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Show LETTERS TO THE EDITOR Delayed Third Cranial Nerve Palsy After Aneurysm Wrapping Third cranial nerve palsy after aneurysm wrapping may be caused by damage to the nerve during surgical dissection, perianeurysmal inflammation related to the cotton used to wrap the aneurysm, or, if fibrin glue is also used, adherence of the wrapping material to the nerve. In almost all cases, the palsy occurs immediately after surgery. We recently examined a 64-year-old woman who developed a third cranial nerve palsy on the side where, nearly 1 year earlier, she had undergone clipping of a 14-mm aneurysm located at the junction of the internal carotid and posterior communicating arteries. At the time of surgery, a small residual area at the aneurysm base had to be wrapped with cotton and secured with fibrin glue. Intraoperative angiography had confirmed almost complete obliteration of the aneurysm. Postopera-tively, the patient had no neurologic or visual deficits. During the year after surgery, she experienced two brief episodes in which, when looking in a mirror, she noticed that her left pupil was dilated. She never had double vision or drooping of her left upper lid at that time. Eleven months after surgery, the patient sustained moderate trauma to her left orbit after she slipped while pushing a metal dolly and struck her head against the handle. She did not lose consciousness or sustain any facial lacerations, but she did develop significant swelling and bruising of the left orbit and face. As the facial swelling resolved during the next month, she noticed binocular double vision and was found to have a partial left third cranial nerve palsy that became complete over the next 5 months. MRI and catheter angiography showed no changes from previous intra-operative imaging, but a lumbar puncture showed an increased protein concentration of 98 mg/dL. The patient was treated with 1 g of intravenous methylprednisolone per day for 3 days, followed by 60 mg of prednisone per day. Two weeks after treatment was started, the patient's third cranial nerve palsy began to improve and continued to improve until the patient stopped treatment because of side effects. Two other cases of delayed third cranial nerve palsy after aneurysm wrapping have been reported (1,2). Onoue et al (1) described a patient who developed a third cranial nerve palsy 6 months after muslin wrapping of an aneurysm located at the junction of the ipsilateral internal carotid and anterior choroidal arteries. Craniotomy disclosed a mass consisting of soft granulomatous tissue mixed with calcified material. Microscopic examination revealed filamentous foreign material and reactive giant cells consistent with a foreign body granuloma. The third cranial nerve palsy resolved several weeks after surgery. Chambi et al (2) described a 71-year-old woman who developed a progressive third cranial nerve palsy 19 months after clipping and wrapping of an aneurysm at the junction of the ipsilateral internal carotid and posterior communi-cating arteries (2). No treatment was offered. Despite partial improvement in ptosis over the next year, palsy of the superior, medial, and inferior rectus muscles was still present 4 years later. We believe that in our patient the combination of wrapping material and fibrin glue resulted in slight adhesion of the aneurysm to the superior aspect of the third cranial nerve that was then exacerbated by the head trauma. Whatever the mechanism, our patient illustrates the fact that such delayed postoperative complications can occur many months after otherwise uncomplicated aneu-rysm treatment, particularly when clipping and wrapping are used. Corticosteroid treatment may be effective. Zina Evy Almer, MD Neil R. Miller, MD The Wilmer Eye Institute Johns Hopkins University Baltimore, Maryland nrmiller@jhmi.edu REFERENCES 1. Onoue H, Abe T, Tashibu K, et al. Two undesirable results of wrapping of an intracranial aneurysm. Neurosurg Rev 1992;15:307-9. 