VINOD K. ANAND, MD, CHARLES SHERWOOD, MD,OSSAMA AL-MEFTY, MD
Visual loss following direct or indirect maxillofacial injuries may result from either reversible or irreversible opticnerve injuries. Optic nerve decompression may be required ~n select reversible inju~es to. the nerve, as well asfor compressive neuropathy in fibrous dysplasia, osteopetrosis, and neoplasms of this region. M~ch cont~oversy
regarding ideal timing and surgical approach, steroid therapy, and the role of shea.th deco~I:resslOn remamsunresolved. Here, we discuss indications and surgical approaches for decompression, specifically thetransethmoidal (external and transantral) and supraorbital craniotomy a~proaches. .KEY WORDS: Decompression/optic canal/optic neuropathy/supraorbltal/transethmoldal.
Visual loss as a consequence of injury to the optic nervewas described over 2,000 years ago when Hippocratesnoted,
Dimness of vision occurs in injuries to the brow, and in thoseplaces slightly above. It is less noticeable the more recent thewounds but as the scar becomes old so the dimness increases."
Approximately 5% of patients with maxillofacial andhead trauma manifest variable degrees of injury to thevisual systern.v" Direct ocular injuries (eg, hypherna,dislocated lens, retinal vitreous hemorrhage, scleral rupture, retrobulbar hematoma, cortical blindness) constitutethe most common cause of traumatic visual loss.However, in a patient having visual loss but no evidenceof direct ocular injury, damage to the optic nerve shouldbe considered and clinically investigated. Managementof optic nerve injury remains a subject of considerabledebate because the degree of severity, which includesmild compressive edema, central retinal artery .occlusion,compressive optic neuropathy, ?r. total avulsion of. theoptic nerve, is frequently ~hffI~U.lt to deten~me.
Furthermore, concomitant proximal Injury, such as In theregion of the optic chiasm, cannot be ascertained.Therefore, the role of surgery in treating traumatic opticneuropathies continues to evolve as new information regarding the pathophysiology of injury co~es t? l~ght.2,4-6Unresolved issues include the appropnate timing andideal approach for decompressive s~rgery, optic s~eath
decompression, and the role of steroid therapy..This article discusses the surgical management of patients requiring optic nerve decompression.
From the Division of Otolaryngology and Departments of Ophthalmology and Neurosurgery, University of Mississippi Medical Center,Jackson, MS.
Address reprint requests to Vinod K. Anand, MD, Division of OtolaryngOlogy. University of Mississippi Medical Center, 2500 N StateSt, Jackson, MS 39216-4505.
Cycle, automobile, and falling accidents most frequentlycause optic nerve injury/ and are almost always accompanied by a period of unconsciousness o~ amnesia.f Theseverity of the injury ~oes no~ ~orrel.at~wI~h the ~eg.ree ~foptic nerve dysfunction. Initial chmcal. Investiga.ti~n ISimportant not only to evaluate the seventy o~ the I~JUry,
but also to determine baseline values by which to Judgeprogression and decide surg~cal i~tervention. .Becausemost patients have sensory impairment, a satisfactoryevaluation may not be possible. .
