Neuro-Ophthalmologic Monitoring of Leaking Arachnoid Cysts

Regarding the excellent JNO publication entitled "Neuro-Ophthalmologic Monitoring in the Management of Increased Intracranial Pressure from Leaking Arachnoid Cysts," we wish to add 2 similar cases that recently came under our care at the same institution.

Letters to the Editor In any case, we acknowledge that the importance of smoking in the pathophysiology of APMPPE-associated vasculitis may have been underrecognized and underreported to date, and we encourage all readers of our report, and of the subsequent discussion associated therewith, to take note of this. We again thank Dr. Knox for astutely raising awareness of this topic. George Harocopos, MD Gregory Van Stavern, MD Departments of Ophthalmology and Visual Sciences, Washington University in St. Louis, St. Louis, Missouri Sonika Dahiya, MD Department of Pathology, Washington University in St. Louis, St. Louis, Missouri Leanne Stunkel, MD Robi Maamari, MD Departments of Ophthalmology and Visual Sciences, Washington University in St. Louis, St. Louis, Missouri 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. The authors report no conflicts of interest. REFERENCES 1. O'Halloran HS, Berger JR, Lee WB, Robertson DM, Giovannini JA, Krohel GB, Meckler RJ, Selhorst JB, Lee AG, Nicolle DA, O'Day J. Acute multifocal placoid pigment epitheliopathy and Neuro-Ophthalmologic Monitoring of Leaking Arachnoid Cysts R egarding the excellent JNO publication entitled “Neuro-Ophthalmologic Monitoring in the Management of Increased Intracranial Pressure from Leaking Arachnoid Cysts,” (1) we wish to add 2 similar cases that recently came under our care at the same institution. 13. 14. central nervous system involvement: nine new cases and a review of the literature. Ophthalmology. 2001;108:861–868. Algahtani H, Alkhotani A, Shirah B. Neurological manifestations of acute posterior multifocal placoid pigment epitheliopathy. J Clin Neurol. 2016;12:460–467. Van Zyl T, Papakostas TD, Sobrin L. Vision loss and paresthesias in a young man. JAMA Ophthalmol. 2015;133:1207–1208. Olin JW. Thromboangiitis obliterans (Buerger's disease). N Engl J Med. 2000;343:864–869. No YJ, Lee EM, Lee DH, Kim JS. Cerebral angiographic findings in thromboangiitis obliterans. Neuroradiology. 2005;47:912– 915. Lippmann HI. Cerebrovascular thrombosis in patients with Buerger's disease. Circulation. 1952;5:680–692. Fakour F, Fazeli B. Visceral bed involvement in thromboangiitis obliterans: a systematic review. Vasc Health Risk Manag. 2019;15:317–353. Puechal X, Fiessinger JN. Thromboangiitis obliterans or Buerger's disease: challenges for the rheumatologist. Rheumatology. 2007;46:192–199. Mohareri M, Mirhosseini A, Mehraban S, Fazeli B. Thromboangiitis obliterans episode: autoimmune flare-up or reinfection? Vasc Health Risk Manag. 2018;14:247– 251. Olin JW, Young JR, Graor RA, Ruschhaupt WF, Bartholomew JR. The changing clinical spectrum of thromboangiitis obliterans (Buerger's disease). Circulation. 1990;82(suppl IV):3–8. Ul haq Keen M, Dass S, Aslam A. Buerger's disease with severe eosinophilia and acute critical ischemia. Rheumatol Adv Pract. 2019;3(suppl 1)40; poster presentation #44. Wolf MD, Folk JC, Panknen CA, Goeken NE. HLA-B7 and HLADR2 antigens and acute posterior multifocal placoid pigment epitheliopathy. Arch Ophthalmol. 1990;108:698–700. McLoughlin GA, Helsby CR, Evans CC, Chapman DM. Association of HLA-A9 and HLA-B5 with Buerger's disease. Br Med J. 1976;2:1165–1166. Shapouri-Moghaddam A, Mohammadi M, Rahimi HR, Esmaeili H, Mahmoudi M, Saeed Modaghegh MH, Tavakol Afshari J. The association of HLA-A, B, and DRB1 with Buerger's disease. Rep Biochem Mol Biol. 2019;8:153–160. somnolent. Repeat MRI 5 months after diagnosis revealed increased thickness of the subdural collection and an organizing membrane within the fluid collection (Fig. 1B). Accordingly, he underwent cystoperitoneal shunting. Within days, he became alert and cheerful. Repeat brain MRI performed 2 days (Fig. 1C) and 1 month (Fig. 1D) after shunt placement showed progressive resolution of the hygroma. Our examination, conducted almost 2 months after shunt placement, showed nearly complete resolution of papilledema and normal visual function. CASE 1 A 14-year-old boy reported new headache