Clinoidal meningiomas

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✓ Anterior clinoidal meningiomas are frequently grouped with suprasellar or sphenoid ridge meningiomas, masking their notorious association with a high mortality and morbidity rate, failure of total removal, and recurrence. To avoid injury to encased cerebral vessels, most surgeons are content with subtotal removal. Without total removal, however, recurrence is expected. Recent advances in cranial-base exposure and cavernous sinus surgery have facilitated radical total removal.

The author reports 24 cases operated on with vigorous attempts at total removal of the tumor with involved dura and bone. This experience has distinguished three groups (I, II, and III) which influence surgical difficulties, the success of total removal, and outcome. These subgroups relate to the presence of interfacing arachnoid membranes between the tumor and cerebral vessels. The presence or absence of arachnoid membranes depends on the origin of the tumor and its relation to the naked segment of carotid artery lying outside the carotid cistern. Total removal was impossible in the three patients in Group I, with postoperative death occurring in one patient and hemiplegia in another. Total removal was achieved in 18 of the 19 patients in Group II, with one death from pulmonary embolism. In the two patients in Group III, total removal without complications was easily achieved.

Abstract

✓ Anterior clinoidal meningiomas are frequently grouped with suprasellar or sphenoid ridge meningiomas, masking their notorious association with a high mortality and morbidity rate, failure of total removal, and recurrence. To avoid injury to encased cerebral vessels, most surgeons are content with subtotal removal. Without total removal, however, recurrence is expected. Recent advances in cranial-base exposure and cavernous sinus surgery have facilitated radical total removal.

The author reports 24 cases operated on with vigorous attempts at total removal of the tumor with involved dura and bone. This experience has distinguished three groups (I, II, and III) which influence surgical difficulties, the success of total removal, and outcome. These subgroups relate to the presence of interfacing arachnoid membranes between the tumor and cerebral vessels. The presence or absence of arachnoid membranes depends on the origin of the tumor and its relation to the naked segment of carotid artery lying outside the carotid cistern. Total removal was impossible in the three patients in Group I, with postoperative death occurring in one patient and hemiplegia in another. Total removal was achieved in 18 of the 19 patients in Group II, with one death from pulmonary embolism. In the two patients in Group III, total removal without complications was easily achieved.

Cushing and Eisenhardt17 clearly distinguished meningiomas of the anterior clinoid as “those of the deep or clinoidal third,” and concurrently, Vincent referred to them as “sphenocavernous meningiomas.”18 Despite this early recognition, these meningiomas are frequently grouped with suprasellar meningiomas or with meningiomas of the sphenoid ridge,6,11,23,24,41,51 masking their ominous course. They are second only to clival meningiomas in surgical mortality and morbidity rates, failure of total removal, and high rate of recurrence. Acknowledging that the best chance for cure comes through radical total removal, most authors, both pioneer and modern, have been content with subtotal removal to avoid the devastating sequelae of injury to the encased cerebral vessels;6,9,17,22,31,43,51,56 hence, repeated surgery and radiation therapy are frequently required. However, unless total removal is achieved, detrimental regrowth is expected in the majority of patients.1,15,17,37,47

Recent advances in cranial-base and cavernous sinus surgery have facilitated total removal, allowing respectable mortality and morbidity rates for these tumors.3,5,20,27,42,46 This report describes 24 cases of clinoidal meningiomas operated on over a period of 7 years, from November, 1981, to October, 1988, with vigorous attempts at total removal (including tumor, dura, and bone) during the first operation. According to the classification system of Simpson,47 the extent of tumor excision was either Grade I (complete macroscopic removal of the tumor, with excision of its dural attachment, and abnormal bone) or Grade II (complete macroscopic removal of the tumor and of its visible extensions, with coagulation of its dural attachment). Our experience with intraoperative anatomical observation led us to distinguish three categories of this tumor (Groups I, II, and III), each with a marked influence on the surgical difficulties, ability to achieve total removal, and outcome. These groups relate to the presence of interfacing arachnoid membranes between the tumor and the cerebral vessels. The presence or absence of this arachnoid membrane depends on the origin of the tumor and its relation to the small intradural carotid artery segment lying outside the carotid cistern.

Anatomical Considerations and Classification

As the carotid artery emerges from the cavernous sinus inferomedial to the anterior clinoid, it enters the subdural space to be vested in the carotid cistern. This cistern is bordered superiorly by the dura over the anterior clinoid process and the frontal lobe, and inferiorly by the dura covering the superior aspect of the cavernous sinus. The arachnoid does not follow the internal carotid artery into the cavernous sinus space, nor is it attached to the anterior clinoid process. A 1-or 2-mm segment of naked internal carotid artery lies between the investment of the carotid cistern and the dura of the cavernous sinus.59 This segment is not to be confused with the extradural segment which lies between the two rings anchoring the carotid artery as it exits the cavernous sinus space.20 Medially, the carotid cistern shares a wall with the chiasmatic cistern and is bounded laterally by the medial temporal lobe and the free margin of the tentorium. The inferior part of the carotid cistern and the superior part of the interpeduncular cistern are in apposition, creating a single Liliequist membrane.

Group I

If the meningioma's origin is proximal to the end of the carotid cistern (Group I), as is the case with a meningioma originating from the inferior aspect of the anterior clinoid, the tumor will enwrap the carotid artery, directly adhering to the adventitia in the absence of an intervening arachnoid membrane (Figs. 1 and 2). As the tumor grows, this direct attachment to the vessel wall continues to the carotid bifurcation and along the middle cerebral artery, advancing the arachnoid membrane ahead of it. This situation makes dissecting the tumor from the carotid artery and the middle cerebral artery branches impossible and explains why some authors describe tumors invading the arterial wall.20,23

Fig. 1.
Fig. 1.

Artist's drawing of a Group I meningioma. The tumor encases the carotid artery and its branches, with direct attachment to the adventitia. The optic nerve maintains an arachnoid plane from the chiasmatic cistern.

Fig. 2.
Fig. 2.

A Group I meningioma. Left: Preoperative computerized tomography appearance. During surgery, no arachnoid membrane was found and dissection of the middle cerebral and carotid arteries was impossible. Right: Lateral carotid arteriogram demonstrating narrowing of the carotid and middle cerebral arteries by the encasing tumor.

