| OCR Text |
Show f. Gin. Neuro-ophthaimol. 3: 221-222,1983. Pupils in Optic Tract Lesions To the Editor: In their interesting paper on pupillary behavior in patients with optic tract hemianopia, O'Connor et al. 1 said that their three patients with thalamic lesions involving the optic tract had "a larger pupil contralateral to the lesion," so that they probably had "Behr's sign." Indeed, Behr insisted that the pupil opposite such lesions often was "enlarged." Behr added that the anisocoria was much more evident in dim than in bright light; and furthermore, in one of his patients the palpebral fissure of the eye opposite the lesion also had been "enlarged." What Behr should have said was that in his patients the pupil on the side of the lesion was somewhat constricted. This would not be surprising since-as in O'Connor's patients-the thalamus or its blood supply can be involved in the pathologic process; and thalamic lesions commonly lead to ipsilateral "central Horner's syndrome." Behr was unlucky in that-at the time he noticed this anisocoria-Karplus and Kreidl had not yet completed their series of experiments which established the existence of diencephalic sympathetic pupillomotor, sudomotor, vasomotor, and other centers, and which have since been confirmed so many times. As to the light reflexes in Behr's patients, the pupil in the eye opposite the lesion did not react less than the ipsilateral pupil, but rather the reverse: that is why the anisocoria was small in bright light ("a fraction of a millimeter") and became much larger in dim light ("up to several millimeters"), as is typical for cases with unilateral sympathetic impairment. In Behr's patients, both pupils reacted more briskly when the eye on the side of the lesion was stimulated (with the smaller pupil, and with only uncrossed chiasmal fibers damaged) than when the light was directed into the opposite eye (with the larger pupil, and with the more numerous crossed chiasmal fibers lost). Furthermore, the reactions to near vision were normal in both eyes. In fact, Behr3 said that he suspected a centripetal (afferent) interruption of the pupillary reflex arc. Somehow, however, he became enmeshed in his own terminology and blamed the contralateral"mydriasis"-and even the"enlarged palpebral fissure"-on the optic tract lesion. He never did come up with an acceptable explanation September 1983 Letters to the Editor for this phenomenon, as pointed out by Weve:J and others. However, that apparently did not bother the many authors who have since cited "Behr's sign." Irene E. Loewenfeld, PhD. Detroit, Michigan References 1. O'Connor, P., Mein, c., Hughes, J., Dorwart, R.H., and Shaklett, D.E.: The Marcus Cunn pupil in incomplete optic tract hemianopias. f. Clin. NeuroOphthaimol. 2: 227-234,1982. 2. Behr, K.: Die Bedeutung der Pupillenstorungen hir die Herddiagnose der homonymen Hemianopsie und ihre Beziehungen zur Theorie der Pupillenbewegungen. Dtsch. Z. Nervenheilk. 46: 88-108, 1913. 3. Weve, H.: Zur PhysioJogie des lichtreflexes der Pupille. von Graefes Arch. Ophthalmol. 100: 137156, 1919. Reply: We very much appreciate Dr. Loewenfeld's letter, because it supplies a rationale explanation for the clinical observation we made of anisocoria in these patients. We did not notice any lid fissure abnormalities in our patients, but it certainly is not an essential feature of sympathetic pathway involvement. At present, we are applying for a grant which will, hopefully, allow us to study the pupillary reactions following section of the brachium of the superior colliculus on one side only. As pointed out by Dr. Loewenfeld, this isolated lesion probably will not result in anisocoria. We all appreciate Dr. Loewenfeld's outstanding contributions to our understanding of the pupil, and will try not to muddy the waters by referring to "Behr's sign" in the future. Patrick S. O'Connor, MD. Jane Hughes, MD. David E. Shacklett, MD. San Antonio, Texas Calvin Mein, Major, USA, M.e. Denver, Colorado Robert H. Dorwart, Major, USAF, M.e. Lackland Air Force Base, Texas 221 |
