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Show journal of Neuro- Ophthalmology 16( 1): 18- 20, 1996. • 1996 Lippincott- Raven Publishers, Philadelphia Presumed Ocular Myasthenia and Micropsia A Case Report Adi Michaeli- Cohen, M. D., Yehoshua Almog, M. D., Anat Loewenstein, M. D., Chaim Stolovitch, M. D., Izaac Gutman, M. D., and Moshe Lazar, M. D. A 68- year- old woman presented with diplopia. Fluctuations of dysfunction of lateral rectus muscles in both eyes were detected on consecutive examinations. The diagnosis of ocular myasthenia was proposed. After the initiation of therapy, the patient complained of disturbing micropsia. The micropsia and diplopia were relieved by occlusion of one eye or by a base- out prism over one of the patient's eyeglass lenses. Mechanisms of micropsia are discussed. Key Words: Diplopia- Micropsia- Ocular myasthenia- Accommodation- Convergence. From the Department of Ophthalmology, Tel- Aviv Sourasky Medical Center, Tel- Aviv, and the Goldschlager Eye Institute ( I. G.), Tel- Hashomer Medical Center, Ramat- Gan, Israel. Address correspondence and reprint requests to Dr. Adi Michaeli- Cohen, Ophthalmology Department, Tel- Aviv Sourasky Medical Center, 6 Weizman Street, Tel- Aviv 64239, Israel. A 68- year- old pharmacist presented to our clinic due to horizontal diplopia. Her past medical history was significant for hypertension and smoking of ~ 20 cigarettes daily for many years. CASE REPORT Ophthalmologic examination revealed corrected visual acuity of 20/ 20, normal intraocular pressure, and normal anterior and posterior segments in both eyes. There was bilateral mild hyperopia (+ 1) and astigmatism ( + 0.75). Pupils were equal and reactive with no apparent miosis. Eyelid position and movements were normal, and there was no fatigue on upward gaze. Examination of eye movements revealed complete palsy of the left lateral rectus muscle. Sedimentation rate, complete blood count, and blood chemistry were within normal limits. A tentative diagnosis of an ischemic sixth cranial nerve palsy was made. The patient was instructed to occlude the left lens of her glasses to avoid the diplopia. She returned 3 weeks later, claiming that eye movements were impaired for both eyes. Nearly complete palsy of the lateral rectus muscle was established in each eye. Neurological examination revealed no abnormal findings. Brain computed tomography scanning demonstrated mild diffuse cortical atrophy while magnetic resonance imaging ( MRI) revealed a lacunar infarct in the white matter of the cerebellum. A Tensilon test was performed twice and was negative both times. The titer of anti- acetylcholine- receptor antibodies was in the upper normal limits. A diagnosis of ocular myasthenia was suspected. The patient was started on a regimen of prednisone, 80 mg/ day, and pyridostigmine bromide was added a few days later. Several hours 18 OCULAR MYASTHENIA AND MICROPSIA 19 after taking the first dose of pyridostigmine bromide, the patient noticed that things appeared to be much smaller than normal. Treatment was discontinued after 3 days; the complaint of micropsia persists until the present- that is, for > 10 months. A striking example of the intensity of the patient's micropsia is that, while shopping, she once mistook cucumbers for green beans. Throughout the past 8 months, the patient has been taking a low maintenance dose of prednisone. There have been many fluctuations of her lateral rectus muscle dysfunction, but paresis has been nearly symmetric and stable for the past 3 months. The range of abduction of both eyes is now limited to about 60% of normal. A prism cover test revealed an esotropia of 25 prism diopters in the primary position as well as for a near target. There is no miosis present to suggest convergence spasm, and the cycloplegic overrefraction is piano bilaterally. The patient noticed that her micropsia disappeared a short while after occluding either eye and reappeared immediately after uncovering the occluded eye. The sensation of micropsia was not present when she used a base- out 20- prism-diopter prism over her eyeglasses. This prismatic correction was suggested to eliminate the diplopia, but the patient fortunately found it very effective in relieving her extremely disturbing micropsia as well. On the most recent examination, the right eye showed no deviation on primary position and there was no limitation of abduction. The left eye showed an esodeviation of 17 prism diopters in the primary position. This means that the patient needs to change the prismatic correction according to the fluctuations of her ocular muscle dysfunction. DISCUSSION This 68- year- old woman was diagnosed as having ocular myasthenia based on the clinical course, which consisted of fluctuations of dysfunction of her lateral rectus muscles in both eyes. The negative Tensilon test and the level of antiacetylcholine antibodies at the upper limits of normal do not contradict the diagnosis of ocular myasthenia. Following a trial of pyridostigmine bromide, the patient started to complain of micropsia that persisted despite drug withdrawal after 72 h. Micropsia is a reduction in the apparent size of a stimulus object of a given retinal angle. It is subjective and thus cannot be