Endoscopic decompression of the optic nerve in pseudotumor cerebri

Endoscopic decompression of the optic nerve in pseudotumor cerebri

Auris Nasus Larynx 32 (2005) 199–203 www.elsevier.com/locate/anl Endoscopic decompression of the optic nerve in pseudotumor cerebri Jose´ Antoˆnio Pa...

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Auris Nasus Larynx 32 (2005) 199–203 www.elsevier.com/locate/anl

Endoscopic decompression of the optic nerve in pseudotumor cerebri Jose´ Antoˆnio Patrocı´nio a, Lucas Gomes Patrocı´nio a,*, Facundo Burgos Ruiz Ju´nior b, Andre´ Rodrigues da Cunha c a

Department of Otorhinolaryngology, Medical School, Federal University of Uberlaˆndia, Rua 15 de Novembro, 327-apt. 1600, Uberlaˆndia, MG, Brazil 38400-214 b Department of Neurology, Medical School, Federal University of Uberlaˆndia, Uberlaˆndia, Brazil c Ocular Health Institute, Uberlaˆndia, Brazil Received 14 September 2004; received in revised form 17 January 2005; accepted 21 January 2005 Available online 23 March 2005

Abstract Pseudotumor cerebri is a neurological condition in which patients develop headaches and visual loss that may not be successfully treated with medication. In these cases surgery is indicated, and decompression of the optic nerve is the preferred surgical procedure. We report a case of decompression of the optic nerve performed through an endonasal endoscopic approach in a patient with pseudotumor cerebri where enhancement of visual acuity was successful. To our knowledge, no previous investigators have reported this approach to treat pseudotumor cerebri. # 2005 Elsevier Ireland Ltd. All rights reserved. Keywords: Pseudotumor cerebri; Surgical decompression; Optic nerve; Endoscopy

1. Introduction Pseudotumor cerebri (PTC), also referred to as idiopathic intracranial hypertension, is characterized by increased intracranial pressure that is not secondary to a spaceoccupying lesion and is accompanied by a normal or small ventricular system, normal neuroimaging, normal composition of cerebrospinal fluid (CSF), and no focal neurologic signs, with the exception of a possible sixth-nerve palsy. Common symptoms include headaches, transient obscurings of vision, intracranial noises and, rarely, diplopia. Medical treatment-strategies include weight loss, serial lumbar puncture, corticosteroids, and diuretics. When visual loss or headaches progress despite maximum medical treatment, surgical therapy should be considered. Recent reports advocate optic nerve decompression (OND) as the preferred treatment [1–4]. Several approaches such as lateral orbitotomy [2], medial orbitotomy [1], and transconjunctival [3,4] procedures have been reported to have comparable effectiveness. Until recently, no * Corresponding author. Tel.: +55 34 3215 1143; fax: +55 34 3215 1143. E-mail address: [email protected] (L.G. Patrocı´nio).

attention has been given in the literature to an endonasal endoscopic approach to OND in PTC. We report a case of OND performed through an endonasal endoscopic approach in a patient with PTC, where enhancement of visual acuity was successfully accomplished.

2. Case report Patient MM, 18 years old, female, Caucasian, from Central Minas Gerais, Brazil, was sent to our service with a diagnosis of PTC. She was treated with corticosteroids and diuretics for 1 year with no improvement. She complained of chronic, severe daily headache and bilateral, progressive visual impairment, more pronounced in the right eye (OD) than in the left eye (OS). Ophthalmologic evaluation showed: visual acuity: 20/50 OD, 20/20 OS; fundoscopy: high-grade papilledema in both eyes; automated perimetry: OD—moderate diminution of retinal sensitivity in the nasal (superior and inferior) and temporal (superior) peripheries; OS—moderate diminution of retinal sensitivity in the superior temporal periphery (Fig. 1). Further examination showed no further alterations.

0385-8146/$ – see front matter # 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.anl.2005.01.014

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Fig. 1. Automated perimetry showing improvement in visual fields following endonasal endoscopic optic nerve decompression. Top left: preoperative, right eye; bottom left: preoperative, left eye; top right: postoperative, right eye; bottom left: postoperative, left eye.

Decompression of the optic nerve was performed in the right eye under general anesthesia. The nasal cavity was prepared with cottonoids soaked with 2% lidocaine with 1:1000 epinephrine. Ten minutes later, 5 ml of 0.5% bupivacaine with 1:100,000 epinephrine was slowly injected into the lateral nasal wall, in a fashion similar to that used during endoscopic total sphenoethmoidectomy. The patient was positioned as if for conventional functional endoscopic sinus surgery, and the right eye was not taped, to permit intraoperative examination of the pupil and palpation of the globe. The operation was performed using a 4 mm 08 telescope. An endoscopic sphenoethmoidectomy was performed using the Messerklinger and Stammberger technique with preservation of the middle turbinate. The sphenoid sinus was entered, and a circular cutting sphenoid punch was used to enlarge the opening. The bulge of the internal carotid artery and the optic nerve was identified. At a distance of 1 mm anterior to the optic tubercle, the lamina papyracea was removed with no injury to the periorbita. Removal of the thick bone at the optic canal was accomplished with a Kerrison forceps and a diamond bur. Bony decompression resulted in a 1808 liberation of the optic nerve on its medial and inferior aspects, from the optic tubercle to near the optic chiasm (Fig. 2). The optic nerve sheath was not incised. Bleeding was minimal during the procedure, and therefore

nasal packing was not necessary. A short course of high-dose steroids was given to decrease postoperative edema. Otorhinolaryngological follow-up was performed for 6 months with no complications. A new ophthalmologic evaluation, 6 months after the surgery, showed: visual acuity: 20/25 OD, 20/20 OS; fundoscopy: OD—no papilledema; OS—mild papilledema; automated perimetry: OD—mild diminution of retinal sensitivity in the nasal (superior and inferior) and temporal (superior) peripheries, suggesting an isopteral contraction; OS—superiorly enlarged blind spot (Fig. 1). Further examination showed no further alterations. Patient’s headaches had lessened dramatically, and she had no complaints at the last evaluation.

