Early phase of pupil dilation is mediated by the peripheral parasympathetic pathway

Pupil diameter fluctuates in association with changes in brain states induced by the neuromodulator systems. However, it remains unclear how the neuromodulator systems control the activity of the iris sphincter (constrictor) and dilator muscles to change the pupil size. The present study compared temporal patterns of pupil dilation during movement when each muscle was pharmacologically manipulated in the human eye. When the iris sphincter muscle was blocked with tropicamide, the latency of pupil dilation was delayed and the magnitude of pupil dilation was reduced during movement. In contrast, when the iris dilator muscle was continuously stimulated with phenylephrine, the latency and magnitude of rapid pupil dilation did not differ from the untreated control eye, but sustained pupil dilation was reduced until the end of movement. These results suggest that the iris sphincter muscle, which is under the control of the parasympathetic pathway, is quickly modulated by the neuromodulator system and plays a major role in rapid pupil dilation. However, the iris dilator muscle receives signals from the neuromodulator system with a slow latency and is involved in maintaining sustained pupil dilation.

Isolated Simultaneous Bilateral Adie’s Pupil

Adie’s pupil, an efferent pupillary defect is caused by injury to parasympathetic pupillomotor nerve supply to Iris sphincter muscle. More commonly seen in young adult females with up to 80% cases having unilateral involvement. According to literature, Adie’s Pupil may occur alone or as a part of a systemic condition or may be associated with a syndromic presentation. Bilateral Adie’s pupil in a female at initial presentation with mild visual symptoms and no syndromic association is sparsely reported in literature.

Anisocoria

A difference in the size of the pupils (anisocoria) is a frequent finding on physical examination. While often a cause for alarm, it is not uncommonly physiologic. In this chapter, we begin by reviewing the innervation of the iris sphincter and dilator muscles. We next introduce clinical strategies that can help to determine the etiology of anisocoria. We describe the components of the pupil examination, which includes an evaluation of pupil size in bright light compared to darkness, as well as evaluation of the pupil shape, response to light, and response to near. We include an algorithm that summarizes the clinical approach to anisocoria. Lastly, we review the clinical features of physiologic anisocoria, which occurs in up to 20% of the normal population and does not require further diagnostic testing.

Modulation of Iris Sphincter and Ciliary Muscles by Urocortin 2

Urocortin 2 (UCN2) is a peptide related to corticotropin-releasing factor, capable of activating CRF-R2. Among its multisystemic effects, it has actions in all 3 muscle subtypes. This study’s aim was to determine its potential role in two of the intrinsic eye muscle kinetics. Strips of iris sphincter (rabbit) and ciliary (bovine) muscles were dissected and mounted in isometric force-transducer systems filled with aerated-solutions. Contraction was elicited using carbachol (10-6 M for iris sphincter, 10-5 M for ciliary muscle), prior adding to all testing substances. UCN2 induced relaxation in iris sphincter muscle, being the effect maximal at 10-7 M concentrations (-12.2 % variation vs. control). This effect was abolished with incubation of indomethacin, antisauvagine-30, chelerytrine and SQ22536, but preserved with L-nitro-L-arginine. In carbachol pre-stimulated ciliary muscle, UCN2 (10-5 M) enhanced contraction (maximal effect of 18.2 % increase vs. control). UCN2 is a new modulator of iris sphincter relaxation, dependent of CRF-R2 activation, synthesis of prostaglandins (COX pathway) and both adenylate cyclase and PKC signaling pathways, but independent of nitric oxide production. Regarding ciliary muscle, UCN2 enhances carbachol-induced contraction, in higher doses.