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Abstract • Five abnormal oculographic patterns were identified in eight patients with either myasthenia gravis or Guillain-Barré syndrome (GBS). These could be differentiated into three intrasaccadic and two postsaccadic abnormalities. From our studies of computer simulations, and considering the established pathophysiology of myasthenia gravis and GBS, we believe that our oculographic findings were a consequence of defects in peripheral neural and neuromuscular conduction, together with a simple adaptive increase in duration of the saccadic burst of central innervation. We conclude that the eye movement abnormalities we observed are explained by intermittent block of peripheral conduction, and suggest that any disease causing intermittent blockage of neural signals to extraocular muscles will produce similar abnormalities of eye movement. References 1. Stark L, Vossius G, Young LR: Predictive control of eye tracking movements . Trans Hum Factors Electronics 1962;3:52-57.Crossref 2. Cook G, Stark L: The human eye movement mechanism: Experiments, modeling and model testing . Arch Ophthalmol 1968;79:428-436.Crossref 3. Clark MR, Stark L: Control of human eye movements: II. A model for the extraocular plant mechanism . Mathematical Biosci 1974;20:213-238.Crossref 4. Hsu FK, Bahill AT, Stark L: Parametric sensitivity analysis of a homeomorphic model for saccadic and vergence eye movements . Comput Programs Biomed 1976;6:108-116.Crossref 5. Yee RD, Cogan DG, Zee DS, et al: Rapid eye movements in myasthenia gravis: II. Electrooculographic analysis . Arch Ophthalmol 1976;94:1465-1472.Crossref 6. Cogan DG, Yee RD, Gittinger J: Rapid eye movements in myasthenia gravis: I. Clinical observations . Arch Ophthalmol 1976;94:1083-1085.Crossref 7. Toyka KV, Drachman DB, Griffin DE, et al: Myasthenia gravis: Study of humoral immune mechanisms by passive transfer to mice . N Engl J Med 1977;296:125-131.Crossref 8. Drachman DB: Myasthenia gravis . N Engl J Med 1978;298:136-142.Crossref 9. Appel SH, Almon RR, Levy N: Acetylcholine receptor antibodies in myasthenia gravis . N Engl J Med 1975;293:760-761.Crossref 10. Lindstrom JM, Lambert EH: Content of acetylcholine receptor and antibodies bound to receptor in myasthenia gravis, experimental autoimmune myasthenia gravis, and Eaton-Lambert syndrome . Neurology 1978;28:130-138.Crossref 11. Wisniewski H, Terry RD, Whitaker JM, et al: Landry-Guillain-Barré syndrome: A primary demyelinating disease . Arch Neurol 1969;21:269-276.Crossref 12. Rasminsky M: Physiology of conduction in demyelinated axons , in Waxman SG (ed): Physiology and Pathobiology of Axons . New York, Raven Press, 1978, pp 361-376. 13. Marshbank RM: Turnover and release of acetylcholine , in Cottrell GA, Usherwood PNR (eds): Synapses . New York, Academic Press Inc, 1977, pp 81-101. 14. Fuchs AF, Luschei ES: Firing patterns of abducens neurons of alert monkeys in relationships to horizontal eye movements . J Neurophysiol 1970;33:382-392. 15. Robinson DA: Oculomotor unit behavior in the monkey . J Neurophysiol 1970;33:393-404. 16. Schmidt D, Dell'Osso LA, Abel A, et al: Myasthenia gravis: Saccadic eye movement waveforms . Exp Neurol 1980;68:346-364.Crossref 17. Shults WT, Stark L, Hoyt WF, et al: Normal saccadic structure of voluntary nystagmus . Arch Ophthalmol 1977;95:1399-1404.Crossref
Archives of Neurology – American Medical Association
Published: Aug 1, 1982
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