Rare Case of a Cervical Ventral Root Filament Neuroma Mimicking a Sequestrated Disc Herniation in Association with Ossification of the Posterior Longitudinal Ligament

Abstract

Spinal neuromas related to chronic irritation or remote trauma may arise from unrecognized repetitive minor injury to the spinal cord or nerve roots, yet detailed descriptions with precise preoperative imaging findings are rare. We report a 59-year-old man with a 6-month history of severe dysesthesia and numbness in the neck and left upper limb, followed by progressive weakness over 2 months. He had undergone splenectomy after a traffic accident 23 years earlier. Computed tomography revealed ossification of the posterior longitudinal ligament, osteophytes, and a disc herniation at the left C5/C6 level. Magnetic resonance imaging demonstrated a slightly enhancing peripheral mass compressing the spinal cord. The differential diagnosis included meningioma and sequestrated cervical disc herniation. During surgery, only the swollen, non-functioning C6 ventral root filaments were resected, while functioning filaments were preserved. Histopathological examination confirmed a neuroma composed of disorganized axonal bundles consistent with chronic irritation- or remote trauma-related changes. The patient showed mild postoperative improvement. Chronic irritation appears to be the predominant contributor. Irritation-related neuromas should be considered in the differential diagnosis of intradural extramedullary lesions arising from C6 ventral root filaments, even when the trauma history is remote.

Introduction

Traumatic neuroma typically arises following nerve injury,^1-7) in which Wallerian degeneration of distal fibers is followed by disorganized proliferation of proximal axons through gaps created by Schwann cell disruption. Repeated attempts at axonal regeneration eventually form a tangled mass of nerve fibers embedded in fibroconnective tissue. Although traumatic neuromas are well described in peripheral nerves, reports involving the spinal cord or spinal nerve roots are rare^1-4,7-12) (see Table 1), and their underlying mechanisms remain poorly understood.

Table 1

Summary of Cervical Traumatic Neuromas

Author, Year	Age Sex	Location	Symptoms	T1WI/T2WI	Gd	Accompanying disease	T/D
AR: anterior nerve root; C: cervical; CMJ: cervicomedullary junction; CS: cervical spinal cord; D: duration from trauma; DM: diabetes mellitus; DR: dorsal nerve root; F: female; Gd: gadolinium; HO: homogenous; HL: hyperlipidemia; HT: hypertension; L: lumbar; M: male; NE: not evaluated; OPLL: Ossification of posterior ligament; P: peripheral; SCS: spinal canal stenosis; T: Trauma; T1WI/T2WI: T1-weighted image/T2-weighted image; TS: thoracic spinal cord; UC: ulcerative colitis; Y: year
Nomura et al. (8), 2002	41 M	C6, AR	-	NE	NE	-	-
	56 F	C7, AR	Pain, numbness	Isointensity/Isointensity	-	NE	-
	68 M	C5, AR	Pain, paresthesia, paresis	Isointensity/Isointensity	-	NE	-
	80 M	C6, AR	-	NE	NE	Parkinsonism, pneumonia	-
Torun et al. (9), 2005	49 F	C2, AR	Pain, hypesthesia	Isointensity/ Hyperintensity	+, HO	-	-
Santagata et al. (12), 2006	50 M	CMJ	Syncope, headache, dizziness	Isointensity/ Isointensity	+, HO	Psoriatic arthritis, HT	+/5.5Y
Johnson and Burger (7), 2009	18 F	CS	NE	NE	NE	Ependymoma	-
	53 F	CS	NE	NE	NE	Ependymoma	-
	53 M	TS	NE	NE	NE	Ependymoma	-
	65 M	NE	NE	NE	NE	Ependymoma	-
	69 M	CS	NE	NE	NE	Ependymoma	-
Arishima et al. (2), 2013	73 F	C6/C7, CS	Gait disturbance	Hypointensity/ Hyperintensity	+, P	Ependymoma	-
Salas et al. (11), 2013	69 F	C8, AR, DR	Pain, paresthesia, hand weakness	Isointensity/NE	+, HO	-	+/a few Y
Su et al. (4), 2013	57 F	C5C6 CS	Tetraparesis	Hypointensity/ Hyperintensity	NE	Spinal cord herniation	+/1Y
McGuire et al. (1), 2017	43 M	C6, CS	Gait disturbance, numbness	NE/Isointensity	+, HO	SCS, foraminal stenosis, and osteophytes	-
Kawajiri et al. (3), 2023	77 M	L1, CS	Gait disturbance, numbness	NE/Hyperintensity	+, HO	DM	-
Elias et al. (10), 2023	54 M	C7, DR	Paresthesia, paresis	Isointensity/ Slightly hyperintensity	+, HO	HT, HL	-
Present report, 2025	59 M	C6, AR	Dysesthesia, paresis	Slightly hyperintensity/ Slightly hypointensity	+, P	DM, UC, OPLL, osteophyte, and disk hernia	+/23Y