Group II

Tumors of Group II originate from the superior and/or lateral aspect of the anterior clinoid above the segment of the carotid invested in the carotid cistern. Thus, as the tumor grows, an arachnoid membrane of the carotid cistern and, distally, of the sylvian cistern separates the tumor from the arterial adventitia. Although the tumor engulfs the vessels, this arachnoid membrane remains intact, making microsurgical dissection feasible despite total encasement of the vessels (Figs. 3 and 4). This observation correlates with reports in the literature concerning the feasibility of tumor dissection despite total vascular encasement.4,23,36

Fig. 3.
Fig. 3.

A Group II meningioma. Left: Artist's drawing showing the tumor encasing the carotid artery and its branches. An arachnoid membrane of the carotid cistern separates the tumor from the adventitia, rendering dissection possible. The optic nerve maintains an arachnoid membrane from the chiasmatic cistern. Right: Retouched operative photograph showing the optic nerve (II), the anterior cerebral artery (A1), the middle cerebral artery (M1), and part of the internal carotid artery (C) dissected free from the encasing tumor (T). Dissection continues on the proximal carotid artery and into the cavernous sinus. The dissection is relatively easy, owing to the presence of the arachnoid membrane of the carotid cistern. R = retractor on the frontal lobe.

Fig. 4.
Fig. 4.

A Group II meningioma. Computerized tomography scan (left) and arteriogram, anteroposterior view (right). Notice the arterial narrowing by the encasing tumor. Dissection and tumor removal were facilitated by the presence of an intervening arachnoid membrane.

The optic chiasm and the optic nerves in both Group I and II tumors are wrapped in the arachnoid membrane of the chiasmatic cistern, and dissecting them free from the tumor is relatively easy with a microsurgical technique. In patients having undergone previous surgery, the arachnoid membrane may be violated; subsequently, the dissection plane is lost and the tumor will be in direct contact with the adventitia. In this case, the difficulty in Group II becomes similar to that in Group I.

Group III

Tumors in Group III originate at the optic foramen, extending into the optic canal and the tip of the anterior clinoid process. These tumors are usually small. The arachnoid membrane is present between the vessels and tumor but may be absent between the optic nerve and the tumor (Figs. 5 and 6).

Fig. 5.
Fig. 5.

A Group III meningioma. Left: Artist's drawing showing the tumor originating in the optic foramen. The tumor is small, separated from the carotid by the carotid cistern, but it extends into the optic canal. Right: Retouched operative photograph showing the carotid cistern intact. The tumor (T) is small and extends into the optic canal. II = optic nerve; C = carotid artery; R = retractor on the frontal lobe.

Fig. 6.
Fig. 6.

Computerized tomography scan of a Group III meningioma (arrow).

Operative Technique

Early in this series, the pterional approach was used in seven patients and subfrontal approach in three. Since 1985, we have exclusively used the orbitocranial approach described elsewhere2,3 for removal of these tumors. This approach provides the following advantages: 1)it brings the surgeon closer to the deep-seated lesion, allowing dissection over the shortest possible distance; 2) it permits a surgical attack via multiple routes: subfrontal, transsylvian, and subtemporal; 3) it consists of a single bone flap, eliminating the need for reconstruction and associated functional and anatomical or cosmetic deficits; 4) its low basilar approach alleviates brain retraction; and 5) it allows early interception of the tumor's blood supply through the sphenoid ridge, thus minimizing blood loss.

Positioning and Scalp Incision

The patient is placed supine and a spinal drainage needle is inserted. The head is rotated 30° to 40° to the opposite side, dropped toward the floor, tilted 5° to 10°, and fixed in the Mayfield headrest. The scalp incision is begun 1 cm anterior to the tragus, proceeding in a curvilinear fashion behind the hairline to the level of the superior temporal line on the opposite side. This results in the superficial temporal artery coursing posterior to the incision while the branches of the facial nerve are located anteriorly. Preservation of the superficial temporal artery is important since the artery may be needed for extracranial-intracranial (EC-IC) anastomosis. The frontal branches of the facial nerve are preserved by intrafascial dissection, as described previously by Yaşargil, et al.60

Bone Removal

The zygomatic arch is dissected in subperiosteal fashion, sectioned at the most anterior and posterior ends, and displaced downward along with its attachment to the masseter muscle. This maneuver allows a more basal approach to the floor of the middle fossa, obviating obstruction by the bulky temporal muscle. The temporal muscle is retracted posteriorly and inferiorly, exposing the junction of the zygomatic, sphenoidal, and frontal bones. Removal of the orbitocranial flap then proceeds as described elsewhere.2,3 The sphenoid ridge is drilled using a high-speed air drill. Drilling is continued to completely remove the sphenoid ridge, unroofing the superior orbital fissure and removing the anterior clinoid extradurally. This maneuver intercepts the arterial feeders coming from branches of the middle meningeal artery. It also assures removal of the involved bone at the insertion and prepares for exposure of the internal carotid upon entry to the cavernous sinus.

Dural Opening and Tumor Exposure

The dura mater is opened with a semicircular incision centered on the pterion; an extension from the main incision is directed posteriorly and inferiorly to the floor of the temporal fossa. Opening the dura under the microscope provides a transitional adjustment of the surgeon's dexterity from bone work to fine microsurgical dissection.

When the dura is opened, brain relaxation is achieved by partial drainage of cerebrospinal fluid (CSF) through the lumbar catheter. The arachnoid over the sylvian fissure is opened, allowing separation of the temporal and frontal lobes. The arachnoid opening is made and extended on the frontal side to preserve the superficial middle cerebral veins when possible. The relaxed frontal lobe is held by a self-retaining retractor. Elevation of the frontal lobe should be minimal — a distance of 1.5 cm or less is adequate for tumor resection. The olfactory nerve is located and preserved by dissecting it for some distance from the base of the frontal lobe. Preservation of the olfactory nerve deters excessive frontal lobe retraction, otherwise resulting in avulsion of the olfactory nerve.

Tumor Debulking

Under the operating microscope, a plane of dissection is established between the tumor and the frontal and temporal lobes. Ultrasonic aspiration is used to debulk large tumors. Caution is used not to carry debulking close to the carotid artery or the middle cerebral artery branches. Tumor removal around this area is continued using only microsurgical dissection with bipolar coagulation and careful piecemeal removal by microdissection.

