Meningiomas of the lateral skull base: Neurotologic manifestations and patterns of recurrence JOHN P. LEONETTI, MO, O. HOWARD REICHMAN, MO, PETER G. SMITH, MO, PhD, ROBERT L. GRUBB, MO, and PETER KAISER, MO, Maywood. Illinois
Theeradication of basicranial meningiomas by traditional surgical techniques is often hindered by neoplastic entanglement with critical neurovascular structures. Apparent, complete tumor resection Is frequently followed by extensive, yet clinically silent, reo current disease with local infiltration of bone, cranial nerves, and brain. Fifty·five cases of sphenoid wing or parasellar meningioma were analyzed to Identify clinical manifestations suggestive of early tumor recurrence. Regrowth patterns were then defined according to preoperative radiographic and intraoperative surgical findings. Medial tumor regrowth, Involving the cavernous sinus, caused neurapraxla of cranial nerves III, IV, or VI, with associated diplopia or ophthalmoplegia. Inferior (caudal) regrowth of disease Involved the infratemporal fossa, pterygomaxlllary space, or paranasal sinuses by bony erosion of the middle cranial fossa floor or through natural anatomic foramina and fissures. Such Inferior extension was manifested clinically by facial hypesthesia, trismus, and referred otalgia caused by trigeminal nerve involvement and by autophony or serous otitis media related to eustachian tube obstruction. Posterior tumor regrowth occurred along the petrous bone and horizontal carotid canal, resulting In Internal aUditory meatus erosion and cerebellopontine angle extension with associated tinnitus, hearing loss, unsteadiness, and occasional facial twitching. While the clinical and radiographic evaluations of any patient with a suspected recurrent basicranial meningioma are critical In planning the method and magnitude of reoperatlon, an understanding of potential recurrence patterns can be used In devising more extensive, combined approaches that may allow complete tumor extirpation at the initial surgical Intervention. (OTOlARYNGOL HEAD NECK SURG 1990;103:972,)
Meningiomas account for approximately 14% of all primary intracranial neoplasms.' While tumor histology, location, and degree of neurovascular invasion have been correlated with overall patient survival, the most significant factor related to long-term treatment
From the Departments of Otolaryngology-Head and Neck Surgery al Loyola University Medical Center (Drs. Leonetti and Kaiser) and at Washington University Medical Center (Dr. Smith). and the Departments of Neurological Surgery at Loyola University Medical Center (Dr. Reichman) and at Washington University Medical Center (Dr. Grubb). Presented at the Annual Meeting of the American Academy of Otolaryngology-Head and Neck Surgery, New Orleans. La., Sept. 24-28. 1989. Received for publication Sept. 23. 1989; revision received Feb. 20. 1990 ~ accepted Feb. 26, 1990. Reprint requests: John P. Leonelli. MD, Department of Otolaryngology-Head and Neck Surgery, Loyla University of Chicago. 2160 South First Ave.. Maywood. II.. 60153. 2311120491
success remains the ability to accomplish complete tumor extirpation. 2-5 The presence of transcranial tumor extension, often associated with meningiomas of the sphenoid ridge. may account for the unusually high incidence of recurrence for surgically treated lesions in this particular region." A clinicoradiographic study with intraoperative correlation was therefore performed in an effort to identify tumor recurrence patterns that might be used in the surgical planning for both advanced primary and extensive recurrent meningiomas of the sphenoid ridge.
CLINICAL METHODS AND MATERIALS Included in this series were 127 patients with the diagnosis of sphenoid ridge meningioma, who were seen at Loyola University Medical Center (LUMC) or Washington University Medical Center between July 1983 and July 1988. Sixty-four patients with newly diagnosed tumors were eliminated from the study, as were 8 additional patients with recurrent tumors that
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AGE AND SEX DISTRIBUTION (N = 55) 20
r-----------------~-.--.-.------.---------
15 N U M
B
10
E R
5
o
-_._---_ ......~---
o - 19
20 - 39
40 - 59
60 - 79
AGE
Fig. 1
_
Male (16)
_
Female (39)
Fig. 1. Age and sex distribution of 55 patients with recurrent sphenoid ridge meningiomas.
were managed with radiotherapy (5) or radiologic observation (3). The hospital charts, radiologic reports, and operative records of the remaining 55 patients with recurrent s.phenoid ridge meningiomas treated by surgical resec~Ion were retrospectively reviewed. Preoperative clinical manifestations and radiographic analysis were correlated with intraoperative findings in order to define patterns of tumor regrowth.
