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Show LETTERS TO THE EDITOR Editor's note: The Journal of Neuro- Ophthalrnology welcomes letters as written or e- mail correspondence. Send e- mail to jdtrobe@ umich. edu. Video Electroencephalogram Monitoring During Paroxysmal Upside Down Reversal of Vision To the Editor: Metamorphosia is a visual illusion that distorts the size, shape, or inclination of objects. It can be a rare manifestation of acute central nervous system ( CNS) disease involving the visual or vestibular pathways ( 1- 5). " Floor- on-ceiling" phenomenon is one of its rare paroxysmal forms, classified as reversal of visual metamorphosia ( RVM). It was first described by Winslow ( 1) in 1868 in a patient with hysteria. It has been also reported in patients with migraine or vertebrobasilar insufficiency ( 1,3,4). Its pathophysiology is uncertain, but the favorable response to anticonvulsants in some cases suggests a possible hyperactivity of cortical or subcortical neurons ( 2). In the few available reports in the medical literature, electroencephalogram ( EEG) findings have been described only during the interictal state ( 1- 4). We report the findings of continuous video EEG monitoring performed while a patient experienced several episodes of " floor- on- ceiling" phenomenon associated with the sensation of body levitation. A 76- year- old man with a history of hypertension and old pontine stroke was admitted to our hospital after being found conscious on the floor by his wife. While in the hospital, he developed multiple episodes of sensing 180° rotation of his visual environment in the coronal plane. Each episode lasted up to 60 minutes and was associated with a sensation of body levitation. He felt as if he was " floating above the bed," while seeing the television set down on the floor. His episodes were initially associated with an intense fear of falling from the bed. They were not associated with confusion, vertigo, speech changes, or other neurologic complaints. His medications included prazosin, aspirin, metoprolol, and Atorvastatin. His neurologic examination was consistent with his previous pontine stroke and revealed mild dysarthria, left facial paresis, and left hemipa-resis with increased tone, hyperreflexia and Babinski sign but no sensory changes. During one of the episodes we asked him to write his name and a sentence on a piece of paper. He was still able to do it correctly although the text was rotated clockwise by about 30 degrees. Brain magnetic resonance imaging revealed an old right pontine stroke but no evidence of acute ischemia. Magnetic resonance angiography was normal. Initially, he was experiencing 1 to 3 episodes/ day. He was started on intravenous heparin, which was later stopped as the episodes persisted. During continuous 24- hour video EEG monitoring, three episodes were recorded. No abnormalities in the surface EEG were observed during the attacks. Subsequently, gabapentin was started and the episodes stopped. One month later, we slowly tapered the gabapentin. No further episodes occurred 9 months after this medication was discontinued. To our knowledge, this is the first report of video EEG findings during episodes of RVM. The response to gabapentin could support the hypothesis of abnormal activity of subcortical nuclei, which could be missed by surface EEG tracings and thus explain the normal EEG recording in our patient. In addition, surface EEG has a relatively poor sensitivity in the confirmation of simple partial seizures, although the temporal clinical pattern does not favor this etiology. It is possible that these episodes represented transient abnormal activity of the vestibular projections, which could have generated an altered body scheme representation in the parieto- occipital cortex ( 1). This case suggests that episodes of RVM are not associated with ictal surface EEG abnormalities. Further studies are necessary to confirm this observation. Francisco de Assis A. Gondim, MD, MSc Enrique C. Leira, MD Mary E. Bertrand, MD Department of Neurology St. Louis University Hospital St. Louis, Missouri E- mail: leiraec@ slu. edu REFERENCES 1. River Y, Ben Hur T, Steiner I. Reversal of vision metamorphopsia. Arch Neurol 1998; 55: 1362- 68. 2. Ringel RA, Brick JF, Riggs J. Upside down epilepsy: a manifestation of second sensory seizures. South Medical Journal 1988; 81: 1466. 