Arterial Dissection

Once the tumor is debulked, the distal branches of the middle cerebral artery are identified under high magnification and, using microdissection, the tumor capsule is removed from the arterial wall. Despite total encasement of these vessels, a thickened arachnoid membrane separated the tumor from the adventitia in Group II tumors. Dissection is carried to the bifurcation of the carotid artery, removing the tumor from the anterior cerebral artery. Careful dissection under high magnification is continued to free the ventriculostriate arteries, the perforator of the anterior cerebral artery, and the internal carotid artery branches to the optic apparatus. Dissection becomes easier along the posterior communicating artery and the anterior choroidal artery, since these two arteries have their own vesting arachnoid membranes.59 Dissection of the third nerve segment, prior to its entry in the lateral wall of the cavernous sinus space, also becomes easier.

When hemorrhage ensues from a tear in a cerebral vessel, as it did in five of our cases, temporary vascular clips (30 gm/mm) are applied distal and proximal to the bleeding point, and the arterial wall is stitched with fine 10-0 sutures. Since the tumor may be supplied by arterial twigs from the cerebral artery, the surgeon first confirms that they are tumor feeders and not hypothalamic perforators or the optic nerve blood supply. Thus, each arterial branch is dissected and followed to ascertain its course. Particular attention is paid to spare the artery of Heubner and the vital branches of the striatum. The Liliequist membrane was intact in all of our cases of Group II tumors; consequently, removal of the tumor from the interpeduncular fossa and the posteriorly displaced basilar artery was usually easy.

Optic Nerve Dissection

The optic nerves in these tumors are displaced in several different ways. The optic nerve may be pushed inferiorly and medially or elevated by the bulk of the tumor coming between the carotid artery and the optic nerve. In seven of our cases, the optic nerve was totally engulfed, but in all cases the optic nerve maintained its arachnoid barrier formed by the wall of the chiasmatic cistern. When the optic nerve is engulfed, it is easier to begin the dissection from the chiasm and continue forward toward the optic canal. Frequently, the tumor extends a bud into the optic canal, requiring unroofing of the optic canal and careful dissection of the tumor. The arterial supply to the optic nerve and chiasm is preserved by the same method of dissection. Particular attention is paid to preserve the inferior group of arteries, which are the sole blood supply to the decussating fibers in the central chiasm.8 Since occasional observations of visual recovery after total blindness have been reported,4,33 the optic nerve was never sacrificed in our patients to obtain better exposure of the tumor, even in a totally blinded eye.

Dissection of the Pituitary Stalk

The pituitary stalk is easily recognized by its distinctive color and vascular network. It is usually displaced backward and to the opposite side. Arachnoidal cleavage is present and careful dissection under the microscope is successful.

Cavernous Sinus Involvement

When the tumor extends into the cavernous sinus, as it did in nine of our cases, proximal and distal control of the carotid artery is necessary. Early in this series, proximal control was achieved by exploring the internal carotid artery in the neck. More recently, this was accomplished by exposing the intrapetrous segment of the carotid artery. The anterior clinoid is already removed, facilitating exposure of the superior aspect of the cavernous sinus. The tumor is then removed through the superior or lateral wall of the cavernous sinus, as reported elsewhere.5

After gross tumor removal, the dura around the anterior clinoid is evaporated with the CO2 laser. Any further bone hyperostosis is drilled with the diamond bit of a high-speed drill. Frequently, this change in the bone is actually invasion by the tumor.9,19 To avoid postoperative CSF leakage through the extended ethmoidal cell, a piece of fascia is applied over this area. The dura is then closed in a watertight fashion, the single bone flap positioned in place, and the skin closed in two layers.

Summary of Cases
Case Material

Twenty-four cases qualifying as clinoidal meningiomas were operated on over a 7-year period, from November, 1981, through October, 1988. There were four other patients with the same pathology who did not have surgery. We excluded from the study meningiomas with origins (as described intraoperatively) on the tuberculum sellae, diaphragma sellae, planum sphenoidale, and middle and lateral sphenoid ridge, as well as hyperostosing en plaque meningiomas. Of the 24 patients studied, 14 have been described in previous publications.4,5 Seventeen were operated on at King Faisal Specialist Hospital in Riyadh, Saudi Arabia, between November, 1981, and December, 1985, and seven were operated on at the University of Mississippi Medical Center between January, 1986, and November, 1988. The patients ranged in age from 26 to 76 years (mean 52 years); there were seven men and 17 women. The symptoms of two women presented during pregnancy. Four patients had previously undergone surgery on their tumors.

Clinical Presentation

Visual disturbances were present in 84% of cases, similar to the typical findings described for tumors at this site (initial unilateral visual loss). Five patients experienced loss of vision on one side only; nine experienced optic atrophy, and six had papilledema. Foster Kennedy syndrome was documented in only one case. Four patients had impairment of the oculomotor or trigeminal nerve, while seizure was present in three patients. Two patients were admitted in a comatose state with giant tumors, and underwent emergency surgery. Visual loss preceded diagnosis by 2 to 44 months (average 25 months); headache preceded surgery by an average of 68 months.

Radiographic Findings

Computerized tomography (CT) scans in all cases revealed the presence of tumor and its extensions. Magnetic resonance (MR) imaging with gadolinium enhancement was used in the last three cases. All patients underwent cerebral angiography to delineate the anatomy of the cerebral circulation, arterial displacement, encasement of major vessels, and blood supply. Angiography revealed an associated internal carotid artery aneurysm in one patient. According to the classification mentioned above,47 there were three Group I tumors, 19 Group II tumors, and two Group III tumors.

The carotid, middle cerebral, and anterior cerebral arteries, as well as the optic apparatus, were all intimately involved with the tumor, being displaced, adherent, or totally engulfed. The carotid artery was totally encased in 11 patients, the branches of the middle cerebral artery were encased in seven, the anterior cerebral artery was encased in three, and the optic nerve was encased in seven. Cavernous sinus invasion occurred in nine patients.

Operative Results

Total removal (tumor, dura, and bone), as judged by intraoperative inspection and confirmed by postoperative CT scans (Fig. 7), was achieved in 18 of the 19 patients with Group II tumors; in the one exception a small nub of tumor was left in the cavernous sinus. There was one death 9 days postoperatively, due to pulmonary embolism, in a patient who was in excellent condition and was ready to be discharged. One patient lost vision in one eye in which she had been able to count fingers preoperatively from 1 ft. Preoperative visual impairment improved in only two patients. One patient had permanent third cranial nerve palsy. Two patients had transient diabetes insipidus, and one patient had permanent diabetes insipidus. One patient was readmitted for repair of a CSF leak, and one required a CSF shunt for hydrocephalus. One other patient had a pulmonary embolism. The one semicomatose and one fully comatose patient at admission both made impressive recoveries postoperatively.