Evaluation should include a best-corrected (by eitherpinhole or spectacle) test of visual acuity, as well as pupilappearance and reacti~ity. The ph~sicia~ sh.ould loo~ fora relative afferent pupillary defect (ie, SWIngIng flashlighttest, Marcus Gunn pupil phenomenon), which is themost reliable sign of optic nerve injury." The ocular fundus is initially normal in posterior optic nerve injury; theoptic disk exhibits pallor only after 3 to 6 weeks. Themore anterior the injury, the earlier the onset of opticnerve atrophy. An abnormality within the ocular fundusmay make optic nerve injury more difficult to establishand follow. No pathognomonic visual field defects existin injuries of the optic nerve. However, because the injuries are anterior to the optic chiasm, visual field defectsare confined to the involved side, respect the horizontalmeridian of the field, and/or involve a central or paracentral scotoma (macular fibers). Formal visual field testing,when possible, is useful to identify and quantify the defects since subsequent visual fields may be compared forprogression of field loss.2,4 The visual evoked responsetest correlates highly with optic nerve injury, showingearly abnormal waveforms with normal latencies,8,9 butits availability and impracticality limit its usefulness.f Intraoperative visual evoked potentials (VEPs) reassure thesurgical team, but are generally considered unnecessarywith the use of a satisfactory technique." Computedtomographic (CT) scans-should be used to rule out a direct component of injury to the optic nerve from bonefragments (Fig 1) and to detect intracranial injuries (Fig2). They are also useful for detecting foreign bodies (Fig
OPERATIVE TECHNIQUES IN OTOLARYNGOLOGy-HEAD AND NECK SURGERY, VOL 2, NO 3 (SEP). 1991: PP 157-166 157
FIGURE 1. Axial CT scan demonstrating right orbitalproptosis and soft tissue edema, mucosal edema andfluid within the sphenoethmoidal sinuses, and afracture fragment of the lateral portion of the rightoptic canal.
FIGURE 2. Coronal CT scan of the patient in Fig 1showing multiple fracture fragments in the orbitalapex region. Note the presence of a small amount ofair in the intracranial cavity.
FIGURE 3. Coronal CT scan of a patient with abullet injury to the intraorbital portion of the opticnerve.
158
FIGURE 4. T-l-weighted axial MR image of a patient with optic nerveinjury. The arrow shows area of compression and enhanced signal in theregion of the optic canal.
OPTIC NERVE DECOMPRESSION
3). However, a normal examination in the face of otherindications for surgery should not defer decompres-
• 4·6 8 10 11 M t' (MR) . ISJOn. . ., agne IC resonance Images comp e-ment CT scans by assessing subtle soft tissue changesalong the optic nerve (Fig 4).
SURGICAL ANATOMY
Each optic nerve is enveloped by all three meningeal layers and is considered a direct prolongation of brain tissue.Measuring approximately 50 mm in length, the nerve extends posteromedial through the optic canal to join theoptic chiasm. It has four anatomical subsegments, theintraocular (1 mm), intraorbital (25 to 30 mm), intracanalicular (about 10 mm), and intracranial (about 10 mm) (Fig5) . The intracanalicular segment, which is the most frequently injured segment and requires decornpression. .will be discussed in detail. The relationship of the opticnerve within the lateral wall of the sphenoid sinus to
other important neurovascular structures is of general familiarity to the otolaryngologist (Figs 6, 7). Here, in 78%of patients, the nerve is covered by only 0.5 mm of bone;in 4%, the nerve is dehiscent into the sphenoid sinus.In contrast, in 8% of patients, the carotid artery is dehiscent within the sphenoid sinus;'?
The optic canal, formed by the two struts of the lessersphenoid wing, is approximately 10 mm long, 4 mmwide, and 5 mm high. The roof of the canal is about 1 to3 mm thick . Dorsally, the proximal opening of the canalis formed by the falciform process, a thin fold of duraoverlying the optic nerve. The anterior clinoid process,which may be pneumatized, lies anterior while the sphenoid sinus lies medial. The optic canal is wider and thinner proximally (7.07 mm) and narrower and thicker distally (4.78 mm); the medial wall is denser in its distalsegment relative to the proximal portion.P The optic foramen lies in the same horizontal meridian of the orbit asthe ethmoid roof and anterior and posterior ethmoidalforamina. The thick distal optic ring requires adequate
Bo to be remove
FIGURE 5. Intracranial, intracanalicular,and intraorbital segments of the opticnerve are shown in this illustration. Thetrochlear nerve is at increased risk ofinjury during superior or transcranialapproaches (right). Bone to be removedduring trans ethmoidal approaches isshown (left).