3. Stracciari A, Guarino M, Pazzaglia P, et al. Acute upside down reversal of vision in vertebrobasilar ischaemia. J Neurol Neurosurg Psych 1993; 56: 423. 4. Arias M, Lema C, Requena I, et al. [ Inverted metamorphopsia: an alteration in the perception of a special situation of objects]. Neu-rologia 2001; 16: 149- 53. 5. Charles N, Froment C, Rode G, et al. Vertigo and upside down vision due to an infarct in the territory of the medial branch of the posterior cerebellar artery caused by dissection of a vertebral artery. J Neurol Neurosurg Pscyh 1992; 55: 188- 9. Copyright © Lippincott Williams & Wilkins. UnauthorizGd reproduction of this article is prohibited. 180 JNeuro- Ophthalmol, Vol. 23, No. 2, 2003 LETTERS TO THE EDITOR JNeuro- Ophthalmol, Vol. 23, No. 2, 2003 Bilateral Distribution of the End Branches of the Pontine Paramedian Branches of the Basilar Artery To the Editor: Recently, within the same week, two elderly patients were admitted to the Massachusetts General Hospital with the acute onset of a bilateral internuclear ophthalmoplegia ( INO) and signs of a unilateral pontine stroke. In light of the unexplained bilaterality of the INO, I was reminded that in the past, when studying the vascular disease underlying lacunar strokes in the pons, I observed that a penetrating paramedian branch of the basilar artery, when approaching the floor of the fourth ventricle, could bifurcate, sending terminal branches to both the ipsilateral paramedian pons and the contralateral mirror territory. Since the medial longitudinal fasciculus lies in the posterior pontine paramedian region on each side, the division of the terminal arterioles described could explain the occurrence of bilateral INOs in an otherwise unilateral pontine stroke. The observations were made in horizontal serial section preparations of the pons in cases of lacunar infarction. The sections were 8 urn thick and the series was continuous. The phosphotungstic acid- hematoxylin staining method was used. Arteries could be traced in continuity down to their finest twigs. This terminal branching was noted in several instances but only in passing, and a methodical study was not made since it was not relevant to the investigation on the nature of the vascular occlusion. My recollection, however, is quite definite. Support for the validity of the present suggestion is provided by a case of proved basilar branch occlusion in which the patient, clinically, had exhibited a one- and- a- half syndrome. ( 1) The matter is important in the stroke field where bilateral signs indicate basilar trunk occlusion and potential disaster, whereas a unilateral lesion is consistent with a less threatening basilar branch occlusion. Also, at times, the precise neuro- anatomic organization at the level of the sixth nerve nuclei seems unclear clinically, possibly because of vascular factors. A restudy of the vasculature using serial sections should be feasible in experienced hands. Pathological study in a clinically studied case of INO would, of course, be preferable. Injection of the paramedian arteries of the freshly removed brain at autopsy could be tried, using India ink or other material. The postmortem radiographic studies of Hassler ( 2) used injection into the basilar artery, thus producing bilateral filling. C. Miller Fisher, MD Massachusetts General Hospital Boston, Massachusetts REFERENCES 1. Fisher CM, Caplan LR. Basilar artery branch occlusion. A cause of pontine infarction. Neurology 1971; 21: 900- 5. 2. Hassler O. Arterial pattern of human brainstem. Neurology 1967; 17: 368- 75 Asymmetric Myopia Developing After Optic Neuritis To the Editor: The relationship between anisometropic refractive error and amblyopia is commonly understood to be that the former may often cause the latter. Some researchers though, have recently postulated the opposite- that amblyopia can actually cause hyperopia to develop in some children, and that it can interfere with a young eye' s expected tendency to become more myopic over time. The patient described here provides anecdotal evidence to support the causative role of amblyopia in the development of anisometropia. A 7- year, 9- month- old girl presented with unilateral optic nerve edema resulting from post- viral optic neuritis. Her visual acuity was correctable to 20/ 