What is pupillary light reflex

The retinal fibers which come from the nasal side of each eye decussate at the optic chiasm into the contralateral optic tract, whereas the retinal fibers from the temporal side of each eye do not cross but instead proceed through the ipsilateral optic tract; thus, each optic tract is composed of the ipsilateral temporal fibers and the contralateral nasal fibers.

This decussation of the nasal, but not the retinal, fibers allows the right half of the visual field to be processed by the left cerebral hemisphere and the left half of the field to proceed to the right hemisphere.

Most of the optic tract fibers synapse in the ipsilateral lateral geniculate nucleus LGN of the thalamus for image processing. A small number of the optic tract fibers arrive at the pretectal nucleus in the midbrain instead of the LGN and participate in the pupillary light reflex. The axons of the LGN project to the calcarine also known as striate cortex as two bundles called temporal and parietal radiations.

The electrochemical signal finally arrives at the calcarine cortex Brodmann area 17 , which is the primary visual cortex in the occipital lobe. The visual information is further processed by the higher-order visual cortex to identify an object.

The pupillary light reflex pathway is similar to the visual pathway; however, the optic tract fibers involved in pupillary light reflexes terminate at the pretectal nucleus in the midbrain and not at the LGN of the thalamus. The nasally aligned fibers decussate at the optic chiasm and transfer the signal to the contralateral pretectal nucleus, whereas the temporally aligned fibers relay the information to the ipsilateral pretectal nucleus.

When each pretectal nucleus projects bilaterally and synapses in both Edinger-Westphal nuclei cranial nerve III , the activated Edinger-Westphal nuclei begin the efferent limb of the reflex by generating action potentials. The axons of these preganglionic parasympathetic neurons send the signals along the oculomotor nerve to the post-ganglionic nerve fibers of the ciliary ganglion. Subsequently, the short ciliary nerves arising from the ciliary ganglion stimulate the pupillary sphincter muscle and cause pupillary constriction.

Even when the light is shined in only one eye, a consensual response occurs in the other eye since the nasal retinal fibers cross at the optic chiasm to reach the contralateral pretectal nucleus. Also, the projection of each pretectal nucleus to both Edinger-Westphal nuclei contributes to the consensual pupillary reflex in the contralateral eye. Each activated Edinger-Westphal nucleus is responsible for the ipsilateral pupillary constriction, and these stimulated nuclei together allow the bilateral pupillary reflex to occur.

In the dim light, pupillary dilator muscle fibers contract and widen the size of the pupil. The postganglionic sympathetic fibers from the long ciliary nerve innervate the dilator muscle. The ocular development of an embryo begins at approximately three weeks into gestation and continues until week The optic cup and optic stalk are the invaginations from the optic vesicle, which develops from the neuroectoderm of the diencephalon of the brain.

The retina, iris, and ciliary body all arise from the optic cup, whereas the optic nerve forms from the optic stalk. The lens placode develops from the thickened surface ectoderm, and this precursor later gives rise to the lens and anterior corneal epithelium. The mesodermal layer forms the white area of the external eye known as the sclera, part of the vitreous body, and extraocular muscles.

The neural crest cells participate in the development of the pupillary muscles of the iris and the ciliary muscle of the lens. The hyaloid artery and vein are the primitive blood vessels that later form the central artery and vein of the retina. The ophthalmic artery is the first arterial branch of the internal carotid artery that provides the blood supply to the majority of components in the eye.

Together with the optic nerve, the ophthalmic artery travels through the optic canal to enter the orbit of the eye. The central retinal artery, the anterior ciliary arteries, and posterior ciliary arteries are the essential vascular branches that arise from the ophthalmic artery.

The central retinal artery pierces the meninges from the inferior aspect of the optic nerve. It emerges from the optic cup of the disc to supply blood to the inner layers of the retina. The posterior ciliary arteries provide blood supply to the head of the optic nerve, choroid, and the outer layers of the retina.

The anterior ciliary arteries are the crucial vasculatures for the iris and ciliary body. Venous drainage of the retina is carried out by the central retinal vein, which travels temporally to the central retinal artery near the head of the optic nerve. From the central vein, the blood drains into the superior ophthalmic vein that projects to the cavernous sinus. The choroidal veins drain into vortex veins, which project to the superior and inferior ophthalmic veins and then to the cavernous sinus.

The optic nerve cranial nerve II is the essential nerve for relaying visual signals to the brain. Pupillary light reflexes require both optic and oculomotor nerve cranial nerve III to constrict pupils upon light exposure. Physical examination determines that touch, vibration, position and pain sensations are normal over the entire the body and over the lower left and right side of his face.

Pathway s affected : You conclude that structures in the following reflex pathway have been affected. The Trigeminal Nerve. Section of the trigeminal nerve will eliminate somatosensory sensation from the face and the eye blink reflex e. However, light touch of the right cornea will elicit a bilateral eye blink. The effect of sectioning the trigeminal nerve is to remove the afferent input for the eye blink reflex.