Proposed etiologies extend beyond a clear history of major trauma and include minor obstetric brachial plexus injury, childhood traction injuries of the upper limb, or unrecognized minor trauma sustained later in life.^8,9) Chronic mechanical irritation from degenerative spinal changes has also been suggested as a potential contributing factor in selected cases. However, characteristic magnetic resonance imaging (MRI) features, differential diagnostic clues, and predisposing clinical conditions remain insufficiently documented.

Here, we report a rare case of a neuroma arising from the C6 ventral root filaments, which converge to form the C6 ventral root in association with ossification of the posterior longitudinal ligament (OPLL), osteophytes, and disc herniation. The lesion developed more than 2 decades after a remote traffic accident, raising important considerations regarding chronic irritation-related mechanisms and the diagnostic challenges these lesions present.

Case Report

A 59-year-old man presented with a 6-month history of neck pain and numbness in the left upper limb. He had diabetes mellitus for 39 years, ulcerative colitis, and had undergone splenectomy due to a traffic accident 23 years earlier. No head or cervical trauma occurred at that time, although there was prior systemic trauma. He experienced severe dysesthesia and numbness in his neck and left arm for 6 months. Two months prior to presentation, he developed progressive muscle weakness in the left upper limb, prompting MRI evaluation (Figure 1), which revealed a suspected spinal tumor at the cervical C5/6 level. He was referred to our department for surgical treatment. His hemoglobin A1c was 8.8% on admission. Despite preoperative corticosteroid administration, his symptoms showed minimal improvement. Physical examination revealed decreased grip strength in the left hand and significant proximal muscle weakness in the left upper limb, particularly in the deltoid and biceps muscles, making sustained arm elevation difficult. The preoperative Medical Research Council (MRC) grades for his left deltoid, biceps, and brachioradialis were 2, 1, and 2, respectively. He was able to use chopsticks for meals, showed improvement of the prior sensory deficits, and exhibited no posterior column dysfunction. Deep tendon reflexes of his bilateral lower extremities were normal.

Figure 1

Preoperative and postoperative spinal MRI findings.

(a) T1WI demonstrates an intradural extramedullary lesion (solid arrow) at the C5/C6 level showing slightly hyperintensity.

(b) T2WI shows the lesion as slightly hypointense.

(c, f) Gadolinium-enhanced T1WI demonstrates peripheral enhancement around the lesion.

(d) Coronal T2WI DRIVE sequence shows a mildly compressive intradural extramedullary lesion (solid arrow).

(e) Postoperative coronal T2WI demonstrates adequate decompression of the spinal cord following resection, with dotted arrows indicating the residual edges of the partially resected left C6 ventral root filaments.

(g-i) Postoperative MRI shows transient C5-C6 spinal cord compression caused by a localized fluid collection (arrowhead) at 1 week (g), which resolved by 3.5 months (h). No recurrence was observed at 22.2 months (i).

Solid arrow: Intradural extramedullary lesion with slightly T1 hyperintensity, slightly T2 hypointensity, and peripheral enhancement.

Dotted arrow: Residual edges of the partially resected left C6 ventral root filaments on postoperative imaging.

Arrowhead: Postoperative fluid collection causing transient C5-C6 spinal cord compression, resolved on follow-up.

