathways after spinal cord compression.

The incorporation of rTMS in neurological rehabilitation reflects the emergence of neuromodulation strategies. Recent evidence suggests that high-frequency rTMS applied to the motor cortex can strengthen corticospinal pathways and promote neuroplasticity following spinal cord injury [22]. A 2025 review of 14 studies demonstrated its beneficial effects on muscle strength and functional outcomes, although larger trials are needed [23].

Our patient’s rapid progression from unilateral weakness to near-complete quadriplegia within hours exemplifies the aggressive nature of cervical SEA. The literature consistently shows 75% medical management failure rates for cervical epidural abscesses, compared with 29% to 41% for the general population with SEA, underscoring the importance of early recognition and urgent surgical intervention [24]. The diagnostic delay in our case, which was initially attributed to a stroke-like presentation, reflects a common pitfall. Velpula et al reported similar cases in which unilateral weakness led to a cerebrovascular workup, with 1 patient undergoing 48 hours of stroke evaluation before spinal imaging revealed an extensive abscess [6]. The key differentiating features include preserved consciousness, absence of cranial nerve involvement, presence of a sensory level, and progression pattern inconsistent with vascular territories.

Conclusions

This case demonstrates the diagnostic complexity of a cervical epidural abscess presenting with stroke-like symptoms and paradoxical sensory level localization. A critical teaching point emerging from this case is that a thoracic sensory level with fever and preserved mentation represents a spinal cord process until proven otherwise. Clinicians should perform urgent spinal MRI in at-risk patients rather than anchoring for a cerebrovascular diagnosis. Early neurosurgical decompression with pathogen-directed antimicrobial therapy remains the cornerstone of cervical SEA management and is most likely responsible for infection control and neurological stabilization in this case. HBOT may be considered in selected complex cases; however, ILIB and rTMS should be regarded as adjunctive approaches rather than standard-of-care for SEA, and their clinical roles require confirmation in controlled studies. As SEA incidence continues to rise, increased awareness of atypical presentations and innovative management strategies is essential to reduce the significant morbidity associated with this potentially devastating condition.