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Show Journal of Clinical Neuro-ophthalmology 7(1): 38-39, 1987. Editorial Comment The Pupil Cycle Time The paper in the December 1986 issue by Hlumen, Feiler-Ofry and Korczyn [6(4):232-4] puts on record that the pupil cycle time is prolonged in an eye with Horner's syndrome. This is not a surprising finding since it is known that the affected pupil is slow to dilate in Horner's syndrome. This slowness is due to loss of innervational tone in the dilator muscle and perhaps also to loss of adrenergic inhibitory impulses to the sphincter muscle. I believe that there are easier ways to confirm Horner's syndrome in the office-"dilation lag," in a young person, can be seen clinically with a hand light, and "upside-down ptosis" is worth looking for-but Blumen's observation is of value and it may lead to new uses for measuring the pupil cycle time. When the "edge-light pupil cycle time" was disinterred in 1978 by Miller and Thompson (1) it was offered as a test of optic nerve function. Induced pupillary oscillations, timed at the slit lamp, were shown to be slowed in optic neuritis (2-5) and in optic nerve compression (6,7), but Ukai and Ishikawa (8) analyzed the oscillations and demonstrated that some of the prolongation of the mean pupil cycle time was due to weak and irregular pupil responses. A regularly bounding pupil is easily kept on the beam, but when the pupillary movements are weak, the pupillary margin sometimes has to be chased by the slit beam and this artificially prolongs the pupil cycle time (9). It could be argued that, by boosting only the bad scores, the slit lamp makes the test more sensitive. But this would do nothing for the specificity of the test, and it is the uncertainty as to what is actually being measured that has kept many of us from using this test (10). Besides, the test takes 5 minutes of the doctor's highly prized examination time. These difficulties prompted Safran (11) to suggest that, in the office, one could put down the stopwatch and simply take note of whether a light placed at the edge of the pupil generated good oscillations. The pupil cycle time measurement was, how~~'(!,)! 1'. w~f1v app~1!IJin.8 because it offered a way of 38 © 1987 Raven Press, New York getting a number from each eye, in the office, using only a slit lamp, a stop watch and a little care (12-16). It seemed clear that anything that disturbed th~ pupillary reflex arC might prolong the pupil cycle time. This included outflow problems as well as input defects; for example, a wide variety of drugs might excite or inhibit neurons in the reflex arc or slow synaptic transfer of information (17), and damage to the neuromuscular junction or to the pre- or postganglionic neurons-either sympathetic or parasympathetic-would also prolong the pupil cycle time. This fact generated some interest in measuring the pupil cycle time in myasthenia gravis (18-22) and it seems that if you take the time to compar~ the cycle time during th~ first and the fifth minutes of edge-light induced oscillation you will observe a fatiguability of the pupillary movements in patients with myasthenia that is not seen in those with normal eyes (21). Measuring the pupil cycle time has also been offered as a handy test for autonomic neuropathy (23,24). This is a natural enough suggestion because the pupils of diabetic patients don't move very well (25,26)-which is prObably due tOa combination of dilator and sphincter muscle denervation. This is all seen from another point of view when you consider the apparent association between narrow angle glaucoma and the signs of autonomic neuropathy: Hahnenberger (27) has suggested that the pupil of a glaucomatous eye tends to be slightly miotic and Clark and Mapstone (28) have found evidence of autonomic neuropathy in 34% (34/99) of ocular hypertensives with wide chamber angles and in 50% (45/90) of ocular hypertensives with narrOw angles, but in only 2.6% (2/74) of a series of control subjects. The same authors demonstrated that an abnormality of edgeinduced pupillary oscillations was frequent in the fellow eye of patients with angle closure glaucoma in one eye (29), and suggested that parasympathetic denervation of the chamber angle may be a contributing factor in angle closure glaucoma (30). This is in line with Mapston~'shypothesis that the EDITORIAL: THE PUPIL CYCLE TIME 39 essential anterior segment event precipitating irido-corneal contact-and therefore angle closure- is a loss of parasympathetic tone (31). Since the pupil cycle time is not affected by timolol (32) it could also be measured in patients with open angle glaucoma. Since the pupil cycle time may be abnormal as a result of either afferent or efferent impairment of the pupil reflex arc, we may be in for a new wave of interest in the ability of the pupil to oscillate as an indicator of the risk of glaucomatous damage to the