and vomiting immediately after a day of ocean bodysurfing. Our examination disclosed normal visual function but bilateral papilledema. Brain MRI revealed a left temporal fossa arachnoid cyst that seemed to be connected to a crescentshaped extra-axial fluid collection diagnosed as a traumatic subdural hygroma (Fig. 1A). Acetazolamide 500 mg twice a day was prescribed to lower intracranial pressure, but over 5 months, the papilledema worsened, and he became more Letters to the Editor: J Neuro-Ophthalmol 2021; 41: e817-825 CASE 2 A 12-year-old boy playing football without a helmet was tackled and slammed into the ground, striking his head. Within hours, he developed a persistent headache. He sought no medical consultation until 2 weeks later, when the headache worsened and vomiting began. Brain computed tomography showed a left temporal fossa arachnoid cyst connected to a prominent subdural fluid collection that was better delineated on a subsequent brain MRI (Fig. 2A, B). Our e821 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Letters to the Editor FIG. 1. Case 1. T2 axial brain MRI performed at presentation (A) shows an arachnoid cyst connected to an extra-axial hygroma (arrow). T2 axial MRI performed 5 months after presentation (B) demonstrates an organizing membrane within the hygroma (arrow). T2 axial MRIs performed 2 days (C) and 1 month (D) after shunt placement, which occurred at 5 months after initial presentation, show progressive shrinkage of the hygroma. FIG. 2. Case 2. T2 axial brain MRI performed at presentation (A) shows an arachnoid cyst connected to a subdural hygroma (arrow), better visualized in a higher axial plane (B). Repeat imaging 4 months after original presentation shows a smaller connection between the hygroma and cyst (C, arrow), but no change in the size of the hygroma (D). We present these cases as further evidence of rupture of an arachnoid cyst after head trauma to form a subdural hygroma that may cause a sudden increase in intracranial pressure. The decision of whether and when to intervene surgically is complex (2,3). A principal consideration is vision-threatening papilledema, as these cases emphasize (1). Adrienne Jarocki, BA University of Michigan Medical School, Ann Arbor, Michigan FIG. 3. Case 2. Fundus photographs performed 4 months after diagnosis of the leaking arachnoid cyst still show papilledema. examination 4 weeks after the collision disclosed normal visual acuity, nerve fiber bundle defects on automated perimetry, and moderate papilledema (Fig. 3). He was treated with acetazolamide 500 mg twice a day. All symptoms resolved within 2 weeks. Our follow-up examination conducted 4 months after diagnosis showed persistent papilledema and stable visual field deficits. MRI at that time disclosed that the hygroma size had not changed (Fig. 2D) but that the connection between the cyst and the hygroma seemed to be smaller (Fig. 2C). Treatment with acetazolamide was continued, and surgical intervention was deferred pending the results of a follow-up MRI. e822 Eric Liao, MD Department of Neuroradiology, University of Michigan Medicine, Ann Arbor, Michigan Lindsey B. De Lott, MD Department is Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan Medicine, Ann Arbor, Michigan The authors report no conflicts of interest. L. B. De Lott's time is funded by Grant NIH K23EY027846. Letters to the Editor: J Neuro-Ophthalmol 2021; 41: e817-825 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Letters to the Editor REFERENCES 1. Deveney TK, Lebas M, Lobo RR, Maher CO, Trobe JD. Neuroophthalmologic monitoring in the management of increased intracranial pressure from leaking arachnoid cysts. J Neuroophthalmol. 