400 in the involved OS, and was 20/ 15 uncorrected in the OD. Six months earlier, an examination had found 20/ 15 uncorrected acuity in OU and no other ocular abnormalities. After normal laboratory and radiologic evaluations, a neuro- ophthalmologist prescribed a short course of prednisone. Within a month, uncorrected visual acuity had returned to 20/ 20 in the affected OS, although color and contrast perception remained subjectively impaired. The unaffected OD gradually became myopic. Within a year, it measured - 0.75 sphere. Two years later, it was - 1.25 sphere, and after seven years, was - 2.25 sphere. Meanwhile, the affected OS became hyperopic, with a cy-cloplegic refraction of+ 0.50 sphere. Axial length also became asymmetric. After 7 years, the myopic OD's axial length was 23.30 mm, while the OS, having recovered from optic neuritis, measured only 22.35 mm. There has been no recurrence of optic nerve inflammation and no sign of an associated systemic disease. The various intertwined factors that control eye growth and emmetropization are poorly understood. Among the many presumptive causes of myopia are genetic factors, excessive near work ( 1), high level of education, perinatal ambient lighting conditions, and ocular occlusion or visual deprivation or defocus ( 2,3). Genetic characteristics and early visual experience seem to determine an eye's eventual axial length and refractive error ( 4). The case described here raises questions that may help to illuminate the relationship between these influences. This child's impaired eye remained emmetropic, while the fellow eye, normal and unaffected by optic neuritis, developed progressive axial myopia. Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 181 JNeuro- Ophthalmol, Vol. 23, No. 2, 2003 LETTERS TO THE EDITOR Emmetropization appears to be an active process that is not yet fully understood ( 5). As a child's eye grows, the refractive error typically becomes less hyperopic and approaches emmetropia. Several studies have shown, however, that normal emmetropization and eye growth can be prevented by various interventions. Myopia can be produced by wearing spectacle lenses that impose hyperopia and by visual deprivation. In chicks, hyperopia can be caused by sectioning the optic nerve or by raising visually immature birds in constantly lighted conditions. In this case, the child's normal eye grew to be about 3.8% longer than the eye affected by optic neuritis. Kiorpes and Wallman ( 6) showed that when experimental unilateral amblyopia was induced in monkeys, hyperopia tended to develop in these eyes within only a few months of the onset of amblyopia. Meanwhile, the untreated normal eyes became myopic, their axial length increasing by an average of 3%> ( 6). In their study, amblyopia seemed to interfere with the eye's normal growth toward myopia. Rather than being a result of the eye's hyperopic error, experimental amblyopia actually seemed to cause the hyperopia to develop. Our case would seem to be a natural experiment that supports the unorthodox view that amblyopia may in some circumstances cause anisometropia, rather than the reverse. Controlled human studies will likely be impossible to perform, but other similar cases might confirm or refute this impression. Acknowledgment The authors thank Josh Wallman, PhD, for his assistance in the preparation of this manuscript. Michael Rotberg, MD Emily Rotberg Charlotte Eye Ear Nose and Throat Associates Charlotte, North Carolina E- mail: mrotberg@ ceenta. com REFERENCES 1. Angle J, Wissmann DA. Age, reading, and myopia. Am J Optom Physiol Optics 1978; 55: 302- 8. 2. Smith EL, Hung LF. The role of optical defocus in regulating refractive development in infant monkeys, Vision Res 1999; 39: 1415- 35. 3. Wildsoet CF. Active emmetropization: Evidence for its existence and ramifications for clinical practice. OphthalPhys Opt 1997; 17: 279- 90. 4. Wallman J. How is emmetropization controlled? Results of research on experimental myopia. In Tokoro T, ed. Myopia Updates: Proceedings of the Sixth International Conference on Myopia. Tokyo: Springer, 1998: 13- 22. 5. McBrien NA, Gentle A, Cottriall C. Optical correction of induced axial myopia in the tree shrew: implications for emmetropization. Optom Vis Sci 1999; 76: 419- 27. 