The Relationship Between Jugular Foramen Schwannoma and Surrounding Membrane Structures and Its Surgical Application

Abstract

BACKGROUND AND OBJECTIVES:

Surgical resection of jugular foramen (JF) schwannomas with minimal neurological complications is challenging because of their difficult-to-access location and complex relationships with surrounding neurovascular structures, even for experienced neurosurgeons. In this article, we elucidate the membranous anatomy of JF schwannomas, with the aim of reducing iatrogenic injury to the lower cranial nerves (LCNs) during surgery.

METHODS:

The clinical data of 31 consecutive patients with JF schwannomas were reviewed. The relationship between the tumor and the surrounding membranous structures was observed during dissection. Samples were analyzed using Masson's trichrome and immunofluorescence staining to study the membranous characteristics. Histological-radiographic correlations were also summarized.

RESULTS:

In this series, we found that all 3 type B, 2 type C, and 8 type D tumors (according to the Kaye-Pellet grading system) were entirely extradural in location, whereas the 18 type A tumors could be subdural (9 cases) or extradural (9 cases), which frequently could not be predicted preoperatively based on whether the tumor had intraforaminal extension. The dural capsule, when present, could be used as an insulating layer to protect LCNs. With this subcapsular dissection technique, postoperative LCN dysfunction occurred in 10 patients (32.3%), which was usually temporary and mild.

CONCLUSION:

The different relationships between the tumor and membranous structures of the JF is related to the distinct point of tumor origin and the complex anatomy of the meningeal dura within the JF. Subcapsular dissection technique is recommended for better preservation of LCNs when the dural capsule is identified.

ABBREVIATIONS:

JF

Jugular foramen

LCN

lower CN.

Jugular foramen (JF) schwannomas only comprise 2.9% to 4% of intracranial schwannomas and can be cured by complete surgical resection.^1,2 However, radical resection poses a risk of lower cranial nerve (LCN) deficits, with an incidence ranging from 11% to 100% as reported in the literature.^3-9 Although dysphagia will resolve eventually and chronic hoarseness can be treated with thyroplasty or vocal cord injection, the short-term considerable morbidity associated with dysfunctional swallowing can be severe and lead to high treatment costs. The relationship between the JF schwannomas and membranous structures of the JF has been a controversial subject of discussion.^10,11 Clear delineation of the tumor in relation to the surrounding membranous structures is essential for identifying the correct surgical cleavage plane. In this study, we describe the intraoperative findings and histological features of the tumor capsule, clarify the rearrangement of membranous structures on the JF schwannoma during its growth, and present our subcapsular dissection technique for better preservation of LCNs.

METHODS

In this retrospective, single-center case series, we included 31 consecutive patients who underwent microsurgical resection of JF schwannomas at Nanfang hospital between April 2018 and August 2023. Demographic profiles, imaging characteristics, operative findings, perioperative complications, and preoperative and postoperative cranial nerve (CN) outcomes were analyzed. The relationships between the tumor, LCNs, and membranous structures of the JF were carefully evaluated during tumor exposure and dissection. In all cases, tumor samples were collected from the safe area of the intracranial tumor and sent for Masson's trichrome and immunofluorescence staining. This study was conducted in accordance with the Declaration of Helsinki. All clinical data and tumor samples were obtained with the patients' written consent and approved by the Ethics Committees of Nanfang hospital. Comparisons between groups were analyzed by Fischer's exact test using GraphPad Prism 10.0 (GraphPad Software), with statistical significance defined as P < .05. This case series has been reported in line with the Preferred Reporting of Case Series in Surgery guideline.¹²