Fig. 7.
Fig. 7.

Contrast-enhanced computerized tomography scans of a patient with a Group II clinoidal meningioma. Left: Preoperative scan. Right: Scan obtained after total removal of the tumor including intracavernous and optic canal extensions. Notice the resection of the anterior clinoid.

The postoperative follow-up period ranged from 1 to 7 years (average 57 months). There was only one asymptomatic recurrence which was observed to be without change on a CT scan 3 years later in the one Group II patient with subtotal removal. Two patients in this group had a second meningioma remote from the first (in the convexity), separated from the first operation by 3 and 6 years, respectively. These were removed surgically.

Only partial but extensive removal was possible in all three Group I patients. One patient developed delayed postoperative vasospasm 7 days postoperatively, which was confirmed by angiography, with a deteriorating ischemic neurological condition and eventual death 4 months later. The second patient had postoperative hemiplegia and was treated for pulmonary embolism. A gradual increase in tumor size over a 3-year period was documented by CT scanning. Radiation therapy was administered upon the patient's refusal of a second operation. The third patient showed some recovery of extraocular movement and received radiation therapy, showing no changes on an MR image 24 months later.

The two patients in Group III had no complications and showed neither clinical changes nor recurrence 7 months and 46 months postoperatively, respectively, according to the last available follow-up report of December, 1985.

Discussion
Distinguishing Clinoidal Meningiomas

To subclassify anterior clinoidal meningiomas into three groups may be surprising since many authors find it difficult to distinguish clinoidal meningiomas from those with more lateral attachment on the sphenoid ridge, and prefer the notion of wide or small attachment.23–25 Stern49 has even advocated the concept of an anatomical continuum of all meningiomas involving the cranio-orbital junction.

In a discussion of meningiomas of the “clinoidal third,” Cushing and Eisenhardt17 stated, “it is not easy, with certainty, to identify these cases in the literature.” This statement is still true today. Only a thorough review of the literature can extract cases of anterior clinoidal meningiomas (Table 1). An analysis of these cases leads to recognition of clinoidal meningiomas as a separate entity with distinguishing clinical, radiological, and surgical considerations. Cushing's series is a typical example: of the 13 patients with anterior clinoidal meningiomas, two were operated on transsphenoidally in 1912 and 1913, resulting in one operative death. There was one other operative death. Only three patients had total removal. Recurrence with eventual death occurred in five patients.

TABLE 1

Summary of major surgical series of anterior clinoid meningiomas*

Authors & YearNo. of CasesPartial or Subtotal RemovalTotal RemovalOperative DeathRecurrence + Eventual DeathKnown Symptomatic Recurrence
Cushing & Eisenhardt, 193811+(2)† 831+(1)† 5
Uihlein & Weyand, 195352 17 5
Holub, 195619 69 
Olivecrona, 196747 153211 3
Guyot, et al., 196713  
Cook, 197111 3 
Fischer, et al., 19736 2 
Ugrumov, et al., 197916 1424 
Cophignon et al., 19796 420 2
Konovalov, et al., 197970 13 
MacCarty & Taylor, 197947  
Bonnal, et al., 19807 73 
Pompili, et al., 198210 5 
Ojemann, 198516 0 15
Hakuba, et al., 19867 0 
Jan, et al., 198619 6 
Sekhar, et al., 198916 3130 1
Al-Mefty, 199024 4212 1

Only available information is entered.

Two patients were operated on transsphenoidally in 1912 and 1913, one of whom was an operative death.

Bonnal, et al.,9 described a similar series, with only subtotal removal possible in all seven patients and three operative deaths. Pompili, et al.,44 reported that only two of their nine patients with inner sphenoid ridge meningiomas (five of which were globus tumors) had excellent results, defined as total removal combined with complete clinical remission and no clinical or radiological sign of recurrence. A striking difference in mortality and morbidity rates, failure of total removal, and recurrence is apparent whenever clinoidal meningiomas are compared with middle and lateral sphenoid tumors or with tuberculum sellae tumors.9,17,26,29,41,44,52

Recognizing these differences, Bonnal, et al.,9 classified sphenoid ridge meningiomas into five groups (A to E), with Group A in their classification representing the meningiomas discussed in this report. They described clinoidal or sphenocavernous meningiomas en masse as: “extended upward into the cranial cavity from the dura of the cavernous sinus, of the anterior clinoid process, and of the internal part of the sphenoidal wings. They were in close contact with the internal carotid artery and its branches, which were shifted, stretched, or embedded, and with the optic nerve and tract. Bone was not involved, except for the anterior clinoid process, nor were the craniofacial cavities.” They conceded that total removal of these meningiomas is difficult even with the help of magnification and ultrasonic aspiration. This group is similar to the first category of Ojemann's sphenoid ridge meningioma.40

Although meningiomas of the anterior clinoid invade the cavernous sinus, there exist meningiomas that are strictly intracavernous, originating from within the cavernous sinus.10,13,34 The latter present with symptoms and signs of cavernous sinus syndrome, and form a separate entity; thus, we have excluded them from this discussion.

Total vs. Subtotal Removal

The surgical mortality rate associated with anterior clinoidal meningiomas has remained unacceptably high. Uihlein and Weyand53 reported a mortality rate of 32% in 1953, comparable to a 42% mortality rate in the series of Bonnal, et al.,9 in 1980. Repeatedly, the operative cause is injury to the major cerebral vessels,9,17,23,41,43,53 a risk that has forced an overwhelming number of surgeons to accept and recommend subtotal removal.6,9,11,17,22,23,31,45,51,52,56

Most neurosurgeons have had the experience of carefully observing slow-growing tumors, and there have been reports of patients who remain in satisfactory condition for years after partial removal of their tumors.9,30,45 On the other hand, the extent of surgical removal is clearly the most determining factor in tumor recurrence and progression.1,37,47,48 In the series of Mirimanoff, et al.,37 sphenoid ridge meningiomas (with a 28% rate of total resection in all sphenoid ridge locations) recurred or progressed with a probability at 5 and 10 years of 34% and 54%, respectively. A second operation carries a significantly higher mortality and failure rate.35,37

Uihlein and Weyand53 have stated that “total removal of these tumors is necessary to prevent recurrence.” Cophignon, et al.,15 stated the point clearly: “to cure a patient from a spheno-orbital meningioma one has to remove the entire intradural tumor, all the involved dura, the orbital tumor, and all the so-called hyperostosis, opening the facial and intracranial sinuses, if necessary.”

