Pupillary Escape Research Articles

The association between pupillary responses and axial length in children differs as a function of season

The association between pupillary responses to repeated stimuli and adult refractive error has been previously demonstrated. This study evaluated whether this association exists in children and if it varies by season. Fifty children aged 8–17 years (average: 11.55 ± 2.75 years, 31 females) with refractive error between + 1.51 and − 5.69 diopters (non-cycloplegic) participated (n = 27 in summer, and n = 23 in winter). The RAPDx pupilometer measured pupil sizes while stimuli oscillated between colored light and dark at 0.1 Hz in three sequences: (1) alternating red and blue, (2) red-only, and (3) blue-only. The primary outcome was the difference in pupillary responses between the blue-only and red-only sequences. Pupillary constriction was greater in response to blue light than to red for those with shorter eyes in summer (β = − 9.42, P = 0.034) but not in winter (β = 3.42, P = 0.54). Greater constriction comprised faster pupillary escape following red light onset and slower redilation following stimulus offset of both colors (P = 0.017, 0.036, 0.035 respectively). The association between axial length and children’s pupillary responses in summer, but not winter may be explained by greater light-associated release of retinal dopamine in summer. Shorter eyes’ more robust responses are consistent with greater light exposure inhibiting axial elongation and reducing myopia risk.

Central retina plays a decisive role in the suppression of pupillary escape

PurposeTo explore the pupil redilation during persistent light exposure (pupillary escape phenomenon) at the macula and periphery with monochromatic light stimuli.MethodsForty healthy subjects aged 18–64 years (24 females) were examined by chromatic pupil campimetry (CPC) using red and blue 4-s stimuli of 10° radius at the center and 20°-peripheral locations one per quadrant. One glaucoma patient and one achromatopsia patient served as disease models. For statistical analyses, linear mixed-effects models were performed followed by post hoc t-tests.ResultsA distinct pupillary escape could be demonstrated peripherally (blue 0.099%*s, red 0.153%*s); at the central healthy retina, there was no relevant escape, neither for blue nor red stimulation. Comparing central versus peripheral stimulation revealed highly significant differences in the escape (difference blue 0.100 ± 0.013, red 0.144 ± 0.013, < 0.0001, respectively). In the periphery, the escape was significantly more pronounced for red compared with blue stimulation (difference 0.054 ± 0.013; p = 0.0001). Enhanced pupillary escape outside of the 95% confidence interval of the linear mixed-effects model of the healthy population could be exemplarily shown in a patient with glaucomatous ganglion cell damage. In the achromatopsia example, no relevant escape was found for blue stimulation, but for red stimulation in the periphery in a comparable range to healthy controls.ConclusionThe results emphasize that an intact inner retinal network of nerve fibers arising from the central macular region is necessary for maintaining pupillary constriction during a bright 4-s light stimulus and preventing increase of pupillary escape. Increasing receptive field sizes towards the periphery on the level of retinal ganglion cells and less input from central 1:1 connections could be one of the driving mechanisms for pupillary escape.

Analysis of retinal function using chromatic pupillography in retinitis pigmentosa and the relationship to electrically evoked phosphene thresholds.

To analyse pupil responses to specific chromatic stimuli in patients with advanced retinitis pigmentosa (RP) to ascertain whether chromatic pupillography can be used as an objective marker for residual retinal function. To examine correlations between parameters of the pupil response and the perception threshold of electrically evoked phosphenes. Chromatic pupillography was performed in 40 patients with advanced RP (visual acuity<0.02 or visual field ≤5°, non-recordable ERGs) and 40 age-matched healthy subjects. Pupil responses to full-field red (605nm) and blue (420nm) stimuli of 28 lx corneal illumination were recorded and analysed for two stimulus durations (1 and 4seconds). The perception threshold of phosphenes to transcorneal electrostimulation was ascertained and correlated to the pupil responses and visual acuity. Patients with RP showed significantly reduced pupil responses to red and blue stimuli compared with the controls. With red stimuli, pupillary escape could be observed; blue stimuli resulted in a well-preserved postillumination pupil response. Phosphene thresholds were significantly increased in patients with RP and correlated with the parameters of the pupil response if all subjects were considered. Within the RP group alone, this relationship was less pronounced and statistically not significant. Chromatic pupillography demonstrated a significant decrease in outer retinal photoreceptor responses but a persisting and disinhibited intrinsic photosensitive retinal ganglion cell function in advanced RP. These phenomena may be useful as an objective marker for the efficacy of any interventional treatment for hereditary retinal diseases as well as for the selection of suitable patients for an electronic retinal implant.

Pupillary responses driven by ipRGCs and classical photoreceptors are impaired in glaucoma.

