This article summarizes tumor control and functional outcomes of stereotactic radiosurgery (SRS) for patients with nonvestibular schwannomas, in comparison with those treated with microsurgical resection. To date, surgical resection has been a common treatment for nonvestibular schwannomas. Because these tumors are generally benign, complete tumor resection is a desirable curative treatment. However, it is almost infeasible to completely remove these tumors without any complications, even for experienced neurosurgeons, because of adherence to surrounding critical structures such as cranial nerves, brainstem, or vessels. SRS provides a good tumor control rate with much less morbidity than microsurgical resection.
Key points
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Stereotactic radiosurgery is one of the reasonable treatment options for patients with small to medium-sized nonvestibular schwannomas without a severe compression of the brainstem.
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Because of tumor origin and surrounding critical structures, it is extremely difficult to completely remove nonvestibular schwannomas without any complications.
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Stereotactic radiosurgery provides a good tumor control for nonvestibular schwannomas.
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Morbidity after stereotactic radiosurgery is much less than that after microsurgery for patients with nonvestibular schwannomas, particularly with facial or jugular foramen schwannomas.
Introduction
Intracranial schwannomas are generally benign tumors that arise from Schwann cells of the nerve sheath. Most of them originate from eighth cranial nerve, so-called vestibular schwannoma. Nonvestibular schwannomas are rare, accounting for less than 10% of intracranial schwannomas, and less than 0.5% of all intracranial neoplasms. Complete tumor resection is the desirable curable approach for these benign tumors. However, it is not always feasible to achieve complete resection without any complications, even for experienced neurosurgeon using recent microsurgical techniques as well as neuromonitoring, because of the tumor origin and surrounding critical structures such as cranial nerves, vessels, and brainstem. Also, the rarity of nonvestibular schwannomas would be one of the reasons why complete resection without worsening of neurologic function is extremely difficult. Accordingly, a relatively high rate of morbidity after surgical resection remains a current major issue despite the potential of “cure.” Because nonvestibular schwannomas are histologically benign, it must be borne in mind that the goal of the management for patients harboring nonvestibular schwannomas is not to achieve complete resection with some neurologic deficits, but to obtain a good tumor control with preservation of neurologic function for their life span. During the last several decades, stereotactic radiosurgery (SRS) has emerged as a minimally invasive alternative to surgical resection. This article addresses the safety and efficacy of SRS for nonvestibular schwannomas.
Introduction
Intracranial schwannomas are generally benign tumors that arise from Schwann cells of the nerve sheath. Most of them originate from eighth cranial nerve, so-called vestibular schwannoma. Nonvestibular schwannomas are rare, accounting for less than 10% of intracranial schwannomas, and less than 0.5% of all intracranial neoplasms. Complete tumor resection is the desirable curable approach for these benign tumors. However, it is not always feasible to achieve complete resection without any complications, even for experienced neurosurgeon using recent microsurgical techniques as well as neuromonitoring, because of the tumor origin and surrounding critical structures such as cranial nerves, vessels, and brainstem. Also, the rarity of nonvestibular schwannomas would be one of the reasons why complete resection without worsening of neurologic function is extremely difficult. Accordingly, a relatively high rate of morbidity after surgical resection remains a current major issue despite the potential of “cure.” Because nonvestibular schwannomas are histologically benign, it must be borne in mind that the goal of the management for patients harboring nonvestibular schwannomas is not to achieve complete resection with some neurologic deficits, but to obtain a good tumor control with preservation of neurologic function for their life span. During the last several decades, stereotactic radiosurgery (SRS) has emerged as a minimally invasive alternative to surgical resection. This article addresses the safety and efficacy of SRS for nonvestibular schwannomas.
Therapeutic options
Treatment options include the wait-and-see approach with serial images, microsurgery, and SRS. If patients have asymptomatic tumors, a wait-and-see approach with serial images may be a reasonable treatment option, particularly in older patients or those with comorbidities, because nonvestibular schwannomas are generally slow-growing tumors. At present, there is little information about long-term natural history of nonvestibular schwannomas because of their rarity. If considering that any intervention after tumor growth may increase the risk of complications, earlier intervention is advisable to reduce complications. Microsurgery was a common treatment before the advent of SRS. Complete resection is an ideal treatment, but is not so easily achievable without any complications. Although recently skull-base surgery has contributed to an increased rate of complete resection, there is no doubt that this is one of the most invasive treatments. SRS is a less invasive treatment option for small to medium-sized nonvestibular schwannomas, with good tumor control as well as a lower complication rate.
Clinical outcomes
Contemporary series of radiosurgery for nonvestibular schwannomas are shown in Table 1 .