Recent advances in skull-base exposure, anesthesia, cerebral protection, microsurgical techniques, imaging, and surgery of the cavernous sinus have assisted in overcoming many of the formidable tasks in dissecting and preserving the vital neural and vascular structures involved with these tumors. Embedded carotid and middle cerebral artery branches can be dissected free under magnification by means of microsurgical techniques.4,20,27,36,46 Extensions into the cavernous sinus can be removed with preservation of the intracavernous carotid artery and the cranial nerves.4,20,46 Involved bone can be extensively drilled away.3,44 Revascularization can be performed by EC-IC anastomosis,38 a saphenous vein graft,50 or direct reconstruction of the carotid artery using an interposed venous graft46 (T Fukushima, personal communication, 1989), providing a means to alleviate ischemia should injury beyond repair occur to major cerebral vessels. Delayed thrombosis of the internal carotid and middle cerebral arteries leading to stroke has been reported after surgery of these tumors.23,43 We do not believe, however, that this potential risk is frequent enough to be a deterrent to arterial dissection.

Olivecrona41 reported no recurrences in 26 surviving patients after complete removal of their medial ridge meningiomas, with a postoperative follow-up period of up to 25 years. Reviewing his long-term results in patients with medial sphenoid ridge meningiomas, Olivecrona concluded, “in the group where the tumor was completely removed the functional results in the survivors were highly satisfactory, whereas in the incompletely removed groups some patients lived for many years but the rate of recurrence was high and the results of secondary operation far from encouraging.” Hence, the controversy surrounding pursuit of total removal does not question its value, but reveals the potentially high price in risk of mortality and morbidity.

The microsurgical technique has clearly improved the incidence of operative mortality and morbidity and the chance of total removal.4,32,33,45,51 This is because the surgeon is able to dissect adherent or encased structures due to the cleavage of the arachnoid membrane, which is recognizable under the microscope. Hence, our classification has a deep impact on surgical decision-making and outcome. When this membrane was absent (Group I in our classification), dissection was impossible; none of the tumors was removed totally and the outcome was a disappointment. In contrast, despite total encasement of arteries and nerves, total removal was possible in Group II, with minimal morbidity. Unlike other suprasellar meningiomas, recovery of visual deficits in clinoidal meningiomas is poor.6,40 This implicates ischemia as the cause of visual loss in clinoidal meningiomas rather than mere optic nerve compression.

Small Meningiomas of the Anterior Clinoid

Cushing and Eisenhardt17 cited an early example of a small anterior clinoidal meningioma found at autopsy and depicted in 1910 by Frotscher. Several cases of these small meningiomas at the anterior clinoid (Group III in our classification) can be found. We were able to isolate 14 such cases9,16,21,40,51,52 in addition to 22 others mentioned by Konovalov, et al.32 These meningiomas are characterized by severe loss of vision with optic atrophy on one side. Prior to high-resolution CT and MR imaging, radiological studies were frequently normal and the tumor was usually found upon exploration for unexplained visual loss. This group of tumors is frequently reported to extend into the optic canal. They are easily removed; however, visual prognosis remains guarded because of the ischemic nature of the optic nerve deficit. These tumors are similar in clinical findings and surgical consideration to intracanalicular meningiomas, which have recently been reviewed by Wilson, et al.57

The Role of Radiation Therapy

The role of radiation therapy cannot be left unaddressed in a discussion of clinoidal meningiomas in which subtotal removal or recurrence are prominent features. Waga, et al.,54 were unable to establish whether prophylactic radiation therapy was effective in preventing recurrence of benign meningiomas, while Yamashita, et al.,58 concluded that irradiation of recurrent meningiomas is of little value, although it might occasionally be beneficial. Recent reports, however, have advocated the effectiveness of radiotherapy in conjunction with subtotal surgical excision.7,12,55 Hence, radiation therapy is a viable adjuvant in treating nonremovable residual or recurring tumors. For smaller residual tumors, stereotactic radiotherapy is an attractive alternative awaiting long-term results.

Acknowledgments

The author is grateful to Julie Hipp for help in preparing the manuscript and to Michael P. Schenk for the drawings.

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    Cook AW: Total removal of large global meningiomas at the medial aspect of the sphenoid ridge. Technical note. J Neurosurg 34:1071131971Cook AW: Total removal of large global meningiomas at the medial aspect of the sphenoid ridge. Technical note. J Neurosurg 34:

  • 15.

    Cophignon JLucena JClay Cet al: Limits to radical treatment of spheno-orbital meningiomas. Acta Neurochir Suppl 28:3753801979Acta Neurochir Suppl 28:

  • 16.

    Craig WMGogela LJ: Meningioma of the optic foramen as a cause of slowly progressive blindness. J Neurosurg 7:44481950J Neurosurg 7:

  • 17.

    Cushing HEisenhardt L: Springfield, Ill: Charles C Thomas1938298319

  • 18.

    David MMahoudeau D: Les méningiomes de la petite aile du sphénoide (considerations anatomo-cliniques et thérapeutiques). Gaz Med France:1111301935Gaz Med France:

  • 19.

    Derome PJGuiot G: Bone problems in meningiomas invading the base of the skull. Clin Neurosurg 25:4354511978Clin Neurosurg 25:

  • 20.

    Dolenc VV: Anatomy and Surgery of the Cavernous Sinus. Wien: Springer-Verlag1989Dolenc VV: Anatomy and Surgery of the Cavernous Sinus.

  • 21.

    Elsberg CADyke CG: Meningiomas attached to the medial part of the sphenoid ridge with syndrome of unilateral optic atrophy, defect in visual field of the same eye and changes in sella turcica and in shape of interpeduncular cistern after encephalography. Arch Ophthalmol 12:6446751934Arch Ophthalmol 12:

  • 22.

    Fischer GFischer CMansuy L: Pronostic chirurgical des méningiomes de l'arête sphénoïdale. Neurochirurgie 19:3233461973Neurochirurgie 19:

  • 23.

    Fohanno DBitar A: Sphenoidal ridge meningioma. Adv Tech Stand Neurosurg 14:1371741986Adv Tech Stand Neurosurg 14:

  • 24.

