Vertical Diplopia and Ptosis from Removal ofthe Orbital Roof in Pterional Craniotomy

Shilpa J. Desai, MD,1 Michael T. Lawton, MD,2 Michael W. McDermott, MD,2 Jonathan C. Horton, MD, PhD1,3,4

Purpose: To describe a newly recognized clinical syndrome consisting of ptosis, diplopia, vertical gazelimitation, and abduction weakness that can occur after orbital roof removal during orbito-zygomatic-pterionalcraniotomy.

Design: Case series.Participants: Eight study patients (7 women), 44 to 80 years of age, with neuro-ophthalmic symptoms after

pterional craniotomy.Methods: Case description of 8 study patients.Main Outcome Measures: Presence of ptosis, diplopia, and gaze limitation.Results: Eight patients had neuro-ophthalmic findings after pterional craniotomy for meningioma removal or

aneurysm clipping. The cardinal features were ptosis, limited elevation, and hypotropia. Three patients also hadlimitation of downgaze and 2 patients had limitation of abduction. Imaging showed loss of the fat layers thatnormally envelop the superior rectus and levator palpebrae superioris. The muscles appeared attached to thedefect in the orbital roof. Ptosis and diplopia developed in 2 patients despite Medpor titanium mesh implants.Deficits in all patients showed spontaneous improvement. In 2 patients, a levator advancement was required torepair ptosis. In 3 patients, an inferior rectus recession using an adjustable suture was performed to treat verticaldiplopia. Follow-up a mean of 6.5 years later revealed that all patients had a slight residual upgaze deficit, butalignment was orthotropic in primary gaze.

Conclusions: After pterional craniotomy, ptosis, diplopia, and vertical gaze limitation can result from teth-ering of the superior rectuselevator palpebrae superioris complex to the surgical defect in the orbital roof. Lateralrectus function sometimes is compromised by muscle attachment to the lateral orbital osteotomy. This syndromeoccurs in approximately 1% of patients after removal of the orbital roof and can be treated, if necessary, by prismglasses or surgery. Ophthalmology 2015;122:631-638 ª 2015 by the American Academy of Ophthalmology.

The development of the fronto-temporal-sphenoidalapproach has greatly facilitated neurosurgical access to le-sions around the base of the skull.1e5 It is also known as thepterional approach because it involves the conjunction of thefrontal, parietal, sphenoid, and temporal bones. In a refine-ment of the pterional approach, an orbitozygomatic crani-otomy was added to allow a more tangential approach tolesions in the anterior cranial fossa, such as aneurysms andmeningiomas.6e9 After surgery, a permanent defect oftenremains in the orbital roof, bringing orbital contents into directcontact with meningeal tissue at the base of the frontal lobe.

Over the past 15 years, we have encountered 8 patientswith a constellation of neurovisual findings that constitutea new clinical syndrome caused by orbito-zygomatic-pterional craniotomy. The patients had various combina-tions of vertical diplopia, limited upgaze, restricteddowngaze, and ptosis after neurosurgical exploration of theanterior cranial fossa. Some patients also had a horizontalcomponent to their gaze misalignment with limited abduc-tion. This article describes the neuro-ophthalmic complica-tions of pterional craniotomy involving the orbit, withemphasis on the likely mechanism, prevention, andtreatment.

� 2015 by the American Academy of OphthalmologyPublished by Elsevier Inc.

Methods

This study was approved by the University of California, SanFrancisco, Institutional Review Board and adhered to the tenets ofthe Declaration of Helsinki. The electronic patient records of a singleneuro-ophthalmologist (J.C.H.) from 1999 through 2013 weresearched to identify patients who were referred after pterionalcraniotomy for either ptosis, diplopia, or limitation of eye move-ments. Patients with a malignancy, benign tumor invading the orbit,or cranial nerve palsy were excluded. There were 8 patients whometthe search criteria (Table 1). In each case, a portion of the orbital roofhad been removed to gain better access to the anterior cranial fossaduring the pterional approach. The operative report, computed to-mography (CT) or magnetic resonance imaging (MRI), intracranialpathologic features, neurovisual examination, ocular deviation, anddegree of ptosis were reviewed. The subsequent course of treatmentwas recorded. Patients were contacted and invited to return to theclinic to document their long-term outcome.

