Note the pupillary constriction of both eyes.

Check the light reflex in each eye, then move the beam swiftly and rhythmically from eye to eye, making sure that each eye receives the same light exposure, from the same angle. It relies on a comparison between the two eyes, and is looking for (and can only detect) an asymmetrical abnormality in the afferent pathway. This compares the direct and consensual pupillary constriction of each eye to look for a difference in the afferent conduction between them, called a relative afferent pupillary defect (RAPD).

A normal result is a brisk, simultaneous, equal response of both pupils in response to light shone in to one or the other eye.

Note whether there is a direct pupillary response (the pupil constricts when the light is shone on to it) and a consensual response (the other pupil also constricts). Illuminate the right eye from the right side and the left from the left side.

Dim the ambient light and ask the patient to fixate a distant target.

This assesses the integrity of the pupillary light reflex pathway. A slight difference will become more apparent.Ī slit lamp will aid more detailed observation of an abnormally shaped pupil. If there seems to be size asymmetry, stand back and observe the red reflex of both eyes simultaneously with the ophthalmoscope. Observe the pupils closely whilst shining a bright light on the patient's face from below (minimise the shadow cast by the nose by placing the light in the midline). Reduce the ambient light and ask the patient to fixate on the far wall.

When pupillary function is normal, pupils are isocoric (equally sized) and react equally to light. Size is measured in millimetres and the normal pupil ranges from 1-8 mm. Note the shape and size of the pupils in ambient bright light. This may provide helpful clues as to the cause of pupillary abnormalities, particularly where there is an underlying neurological cause. See also the separate Examination of the Eye article. There is a secondary sympathetic effect modulated by adrenergic receptors in the Edinger-Westphal nucleus which are inhibited by the direct action of sympathetic amines. The sympathetic fibres then travel with the trigeminal nerve through the superior orbital fissure to the ciliary muscle. Postsynaptic neurons travel down all the way through the brain stem on each side and finally exit through the cervical sympathetic chain, travel over the lung apices, and ascend to the superior cervical ganglia with the carotid artery, then onwards as a plexus around the internal carotid artery, passing through the cavernous sinus. The sympathetic input then comes from the hypothalamus with the first synapse at the ciliospinal centre at C8-T1 level. During sleep the pupils are partially constricted but still react to light. The pathway begins in the cortex, which exerts a modulatory effect on constriction which is lost during drowsiness and sleep but increased during intense concentration and arousal. Pupillary dilatation is controlled by the sympathetic system and is efferent only.

Short ciliary nerves then innervate the iris sphincter and muscles of accommodation.

They travel in the superficial part of the oculomotor nerve via the cavernous sinus and the superior orbital fissure to synapse in the ciliary ganglia. From each Edinger-Westphal nucleus, preganglionic parasympathetic fibres exit with the oculomotor nerve. Each pretectal nucleus has two pupillary motor outputs, one to the Edinger-Westphal nucleus on its own side and one to the other side. The efferent limb for pupillary constriction comes from the pretectal nucleus via the Edinger-Westphal nucleus (also in the midbrain) to the ciliary sphincter muscle of the iris. The afferent limb is made up of the retina, the optic nerve and the pretectal nucleus in the midbrain, all on the same side. The pathway for pupillary constriction for each eye has an afferent limb taking sensory information to the midbrain, and two efferent limbs (one to each eye).

Pupil constriction reatment