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. 2024 Feb 24;23:100312. doi: 10.1016/j.wnsx.2024.100312

Spinal calcifying pseudoneoplasms of the neuraxis: A case report and review of the literature

Ajay Chatrath a,#, Mackenzie Lemieux a,#, Rujvee P Patel a, Kaleigh F Roberts b, Sonika Dahiya b, Brenton Pennicooke a,∗
PMCID: PMC10937954  PMID: 38497058

Abstract

Calcifying pseudoneoplasms of the neuraxis (CAPNON) are rare, non-neoplastic, slow-growing tumors that can present anywhere throughout the central nervous system. While the etiology of these lesions remains unknown, the mainstay of treatment is surgical excision. We describe a case of CAPNON at our institution in a 66 year-old female patient who presented with 5 months of pain and burning sensation in her thigh. On MRI, an intradural extramedullary lesion was identified at the level of T11-T12. The mass was surgically excised and the patient reported resolution of her symptoms by her six week follow-up appointment. We reviewed 79 spinal CAPNON cases, covering all cases reported in the literature thus far. In summary, we find that spinal CAPNON are most commonly lumbar and extradural in location, with pain as the most common presenting symptom. Lesions are well-defined and hypointense on T1 and T2 MRI sequence. The majority of cases had favorable surgical outcomes with near complete resolution of pain and associated symptoms.

Keywords: Calcifying pseudoneoplasms of the neuraxis(CAPNON), Surgical excision, Central nervous system, Intradural extramedullary lesion, Pain and sensory symptoms, Pathognomonic imaging findings, Favorable surgical outcomes

Abbreviations

CAPNON

Calcifying pseudoneoplasms of the neuraxis

MRI –

Magnetic Resonance Imaging

CNS –

Central Nervous System

GFAP –

Glial Fibrillary Acidic Protein

S-100 –

Schwannian Marker protein soluble in saturated (100%) ammonium sulfate solution

CKD –

Chronic Kidney Disease

NSAIDs –

Non-Steroidal Anti Inflammatory Drugs

CT –

Computed tomography

CD68 –

Cluster of Differentiation 68

EMA –

Epithelial Membrane Antigen

1. Introduction

Calcifying pseudoneoplasms of the neuraxis (CAPNON), first pathologically described in 1978 by Rhodes and Davis, are rare, benign, calcified lesions that arise within the central nervous system (CNS). With less than 150 total reported cases, the epidemiology and pathogenesis of CAPNON is poorly understood. Given the rarity of these lesions, diagnosing CAPNON is difficult and little research is available to guide treatment decisions. Since CAPNON often mimic other more common CNS lesions on imaging, it is often misdiagnosed as meningioma, metastasis, hematoma, vascular malformations and even more rare occurrences like neurocysticercosis.

Beyond mimicking more common lesions on imaging, spinal CAPNON in particular may not be initially worked up as presenting symptoms caused by spinal CAPNON such as back pain or sciatica are not specific which can delay identification.1,2,3,4,5 Other presentations of spinal CAPNON include radiculopathy, myelopathy, paraparesis, tetraparesis, and gait changes.6,7 Given the non-specific presentations and imaging findings, a better understanding and characterization of CAPNON cases is important to inform medical and surgical decision making.

Despite frequent uncertainty in diagnoses, the majority of spinal CAPNON are treated surgically with favorable outcomes and often total relief of symptoms.5 Definitive diagnosis of CAPNON often occurs after the lesion is resected and analyzed histologically. Common histologic findings associated with CAPNON are calcifications, palisading of histiocytes, multinucleated giant cells, fibrocellular stroma, positive immunohistochemical stain for EMA and Vimentin and negative stain for GFAP and S-100.8, 9, 10, 11,12,13 The granulomatous appearance on histology in addition to the good clinical outcomes, has led to the hypothesis that the pathogenesis of CAPNON is a reactive process as opposed to a neoplastic one.1 However, the exact pathogenesis of CAPNON is unknown.

In this case report, we present a case of spinal CAPNON treated at our institution and review the literature to identify all cases of spinal CAPNON cases that have been published thus far to summarize the diagnosis and management of these cases.