The operative technique varied from case to case, depending onthe lesion being resected. The patient was placed supine on theoperating room table with the head stabilized in a Mayfield headholder and turned 45� to the side. A pterional skin incision wasmade with a scalpel and clips were applied to the skin edges forhemostasis. The scalp was elevated anteriorly and the superficialtemporal fascia was dissected as a free flap from the deep

631http://dx.doi.org/10.1016/j.ophtha.2014.09.011ISSN 0161-6420/14

Table 1. Summary of Patients with Neuro-ophthalmic Complications Resulting from Orbital Roof Removal During Pterional Craniotomy

PatientNo.

Age(yrs) Gender Neurosurgical Lesion Motility Deficit Primary Gaze Deviation Ptosis Follow-up/Intervention

1 55 M Anterior communicating arteryaneurysm

Right elevation &abduction

30 PD right hypotropia & 12PD right esotropia

No Left inferior rectus recession

2 69 F Right sphenoid wingmeningioma

Right elevation &depression

Orthotropia Yes Levator repair

3 58 F Right sphenoid wingmeningioma

Right elevation 20 PD right hypotropia Yes Prism glasses

4 44 F Right supraclinoid internalcarotid artery aneurysm

Right elevation &depression

Right hypotropia Yes No light perception right eye,no intervention

5 53 F Anterior communicating arteryaneurysm

Right elevation 10 PD right hypotropia Yes Right inferior rectus recession& levator repair

6 55 F Anterior communicating arteryaneurysm

Left elevation Orthotropia Yes No treatment needed

7 54 F Left middle cranial fossameningioma

Left elevation &abduction

25 PD left hypotropia & 25 PDleft esotropia

Yes Left inferior & medial rectusrecession

8 80 F Left sphenoid wing meningioma Left elevation &depression

40 PD left hypertropia Yes Monitoring

F ¼ female; M ¼ male; PD ¼ prism diopters.

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temporalis fascia to protect the facial nerve. After the zygoma andthe superior and lateral orbital rims were exposed, the periorbitawas dissected away from the inner surface of the orbital wall. Thetemporalis muscle was reflected inferiorly. A pterional craniotomywas performed with a Midas Rex drill saw (Medtronic, Minneap-olis, MN) equipped with a footplate attachment. After the bone flapwas removed, the dura was opened and tacked up circumferentiallyto the bone edge.

At this point, a series of osteotomy cuts with a reciprocatingsaw were made to release the superior and lateral orbital wall as asingle unit. These consisted of a linear, parasagittal cut in themedial orbit, a perpendicular cut in the posterior orbit extendingmediolaterally, and a cut in the lateral orbital wall from the inferiororbital fissure to the pterion (Fig 1). Additional bone was removedfrom the orbital roof as necessary using a Lempert rongeur. Theintraorbital contents were retracted from the orbital roof with amalleable retractor to guard them from injury during the saw cuts.Moist Telfa pads or cottonoid sponges were placed over the orbitaltissues for protection. The dura was opened in a curvilinear fashionover the orbital roof to provide access to the tumor or aneurysmlocated underneath the frontal lobe.

After lesion resection, the durawas closedwith running 4-0Dexonsuture. The pterional bone flap and orbital bone fragment werereplaced with hydroxyapatite cement, plates, and screws. In somepatients a Medpor titanium mesh (Stryker, Kalamazoo, MI) was usedto close the orbital roof defect. The temporalis muscle and its fasciawere reapproximated with interrupted 3-0 Dexon sutures and thegalea was closed with running 2-0 Dexon sutures. A subgaleal drainwas placed and brought out through a separate skin incision.

Results

Patient 1

Patient 1 is a 55-year-old man who underwent clipping of aruptured anterior communicating artery aneurysm. The patient re-ported vertical diplopia immediately after the operation. One yearlater, there was nearly complete absence of elevation (Fig 2). Inprimary position, there were 30 prism diopters (PD) of righthypotropia and 12 PD of right esotropia. In upgaze, there were 45PD of right hypotropia. In downgaze he could fuse. Horizontal

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gaze was full, except for slight limitation of abduction in the righteye. Surprisingly, there was no appreciable ptosis.

A 3-dimensional CT reconstruction showed a 2-cm defect in theroof of the orbit (Fig 3). An oblique CT image revealed that thesuperior rectus muscle followed an abnormal trajectory to theorbital apex. It was tented upward in mid course, where it appearedadherent to soft tissue filling the bony defect. A coronal T1-weighted MRI scan showed disruption of the superior rectus andlevator palpebrae superioris muscles (Fig 4A). The normal fatplane between the 2 muscles could not be identified. In addition,the layer of fat that usually surrounds the 2 muscles was absent. Acontrast-enhanced image confirmed that the superior rec-tuselevator palpebrae superioris complex was damaged (Fig 4B).In addition, the lateral rectus appeared displaced toward the tem-poralis muscle.