RESULTS

Patient Characteristics

From April 2018 to August 2023, 31 consecutive patients with JF schwannomas were operated by a single senior neurosurgeon at Nanfang hospital. The mean age of patients was 39.6 years (range, 22-68 years), and the mean tumor size in the maximum dimension was 4.4 cm. The most common initial symptom was hearing loss/tinnitus (58.1%), followed by dizziness (41.9%), headache (29%), and unstable gait (19.4%). Cranial nerve deficits were found on CN VIII in 21 patients (67.7%), CN IX-X in 5 patients (16.1%), CN VII in 3 patients (9.7%), CN XII in 2 patients (6.5%), CN V in 1 patient (3.2%), and CN XI in 1 (3.2%) patient. JF schwannomas were classified into 4 types according to the Kaye-Pellet grading system^5,13: type A in 18 cases, type B in 3 cases, type C in 2 cases, and type D in 8 cases. Additional details of the study population are presented in Tables 1 and 2.

TABLE 1.

Clinical Data of 9 Subdural Jugular Foramen Schwannomas

Case no.	Age (y)	Sex	Tumor size (cm)	Tumor type	Chief complaints	Preoperative cranial nerve deficits	Tumor origin	Tumor removal	Additional therapy	Surgical complications
										≤3 mo	>3 mo
1	68	M	3.1	A	Decreasing hearing, headache	VIII	X	GTR	No	No	No
2	60	M	1.8	A	Dizziness	—	X	GTR	No	No	No
3	30	M	1.9	A	Tinnitus, dizziness	—	IX	GTR	No	No	No
4	27	F	5.0	A	Dizziness, headache	—	X	GTR	No	No	No
5	46	F	4.2	A	Tinnitus, decreasing hearing, dizziness, gait disturbance	VIII	IX	GTR	No	No	No
6	45	F	4.7	A	Decreasing hearing, dizziness	VIII, IX-X	X	GTR	No	Hoarseness, dysphagia	Hoarseness, dysphagia
7	55	F	3.6	A	Tinnitus, decreasing hearing	VIII	IX	GTR	No	No	No
8	50	F	3.5	A	Dizziness, gait disturbance	VIII	X	GTR	No	No	No
9	24	M	7.0	A	Decreasing hearing, headache	VIII	IX	GTR	No	No	No

GTR, gross total resection.

TABLE 2.

Clinical Data of 22 Extradural Jugular Foramen Schwannomas

Case no.	Age (y)	Sex	Tumor size (cm)	Tumor type	Chief complaints	Preoperative cranial nerve deficits	Tumor origin	Tumor removal	Additional therapy	Surgical complications
										≤3 mo	>3 mo
10	37	M	6.3	D	Tinnitus, decreasing \hearing, hoarseness, dysphagia	VIII, IX-X	Unknown	GTR	No	Cerebrospinal fluid leak	No
11	48	M	3.0	A	Hoarseness, dysphagia, gait disturbance	IX-X, XI	XI	GTR	No	Hoarseness, dysphagia	No
12	33	F	3.6	D	Decreasing hearing, dizziness	VIII	Unknown	MSR	Gamma knife + reoperation	No	No
13	35	M	4.7	A	Decreasing hearing, headache, gait disturbance	VIII	IX	GTR	No	No	No
14	47	F	4.0	B	Tinnitus, decreasing hearing, dizziness, headache	VIII	IX	STR	No	No	No
15	46	M	4.5	A	Tinnitus, decreasing hearing, dizziness, gait disturbance	VIII	X	GTR	No	Hoarseness	No
16	29	F	6.1	C	Tongue deviation, headache	V, VII, VIII, XII	Unknown	MSR	Cyber knife	Hoarseness, dysphagia	No
17	22	M	1.6	A	Dizziness, headache	IX-X	Unknown	GTR	No	No	No
18	47	F	4.0	A	Tinnitus, decreasing hearing	VIII	IX	NTR	Gamma knife	No	No
19	40	F	3.9	B	Hemifacial spasm	VII	Unknown	NTR	Gamma knife	No	No
20	38	F	3.0	D	Hemifacial spasm	VII	Unknown	MSR	Gamma knife	Hoarseness, dysphagia	No
21	54	M	9.8	C	Decreasing hearing	VIII	Unknown	MSR	No	No	No
22	37	F	6.8	D	Tongue deviation	VIII, XII	Unknown	MSR	Gamma knife	Hoarseness, dysphagia	No
23	29	F	4.9	D	Tinnitus, decreasing hearing	VIII	Unknown	MSR	Gamma knife	Hoarseness, dysphagia	Hoarseness
24	61	M	5.2	D	Headache	VIII	Unknown	MSR	No	No	No
25	38	F	4.8	D	Decreasing hearing, dizziness	VIII, IX-X	Unknown	MSR	Gamma knife	No	No
26	34	F	3.4	A	Decreasing hearing, dizziness	VIII	Unknown	STR	Gamma knife	No	No
27	24	M	3.9	A	—a	—	Unknown	GTR	No	Dysphagia	No
28	22	M	3.6	A	Tinnitus, decreasing hearing	VIII	IX	NTR	No	No	No
29	36	M	4.4	A	Dizziness, headache	—	Unknown	GTR	No	Hoarseness, dysphagia	Hoarseness, dysphagia
30	31	M	5.7	D	Gait disturbance	—	Unknown	MSR	No	No	No
31	35	F	4.4	B	Tinnitus, decreasing hearing	VIII	Unknown	STR	Gamma knife	Hoarseness	Hoarseness