Sphenoidsinus
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ptic ner e
p ic canal
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FIGURE 7. Surgical relationships of the optic canal and theoptic nerve to the sphenoid sinus (S.s.) are shown in thisartist's rendition. Abbreviations: O.n., optic nerve; P, pituitarygland; Ca., internal carotid artery.
/.c.:»
Sp enoid sinus
FIGURE 6. Sagittal illustration of the relationship of the opticnerve within the lateral wall of the sphenoid sinus to thecarotid artery (Ca.) and the maxillary division of thetrigeminal nerve (VI)'
ANAND, SHERWOOD, AL-MEFTY 159
SURGICAL APPROACHES
The authors have used the following approaches for surgical decompression of the optic nerve: 1) a medial approach by external ethmoidectomy; 2) an inferomedialapproach via a transantral-transethmoidal avenue; and 3)a supraorbital-cranial approach. The lateral approachwas not used because important orbital neurovascularstructures impede access to the nerve'" (Fig 8). We have
covered.v?" Unequivocal roles for steroids and surgical decompression wiII not be resolved without controlledprospective trials.2,7,10,16 Recent research has demonstrated dose-related benefits of "megadose" methylprednisolone in acute spinal cord injury when given within 8hours of injury; these effects are not explained by themodulation of the steroid molecule interaction of glucocorticoid receptors."
All prior recommendations for steroid therapy in traumatic optic neuropathy have been based on clinical andexperimental therapy of brain and spinal cord injury.5,6Our recommendations incorporate this new informationwith previous clinical conclusions about the role and timing of steroids and optic can al decompression in treatingtraumatic optic neuropathy,2 which follow.
1. Patients with demonstrable bone or foreign bodyfragments impinging on the optic canal or optic nerveaccompanied by optic nerve dysfunction should undergooptic nerve decompression in conjunction with spinalcord injury dose (SCID) steroid therapy.
2. Surgical decompression is indicated for visual lossthat develops after injury and fails to reverse with SCIDsdoses of methylprednisolone (30 mg/kg bolus followed by54 mg/kg infusion for 23 hours).
3. Decompression is required for deterioration of visual acuity or visual fields from baseline on steroids.
4. Patients who present with visual acuity of no lightperception from time of injury should be given a trial ofSCID steroids followed by optic canal decompression ifthere is no response to SCID steroids. Patients presenting after 1 week followin9 injury should not undergooptic canal decompression. 0
Infe lororb ita lfiss ire
Superior-orbitaltis urept ic forame
PATHOPHYSIOLOGY
The merging of the dural sheath of the optic nerve withthe periorbita of the canal tethers the nerve, which ismobile intraorbitally and intracranially," accounting fornerve injuries in this segment. The intracranial segmentof the nerve seldom gets injured. Dense fibrous bands(or adhesions) throughout the subarachnoid space of theoptic nerve are especially heavy in the canal, making thisarea a natural pressure valve for CSF.15 The intracanalicular segment of the nerve receives small perforatingbranches from the ophthalmic artery in its course throughthe inferolateral canal; the superior aspect of the nerve isthe greatest distance from this supply.I" Extrinsic compressive lesions impair optic nerve function through acombination of altered CSF circulation, direct axoplasmictransport interruption, and ischemia from vascularocclusion. 15 Direct and indirect trauma subject the intracanalicular nerve to additional injury from torsional andstretch tearing, axonal shearing from bony canal fractures, and intrinsic compression from inter- and intraneuronal edema and hemorrhage." Indirect optic nerve injury (associated with closed head trauma) should be considered separately from direct injury (induced by apenetratinp foreign object or fracture of the bony canal) .Kline et al have divided indirect traumatic optic neuropathies into two types, anterior (associated with visibleocular injury) and posterior.