The aim was to investigate the involvement of intrinsically photosensitive retinal ganglion cells (ipRGCs) in patients with manifest glaucoma and ocular hypertension (OH) using specific parameters of the pupil light reflex to chromatic stimuli. Twenty-five patients with manifest glaucoma, 16 patients with OH and 16 healthy control subjects were stimulated with 28lx red (605nm) or blue (420nm) light with a duration of either 1s or 4s. The consensual pupil light reaction was recorded by means of infrared pupillometry. The maximal relative amplitude (MRA), the post-illumination pupil response PIPRblue-red, and the slope of the response during exposure to the 4s red stimulus (SORRS) were calculated and compared using ANOVA and Tukey-Kramer post-hoc tests. Correlations between pupil parameters and visual field defects were analyzed using Pearson correlation coefficient r. PIPRblue-red was reduced in glaucoma patients compared to normals (p < 0.001) and OH (p < 0.01). There was no significant difference between OH and normals. Glaucoma patients showed additionally reduced MRA for red and blue light (p < 0.05) and a pupillary escape during exposure to red light (increased SORRS, p < 0.0005). This pupillary escape could also be seen in single subjects with OH. Significant correlations between pupil parameters and visual field defects were detected. The reduced PIPRblue-red indicates a characteristic impairment of the melanopsin-driven pathway of ipRGCs in glaucoma patients, whereas the reduced MRA and increased SORRS suggest a disturbed synaptic function and altered interaction between outer photoreceptors, RGCs, and ipRGCs.

The Perils of PERRLA

Letters17 April 2007The Perils of PERRLALeonard A. Levin, MD, PhDLeonard A. Levin, MD, PhDFrom University of Wisconsin Medical School and University of Montréal; Montréal, Québec, Canada.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-146-8-200704170-00022 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Background: The pupillary examination is arguably the single most useful clinical test of the nervous system in the conscious or unconscious patient. When properly done with a few swings of a light, the examination can assess the functional status of the retina, optic nerve, contralateral optic tract, cranial nerve III, dorsal midbrain, and sympathetic chain from the hypothalamus down to the lower cervical spinal cord and up to the cavernous sinus and orbit. The results of normal pupil testing are frequently documented with PERRLA (pupils equal, round, reactive to light, and accommodation). But PERRLA is not only incorrect and inexact—it ...Reference1. Levatin P. Pupillary escape in disease of the retina or optic nerve. Arch Ophthalmol. 1959;62:768-79. [PMID: 14416133] CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAuthors: Leonard A. Levin, MD, PhDAffiliations: From University of Wisconsin Medical School and University of Montréal; Montréal, Québec, Canada.Disclosures: None disclosed. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 17 April 2007Volume 146, Issue 8Page: 615-616KeywordsDenervationOptic nerveOptic neuropathyParalysisReflexesRetinaSpinal cordSympathetic nervous systemVisionVisual impairments ePublished: 17 April 2007 Issue Published: 17 April 2007 Copyright & PermissionsCopyright © 2007 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...

Greater pupillary escape differentiates central from peripheral visual field loss

ObjectiveTo test whether pupil escape observed during a constant light stimulus was greater in eyes with central visual field loss compared to eyes with peripheral visual field loss and normal eyes. DesignComparative, observational case series. ParticipantsTwenty-seven normal subjects, 5 patients with central field loss, 11 patients with peripheral field loss, and 8 patients with combined loss (central and peripheral visual field loss) were tested. MethodsA dual-channel infrared pupillograph was used to simultaneously record the right and left pupil diameters at a rate of 60 Hz to characterize the initial, phasic pupil contraction, and the sustained, or prolonged, pupil contraction in response to a 5-second light stimulus. Full-field light stimuli with a diameter of 30° were presented to each eye at seven different intensities. Main outcome measuresThe amplitude of the phasic pupil contraction was compared with the amplitude of the sustained pupil contraction at the four brightest intensities (slope of phasic versus sustained contraction) in the normal eyes and in eyes with visual field loss in the center and the periphery. ResultsThe sustained pupillary contraction showed a statistically greater reduction in proportion to the phasic component in eyes with central field loss compared to those with peripheral field loss, combination central and peripheral field loss, and normal eyes. ConclusionsAfferent neurons from the central retina normally contribute a substantial component to the sustained pupil response. Eyes with central field loss can be distinguished from eyes with peripheral field loss by a relatively greater loss of the sustained response, causing greater pupil escape. This study showed that pupil movements in response to a nonperimetric full-field light stimulus may provide some degree of mapping of retinotopic sensitivity. This information may be of use in interpreting the pupillary movements during the swinging flashlight test and may help predict the pattern of visual field loss.

Pupillary escape

Pupillary escape

Estimation of autonomic nervous activity using the inverse dynamic model of the pupil muscle plant.

In order to elucidate the mechanism of the pupillary control system, the internal property of the pupillary muscle plant, as well as the autonomic nervous input to the muscle plant, must be analyzed. In this study, we approach the problem first by constructing a new homeomorphic biomechanical model for the human pupillary muscle plant (forward dynamic model). We showed that the model is able not only to reproduce various experimental results that exhibit various nonlinearities but also to explain how such nonlinear responses are generated in terms of the internal property of the model. Then, we contrive a possible method to estimate the autonomic nervous input to the muscle plant. This method utilizes the inverse dynamic model of the pupillary muscle plant so that the autonomic nervous input can be estimated from the pupillary response. We applied this method to the experimental step responses, and showed that the estimated neural input indicates characteristics quite similar to the results of the physiological experiment. Last, we discuss the origin of the pupillary escape and capture as well as the sustained and transient components of the pupillary response, based on the analysis of the forward and/or inverse dynamic model.

Pupillary escape

I performed a pupillographic study of pupillary escape to determine its effectiveness in detecting optic nerve and retinal disease. Fourteen patients and 39 normal subjects were included in the study. Only one patient had abnormal pupillary escape, even though 13 patients had relative afferent pupillary defects. Testing for pupillary escape is not a reliable clinical technique.

Neuronal population model for the pupil-size effect

The human pupil has been widely studied as an example of nonlinear biological systems. Many systems, or “black box,” models have been proposed to describe the nonlinear phenomena called “pupillary escape,” “pupillary capture,” the response asymmetry, and, more recently, the “pupil-size effect.” A new neuronal population model is given here which is more homeomorphic than previous models, while retaining the accurate description of the nonlinear responses of the pupil. A signal controlling steady-state pupil size is used to control the recruitment of neuron populations from an inverse “Henneman-coded” pool. Multiple configurations of this neuronal pool are explored by comparing experimental data with computer simulations of the model.

Dynamic pupillary response controlled by the pupil size effect

Pupillary escape has been described as an initial contraction followed by a slow redilatation, occurring in response to a step stimulus of low-intensity light. When the initial pupil size is small, the response to the same step stimulus is pupillary capture, a steady and sustained contraction. In this experiment a comparison was made between three modes of controlling pupil size and thereby of regulating the pupillary response: contralateral light background level, ipsilateral light background level, and accommodative level with which there is no change in retinal adaptation. All three level setting modes showed similar results in illustrating the pupil size effect. In addition, an inhibitory effect was found with both ipsilateral and contralateral light backgrounds that is independent of Weber's Law in the contralateral case. Our results lead to the formulation of a binocular model, featuring an internal parameter control whereby a signal dependent on the static pupil size regulates the gains of the parallel phasic and tonic pathways, the former responsive to transient changes of light, and the latter to background levels of light and accommodative levels. Our findings also raise interesting questions concerning the loci of these complex interactions in the simple neuroanatomy of the pupillary pathways.

A systems model for the pupil size effect. I. Transient data.

The human pupillary control system is a paradigm for linearized biological control systems. It also exhibits a series of interesting nonlinear behaviors, particularly asymmetry, "pupillary escape," and "pupillary capture." We present a nonlinear model in which a signal dependent upon pupil size is fed back internally to cause a change in system parameters related to gains and rates of light adaptation. The model was simulated on a digital computer, a variety of experimental data was well matched, and improvements over previous pupil models demonstrated. A candidate physiological mechanism for adaptive components of the model might have the form of an inverse "Henneman coded" neuronal pool.

Pupillary escape intensified by large pupillary size

Pupil responses to light are greatly influenced by initial pupil size. Small pupils, operating under photopic conditions, show tonic responses to step increases of light and high gains; thus the pupil is a good regulator of light. Large pupils, operating under mesopic or scotopic conditions show phasic responses, “pupillary escape”, and smaller gains; the pupil only transiently influences retinal flux. By using accommodation level to set the size of the pupil, the mechanism of the “pupil size effect” is shown to be dependent on retinal light level only so far as retinal activity sets pupil size.

Interpretation of kernels. III. positive off-diagonal Kernels as correlates of the dynamic process of pupillary escape

Pupillary escape to on-step light stimulus is a well-known nonlinear dynamic phenomenon. Using adequate-bandwidth noise and a spectral computational technique, the 1st- and 2nd-degree kernels of the pupillary system were estimated. Nonlinear heuristic models, composed of cascades of linear elements, were then simulated. These heuristic models produced varying amounts of pupillary-escape-like effect for step inputs. Kernels of these heuristic models were determined with a biimpulse technique. Comparison of simulation results showed direct correspondence between positive off-diagonal 2nd-degree kernel values and the pupillary-escape-like effect demonstrated by the heuristic model. This supports the ability to interpret kernel shapes in general by relating them to the dynamics of nonlinear systems.

Pupillary escape in disease of the retina or optic nerve.

Duke-Elder,¹in discussing the clinical picture of optic neuritis, mentions "a peculiar pupillary reaction common to all forms of conduction interference, wherein, although both the direct and consensual reactions are present the contraction is not maintained under bright illumination so that the pupil slowly dilates again while the light is still kept upon the eye." This seemingly paradoxical light reaction of the pupil was observed in retrobulbar neuritis by Marcus Gunn (1904), who attributed it to the consensual reaction of the pupil to darkness. In this paper is presented a simple and sensitive method for demonstrating the Marcus Gunn sign and, also, a hypothesis to show that there is nothing peculiar or paradoxical about this pupillary reaction, which should be expected whenever the light sense is reduced by disease of the retina or optic nerve. <h3>Hypothesis</h3> Assume that the pupillomotor impulses produced by visible light (and hence the stimuli