GTR, gross total resection; MSR, maximally safe resection, including complete resection of the intracranial component and safe maximal removal of the intrapetrous tumor; NTR, near-total resection; STR, subtotal resection.

^aTumor of this patient was accidently found by plain computed tomography scan after a craniocerebral injury.

Surgical Approaches

The retrosigmoid suboccipital approach was performed for all type A and B tumors. To remove the tumor component within the JF in type A cases and tumors within the bone in type B tumors, direct visualization was obtained by drilling the petrous bone lateral to the JF (3 cases) or using angled endoscope (6 cases). A similar approach was used in 9 of the 10 patients with type C or D tumors for conservative resection consisting of complete removal of intracranial tumor and safe maximal removal of intrapetrous tumor. In one patient with a type D tumor, a combined lateral suboccipital retrosigmoid and transmastoid transjugular approach with endoscopic high cervical dissection was applied to pursue the goal of radical resection. The choice was made by patients after being informed of the short-term and long-term benefits and risks of both strategies. Electromyograms of the vagal nerve and facial nerve, auditory brainstem response, and motor and somatosensory evoked potentials were monitored during surgery.

Intraoperative and Pathological Findings Related to the Membranous Structures

When the cerebrospinal fluid was released from the cerebellopontine angle cistern and the cerebellum fell back, LCNs at the inferior pole of the intracranial tumor were first observed (Figure 1). When there were only a few, it could not only predict the possible origin of nerves X-XI but also highlight the possibility of fine nerve rootlets on the surface of the intracranial tumor. The relationship between the tumor and the dura was then inspected and classified into subdural and extradural types based on whether the intracranial tumor was entirely covered by a dural capsule.

FIGURE 1.

Intraoperative images showing the distribution of LCNs. A and B, A large number of LCN rootlets (white arrows) were found on the upper part of the intracranial tumor, and the CN XI was confirmed as the originating nerve. The white asterisk in B, indicates the dural capsule. C, This tumor originated from CN glossopharyngeal nerve, and most of the LCN rootlets (white arrows) gathered at the inferior pole of the tumor. Sides of lesions were labeled as L (left) and R (right). CN, cranial nerve; LCN, lower CN; XI, accessory nerve.

There were 9 subdural tumors in this series. In these cases, the arachnoid enveloped the lateral pole of the tumor, which is a characteristic feature of subdural tumors. In this type of tumor, the location of the LCNs and their relationship with the tumor could be best appreciated at the JF (Figure 2). The debulking and dissection were proceeded as those used in vestibular schwannomas.

FIGURE 2.