Posterior traumatic indirect optic neuropathy (PIlON)almost invariably involves a blow to the forehead, supraorbital rim, or malar eminence; the temporal region isoccasionall~ involved, but the parietal or occipital areasrarely are. Anderson et al5 experimentally demonstrated the force transmitted around the optic canal fromthe initial force delivered to anterior aspects of the humanskull.
decompression for surgery to be successful. However,extreme care must be taken to avoid cerebrospinal fluid(CSF) leakage into the sphenoethmoid region.
After leaving the optic chiasm, the nerve travelsthrough the intracranial subarachnoid space, where it invests in the pia mater upon entering the optic canal. Thedura mater and the periosteal layer of the optic canalcontinue anteriorly as the periorbita. The fibrous annulus of Zinn begins at the orbital apex where the pia andarachnoid fuse. The patency of the subarachnoid space ismaintained until the space fuses with the pia mater at theposterior margin of the globe. The ophthalmic artery,which provides the major blood supply, lies inferolateralto the nerve in the bony canal, eventually assuming amore medial position behind the glove. About 10 mmbehind the globe, it gives off the central retinal artery,which traverses the dural sheath obliquely to enter theoptic nerve medlally.J" Understanding the relationshipof this artery to the nerve's blood supply is essential forperforming medial decompression of the optic nerve.The trochlear nerve, which is at risk of injury during superior approaches, crosses lateral-to-medial above the optic nerve and immediately under the periorbita.
SURGICAL INDICATIONS
The role of surgery continues to evolve as informationconcerning the pathophysiology of the optic nerve is dis-
FIGURE 8. Notice the superomedial position of the opticforamen in the orbit and its proximity to the superior orbitalfissure and its contents , A lateral approach to the optic nerveis treacherous because of the presence of importantneurovascular structures in the superior orbital fissure.
160 OPTIC NERVE DECOMPRESSION
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FIGURE 9. Transcutaneous-transethrnoidal approach tooptic nerve decompression. (A) Skin incision may becurvilinear or an M-plasty to avoid longitudinal scarcontracture. (B) Following division of the medial palpebralligament, the frontal ethmoidal suture line is identified,and the anterior and posterior ethmoidal neurovascularbundles are coagulated using bipolar cautery. (C) Anethmoidectomy is performed using a microdrill to enlargethe operative field and minimize globe retraction. (D)Artist's rendition of an ethmoidectomy. Minimal globeretraction is employed. The periorbita must bemeticulously handled to avoid orbital fat herniation intothe operative field. (E) Intraoperative enhancedphotograph demonstrating the degree of left optic nervedecompression in the canal achieved by this route.Abbreviations: 0. optic nerve; 5, sphenoid; E, ethmoid; P,
periorbita; R, orbital retractor.
ANAND, SHERWOOD, AL-MEFTY 161
not found it necessary to employ the medial approachdescribed by Sofferrnan.""
APPROACH SELECTION
or osteopetrosis, the authors favor use of the supraorbitalapproach. If any intracranial injuries require surgicaltreatment (for example, evacuation of subdural or epidural hematoma), approach selection is simplified.
The advantages of an extracranial approach includeavoiding frontal lobe elevation and injury to the olfactorynerves, rapid recovery, and minimal external scars. Themedial approaches are ideal for patients with demonstrable fracture fragments impinging medially who have noother cranial injuries.