RESULTS Patient data. Patient age and sex distribution are shawn in Fig. 1. Roughly 90% (50 of 55) of the patients were Over the age of 40 years. There were 39 women and 16 men, a sex ratio of 4.1: I. All underwent at least one earlier surgical procedure at another institution (41 patients) or at one of the study centers (14 patients). Six patients had undergone more than one previous operation. Tumor resection at the most recent procedure, as determined by the operating s~rgeon, was complete in 39 cases, subtotal in II patients, and not stated in five instances. Postoperative radiotherapy was used in three patients with subtotal tumor removal, two cases in which tumor resection was determined to be complete, and in one patient with an unspecified degree of tumor removal. . The length of time for tumor recurrence or progresSIon of residual disease is demonstrated in Fig. 2. The
majority of patients manifested regrowth of disease 4 to 6 years after initial surgical resection. Presenting symptoms. Facial hypesthesia and headache were the most common presenting symptoms, in addition to various otologic and ophthalmologic manifestations. Asymptomatic tumor recurrence developed in roughly one third (18 of 55) of the cases. Other presenting symptoms are shown in Table I. Presenting signs. Absent or abnormal facial sensation, the most common presenting sign, occurred in the distribution of VI in eight patients, V 2 in four patients, VI in one patient, and in a combination of sensory distributions in 14 cases. Unilateral ophthalmoplegia occurred in three patients, while isolated trochlear or abducens paresis was noted in two and three patients, respectively. Four patients had a combined IV-VI neuropathy, and seven patients demonstrated unilateral proptosis. Middle ear effusion with associated conductive hearing loss' was identified in nine patients, while two individuals manifested new-onset sensorineural hearing loss. Progressive hemifacial spasm occurred in one patient and an isolated blepharospasm was seen in one individual. Six patients presented with a bony (4) or soft tissue (2) temporal mass. Approximately 42% (23 of 55) of the patients had no new physical findings associated with recurrent disease, as summarized in Table 2.
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LENGTH OF TIME FOR TUMOR RECURRENCE OR PROGRESSION (N • 55) 25
20 N U M
15
E
10
B
R
5
0 c
2
2-4
4-6
6-8
)8
YEARS
Fig. 2
Fig. 2. Time for tumor recurrence or progression in 55 cases of recurrent sphenoid ridge meningiomas.
RADIOGRAPHIC ANALYSIS IN 55 PATIENTS WITH RECURRENT MENINGIOMA
CT (55)
MRI (48)
Table 1. Presenting symptoms In 55 patients with recurrent sphenoid ridge meningiomas Symptom
No.
Facial hypesthesia Headache Diplopia Blurred vision Hearing loss Otalgia Seizures Trismus Tinnitus Unsteadiness None
21 16 12 11 11 8
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7 5
5 3 18
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FIg. 4. Contrast-enhanced computed tomographic view of a recurrent spheno id ridge meningioma with A. cavernous sinus (cuNed onow) Infratemporal and B. paranasal sinus extension. Note the hyperostotic sphenoid ridge (straight a"ow).
Fig. S. Magnetic resonance imaging view of a recurrent sphenoid ridge meningioma with A. cavernous sinus and B, infratemporal extension.
~agnetic resonance imaging outlined: cavernous si~us Invasion (10 cases), encroachment of cranial nerves II and VIII (2 cases), infratemporal fossa extension (5 cases), orbital and paranasal sinus involvement (4 c(aF~es), and multidirectional tumor regrowth in 22 cases Ig.5).
Angiography helped identify displacement or narrowing of the internal carotid (7 cases) or middle cerebral (6 cases) arteries (Fig . 6) . Petrous carotid artery involvement, noted in nine patients, was best determined by using a combination of all three radiographic techniques .
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Fig . 6. Recurrent sphenoid ridge mening ioma with internal carotid artery compression demonstrated by cervicocerebral angiography in the A, frontal and B, sagitta l views. The arrow in panel B po ints to the petrous carotid artery.
Table 2. Presenting signs In 55 patlents with recurrent sphenoid ridge meningiomas Signa
Cranial neuropathy III, IV, VI
V VII VIII Middle ear effusion Papilledema Proptosis Mass None
No.
12
27 2 2 9 7 7 6
23
Surgical approach and operative findings. Twenty-six patients with recurrent tumors that were clinicoradiographically localized to the sphenoid ridge or cavernous sinus underwent a direct pterional approach, while an equal number of patients with transcranial recurrent disease were approached through a combined subtemporal-infraternporal technique." Orbital exenteration was required , with and without maxiIlectomy, in two and one cases , respectively.
Medial tumor regrowth resulted in lateral wall displacement (4 cases) or direct invasion (9 cases) of the cavernous sinus. Petrous bone erosion , noted in II patients, resulted in bony dehiscence of the carotid canal (8 cases) , cerebellopontine angle extension (3 cases) , and internal auditory canal erosion (l case). Such posterior regrowth occurred along the roof or medial face of the petrous pyramid or both. Inferior or caudal spread of tumor occurred through the foramen ovale or rotundum in nine patients, whereas infratemporal fossa extension via middle cranial fossa floor erosion was identified in 17 cases . Orbital or paranasal sinus tumor was found in six patients. Of the 55 patients reviewed , 16 were determined to have unidirectional (medial, posterior, or inferior) tumor recurrence and 30 were noted to have a multidirectional pattern of recurrence. Insufficient data were available in the operative reports of the remaining nine cases to comment on the extent or direction of recurrent disease . Tumor resection was considered complete in 33 patients, subtotal in 14 cases, and undocumented in eight instances. Postoperative radiotherapy was used in nine of the 14 patients with subtotal tumor removal.