3. Discussion Decompression of the optic nerve was first reported in 1911 by Kronlein, who used the lateral orbitotomy approach. In 1916, Pringle described OND via a craniotomy approach [6]. Decompression of the nerve medially through the lateral wall of the ethmoid and sphenoid sinus was originally described by Sewall in 1926 and was developed by Niho et al. in the 1960s [7]. A transantral ethmoid access to the medial optic canal has been reported by Kennerdell

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Fig. 2. Schematic drawing of the steps involved in endonasal endoscopic optic nerve decompression. (a) Anterior ethmoidectomy, (b) posterior ethmoidectomy, (c) sphenoidotomy, (d) removal of anterior wall of the sphenoid sinus (S) using a punch forceps (arrow), and (e) optic nerve (ON) decompression using a diamond burr (B) (adapted, with permission, from [5]).

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Fig. 3. Computed tomography showing the optic nerve (arrows) exposed in the sphenoid sinus bilaterally.

et al. [8]. Takahashi et al. reported success using a microscopic endonasal approach to OND [9]. Endoscopic OND is probably the most often indicated approach when surgical intervention is needed. The endoscopic technique offers several advantages over other surgical approaches, as it provides excellent visualization of the surgical site and avoids the morbidity associated with intracranial and external extracranial approaches. Recently, some authors have demonstrated its advantages (decreased morbidity, preservation of olfaction, rapid recovery time, no external scars, less operative stress) and efficacy in treating traumatic optic neuropathy [10–12]. We could not find any report of endonasal endoscopic OND for PTC. The pathophysiology of this disorder is unclear. A relative resistance to the absorption of cerebrospinal fluid across the arachnoid villi is widely presumed to be present. Other theories support an abnormality in the cerebral circulation with a resulting increase in the brain’s water content. The subsequent increase in the intracranial pressure is transmitted to the structures within the intracranial cavity, including the optic nerves [13–14]. In the present case, we performed OND in the right eye of a patient with PTC through an endoscopic approach. Six months after the surgery her visual acuity and visual field had returned to normal; this was associated with a marked improvement in papilledema. Headaches had clinically disappeared. There were no complications. These data are comparable to those in previously published studies by other authors who used different surgical approaches (intracranial or extracranial external), especially comparable in relation to visual improvement and resolution of papilledema [1–4]. Slitting and/or fenestration of the optic nerve are controversial procedures for which there are no studies to indicate proper patient-selection [10]. We preferred not to perform it. The mechanism by which OND improves visual function is also debated. Seif and Shah [15], Davidson [13], and

Keltner [14] suggest that obliteration of the subarachnoid space surrounding the optic nerve by fibroblast proliferation prevents CSF pressure distal to the operative site. On the other hand, after histologic and ultrasonic examination, Tsai et al. [16] postulate CSF filtration through a fibrotic bleb. Surgery in one eye will often benefit the other eye. This contralateral effect has been hypothesized to be due filtration of CSF through the posterior orbit and chiasm [14]. Seif and Shah [15] demonstrated with a biomechanical model that such mechanism has validity. Relief of headache due to increased intracranial pressure following OND has been reported by some authors, but is variable and the matter remains unsettled to date [1–4,13–15]. If a patient’s primary problem is headache, then a lumboperitoneal shunt should be performed. Decompression of the optic nerve via an endonasal endoscopic approach may be an useful surgical treatment to reverse and prevent visual deterioration in PTC. Therefore, we believe that this approach merits consideration by surgeons. Caution should be taken to avoid iatrogenic injury to the ophthalmic artery or to the optic nerve itself (specially when it is dehiscent, as shown in Fig. 3), resulting in additional damage. Thus, we believe this procedure should only be undertaken by most experienced endoscopists. When a patient faces visual loss, efforts by a team of sub-specialists are most likely to yield optimal results [17].

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J.A. Patrocı´nio et al. / Auris Nasus Larynx 32 (2005) 199–203 [11] De Ganseman A, Lasudry J, Choufani G, Daele J, Hassid S. Intranasal endoscopic surgery in traumatic optic neuropathy—the Belgian experience. Acta Otorhinolaryngol Belg 2000;54(2):175–7. [12] Kountakis SE, Maillard AA, El-Harazi SM, Longhini L, Urso RG. Endoscopic optic nerve decompression for traumatic blindness. Otolaryngol Head Neck Surg 2000;123(1 Pt 1):34–7. [13] Davidson SI. A surgical approach to pleocephalic disc oedema. Trans Ophthalmol Soc UK 1970;89:669–90. [14] Keltner JL. Optic nerve sheath decompression: how does it work? Has its time come?. Arch Ophthalmol 1988;106:1365–9.

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