Knowledge of pupillary responses is critical to neuro-foundational ophthalmology’s concepts and pupil measurement. It is a skill needed in eye emergencies, clinics, and, most significantly, examinations. To begin, the pupil is the iris’s central opening, which controls the quantity of light that reaches the retina, ranging in diameter from roughly 1 to 8 millimeters in diameter.
Interaction among the sympathetic and parasympathetic nervous systems is responsible for the interaction that results in pupil size. A reliable and proper diagnosis can only be made by examining the pupils and pupillary reflexes during a clinical exam.
Normal pupil reflexes
Constriction of the pupillary muscles is caused by the activity of the parasympathetic nervous system. It is a typical response to two stimuli: light falling on retinal photoreceptors and the exertion of performing near reflexes and accommodation.
The contraction of the pupils in response to light is mediated by four different types of neurons. The afferent route begins in the ganglion cell layer of the retina, where it gives birth to the optic nerves and then continues to the brain. After exiting the optic chiasm, the fibers continue to both optic tracts, ending in the pretectal nuclei. Internuncial neurons connect each pretectal nucleus to the ipsilateral Edinger-Westphal nucleus on each side of the brain. The posterior commissure is used to access the contralateral Edinger-Westphal nucleus on the other side of the brain.
Since the input to one optic nerve is received by both Edinger-Westphal nuclei, this route results in direct and indirect light reflexes. In the oculomotor nerve, preganglionic parasympathetic fibers enter, depart the branch to the inferior oblique, and synapse in the ciliary ganglion. Post-ganglionic fibers run in the short ciliary nerves and penetrate the iris to feed the sphincter pupillae, located at the iris’s base.
The afferent limb of the reflex travels from the retina to the occipital lobe through the lateral geniculate body. There are fibers in the midbrain that activate the Edinger-Westphal nucleus and the vergence cells of the reticular formation, which traverse the occipital lobe. If you don’t have eyesight, you can still make accommodations.
Bilateral stimulation of the Edinger-Westphal nuclei from pre-striate cortex area 19 may provide the same results. This stimulus results in three responses: contraction of the ciliary muscles, relaxation of the zonules, and an increase in the lens’ refractive power; an increase in the lens’ refractive power and a decrease in its globularity; and contraction of the ciliary muscles, relaxation of the zonules, and an increase in the lens’ globularity. At the same time, the sphincter pupillae contract, obstructing light from flowing through the lens’s peripheral portion. Reticuli grows more intense, causing the eyes to become more concentrated on the same subject, which is vital in pupillary evaluation.
On the other hand, the dilation of the pupils is a consequence of sympathetic activity. An essential part of this route may be traced back to the innervation of the posterior hypothalamic nucleus, which is linked to the sympathetic nerves that descend from their respective spinal cord branches.
The pre-ganglionic neuron develops from the first thoracic ventral nerve root to join the paravertebral sympathetic chain, which travels up to the superior cervical ganglion. The external and internal carotid arteries are both covered by post-ganglionic fibers. A portion of the sympathetic fibers joins the trigeminal nerve ophthalmic division in the cavernous sinus before passing via the long ciliary nerve to feed the dilator pupillae.
Pupils dilate as a reaction to the far response or in the presence of stress, worry, or fear, and these come into play when clinicians measure pupil size.
Pupil reactivity eye disorders
Adie’s tonic pupil
An anisocoria known as Adie’s tonic pupil is characterized by an abnormally large pupil that does not contract in response to light but does so gradually in response to accommodation and pupil reactivity.
Light-near dissociation is the term for this. It is common for the pupil to demonstrate a gradual constriction and re-dilation to distance after prolonged near exertion. The parasympathetic route has been damaged by post-ganglionic fiber injury. It begins as a unilateral problem in 90% of individuals before spreading to both sides.
This so-called “little old Adie’s pupil” eventually develops into a tonic and even miotic state. This is a common ailment that affects women and may be caused by a viral infection, diabetes, or trauma, although generally idiopathic. Holmes Adie syndrome is a condition in which there is a decline in the reflexes of the tendons. To be sure, an average pupil will not be impacted by denervation hypersensitivity to mild cholinergic drugs (0.125 percent pilocarpine), but an aberrant one will.
Acute angle-closure glaucoma
Because of the crowding of the peripheral iris, when the pupil has been semi-dilated, the anterior chamber angle is automatically closed by this crowding. A tumor in the eye might cause, as could the creation of anterior or posterior synechiae after uveitis or rubeotic glaucoma due to fibrovascular growth in the chamber angle produced by retinal ischemia (diabetes and central retinal vein occlusion classically). A slit-lamp examination is necessary to establish the diagnosis of this ocular emergency, which is typically assumed based on the patient’s history alone. The ophthalmologist should be contacted promptly if a patient has this issue. A glaucoma drop, intraocular pressure-lowering medications, topical miotics, and iridotomy may be utilized to reduce eye pressure in these individuals.
Third nerve palsy
There are two types of third-nerve palsy: full and partial. Third nerve palsy is characterized by a wholly dilated pupil, ‘down and out’ eye, ptosis, and no light or accommodation constrictions in the affected eye. The efferent route may be confirmed by flashing light into the affected eye and seeing that the pupil does not contract. Still, the consensual light response in the opposite eye is intact. Some causes include microvascular infarction (occlusion of the vasa nervorum), compressive lesions (aneurysms, tumors, and trauma), hypertension, and diabetes. Minor third-nerve palsy symptoms may indicate an imminent medical emergency despite their mildness. As intracranial pressure rises rapidly, the third nerve is often compressed against the crest of the petrous temporal bone. When the parasympathetic fibers, located close to the surface, get inflamed, they cause the pupil to dilate on the afflicted side. A CT angiography to screen for intracranial aneurysms is nearly always required when there is an urgent need for surgical decompression of the brain due to pupillary dilatation.