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with cavernous sinusInVOlVement. Fig. 7. Medial recurren ce pattern of sphenoi d ridge mening iomas
.C ompllc atlons. Two deaths in the early postope ratl~e period resulted from major cerebral infarctions, WhIle transient or persistent hemiparesis occurre d in six and two patients, respectively. Postoperative extradural (~) or intradural hemorrhage (I) required emergent surgical re-exploration . Additional untoward sequelae are noted in Table 3. .Results. Patient followup ranged from I to 6 years, With a mean of 3.7 years. Twenty-nine of 33 patients (88%) who underwent comple te tumor resection are .h aliv Wit out disease, whereas tumor recurrence has . e SInce developed in two patients in this group. Twelve of the 14 patients who underwent subtotal resection are alive . Four of these patients have evidence of slow tumor progression, while eight patients have radiographically stable disease . Of the nine patients in this group. Who received postoperative radiotherapy, seven are ahve with stable disease , one patient has tumor progression, and one individual has died from an un~elated cause. The overall pat ient status is summarized In Table 4.
DISCUSSION
Mening iomas of the sphenoid ridge, which account for approximately 20% of all intracranial mening iomas, have a notoriously high local recurrence rate of 38% to 60%.4.6.9 Several authors have conclud ed that the risk of tumor regrowth is directly related to the completeness of surgical resection .t -" 10. I I Almost 50% (63 of 127) of the patients with sphenoid ridge meningiomas seen at the two study centers in this review had recurrent disease . Tumor involve ment of adjacent neurova scular structures may result in associated clinical manifestations as early evidence of mening ioma recurrence . Medial tumor regrow th, for exampl e, may involve the caverno us sinus and related cranial nerves III, IV, and Vp2 (Fig. 7) . Nine of the 12 patients in this series who manifes ted diplopia were noted to have direct cavernous sinus invasion. Optic nerve or tract involve ment was seen in 11 patients with more advanc ed medial tumor extension . Posterio r regrowth of sphenoid ridge meningiomas
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J J
Fig. 8. Posterior recurrence pattern of spheno id ridge meningiomas along the petrous bone.
Table 3. Perioperatlve complications In 55 patients with recurrent sphenoid ridge meningiomas Compllcallon
No.
Death Neurologic def icit Transient hemiparesis Persistent hemipa resis Dysphas ia Seizures CSF leak Wound infection Flap necrosis Hemorrhage Pneumocephalus
2
6 2 2
4
3 2 2 2 1
occurs along the petrou s bone, where it forms the middle cranial fossa floor " (Fig . 8). Clinical evidence suggestive of posterior tumor extension included the . trigeminal nerve findings of facial hypesthesia and trismus in 2 I and 5 patients, respectively. Cerebellopontinc
angle or internal auditory canal involvement by recurrent tumor resulted in unsteadiness, tinnitus, or sensorineural hearing loss in six patients and facial twitching in two instances . The most advanced recurrent tumors were found in patients with inferior (caudal) transcranial regrowth through the foramina ovale or rotundum and the infraorbital fissure (Fig. 9) . Infratemporal tumor extension commonly resulted in facial hype sthesia, trismu s. and referred otalgia, as well as middle ear effu sion secondary to eustachian tube obstruction . Five patients in this group had direct tumor invasion of the pterygoid musculature , and six patients had a bony or soft tissue mass in the temporal fossa . While many patients had clinical manifestations suggestive of tumor recurrence, almost one third (18 of 55) of the patients were asymptomatic at the time of diagnosis. Contrast-enhanced computed tomography, performed in the axial and coronal planes. can identify cavernous sinus tumor extension, middle cranial fossa floor erosion, and areas of neoplastic hyperostosis."
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Fig. 9. Inferior recurrence pattern of sphenoid ridge meningiomas with infratemporal or poranasal sinus extension.
~ble 4. Patient status In 55 cases of recurrent sphenoid ridge meningiomas
-
Tumor resection Complete (33) SUbtotal (14) Unspecified (8)
Alive without disease
Alive WIth disease
Dead of disease
Dead of other cause
29
o
2 12
o
2
4
1
1* 1*
2
1
*Perioperali ve deaths (see Tab le 3).