2021;41:e535–540. Comments on Disorders of the Fourth Cranial Nerve I read with interest the recent article by Kline et al (1) and commend the authors for their thorough update of superior oblique palsy (SOP). I have 2 comments, both relating to the cyclotorsion accompanying SOP. The authors mention objective testing using fundus photography or indirect ophthalmoscopy and subjective testing using the double Maddox rod for confirming and quantifying cyclotorsion. Whereas objective testing determines the anatomic position of the eye(s) by estimating the position of the fovea relative to the optic disc, and subjective testing determines the patient's sensory adaptation, if any, to the cyclotorsion (2–6). A comparison of objective and subjective findings can therefore help determine probable age of onset of the SOP along with the other clinical findings mentioned by Kline et al (1). Objective testing reveals excyclotorsion of the paretic eye(s) regardless of the age of onset and duration of the SOP, whereas the absence of subjective excyclotorsion is more likely in patients having history of congenital SOP (3–5). Distinguishing acquired SOP from symptomatic decompensated congenital SOP that can present initially in adulthood is an essential part of the evaluation for patients with presumed SOP (7). The early onset of the latter permits the patient to develop a sensory adaptation to the torsion entering the patient's conscious awareness. Cyclotorsion accompanying SOP can alter the patient's refractive correction. The eyes will rotate around the line of sight to the physiological position of rest under monocular viewing conditions, but under fused binocular viewing conditions, a cyclofusional movement will occur. Because most clinicians perform astigmatic axis measurements while the patient is viewing monocularly, there can conceivably be a change in the axis when testing is performed under binocular viewing conditions. To investigate this presumption, Rutstein and Eskridge (8) measured the astigmatic axis both with monocular and binocular viewing for adults with acquired SOP. All patients had 3° or more subjective excyclotorsion, 1 diopter or more of astigmatism, and manifested fusion with stereopsis. The aver- Letters to the Editor: J Neuro-Ophthalmol 2021; 41: e817-825 2. Maher CO, Garton HJ, Al-Holou WN, Trobe JD, Muraszko KM, Jackson EM. Management of subdural hygromas associated with arachnoid cysts. J Neurosurg Pediatr. 2013;12:434–443. 3. Parsch CS, Krauss J, Hofmann E, Meixensberger J, Roosen K. Arachnoid cysts associated with subdural hematomas and hygromas: analysis of 16 cases, long-term follow-up, and review of the literature. Neurosurgery. 1997;40:483–490. age change in astigmatic axis was 5° (difference between monocular viewing and binocular viewing), and the average excyclotorsion determined with the double Maddox rod test was 5.2°. Interestingly, that cyclotorsion can alter the refractive correction has been brought to the attention of cataract surgeons. Because toric intraocular lenses are frequently used for patients with high astigmatism, if the patient also has pre-existing SOP and excyclotorsion, the surgeon must take into account the variation in astigmatic axis between monocular and binocular viewing conditions (9). Robert P. Rutstein, OD School of Optometry, University of Alabama at Birmingham, Birmingham, Alabama The author reports no conflicts of interest. REFERENCES 1. Kline LB, Demer JL, Vaphiades MS, Tovakoli M. Disorders of the fourth cranial nerve. J Neuroophthalmol. 2021;41:176–193. 2. von Noorden GK, Murray E, Wong SY. Superior oblique paralysis: a review of 270 cases. Arch Ophthalmol. 1986;104:1271–1276. 3. Dale RT. Fundamentals of Ocular Motility and Strabismus. Vol 180. New York, NY: Grune & Stratton, 1982:246–247, 307– 310. 4. Guyton DL, von Noorden GK. Sensory adaptations to cyclodeviations. In: Reinecke RD, ed. Proceedings of the Third Meeting of the International Strabismological Association, Kyoto 1978. New York, NY: Grune & Stratton, 1978;399–403. 5. Rutstein RP, Corliss DA. The relationship between duration of superior oblique palsy and vertical fusional vergence, cyclodeviation, and diplopia. J Am Optom Assoc. 1995;66:442– 448. 6. Ruttum M, von Noorden GK. Adaptation to tilting of the visual environment in cyclotropia. Am J Ophthalmol. 1983;96:229– 237. 7. Dosunmu EO, Hatt SR, Leske DA, Holmes JM. Incidence and etiology of presumed fpurth cranial nerve palsy: a population based study. Am J Ophthalmol. 2018;185;110–114. 8. Rutstein RP, Eskridge JB. Effect of cyclodeviation on the axis of astigmatism (for patients with superior oblique paresis). Optom Vis Sci. 1990;67:80–83. 9. Seif R, Bleik J, Jabbur N. Digital marking for toric intraocular lenses in a patient with cyclodeviation. Case Rep Ophthalmol Med. 2021;2021:3671951. e823 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.