2. Case report

BS was a 66 year old female with a history of hypertension, hypercholesterolemia, malnutrition, CKD, and depression who initially presented to an outside clinic with right anterior thigh pain in the L2-L3 distribution which began 5 months prior to her presentation to the clinic in March 2022. She had previously had pain 8 years ago that lasted 3 months and then resolved spontaneously. Her pain had been managed with NSAIDs and gabapentin. She was neurologically intact on exam. Her primary care physician ordered an MRI of the spine without contrast which demonstrated an intradural extramedullary mass on the right at the level of T11-T12. The patient was then referred to a neurosurgeon at an outside clinic. Upon retrospective review by the neurosurgeon of the patient's prior lumbar MRI performed 2 years ago due to low back pain, the lesion was present on her MRI performed 10 years ago, though the lesion had been slightly smaller at that time. The lesion was also apparent in retrospect on CT of the abdomen and pelvis ordered at the same time as the MRI which demonstrated a partially calcified intradural extramedullary mass on the right from T11-T12. The neurosurgeon at that time believed that the most likely diagnosis was a meningioma given the appearance of the lesion and its slow growth over the past decade. Neurofibroma and schwannoma were considered to be less likely diagnoses. The neurosurgeon discussed expectant management and surgical resection of the mass with the patient and the patient favored expectant management at that time.

Two years later, the neurosurgeon referred the patient to our institution for evaluation for resection of the lesion given the patient's worsening proximal leg pain and burning. The patient remained neurologically intact on our exam. CT of the thoracic spine and MRI of the spine with contrast was performed. CT of the thoracic spine demonstrated a calcified intradural lesion of the right aspect of the spinal cord at the level of T11-T12 that was up to 1.1 cm in length (Fig. 1). MRI of the thoracic spine with contrast demonstrated an intradural extramedullary calcified lesion at T11-T12 with nodular peripheral enhancement and mass effect on the spinal cord with associated dorsal spinal cord edema from T10-T12 (Fig. 2). The neuroradiologist at our institution believed that this finding was most likely consistent with meningioma given the slow growth of the lesion. The differential diagnosis at that time also included calcified vascular malformation or a calcified metastatic lesion. The patient ultimately elected for neurosurgical resection of the lesion following discussions of the risks and benefits of the procedure.

Fig. 1.

Fig. 1

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Sagittal (A) and axial (B) sections of a pre-operative CT scan without contrast of the thoracic spine demonstrating a 1.1 × 0.9 × 1.1 cm calcified intradural lesion at T11-T12.

Fig. 2.

Fig. 2

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Sagittal T1W (A), T2W (B) and axial T11-12 disc space (C) sections from a MRI of the thoracic spine with and without contrast demonstrating an intradural, extramedullary calcified lesion with peripheral nodular enhancement at T11-T12 with mass effect on the spinal cord.

We elected to perform a posterior thoracic laminectomy from T11-T12 with resection of the intradural, extramedullary spinal tumor and placement of a lumbar drain. Intraoperative neural monitoring was used. Following the T11-T12 laminectomy, the tumor was easily visualized. The tumor was attached to the dura and was found to be highly calcified. The tumor was easily dissected from the spinal cord. The frozen specimen sent from the operating room came back as meningioma with extensive calcification. Motor evoked potentials and somatosensory-evoked potentials remained stable throughout the case. Inspection of the surgical site and ultrasound showed that the spinal cord was completely decompressed. In a patient who presented with myelomalacia resulting from a decade-long spinal cord compression, we opted for a 2-level laminectomy instead of a hemilaminectomy. This choice provided superior access for the resection of the pathology without requiring any significant retraction of the spinal cord. Additionally, it facilitated a more thorough spinal cord decompression, minimizing the risk of re-compression in the event of an incomplete resection of the CAPNON.

Postoperatively, the patient was neurologically intact at the time of discharge. Her proximal leg pain had almost entirely resolved. She continued to exhibit resolution of her right proximal anterior thigh pain at her follow-up appointment 6 weeks after the surgery. Final pathology demonstrated chondromyxoid matrix with fibrillary appearance, calcifications and ossification (osseous metaplasia), as well as reactive fibroconnective tissue on hematoxylin and eosin staining, overall most consistent with CAPNON (Fig. 3). Immunohistochemical staining demonstrated that the lesion was negative for progesterone receptor with only rare foci of epithelial membrane antigen (EMA) positivity favored to represent entrapped arachnoid cap cells. S100 was negative in the lesion. CD68 highlighted numerous histiocytes. Follow-up imaging 3 months later demonstrated T11 laminectomy for partial resection of a heterogeneously calcified mass with decreased mass effect on the spinal cord (Fig. 4).

Fig. 3.

