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Pupillary Responses

Pupillary Constriction

The physiology behind a “normal” pupillary constriction is a balance between the sympathetic and parasympathetic nervous systems.

Parasympathetic innervation leads to pupillary constriction.  A circular muscle called the sphincter pupillae accomplishes this task.  The fibers of the sphincter pupillae encompass the pupil.  The pathway of puillary constriction begins at the Edinger-Westphal nucleus near the occulomotor nerve nucleus.  The fibers enter the orbit with CNIII nerve fivers and ultimately synapse at the cilliary ganglion.  The muscle itself is innervated by the short cilliary nerves. Note that the entire parasympathetic innervations happens at the brainstem level, whereas the sympathetic innervation takes a long circuitous route to get to the pupil!

Sympathetic innervation leads to pupillary dilation.  Dilation is controlled by the dilator pupillae, a group of muscles in the peripheral 2/3 of the iris.  Sympathetic innervation begins at the cortex with the first synapse at the cilliospinal center (also known as Budge’s center after German physiologist Julius Ludwig Budge).  Post synaptic neurons travel down all the way through the brain stem and finally exit through the cervical sympathetic chain and the superior cervical ganglion.  They synapse at the superior cervical ganglion where third-order neurons travel through the carotid plexus and enter into the orbit through the first division of the trigeminal nerve.

If the postganglionic sympathetic fibers are interrupted anywhere along the internal carotid arteries or if the superior cervical ganglion is suffers a lesion, the result is miosis, drooping of the eyelid, and abolition of sweating over one side of the face; this constellation is known as Horner’s syndrome.

Hippus (physiologic pupillary unrest) is an irregular wavering between constricting and dilating that occurs through the opposed actions of the sphincter and dilator muscles. Of no clinical consequence.

Performing the Exam

When performing a pupillary exam, it sometimes helps to illuminate pupils indirectly from the side, so you can actually see what is happening.

1. Observe the pupil size and shape at rest

2. Observe the direct response (constriction of the illuminated pupil)

-Failure of direct response is often due to defects of the ipsalateral visual pathway.  Including the optic nerve, pretectal area, the pupillary constrictor muscles, and the parasympathetic fibers iin CN III

3. Observe the consensual response (constriction of the opposite pupil)

-Improper responses are often due to defects in the contralateral visual pathway. Including the optic nerve, pretectal area, the pupillary constrictor muscles, and the parasympathetic fibers in CN III

4. Repeat with the opposite pupil

RAPD (relative afferent pupillary defect)

An RAPD is a defect in the direct response.  It is due to damage in the afferent pupillary light pathway.  This is often due to an asymmetric defect in light detection by the diseased retina or more commonly by a decrease in signal transmission through the optic tract and into the E-W nucleus or the geniculate ganglia.

It is important to be able to differentiate whether a patient is complaining of decreased vision from an ocular problem such as catarct or from a defect of the optic nerve.  If an optic nerve lesion is present the affected pupil will not directly constrict to light as effectively as the healthy pupil.  However, it will still consensually constrict to light normally. The swinging flashlight test is helpful in separating these two etiologies as only patients with optic nerve damage will have an RAPD.

Rapid Flashlight Test

1. Swing a light back and forth in front of the two pupils and compare the reaction to stimulation in both eyes.

2.  When light reaches a pupil there should be a normal direct and consensual response.

3. An RAPD is diagnosed by observing paradoxical dilatation when light is directly shone in the affected pupil after being shone in the healthy pupil.

In this imagine demonstrating the swinging flashlight test panel C is demonstrating an RAPD of the L eye.

This decrease in constriction or widening of the pupil is due to reduced stimulation of the visual pathway by the pupil on the affected side.  By not being able to relay the intensity of the light as accurately as the healthy pupil and visual pathway, the diseased side causes the visual pathway to mistakenly respond to the decrease in stimulation as if the flashlight itself were less luminous.  This explains the healthy eye is able to undergo  both direct and consensual dilatation seen on the swinging flashlight test.