| No. of Patients | Methods | CN (No. of Lesions) | Tumor Volume [Range] (cm 3 ) | Marginal Dose [Range] (Gy) | Follow-Up (mo) | Tumor Control Rate (%) | Improvement of Clinical Symptoms/Signs (%) | New or Worsening Symptoms (%), No. of Patients |
|---|---|---|---|---|---|---|---|---|
| 56 | GK | V | 8.7 (mean) [0.8–33] | 13.3 (mean) [10–15] | 68 (mean) | 93 (crude) | 39 (70%) | 9 (16%) |
| Facial numbness, 5 | ||||||||
| Masseter muscle atrophy, 4 | ||||||||
| 37 | GK | V | 10.3 (mean) [1.2–40.4] | 14.2 (mean) [11–16] | 54 (mean) | 84 (5, 10-y) | 14 (40%) | 5 (14%) |
| Facial numbness, 3 | ||||||||
| Facial pain, 3 | ||||||||
| Corneal ulcer, 1 | ||||||||
| Abducens palsy, 1 | ||||||||
| 33 | GK | V | 4.2 (median) [0.5–18.0] | 15 (median) [12–20] | 72 (mean) | 82 (5,10-y) | 11 (33%) | 3 (9%) |
| Facial sensory loss, 1 | ||||||||
| Facial pain, 1, Unknown, 1 | ||||||||
| 74 | GK | V | 5.3 (mean) [0.4–19.9] | 16.4 (mean) [12–30] | 48.2 (mean) | 93 (5-y) | 8 (11%) | 7 (9%) |
| 79 (10-y) | Diplopia, 1 | |||||||
| Permanent facial paresthesia, 3 | ||||||||
| Permanent facial numbness, 2 | ||||||||
| Transient facial numbness, 1 | ||||||||
| 14 | GK | VII | 5.5 (mean) [1.0–20.8] | 12.9 (mean) [11–16] | 31.4 (mean) | 100 (crude) | 5 (42%) | 1 (7%) |
| Facial palsy, 1 | ||||||||
| 11 | GK | VII | 0.9 (mean) [0.05–2.3] | 13 (mean) [10–16] | 39 (mean) | 91 (crude) | 3 (38%) a | None |
| 34 | GK | JF | 4.2 (median) [0.6–10.4] | 14 (median) [12–18] | 84 (median) | 97 (5-y) | (20%) b | 1 (3%) |
| 94 (10-y) | NA | |||||||
| 17 | GK | JF | 5.9 (mean) [1.1–12.3] | 13 (mean) [10–16] | 64 (mean) | 100 (crude) | 6 (35%) | 1 (6%) |
| Transient hoarseness, 1 | ||||||||
| 49 | Linac | III (2) | 4.8 (median) [0.35–15.1] | 12.5 (median) [10–15] | 37 (median) | 83 (5-y) | 11 (26%) | 5 (12%) |
| V (25) | Facial numbness, 2 | |||||||
| VII (2) | Mild anesthesia dolorosa, 1 | |||||||
| XII (1) | Facial palsy, 1 | |||||||
| JF (18) | Transient diplopia, 1 | |||||||
| RS (1) | ||||||||
| 40 | CK (single- and multisession) | IV (1) | 3.2 (median) [0.1–23.7] | 18 (median) [15–33] | 29 (median) | 96 (3-y) | 5 (14%) | 2 (5%) |
| V (18) | Jaw weakness and facial numbness, 1 | |||||||
| VII (6) | 17.5 (1 fraction) | |||||||
| X (5) | 20 (2 fractions) | Facial weakness and tinnitus, 1 | ||||||
| XII (2) | 18 (3 fractions) | |||||||
| JF (8) | ||||||||
| CS (2) | ||||||||
| 36 | GK | III (1) | 2.9 (median) [0.07–8.8] | 13.5 (median) [9.3–20] | 37 (median) | 91 (2-y) | 21 (64%) | 4 (12%) |
| IV (1) | 78 (5-y) | Facial paresthesia, 2 | ||||||
| V (25) | Lower and upper extremity tremors, paresthesia, slurred speech, tongue deviation and | |||||||
| VI (2) | ||||||||
| VII (6) | ||||||||
| IX (1) | Drooling, 1 | |||||||
| XII (3) | Died, 1 | |||||||
| JF (2) | ||||||||
a 3 of 8 patients who had facial palsy before treatment.
b 22 of 105 ipsilateral motor cranial nerves including IX,X,XI and XII.
Trigeminal Schwannomas
At the author’s institution, 37 trigeminal schwannoma patients treated with gamma-knife radiosurgery (GKRS) were evaluated. Of these patients, 23 (38%) had solid tumors and 14 (62%) had tumors with a cystic component. Seventeen tumors (46%) were located predominantly in the middle fossa, 12 (32%) were located predominantly in the posterior fossa, and 8 (22%) were dumbbell-shaped lesions involving the middle and posterior fossa. Twenty patients (54%) underwent GKRS as an initial treatment. Mean tumor volume was 10 cm 3 and mean marginal dose was 14 Gy. During the mean follow-up period of 54 months (range 12–140 months), 4 patients (11%) achieved complete remission, 20 (54%) had partial remission, 8 (22%) had stable tumors, and 5 (14%) developed tumor progression or uncontrollable facial pain requiring surgical resection. With a Kaplan-Meier method, actuarial progression-free survival was 84% at both 5 and 10 years. Excluding 2 cases whereby only partial treatment was given because of large tumor volume, these rates increased to 91%. A typical case of trigeminal schwannoma is shown in Fig. 1 . Of 35 patients who had neurologic symptoms before GKRS, 14 (40%) exhibited some degree of improvement in their symptoms, including reduced facial numbness in 12 patients, resolved facial pain in 6, and resolved diplopia in 4. On the other hand, 5 patients (14%) had newly developed or worsened preexisting symptoms, including facial numbness in 3, facial pain in 3, corneal ulcer in 1, and abducens palsy in 1. Among these patients, 4 developed neurologic deterioration caused by tumor progression while 1 patient developed facial numbness despite tumor regression, thought to be due to adverse radiation effects. Similarly, Kano and colleagues reported the results of GKRS in 33 patients with trigeminal schwannomas. The median radiosurgery target volume was 4.2 cm 3 and the median marginal dose was 15 Gy. At a mean follow-up period of 6 years (range 7–148 months), actuarial progression-free survival was 82% at both 5 and 10 years. Eleven of 33 patients (33%) achieved improved symptoms or signs, and 3 (9%) developed neurologic deterioration.
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