Prism glasses were prescribed but were unsatisfactory forrestoration of fusion in primary gaze. An 8-mm recession of theinferior rectus muscle was performed 16 months after the pterionalcraniotomy using an adjustable suture technique. Forced ductionsunder anesthesia just before the muscle surgery showed restrictionof elevation. After surgery, the patient was able to fuse in primarygaze.

Patient 2

Patient 2 is a 69-year-old woman with a history of vision loss in theright eye resulting from a sphenoid wing meningioma. The lesionwas resected via a right fronto-temporal-sphenoidal craniotomy.The orbital roof was removed up to the superior orbital fissureusing rongeurs. Difficulty was encountered because of theabnormal thickness of the sphenoid bone. A Midas Rex drill wasused, requiring bipolar cautery, bone wax, and Surgicel (Ethicon,Somerville, NJ) to achieve hemostasis. Although the orbital con-tents were protected with cottonoid sponges, the levator palpebraesuperioris and superior rectus muscles were damaged.

Immediately after surgery, the patient had complete right ptosisand little vertical eye movement. Ten weeks later, the ptosis wasstill complete. There was 80% elevation and 30% depression of theglobe. Six months later, the right palpebral fissure measured 5 mm.The eyelid just cleared the pupil and the patient reported nodiplopia in primary gaze. However, there was still limitation of

Figure 1. Photograph showing how pterional craniotomy (gray shading)and orbitozygomatic craniotomy (yellow shading) allow removal of 2separate bone pieces for optimal exposure of lesions in the anterior cranialfossa. Additional bone (dashed line) often is removed piecemeal from theorbital roof, leaving a defect.

Desai et al � Diplopia and Ptosis in Pterional Craniotomy

vertical ductions, with corresponding diplopia. A levator muscleadvancement was performed to correct the ptosis.

The patient was examined again 8 years after meningiomaresection. She reported diplopia only on upgaze. The ductions inthe right eye were full, except for 90% elevation with 10 PD ofhypotropia in upgaze. A coronal flair MRI scan showed directcontact between the levator palpebral superiorisesuperior rectusmuscle and the basal meninges of the frontal lobe, with peaking ofthe muscle (Fig 5A). Abnormal gadolinium enhancement of thebasal meninges was seen, which merged with the muscle complex(Fig 5B). The dark cleft representing the bony orbital roof wasabsent on the right side. The layer of adipose tissue that normallyinsulates the muscle complex from the orbital roof also was absent.

Patient 3

Patient 3 is a 58-year-old woman who underwent removal of a rightsphenoid wing meningioma via a right fronto-temporal-sphenoidal

Figure 2. Photographs of patient 1 showing limited elevation in the right ecraniotomy. There is essentially no ptosis. Horizontal gaze shows slight limitati

craniotomy. The orbital roof and lateral wall were removed to theorbital fissures using a rongeur. The optic canal then was exposedunder the operating microscope using a drill. After tumor removal,FloSeal hemostatic matrix (Baxter, Deerfield, IL) was applied to theundersurface of the frontal lobe. The defect in the orbital roof wasclosed with a titanium mesh Medpor implant.

Examination 2 months after surgery showed 5 mm of ptosis inthe right eye. There was only 50% elevation of the right eye, with20 PD of hypotropia in primary gaze. An orbital MRI scan showeddisruption of the superior rectus/levator muscles and loss of the fatlayer separating them from the Medpor implant. Four months aftersurgery, the ptosis had resolved completely. There was a persistentelevation paresis, with 7 PD of right hypotropia in primary gaze.Prism glasses were prescribed. By 5 months after surgery, thepatient had regained fusion in primary gaze without prisms.

The patient was evaluated 7.5 years after the meningiomaresection. There was still slight limitation of elevation, manifestedby 10 PD of right hypotropia on upgaze.

Patient 4

Patient 4 is a 44-year-old woman in whom vision loss developed inthe right eye from a 2.5-cm right supraclinoid internal carotid ar-tery aneurysm. The lesion was clipped via a pterional craniotomy.The optic strut was drilled out to expose the siphon of the internalcarotid artery. In addition, a superior orbitotomy was performed.Four clips were required to obliterate the aneurysm.