MRI: magnetic resonance imaging; T1WI: T1-weighted imaging; T2WI: T2-weighted imaging

His Japanese Orthopedic Association score for cervical myelopathy (C-JOA)^13,14) was 12/17. Preoperative somatosensory evoked potential (SEP) monitoring showed no delayed latency of peripheral and central conduction time (data not shown).

Image findings

A spinal computed tomography (CT) scan demonstrated OPLL from C4 to C7 (Figure 1). Spinal MRI revealed a nodular lesion at the C5/6 level, appearing slightly hyperintense on T1-weighted imaging (T1WI) and slightly hypointense on T2-weighted imaging (T2WI). Posterior disc protrusion was observed at C4/5 and C5/6. T2-DRIVE imaging showed spinal cord compression caused by the nodular lesion and lateral displacement of the C6 nerve root. On T1-contrast imaging, the lesion demonstrated faint peripheral enhancement, and axial imaging suggested continuity with the ventral dura (Figure 1). Preoperative CT images revealed segmental-type OPLL from C4 to C7. Sagittal cervical CT confirmed K-line-positive OPLL lesions. Axial measurements showed an ossification occupancy rate of 36.4% (4.43 mm/12.18 mm), reflecting moderate canal compromise (Supplementary Figure 1). Differential diagnoses included an intradural extramedullary lesion arising from C6 ventral root filaments, such as meningioma or schwannoma, as well as sequestrated cervical disc herniation.

Intraoperative electrophysiological monitoring

Intraoperative neurophysiological monitoring was performed under total intravenous anesthesia and included transcranial motor evoked potentials (TcMEPs), lower-extremity SEPs, and monopolar direct nerve root stimulation. TcMEPs were elicited using C3/C4 scalp electrodes with a train of 5 pulses (interstimulus interval, 2 ms; intensity 300-600 V) and recorded bilaterally from upper- and lower-extremity muscles. SEPs were obtained by stimulating the posterior tibial nerve with cortical recordings at Cz′-Fpz. Alarm criteria consisted of a persistent ≥50% decrease or loss of TcMEP amplitude and/or a ≥50% decrease in SEP amplitude or ≥10% increase in latency relative to baseline.

For functional assessment of the cervical ventral root filaments, monopolar direct nerve root stimulation was applied using a handheld probe delivering cathodal pulses (0.2 ms duration, 4.1 Hz) at incremental intensities up to 1.0 mA. This technique follows physiological principles used for assessing spinal motor pathway excitability, allowing identification of functioning motor fibers within the stimulated root filaments. A reproducible compound muscle action potential elicited at ≤0.5 to 1.0 mA was interpreted as indicating preserved functional fibers, whereas the absence of a response at 1.0 mA suggested non-functional or severely injured fibers. These criteria guided selective resection while minimizing the risk of postoperative motor deficits.

Surgical findings

A posterior approach was performed via a midline cervical incision (Figure 2). Following laminectomy from the lower half of C4 through the upper half of C7, the dura was opened, revealing an elastic, soft, whitish mass originating from the left C6 ventral root filaments beneath the left C6 dorsal filaments. Upon mobilization of the dorsal root filaments to visualize the ventral aspect, the lesion was well demarcated and independent of the dura, forming a focal fusiform-like enlargement of the C6 ventral root filaments. Intraoperative neurophysiological monitoring, including motor evoked potentials and SEPs, was preserved without elongation of peripheral or central nerve conduction times during resection of the mass lesion. Direct nerve stimulation was also used to differentiate functional motor nerves from non-functional ones, as no reactive motor evoked potential at 1 mA nerve stimulation, allowing selective resection of the lesion while preserving the functional C6 ventral root filament.

Figure 2

Intraoperative findings of the cervical ventral root filament neuroma.

After performing a laminectomy from the lower half of C4 through the upper half of C7, the C5 dorsal root filaments (black dotted arrows) and the C6 dorsal root filaments (black arrows) were exposed.

(a-c) The thick black arrowhead indicates the neuroma, which presents as fusiform-like enlargement involving the C6 ventral root filaments.

Most of the neuroma (c) was removed while preserving the functional C6 ventral root filaments, confirmed through intraoperative neurophysiological monitoring.

(d) The thick black arrowhead indicates the cut edge of the resected neuroma adjacent to preserved C6 ventral root filaments.