The patient complains of pain in her left eye. Her left pupil appears dilated and is not reactive to light directed at either the left or right eye Figure 7. The right pupil appears normal in size and reacts to light when it is directed in the right or left eye. Both eyelids can be elevated and lowered and both eyes exhibit normal movement. Touch, vibration, position and pain sensations are normal over the entire the body and face.

Parasympathetic Innervation of the Eye. Section of the parasympathetic preganglionic oculomotor nerve or postganglionic short ciliary nerve innervation to one eye will result in a loss motor of both the direct and consensual pupillary light responses of the denervated eye. Section of the left short ciliary nerve or a benign lesion in the left ciliary ganglion will result in no direct response to light in the left eye and no consensual response in the left eye when light is directed on the right eye a.

When the damage is limited to the ciliary ganglion or the short ciliary nerve, eyelid and ocular mobility are unaffected.

The patient presents with a left eye characterized by ptosis, lateral strabismus, and dilated pupil. When asked to rise his eyelids, he can only raise the lid of the right eye. When asked to close both eyes, both eyelids close fully.

His left pupil does not react to light directly or consensually Figure 7. When asked to look to his right, his left eye moves to a central position, but no further. The right eye is fully mobile. When the patient is asked to look straight ahead, you note his left eye remains directed to the left and depressed. Observe the reaction of the patient's pupils to light directed in the left or right eye. The Oculomotor Nerve. Section of the oculomotor nerve produces a non-reactive pupil in the ipsilesional side as well as other symptoms related to oculomotor nerve damage e.

Section of the oculomotor nerve on one side will result in paralysis of the superior levator palpebrae, which normally elevates the eyelid. The parasympathetic preganglionic axons of the Edinger-Westphal nucleus, which normally travel in the oculomotor nerve, will be cut off from the ciliary ganglion, disrupting the circuit normally used to control the iris sphincter response to light.

The patient complains of reduced vision in the left eye. Pupil size in both eyes appears normal. However, both pupils do not appear to constrict as rapidly and strongly when light is directed into his left eye Figure 7.

That is, compared to the response to light in the left eye, light in the right eye produces a more rapid constriction and smaller pupil in both eyes. The Optic Nerve. Partial damage of the retina or optic nerve reduces the afferent component of the pupillary reflex circuit.

The reduced afferent input to the pretectal areas is reflected in weakened direct and consensual pupillary reflex responses in both eyes a. Section of one optic nerve will result in the complete loss of the direct pupillary light reflex but not the consensual reflex of the blinded eye. That is, if the left optic nerve is sectioned, light directed on the left blind eye will not elicit a pupillary response in the left eye direct reflex or the right eye consensual response. However, light directed in the right eye will elicit pupillary responses in the right eye and the left blind eye.

The effect of sectioning one optic nerve is to remove the afferent input for the direct reflex of the blinded eye and the afferent input for the consensual reflex of the normal eye. Section of one optic tract will not eliminate the direct or consensual reflex of either eye as the surviving optic tract contains optic nerve fibers from both eyes. However, the responses to light in both eyes may be weaker because of the reduced afferent input to the ipsilesional pretectal area.

A patient who is suffering from the late stages of syphilis is sent to you for a neuro-ophthalmological work-up. His vision is normal when corrected for refractive errors. He has normal ocular mobility and his eyelids can be elevated and depressed at will.

Examination of his pupillary responses indicates a loss of the pupillary light reflex no pupil constriction to light in either eye but normal pupillary accommodation response pupil constricts when the patient's eyes are directed from a distant object to one nearby.

Observation : You observe that the patient has normal vision but that his pupils. This area was spared by syphilis. In the Argyll Robertson response, there is an absence of the pupillary light reflex with a normal pupillary accommodation response.

The Argyll Robertson response is attributed to bilateral damage to pretectal areas which control the pupillary light reflex with sparing of the supraoculomotor area which controls the pupillary accommodation reflex. The accommodation response involves many of the structures involved in the pupillary light response and, with the exception of the pretectal area and supraoculomotor area, damage to either pathway will produce common the symptoms.

The most common complaint involving the accommodation response is its loss with aging i. Recall that presbyopia most commonly results from structural changes in the lens which impedes the lens accommodation response. This chapter described three types of ocular motor responses the eye blink, pupillary light and accommodation responses and reviewed the nature of the responses and the effectors, efferent neurons, higher-order motor control neurons if any , and afferent neurons normally involved in performing these ocular responses.

Table I summarizes these structures and the function s of these ocular motor responses. Readers should understand the anatomical basis for disorders that result from damage to components of neural circuit controlling these responses. Reticular Formation bilaterally to. The reflex describes the finding of pupillary constriction in darkness or as part of closing eyelids when going to sleep. It is hypothesized that it is due to oculomotor disinhibition.

The ciliospinal reflex is pupillary dilation in response to noxious stimuli, such as pinching, to the face, neck, or upper trunk. Pathway: The trigeminal nerve or cervical pain fibers, which are part of the lateral spinothalamic tract, carry the afferent inputs of the ciliospinal reflex.