The following criteria for adequate decompressionwere outlined by Sofferman19: 1) removal of half of thecircumference of the osseous canal in its entire length,and 2) complete incision of the sheath to include thethickened annulus tendon at the orbital end.20 The extracranial approaches described satisfactorily achievethese objectives. However, when extensive decompression of the optic canal is desired, as in some circumferential stenosis of the canal observed in fibrous dysplasia
Transcutaneous-Transethmoidal ApproachSewalf" first discussed the possibility of transethmoi
dal access to the optic nerve in a procedure that has beensuccessfully used by several surgeons with acceptablerisk. The operation is performed under general anesthesia, although it can be done under local anesthesia.Avoiding general anesthesia has been advocated to allowspecific observations of visual acuity intraoperativeJr andassessment of the adequacy of decornpression.P: Aninfiltration of 1% lidocaine with 1:100,000 epinephrine ismade over the proposed site of incision. The incision ismade .5 to 1 em medial to the medial canthus of the eye,curving laterally and below the eyebrow. An M-plastyincision avoids vertical scar contracture (Fig 9A). Themedial palpebral ligament is exposed and divided after
s
FIGURE 10. Transantraltransethmoidal approach foroptic nerve decompression.(A) Operative photoshowing transantralexposure of themaxilloethmoidal recess.Note the self-retainingretractor. (B) Enhancedphoto showing emergence ofinfraorbital (1.0.)neurovascular bundle andexposure of the periorbita .(r), posterior ethmoidal (Pe),and sphenoid (s) air spaces.(C) Depiction oftransantral-transethrnoidalaccess to the inferomedialregion of the optic canal.Removing the floor of theorbit medial to theinfraorbitalnerve is requiredto achieve a satisfactoryoperative field. (D) Coronalsection of the inferomedialdirection of optic canalaccess via this route.
tl nerve
Maxill ryin s
162 OPTIC NERVE DECOMPRESSION
adequate labelling with silk sutures to facilitate the exactapproximation at the end of the procedure. The underlying periosteum of the medial wall of the orbit is thencarefully elevated. The trochlea is identified and the superior oblique muscle is carefully displaced. The globe isretracted with malleable orbital retractors. After identification of the frontoethmoidal suture line, the anteriorethmoidal vessels are coagulated using bipolar coagulation and divided. The posterior ethmoidal vessels can besimilarly managed (Fig 9B). The optic tubercle is identified about 4 to 6 mm posterior to the posterior ethmoidalforamen. Extreme care is exercised throughout to avoidinjury to the periorbita and subsequent orbital fat herniation (Fig 9C).
The operative field is enlarged through an external ethmoidectomy using a microdrill and the microscope isbrought in (Fig 90). If there is a fracture, some discoloration of bone will be noted. Decompression is performedunder magnification by removing the medial lip of theoptic foramen with a microcurette or drill (Fig 9E). Theanterior portion of the optic foramen is usually very thick.However, as the thin posterior proximal portion is encountered, drilling is frequently unnecessary. A rotatedfragment of bone may result, which requires gentle removal with a curette.
An improvement in visual acuity can be seen in patients undergoing this procedure under local anesthesia.Drainage is generally not necessary if an adequate ethmoidectomy has been performed.
Transantral-Transethmoidal ApproachThe transantral-transethmoidal approach for optic
nerve decompression was first described by Kennerdell etal24 and is an extension of Hamberger'sf' transsphenoidalapproach to the pituitary gland. A sublabial incision ismade in the gingiva, extending from the canine regionposteriorly to the molar region (Fig 10). The mucoperiosteum from the anterolateral aspect of the maxilla is elevated and the infraorbital neurovascular bundle is identified. From this point on, retraction must be careful toavoid injury to this structure. Entrance to the maxillaryantrum is gained by creating a bony window, which isenlarged to the maximal size possible, leaving a small
shell of bone around the infraorbital foramen (Fig lOA).Adequate retraction using a McCabe retractor is helpful.The microscope is brought into the field at this point.Entrance to the ethmoid is gained with a curette. Carefuldrilling is performed in the medial roof of the maxillaantrum, exposing the periorbita in the inferomedial aspect of the orbit. The bone up to the infraorbital bundlemay be removed to gain maximal exposure. The ethmoidair cells are also carefully removed (Fig lOB). The ethmoidal neurovascular bundles can be identified after theglobe is retracted; these are carefully coagulated and divided with microscissors. A biplanar image intensifierfacilitates locating the sphenoid sinus and the region of