6. Kiorpes L, Wallman J. Does experimentally- induced amblyopia cause hyperopia in monkeys? Vision Res 1995; 35: 1289- 97. Migraine- like Visual Hallucinations in Occipital Lesions of Cysticercosis To the Editor: I read with great interest the article by Sharma et al ( 1) about migraine- like visual hallucinations in occipital lobe lesions of cysticercosis. All four patients presented with episodic visual hallucinations. Neuroimaging revealed single enhancing computed tomographic ( CT) or magnetic resonance ( MR) imaging lesions. Such single enhancing CT/ MR lesions are the most common imaging abnormality in Indian patients with new- onset seizures ( no relevant references are provided by the authors). The seizures are often partial ( motor > sensory) with or without secondary generalization. If the lesion is located in the occipital lobe, episodic visual hallucinations may be the only ictal manifestation. More often, visual manifestations precede motor convulsions ( 2- 4). Histopathologic studies of these lesions in India and even in some developed countries have revealed that neurocysticercosis is the most likely cause, provided they fulfill a rigid set of clinical and radiologic criteria. Single cysticercus granulomas measure less than 20 mm in diameter, may be associated with cerebral edema not severe enough to displace midline, and occur in patients with seizures, a normal neurologic examination and no evidence of active systemic disease. The next most common cause of these lesions is tuberculosis; clinical and imaging features are similar to cysticercosis ( 5,6). Because of similarities in clinical and imaging characteristics, it is difficult to differentiate between tuberculoma and single cysticercus granuloma ( 7,8). Serological tests for cysticercosis, enzyme- linked immunosorbent assay ( ETISA), and the enzyme- linked immunotrans-fer- blot ( EITB or immunoblot) display poor sensitivity in detecting antibodies in cases of single lesions and sensitivity is very low ( range 14- 45%) ( 2). The most interesting feature of single cysticercus granuloma is their spontaneous disappearance within a few weeks or months ( 2- 4). Some lesions heal with calcification. These patients need only an-tiepileptic therapy. Antiepileptic drugs may safely be withdrawn after CT lesions have disappeared ( 9). Contrary to what has been done in this series ( 1) treatment with albendazole has not been found effective. Padma et al. ( 10) in a placebo- controlled study observed that treatment with albendazole did not hasten the resolution of CT lesion. Ravindra Kumar Garg, MD, DM Sri Ram Sharma, MD Department of Neurology King George's Medical College Lucknow, India Copyright © Lippincott Williams & Wilkins. UnauthorizGd reproduction of this article is prohibited. 182 © 2003 Lippincott Williams & Wilkins LETTERS TO THE EDITOR JNeuro- Ophthalmol, Vol. 23, No. 2, 2003 REFERENCES 1. Sharma K, Wahi J, Phadke RV, et al. Migraine- like visual hallucinations in occipital lesions of cysticercosis. J Neuroophthalmol 2002; 22: 82- 7. 2. Garg RK, Singh MK, Misra S. Single enhancing CT lesions in Indian patients with seizures: a review. Epilepsy Res 2000; 38: 91- 104. 3. Singh MK, Garg RK, Nath G, et al. Single small enhancing computed tomographic ( CT) lesions in Indian patients with new- onset seizures: a prospective follow- up in 75 patients. Seizure 2001; 10: 573- 8. 4. Chopra JS, Sawhney IMS, Suresh N, et al. Vanishing CT lesions in epilepsy. J Neurol Sci 1992; 107: 40- 9. 5. Rajshekhar V, Haran RP, Prakash GS, et al. Differentiating solitary small cysticercus granuloma and tuberculoma in patients with epilepsy: clinical and computerized tomographic criteria. JNerurosurg 1993; 78: 402- 7. 6. Rajshekhar V, Chandy MJ. Validation of diagnostic criteria for solitary cysticercus granuloma in patients presenting with seizures. Acta Neurol Scand 1997; 96: 76- 81. 7. Shah GV. Central nervous system. Tuberculosis. Neuroimaging Clin North Am 2000; 10: 355- 74. 8. Garg RK. Proposed diagnostic criteria for neurocysticercosis ( letter). Neurology 2002; 58: 1315. 9. Murthy JMK, Subha Reddy YV. Prognosis of epilepsy associated with single CT enhancing lesion: a long- term follow- up study. J Afewo/ Scz 1998; 159: 151- 5. 10. Padma MV, Behari M, Misra NK, et al. Albendazole in single CT ring lesions in epilepsy. Neurology 1994; 44: 1344- 6. Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 183 |