Dysplasia of pupils (anisocoria)
Last reviewed: 23.04.2024
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
The study of pupils is of particular importance for the diagnosis of a large number of pathological conditions.
A small difference in the size of the pupils occurs in 15-20% of healthy people and is congenital in nature. The pronounced anisocoria can have a twofold origin:
- I. "Ophthalmologic": structural defect in the muscles of the iris, the effects of iritis, uveitis, trauma, refraction disorders, etc. This often reveals a different visual acuity in the left and right eye.
- II. Neurological anisocoria:
- anisocoria is more pronounced in the dark
- anisocoria is more pronounced in bright light.
To examine pupils in darkness (darkened room), turn off all light sources and hold a flashlight near the patient's chin, giving a quantity of scattered light so that the size of the pupil can be measured.
A bright light is provided by switching on the light sources and directing the flashlight beam directly into the pupil.
[I. Anisocoria is more pronounced in the dark
In this situation, the pupil is smaller, since it is difficult to dilate. Here it is necessary to differentiate four possible situations.
A simple (physiological) anisocoria is observed in 20% of healthy people. Pupils of the correct form with a living 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, myosis and anhidrosis). Myoz is small, so 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 the delay in the expansion of the myotmic pupil in comparison with the normal pupil when observed for 15-20 seconds in the dark.
Aberrant Regeneration. In non-ischemic damage to the oculomotor nerve (trauma, compression), the regenerating axons of the latter (for example, to the lower rectus muscle) can grow aberrantly, reaching m. Sphincter iris. In this case, when you try to look down, the pupil will also taper. This narrowing of the pupil is synkinesia. Although anisocoria in aberrant regeneration is more pronounced in the dark, the abnormal pupil is narrower in the dark and wider in bright light.
The persistent tonic (wide) pupil of Edie (Adie) is the result of prolonged denervation (pupilotonia). He can become less than a normal pupil. When pupillotonia, the pupil does not expand into light, or a flaccid reaction to light is observed. Its cause is not completely known.
II. Anisocoria is more pronounced in bright light
In this situation, the abnormal here is a pupil of a larger size, since it has difficulty in constriction. This situation is possible in the following three cases.
Eddie's tonic pupil. 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 broad and reacts poorly to light. In addition, reading disorders are difficult due to a violation of accommodation.
A few days after denervation, cholinergic hypersensitivity and aberrant regeneration of parasympathetic fibers develop, leading to segmental paralysis and a reduction in the sphincter with vermicular movements and slow tonic abbreviations of the sphincter when attempting accommodation. After months or years, the size of the tonic pupil becomes smaller and there is segmental paralysis of the sphincter with a poor response to light, the tonic reaction of the pupil 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 his defeat include ptosis, mydriasis and ophthalmoplegia. The pupil is more than normal and reacts poorly to light.
Pharmacological mydriasis. Pupillary dilatation can be the result of the use of sympathomimetics, stimulating the dilator, or anticholinergics blocking the constrictor (cocaine, amphetamine, atropine, scopolamine, etc.)
Isolated fixed dilated pupil. If there are no signs of ophthalmoparesis, the probability of damage to the III nerve, as the cause of an isolated fixed dilated pupil, becomes very small. Consider the options for the tonic pupil or pharmacological mydriasis.