Intraoperative images of subdural jugular foramen schwannomas. The intracranial tumors had no dural capsule. The spinal accessory nerve was constantly located at the inferior pole of the tumor, but other lower cranial nerves could be pushed to any direction. A, The IX nerve, X nerve, and cranial roots of XI nerve were located at different directions of the tumor. B, All the IX nerve, X nerve, and cranial roots of XI nerve were found on the posterior surface of the tumor. T, tumor; IX, glossopharyngeal nerve; X, vagus nerve; XI, accessory nerve. Sides of lesions were labeled as L (left) and R (right).

Pathological findings in these 9 cases were consistent with typical schwannomas, with no sign of dural layer on the surface of the tumor (Figure 3).

FIGURE 3.

Photomicrographs of a subdural sample. There was no sign of dura mater on the free surface of the tumor. A, Low-magnification image of MT staining. High-magnification images of B, Masson's trichrome and C and D, immunofluorescence staining of the red-framed area in image A. Tumor was positively stained by S100, whereas nerve fibers were positively stained by neurofilament and myelin basic protein. DAPI, 4',6-diamidino-2-phenylindole; MBP, myelin basic protein; NF, neurofibromatosis.

In the 22 extradural tumors, arachnoid invagination revealing as a fold of arachnoid along the edge of JF could be seen. The capsule thickness varied significantly (Figure 4A and 4B). In tumors did not appear to have a distinct capsule, a crater-like dural invagination along the edge of JF (peripheral part) might be seen, which was not circumferential and served as a reliable indicator for locating the LCNs, especially the X-XI rootlets (Figure 4C-4E). In these tumors, there consistently existed an intact dural capsule enveloping the entire intracranial tumor (dome part), no matter how thick or thin. The posterior part of the capsule was opened at the nerve-free area. After tumor debulking, the surgical cleavage plane was developed between the tumor and the dural capsule. Regardless of the thickness, the dural capsule was continuous with the dura mater of the JF. In some cases, 2 dural layers were found near the intracranial opening of the JF, with the LCN rootlets sandwiched between them (Figure 4F). The inner layer was the inward-bulging dural sheath of the tumor-originating nerve (dome part), whereas the outer layer was the invaginated dura along the edge of the intracranial opening of the JF (peripheral part). The dissection was then returned to the cleavage plane between the inner layer and the tumor to protect the unaffected LCN rootlets. In some cases, extensive adhesion existed between the dural capsule and the LCN fibers. Within the JF, we performed subcapsular dissection and avoided applying excessive pressure to the capsule during dissection to preserve the unaffected LCN fibers within the capsule. If we perceived a high risk of LCN injury, we would cease resection and achieving a maximally safe resection instead.

FIGURE 4.

Intraoperative images of extradural JF schwannomas. The intracranial parts of the tumors were entirely encased by the dural capsule with active angiogenesis. The dural capsule might be A, thin and translucent or B, thick and whitish. White arrowheads in A, indicate the cutting edge of the dural capsule at the intracranial orifice of the JF, whereas black arrows indicate the fold of arachnoid. C-E, Photographs showing the crater-like dural invagination (black asterisk) along the edge of JF. It most commonly appeared at the C, posteroinferior part of the dural capsule and occasionally at the D and E, posterosuperior part. The dural invagination could serve as a reliable indicator for locating the LCNs (white arrows). F, Image showing 2 dural layers (white arrowheads) on the surface of the tumor near the intracranial JF opening, with LCN rootlets (white arrow) between them. X, vagus nerve; XI, accessory nerve. Sides of lesions were labeled as L (left) and R (right). JF, jugular foramen; LCNs, lower cranial nerves.

Tumor samples collected from the intracranial parts of the 22 extradural cases were all covered with a dural capsule formed by curled, cord-like fibers that stained blue on Masson's trichrome staining. The thickness of this dural capsule varied from 50 to 1300 µm (Figure 5A-5D). The integrity of the dural capsule was reconfirmed by histopathological staining of 7 en bloc removed intracranial tumor samples. In 2 of these samples, we found 2 layers of dura near the edge of the specimen, with nerve fibers between them, as observed intraoperatively (Figure 5E-5H).