    Grant FC: Intracranial meningiomas. Surgical results. Surg Gynecol Obstet 85:4194311947Grant FC: Intracranial meningiomas. Surgical results. Surg Gynecol Obstet 85:

  • 25.

    Guthrie BLEbersold MJScheithauer BW: Neoplasms of the intracranial meningesYoumans JR (ed): Neurological Surgeryed 3. Philadelphia: WB Saunders1990532503281

  • 26.

    Guyot JFVouyouklakis DPertuiset B: Méningiomes de l'arête sphénoïdale. A propos de 50 cas. Neurochirurgie 13:5715841967Neurochirurgie 13:

  • 27.

    Hakuba ALiu SSNishimura S: The orbitozygomatic infratemporal approach: a new surgical technique. Surg Neurol 26:2712761986Surg Neurol 26:

  • 28.

    Holub K: Intrakranielle meningeome. Acta Neurochir 4:3554011956Holub K: Intrakranielle meningeome. Acta Neurochir 4:

  • 29.

    Jan MBazézé VSaudeau Det al: Devenir des méningiomes intracrâniens chez l'adulte. Etude rétrospective d'une série médico-chirurgicale de 161 méningiomes. Neurochirurgie 32:1291341986Neurochirurgie 32:

  • 30.

    Jefferson AAzzam N: The suprasellar meningiomas: a review of 19 years' experience. Acta Neurochir Suppl 28:3813841979Acta Neurochir Suppl 28:

  • 31.

    Kempe LG: Operative Neurosurgery. New York: Springer-Verlag19681109118Kempe LG: Operative Neurosurgery.

  • 32.

    Konovalov ANFedorov SNFaller TOet al: Experience in the treatment of the parasellar meningiomas. Acta Neurochir Suppl 28:3713721979Acta Neurochir Suppl 28:

  • 33.

    Koos WTKletter GSchuster Het al: Microsurgery of suprasellar meningiomas. Adv Neurosurg 2:62671975Adv Neurosurg 2:

  • 34.

    Lesoin FJomin MBouchez Bet al: Management of cavernous sinus meningiomas. Neurochirurgia 28:1951981985Neurochirurgia 28:

  • 35.

    MacCarty CSTaylor WF: Intracranial meningiomas: experiences at the Mayo Clinic. Neurol Med Chir 19:5695741979Neurol Med Chir 19:

  • 36.

    Malis LI: Tumors of the parasellar region. Adv Neurol 15:2812991976Malis LI: Tumors of the parasellar region. Adv Neurol 15:

  • 37.

    Mirimanoff RODosoretz DELinggood RMet al: Meningioma: analysis of recurrence and progression following neurosurgical resection. J Neurosurg 62:18241985J Neurosurg 62:

  • 38.

    Moritake KHanda HYamashita Jet al: STA-MCA anastomosis in patients with skull base tumours involving the internal carotid artery — haemodynamic assessment by ultrasonic Doppler flowmeter. Acta Neurochir 72:951101984Acta Neurochir 72:

  • 39.

    Ojemann RG: Meningiomas: clinical features and surgical managementWilkins RHRengachary SS (eds): Neurosurgery. New York: McGraw-Hill19851635654Neurosurgery.

  • 40.

    Ojemann RG: Meningiomas of the basal parapituitary region: technical considerations. Clin Neurosurg 27:2332621980Ojemann RG: Meningiomas of the basal parapituitary region: technical considerations. Clin Neurosurg 27:

  • 41.

    Olivecrona H: The surgical treatment of intracranial tumorsOlivecrona HTönnis W (eds): Handbuch der Neurochirurgie. Berlin: Springer-Verlag19671301Handbuch der Neurochirurgie.

  • 42.

    Pellerin PLesoin FDhellemmes Pet al: Usefulness of the orbitofrontomalar approach associated with bone reconstruction for frontotemporosphenoid meningiomas. Neurosurgery 15:7157181984Neurosurgery 15:

  • 43.

    Pertuiset BFarah SClayes Let al: Operability of intracranial meningiomas. Personal series of 353 cases. Acta Neurochir 76:2111985Acta Neurochir 76:

  • 44.

    Pompili ADerome PJVisot Aet al: Hyperostosing meningiomas of the sphenoid ridge — clinical features, surgical therapy, and long-term observations: review of 49 cases. Surg Neurol 17:4114161982Surg Neurol 17:

  • 45.

    Probst C: Possibilities and limitations of microsurgery in patients with meningiomas of the sellar region. Acta Neurochir 84:991021987Probst C: Possibilities and limitations of microsurgery in patients with meningiomas of the sellar region. Acta Neurochir 84:

  • 46.

    Sekhar LNSen CHJho HDet al: Surgical treatment of intracavernous neoplasms: a four-year experience. Neurosurgery 24:18301989Neurosurgery 24:

  • 47.

    Simpson D: The recurrence of intracranial meningiomas after surgical treatment. J Neurol Neurosurg Psychiatry 20:22391957Simpson D: The recurrence of intracranial meningiomas after surgical treatment. J Neurol Neurosurg Psychiatry 20:

  • 48.

    Skullerud KLöken AC: The prognosis in meningiomas. Acta Neuropathol 29:3373441974Acta Neuropathol 29:

  • 49.

    Stern WE: Meningiomas in the cranio-orbital junction. J Neurosurg 38:4284371973Stern WE: Meningiomas in the cranio-orbital junction. J Neurosurg 38:

  • 50.

    Sundt TM JrPiepgras DGMarsh WRet al: Saphenous vein bypass grafts for giant aneurysms and intracranial occlusive disease. J Neurosurg 65:4394501986J Neurosurg 65:

  • 51.

    Symon LRosenstein J: Surgical management of suprasellar meningioma. Part 1: The influence of tumor size, duration of symptoms, and microsurgery on surgical outcome in 101 consecutive cases. J Neurosurg 61:6336411984J Neurosurg 61:

  • 52.

    Ugrumov VMIgnatyeva GEOlushin VEet al: Parasellar meningiomas: diagnosis and possibility of surgical treatment according to the place of original growth. Acta Neurochir Suppl 28:3733741979Neurochir Suppl 28:

  • 53.

    Uihlein AWeyand RD: Meningiomas of anterior clinoid process as a cause of unilateral loss of vision. Surgical considerations. Arch Ophthalmol 49:2612701953Arch Ophthalmol 49:

  • 54.

    Waga SYamashita JHanda H: [Recurrence of meningiomas.] Neurol Med Chir 17:2032081977 (Jpn)Neurol Med Chir 17:

  • 55.

    Wara WMSheline GENewman Het al: Radiation therapy of meningiomas. AJR 123:4534581975AJR 123:

  • 56.

    Watts C: Sphenoid wing meningiomaLong DM (ed): Toronto: CV Mosby19851416

  • 57.

    Wilson WBGordon MLehman RAW: Meningiomas confined to the optic canal and foramina. Surg Neurol 12:21281979Surg Neurol 12:

  • 58.

    Yamashita JHanda HIwaki Ket al: Recurrence of intracranial meningiomas, with special reference to radiotherapy. Surg Neurol 14:33401980Surg Neurol 14:

  • 59.

    Yaşargil MG: Microneurosurgery. Stuttgart: Georg Thieme Verlag198412632Yaşargil MG: Microneurosurgery.

  • 60.

    Yaşargil MGReichman MVKubik S: Preservation of the frontotemporal branch of the facial nerve using the interfascial temporalis flap for pterional craniotomy. Technical article. J Neurosurg 67:4634661987J Neurosurg 67:

Article Information

Address reprint requests to: Ossama Al-Mefty, M.D., Department of Neurosurgery, University of Mississippi Medical Center, 2500 North State Street, Jackson, Mississippi 39216-4505.

© AANS, except where prohibited by US copyright law.

Headings

Figures

  • View in gallery

    Artist's drawing of a Group I meningioma. The tumor encases the carotid artery and its branches, with direct attachment to the adventitia. The optic nerve maintains an arachnoid plane from the chiasmatic cistern.

  • View in gallery

    A Group I meningioma. Left: Preoperative computerized tomography appearance. During surgery, no arachnoid membrane was found and dissection of the middle cerebral and carotid arteries was impossible. Right: Lateral carotid arteriogram demonstrating narrowing of the carotid and middle cerebral arteries by the encasing tumor.

  • View in gallery

    A Group II meningioma. Left: Artist's drawing showing the tumor encasing the carotid artery and its branches. An arachnoid membrane of the carotid cistern separates the tumor from the adventitia, rendering dissection possible. The optic nerve maintains an arachnoid membrane from the chiasmatic cistern. Right: Retouched operative photograph showing the optic nerve (II), the anterior cerebral artery (A1), the middle cerebral artery (M1), and part of the internal carotid artery (C) dissected free from the encasing tumor (T). Dissection continues on the proximal carotid artery and into the cavernous sinus. The dissection is relatively easy, owing to the presence of the arachnoid membrane of the carotid cistern. R = retractor on the frontal lobe.

  • View in gallery

    A Group II meningioma. Computerized tomography scan (left) and arteriogram, anteroposterior view (right). Notice the arterial narrowing by the encasing tumor. Dissection and tumor removal were facilitated by the presence of an intervening arachnoid membrane.

  • View in gallery

    A Group III meningioma. Left: Artist's drawing showing the tumor originating in the optic foramen. The tumor is small, separated from the carotid by the carotid cistern, but it extends into the optic canal. Right: Retouched operative photograph showing the carotid cistern intact. The tumor (T) is small and extends into the optic canal. II = optic nerve; C = carotid artery; R = retractor on the frontal lobe.

  • View in gallery

    Computerized tomography scan of a Group III meningioma (arrow).

  • View in gallery

    Contrast-enhanced computerized tomography scans of a patient with a Group II clinoidal meningioma. Left: Preoperative scan. Right: Scan obtained after total removal of the tumor including intracavernous and optic canal extensions. Notice the resection of the anterior clinoid.

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Cook AW: Total removal of large global meningiomas at the medial aspect of the sphenoid ridge. Technical note. J Neurosurg 34:1071131971Cook AW: Total removal of large global meningiomas at the medial aspect of the sphenoid ridge. Technical note. J Neurosurg 34:

15.

Cophignon JLucena JClay Cet al: Limits to radical treatment of spheno-orbital meningiomas. Acta Neurochir Suppl 28:3753801979Acta Neurochir Suppl 28:

16.

Craig WMGogela LJ: Meningioma of the optic foramen as a cause of slowly progressive blindness. J Neurosurg 7:44481950J Neurosurg 7:

17.

Cushing HEisenhardt L: Springfield, Ill: Charles C Thomas1938298319

18.

David MMahoudeau D: Les méningiomes de la petite aile du sphénoide (considerations anatomo-cliniques et thérapeutiques). Gaz Med France:1111301935Gaz Med France:

19.

Derome PJGuiot G: Bone problems in meningiomas invading the base of the skull. Clin Neurosurg 25:4354511978Clin Neurosurg 25:

20.

Dolenc VV: Anatomy and Surgery of the Cavernous Sinus. Wien: Springer-Verlag1989Dolenc VV: Anatomy and Surgery of the Cavernous Sinus.

21.

Elsberg CADyke CG: Meningiomas attached to the medial part of the sphenoid ridge with syndrome of unilateral optic atrophy, defect in visual field of the same eye and changes in sella turcica and in shape of interpeduncular cistern after encephalography. Arch Ophthalmol 12:6446751934Arch Ophthalmol 12:

22.

Fischer GFischer CMansuy L: Pronostic chirurgical des méningiomes de l'arête sphénoïdale. Neurochirurgie 19:3233461973Neurochirurgie 19:

23.

Fohanno DBitar A: Sphenoidal ridge meningioma. Adv Tech Stand Neurosurg 14:1371741986Adv Tech Stand Neurosurg 14:

24.

Grant FC: Intracranial meningiomas. Surgical results. Surg Gynecol Obstet 85:4194311947Grant FC: Intracranial meningiomas. Surgical results. Surg Gynecol Obstet 85:

25.

Guthrie BLEbersold MJScheithauer BW: Neoplasms of the intracranial meningesYoumans JR (ed): Neurological Surgeryed 3. Philadelphia: WB Saunders1990532503281

26.

Guyot JFVouyouklakis DPertuiset B: Méningiomes de l'arête sphénoïdale. A propos de 50 cas. Neurochirurgie 13:5715841967Neurochirurgie 13:

27.

Hakuba ALiu SSNishimura S: The orbitozygomatic infratemporal approach: a new surgical technique. Surg Neurol 26:2712761986Surg Neurol 26:

28.