measured objectively. Factors that are known to induce micropsia include optical factors ( myopic correction with minus sphere lenses can produce minification of objects); central nervous system pathology [ e. g., brain infarcts or brain lesions ( 1) and multiple sclerosis ( 2)]; retinal factors [ e. g., reattached macula following surgery for retinal detachment ( 3), macular edema ( 4), and central serous choroidopathy ( 5)]; and physiological factors [ accommodation- convergence micropsia- that is, the minification of an approaching figure as convergence and accommodation become more prominent ( 6- 10)]. The patient's MRI demonstrated a lacunar infarct in the cerebellum. Although micropsia is a known manifestation of CNS diseases, no specific location in the brain has been established as the locus of injury when micropsia is present. Therefore, the location of the lacunar infarct in our case could not contribute to the establishment of a central origin for the micropsia. Moreover, that occlusion or a prism correction effectively relieved the micropsia is suggestive of a more peripheral pathology rather than a central lesion affecting high visual centers. There was no retinal pathology that might explain the micropsia. The patient was hyperopic ( + 1.0), but no residual accommodative amplitude could be detected, as expected in a 68- year- old person, indicating that accommodation drive was not a viable explanation. As for pyridostigmine bromide as the cause of micropsia, we are not aware of any description of micropsia as a side effect of this drug. In a study conducted on four healthy men who ingested pyridostigmine bromide, 30 mg t. i. d. for 3 days, there was no mentioning of micropsia as a side effect ( 11). A slight constriction of the pupils was reported, and a slight myopic shift attributed to ciliary spasm causing excessive accommodation was found. Such phenomena can certainly be excluded in our presbyopic patient. Another factor against the drug being the cause of the micropsia is that the micropsia persisted after the medication was stopped. We suggest the following theory of the etiology of our patient's micropsia. Convergence is a known strong stimulator of micropsia ( 6- 9). The brain uses the micropsia generated by convergence to prevent the sensation of enlargement when an object is approaching the eye. When there is an excessive convergence drive while looking at an object that is not close enough to justify such a degree of convergence, micropsia should appear. Our patient was esotropic due to bilateral lateral rectus paresis, and so we would not expect there to ] Neuro- Ophthalmol, Vol. 16, No. 1, 1996 20 A. MICHAEL1- C0HEN ET AL. be excessive convergence in trying to fuse the double images she was seeing. It is possible that she did use convergence to enlarge her angle of esotropia and thus drove the two images apart- which was probably more comfortable than seeing them close to each other. The micropsia might have possibly been brought on by convergence, which increased her esotropia and made the diplopia more bearable. This hypothesis is supported by the fact that the micropsia disappears when diplopia is eliminated by occlusion or by prisms. When the drive for convergence is abolished, objects are seen in their normal size again. It is our belief that it is not the convergence itself that produces the micropsia, but rather the drive to converge, which is generated by neuronal impulses that bring to the brain the message that convergence is in process; this produces the sensation of micropsia. The brain interprets the image as being closer than it actually is, and the visual angle under which the object is seen is then relatively too small, producing a microptic perception of the object. REFERENCES 1. Cohen L, Gray F, Meyrignac C, Dehaene S, Degos JD. Selective deficit of visual size perception: two cases of hemi-micropsia. / Neurol Neurosurg Psychiatry 1994; 57: 73- 8. 2. Cendrowski W. Micropsia in multiple sclerosis [ Abstract]. Neurol Neurochir Pol 1992; 26: 729- 31. 3. Sjostrand J, Anderson C. Micropsia and metamorphopsia in the re- attached macula following retinal detachment. Acta Ophthalmol ( Copenh) 1986; 64: 425- 32. 4. Frisen L, Frisen M. Micropsia and visual acuity in macular edema. A study of the neuro- retinal basis of visual acuity. Graefes Arch Clin Exp Ophthalmol 1979; 210: 69- 77. 5. Avci R, Deutman AF. Treatment of central serous choroidopathy with the beta receptor blocker metoprolol ( preliminary results). Klin Monatsbl Augenheilkd 1993; 202: 199- 205. 6. Smith G, Meehan JW, Day RH. The effect of accommodation on retinal image size. Hum Factors 1992; 34: 289- 301. 7. Hollins M. Does accommodative micropsia exist? Am J Psychol 1976; 89: 443- 54. 8. Alexander KR. On the nature of accommodative micropsia. Am J Optom Physiol Opt 1975; 52: 79- 84. 9. McCready DW. Size- distance perception and accommodation- convergence micropsia- a critique. Vision Res 1965; 5: 189- 206. 10. Ehlers N. A case of horizontal micropsia and ocular instability. Acta Ophthalmol 1968; 46: 75- 8. 11. Wiley RW, Kotulak JC, Behar I. The effects of pyridostigmine bromide on visual performance. Aviat Space Environ Med 1992; 63: 1054- 9. / Neuro- Ophthalmol, Vol. 16, No. 1, 1996 |