Black dotted arrows: C5 dorsal root filaments exposed after laminectomy.

Black arrows: C6 dorsal root filaments.

Thick black arrowhead: Neuroma (a-c) and cut end of the lesion after resection (d).

C6 ventral root filaments: Functionally preserved, verified using intraoperative neurophysiological monitoring.

Histopathological findings

To rule out tumor pathology and demyelinating disease, hematoxylin and eosin (H&E), Klüver-Barrera (KB), silver staining, and immunohistochemical staining for neurofilament and S100 protein were performed.

H&E staining demonstrated disorganized bundles of axons surrounded by Schwann cells within fibrous stroma, showing a mixture of transverse and longitudinal orientations with well-defined boundaries and no cellular atypia (Figure 3).

Figure 3

Histopathological findings.

(a) Hematoxylin-eosin staining (low magnification) shows irregular, crossing bundles of axons circumscribed by Schwann cells.

(b) Klüver-Barrera stain and (c) silver stain highlight the neural fibers.

(d) Immunohistochemistry demonstrates neurofilament-positive axons.

(e) S100 protein expression is strongly positive in Schwann cells at high magnification.

(f, g) MIB-1 (Ki-67) staining at low (f) and high (g) magnification shows a proliferation index of 0%.

The lesion consists of randomly oriented neural fibers without evidence of neoplasia, supporting the diagnosis of a neuroma.

KB and silver stains highlighted both myelinated and non-myelinated fibers, whereas neurofilament immunostaining confirmed axonal components. S100 was strongly positive in Schwann cells. No neoplastic proliferation or demyelinating changes were identified.

These findings are characteristic of a neuroma composed of non-neoplastic but disorganized regenerating nerve fibers. Such morphology is classically described in traumatic neuroma, a category that encompasses neuromas resulting from prior injury as well as those associated with chronic mechanical irritation.

Postoperative course

Postoperatively, the patient showed gradual improvement in left upper extremity strength. Detectable voluntary contraction returned in the deltoid and biceps muscles, with MRC grades improving to 3 in the deltoid, 3 in the biceps, and 5 in the brachioradialis at follow-up. His postoperative C-JOA score was 15.5/17, representing a 3.5-point improvement compared with the preoperative score. He regained the ability to elevate his left upper limb, demonstrated no hand clumsiness, and maintained a stable gait. However, numbness in the left arm remained unchanged, and no improvement was noted in left hand grip strength.

Shortly after surgery, he developed transient numbness and hypoesthesia involving the back, bilateral buttocks, and toes. Given that these symptoms persisted, a postoperative MRI performed at 1 week demonstrated C5-C6 spinal cord compression caused by a localized transient fluid collection adjacent to the operative field (Figure 1g). This finding likely accounted for his temporary symptoms, suggesting transient postoperative myelopathy related to cord manipulation, traction, or edema. The fluid collection resolved by 3.5 months (Figure 1h), paralleling gradual resolution of symptoms. No recurrence was seen on MRI at 22.2 months (Figure 1i).

MRI also confirmed resolution of spinal cord compression and improvement in lateral displacement of the left C6 ventral root filaments (Figure 1e). Partial resection of the proximal portions of the left C6 ventral root filaments was visualized (Figure 1e). Consistent with the imaging findings and postoperative neurological examination, the C6 root contribution to deltoid function was greater than C5 in this patient.

Regarding postoperative cervical alignment, dynamic radiographs demonstrated no evidence of instability and no progression to kyphosis at 33 months after C4-C7 laminectomy (Supplementary Figure 2). Clinically, there were no symptoms suggestive of mechanical neck pain, radiculopathy, or myelopathic deterioration during follow-up. The patient continued rehabilitation under outpatient supervision and showed stable functional improvement.

Discussion

Mechanisms of neuroma formation

Cervical neuromas attributed to trauma or chronic irritation are rare, with only 18 reported cases, including the present one^1-4,7-12) (see Table 1). These lesions have originated from ventral root filaments, dorsal roots, both roots, or even from within the spinal cord parenchyma. A clear history of trauma is not universal; many reported cases coexist with degenerative or compressive pathologies such as osteophytes, disc herniation, OPLL, or canal stenosis. Collectively, these observations support the concept that chronic mechanical irritation may play a central role in neuroma formation.

