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Paola Diaz, O.D. Ocular Disease Resident University of Houston College of Optometry Cedar Springs Eye Clinic Abnormal Pupils Why? Test the neurological integrity Aid in the determination for vision loss Clues to ocular diseases When? Comprehensive exams Prior to dilation and after dilation Symptoms: Vision loss Visual field loss Diplopia Ocular pain Evaluating neuro‐visual function /neurological status The Pupil An aperture in the center of the iris which regulates the amount of light that reaches the retina. The Pupil: Facts Size varies with: Age Larger in teenagers/middle‐aged Smaller in the very young and older Sex Larger in females Iris color Larger in blue iris vs brown Refractive error Larger in myopes Intensity of ambient light Emotions Medication The Pupil: Facts Normal size: 2‐4mm in the light 4‐8mm in the dark Pupillary light reaction @ 31 weeks of gestation Allows aqueous humor flow Improves visual acuity by preventing irregular refraction and increasing depth of focus The Nervous System Sphincter and Dilator Muscle Smooth muscle located in the iris derived from neural ectoderm Regulates the size of the pupil Autonomic NS Iris Smooth Muscle Sphincter Dilator Autonomic Nervous System Parasympathetic Sympathetic Action Constriction Dilation Pathways Pupillary Light Reflex Sympathetic Pupillary Near Pupillary Reflex Pupillary Light Reflex (PLR) Afferent Pathway Efferent Pathway Parasympathetic Pupillary Pathway Homonymous= Same Side Hemianopsia=half of the field Congruent=Same pattern Incongrunet=Different pattern Sympathetic Pathway Central 1st Preganglionic 2nd Postganglionic 3rd Sympathetic Pathway: Pupillary dilator‐ pupil dilation Muller’s muscle‐lid retraction (upper and lower) Facial sweating Lacrimal gland‐lacrimation Vessels of conjunctiva‐ vasoconstriction Iris melanin development in early life Near Pupillary Reflex Constriction of pupil when gaze from distance to near object Independent of illumination Triad response: Accommodation, convergence, and miosis Pathway poorly understood Final pathway is shared with the efferent pathway of the pupillary light reflex Bypassing the pretectal nuclei Lesion in the dorsal midbrain/ pretectal nucleus = light near dissociation) Afferent (Sensory) Pathway: Carry information to the CN Input from: retina, optic nerve, and the anterior visual pathway (chiasm, optic tract, and midbrain) Assess integrity of anterior visual system Afferent Pupillary Defects: Interference with: retinal layers, optic nerve, chiasm, optic tract, or midbrain pretectal area. Impairs the PLR and reduces the amplitude of pupil movement in response to light stimulus. Swinging flashlight test. Does NOT cause anisocoria. Does NOT affect near response. Efferent (Motor) Pathway: Autonomic NS Parasympathetic Sympathetic Information from CNS to the target organ Efferent Pupillary Defects: Any damage to the pathway innervating the sphincter or dilator muscle. Causes anisocoria. Reduced response to light AND near. Equipment/Technique Transilluminator Penlight BIO If inadequate brightness Pupil size card Burton lamp or ultraviolet light ***DO NOT shine light directly into the eye…should be directed from slightly inferior and upward toward the patient's pupil. source Dark irides Infrared pupillometer(CPT 0341T) Size of pupil Neutral density filers /crossed polarized neutral density filters Quantify APD Examination: Order Matters 1. Size 2. Reaction 3. Color 4. Shape PERRLA 5. Position Size Performed first 1.0 mm of anisocoria= 0.1 log induced APD Technique Pupil size cards Target‐ distance vs. near Illumination‐ bright vs. dark Looking for pupil symmetry Anisocoria 20% of Pop. < 1 mm Induced Pathology Physiological Innervations Structure Efferent Trauma Parasympathetic Sympathetic Medication Toxins Drugs Never Afferent Defect!!!! Anisocoria Determine which pupil is the abnormal one Present= measure