Magnetic resonance imaging with gadolinium enhancement also provides accurate assessment of tumor invasion of the cavernous sinus , brain, cranial nerve bundles, and soft tissue compartments in the infratemporal fossa. IS Tumor mapping with HRCT and MRI can be augmented with cervicocerebral carotid angiographic d?monstration of neoplasm-vessel relationships , vessel dIstortion, and isolated feeding vessels for possible preoperative embolization. A meticulous review of clinical manifestations and r~diographic findings should provide an accurate mapPing of tumor extent, which is mandatory for optimum sur~ical planning . Recurrent meningiomas that are 10cahzed to the sphenoid ridge or cavernous sinus may be completely resected through a direct pterional ap7 proach . Of the 26 patients in this series who underwent
this procedure, c1inicoradiographic analysis failed to demonstrate cavernous sinus involvement in only one patient and infraorbital extension in two cases. Additional surgical exposure was easily obtained, without added morbidity, in all three cases. Transcranial tumor recurrence , present in 29 patients in this series, requires a more extensive combined approach to achieve complete tumor extirpation ." Two patients in this category had infratemporal disease not determined radiographically that required additional surgical exposure through a subtemporal-infratemporal approach after initial pterional dissection . One additional patient in this group , believed to have infratemporal tumor extension radiographically, was found to have localized sphenoid ridge disease and atrophic temporalis muscle lining the middle cranial fossa floor that
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was misinterpreted as tumor recurrence on computed tomography. While a discussion of the roles for radiotherapy, 16 stereotactic radiosurgery, 17 or radiologic observation in the management of recurrent sphenoid ridge meningiomas is beyond the scope of this review, we believe an understanding of the clinicoradiographic features associated with this difficult problem will assist in the treatment planning, regardless of the modality used.
SUMMARY Recurrent meningiomas may cause a myriad of neurotologic signs or symptoms related to the direction and degree of tumor regrowth. The full extent of disease in these patients, and those with asymptomatic recurrence, can best be ascertained by combined radiologic analysis using CT, MRI, and arteriography. Tumor regrowth may occur medially to involve the cavernous sinus, posteriorly along the petrous ridge, or inferiorly to invade the infratemporal fossa. The method and magnitude of re-operation should be based upon clinicoradiographic analysis and a knowledge of potential tumor recurrence patterns. We would like to thank Ms. Jackie Burns for preparing this manuscript and Ms. Sue Cottrill for designing the detailed illustrations used in this work. REFERENCES
I. Russell DS. Rubinstein LJ. Pathology of tumors of the nervous system. 4th ed. London: Edward Arnold. 1977:66-91. 2. Simpson D. The recurrence of intracranial meningiomas after surgical treatment. Neurol Neurosurg Psychiatry 1957:20:22-39.
3. Yamashita J. Handa H. Iwaki K. Recurrence of intracranial meningiomas with special reference to radiotherapy. Surg Neurol 191\0: 14:33-40. 4. Mirimanoff RO. Dosoretz DE. Linggood RM. Ojemann RG. Martuza RL. Meningioma: analysis of recurrence and progression following neurosurgical resection. J Ncurosurg 1985:62:\824. 5. Crompton MR. Gautier-Smith PC. The prediction of recurrence in meningiomas. J Ncurol Neurosurg Psychiatry 1970;33:80-7. 6. Adegbitc AB. Khan MI. Paine DW, Tan LK. The recurrence of intracranial meningiomas after surgical treatment. J Neurosurg 1983:58:51-6. 7. Dolenc V. Microsurgical removal of large sphenoidal bone meningiomas. Acta Neurochirurgica 1979:21\:391-6. 8. Sekhar LN. Schramm VL. Jones NF. A subtemporal and preauricular infratcmoral fossa approach to large lateral and posterior cranial base neoplasms. J Neurosurg 1987;67:488-99. 9. Raaf J. Parsons WR. Intracranial meningiomas. Arch Surg 1971:102:380-4. 10. Melamed S. Sahar A. Beller AJ. The recurrence of intracranial meningiomas. Neurochivurgia (Stuttg) 1979:22:47-51. II. Skullerud K. Loken AC. The prognosis in meningiomas. Acta Neuropathol 1974;29:337-44. 12. Umansky F. Nathan H. The lateral wall of the cavernous with special reference to the nerves related to it. J Neurosurg 1982:56:228-34. 13. Bonnal J. Thibaut A. Brotchi J. Invading meningiomas of the sphenoid ridge. J Neurosurg 1980:53:51\7-99. 14. Kline LB. Acker JD. Post MJ. Computed tomographicevaluation of the cavernous sinus. Ophthalmology 1982;89:374-85. 15. Levine PA. Paling MR. Black WC. Cantrell RW. MRI vs. high resolution CT scanning: evaluation of the anterior skull base. OTOLARYNGOL HEAD NECK SURG 1987;96:260-7. 16. Carella RJ. Ransohoff J. Newall J. Role of radiation therapy in the management of meningioma. Neurosurg 1982:10:332-9. 17. Lunsford DL. Flickinger J. Lindner G. Maitz A. Stereotactic radiosurgery of the brain using the first United States 201 Cobalt60 source gamma knife. Neurosurg 1989;24:151-9.