Inflammation of the Eye

Inflammatory disorders of the eye range from ubiquitous to rare and also from benign to emergent.  In this table the salient features that help the clinician separate the various inflammatory disorders of the eye are highlighted.

Common Causes of Red Eye
Acute Conjunctivitis Acute Anterior Uveitis (Iritis) Acute Angle-Closure Glaucoma Corneal Trauma or Infection
Incidence Extremely common Common Uncommon Common
Discharge Moderate to copious None None Watery or purulent
Vision No effect on vision Often blurred Markedly blurred Usually blurred
Pain Mild Moderate Severe Moderate to severe
Conjunctival injection Diffuse; more toward fornices Mainly circumcorneal Mainly circumcorneal Mainly circumcorneal
Cornea Clear Usually clear Steamy Clarity change related to cause
Pupil size Normal Small Moderately dilated and fixed Normal or small
Pupillary light response Normal Poor None Normal
Intraocular pressure Normal Usually normal but may be low or elevated Markedly elevated Normal
Smear Causative organisms No organisms No organisms Organisms found only in corneal infection

Riordan-Eva Paul, “Chapter 7. Disorders of the Eyes & Lids” (Chapter). McPhee SJ, Papadakis MA: CURRENT Medical Diagnosis & Treatment 2011:

Horner’s Syndrome

Horner’s syndrome is a constellation of physical exam findings which relate to disruption of sympathetic fibers anywhere from the sympathetic plexus surrounding the carotid artery to the brainstem.  Horner’s syndrome is defined as ptosis (drooping eyelid), miosis (pupillary constriction), and anhidrosis (decreased sweating) all ipsalateral to the sympathetic disruption.  Other clinical symptoms may occur depending on the site of the sympathetic nerve disruption.

Ptosis: The superior tarsal muscle requires sympathetic innervation to keep the eyelid retracted

Miosis: A loss of sympathetic input causes unopposed parasympathetic stimulation which leads to pupillary constriction.  This degree of miosis may be subtle and require a  dark room.

Anhidrosis:  Also caused by a loss of sympathetic activity.  The pattern of anihidrosis may help identify the lesion.  Anhidrosis of the entire face is often associated with a lesion at the level of the carotid artery.  Partial anhidrosis involving only the medial aspect of the forehead ipsalateral side of the nose is associated with a lesion distal to the carotid bulb.

Clinical-radiographic correlate

When attempting to identify the causes of Horner’s syndrome often consultation with a radiologist is helpful.  It is helpful for the clinician to provide a logical differential diagnosis due to the variety of causes and locations that can cause Horner’s syndrome.  This table, summarized from statdx, covers many of the common causes of Horner’s syndrome.

Cause Clinical Radiographic
Carotid Artery Dissection Horner’s triad +/- Periorbital pain, ispalateral visual loss, and recent                                     trauma CTA: Narrowing of the ICA lumen with subintimal hematoma
Nasopharyngeal Carcinoma Look for other acute causes Carotid Sinus(CS) involvement of tumor
Cavernous Sinus Thrombosis Sharp headache, periorbital edema, Lateral gaze palsy (CN VI) Non-enhancing clot in an enlarged CS. Possible large superior ophthalmic vein
Fibromusclar Dysplasia Concern in young women r/o carotid dissection and image other arteries Multifocal stenosis, single wall outpouching, tubular stenosis
Pancoast Tumor Smoking history, pleuritic chest pain Apical mass invading cervical-thoracic outlet
Brachial Plexus Injury Traumatic severe shoulder injury Avulsion of one or more brachial plexus roots
Lymphoproliferative disorders Mostly Non-Hodgkin’s lymphoma Enhancing solid mass in any area of the orbit

About the Author

Amar Trivedi, BA  is a fourth-year medical student at Stanford.  He is applying in Internal Medicine with an interest in the philosophy of medicine, bioethics, and using new technology at the bedside.


Written by stanford25admin

June 7, 2010 at 3:22 pm

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