FIGURE 11. Artist's illustration of patient's position. Thehead is elevated about 20° and the lumbar spinal needle is inplace. The neck is extended to allow the frontal lobe to fallbackward. The head is kept straight to facilitate orientation inthe suprasellar area. (Reprinted with permission.P)
.- - -
163
FIGURE 12. Artist's illustrationdemonstrating the supraorbitalapproach. The midline hole and thekeyhole are connected by a cutthrough the frontal bone using thecraniotome and through the orbital~f using a Gigli saw. (Uppertnset) The position of the keyhole.<Lower inset) Freeing the6Upraorbital nerve from its canal.«Reprinted with permission.i")
ANAND, SHERWOOD, AL·MEFTY
,
the optic foramen .. Using small curette.sand a ~icrod~lI,the optic foramen IS accessed from the intrarnedial region(Fig lOC, D) and the overlying bone is removed. Theentire length of the optic canal is .drilled in this mannerfrom an anteroposterior direction (Fig 10C). The woundis irrigated and the gingival mucosa is closed, using ab-
FIGURE 13. Operative photograph of a patient withosteopetrosis. The cranial flap is removed and the thick andhighly domed orbital roof (OR) exposed. FD, dura of thefrontal lobe.
sorbable material. In four patients in whom these approaches were used for traumatic neuropathies, two visual recoveries were observed.
Supraorbital-Cranial ApproachThe supraorbital-cranial approach to optic nerve de
compression provides direct visualization of the optic canal and nerve, allowing unroofing of the canal and widedecompression of the optic nerve both medially and laterally. It is specifically applied in patients requiring acraniotomy for any associated cranial injuries. To alleviate brain retraction, which is the main disadvantage ofthe cranial approach, we use the supraorbital approachdescribed herein.26
The patient is placed supine. A spinal needle is inserted through a split mattress and connected to a sterileconnection bag. A flow control clamp is applied to thedraining tube to avoid rapid loss of CSF. The table isadjusted so the patient's trunk and head are elevated 20°.The head is then hyperextended and fixed in a Mayfieldhead rest, allowing the frontal lobe to fall backward. Thehead is kept straight to facilitate orientation (Fig 11).
After making a bicoronal incision behind the hairline,the scalp flap is turned. The incision extends from thelevel of the zygomatic arch on the operated side to as faras the superior temporal line on the other side. The superficial temporal artery and the frontal branches of thefacial nerve are preserved through subfascial dissection.The temporalis muscle is detached from its insertion anteriorly to as far as the zygomatic arch; the muscle is thenretracted posteriorly, exposing the junction of the zygomatic, sphenoidal, and frontal bones. .
A pericranial flap is incised posteriorly, dissected forward, and reflected over the anteriorly turned scalp flap.The intact base of this pericranial flap is then dissectedfree from the roof and lateral wall of the orbit. It may benecessary to use a high-speed air drill around the supraorbital notch to free the supraorbital nerve (Fig 12,lower inset).
To begin the supraorbital approach, two bur holes aredrilled. The first , MacCarty's keyhole, is made in the
FIGURE 14. Enhanced operativephotograph. Both optic canals are widelydecompressed superiorly, medially andlaterally. The optic sheath remains to protectthe nerve. Abbreviations: II, optic nerve; D,
drill; R, retractor.
164 OPTIC NERVE DECOMPRESSION
FIGURE 16. A cr scan of limited fibrous dysplasia with opticnerve encroachment.
,
FIGURE 17. Axial cr scan and perpendicular reconstructionacross the optic canal in a patient with osteopetrosis. Noticethe sclerotic bone at the skull base and severe narrowing ofthe optic canal (arrows).
periorbita, the two membranes being separated by theroof of the orbit (Fig 12, upper inset.) The second hole ismade in the frontal bone above the nasion. To keep it assmall as possible, this hole is made with a high-speeddrill such as the Midas Rex (Fort Worth, TX). In adults,this hole will invariably pass through the anterior andposterior walls of the frontal sinus. The mucosa is exenterated, the sinus is cranialized, and the frontal duct ispacked with a small piece of temporalis muscle.