Fig. 3

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Hematoxylin and eosin-stained formalin fixed paraffin embedded sections show abundant hypocellular basophilic amorphous to fibrillated material with ghost cells, consistent with the characteristic chondromyxoid fibrillary matrix of CAPNON. There are areas of coarse and amorphous calcifications (A and C) and osseous metaplasia (B and D). There is intervening reactive fibrous stroma with focal areas of palisading epithelioid cells with eccentric nuclei at the periphery of the chondromyxoid matrix (D).

Fig. 4.

Fig. 4

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Sagittal sections from a post-operative CT scan without contrast (A), T2W MRI (B), axial T11-12 sections CT scan without contrast (C) and T2W MRI (D) of the thoracic spine demonstrating T11 laminectomy for partial resection of a heterogeneously calcified mass with decreased mass effect on the spinal cord.

3. Methods

3.1. Statistical analysis

All statistical analyses were performed using GraphPad Prism version 9.0.0 for macOS, GraphPad Prism Software, La Jolla California USA, www.graphpad.com. Fisher's exact test of independence was performed for 2x2 contingency tables and Pearson's Chi-square test was performed for contingency tables with greater than 2 rows. In all of our statistical analyses, we compared expected values based on the null hypothesis to actual values obtained through the literature review. Our expected values are based on the assumption that the number of patients in each group is equal, and thus the null hypothesis is no significant difference between groups. p values of <0.05 were regarded as significant.

4. Discussion

CAPNON is a rare benign calcified lesion first described intracranially in 197814; subsequent reports have also described its spinal manifestation.15 Here, we describe a spinal CAPNON case surgically treated at our institution, adding one more case to the stark CAPNON literature.

Our extensive review of spinal CAPNON cases has found that to date, including our patient case, there have been 80 instances of CAPNON reported in the spine (Table 1). In summarizing these cases, we find that CAPNON can occur across the lifespan, reportedly diagnosed in patients from one to 90 years of age, with the majority (70.1%) occurring over the age of 49. Before a recent surge in spinal CAPNON cases reported in the literature between 2020 and 2022,16,17,18,19 there was a male predominance in CAPNON.6 With the most recent cases included, we find a female predominance in spinal CAPNON, with 55.7% female cases and 44.3% male cases (p = 0.5264).

Table 1.

Clinical, radiological, surgical, pathological, and post-operative information from all cases of spinal CAPNON in the literature.