FIGURE 5.

Photomicrographs of extradural samples. Tumors were covered by dura mater (black arrows). A and C, MT and B and D, IF staining showing a significant difference in thickness of the dural capsule between 2 extradural tumors. E, Low-magnification image of MT staining showing the dural capsule had encased the entire intracranial tumor. High-magnification images of F, MT and G and H, IF staining of the red-framed area in E. There were 2 layers of dura mater (red dotted line indicated the boundary) at the peripheral part of the dural capsule, with nerve fibers (black arrowheads) between them. Nerve fibers were positively stained by NF and MBP, and tumor was positively stained by S100, whereas dura mater was stained negative by all these markers. DAPI, 4',6-diamidino-2-phenylindole; IF, immunofluorescence; MBP, myelin basic protein; MT, Masson's trichrome; NF, neurofilament.

Histological-Radiographical Correlation

As summarized in Tables 1 and 2, without exception, the dural capsule was found on the surface of the intracranial tumor in all type B, C, and D cases in this series. However, the relationship between the tumor and membranous structures varied in type A tumors (Figure 6). When the tumor was confined within the cerebellopontine cistern and did not come into contact with the JF, it was a subdural tumor. This was the case in 4 of the 18 type A tumors. However, when the tumor involved the JF, even just the recess, it could not be predicted preoperatively. In 8 cases, the tumor just filled the recess. Half of these tumors were subdural, and the others were extradural. Interestingly, all the 4 extradural tumors attached to the intracranial orifice of the vagus meatus. Among the remaining 6 tumors with deeper intraforaminal components, there were 5 extradural tumors and 1 subdural tumor; the latter entered the glossopharyngeal meatus.

FIGURE 6.

Variety of membranous characteristics in Kaye-Pellet type A tumors. A, Preoperative contrast-enhanced T1-weighted MRI showed a small round lesion in cerebellopontine cistern without JF involvement, and B, it was demonstrated to be a subdural tumor intraoperatively. C-E. Preoperative thin-sliced T2-weighted MRI revealed that the tumor just filled the recess of vagus meatus (D, white arrowhead) but did not involve the glossopharyngeal meatus (C, red arrowhead). E, Intraoperatively, the tumor has a distinct dural capsule with active angiogenesis. F, Preoperative contrast-enhanced T1-weighted MRI showed that the tumor had deeply extended into the JF, yet G, the intracranial tumor had no dural capsule. JF, jugular foramen.

Surgical Outcomes and Follow-up

The follow-up results of the 31 patients are summarized in Tables 1 and 2. Tumors of the 9 subdural cases were all completely resected. As for the 22 extradural cases, gross total resection was achieved in 7 (31.8%), near-total resection in 3 (13.6%), and subtotal resection in another 3 (13.6%). The remaining 9 patients (40.9%, 2 type C and 7 type D tumors) achieved maximally safe resection, including complete resection of the intracranial component and safe maximal removal of the intrapetrous tumor. Of the 15 cases with residual tumors, 5 were monitored through regular enhanced MRI examinations because of the small remnant size and good patient compliance. For patients with larger tumor remnants or those who had difficulty in returning to the hospital because of the lockdown restrictions during the COVID-19 pandemic, stereotactic radiosurgery was arranged as soon as possible. Gamma Knife was applied in 9 cases, whereas Cyber Knife was conducted for the remaining 1 patient, in whom the inferior pole of the extracranial tumor was beyond the capabilities of Gamma Knife.

