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Show Journal of Clinical Neuro- ophthalmology 11( 3): 173- 174, 1991. Editorial Comment: Pretectal Pupillary Defects © 1991 Raven Press, Ltd., New York Dr. Miller and his co- workers have added several pieces to this fascinating puzzle in the past, and in this case report they add yet another. They show that when the dorsal midbrain is damaged on one side from top to bottom ( that is, from the pretectum down to below the inferior colliculi), both the pupillary reflex arc and the fourth nerve may be involved, and this produces a clinically recognizable combination of signs. A contralateral relative afferent pupillary defect seems to be characteristic of a unilateral pretectal lesion, and in trying to explain this input asymmetry of the pupillary light reflex, the main emphasis up to now, has been on the asymmetry of the chiasmal decussation. The logic has gone something like this: Damage to the pretectal nucleus ( or to the brachium of the superior colliculus) is, as far as the pupillary light reflex is concerned, identical to damage to the optic tract on that side, because a lesion in any of these locations disconnects the same two homonymous hemiretinas from the light reflex arc. The contralateral hemiretina always fires off more impulses than the ipsilateral hemiretina, just because nasal herniretinas cover more area than temporal hemiretinas and carry slightly more ganglion cells per square millimeter. It is for this reason that there are more crossed than uncrossed fibers in the chiasm. Since more pupillary fibers have been cut off from the contralateral eye than from the ipsilateral eye, a relative afferent pupillary defect will be visible to the clinician when the contralateral eye is stimulated. But the chiasmaI decussation is not the only crossing of the light reflex path; a lesion in the area of the pretectal nucleus might also produce ( or perhaps the right word is " reveal") an asymmetry in the dorsal midbrain decussation of the pupillary pathways. If the light reflex fibers leaving each pretectal nucleus are more crossed than not ( and to the same degree on each side), then each EdingerWestphal nucleus should receive the same total amount of pupil constrictor stimulus when both eyes are open in a lighted room, and the pupils should remain equal in size. If one optic tract or 173 pretectal nucleus is shut down, the pupils will still react to light, but all the impulses will be coming through the only remaining pretectal nucleus, and that nucleus may distribute more impulses to the contralateral Edinger- Westphal nucleus than to the ipsilateral Edinger- Westphal, producing a small anisocoria. Our knowledge of the neuroanatomy of the human pupillary pathways has not changed much in the last 90 years, and Carl Behr, who worked on this subject from 1908 to 1925, also assumed that the two hemidecussations of the pupillary reflex arc were more crossed than uncrossed. This led him to state that in a tract hemianopia there was a consistent anisocoria ( a) that decreased with the passage of time; ( b) that was more pronounced in dim illumination; and ( c) that always had the wider pupil on the side of the homonymous hemianopia, that is, contralateral to the tract lesion ( 1). The handful of cases Behr offered in support of this hypothesis may have, in retrospect, included some cases of central Horner's syndrome on the side of the tract lesion- which might explain the greater anisocoria in dim light ( 2). Behr also stated that when the eye with the wider pupil was stimulated, the pupil reactions were clearly weaker than when the same stimulus was applied to the eye with the smaller pupil ( 3). I read this as a relative afferent pupillary defect contralateral to the tract lesion. Behr does not seem to have seen with any clarity that this afferent defect was due to the asymmetry of the chiasmal hemidecussation, and that the anisocoria was due to the asymmetry of the midbrain hemidecussation. To get back to the case report under discussion: If it is indeed true that in primates there are always more crossed than uncrossed fibers in the midbrain pupil hemidecussation, then every lesion of the optic tract, brachium of the superior colliculus, and pretectal nucleus should result in a " consensual deficit" in which the direct response is stronger than the consensual- at least when the eye on the side of the tract lesion is stimulated. Let's go over that again, starting with a patient who is equipped with a 60% crossed and 40% uncrossed midbrain decussation of the pupillary light reflex, so that each pretectal nucleus sends more pupillary information to the contralateral iris 174 EDITORIAL COMMENT sphincter nucleus. Let's give this hypothetical patient a complete right tract lesion, so that no pupillomotor input reaches the right pretectal nucleus. This means that, whichever eye is stimulated, the pupillary impulses will come through the left pretectal nucleus- and the right EdingerWestphal nucleus will always get the lion's share of the stimulation. When the stimulus light falls on this patient's right eye, only the nasal hemiretina will send out pupillary impulses, and there will be a " consensual deficit" due to the asymmetry of the midbrain hemidecussation. This will result in a " contraction anisocoria." Conversely, when the left eye is stimulated, there should be a " consensual excess" of some degree, and a reverse contraction anisocoria might be expected to appear. Now imagine doing an alternating light test on this patient- trying to measure the relative afferent pupillary defect. The right pupil will always seem to be reacting better to light than the left pupil, because the left pupil is getting the short end of the stick- in this patient the left pupil is getting only 40% of the output, while the right pupil gets 60%. Clinically, we tend to watch the illuminated pupil, and we don't go out of our way to look for a fluctuating anisocoria that might be mixing a little efferent asymmetry in with the afferent asymmetry we are trying to measure. This is why Cox recommended that the clinician just watch the eye suspected of having an input defect and compare its direct and its consensual responses ( 4). Of course, one would expect a patient with an isolated, complete tract lesion to have a contralateral relative afferent pupillary defect because of the asymmetry of the chiasmal hemidecussation. The question is whether a component of this clinically visible relative afferent pupillary defect is an illusion caused by an asymmetry of the distribution of J '_. the pupillomotor outflow from the pretectal nucleus. Of the four probable " pretectal afferent defects" described in the literature, only the report by Forman et al. ( 5) included a pupillogram, and this showed a clear consensual deficit when one eye was stimulated. Was this because the lesion left the patient with only one working pretectal nucleus- a nucleus whose output was more crossed than uncrossed? Or did the asymmetry of the midbrain crossing antedate the lesion? Does a pretectal nucleus care which eye its input is coming from? Are some of its cells connected to the contralateral nasal hemiretina and some to the ipsilateral temporal hemiretina, so that stimulating one eye produces a different response from stimulating the other eye? Has the lesion ( as Helmut Wilhelm suggests) caused a loss of inhibition of the ipsilateral Edinger- Westphal nucleus, so that the pupil on the same side is smaller and reacts better? Do these patients all have a homonymous pupillary hemifield loss? ( that is, a " homonymous pupillary hemiakinesia" or a " hemianopische Pupillenstarre," as it was called in the old German literature)? There are still more questions than there are answers. H. Stanley Thompson, M. S., M. D. Randy H. Kardon, M. D., Ph. D. Iowa City, Iowa REFERENCES 1. Behr C. Oil.' uhre " Oil dell Plipillenbewegungen. Berlin: Verlag von julius Springer, 1924: 64. 2. Loewenfeld IE. Pupils in optic tract lesions ( letter to the editor). I Gill Nellro- ophthalmol 1983; 3: 211- 2. 3. Behr C. Oil.' uhre " Oil dell Plipillenbeu'egungen. Berlin: Verlag von julius Springer, 1924: 65. 4. Cox TA. Pupillography of a relative afferent pupillary defect. Am I Ophthalmol 1986; 101: 320- 4. 5. Forman S, Behrens MM, Odel jG, Spector RI, Hilal S. ReIabve afferent pupillarv defect with normal visual function. Arch 01' hthalmol 1990j08: 1074- 5. |