Author Age (year), Sex Presentation Location, relationship to dura Pre-op diagnosis MRI CT Maximum Dimension (mm) Extent of Resection Adherence to spinal cord Recurrence (months) Follow-up Follow-up Length (months)
Bertoni, 19901 50, M NP FM, e N/A N A 42
Bertoni, 1990 23, M BP T10, e N/A N L
Bertoni, 1990 58, M Pp C2, e N/A N A 112
Bertoni, 1990 12, M NP C6, e N/A N A 39
Bertoni, 1990 32, M BP L4, e N/A N A 84
Bertoni, 1990 33, F BP T9, e N/A N L
Bertoni, 1990 68, F Sc L4, e N/A N S 16
Bertoni, 1990 20, F I C2, e N/A N L
Bertoni, 1990 56, F BP L4, e N/A N L
Smith, 19944 48, M Sc L2, e HOI 8 N/A N
Moser et al 199420 68, M AP C7, e C8 R HRI/HRI/Well-defined HOI/C 10 GTR AD A
Shrier, 19997 59, M SG, ΔS (LUE), Tp FM, e MG HOI/HOI + HRI/E 20 GTR S 24
Qian et al 199921 49, M LUE and LLE –S clivus region 40 GTR I 90
Qian et al 1999 59, M NP, SG, ΔS (LUE) C1-2, ea N/A 46
Chang, 200022 60, M NP C3, io HOI/HOI/E N/A 24
Mayr, 20002 58, M BP, UMN T10, e DH, HTc, MG HOI/HOI/C C 40 STR A 48
Mayr, 2000 63, M -S (LUE), Tp C3, e HOI C N/A AD A 60
Liccardo, 200323 40, M BP, W T8, e HOI/HOI HRI/C 50 GTR I 36
Park, 200824 59, F NP +(LUE), R C7, e CM IOI/IOI/C GTR AD
Apostolopoulos, 200925 53, M BP, HP, P(LLE) L1 MG, NF C 15 GTR AS
Tong, 201026 67, F BP, Cl, W L4, e SOA (CPP) C N/A
Rusleh et al, 201115 43, F BP L3 HOI/HOI/well-defined 5 GTR AS I 10
Ozdemir, 201127 53, M Mp FM, i E/C/Well-defined 20 GTR
Naidu et al 201228 43, M BP, +(LLE) L4, e HTc, MG, NST, TB, IOI to HRI/HRI/C C/Well-defined N/A
Muccio, 20123 57, M BP, Pp T10-11, e HRI/HRI/E/Well-defined HRI/C/Well-defined 24 GTR P 2
Nathoo et al, 201229 44, F BP (L) FMT, HTc, LM, NF, Sc C GTR AP 18
Kwan et al 201230 48, M BP +(LLE) T9 HOI/HOI IOI/C 18 N/A A
Jentoft et al, 201231 26, F BP L1-L2 SW HOI/HOI 8 GTR AS
Bartanusz et al 201332 1.83, F NP C1-2 HOI/HOI/C C 10 STR A 12
Kocovsky et al 201533 64, F BP +(LLE) L5-S1, e HOI/HOI/Well-defined C 38
Reinard et al 201534 44, M BP, P(LLE) L4, e A, CM, DH, HTc, MG, SyC, SD, SW, TB HOI/HOI/E C/well-defined GTR AS A 48
Song, 201535 77, F BP T12, e HOI/HOI C GTR AD I 5
Song, 2015 67, F L3 R (R) L2-3, e C 10.4 GTR
Song, 2015 78, F BP L1, e C/well-defined 8.5 GTR
Lopes et al 201636 72, F BP, CES L2, i HOI/HOI HRI GTR N <1
Garcia Duque et al 20166 51, F BP L2, i, em HOI/HOI C GTR AD I 12
Garcia Duque et al 2016 46, F NP C3, io C GTR 27
Garcia Duque et al 2016 73, M Pp T2, i, em HOI/HOI/well-defined C GTR A 12
Singh, 201637 90, F Wk (LUE) C7-T1, i well-defined N/A AD I 2
Giardinaet al. 201638 68, M R L4-5 SyC HOI to IOI/HOI to IOI C GTR I 60
Wu et al 201739 39, F SP S2, subdural HOI/E/well-defined C GTR N A 36
Lu et al 202018 51, F BP L3-4, epi HOI/HOI + HRI/C 65 N/A
Yang et al 202019 64, F NP (L) C3, epi HOI/HOI C 11.4 N/A 2
Yang et al 2020 60, M CM C7, epi IOI/IOI/C/well-defined 17.3 N/A S 7
Yang et al 2020 64, F BP (L) L5-S1, epi HOI C/well-defined 38 N/A I 6
Ho et al 202016 75, M T11 N/A
Ho et al 2020 52, M T7-T8 N/A
Ho et al 2020 74, F L5-S1 N/A
Ho et al 2020 68, F L4-L5 N/A
Ho et al 2020 49, M L5-S2, i HOI/HOI/Well-defined N/A
Ho et al 2020 43, F T10-T11, e HOI/Well-defined N/A
Ho et al 2020 70, F L4-L5, t HOI N/A
Ho et al 2020 67, F L4-L5, e Well-defined N/A
Ho et al 2020 83, F L4-L5, e HOI/Well-defined N/A
Ho et al 2020 71, F L5-S1, t Well-defined, N/A
Ho et al 2020 50, F L5-S1, e -/HOI N/A
Ho et al 2020 39, F T9-T10, e -/HOI/Well-defined, N/A
Ho et al 2020 65, M L2-L3, e N/A
Ho et al 2020 7, F T2-T3, e HOI/HOI/Well-defined N/A
Ho et al 2020 78, M T9-T10, e HOI/HOI/Well-defined N/A
Ho et al 2020 58, M L2-L3, i -/HOI N/A
Ho et al 2020 77, M C7-T1, e -/HOI N/A
Ho et al 2020 65, M L3-L4, t HOI/HOI N/A
Ho et al 2020 71, F L1-L2, i HOI/HOI N/A
Ho et al 2020 66, M L4-L5 N/A
Ho et al 2020 75, M T8-T9 N/A
Ho et al 2020 82, F L4-L5 N/A
Ho et al 2020 77, F L4-L5 N/A
Ho et al 2020 56, F L4-L5, t N/A
Ho et al 2020 45, F L4-L5, e N/A
Ho et al 2020 43, M T9-T10, e C N/A
Ho et al 2020 52, F C7-T1, e HOI/HOI/C/Well-defined N/A
Ho et al 2020 64, M C6 N/A
Ravi and Srinath, 202140 53, F L4-L5 R L5, i, em IOI/IOI N/A AD A 6
Lu et al 202217 71, F BP, LP (L) L1-2 HOI + HRI/HOI C 46.5 N/A
Lu et al 2022 78, F Wk (LE) T11 HOI/HOI 7.5 N/A
Lu et al 2022 62, F LP (R) L4-L5 HOI/HRI 11 N/A
Lu et al 2022 76, F LP (L), U L3-L4 HOI/HRI 18.7 N/A
Lu et al 2022 77, F (same person as above) BP +(RLE) L3-L4 HOI/HRI 13.9 N/A
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Presentations: AP, arm pain; BP, back pain; Cl, claudication; CES, cauda equina syndrome; CM, cervical myelopathy; HP, hip pain; I, incidental; LE, lower extremity; LP, leg pain; UE, upper extremity pain; Mp, monoparesis; NP, neck pain; P, pain; Pp, paraparesis; R, radiculopathy; Sc, sciatica; SG, shuffling gate; SP, sacrococcygeal pain; Tp, tetraparesis; U, urinary urgency; UMN, upper motor neuron signs; W, difficulty walking; Wk, weakness; ΔS, change in sensation; –S, sensory loss; +, radiating; (L), left; (R), right Location: e, extradural; ea, extraaxial; em, extramedullary; epi, epidural; i, intradural; io, intraosseous; t, transdural Pre-operative diagnosis A, abscess; CM, cancer metastasis; CPP, calcium pyrophosphate; DH, disc herniation; FMT, fibromyxoid tumor; HTc, hematoma calcified; LM, leiomyoma; MG, meningioma; NF, neurofibroma; NST, nerve sheath tumor; SCc, sarcoma calcified; SD, sarcoidosis; SOA, synovial osteochondromatosis and arthropathies; SW, schwannoma; SyC, synovial cyst; TB, tuberculosis infection Imaging AL, anterolateral; C, calcified density; DDD, degenerative disc disease; FM, foramen magnum; E, contrast enhancing; HOI, hypointense; HRI, hyperintense; IOI, isointense Extent of Resection GTR, gross total resection; STR, subtotal resection Adherence to spinal cord AS, adherence to spinal cord; AD, adherence to dura; AP, adherence to periosteum; N, non-adherent Follow-up A, asymptomatic; S, stable; I, improved; P, partially improved Follow-up Length L, lost to follow-up.