in the light and dark Aniso > in LIGHT= Larger pupil abnormal (Parasympathetic Disorder) Aniso > in DARK= Smaller pupil abnormal (Sympathetic Disorder) Aniso = in the DARK AND LIGHT= Physiological Size Gross observation Observe lid position (Horner’s/CN III Palsy) EOM motility Reasons to suspect: Patient CC Lung cancer Carotid surgery Neck trauma Other S/S or Hx indicative of Horner’s or CN III palsy Size Smaller pupil abnormal Horner syndrome Argyll Robertson pupil Long‐standing Adie pupil Iritis Miotic drugs (eg. Pilocarpine) Size Larger pupil abnormal Third nerve palsy Adie pupil Iris sphincter damage Mydriatic drugs (eg. Atropine) Horner Syndrome‐small pupil Symptoms Ptosis Miosis Anhydrosis Often asymptomatic Signs Anisocoria greater in the DARK Mild ptosis (2mm)/lower eyelid elevation, ipsilateral Lower IOP Lighter iris color (congenital cases) Transient inc in accommodation Dilation Lag Etiology‐>Sympathetic Disorder Pre‐ganglion disorders: Trauma Aortic dissection Carotid dissection Tuberculosis Pancoast tumor Post‐ganglion disorders: Trauma Cluster migraine headache Neck surgery Thyroid surgery Congenital‐>birth trauma Horner Syndrome Horner Syndrome Diagnosis‐> Pharm testing Test Cocaine 10% Abnormal Pupil Response No dilation Hydroxy‐ amphetamine Dilation 1% Hydroxy‐ amphetamine No dilation 1% Apraclonidine 0.5% or 1% Reversal Treatment Treat underlying disorder Ptosis surgery may be Location performed electively Work‐up acute Horner syndromes ASAP to r/o Non Specific life threatening causes MRA ‐>done same day for Preganglionic dissection, other test can be done within 1‐2 days Postganglionic Chronic Horner syndrome evaluated with less urgency Non Specific Horner Syndrome Argyll Robertson‐small pupil Symptoms Asymptomatic Signs Miosis Light‐near dissociation Dilate poorly in darkness/mydriatic agents Etiology Hallmark for tertiary syphilis (80% w/ neurosyphilis will have AR) Tabes diabetica MS Encephalitis Sarcoidosis Chronic alcoholism Trauma Neoplasm Diabetes mellitus Testing Light reaction and near reaction Look for interstitial keratitis DFE: Chorioretinitis, papillitis, uveitis FTA‐ABS, MHA‐TP, RPR, VDRL laboratory test Lumbar puncture Treatment Treat active underlying disease Third Nerve Palsy‐large pupil Symptoms Diplopia Droopy eyelid Difficulty reading/focusing Eye or hemicranial pain Signs Complete: ptosis, down and out eye, EOM restriction (minus abduction and intorsion), pupil fixed and dilated Superior division: ptosis with up‐gaze restriction Inferior division: down gaze and adduction restriction, pupil dilation Aberrant regeneration Loss of accommodation Loss of near‐light reflex Etiology Pupil involving Aneurysm (PCAA) more common Tumor Trauma Congenital Cavernous sinus mass Pupil sparing Ischemic microvascular disease more common Cavernous sinus syndrome or Giant cell less common Testing Good Hx Preliminary testing (pupils/ EOM’s) Pilocarpine 1%‐> constriction if III palsy Neurological examination CNS imaging to r/o mass/aneurysm Blood laboratory testing Third Nerve Palsy Treatment Treat underlying condition Patch for diplopia Strabismus surgery Pupil sparing observe daily for 14 days for involvement and then every 1 month until resolved Ischemic in nature resolved by 3 months If does not improve by 3 months, get pupil involvement, or worse refer for imaging If pupil involved and imaging /angiography negative = order lumbar puncture Adie (Tonic) Pupil‐large pupil Symptoms Difference in pupil size Blurry near vision Photophobia Asymptomatic Signs Pupil: Minimal to no reaction to light Pupil: Slow, tonic constriction with convergence, and slow re‐ dilation Typically unilateral initially‐>may become bilateral More common in young women Over time the affected pupil may become smaller than normal pupil Etiology Idiopathic‐>more common Trauma Surgery Zoster infection Testing Evaluate pupil reaction Test for cholinergic hypersensitivity: 