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Theeradication of basicranial meningiomas by traditional surgical techniques is often hindered by neoplastic entanglement with critical neurovascular structures. Apparent, complete tumor resection Is frequently followed by extensive, yet clinically silent, reo current disease with local infiltration of bone, cranial nerves, and brain. Fifty·five cases of sphenoid wing or parasellar meningioma were analyzed to Identify clinical manifestations suggestive of early tumor recurrence. Regrowth patterns were then defined according to preoperative radiographic and intraoperative surgical findings. Medial tumor regrowth, Involving the cavernous sinus, caused neurapraxla of cranial nerves III, IV, or VI, with associated diplopia or ophthalmoplegia. Inferior (caudal) regrowth of disease Involved the infratemporal fossa, pterygomaxlllary space, or paranasal sinuses by bony erosion of the middle cranial fossa floor or through natural anatomic foramina and fissures. Such Inferior extension was manifested clinically by facial hypesthesia, trismus, and referred otalgia caused by trigeminal nerve involvement and by autophony or serous otitis media related to eustachian tube obstruction. Posterior tumor regrowth occurred along the petrous bone and horizontal carotid canal, resulting In Internal aUditory meatus erosion and cerebellopontine angle extension with associated tinnitus, hearing loss, unsteadiness, and occasional facial twitching. While the clinical and radiographic evaluations of any patient with a suspected recurrent basicranial meningioma are critical In planning the method and magnitude of reoperatlon, an understanding of potential recurrence patterns can be used In devising more extensive, combined approaches that may allow complete tumor extirpation at the initial surgical Intervention. (OTOlARYNGOL HEAD NECK SURG 1990;103:972,)
Meningiomas account for approximately 14% of all primary intracranial neoplasms.' While tumor histology, location, and degree of neurovascular invasion have been correlated with overall patient survival, the most significant factor related to long-term treatment
From the Departments of Otolaryngology-Head and Neck Surgery al Loyola University Medical Center (Drs. Leonetti and Kaiser) and at Washington University Medical Center (Dr. Smith). and the Departments of Neurological Surgery at Loyola University Medical Center (Dr. Reichman) and at Washington University Medical Center (Dr. Grubb). Presented at the Annual Meeting of the American Academy of Otolaryngology-Head and Neck Surgery, New Orleans. La., Sept. 24-28. 1989. Received for publication Sept. 23. 1989; revision received Feb. 20. 1990 ~ accepted Feb. 26, 1990. Reprint requests: John P. Leonelli. MD, Department of Otolaryngology-Head and Neck Surgery, Loyla University of Chicago. 2160 South First Ave.. Maywood. II.. 60153. 2311120491
success remains the ability to accomplish complete tumor extirpation. 2-5 The presence of transcranial tumor extension, often associated with meningiomas of the sphenoid ridge. may account for the unusually high incidence of recurrence for surgically treated lesions in this particular region." A clinicoradiographic study with intraoperative correlation was therefore performed in an effort to identify tumor recurrence patterns that might be used in the surgical planning for both advanced primary and extensive recurrent meningiomas of the sphenoid ridge.
CLINICAL METHODS AND MATERIALS Included in this series were 127 patients with the diagnosis of sphenoid ridge meningioma, who were seen at Loyola University Medical Center (LUMC) or Washington University Medical Center between July 1983 and July 1988. Sixty-four patients with newly diagnosed tumors were eliminated from the study, as were 8 additional patients with recurrent tumors that
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AGE AND SEX DISTRIBUTION (N = 55) 20
r-----------------~-.--.-.------.---------
15 N U M
B
10
E R
5
o
-_._---_ ......~---
o - 19
20 - 39
40 - 59
60 - 79
AGE
Fig. 1
_
Male (16)
_
Female (39)
Fig. 1. Age and sex distribution of 55 patients with recurrent sphenoid ridge meningiomas.
were managed with radiotherapy (5) or radiologic observation (3). The hospital charts, radiologic reports, and operative records of the remaining 55 patients with recurrent s.phenoid ridge meningiomas treated by surgical resec~Ion were retrospectively reviewed. Preoperative clinical manifestations and radiographic analysis were correlated with intraoperative findings in order to define patterns of tumor regrowth.
