And when you have a unilateral Adie tonic pupil or a bilateral, what we are looking for is a sector paresis so one part of the iris might be paralyzed and the other parts can still move and the other parts that still move have hippus, the normal change and reactivity of the pupil and that can look like there is a worm, a vermiform, a worm-like movement in the pupil and so when we see the combination of a sector paresis, a vermiform movement, and a tonic reaction of the pupil at near with a poor light reaction or no light reaction, these are the key differentiating features of Adie's tonic pupil. When it is unilateral, it makes it a lot less likely to be central because the central causes of light-near dissociation are usually bilateral and not unilateral. In the Adie tonic pupil, it is usually unilateral initially and then becomes bilateral over time in some percentage of patients. So when we see a light-near dissociation of the pupils, we'd like to know is it unilateral or bilateral. So what we have is a light reaction that is either poor or absent, but a preserved near reaction and that finding is called light-near dissociation. So in the Adie Tonic pupil, what we are looking for is the increased tone on the near response. The key part is the tonic part and what tone means is the pupil constricts but then stays tonically constricted and that tonic constriction is the feature that differentiates the tonic pupil from other common causes of pupil dysfunction where the pupil doesn't react well to light. So today we are talking about the Adie Tonic pupil. Lee lectures medical students on Adie's tonic pupil. Lee, MD, Chairman, Department of Ophthalmology, The Methodist Hospital, Houston, TX Professor of Ophthalmology, Weill Cornell Medicine Jaijo Vennatt, Baylor College of Medicine Class of 2021ĭr. This suggests that hippus originates from central PNS activity, and not from SNS activity, or oscillations in the balance between PNS and SNS at the pupil.Pathology Neuroanatomy Signs and SymptomsĪndrew G. Pupillary hippus can be extinguished by antagonizing the PNS, whereas agonizing the SNS dilates the pupil without affecting hippus. Hippus magnitude (treatment eye relative to control eye) decreased in the TL (-72.8 ± 4.7%, P < 0.0001) and TD (-71.3 ± 2.6%, P < 0.0001) groups, but did not change in the PL (+5.4 ± 13.7%, P = 0.173) group, despite PL pupils dilating to a proportion similar to TD. Pupillary hippus with a distinct dominant frequency was present in all measures at baseline (mean: 0.62 Hz, SD: 0.213 Hz), and that frequency did not change in any group (P = 0.971). Hippus, analyzed in both time and frequency domains, was compared between eyes and cohorts. Measures were taken at baseline, then every 5 minutes for 40 minutes. Bilateral measures of pupil size and dynamics were made over 2.6 seconds using an infrared eye-tracker sampling at 500 Hz. Each subject received one drop to the randomly determined treatment eye, while the other eye served as control. We used a paired-eye control study design with three cohorts receiving either 1.0% tropicamide (PNS antagonist) in light (TL), 1.0% tropicamide in dark (TD), or 10% phenylephrine (SNS) in light (PL), n = 12 in each. The purpose of this study was to determine the relative roles of the sympathetic (SNS) and parasympathetic nervous system (PNS) in pupillary hippus.
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