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Show Waldenstrom Macroglobulinemia Mimicking Temporal Arteritis I read with great interest the very interesting article by Hughes et al (1) on "Isolated optic nerve, chiasm and tract involvement in Bing-Neel syndrome." In 1985, we reported a case of a 65-year-old woman who reported sudden visual loss in 1 eye associated with an inferior altitudinal visual field defect and optic disc edema with peripapillary and periph-eral retinal hemorrhages (2). Over the preceding months, she experienced malaise, intermittent fever, and muscle pains. Her evaluation revealed a hypochromic anemia and sedimentation rate of 122 mm/h. Although giant cell arteritis was believed to be a likely diagnosis, the findings of hepatomegaly, lymphade-nopathy, a reversed albumin/globulin ratio, and an elevated serum concentration of immunoglobulin M led to a diagnosis of Waldenstrom macroglobulinemia. Despite appropriate treat-ment, including plasmapheresis, the patient experienced ische-mic optic neuropathy in the fellow eye. The ischemic events likely were triggered by hyperviscosity due to Waldenstrom macroglobulinemia although other potential mechanisms in-cluded an autoimmune reaction or invasion of the optic nerve and brain by lymphocytoplasmoid cells. This case teaches us that even when facing signs and symptoms which perfectly match a likely diagnosis (giant cell arteritis in our patient), we should not close our mind to other diagnostic possibilities. Frenchmen have a saying: "En medicine comme dans l-amour Il n'y a pas de jamais il n'y a pas de toujours" (In medicine, like in love, there is not such a thing as never, there is not such a thing as always). Riri S. Manor, MD Neuro-Ophthalmology Unit, Department of Ophthalmology, Rabin Medical Center, Sharon Campus, Petah Tikva, Israel The author reports no conflicts of interest. REFERENCES 1. Hughes MS, Atkins AJ, Cestair DM, Stacy RC, Hochberg F. Isolated optic nerves, chiasm and tract involvement in Big-Neel Syndrome. J Neuroopthalmol. 2014;34;340-345. 2. Manor RS, Axer-Sigel R, Hart M. Anterior ischemic optic neuropathy. Am J Ophthalmol. 1985;99:608-609. Palinopsia and Other Reversible Visual Disturbances Induced by Topiramate We read with interest the article by Yun et al (1) de-scribing 9 new patients with topiramate-induced pal-inopsia. Palinopsia, consisting of the persistence of visual images after the removal of the initial stimulus, may be ob-served in different medical conditions, especially migraine (2), but may also be provoked by different medications. Topira-mate is an antiepileptic drug useful for migraine prophylaxis and for the treatment of both partial and generalized seizures (3). Topiramate has been rarely associated with adverse ocular events, in particular ciliochoroidal effusion syndrome, but patients with transitory visual disturbances induced by top-iramate are being increasingly recognized (1). We evaluated 2 patients with other types of visual disturbances that were severe but transitory and fully reversible and appear related to beginning topiramate or dosage increase of the medication. Patient 1: A 19-year-old woman had a 1-year history of migraine with aura. Her headaches usually were preceded by visual symptoms (teichopsia or visual distortion) lasting for about 20-30 minutes and occurred monthly. Topiramate was started at a daily dose of 25 mg.Within 5 days, she complained as if looking "through a veil." This visual disturbance was continuous, and she was not taking any other medications. A complete ophthalmologic examination was unremarkable. Physical examination, numerous blood tests, brain magnetic resonance imaging (MRI), and electroencephalography were normal. Topiramate was discontinued, and within 2 days, her visual symptoms completely disappeared. She was pre-scribed amitriptyline for migraine prophylaxis. There was no recurrence of her visual symptoms in 6 years of follow-up. Patient 2: A 21-year-old man had a 6-year history of juvenile myoclonic epilepsy. Initially, he was treated with levetiracetam 3 g/d, with reduction of seizure frequency. At age 20 years, topiramate 100 mg/d was added, and he remained seizure-free for 5 months. He then experienced 2 generalized tonic-clonic seizures, and his topiramate was gradually increased by 50 mg/ wk up to 200 mg/d. Two days after reaching the maximal dosage, the patient complained of severe blurred vision ("I see all black") that lasted for approximately 30 minutes. He had no similar symptoms in the past and was taking no other medications. Neurologic and ophthalmologic examinations were normal. Topiramate was gradually reduced to 50 mg/ d and valproate was given at 1,000 mg/d. In the ensuing 9 years, he has not experienced seizures or visual disturbances. Our 2 patients had reversible visual disturbances associ-ated with use of topiramate. In our