Immediately after the surgery, the patient had no light percep-tion in the right eye. The eyelids were closed because of periorbitaledema. Despite treatment with high doses of glucocorticoids, therewas no recovery of visual function. One month after surgery, therewere 5 mm of ptosis. Ductions showed 50% elevation and 90%depression. In primary gaze, there was a right hypotropia. A CTscan showed extensive postoperative changes, clip artifacts, and adefect in the orbital roof.

Examination 9 years later showed slightly limited elevation ofthe right globe. There were 20 PD of sensory exotropia.

Patient 5

Patient 5 is a 53-year-old woman who experienced a subarachnoidhemorrhage from a 4-mm anterior communicating artery aneu-rysm. Four days later, she underwent a right orbital-pterionalcraniotomy. A portion of the orbital roof extending back to theanterior clinoid process was removed. In addition, a small part ofthe gyrus rectus was removed to improve exposure. After the lesion

ye, with 30 prism diopters of hypotropia in primary gaze after pterionalon of abduction in the right eye, producing a small esodeviation.

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Figure 3. Images from patient 1. A, Computed tomography reconstructionrevealing right orbital roof defect. B, Oblique cut demonstrating tenting ofthe superior rectuselevator palpebrae superioris complex (white arrow). C,Corresponding image through the other orbit showing normal trajectory ofthe muscle complex (black arrow).

Figure 4. Images from patient 1. A, Coronal T1-weighted magneticresonance imaging scan showing abnormal right superior rectus and levatorpalpebrae superioris. The normal fat signal that surrounds the muscles onthe left side (white arrows) is disrupted on the right side. B, Contrast-enhanced image showing bowing of the right lateral rectus (black arrow).

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was clipped, the orbital bone was repositioned using titaniumplates and screws. The defect in the orbital roof was left open.After surgery, hydrocephalus developed that required placement ofa ventriculoperitoneal shunt.

Examination 8 months later showed 4 mm of ptosis of the righteyelid and only 50% elevation of the globe. Ocular alignment wasachieved with a 12-PD base-up prism in the right eye. An MRIexamination of the orbits showed loss of the fat signal in the su-perior orbit and alteration in the appearance of the superior rectusand levator muscles. The patient declined prism glasses. Ocularalignment was restored by performing a 5-mm recession of theinferior rectus muscle using an adjustable suture technique. The

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ptosis was repaired by advancement of the levator palpebraesuperioris.

The patient was contacted by telephone 12 years later. Shereported double vision only on extreme upgaze.

Patient 6

Patient 6 is a 55-year-old woman who experienced a subarachnoidhemorrhage from a 7-mm anterior communicating artery aneu-rysm. It was clipped by a left orbitalepterional approach, withremoval of additional bone from the back of the orbit with a ron-geur. A small portion of the left gyrus rectus was sacrificed toimprove exposure of the base of the aneurysm. After the aneurysmwas clipped, the bone flap and orbital osteotomy were replacedusing cement plates and screws, without closure of the defect in theorbital roof.

Examination 2 months after surgery revealed 1 to 2 mm ofptosis of the left upper eyelid. Ductions were intact except eleva-tion, which showed only 90% of the normal range. Alignment wasorthotropic in primary gaze, but a small left hypotropia developedin upgaze. No treatment was necessary. The only neuroimagingavailable after surgery was an axial CT scan obtained on the firstpostoperative day. The orbital images were not of adequate qualityto determine the cause of her elevation deficit.

A follow-up examination 12 years later showed persistence of asmall elevation deficit in the left eye with vertical diplopia onextreme upgaze.

Patient 7

Patient 7 is a 54-year-old woman who experienced slowly pro-gressive vision loss in the left eye. An MRI scan showed a large

Figure 5. Images from patient 2. A, Coronal flair magnetic resonanceimaging scan obtained 8 years after surgery showing direct contact betweenthe right superior rectuselevator palpebrae superioris complex and thebasal meninges of the frontal lobe, with peaking of the muscle complex(white arrow). Note abnormal bright signal in frontal white matter frombrain retraction during pterional craniotomy. B, Postgadolinium imageshowing abnormal enhancement of the basal meninges (black arrowheads),which is contiguous with the superior rectuselevator complex. On thenormal side, the dark contour representing the orbital roof is intact (whitearrowheads), along with the fat cushion between the orbital roof andmuscle complex.

Figure 6. Images from patient 8. A, Computed tomography scan showingsaw cut (black arrow) in the left orbital roof with incarcerated soft tissuethat appears to draw upward the superior rectuselevator palpebrae supe-rioris complex (see insets comparing normal and altered sides). B, A moreposterior cut, showing a vertically distorted superior rectuselevatorcomplex. The roof defect has been closed with a Medpor implant (whitearrows), but incompletely.

Desai et al � Diplopia and Ptosis in Pterional Craniotomy

sphenoid wing meningioma compressing the left optic nerve. Sheunderwent a left pterional craniotomy with removal of the lateraland superior orbital walls. The orbital roof was left open afterclosure of the craniotomy.

Examination 6 weeks after surgery showed a left frontalismuscle palsy, 50% elevation deficit, and a nearly total abductiondeficit. In primary gaze, there were 25 PD of left hypotropia and 25PD of left esotropia. An MRI examination showed a large defect inthe left orbital roof and postoperative changes in the appearance ofthe lateral rectus and the levator palpebrae superioris and superiorrectus muscles.

One year after removal of the meningioma, the patient under-went an 8-mm recession of the inferior rectus muscle and an 8-mmrecession of the medial rectus muscle to correct her diplopia. Anadjustable suture technique was used for both muscles. She couldnot be reached to obtain follow-up information.

Patient 8

Patient 8 is an 80-year-old woman who reported gradual proptosisof the left eye. An MRI scan showed a left sphenoid wing me-ningioma. It was resected via a left pterional craniotomy with afrontozygomatic and supraorbital osteotomy. After tumor removal,the orbital roof defect was reconstructed with a titanium meshMedpor implant.

The day after surgery, the patient reported vertical doublevision. There was eyelid swelling with ptosis. Globe elevation wasreduced slightly and depression was absent. Forced ductionsshowed restriction of depression. There were 40 PD of lefthypertropia in primary gaze. A CT scan obtained 2 days aftersurgery showed air in the left orbit (Fig 6A). There was soft tissueincarcerated in the supraorbital bone incision, with the levatorpalpebrae superioris and superior rectus muscles pulled upward. Amore posterior cut (Fig 6B) showed the Medpor implant, withvertical distortion of the muscles. Three months after surgery, therewas a persistent depression deficit with a left hypertropiameasuring 10 PD.

Discussion

The pterional approach has undergone numerous modifica-tions to improve access to the sellar region and the anteriorcranial fossa.8 The most critical advance has been the dis-covery that temporary removal of the superior and lateralwalls of the orbit can reduce the brain retraction required forexposure of lesions, such as sphenoid wing meningiomasand circle of Willis aneurysms.9 Violation of the orbit,however, carries the risk of disturbing eyelid function, globemotility, and ocular alignment. We report 8 patients withneurovisual symptoms that occurred immediately afterpterional craniotomy. All but 1 patient had ptosis,

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presumably from compromise of the levator palpebraesuperioris. Every patient had limitation of globe elevation,most with a corresponding hypotropia. The mechanism isuncertain, but imaging showed attachment of the superiorrectus to the defect in the orbital roof (Figs 3e6). We pro-pose that adhesion of the muscle to the orbital roof mayreduce its ability to rotate the globe in a manner similar tothe action of a posterior fixation suture.10 Physical injuryduring surgery also may cause paresis of the superior rectusmuscle. Three patients also displayed restricted globedepression. In these individuals, scarring of the superiorrectus may have restricted downward eye rotation. Inaddition, 2 patients had limited abduction with esotropia. Inthese cases, removal of the lateral orbital wall seemed tocause adhesion of the lateral rectus muscle (Fig 3).

Kaeser and Klainguti11 were the first to recognize theproblem of vertical diplopia resulting from pterional crani-otomy. They described a single patient with upgaze limita-tion and corresponding hypotropia, with adhesion of thesuperior rectus and levator palpebrae to the orbital roofdefect. In the neurosurgery literature, a review of 75 patientswho underwent pterional surgery identified 2 cases (2.6%)of extraocular muscle restriction and 3 cases (4.0%) ofptosis.12 The true rate of neuro-ophthalmic complicationsafter pterional craniotomy is difficult to estimate. Weencountered 8 patients with diplopia and ptosis over a15-year period, during which 980 pterional craniotomieswith orbital takedown were performed by 2 neurosurgeons.This corresponds to a 0.81% rate of neurovisual complica-tions but does not include patients whose symptomsresolved before referral to our clinic or who were evaluatedelsewhere.