Experimental and clinical studies^1,15-17) indicate that repeated microinjury to nerve roots-through compression, traction, or friction-induces cycles of Wallerian degeneration followed by disorganized axonal regeneration. In our patient, the combination of OPLL, osteophytes, and disc herniation likely resulted in sustained irritation of the left C6 ventral root filaments, promoting neuroma development over the years. Although the patient's remote trauma history raises the possibility of post-injury regenerative changes, the 23-year interval makes chronic mechanical irritation the more plausible predominant factor.

Importantly, the histopathological pattern fulfilled established criteria for traumatic neuroma, a designation that is rooted in morphological characteristics rather than strict etiological certainty. Thus, while the precise causal contribution of the remote trauma cannot be definitively established, it may have increased susceptibility to subsequent degenerative stress without contradicting the final pathological diagnosis.

Neuromas occurring within the spinal cord have been associated with microvascular injury, diabetes-related Schwann-cell proliferation, or neoplasms.^7,18-21) The patient exhibited no evidence of diabetic neuropathy or intramedullary pathology. Taken together, these findings support a multifactorial mechanism in which chronic degenerative compression served as the principal driver of neuroma formation, with remote trauma functioning as a possible background contributor.

Differential diagnosis

The preoperative diagnosis of neuroma is often difficult because MRI findings are non-specific. Many previously reported cases were initially misdiagnosed as sequestrated disc herniation,^22-25) meningioma,^26,27) or schwannoma.^28,29) In our case, slight peripheral enhancement suggested either a sequestrated disc herniation or a ventral meningioma. However, the intrinsic signal characteristics-T1 hyperintensity and T2 hypointensity-were atypical for both tumors.

Typical schwannomas generally demonstrate iso- to hypointensity on T1-weighted imaging and hyperintensity on T2-weighted imaging, often with variable but pronounced enhancement, as described in large imaging reviews of schwannomatosis and intraosseous schwannomas.³⁰⁾ Likewise, typical meningiomas appear isointense on both T1- and T2-weighted sequences and enhance homogeneously with gadolinium, frequently showing a dural tail sign.³¹⁾ Given that these characteristic MRI patterns were absent in our case, schwannoma and meningioma were considered less likely.

Slight peripheral enhancement maintained the possibility of a sequestrated disc herniation or ventral meningioma; however, intraoperative exploration revealed fusiform enlargement of the C6 ventral root filaments without tumor tissue or disc material. These findings supported the diagnosis of a neuroma rather than a neoplasm. Therefore, chronic irritation-related neuroma should be included in the differential diagnosis of cervical intradural extramedullary lesions when MRI signal characteristics are non-classical and when the lesion is located adjacent to ventral compressive structures such as OPLL, osteophytes, or disc herniation. Intraoperative neurophysiological monitoring assists in identifying functioning nerve root components and facilitates selective resection.

The role of intraoperative electrophysiological monitoring

Direct stimulation techniques used to assess motor pathway integrity-typically employing single or short pulse trains with triggered electromyography-have shown that non-functional or severely degenerated neural tissue often fails to elicit muscle responses even when current is increased up to approximately 1.0 mA,^32-34) whereas reproducible motor responses reliably appear near preserved functional fibers. Based on this physiological principle, regions that remain unresponsive at 1.0 mA are generally considered non-functional and may be resected with a low risk of postoperative motor deficits.

However, whether lesions suspected to represent chronic irritation-related or traumatic neuromas should be resected solely on the basis of intraoperative stimulation response remains controversial. The absence of an elicited response does not necessarily indicate complete loss of neural function, as neuromas may contain heterogeneous components, including viable but electrically silent fibers. Therefore, the extent of resection should be determined individually, integrating clinical presentation, radiological findings, intraoperative anatomical assessment, and electrophysiological data.

In the present case, intraoperative decision-making was performed without pathological confirmation, as the diagnosis was established only on postoperative histological examination. Surgical strategy therefore relied on the patient's progressive motor weakness, the radiological suspicion of ventral root filament involvement, and real-time anatomical and neurophysiological assessments. Given the diagnostic uncertainty, particular care was taken to avoid unnecessary sacrifice of potentially functioning neural elements.