eye. It should not be forgotten that when the pupil cycle time is measured at the slit lamp no effort is made to rigorously control the level of retinal illumination. The amount of light that spills over the pupillary margin varies with the width and height of the beam. It is probably because this factor was not carefully controlled that Miller and I (1) were unable to detect any change in the pupil cycle time when we introduced neutral density filters into the beam. Glenn Myers (33) has recently shown that the pupil cycle time is indeed influenced by changes in the level of retinal illumination, so this will have to be controlled in any device that is to be constructed to measure the rate of these oscillations. H. Stanley Thompson, M.D. University of Iowa Iowa City, Iowa 52242 REFERENCES 1. Miller SD, Thompson HS. Edge-light pupil cycle time. Br J OphthalmoI1978;62:495-500. 2. MiIler SD, Thompson HS. Pupil cycle time in optic neuritis. Am J OphthalmoI1978;85:635-42. 3. Hamilton W, Drewry RD Jr. Edge-light pupil cycle time and optic nerve disease. Ann OphthalnzoI1983;15:714-21. 4. Kirkham TH, Coupland Sc. Multiple regression analysis of diagnostic predictors in optic nerve disease. Can J Neurol Sci 1981;8:67. 5. Manor RS, Yassur Y, Ben-Sira 1. Pupil cycle time in noncompressive optic neuropathy. Ann Ophthalmol 1982;14: 546. 6. Weinstein JM, Van Gilder J, Thompson HS. Pupil cycle time in optic nerve compression. Am J Ophtha/mol 1980;89: 263-7. 7. Manor RS, Yassur Y, Ben-Sira 1. Pupil cycle time in space occupying lesions of anterior visual pathways. Ann OphthalmoI1982; 14:1030. 8. Ukai K, Higashi JT, Ishikawa S. Edge-light pupil oscillation of optic neuritis. Neuro-ophthalmologIl1980;1:33. 9. Thompson HS. The pupil. In: LesselI 5, van Dalen JTW, eds. Neuro-ophthalmology. Vol. 3. Amsterdam: Excerpta Medica, 1984:232. 10. Cox TA, Thompson HS, Hayreh 55, Snyder JE. Visual evoked potential and pupiIlary signs: a comparison in optic nerve disease. Arch OphthalmoI1982;100:1603-7. 11. Safran AB, Walser A, Roth A, Gauthier G. Pupil cycle induction test: a way of evaluating the pupil light reflex. Ophthalmologica 1981;183:205. 12. Manor RS, Yassur Y, Siegal R, Ben-Sira 1. The pupil cycle time test: age variations in normal subjects. Br J Ophthalmol 1981;65:750. 13. Higashi JT, Ishikawa 5, Mukuno K, Watanabe A. Pupillary analysis in Graves' disease. Jpn J OphthalmoI1982;26:213. 14. Namba K, Utsumi T, Kanamura K. PupiIlary dynamics in Graves' disease. JJpn Ophthalmol Soc 1982;86:358. 15. Hreidarsson AB, Laurberg P. Evaluation of pupiIlary function in thyroid disease. Acta Ophthalmol (Copenh) 1981;60:641. 16. Sood AK, Mithal 5, Elhence A, Maini A. Pupil cycle time. Indian J OphthalmoI1985;33:41-3. 17. Safran AB, Walser A, Roth A, Gauthier G. Influence of central depressant drugs on pupil function: an evaluation with the pupil cycle induction test. Ophthalmologica 1981;183:214. 18. Yamazaki A, Ishikawa S. Abnormal pupiIlary responses in myasthenia gravis: a pupillographic study. Br J Ophthalmol 1976;60:575. 19. Lepore FE, Sanborn GE, Slevin JT. Pupillary dysfunction in myasthenia gravis. Ann. Neurol. 1979;6:29. 20. Lepore FE, Sanborn GE, Slevin JT. Reply to letter by R. C. Bryant. Ann NeuroI1980;7:289. 21. Dutton GN, Garson JA, Richardson RB. PupiIlary fatigue in myasthenia gravis. Trans Ophtllalmol Soc UK 1982;102:510. 22. Lu Chuan-zhen, Hao Zhong-shun, Liu Hao-kun, Zhang Ming-kui. Dynamic pupillary response to positive differential light stimulation in myasthenia gravis. Chin Medical J [Engl] 1985;98:405-8. 23. Martyn CN. Edge-light pupil cycle time: a quantifiable autonomic reflex. J Neurol Neurosurg Psychiatry 1985;48:602. 24. Gadoth N, Schlaen N, Maschkowski D, Bechar M. The pupil cycle time in familial dysautonomia. Metab Pediatr Syst OphthalmoI1983;7:131-4. 25. Smith SA, Smith SE. Reduced pupiIlary light reflexes in diabetic autonomic neuropathy. Diabetologia 1983;24:330-2. 26. Alexandridis E, Hain G. Frequenz der F1immerlichtabhangigen Pupillenoszillationen bei Diabetikern. Fortschr Ophthalmol 1985;82:187-8. 27. Hahnenberger R. Anisocoria in untreated unilateral openangle glaucoma. Acta OphthalmoI1984;62:135-41. 28. Clark CV, Mapstone R. Autonomic neuropathy in ocular hypertension. Lancet 1985;2:185-6. 29. Clark CV, Mapstone R. Pupil cycle time in primary closedangle glaucoma. Call J Ophtha/mol 21:88-91. 30. Editorial: The autonomic nervous system and the eye. Lancet 1985;2:591-2. 31. Mapstone R, Clarke CV. The prevalence of autonomic neuropathy in glaucoma. Trans Ophthalmol Soc UK 1985;104: 265-9. 32. Kirkham TH, Coupland SC, Blanchet L-M, Nelson DE. Effect of timolol maleate on intraocular pressure and pupil cycle time in normal eyes. Can JOphthalnzoI1981;16:132-5. 33. Myers G. Interactive control of pupil size by light and target distance [Dissertation]. Berkeley, California: University of California, 1985. J Clin Neuro-ophthalmol, Vol. 7, No.1, 1987 |