RESULTS Patient data. Patient age and sex distribution are shawn in Fig. 1. Roughly 90% (50 of 55) of the patients were Over the age of 40 years. There were 39 women and 16 men, a sex ratio of 4.1: I. All underwent at least one earlier surgical procedure at another institution (41 patients) or at one of the study centers (14 patients). Six patients had undergone more than one previous operation. Tumor resection at the most recent procedure, as determined by the operating s~rgeon, was complete in 39 cases, subtotal in II patients, and not stated in five instances. Postoperative radiotherapy was used in three patients with subtotal tumor removal, two cases in which tumor resection was determined to be complete, and in one patient with an unspecified degree of tumor removal. . The length of time for tumor recurrence or progresSIon of residual disease is demonstrated in Fig. 2. The
majority of patients manifested regrowth of disease 4 to 6 years after initial surgical resection. Presenting symptoms. Facial hypesthesia and headache were the most common presenting symptoms, in addition to various otologic and ophthalmologic manifestations. Asymptomatic tumor recurrence developed in roughly one third (18 of 55) of the cases. Other presenting symptoms are shown in Table I. Presenting signs. Absent or abnormal facial sensation, the most common presenting sign, occurred in the distribution of VI in eight patients, V 2 in four patients, VI in one patient, and in a combination of sensory distributions in 14 cases. Unilateral ophthalmoplegia occurred in three patients, while isolated trochlear or abducens paresis was noted in two and three patients, respectively. Four patients had a combined IV-VI neuropathy, and seven patients demonstrated unilateral proptosis. Middle ear effusion with associated conductive hearing loss' was identified in nine patients, while two individuals manifested new-onset sensorineural hearing loss. Progressive hemifacial spasm occurred in one patient and an isolated blepharospasm was seen in one individual. Six patients presented with a bony (4) or soft tissue (2) temporal mass. Approximately 42% (23 of 55) of the patients had no new physical findings associated with recurrent disease, as summarized in Table 2.
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LENGTH OF TIME FOR TUMOR RECURRENCE OR PROGRESSION (N • 55) 25
20 N U M
15
E
10
B
R
5
0 c
2
2-4
4-6
6-8
)8
YEARS
Fig. 2
Fig. 2. Time for tumor recurrence or progression in 55 cases of recurrent sphenoid ridge meningiomas.
RADIOGRAPHIC ANALYSIS IN 55 PATIENTS WITH RECURRENT MENINGIOMA
CT (55)
MRI (48)
Table 1. Presenting symptoms In 55 patients with recurrent sphenoid ridge meningiomas Symptom
No.
Facial hypesthesia Headache Diplopia Blurred vision Hearing loss Otalgia Seizures Trismus Tinnitus Unsteadiness None
21 16 12 11 11 8
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7 5
5 3 18
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FIg. 4. Contrast-enhanced computed tomographic view of a recurrent spheno id ridge meningioma with A. cavernous sinus (cuNed onow) Infratemporal and B. paranasal sinus extension. Note the hyperostotic sphenoid ridge (straight a"ow).
Fig. S. Magnetic resonance imaging view of a recurrent sphenoid ridge meningioma with A. cavernous sinus and B, infratemporal extension.
~agnetic resonance imaging outlined: cavernous si~us Invasion (10 cases), encroachment of cranial nerves II and VIII (2 cases), infratemporal fossa extension (5 cases), orbital and paranasal sinus involvement (4 c(aF~es), and multidirectional tumor regrowth in 22 cases Ig.5).
Angiography helped identify displacement or narrowing of the internal carotid (7 cases) or middle cerebral (6 cases) arteries (Fig . 6) . Petrous carotid artery involvement, noted in nine patients, was best determined by using a combination of all three radiographic techniques .
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Fig . 6. Recurrent sphenoid ridge mening ioma with internal carotid artery compression demonstrated by cervicocerebral angiography in the A, frontal and B, sagitta l views. The arrow in panel B po ints to the petrous carotid artery.
Table 2. Presenting signs In 55 patlents with recurrent sphenoid ridge meningiomas Signa
Cranial neuropathy III, IV, VI
V VII VIII Middle ear effusion Papilledema Proptosis Mass None
No.
12
27 2 2 9 7 7 6
23
Surgical approach and operative findings. Twenty-six patients with recurrent tumors that were clinicoradiographically localized to the sphenoid ridge or cavernous sinus underwent a direct pterional approach, while an equal number of patients with transcranial recurrent disease were approached through a combined subtemporal-infraternporal technique." Orbital exenteration was required , with and without maxiIlectomy, in two and one cases , respectively.
Medial tumor regrowth resulted in lateral wall displacement (4 cases) or direct invasion (9 cases) of the cavernous sinus. Petrous bone erosion , noted in II patients, resulted in bony dehiscence of the carotid canal (8 cases) , cerebellopontine angle extension (3 cases) , and internal auditory canal erosion (l case). Such posterior regrowth occurred along the roof or medial face of the petrous pyramid or both. Inferior or caudal spread of tumor occurred through the foramen ovale or rotundum in nine patients, whereas infratemporal fossa extension via middle cranial fossa floor erosion was identified in 17 cases . Orbital or paranasal sinus tumor was found in six patients. Of the 55 patients reviewed , 16 were determined to have unidirectional (medial, posterior, or inferior) tumor recurrence and 30 were noted to have a multidirectional pattern of recurrence. Insufficient data were available in the operative reports of the remaining nine cases to comment on the extent or direction of recurrent disease . Tumor resection was considered complete in 33 patients, subtotal in 14 cases, and undocumented in eight instances. Postoperative radiotherapy was used in nine of the 14 patients with subtotal tumor removal.