Holub K: Intrakranielle meningeome. Acta Neurochir 4:3554011956Holub K: Intrakranielle meningeome. Acta Neurochir 4:

29.

Jan MBazézé VSaudeau Det al: Devenir des méningiomes intracrâniens chez l'adulte. Etude rétrospective d'une série médico-chirurgicale de 161 méningiomes. Neurochirurgie 32:1291341986Neurochirurgie 32:

30.

Jefferson AAzzam N: The suprasellar meningiomas: a review of 19 years' experience. Acta Neurochir Suppl 28:3813841979Acta Neurochir Suppl 28:

31.

Kempe LG: Operative Neurosurgery. New York: Springer-Verlag19681109118Kempe LG: Operative Neurosurgery.

32.

Konovalov ANFedorov SNFaller TOet al: Experience in the treatment of the parasellar meningiomas. Acta Neurochir Suppl 28:3713721979Acta Neurochir Suppl 28:

33.

Koos WTKletter GSchuster Het al: Microsurgery of suprasellar meningiomas. Adv Neurosurg 2:62671975Adv Neurosurg 2:

34.

Lesoin FJomin MBouchez Bet al: Management of cavernous sinus meningiomas. Neurochirurgia 28:1951981985Neurochirurgia 28:

35.

MacCarty CSTaylor WF: Intracranial meningiomas: experiences at the Mayo Clinic. Neurol Med Chir 19:5695741979Neurol Med Chir 19:

36.

Malis LI: Tumors of the parasellar region. Adv Neurol 15:2812991976Malis LI: Tumors of the parasellar region. Adv Neurol 15:

37.

Mirimanoff RODosoretz DELinggood RMet al: Meningioma: analysis of recurrence and progression following neurosurgical resection. J Neurosurg 62:18241985J Neurosurg 62:

38.

Moritake KHanda HYamashita Jet al: STA-MCA anastomosis in patients with skull base tumours involving the internal carotid artery — haemodynamic assessment by ultrasonic Doppler flowmeter. Acta Neurochir 72:951101984Acta Neurochir 72:

39.

Ojemann RG: Meningiomas: clinical features and surgical managementWilkins RHRengachary SS (eds): Neurosurgery. New York: McGraw-Hill19851635654Neurosurgery.

40.

Ojemann RG: Meningiomas of the basal parapituitary region: technical considerations. Clin Neurosurg 27:2332621980Ojemann RG: Meningiomas of the basal parapituitary region: technical considerations. Clin Neurosurg 27:

41.

Olivecrona H: The surgical treatment of intracranial tumorsOlivecrona HTönnis W (eds): Handbuch der Neurochirurgie. Berlin: Springer-Verlag19671301Handbuch der Neurochirurgie.

42.

Pellerin PLesoin FDhellemmes Pet al: Usefulness of the orbitofrontomalar approach associated with bone reconstruction for frontotemporosphenoid meningiomas. Neurosurgery 15:7157181984Neurosurgery 15:

43.

Pertuiset BFarah SClayes Let al: Operability of intracranial meningiomas. Personal series of 353 cases. Acta Neurochir 76:2111985Acta Neurochir 76:

44.

Pompili ADerome PJVisot Aet al: Hyperostosing meningiomas of the sphenoid ridge — clinical features, surgical therapy, and long-term observations: review of 49 cases. Surg Neurol 17:4114161982Surg Neurol 17:

45.

Probst C: Possibilities and limitations of microsurgery in patients with meningiomas of the sellar region. Acta Neurochir 84:991021987Probst C: Possibilities and limitations of microsurgery in patients with meningiomas of the sellar region. Acta Neurochir 84:

46.

Sekhar LNSen CHJho HDet al: Surgical treatment of intracavernous neoplasms: a four-year experience. Neurosurgery 24:18301989Neurosurgery 24:

47.

Simpson D: The recurrence of intracranial meningiomas after surgical treatment. J Neurol Neurosurg Psychiatry 20:22391957Simpson D: The recurrence of intracranial meningiomas after surgical treatment. J Neurol Neurosurg Psychiatry 20:

48.

Skullerud KLöken AC: The prognosis in meningiomas. Acta Neuropathol 29:3373441974Acta Neuropathol 29:

49.

Stern WE: Meningiomas in the cranio-orbital junction. J Neurosurg 38:4284371973Stern WE: Meningiomas in the cranio-orbital junction. J Neurosurg 38:

50.

Sundt TM JrPiepgras DGMarsh WRet al: Saphenous vein bypass grafts for giant aneurysms and intracranial occlusive disease. J Neurosurg 65:4394501986J Neurosurg 65:

51.

Symon LRosenstein J: Surgical management of suprasellar meningioma. Part 1: The influence of tumor size, duration of symptoms, and microsurgery on surgical outcome in 101 consecutive cases. J Neurosurg 61:6336411984J Neurosurg 61:

52.

Ugrumov VMIgnatyeva GEOlushin VEet al: Parasellar meningiomas: diagnosis and possibility of surgical treatment according to the place of original growth. Acta Neurochir Suppl 28:3733741979Neurochir Suppl 28:

53.

Uihlein AWeyand RD: Meningiomas of anterior clinoid process as a cause of unilateral loss of vision. Surgical considerations. Arch Ophthalmol 49:2612701953Arch Ophthalmol 49:

54.

Waga SYamashita JHanda H: [Recurrence of meningiomas.] Neurol Med Chir 17:2032081977 (Jpn)Neurol Med Chir 17:

55.

Wara WMSheline GENewman Het al: Radiation therapy of meningiomas. AJR 123:4534581975AJR 123:

56.

Watts C: Sphenoid wing meningiomaLong DM (ed): Toronto: CV Mosby19851416

57.

Wilson WBGordon MLehman RAW: Meningiomas confined to the optic canal and foramina. Surg Neurol 12:21281979Surg Neurol 12:

58.

Yamashita JHanda HIwaki Ket al: Recurrence of intracranial meningiomas, with special reference to radiotherapy. Surg Neurol 14:33401980Surg Neurol 14:

59.

Yaşargil MG: Microneurosurgery. Stuttgart: Georg Thieme Verlag198412632Yaşargil MG: Microneurosurgery.

60.

Yaşargil MGReichman MVKubik S: Preservation of the frontotemporal branch of the facial nerve using the interfascial temporalis flap for pterional craniotomy. Technical article. J Neurosurg 67:4634661987J Neurosurg 67:

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