Intraoperative electrophysiological monitoring was thus used as an adjunct rather than an absolute determinant of resection margins. This multimodal approach allowed selective resection of non-functional ventral root filaments while attempting to preserve fibers contributing to upper extremity motor function. Although the precise contribution of the preserved root components to postoperative neurological recovery cannot be fully determined, the patient's clinical improvement supports the role of combining electrophysiological monitoring with careful anatomical judgment to balance symptom relief and preservation of neurological function.

Rationale for selecting a posterior intradural approach

Preoperative imaging could not definitively differentiate between a ventral cervical meningioma and a sequestrated disc herniation. Given that an intradural lesion could not be excluded-based on the peripheral enhancement pattern, the continuity with the dura, and the lesion's anatomical relationship to the ventral root filaments-we selected a posterior intradural approach to achieve both definitive diagnosis and treatment within a single procedure. An anterior approach was considered; however, adequate access to the ventral pathology would have required multilevel anterior decompression and fusion. Given the diagnostic uncertainty, such an invasive anterior procedure posed a substantial risk of unnecessary morbidity if the lesion proved to be nonneoplastic or intradural in nature.

To safely approach the ventral intradural space, we performed expansive laminectomy from the lower half of C4 to the upper half of C7. This multilevel decompression provided sufficient spinal cord mobility and working space, which were essential for controlled spinal cord rotation after sectioning the dentate ligaments. This exposure minimized the need for direct spinal cord retraction and enabled a safe intradural procedure, particularly in the presence of OPLL and other ventral compressive elements.

Posterior fixation was not required because the facet joints were fully preserved, and postoperative imaging confirmed maintenance of cervical alignment without instability. Following surgery, the patient experienced transient bilateral numbness involving the back, buttocks, and toes. This neurological deterioration was attributed to postoperative myelopathy associated with a temporary fluid collection around the manipulated spinal cord. The symptoms improved spontaneously in parallel with the radiographic resolution of the fluid collection, and follow-up MRI showed no hematoma, pseudomeningocele, or compressive cyst (Figure 1h).

Intraoperative neurophysiological monitoring was useful for distinguishing functioning from non-functioning ventral root filaments, allowing selective resection of the abnormal rootlets. Although limited to a single case, this report highlights that spinal neuromas associated with chronic irritation or remote trauma should be considered in the differential diagnosis of intradural mass lesions, especially when they are surrounded by ventral offending structures. Additional accumulation of similar cases is warranted to clarify diagnostic indicators, underlying mechanisms, and contributory factors related to degenerative pathology or long-standing mechanical stress.

Conclusion

We presented a rare case of a cervical neuroma likely related to chronic mechanical irritation from OPLL, osteophytes, and disc herniation, occurring decades after remote trauma. Although the precise etiology remains uncertain, long-standing degenerative compression may have contributed to repeated minor nerve injuries, predisposing the ventral root filaments to neuroma formation. Given that preoperative MRI findings are non-specific, irritation-related neuroma should be considered when an intradural extramedullary lesion displays atypical signal characteristics and is surrounded by ventral compressive structures, even when the traumatic event is remote.

Acknowledgments

We want to thank Editage (www.editage.jp) for their English language editing service of this manuscript.

Author Contributions

Conception and design: Takao Tsurubuchi. Drafting of the article: Kazuki Akutagawa and Takao Tsurubuchi. Analysis and interpretation of the data: Kazuki Akutagawa, Takao Tsurubuchi, Ryutaro Sekimoto, Noriaki Sakamoto, and Daisuke Matsubara. Critically revising the article and supervision: Shunichiro Miki and Eiichi Ishikawa.

Conflicts of Interest Disclosure

All authors have no conflict of interest.

Ethical Approval

This single-patient case report did not require formal review by an ethics committee because it does not constitute human-subject research. All procedures were conducted in accordance with the ethical standards of the Declaration of Helsinki and its later amendments.

Patient Consent

Written informed consent for publication of this case report and all accompanying images was obtained from the patient. All identifying information has been removed to protect patient confidentiality.

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