Prior reports have shown that the majority of CAPNON are more likely to be extradural than intradural (p = 0.0024). Interestingly, our case is one of the few intradural extramedullary cases described. Only nine of the 80 described cases are intradural, and four, including this current case, report intradural extramedullary tumor location. Further, CAPNON were more likely to be located in the lumbar spine (51.9%) compared to cervical (20.2%) or thoracic (21.5%) (p = 0.0336). We found that CAPNON rarely localize to the most caudal and rostral ends of the spinal cord, with only one case in the sacral region and four cases in the upper clivus/foramen magnum region (Table 1).

Tumor location was related to clinical presentation as the patients suffered from pain or dysfunction in a dermatomal or myotomal distribution associated with their lesion location (Table 1). Instances of reported back pain and neck pain had corresponding spinal CAPNON located within the range of T8 to L5 and between the foramen magnum and C7, respectively. Patients were more likely to report back pain than neck pain or leg pain (p = 0.0123), likely due to spinal CAPNONs most frequently occurring in the lumbar spine. We found that patients were more likely to present with pain as a symptom of CAPNON than other presentations, such as sensory changes, paresis, or radiculopathy (p = 0.0010). While our patient's descriptions of burning sensation and pain were common among patients with CAPNON, her neurological manifestations did not correspond precisely to the tumor location. Interestingly, the pain described by our patient was in the L2-L3 distributions despite the tumor being located at the T11-T12 spinal cord level. Difficulty walking was noted as a predominant symptom in one patient with lumbar CAPNON. A shuffling gate was noted twice with CAPNON located in the upper cervical spine and the foramen magnum, likely reflecting the patient's cervical myelopathy from spinal cord compression.

Imaging reports from X-ray, CT, and MRI led to misdiagnoses of CAPNON, such as disc herniation, meningioma, calcified hematoma, cancer metastasis, or abscess (Table 1). While CAPNON can mimic these other spinal pathologies on imaging, we found that CAPNON does have some pathognomonic imaging findings (Table 1, Supplementary Table 1.). On MRI, CAPNON lesions of the spine were predominantly T1 and T2 hypointense. We found that for T1 weighted sequences, CAPNON lesions were more likely to be hypointense than iso- or hyperintense (p = 0.0001). When looking at T2 weighted sequences, again, lesions were more likely to be hypointense than iso- or hyperintense (p = 0.0003). Imaging reports further suggest that CAPNON are well-defined lesions with widely variable sizes. The average size was 18.68 mm, with a standard deviation of 15.55 mm. The largest spinal CAPNON described in the literature is 65 mm × 56 mm × 56 mm, while the smallest was reported as 5 mm (Table 1).