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with cavernous sinusInVOlVement. Fig. 7. Medial recurren ce pattern of sphenoi d ridge mening iomas
.C ompllc atlons. Two deaths in the early postope ratl~e period resulted from major cerebral infarctions, WhIle transient or persistent hemiparesis occurre d in six and two patients, respectively. Postoperative extradural (~) or intradural hemorrhage (I) required emergent surgical re-exploration . Additional untoward sequelae are noted in Table 3. .Results. Patient followup ranged from I to 6 years, With a mean of 3.7 years. Twenty-nine of 33 patients (88%) who underwent comple te tumor resection are .h aliv Wit out disease, whereas tumor recurrence has . e SInce developed in two patients in this group. Twelve of the 14 patients who underwent subtotal resection are alive . Four of these patients have evidence of slow tumor progression, while eight patients have radiographically stable disease . Of the nine patients in this group. Who received postoperative radiotherapy, seven are ahve with stable disease , one patient has tumor progression, and one individual has died from an un~elated cause. The overall pat ient status is summarized In Table 4.
DISCUSSION
Mening iomas of the sphenoid ridge, which account for approximately 20% of all intracranial mening iomas, have a notoriously high local recurrence rate of 38% to 60%.4.6.9 Several authors have conclud ed that the risk of tumor regrowth is directly related to the completeness of surgical resection .t -" 10. I I Almost 50% (63 of 127) of the patients with sphenoid ridge meningiomas seen at the two study centers in this review had recurrent disease . Tumor involve ment of adjacent neurova scular structures may result in associated clinical manifestations as early evidence of mening ioma recurrence . Medial tumor regrow th, for exampl e, may involve the caverno us sinus and related cranial nerves III, IV, and Vp2 (Fig. 7) . Nine of the 12 patients in this series who manifes ted diplopia were noted to have direct cavernous sinus invasion. Optic nerve or tract involve ment was seen in 11 patients with more advanc ed medial tumor extension . Posterio r regrowth of sphenoid ridge meningiomas
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Fig. 8. Posterior recurrence pattern of spheno id ridge meningiomas along the petrous bone.
Table 3. Perioperatlve complications In 55 patients with recurrent sphenoid ridge meningiomas Compllcallon
No.
Death Neurologic def icit Transient hemiparesis Persistent hemipa resis Dysphas ia Seizures CSF leak Wound infection Flap necrosis Hemorrhage Pneumocephalus
2
6 2 2
4
3 2 2 2 1
occurs along the petrou s bone, where it forms the middle cranial fossa floor " (Fig . 8). Clinical evidence suggestive of posterior tumor extension included the . trigeminal nerve findings of facial hypesthesia and trismus in 2 I and 5 patients, respectively. Cerebellopontinc
angle or internal auditory canal involvement by recurrent tumor resulted in unsteadiness, tinnitus, or sensorineural hearing loss in six patients and facial twitching in two instances . The most advanced recurrent tumors were found in patients with inferior (caudal) transcranial regrowth through the foramina ovale or rotundum and the infraorbital fissure (Fig. 9) . Infratemporal tumor extension commonly resulted in facial hype sthesia, trismu s. and referred otalgia, as well as middle ear effu sion secondary to eustachian tube obstruction . Five patients in this group had direct tumor invasion of the pterygoid musculature , and six patients had a bony or soft tissue mass in the temporal fossa . While many patients had clinical manifestations suggestive of tumor recurrence, almost one third (18 of 55) of the patients were asymptomatic at the time of diagnosis. Contrast-enhanced computed tomography, performed in the axial and coronal planes. can identify cavernous sinus tumor extension, middle cranial fossa floor erosion, and areas of neoplastic hyperostosis."
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Fig. 9. Inferior recurrence pattern of sphenoid ridge meningiomas with infratemporal or poranasal sinus extension.
~ble 4. Patient status In 55 cases of recurrent sphenoid ridge meningiomas
-
Tumor resection Complete (33) SUbtotal (14) Unspecified (8)
Alive without disease
Alive WIth disease
Dead of disease
Dead of other cause
29
o
2 12
o
2
4
1
1* 1*
2
1
*Perioperali ve deaths (see Tab le 3).