The two holes are joined by two bony cuts. The firstcut is made with a craniotome, which passes through thefrontal bone about 4 cm above the superior orbital rim asshown in Fig 12. The second cut requires the use of a
temporal fossa at the frontosphenoidal junction, just behind the zygomatic process of the frontal bone. Whenthe hole is drilled, the surgeon will see that its upper halfexposes the dura mater and its lower half exposes the
FIGURE 15. Enhanced operative photographs during theremoval of an optic sheath meningioma. (A) The tumor (T) isbeing dissected from the nerve (II). Abbreviations: c, cartoidartery; R, retractor on the frontal lobe. (B) After tumorremoval. Abbreviations: G, globe; c, carotid artery; II, opticnerve; R, retractor on the frontal lobe.
ANAND, SHERWOOD, AL-MEFTY 165
Gigli saw. With a fine bit high-speed air drill, a groove ismade from the bur hole through the medial part of thesuperior orbital rim, preserving the trochlea. This groovehelps direct the Gigli saw as it cuts through the orbitalroof. A Gigli saw guide is then passed between the twobur holes over the roof of the orbit in the epidural space.The orbital roof is cut as shown in Fig 12. This bonyincision is carried laterally and inferiorly and is continuedthrough the lateral orbital rim. During this process,the contents of the orbit are protected with a brain spatula. The surgeon should pay particular attention to keeping the periorbita intact. Injury to the supraorbital nerveand the trochlear attachment of the superior oblique muscle should be avoided. The removed and preserved craniotomy flap thus includes the superior and the upperhalf of the lateral orbital rim, the anterior portion of t~e
orbital roof, and the adjacent frontal bone.Once the cranial flap is removed, the surgeon may de
compress the optic nerve either intradurally or extradurally, depending on the lesion and the need for intraduralorientation. To minimize frontal lobe retraction, the irregular, highly domed orbital roof encountered in somediseases such as osteopetrosis is smoothed by drillingbefore opening the dura mater (Fig 13). When the duramater is opened, CSF is released, and the optic nerves areidentified. The dura mater over the optic canals is coagulated and dissected away. The thick but fragile bone ofthe optic canal is drilled away with a high-speed air drill,using the diamond bit when approaching the optic nerve(Fig 14). Decompression should be extensive and includenot only unroofing the optic canal, but also drilling awaybone on both sides of the nerve. The nerve sheathshould be kept intact. Once drilling is complete, the thinshell of bone covering and protecting the optic nervesheath is removed with a micro dissector. Both opticnerves can be decompressed during the same surgicalprocedure. If the lesion is an optic sheath meningioma,the dura propria is opened, the annulus of Zinn is longitudinally incised, and the tumor is removed through microdissection (Fig 15).
At the conclusion of the procedure, a piece of temporalfascia is applied intradurally, particularly covering anyentry into the ethmoid sinus, and the dura mater is closedwatertight. To avoid rhinorrhea, the preserved pericranial flap is turned over the frontal sinus and sutured tothe dura mater. A heavy suture is used to reattach thebone flap to the cranial vault. The temporalis muscle issutured back to the fascia at the lateral orbital rim and theskin is closed in two layers.
This technique has been used to decompress the opticnerve in 15 patients (22 nerves), including 6 patients (12nerves) with osteopetrosis-" (Fig 16), 4 patients (5 nerves)with fibrous dysplasia (Fig 17), 4 patients with optic canalmeningiomas, and 1 patient with a bony fragment in thecanal after trauma. There was no incidence of mortalityor morbidity and no patient suffered visual deterioration.Vision improved in 5 patients with osteopetrosis, 1 withfibrous dysplasia, and 1 with trauma.
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