Pupil equality disorder (anisocoria)

Examination of the pupils is of particular importance for the diagnosis of a large number of pathological conditions.

A slight difference in pupil size occurs in 15-20% of healthy people and is congenital. Expressed anisocoria can have two origins:

• I. "Ophthalmological": structural defect of the iris muscles, consequences of iritis, uveitis, trauma, refractive errors, etc. In this case, different visual acuity is often detected in the left and right eyes.
• II. "Neurological" anisocoria:
  • anisocoria is more pronounced in the dark
  • anisocoria is more pronounced in bright light.

To examine the pupils in the dark (a darkened room), turn off all light sources and hold a flashlight near the patient's chin, providing enough diffused light to measure the pupil size.

Bright light is provided by turning on light sources and directing the beam of a flashlight directly into the pupil.

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I. Anisocoria is more pronounced in the dark

In this situation, the abnormal pupil is the smaller one, since it has difficulty dilating. Here, it is necessary to differentiate four possible situations.

Simple (physiological) anisocoria is observed in 20% of healthy people. Pupils are of regular shape with a lively reaction to light. Sometimes it takes the form of a "swing" ("alternating" anisocoria). The size of anisocoria is usually less than 1 mm.

Horner's syndrome (ptosis, miosis and anhidrosis). Miosis is small, so that anisocoria averages about 1 mm in a lighted room, it becomes smaller in bright light and more noticeable in the dark. The most specific sign of Horner's syndrome is a delay in the dilation of the miotic pupil compared to the normal pupil when observing them for 15-20 seconds in the dark.

Aberrant regeneration. In case of non-ischemic damage to the oculomotor nerve (trauma, compression), the regenerating axons of the latter (for example, to the inferior rectus muscle) can grow in an aberrant way, reaching m. sphincter iris. In this case, when trying to look down, the pupil will also constrict. This constriction of the pupil is synkinesis. Although anisocoria in aberrant regeneration is more pronounced in the dark, the abnormal pupil is narrower in the dark and wider in bright light.

Adie's persistent tonic (wide) pupil is the result of long-term denervation (pupilotonia). It may also become smaller than a normal pupil. In pupillotonia, the pupil does not dilate to light or has a sluggish response to light. Its cause is not fully known.

II. Anisocoria is more pronounced in bright light

In this situation, the abnormality here is the larger pupil, since it has difficulty constricting. This situation is possible in the following three cases.

Tonic pupil of Eddie. The mechanism of the tonic pupil is twofold. First, damage to the ciliary body leads to postganglionic parasympathetic denervation of the sphincter and ciliary muscle. If these muscles are denervated, the affected pupil becomes dilated and poorly responsive to light. In addition, due to the disturbance of accommodation, reading is difficult.

Within days of denervation, cholinergic hypersensitivity and aberrant regeneration of parasympathetic fibers develop, resulting in segmental paralysis and sphincter contraction with worm-like movements and slow tonic contractions of the sphincter during attempted accommodation. After months or years, the tonic pupil becomes smaller and segmental sphincter paralysis occurs with poor response to light, tonic pupillary response to accommodation, and cholinergic hypersensitivity.

Paralysis of the oculomotor (III) nerve. The oculomotor nerve includes preganglionic parasympathetic fibers to the sphincter and ciliary muscle, innervates m. levator palpebrae, m. rectus superior, m. rectus medialis and m. obliqus inferior. Clinical manifestations of its damage include ptosis, mydriasis and ophthalmoplegia. The pupil is dilated more than normal and reacts poorly to light.

Pharmacological mydriasis. Pupil dilation may result from the use of sympathomimetics, which stimulate the dilator, or anticholinergics, which block the constrictor (cocaine, amphetamine, atropine, scopalamin, etc.)

Isolated fixed dilated pupil.In the absence of signs of ophthalmoparesis, the probability of damage to the third nerve as a cause of isolated fixed dilated pupil becomes very insignificant. Variants of tonic pupil or pharmacological mydriasis should be considered.