The most common postoperative complication was LCN dysfunction, which occurred in 10 cases (32.3%). There was a nonstatistically significantly higher incidence of postoperative LCN dysfunction in extradural tumors than subdural tumors (40.9% vs 11.1%, P = .2055). Newly developed LCN deficits were found in 9 patients (29%), including 2 with hoarseness, 1 with dysphagia, and the remaining 6 exhibiting both symptoms. In one patient (3.2%), pre-existing hoarseness and dysphagia were temporarily exacerbated postoperatively. For the 8 patients with postoperative dysphagia, nasogastric tubes were inserted to provide enteral nutrition and prevent aspiration until oral feeding was feasible. The tubes were removed within 2 weeks for half of the patients, whereas the remainder required nasogastric feeding for 2 to 4 weeks. None of the patients required tracheostomy after surgery. By the time of the last follow-up, only 4 patients had surgical-related mild hoarseness; 2 of them also complained of occasional difficulty in swallowing solid foods. One patient (the patient with a type D tumor who underwent radical resection) had suffered from postoperative cerebrospinal fluid leak, which ceased after 3 weeks of lumbar drainage. No intracranial infection occurred in any case. There was no operative mortality.

During a mean follow-up of 19.9 months (range, 3.9-54.5 months), tumor recurrence occurred in only one patient (17 months after the first surgery, 12 months after Gamma-Knife therapy). Reoperation of this patient had achieved gross total resection by using a combined lateral suboccipital retrosigmoid and transmastoid transjugular approach with high cervical dissection. The patient experienced severe hoarseness and dysphagia after the second surgery. A tracheostomy tube was placed for approximately 3 months until LCN function had recovered to a satisfactory level. At the last follow-up visit, the patient only presented with mild hoarseness.

DISCUSSION

The anatomy of the JF has been well described by various authors.^14-19 Briefly, within the glossopharyngeal meatus of the JF, CN IX runs from a medial and horizontal trajectory to a lateral and vertical one, with the genu being the superior ganglion. By contrast, CN X-XI run obliquely without sharp turns. The meningeal (inner) layer of the dura mater evaginates to form the sheath enveloping the LCN (epineurium).^20,21 Distal to the end of the tubular or funnel-shaped meningeal dural sheath, the subarachnoid space disappears, and bundles of nerve fibers are enclosed and separated from others by fibrous tissue within the dural sheath (perineurium).^22,23 For the convenience of the following discussion, the intraforaminal segment of the LCN is divided into a proximal and distal part by the genu of the IX nerve and the transition area from the tubular dural sheath to the multichanneled peripheral sheath of the X-XI nerves.

Although schwannomas commonly arise from Schwann cells around the ganglion, they can also arise from the cisternal segment of LCNs because some of them are found to be completely in the subarachnoid space without JF extension (Figure 6A and 6B).

The growth pattern of JF schwannomas arising from the intraforaminal segment of LCNs is complicated and affected by several factors, including but not limited to the path of least resistance, the relationship between the origin site and the sharp turn of the IX nerve, and the guidance by the dural sheath.

When the tumor originates from the proximal intraforaminal segment of LCNs (Figure 7, origin points 1 and 2), it may grow into the subdural space under the guidance of the dural sheath. Under these circumstances, the principle of least resistance prevails, and the tumor only has a minor part within the JF.

FIGURE 7.

Schematic drawings showing different growth patterns of JF schwannomas depending on their exact origin in relationship to the membranous structures of the JF. Tumor originating from the proximal intraforaminal segment of LCNs (origin points 1 and 2) may grow into the subdural space under the guidance of the dural sheath. On the contrary, tumor arising from the distal intraforaminal segment (origin points 3, 4, and 5) would develop into extradural tumor eventually. When the tumor originates from the distal intraforaminal segment of the IX nerve (origin point 3), the dural sheath is expanded and folds on the horizontal segment as the tumor extends intracranially. If the tumor origin locates deeply inside the JF (origin points 3 and 5), the dura at the edge of the intracranial opening of the JF may be expanded subsequently and becomes the peripheral part of the dural capsule as the tumor extends intracranially. In this scenario, the remaining rootlets of the LCN are sandwiched between the peripheral and dome parts of the dural capsule. IX, glossopharyngeal nerve; X, vagus nerve; XI, accessory nerve. The copyright of Figure 7 belongs to Xi'an Zhang. JF, jugular foramen; LCNs, lower cranial nerves.

