Pupil Assessment
Pupil size, shape, and reactivity — direct and consensual response, swinging-flashlight test, and afferent pupillary defects.
The Pupil Exam in Four Steps
Pupils are examined BEFORE any drops, in a dim room, with the patient fixing a distant target (near fixation constricts pupils) and the light brought in from below or the side.
Size and shape — measure both pupils in dim and bright light with a pupil gauge, in millimeters; note irregularity (surgical, traumatic, or synechiae from old iritis).
Direct and consensual response — light in one eye should constrict both: the illuminated eye's constriction is the direct response, the fellow eye's is the consensual response. Both exist because each eye's signal is distributed to both CN III nuclei.
Swinging-flashlight test — alternate the light between eyes every 2–3 seconds with equal illumination. Both pupils dilating when the light reaches one eye is a relative afferent pupillary defect (RAPD, Marcus Gunn pupil).
Near response — convergence, accommodation, and miosis together. Only chart the 'A' in PERRLA if it was actually tested; many clinics prefer PERRL plus an explicit APD statement.
A complete entry: "Pupils 4→2 mm OU, brisk, no APD." Sizes, reactivity, APD status — comparable at every future visit.
The Abnormal Pupil: Pattern Recognition
First check the drop history — a pharmacologically dilated or constricted pupil tells you about the drop, not the patient. Then use lighting to localize:
| Pattern | Think of | Notes |
|---|---|---|
| Anisocoria same in light and dark, brisk reactions | Physiologic anisocoria | ~1 in 5 people; benign |
| Anisocoria worse in the DARK (small pupil abnormal) | Horner syndrome | Ptosis + miosis + anhidrosis; dilation lag; always worked up |
| Anisocoria worse in the LIGHT (large pupil abnormal) | Adie tonic pupil, CN III palsy, pharmacologic | The can't-constrict pupil stands out in brightness |
| Large pupil, poor light response, slow tonic near response | Adie tonic pupil | Benign; often young women; slow redilation |
| Large pupil + ptosis + eye down-and-out | Third-nerve palsy | EMERGENCY — aneurysm until proven otherwise |
| Fixed dilated pupil unresponsive even to pilocarpine | Pharmacologic blockade | Scopolamine patch, plant/drop exposure — history solves it |
| Small irregular pupils, react to near but not light | Argyll Robertson | Classic light-near dissociation of neurosyphilis |
| Rhythmic size oscillation under steady light | Hippus | Normal; no workup |
| Bilateral symmetric sluggish pupils | Systemic medications | Anticholinergics (antihistamines, TCAs) — think drugs before lesions; opioids cause the opposite (bilateral miosis) |
New anisocoria with ptosis, diplopia, or pain goes to the physician immediately.
RAPD: The Assistant's Most Important Catch
What it means — the two eyes deliver unequal afferent signal: asymmetric optic-nerve disease (optic neuritis, ischemic optic neuropathy, advanced glaucoma) or widespread retinal dysfunction (large detachment, vascular occlusion).
What it does NOT come from — refractive error, amblyopia (usually trace at most), or cataract. Even a dense white cataract transmits enough light: an RAPD behind a cataract means something else is wrong — retina or nerve — and changes surgical counseling.
Why the pupils stay EQUAL — each eye's input drives both pupils, so an afferent defect never causes anisocoria. The RAPD is purely a dynamic finding in the swinging light; unequal pupils point to efferent or structural causes instead.
Technique discipline — equal brightness, equal duration (2–3 s), same angle and distance on each eye, brisk transit across the nose. Sloppy technique both creates false RAPDs and hides real ones.
Grading — neutral-density filters over the better eye until the response balances quantify the defect in log units, letting the practice track optic-nerve disease over time.