Restriction or paresis of eye muscles are commonsequelae after any event that results in fracture of an orbitalwall. The most common cause is a blowout fracture of theorbital floor or medial wall resulting from blunttrauma.13e16 Diplopia may occur from muscle entrapment,neuromuscular trauma, or extraocular muscle scarring.Kushner17 emphasized that the vertically acting muscle canshow either restriction or paresis. In surgical decompressionfor thyroid eye disease, bony apertures are left deliberatelyin the orbital walls. Diplopia and gaze limitation occur in2% to 43% of cases.18e25 Vertical diplopia and ptosis havebeen reported in patients with fibrous dysplasia afterremoval of the orbital roof and lateral wall.26,27 Diplopiaalso has been described in patients undergoing medial andsuperior orbital periosteum removal for frontal sinus, ante-rior skull base, and craniofacial procedures.28,29 In suchcases, diplopia is believed to result from tethering of thesuperior oblique tendon or malposition of the trochlea.Finally, postoperative diplopia has been reported afterbreach of the orbital wall during endoscopic paranasal sinussurgery.30e32

Although Yasargil8 was among the first to remove theorbital roof to improve exposure, he later discarded thisstrategy after he recognized the risk of postoperativediplopia. Removal of bone has the advantage of reducingthe amount of frontal lobe retraction required to expose alesion during neurosurgery.33 Even with bone removal,some patients show persistent frontal lobe imaging

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abnormalities from retraction (Fig 5A). The gyrus rectus canbe removed to gain better exposure, but one must balancethe loss of brain tissue against the risks posed by removal ofthe orbital roof.34e37 It is likely that orbital roof removalwill remain a necessary tactic for some pterional operations.Therefore, it is important to devise methods to minimizepostoperative diplopia and ptosis. When possible, the orbitalperiosteum should be left intact to create a barrier betweenthe dura mater and the orbital contents. In a recent study oforbital decompression in thyroid eye disease, Mainville andJordan38 reported only an 11.8% rate of diplopia when theperiorbita was left intact, compared with a 40.0% rate whenit was violated. The orbital fat overlaying the superior rec-tuselevator complex should be disturbed as little aspossible. Animal models have confirmed that changes in fatlocalization and subsequent tethering of tissues can lead toextraocular movement dysfunction.39,40

After the orbital bone fragment is removed, additionalroof often is resected using a rongeur. This technique shouldbe used sparingly to minimize the orbital roof defect.Extraocular muscles have a natural tendency to adhere todura mater because it is histologically identical to sclera. Infact, extraocular muscle flaps have been exploited to repairbony orbital defects.41 By limiting the size of the bonydefect, one may reduce the risk of muscle adhesion to theorbital roof and frontal meninges.

An implant is sometimes used to close orbital wall de-fects, although it is not proven that leaving a defect openresults in a higher incidence of diplopia. Implants have beenconstructed from a wide variety of materials, includingautologous bone, cartilage, dura mater, hydroxyapatite, ti-tanium mesh, polydioxanone, polyethylene, polytetra-fluoroethylene, nylon, glass, silastic rubber, and polyester.42

Porous implants become incorporated into surrounding tis-sues, which seems to reduce the rate of extrusion, migration,and fibrous encapsulation.43,44 However, which material isoptimal for orbital wall reconstruction remains unclear. Twopatients in our series demonstrated ptosis and diplopia,despite repair with a Medpor titanium mesh implant.

In all 8 cases, ptosis and limited ductions improved in themonths after surgery. Prism glasses were prescribed toalleviate diplopia. Surgical correction of ptosis or diplopiawas necessary in half the patients. Rather than operating tofree the adherent superior rectus muscle, we performedinferior rectus muscle recession using an adjustable suturetechnique. Ptosis was repaired by advancement of the le-vator palpebrae superioris. Normal function can be achievedfor patients in primary gaze, but follow-up data collected amean of 6.5 years after surgery revealed slight limitation ofglobe elevation or depression in every patient.

References

1. Scholz M, Parvin R, Thissen J, et al. Skull base approaches inneurosurgery. Head Neck Oncol [serial online] 2010;2:16.Available at: http://www.headandneckoncology.org/content/2/1/16. Accessed September 8, 2014.

2. Wen DY, Heros RC. Surgical approaches to the brain stem.Neurosurg Clin N Am 1993;4:457–68.

Desai et al � Diplopia and Ptosis in Pterional Craniotomy

3. Marchal JC, Civit T. Neurosurgical concepts and approachesfor orbital tumours. Adv Tech Stand Neurosurg 2006;31:73–117.

