How Ophthalmologists Analyze Causation in Vision Loss Claims

Marc H. Shomer, MD, PhD, QME · Published August 2, 2026 · Last reviewed August 2, 2026

Association Is Not Causation

The starting discipline is the oldest one in medicine: after does not mean because. Vision declines for many reasons on many timescales — cataract progresses, macular degeneration advances, diabetic retinopathy evolves, glaucoma erodes the field — and any of these can first come to a person's attention shortly after a memorable event, because the event prompts attention to the eyes. The temporal sequence "incident, then noticed vision loss" is consistent with causation, but it is equally consistent with pre-existing disease newly noticed. The analysis exists to distinguish the two, and an evaluator who treats sequence as proof has skipped the analysis entirely.

Step One: Establish the Baseline

Every causation opinion is a comparison against baseline, so the first task is documentary: what did the records show before the event? Prior ophthalmology and optometry charts, refraction histories, and even DMV screenings establish pre-incident acuity; earlier OCT scans (optical coherence tomography — cross-sectional retinal imaging) and visual fields establish pre-incident structure and function. A well-documented healthy baseline makes a later deficit meaningful. A baseline showing the disease already present reframes the question as aggravation, not causation. And an absent baseline weakens every downstream inference, which is why locating prior records is worth real effort — the point pressed in What Records to Provide.

Step Two: Assess Mechanism Plausibility

The alleged cause must be physically capable of producing the claimed effect. Ophthalmology is well supplied with established injury mechanisms: blunt trauma can cause angle recession, lens dislocation, and retinal tears; penetrating injury follows the geometry of the wound; alkali burns penetrate ocular tissue progressively; certain drugs have well-characterized retinal or optic nerve toxicity. Mechanism analysis asks whether the claimed exposure, at the claimed magnitude, produces the claimed lesion in the medical literature and clinical experience. A minor contusion blamed for a pattern of damage seen only in severe crush injury fails this test; a documented blunt trauma followed by classic contrecoup retinal findings passes it. Where mechanism is uncertain, the opinion must say so rather than paper over the gap.

Step Three: Examine the Temporal Course

Beyond mere sequence, causation analysis asks whether the tempo of the deficit fits the alleged cause. Ophthalmic conditions have characteristic clocks. Traumatic optic neuropathy produces immediate loss with nerve fiber layer thinning that develops over subsequent weeks. Retinal detachment after trauma may lag days to weeks behind the inciting tear. Chemical injury declares itself immediately. Degenerative disease progresses over years. When the documented course matches the expected clock of the alleged mechanism, causation strengthens; when a claimant was documented seeing well for months after the incident and the deficit appears later without a bridge, the alleged mechanism must explain the gap or yield to a better explanation. Serial records are decisive here, which is another reason complete charts matter more than summaries.

Step Four: Correlate with Objective Structure

Vision is a function; functions have anatomy. The strongest causation opinions tie the claimed functional loss to a structural correlate that objective testing can date and localize: RNFL thinning on OCT matching an optic nerve insult, photoreceptor disruption underlying a central scotoma, angle recession on gonioscopy (mirrored-lens examination of the eye's drainage angle) marking old blunt trauma. Structure serves two purposes. It corroborates that the loss is real, and it timestamps the damage — established atrophy days after an incident is old damage; progressive change on serial scans after a documented insult is new. The evidentiary power and the limits of this imaging are detailed in OCT as Evidence.

Step Five: Weigh the Alternatives Honestly

A causation opinion is only as strong as its treatment of the alternatives. The evaluator lists the other conditions capable of producing the same picture — pre-existing disease, age-related change, independent illness, medication effects, non-organic overlay — and tests each against the record. Some are excluded by the evidence; some are quantified as contributing factors; occasionally one turns out to be the better explanation. In California workers' compensation this weighing is not optional but statutory: apportionment under Labor Code sections 4663 and 4664 requires the evaluator to assign permanent disability to its causes, industrial and non-industrial alike. In civil matters the same reasoning appears as the differential analysis opposing counsel will probe at deposition. An opinion that never seriously engaged the alternatives tends not to survive that probing.

Putting It Together — and Saying What Cannot Be Said

The synthesis is a judgment to a reasonable degree of medical probability: given the baseline, a plausible mechanism, a consistent temporal course, corroborating structure, and the weighed alternatives, is the alleged cause the probable one? Sometimes the answer is a well-supported yes. Sometimes it is a well-supported no — the structure predates the incident, or an alternative explains the findings better. And sometimes the honest answer is that the records permit no confident conclusion, most often because baseline documentation is missing. All three are legitimate outcomes of the analysis; only the unsupported ones are not. This is the framework Dr. Shomer applies in causation consulting for plaintiff and defense counsel alike, and it is the framework attorneys should expect any candid evaluator to show their work within.

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