2. Chambi I, Tasker RR, Gentili F, et al. Gauze-induced granuloma (‘‘gauzoma''): an uncommon complication of gauze reinforcement of berry aneurysms. J Neurosurg 1990;72:163-70. Anticholinergic Esotropia In this journal, Oh and Shin (1) recently described a patient who developed esotropia and mydriasis 7 days after beginning treatment with haloperidol and benztropine mesylate. They attributed the esotropia to convergence caused by the excessive accommodative effort required to overcome the anticholinergic effects of these medications. Another case of anticholinergic esotropia has just been reported in a 5-year-old girl taking oxybutynin (Ditropan) for enuresis (2). We recently examined a patient whose clinical history casts further light on this phenomenon. J Neuro-Ophthalmol, Vol. 28, No. 4, 2008 359 J Neuro-Ophthalmol, Vol. 28, No. 4, 2008 Letters to the Editor A 29-year-old woman presented with a 1-month his-tory of horizontal diplopia. She had had esotropia in early childhood that gradually evolved into a consecutive exotropia. She also had a history of schizophrenia, depres-sion, and anxiety and was being treated for these condi-tions with escitalopram (Lexapro), benztropine mesylate (Cogentin), quetiapine (Seroquel), aripiprazole (Abilify), hydroxyzine pamoate (Vistaril), cyclobenzaprine (Flexeril), and lamotrigine (Lamictal). She had asthma and used an albuterol inhaler. Ophthalmologic examination revealed a distance vi-sual acuity of 20/30 in the right eye and 20/25 in the left eye. Pupils measured 6 mm bilaterally in dim illumination and reacted sluggishly to direct light, constricting only to 5 mm. Dynamic retinoscopy showed decreased accommodation bilaterally. Horizontal optokinetic testing showed asymmet-rical monocular responses that were greater nasally than temporally, indicating ocular misalignment within the first year of life. Prism and alternate cover testing showed an esotropia of 20 prism-diopters when fixating on a distance target and 45 prism-diopters when fixating on a near target. Cycloplegic refraction showed no significant refractive error. She had no latent nystagmus, dissociated vertical deviation, or cross fixation. Extraocular movements were full with 1+ inferior oblique muscle overaction bilaterally. Anterior and posterior segment examinations were normal. We informed the patient that she would probably require strabismus surgery. However, we suspected that the anticholinergic medication might be contributing to the esotropia, especially benztropine mesylate, hydroxyzine pamoate, and cyclobenzaprine. We discussed the issue of overmedication with her psychiatrist, who elected to dis-continue her quetiapine, lamotrigine, cyclobenzaprine, aripiprazole, and hydroxyzine pamoate. The dose of benztropine mesylate was reduced. On follow-up examination 2 months later, the patient reported that her diplopia had resolved. Dynamic retinos-copy showed improved accommodation. Prism and alternate cover testing now showed a constant exotropia of 12 prism-diopters when fixating at distance and 9 prism-diopters when fixating at near. Our patient's treatment with multiple psychotropic medications had converted her long-standing exotropia to an esotropia with associated diplopia. Reducing the anticholinergic medications allowed her eyes to revert to their baseline exotropic position and produced resolution of her diplopia. We agree with the pharmacological mechanism proposed by Oh and Shin (1) in which anticholinergic-induced paresis of accommodation leads to excessive accommodative effort with a corresponding excess of accommodative convergence. In children with accommo-dative esotropia, it is common to see a large-angle esotropia develop in the waiting room after administration of topical anticholinergic medications to dilate the pupils. Conversely, phospholine iodide, a cholinesterase inhibitor that enhances the effect of acetylcholine on the ciliary muscle, is used in topical form to eliminate small-angle esotropia (3). Given that so many widely used medications have anticholinergic properties, it is surprising that anticholin-ergic esotropia is not reported more regularly. Our patient's preexisting strabismus and absence of fusion rendered her susceptible to this complication. As Oh and Shin (1) noted, their patient may have also had several predisposing neurologic factors. The need for an intrinsic predisposition for anticholinergic esotropia would best explain the striking rarity of this complication. Since examining our patient and reading the similar report by Oh and Shin (1), we have begun routinely screening for anticholinergic medications in patients with esotropia before planning strabismus surgery. Jennifer M. Anderson, MD Department of Ophthalmology University of Arkansas Little Rock, Arkansas Michael C. Brodsky, MD Department of Ophthalmology Mayo Clinic Rochester, Minnesota brodsky.michael@mayo.edu REFERENCES 1. Oh S-Y, Shin B-S. Benztropine-induced esotropia and mydriasis. J Neuroophthalmol 2007;27:312-3. 2. Wong EYH, Harding A, Kowal L. Oxybutynin-associated esotropia. J AAPOS 2007;11:624-37. 3. von Noorden GK. Binocular Vision and Ocular Motility. Theory and Management of Strabismus. 5th ed. St. Louis: CV Mosby; 1996: 95-6. 360 J Neuro-Ophthalmol, Vol. 28, No. 4, 2008 |
