One may learn a lot about the patient’s reaction by taking an evaluation of pupillary reaction. In order to get an idea of a patient’s eye health and visual pathways, it’s best to look at the patient’s pupils first. Before examining anomalies of the pupillary response, we need to understand pupil examinations and how they work.
In a typical pupil evaluation, both pupils will contract equally regardless of whose eye the light is aimed towards, demonstrating a direct and consensual pupillary light reaction.
When light is flashed into the unaffected eye, there is less pupillary constriction in both eyes (direct and consensual responses). This is known as an afferent pupillary deficit (APD). In other words, an APD occurs when the reaction of an eye to a stimulus is larger than the response of the eye to the stimulus. Since the opposite eye will always be the reference point for an APD, it’s important to remember that (i.e., a bilateral APD is not possible). When the light is swayed from the unaffected eye to the afflicted eye, a pupil with an APD will constrict less, making it seem to partly dilate.
Notably, an APD is not always present in the case of a stationary pupil. You don’t need to worry about an APD if you get an equal reaction from both eyes when the light is flashed into one.
You may employ neutral density filters of progressively higher densities over the unaffected eyes until the swinging flashlight test results are equal. The shift in the relative depth of an APD may be quantified in this way. However, clinically, a subjective grading system is frequently employed instead. The descriptors used in the grading system explain how the pupil with an APD reacts when the light is swung from the unaffected to the afflicted one.
It should be noted that anisocoria by itself is not a sign of APD; most of the time, the two go hand in hand. Although they may coexist, anisocoria is not usually caused by an APD.
If there is a disparity in pupil size of at least 0.4 millimetres when doctors measure pupil size, it is considered to be anisocoria. It is estimated that 20% of the population has anisocoria, which has a difference of less than one millimetre between the pupils. An unhealthy efferent route is indicated by nonphysiologic anisocoria, which will be examined later.
Pupillary fibres from the Edinger-Westphal nucleus to the iris sphincter may be disrupted at any point along their course, resulting in an abnormally dilated pupil. Due to insufficient constriction of the bigger (affected) pupil, this will result in anisocoria that is greater in the light than in the dark. Trauma, recent ocular surgery, angle-closure, or interaction with pharmacologic substances may all cause an excessively dilated pupil.
Adie’s tonic pupil
Post-ganglionic denervation of the iris sphincter and ciliary body causes Adie’s tonic pupil. Typically, the pupil is unusually dilated, has little or no sensitivity to light, and re-dilates slowly. Additionally, there is usually no or just a delayed or absent reaction from both parties’ pupils during a pupillary evaluation. Similar to accommodative tonicity, the ciliary body relaxes slowly following near concentration. More brain fibres govern the near than light pupillary reflex, which explains why the near response is still present. This light-near dissociation may also be caused by an abnormal regeneration of accommodating fibres that reroute to the iris sphincter. Due to segmental constriction, Adie’s pupil has a vermiform pupil response best viewed with a slit light.
Anywhere in the sympathetic nervous system may be the source of Horner’s syndrome, whether inherited or acquired. The ipsilateral Horner’s syndrome will occur if this route is disrupted. Ptosis, miosis, and anhydrosis are symptoms of Horner’s syndrome, which is caused by the paralysis of Mueller’s muscle. In order to produce anhydrosis, nerve fibres from the external carotid artery must be damaged in the central or preganglionic neurons. Congenital or apparent enophthalmos may also cause Horner’s syndrome to result in heterochromia. Due to a lack of activity in the pupillodilator muscle, the pupil dilates slowly in the dark because of the passive release of the sphincter in the light.
Argyll Robertson pupil
Light-near dissociation, which occurs when a pupil reacts poorly to light but responds quickly close during pupillary size measurement, is an Argyll Robertson pupil signature. An Argyll Robertson pupil is often miotic and irregularly shaped; this tends to be bilateral but may be asymmetrical.
Apart from the Argyll Robertson pupil and abnormal regeneration following a CN III palsy, which have already been discussed, light-near dissociation can be observed in a variety of other diseases involving midbrain pathology, including neoplasms (particularly pinealomas), brainstem stroke, midbrain haemorrhages, arteriovenous malformations, alcoholic midbrain degeneration, encephalitis, hydrocephalus, and trauma. In addition, affected patients with dorsal midbrain (Parinaud) syndrome have mid-dilated pupils bilaterally with light-near dissociation, which is often caused by direct or compressive injury to the dorsal midbrain, often caused by pinealomas. This syndrome is also associated with eyelid retraction, supranuclear upgaze paralysis and convergence retraction nystagmus, among other symptoms.
Any newly discovered anisocoria should be subjected to further investigation to establish if the anisocoria is physiologic or pathologic. The importance of a good case history cannot be overstated. This chart will serve as guidance for practitioners as they go through their anisocoria assessment process, in addition to the discussion above.