4. Madhugiri VS, Ambekar S, Pandey P, et al. The pterional andsuprabrow approaches for aneurysm surgery: a systematic re-view of intraoperative rupture rates in 9488 aneurysms. WorldNeurosurg 2013;80:836–44.

5. Yasargil MG, Fox JL, Ray MW. The operative approach toaneurysms of the anterior communicating artery. Adv TechStand Neurosurg 1975;2:113–70.

6. McDermott MW, Durity FA, Rootman J, Woodhurst WB.Combined frontotemporal-orbitozygomatic approach for tu-mors of the sphenoid wing and orbit. Neurosurgery 1990;26:107–16.

7. Seckin H, Avci E, Uluc K, et al. The work horse of skull basesurgery: orbitozygomatic approach. Technique, modifications,and applications. Neurosurg Focus 2008;25:E4.

8. Altay T, Couldwell WT. The frontotemporal (pterional)approach: an historical perspective. Neurosurgery 2012;71:481–91. discussion 491e2.

9. Yasargil MG, Fox JL. The microsurgical approach to intra-cranial aneurysms. Surg Neurol 1975;3:7–14.

10. Buckley EG, Meekins BB. Faden operation for the manage-ment of complicated incomitant vertical strabismus. Am JOphthalmol 1988;105:304–12.

11. Kaeser PF, Klainguti G. Management of diplopia secondary toneurosurgical injury of the orbital roof. Klin Monbl Augen-heilkd 2008;225:507–9.

12. Youssef AS, Willard L, Downes A, et al. The frontotemporal-orbitozygomatic approach: reconstructive technique andoutcome. Acta Neurochir (Wien) 2012;154:1275–83.

13. Thiagarajah C, Kersten RC. Medial wall fracture: an update.Craniomaxillofac Trauma Reconstr 2009;2:135–9.

14. Kum C, McCulley TJ, Yoon MK, Hwang TN. Adult orbitaltrapdoor fracture. Ophthal Plast Reconstr Surg 2009;25:486–7.

15. Loba P, Kozakiewicz M, Nowakowska O, et al. Managementof persistent diplopia after surgical repair of orbital fractures.J AAPOS 2012;16:548–53.

16. Gosse EM, Ferguson AW, Lymburn EG, et al. Blow-outfractures: patterns of ocular motility and effect of surgicalrepair. Br J Oral Maxillofac Surg 2010;48:40–3.

17. Kushner BJ. Paresis and restriction of the inferior rectusmuscle after orbital floor fracture. Am J Ophthalmol 1982;94:81–6.

18. Siracuse-Lee DE, Kazim M. Orbital decompression: currentconcepts. Curr Opin Ophthalmol 2002;13:310–6.

19. Mehta P, Durrani OM. Outcome of deep lateral wall rim-sparing orbital decompression in thyroid-associated orbitop-athy: a new technique and results of a case series. Orbit2011;30:265–8.

20. Clauser LC, Galie M, Tieghi R, Carinci F. Endocrine orbit-opathy: 11 years retrospective study and review of 102 pa-tients & 196 orbits. J Craniomaxillofac Surg 2012;40:134–41.

21. O’Malley MR, Meyer DR. Transconjunctival fat removalcombined with conservative medial wall/floor orbital decom-pression for Graves orbitopathy. Ophthal Plast Reconstr Surg2009;25:206–10.

22. McNab AA. Extracranial orbital decompression for opticneuropathy in Graves’ eye disease. J Clin Neurosci 1998;5:186–92.

23. West M, Stranc M. Long-term results of four-wall orbitaldecompression for Graves’ ophthalmopathy. Br J Plast Surg1997;50:507–16.

24. Roberts CJ, Murphy MF, Adams GG, Lund VJ. Strabismusfollowing endoscopic orbital decompression for thyroid eyedisease. Strabismus 2003;11:163–71.

25. Paridaens D, Hans K, van Buitenen S, Mourits MP. Theincidence of diplopia following coronal and translid orbitaldecompression in Graves’ orbitopathy. Eye (Lond) 1998;12:800–5.

26. Goisis M, Biglioli F, Guareschi M, et al. Fibrous dysplasia ofthe orbital region: current clinical perspectives in ophthal-mology and cranio-maxillofacial surgery. Ophthal PlastReconstr Surg 2006;22:383–7.

27. Moore AT, Buncic JR, Munro IR. Fibrous dysplasia of theorbit in childhood. Clinical features and management.Ophthalmology 1985;92:12–20.