0.125% pilocarpine ‐> Adie’s pupil will constrict, normal no change If unilateral, no further testing indicated If bilateral, laboratory testing indicated If in younger than 1 year old, consult with pediatic neurologist to r/o Riley‐Day syndrome Adie (Tonic) Pupil Treatment Pilocarpine 0.125% bid to qid for cosmesis and accommodation or Brimonidine If diagnosis certain, f/u is routine Examination 1. Size 2. Reaction 3. Color 4. Shape 5. Position Reaction to light Direct/Consensual Response Relative Afferent Pupillary Defect Reaction to light Direct and Consensual Response Technique Dim to dark illumination Distant target Shine light at pupil, observe response for eye which light is shown and other eye when not exposed to light Repeat other eye Reaction to light Direct and Consensual Response Observation Pupil response Absent Reduced/sluggish Brisk If abnormal= afferent (Must r/o efferent= anisocoria first) Afferent Defect= retinal, optic nerve, optic chiasm, or optic tract defect Reaction to light Direct and Consensual Response Reaction to light Relative Afferent Pupillary Defect (RAPD) Technique Dim to dark illumination Distant target Use a bright light source Too bright‐>poor re‐dilation. Fix by inc distance Shine light directly to one eye for 2‐3 sec then swing to other eye 2‐3 sec Repeat at least 3 times Reaction to light Relative Afferent Pupillary Defect (RAPD) Observation Compare direct pupil response in one eye to the direct pupil response in the other eye Speed, magnitude, and escape (+) APD: the affected pupil will dilate when the flashlight is moved from the normal eye to the abnormal eye RAPD Results from significant unilateral or asymmetric visual deficit caused by retinal or optic nerve disease Bilateral APDs do not exist Reaction to light: RAPD Most common causes: Other causes: Optic nerve disease Little ON damage‐>large APD May/may not visualize Chiasmal disease Retrobulbar? Time? Extensive retinal damage Large macular/retinal lesion ‐>little APD Will not miss it! Gross macular disease Large retinal lesions RD BRAO/CRAO Ischemic Vein Occlusions *Cataracts rarely produce APDs Reaction to light: RAPD RAPD Grading System 4+ little to none light response in affected eye ‐>big difference in light reflexes between the two eyes 3+ some light response (near normal) but quicker than normal pupil escape 2+ slight response to light in one eye 1+ very slight difference between the two eyes light responses Reaction to light: RAPD Neutral Density Filters Filter placed over good eye Keep increasing until no asymmetry present, go over= reversal Loss of central 5 degrees of VF = RAPD of 0.3 log units Loss of entire central area of field (10 degrees) =RAPD of 0.6‐0.9 log units Each VF quadrant outside of the macula is a 0.3 log units Examination 1. 2. Size Reaction 3. Color 4. Shape 5. Position Color Iris Pupil Check for heterochromia Physiological Trauma Disease Greyish/black‐ Normal Jet black‐ Aphakia Greyish/white‐ Cataract Whitish‐ Retinoblastoma Reddish‐ Albinism Shape Round shape‐ Normal D‐Shaped‐ Iridodialyis Festooned on DFE‐ Posterior synaechia Pear shaped‐ Leukoma adherent Key hole‐ Sector iridectomy Peaked‐Trauma Position Normally in the center of the iris (slightly 0.5mm inferonasal) Corectopia‐ displacement of the pupil •Bilateral displacement of the pupil •Lens dislocation in the opposite direction •Poor pupillary dilation w/ mydriatics Ectopia Lentis et Pupillae Key Points To Remember Afferent pupillary light pathway follows the visual pathway as far as the posterior optic tract Afferent defect do NOT cause anisocoria Always measure size first, then pupil reaction Efferent defects cause anisocoria and a reduced response to light and near Near reflex fibers bypass the pretectal nuclei = causing a light‐near dissociation Do not forget gross observation Pupil defects can be due to life threatening conditions Do not forget about the PUPILS! QUESTIONS????