Surgical resection was the most common treatment of CAPNON, except for one case treated medically with indomethacin. Gross total resection was more likely to be performed than subtotal resection (p = 0.0034). Of the 24 cases describing the extent of resection, only two cases had subtotal resection because the capsule was densely adherent to the dura, as it was in our case. Overall, both patients had good outcomes despite subtotal resection with relief of symptoms at follow-up appointments at 1 and 2 years post-operatively.

Pathological findings were overall consistent across cases. Immunohistochemical staining was not frequently reported, but of the cases with GFAP staining, 2 were positive and 2 were negative. Of cases with S-100 staining, there were 2 positive and 2 negative. Lastly, of cases with EMA staining, there were 3 positive and 2 negative. In our case, we report negative S-100 and rare focal EMA staining, but the field has yet to find one consistent and reliable immunohistochemical marker for CAPNON lesions of the spine.

The literature suggests that the prognosis for CAPNON is very favorable. In our review, only one case22 showed local progression of a pre-existing lesion. This case was unique in that it required 2 operations. First, a total laminectomy with occipitocervical fusion was performed, followed by curettage with an autogenous iliac bone graft one month later. While the patient was symptom-free at 3 months after the second operation, there was evidence of recurrence at the 24-month follow-up. Of cases with information on post-operative imaging and post-operative follow-up of symptoms, the majority showed no evidence of tumor or growth of the residual lesion. Of the 20 cases that reported specifically about recurrence rates, 19 of them (95%) reported no recurrence at follow-up appointments. Of the 25 cases that reported findings at follow-up, 23 (92%) reported complete relief of symptoms or substantial improvement. Of the two cases that reported continued symptom burden, one reported a continued gate disturbance at 24 months with no recurrence,7 and the other reported minimal improvement in symptoms at 2 months with imaging confirming no recurrence.3 Given that no controlled studies exist, it is uncertain whether 2 months is a long enough recovery time to assess symptomatic improvement post-operatively. Previous reports noted improvement as quickly as the day of hospital discharge39 to as long as 9 years postoperatively due to delayed follow-up time.1 Overall, the average follow-up time was ∼30 months. The patient in our case reported symptomatic improvement at the time of discharge, adding to the large number of cases that show quick symptomatic improvement with surgical excision of CAPNON.

5. Conclusions

Although spinal CAPNON are very rare, it is important to synthesize our understanding of the disease and the most optimal treatment approach for patients. Through our comprehensive literature review, we show that majority of spinal CAPNON are located in the lumbar spine, are often extradural, and are well-defined lesions imaging. On T1 and T2 MRI sequence, CAPNON are mostly hypointense. While pain is the most common presenting symptom, symptomatic improvement is the most likely surgical outcome (Fig. 5). We show that overall, patient outcomes are highly favorable with complete or near complete symptomatic relief shortly after surgical resection.

Fig. 5.

Fig. 5

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Graphical depiction of core characteristic of spinal CAPNON determined from extensive literature review.

CRediT authorship contribution statement

Ajay Chatrath: Writing – review & editing, Writing – original draft, Visualization, Validation, Software, Methodology, Investigation, Formal analysis, Data curation, Conceptualization. Mackenzie Lemieux: Writing – review & editing, Writing – original draft, Visualization, Validation, Software, Formal analysis, Data curation, Conceptualization. Rujvee P. Patel: Writing – review & editing, Writing – original draft, Data curation. Kaleigh F. Roberts: Writing – review & editing, Data curation. Sonika Dahiya: Writing – review & editing, Data curation. Brenton Pennicooke: Writing – review & editing, Writing – original draft, Visualization, Validation, Supervision, Software, Resources, Project administration, Methodology, Investigation, Formal analysis, Data curation, Conceptualization.

Declaration of competing interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Footnotes

Appendix A

Supplementary data to this article can be found online at https://doi.org/10.1016/j.wnsx.2024.100312.

Appendix A. Supplementary data

The following is the Supplementary data to this article.

Multimedia component 1
mmc1.docx (66.6KB, docx)

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