28. Trobe JD, Tao AH, Schuster JJ. Perichiasmal tumors: diag-nostic and prognostic features. Neurosurgery 1984;15:391–9.

29. Bartley J, Eagleton N, Rosser P, Al-Ali S. Superior obliquemuscle palsy after frontal sinus mini-trephine. Am J Otolar-yngol 2012;33:181–3.

30. Bhatti MT, Schmalfuss IM, Mancuso AA. Orbital complica-tions of functional endoscopic sinus surgery: MR and CTfindings. Clin Radiol 2005;60:894–904.

31. Eitzen JP, Elsas FJ. Strabismus following endoscopic intra-nasal sinus surgery. J Pediatr Ophthalmol Strabismus 1991;28:168–70.

32. Thacker NM, Velez FG, Demer JL, Rosenbaum AL. Stra-bismic complications following endoscopic sinus surgery:diagnosis and surgical management. J AAPOS 2004;8:488–94.

33. Chi JH, Parsa AT, Berger MS, et al. Extended bifrontalcraniotomy for midline anterior fossa meningiomas: minimi-zation of retraction-related edema and surgical outcomes.Neurosurgery 2006;59(suppl):ONS426–33. discussionONS433e4.

34. Hyun SJ, Hong SC, Kim JS. Side selection of the pterionalapproach for superiorly projecting anterior communicatingartery aneurysms. J Clin Neurosci 2010;17:592–6.

35. Inci S, Ozgen T. Multiple aneurysms of the anterior commu-nicating artery: radiological and surgical difficulties.J Neurosurg 2005;102:495–502.

36. Kashimura H, Kubo Y, Ogasawara K, et al. Easy dissection ofthe interhemispheric fissure for treatment of the anteriorcommunicating artery aneurysm by the pterional approach.World Neurosurg 2010;73:688–90.

37. Horikoshi T, Nukui H,Mitsuka S, KanekoM. Partial resection ofthe gyrus rectus in pterional approach to anterior communicatingartery aneurysms. Neurol Med Chir (Tokyo) 1992;32:136–9.

38. Mainville NP, Jordan DR. Effect of orbital decompression ondiplopia in thyroid-related orbitopathy. Ophthal Plast ReconstrSurg 2014;30:137–40.

39. Kerr NC. Fat adherence syndrome: an animal model.J AAPOS 2004;8:349–56.

40. Brooks SE, Yu JC, Preston D, Johnson MH. Restricted ocularmotility after orbital traumadstudies with an animal model.J AAPOS 1998;2:246–52.

41. Bartley GB, Kasperbauer JL. Use of a flap of extraocularmuscle and fat during subtotal exenteration to repair bonyorbital defects. Am J Ophthalmol 2002;134:787–8.

42. Avashia YJ, Sastry A, Fan KL, et al. Materials used forreconstruction after orbital floor fracture. J Craniofac Surg2012;23(suppl):1991–7.

43. Aldekhayel S, Aljaaly H, Fouda-Neel O, et al. Evolving trendsin the management of orbital floor fractures. J Craniofac Surg2014;25:258–61.

44. Bratton EM, Durairaj VD. Orbital implants for fracture repair.Curr Opin Ophthalmol 2011;22:400–6.

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Ophthalmology Volume 122, Number 3, March 2015

Footnotes and Financial Disclosures

Originally received: June 14, 2014.Final revision: July 29, 2014.Accepted: September 8, 2014.Available online: November 3, 2014. Manuscript no. 2014-932.1 Department of Ophthalmology, University of California, San Francisco,San Francisco, California.2 Department of Neurosurgery, University of California, San Francisco, SanFrancisco, California.3 Department of Neurology, University of California, San Francisco, SanFrancisco, California.4 Department of Physiology, University of California, San Francisco, SanFrancisco, California.

Financial Disclosure(s):

The author(s) have no proprietary or commercial interest in any materialsdiscussed in this article.

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Supported by the National Eye Institute (grants EY10217 and EY02162),National Institutes of Health, Bethesda, Maryland, and Research to PreventBlindness, Inc., New York, New York.

Abbreviations and Acronyms:CT ¼ computed tomography; MRI ¼ magnetic resonance imaging;PD ¼ prism diopters.

Correspondence:Jonathan C. Horton, MD, PhD, Beckman Vision Center, University ofCalifornia, San Francisco, 10 Koret Way, San Francisco, CA 94143-0730.E-mail: hortonj@vision.ucsf.edu.