When the tumor arises from the distal part (vertical segment) of the intraforaminal segment of the IX nerve (Figure 7, origin point 3), it cannot simply extend along the dural sheath because of the presence of the genu. Instead, it expands its dural sheath and folds on the horizontal segment.

JF schwannomas arising from the distal part of the intraforaminal segment of X-XI (Figure 7, origin point 4 and 5) are extradural in origin. As the tumor grows intracranially, the epineurium and perineurium enveloping the origin nerve, as well as the meningeal dura covering the transition area of the recess of the vagus meatus, cover the tumor circumferentially to form the dural capsule.

When the tumor originates deep inside the JF (Figure 7, origin point 3 and 5) and extends intracranially, the dura at the edge of the intracranial opening of the JF (including both meningeal and periosteal layers) is subsequently expanded and becomes the peripheral part of the dural capsule. In this case, the remaining rootlets of the LCN are sandwiched between the peripheral and dome parts of the dural capsule. The tumor may also be confined within the petrous bone or extend extracranially.

Theoretically, if a JF schwannoma originates from the genu of the intraforaminal segment of the IX nerve, it might grow bidirectionally, developing an intracranial subdural and an extracranial extradural component. This was proposed as type D (epi-subdural) tumor by Sutiono et al.¹⁰ However, they did not perform histological examination of the surgical specimens. No such cases were found in the present series. In our opinion, this type may be rare, if not impossible.

In the preoperative evaluation, the relationship between the tumor and dura can be predicted in the majority of cases and is problematic only in Kaye-Pellet type A tumors with JF extension, as described previously. Fortunately, this does not change much of the preoperative decision-making regarding surgical approaches. High-resolution T2 imaging such as thin-cut constructive interference steady state/ fast imaging employing steady state acquisition might help identify membranous characteristics of the tumor preoperatively.

Intraoperatively, we emphasize the early identification of unaffected LCNs and assess the relationship between the tumor and dura before intracranial tumor debulking and dissection to evaluate the possible origin of the tumor and the relationship with LCNs. Subcapsular dissection was performed if the tumor was located extradurally. The dural capsule was used as an insulating layer to protect the LCN rootlets sandwiched between the peripheral and dome parts of the dural capsule, particularly at or near the inferior pole of the intracranial tumor. When the JF is filled by the tumor, the dural sheath encasing the LCN rootlets expands to form the tumor capsule. The intraforaminal course of LCNs is not predictable enough to facilitate preserving them during tumor resection. Therefore, the subcapsular removal of intraforaminal tumors and preservation of the tumor capsule as much as possible are crucial. The postoperative LCN deficits seem to be related to intraforaminal tumor size rather than the surgical approach because manipulation of the thinner capsule increases the risk of damaging the nerve fibers within the capsule.

Limitations

Because of the rarity of JF schwannomas, this study was limited by the small sample size, and the conclusions we drew need to be further verified. Multi-institutional studies with larger patient samples could further confirm our findings on this rare disease.

CONCLUSION

In this study, JF schwannomas in Kaye-Pellet types B, C, and D were completely extradural in location, whereas type A tumors could be either subdural or extradural. The different relationships between the tumor and membranous structures of JF may be a result of the distinct sites of tumor origin. When present, the dural capsule can be used as an insulating layer to protect LCNs. Our findings can help any neurosurgeon operating on this challenging tumor, no matter whether he/she is an experienced hand.

Funding

This research was supported by the Natural Science Foundation of Guangdong Province, China (Grant no. 2023A1515011775); by the Science and Technology Program of Guangzhou, China (Grant no. 201903010048); by the President Foundation of Nanfang Hospital, Southern Medical University (Grant no. 2022A012); and by the National Natural Science Foundation of China (Grant No. 82303932).

Disclosures

The authors have no personal, financial, or institutional interest in any of the drugs, materials, or devices described in this article.