Magnetic resonance imaging with gadolinium enhancement also provides accurate assessment of tumor invasion of the cavernous sinus , brain, cranial nerve bundles, and soft tissue compartments in the infratemporal fossa. IS Tumor mapping with HRCT and MRI can be augmented with cervicocerebral carotid angiographic d?monstration of neoplasm-vessel relationships , vessel dIstortion, and isolated feeding vessels for possible preoperative embolization. A meticulous review of clinical manifestations and r~diographic findings should provide an accurate mapPing of tumor extent, which is mandatory for optimum sur~ical planning . Recurrent meningiomas that are 10cahzed to the sphenoid ridge or cavernous sinus may be completely resected through a direct pterional ap7 proach . Of the 26 patients in this series who underwent
this procedure, c1inicoradiographic analysis failed to demonstrate cavernous sinus involvement in only one patient and infraorbital extension in two cases. Additional surgical exposure was easily obtained, without added morbidity, in all three cases. Transcranial tumor recurrence , present in 29 patients in this series, requires a more extensive combined approach to achieve complete tumor extirpation ." Two patients in this category had infratemporal disease not determined radiographically that required additional surgical exposure through a subtemporal-infratemporal approach after initial pterional dissection . One additional patient in this group , believed to have infratemporal tumor extension radiographically, was found to have localized sphenoid ridge disease and atrophic temporalis muscle lining the middle cranial fossa floor that
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was misinterpreted as tumor recurrence on computed tomography. While a discussion of the roles for radiotherapy, 16 stereotactic radiosurgery, 17 or radiologic observation in the management of recurrent sphenoid ridge meningiomas is beyond the scope of this review, we believe an understanding of the clinicoradiographic features associated with this difficult problem will assist in the treatment planning, regardless of the modality used.
SUMMARY Recurrent meningiomas may cause a myriad of neurotologic signs or symptoms related to the direction and degree of tumor regrowth. The full extent of disease in these patients, and those with asymptomatic recurrence, can best be ascertained by combined radiologic analysis using CT, MRI, and arteriography. Tumor regrowth may occur medially to involve the cavernous sinus, posteriorly along the petrous ridge, or inferiorly to invade the infratemporal fossa. The method and magnitude of re-operation should be based upon clinicoradiographic analysis and a knowledge of potential tumor recurrence patterns. We would like to thank Ms. Jackie Burns for preparing this manuscript and Ms. Sue Cottrill for designing the detailed illustrations used in this work. REFERENCES
I. Russell DS. Rubinstein LJ. Pathology of tumors of the nervous system. 4th ed. London: Edward Arnold. 1977:66-91. 2. Simpson D. The recurrence of intracranial meningiomas after surgical treatment. Neurol Neurosurg Psychiatry 1957:20:22-39.
3. Yamashita J. Handa H. Iwaki K. Recurrence of intracranial meningiomas with special reference to radiotherapy. Surg Neurol 191\0: 14:33-40. 4. Mirimanoff RO. Dosoretz DE. Linggood RM. Ojemann RG. Martuza RL. Meningioma: analysis of recurrence and progression following neurosurgical resection. J Ncurosurg 1985:62:\824. 5. Crompton MR. Gautier-Smith PC. The prediction of recurrence in meningiomas. J Ncurol Neurosurg Psychiatry 1970;33:80-7. 6. Adegbitc AB. Khan MI. Paine DW, Tan LK. The recurrence of intracranial meningiomas after surgical treatment. J Neurosurg 1983:58:51-6. 7. Dolenc V. Microsurgical removal of large sphenoidal bone meningiomas. Acta Neurochirurgica 1979:21\:391-6. 8. Sekhar LN. Schramm VL. Jones NF. A subtemporal and preauricular infratcmoral fossa approach to large lateral and posterior cranial base neoplasms. J Neurosurg 1987;67:488-99. 9. Raaf J. Parsons WR. Intracranial meningiomas. Arch Surg 1971:102:380-4. 10. Melamed S. Sahar A. Beller AJ. The recurrence of intracranial meningiomas. Neurochivurgia (Stuttg) 1979:22:47-51. II. Skullerud K. Loken AC. The prognosis in meningiomas. Acta Neuropathol 1974;29:337-44. 12. Umansky F. Nathan H. The lateral wall of the cavernous with special reference to the nerves related to it. J Neurosurg 1982:56:228-34. 13. Bonnal J. Thibaut A. Brotchi J. Invading meningiomas of the sphenoid ridge. J Neurosurg 1980:53:51\7-99. 14. Kline LB. Acker JD. Post MJ. Computed tomographicevaluation of the cavernous sinus. Ophthalmology 1982;89:374-85. 15. Levine PA. Paling MR. Black WC. Cantrell RW. MRI vs. high resolution CT scanning: evaluation of the anterior skull base. OTOLARYNGOL HEAD NECK SURG 1987;96:260-7. 16. Carella RJ. Ransohoff J. Newall J. Role of radiation therapy in the management of meningioma. Neurosurg 1982:10:332-9. 17. Lunsford DL. Flickinger J. Lindner G. Maitz A. Stereotactic radiosurgery of the brain using the first United States 201 Cobalt60 source gamma knife. Neurosurg 1989;24:151-9.
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