first patient, visual complaints began after institution of topiramate, whereas in the second patient, visual symptoms were associated with an increase in the dose of medication. Either discontinuing the medication (patient 1) or lowering the dose (patient 2) led to Letters to the Editor: J Neuro-Ophthalmol 2015; 35: 329-332 329 Letters to the Editor Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. cessation of the visual disturbances. The symptoms experi-enced by our patients expand the spectrum of visual complaints experienced by patients taking topiramate. Vincenzo Belcastro, MD, PhD Neurology Unit, Department of Medicine, S. Anna Hospital, Como, Italy Umberto Aguglia Department of Medical and Surgical Sciences, Magna Graecia University of Catanzaro, Catanzaro, Italy Regional Epilepsy Center, Bianchi-Melacrino-Morelli Hospital, Reggio Calabria, Italy Laura R. Pisani, MD IRCCS, Centro Neurolesi "Bonino-Pulejo," Messina, Italy Edoardo Ferlazzo Department of Medical and Surgical Sciences, Magna Graecia University of Catanzaro, Catanzaro, Italy Regional Epilepsy Center, Bianchi-Melacrino-Morelli Hospital, Reggio Calabria, Italy The authors report no conflicts of interest. REFERENCES 1. Yun SH, Lavin PJ, Schatz MP, Lesser RL. Topiramate-induced palinopsia: a case series and review of the literature. J Neuroophthalmol. 2015;35:148-151. 2. Belcastro V, Cupini LM, Corbelli I, Pieroni A, D'Amore C, Caproni S, Gorgone G, Ferlazzo E, Di Palma F, Sarchielli P, Calabresi P. Palinopsia in patients with migraine: a case-control study. Cephalalgia. 2011;31:999-1004. 3. Crespel A, Gelisse P, Reed RC, Ferlazzo E, Jerney J, Schmitz B, Genton P. Management of juvenile myoclonic epilepsy. Epilepsy Behav. 2013;28(suppl 1):S81-S86. Asymmetric Papilledema in Idiopathic Intracranial Hypertension: Comment We would like to congratulate Bidot et al (1) for their article on asymmetric papilledema. Their study is the first to demonstrate a morphological difference in the diameter of the optic canals in patients with asymmetric papilledema. The optic canal consists of 2 components: bone and meningothelial cells (2). Although bone is rigid, the meningothelial cells of the pia-arachnoid react to a variety of biological and mechanical stimuli (3,4). For example, increased intracranial pressure (ICP) causes proliferation of the number of meningothelial cells as well as an in-crease in their size (4). This, in turn, can result in thick-ening of the meningothelial cell layer, leading to narrowing of the subarachnoid space (SAS) surrounding the optic nerve and, eventually, to optic nerve compart-mentation, perhaps protecting the optic nerve from the effects of increased ICP. This process has been demon-strated in an animal model (5) as well as in patients with papilledema who have undergone computed tomographic cisternography before and after intrathecal (spinal) injec-tion of iodinated contrast material (6,7). In these patients, there is a decreased gradient of contrast between the lum-bar SAS and the SAS surrounding the optic nerve (7). It would be interesting to see whether the Frisén grade of papilledema correlates with the contrast gradient. A fur-ther interesting aspect of the work by Bidot et al is that the visual field in the eye with the larger optic canal was more affected, although visual acuity was the same in both eyes. This finding also suggests that compartmentation might offer at least a temporary protective effect on the optic nerve; however, the effect of chronic compartmentation on cerebro-spinal fluid circulation needs to be studied further. In addition to patients with increased ICP and papil-ledema, it might be worthwhile assessing the diameters of the optic canals in astronauts in whom optic disc swelling has developed during prolonged spaceflight (8) and com-paring them with the optic canals of astronauts who never developed optic disc swelling. If the size of the optic canal is a major determinant of whether or not an individual devel-ops optic disc swelling from increased ICP or another cause, one would expect that astronauts in whom disc swelling has been observed should have larger canals than those in whom optic disc swelling has not developed. In the meantime, we agree with Bidot et al that asymmetry of the diameter of the bony optic canal may produce a compartmentation phenomenon that protects the optic nerve from the effects of increased ICP and would add that it is possible that an increase in the thickness of meningothelial cell layer caused by a reaction to increased ICP may play a role as well, both in this setting and possibly in other optic nerve disorders (9). Hanspeter E. Killer, MD Kantonsspital Aarau, Aarau, Switzerland The author reports no conflicts of interest. 330 Letters to the Editor: J Neuro-Ophthalmol 2015; 35: 329-332 Letters to the Editor Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |
