How I read the history

• Seen only with blinking. A blink causes lid pressure, a brief tear-film change, and a small jolt to the vitreous.
• Seen only against a light source or screen, not in the dark. True retinal photopsia from vitreous traction is usually worse in the dark and with eye movement. Cecil describes flashes that "may be more pronounced in the dark and with rapid eye movement" (Goldman-Cecil Medicine, Sensation of Flashing Lights). Wills Eye says the same: flashes are "more common in dim illumination or with eye movement" (Wills Eye Manual, 11.1). So the light-dependence points toward an optical or anterior segment cause, but it does not exclude retinal disease.
• The spot shifts with gaze. I'm assuming it stays fixed relative to the eye as he looks right or left. That means it comes from the eye's own structures, not the outside world. Please confirm this with him.
• Duration of one day, with no pain, redness, watering or trauma. This rules out most inflammatory and surface-injury causes. It does not rule out an early vitreoretinal event.

Differential diagnosis

1. Acute posterior vitreous detachment (PVD) with vitreoretinal traction, with or without a retinal tear.
   • Sudden-onset flashes suggest vitreous traction on the peripheral retina, sometimes with a resulting tear. Because a tear can progress to detachment, Cecil calls for urgent ophthalmology review.
   • PVD is uncommon under 50 (less than 10%) (Kanski). At 31 it is more likely if he has high myopia, previous eye surgery or YAG laser, trauma, or a family history of detachment.
   • Roughly 8% to 26% of acute symptomatic PVDs have a retinal break (Wills Eye).
2. Retinal tear, lattice degeneration or early retinal detachment. Look for new floaters, a curtain or shadow, or field loss.
3. Posterior uveitis or white dot syndromes (MEWDS, AZOOR, etc.). These typically cause unilateral photopsia in young adults, often with floaters or a blind spot. Wills Eye notes that many uveitides present with floaters and photopsias.
4. Optic neuritis or optic nerve disease. Phosphenes with eye movement can occur. Ask about colour desaturation, pain on eye movement, and a relative afferent pupillary defect (RAPD). Bradley and Daroff list optic nerve disease among causes of photopsia.

• This is my leading benign explanation. It fits being visible only against a light source, only with blinking, and moving with gaze.
• Ask about contact lens wear, dry eye, and screen time.

1. Early lens or media opacity. Examples are a posterior subcapsular or cortical change, a vitreous opacity, or a Weiss ring. These can produce glare or sparkle against bright light.
2. Entoptic or flicker phenomena. Blinking in front of a PWM-dimmed screen or LED creates stroboscopic bright images and afterimages. This is common and harmless.
3. Migraine visual aura. Unlikely, because it is monocular, brief, and tied to blinking. Wills Eye describes aura as multicoloured zig-zags lasting about 20 minutes with a normal fundus.
4. Macular causes, such as central serous chorioretinopathy or vitreomacular traction. Ask about distortion or micropsia.
5. Drugs. Digitalis is listed in Bradley and Daroff. Ask about any new medications or supplements.

Next steps

• Is it monocular? Cover each eye in turn.
• Any floaters, curtain or shadow, field loss, distortion, or reduced vision?
• Myopia and its degree, contact lenses, previous eye surgery or YAG laser, trauma, family history of detachment.
• Headache, neurological symptoms, systemic or infective illness, new drugs.

1. Visual acuity, pupils (check for RAPD), colour vision, confrontation fields, and an Amsler grid.
2. Intraocular pressure.
3. Slit-lamp exam of the tear film, cornea (with fluorescein), anterior chamber, and lens. Look specifically for pigmented cells in the anterior vitreous (Shafer sign or "tobacco dust"). Wills Eye states that these, or vitreous haemorrhage, with an acute PVD carry a more than 70% chance of a coexisting retinal break.
4. Dilated fundus exam with indirect ophthalmoscopy and scleral depression. This is the key test. It rules out a retinal break or detachment and looks for a PVD, a Weiss ring, lattice degeneration, and chorioretinal lesions. Examine the fellow eye too.

• Macular OCT, which can confirm or exclude PVD, vitreomacular traction, and macular pathology. Hyperreflective vitreous dots ("falling ash sign") correlate with peripheral breaks.
• B-scan ultrasound if the view of the retina is poor, for example from vitreous haemorrhage.
• Widefield fundus photography or autofluorescence, and fluorescein or ICG angiography if a white dot syndrome is suspected.
• Automated visual field testing, with MRI of the brain and orbits if there are neurological features. Do this if optic neuritis or a neurological cause is suspected, or if a field defect or RAPD is found.
• Dry eye assessment (tear break-up time, staining) if everything else is normal.

Disposition by findings

• No break, no haemorrhage: reassure, give clear retinal detachment warning symptoms, and repeat the dilated exam with scleral depression in 4 to 6 weeks. There is a 2% to 5% risk of a new break after an initially normal exam (Wills Eye).
• Mild vitreous haemorrhage or peripheral punctate retinal haemorrhages: repeat the exam in about 2 weeks.
• Significant vitreous haemorrhage or pigmented anterior vitreous cells: repeat the exam within 24 hours by a retina specialist.
• Retinal break found: laser or cryotherapy, per retina service.
• Normal retina with tear-film debris or dry eye: lubricants and lid hygiene.

Recent evidence check