The methods of pupil diameter measurement in neuro-foundational ophthalmology rely heavily on understanding pupillary responses.
When dealing with an eye emergency, a doctor will need to know how to do exams. When it comes to controlling light exposure, the pupil is the iris’s primary aperture, ranging from around 1 to 8 millimeters in diameter. The result is a larger pupil when the sympathetic and parasympathetic neural systems work together.
A correct diagnosis can be made only by observing the pupils and pupillary reflexes during a clinical examination.
Normal pupillary reflexes
The parasympathetic nervous system is the reason behind the contraction of the pupillary muscles. Light hitting retinal photoreceptors and the effort required to perform near-reflexes and accommodation trigger this reaction.
Pupillary light reflex
In reaction to light, four separate neurons cause the pupil to constrict.
It develops in the retina’s ganglion cell layer, where the optic nerves are formed and then proceeds to the brain. Afferent pretectal nuclei are the ends of the optic chiasm fibers. Internuncial neurons link the pretectal nucleus to the Edinger-Westphal nucleus on either side of the brain.
The contralateral Edinger-Westphal nucleus can be reached through the posterior commissure on the opposite side of the brain.
Direct and indirect light reflexes are possible because the input to one optic nerve is received by both Edinger-Westphal nuclei.
Ocular motor nerve pre-ganglionic parasympathetic fibers enter the inferior oblique and synapse with the ciliary ganglion in the oculomotor nerve. Sphincter pupillae are fed by post-ganglionic fibers via the short ciliary nerves and into the iris.
The lateral geniculate body serves as a conduit for the reflex’ afferent limb, from the retina to the occipital lobe.
The Edinger-Westphal nucleus and the vergence cells of the reticular formation are activate by fibers in the midbrain that cross the occipital lobe. Even if the patient is blind, there are workarounds available.
Similar findings may be obtain by stimulating the Edinger-Westphal nuclei on both sides of the pre-striate cortical region.
Responses include contraction of ciliary muscles, relaxation of the zonules, a rise in globularity, an increase in globularity, and a reduction in refractive power, which are all three possible outcomes of this stimulation. The sphincter pupillae close simultaneously, blocking light from passing through the lens’s periphery section.
During the pupillary assessment, the doctor will measure pupil size. This procedure relies on the eyes being increasingly focus on a single object as the reticuli intensify.
It’s also possible that the pupils dilate due to sympathetic activity.
The innervation in the posterior hypothalamus nucleus is connect to sympathetic nerve roots that exit the spinal cord, making this pathway an essential element of the chain of action. To get to the superior cervical ganglion, the paravertebral sympathetic chain must connect to the first thoracic ventral nerve root’s pre-ganglionic neuron.
Post-ganglionic fibers protect the internal and external carotid arteries.
The trigeminal nerve ophthalmic division in the cavernous sinus receives a part of the sympathetic fibers before traveling via the long ciliary nerve to supply the dilator pupillae. This pathway and Muller’s muscles nourish the eyelid muscles and face sweat glands through Muller’s muscles.
Pupils dilate in response to stress, anxiety, or fear. These factors are taken into account when physicians estimate pupil size.
Pupil reactivity and eye disorders
Adie’s tonic pupil
An anisocoria, Adie’s tonic pupil, is characterize by an excessively large pupil that does not contract in reaction to light but does so gradually in response to accommodation and pupil reactivity.
This condition affects a person’s ability to see in dim light. This phenomenon is refer to as light-near dissociation. After sustained effort at a close distance, it is not uncommon for the pupil to gradually constrict and then re-dilate to the distance. This phenomenon is call accommodation.
Injury to the post-ganglionic fibers has caused disruptions in the parasympathetic pathway.
In 90% of cases, the issue manifests itself on just one side of the body before spreading to the other. This condition, often referred to as “little old Adie’s pupil,” will ultimately mature into a tonic and even a miotic state. This is a frequent condition that primarily affects females and may be brought on by a viral infection, diabetes, or trauma.
However, in most cases, it is the result of unknown causes.
Adie syndrome is characterize by a gradual weakening of the reflexes that control the tendons. Denervation hypersensitivity to modest cholinergic medications (0.125% pilocarpine) will not affect a typical pupil; nevertheless, it will have an effect on a pupil with abnormal characteristics.
Third nerve palsy
Full and partial third-nerve palsy are both forms of this condition.
Ptosis dilate pupils, and no-light or accommodation constrictions are symptoms of third nerve palsy, which is characterize by a completely dilate pupil. It is possible to confirm the efferent pathway to the eye by flashing a bright light into it and seeing that the pupil does not dilate. Even so, the opposite eye’s consensual light response remains intact.
There are several possible reasons, including aneurysms, tumors, trauma, hypertension, and diabetes.
Even moderate signs of third-nerve palsy might point to an impending medical problem. The third nerve is often squeeze against the petrous temporal bone’s crest when intracranial pressure increases fast. Inflamed parasympathetic fibers at the eye’s surface produce dilation of the affected eye’s pupil.
If there is an urgent need for surgical decompression of the brain, a CT angiography to screen for intracranial aneurysms is usually necessary.