If the pupillary dilation is due to the ciliospinal reflex, prolonged pupillary light stimulation should constrict the pupils [8] However, prolonged light stimulation cannot overcome pupillary dilation caused by bilateral third nerve palsies and midbrain dysfunction [8].

It consists of a pupillary accommodation reflex, lens accommodation reflex, and convergence reflex. Afferent pathway for pupillary constriction, lens accommodation, and convergence: Afferent input from the retina is sent to the lateral geniculate nucleus via the optic tract [2].

Fibers from the LGN then project to the visual cortex. Efferent pathway for pupillary constriction: Efferent parasympathetic fibers from the E-W nucleus project via the oculomotor nerve to the ciliary ganglion and then short ciliary nerves to innervate the iris sphincter muscle to cause pupillary constriction [2].

Efferent pathway for lens accommodation: Efferent parasympathetic fibers from the E-W nucleus project via the oculomotor nerve to the ciliary ganglion and then short ciliary nerves to innervate the ciliary muscle to cause contraction [2]. Contraction of the ciliary muscle allows the lens zonular fibers to relax and the lens to become more round, increasing its refractive power.

Efferent pathway for convergence: Efferent fibers from the medial rectus subnucleus of the oculomotor complex in the midbrain innervate the bilateral medial rectus muscles to cause convergence [2]. Ophthalmologic considerations: Deficits in accommodation are usually acquired due to aging and presbyopia [4]. Isolated accommodation deficits can occur in healthy persons or in patients with neurological or systemic conditions such as in children after a viral illness and in women before or after childbirth.

Accommodation insufficiency is also less commonly associated with primary ocular disorders e. Light-near dissociation describes constriction of the pupils during the accommodative response that is stronger than the light response, and it is the primary feature of Argyll Robertson pupils in patients with neurosyphilis [4].

Immediately following denervation injury, there is a dilated pupil that is unresponsive to light or near stimulation. Ciliary muscle dysfunction gradually improves over several months as injured axons regenerate and reinnervate the ciliary muscle, and the pupil becomes smaller over time. While the near response of the pupil begins to improve, the light response remains impaired, causing light-near dissociation.

The corneal reflex causes both eyes to blink in response to tactile stimulation of the cornea [2]. Pathway: Inputs are first detected by trigeminal primary afferent fibers i. These primary afferent fibers synapse on secondary afferent fibers in the spinal trigeminal nucleus, which send axons to reticular formation interneurons, which travel to the bilateral facial nuclei.

Fibers from the facial nuclei motor neurons send axons through the facial nerve to the orbicularis oculi muscle, which lowers the eyelid. Ophthalmologic considerations: The corneal reflex can be utilized as a test of corneal sensation in patients who are obtunded or semicomatose [4]. However, an abnormal corneal reflex does not necessarily indicate a trigeminal nerve lesion, as unilateral ocular disease or weakness of the orbicularis oculi muscle can also be responsible for a decreased corneal response [4].

An abnormal blink reflex may be present in patients with various posterior fossa disorders, including acoustic neuroma, multiple sclerosis, Parkinson disease, trigeminal nerve lesions, and brainstem strokes, tumors, or syrinxes [4].

The vestibulo-ocular reflex VOR allows for eye movements in the opposite direction of head movement to maintain steady gaze and prevent retinal image slip [4]. Horizontal VOR involves coordination of the abducens and oculomotor nuclei via the medial longitudinal fasciculus.

VOR can be assessed in several ways. VOR can be evaluated using an ophthalmoscope to view the optic disc while the patient rotates his or her head; if the VOR is abnormal, catch-up saccades will manifest as jerkiness of the optic disc. Caloric stimulation can also be used to examine the VOR [4]. Irrigation of the external auditory meatus with ice water causes convection currents of the vestibular endolymph that displace the cupula in the semicircular canal, which induces tonic deviation of the eyes toward the stimulated ear [4].

Examination of the VOR via head rotation or caloric stimulation can be useful in the evaluation of unconscious patients, as tonic eye deviation indicates preserved pontine function [4]. Pathway: Afferent fibers are carried by facial nerve. Efferent fibers travel in the oculomotor nerve to the superior rectus muscle to cause an upward deviation of the eyes. This reflex is especially visible in patients with Bell palsy, an acute disorder of the facial nerve, due to failure of adequate eyelid closure [10].

An absent reflex may be the only neurological abnormality in patients with idiopathic epilepsy, Sturge-Weber syndrome, and tuberous sclerosis. The lacrimatory reflex causes tear secretion in response to various stimuli: 1. Pathway: Afferent signals are from the ophthalmic branch of the trigeminal nerve [1]. The superior salivatory nucleus in the pons gives off parasympathetic fibers that join other parasympathetic efferents from the salivatory nucleus [1].

These fibers run with gustatory afferents parallel to the facial nerve as the nervus intermedius and exit at the geniculate ganglion [12] [13].

The parasympathetic fibers then leave CNVII as the greater superficial petrosal nerve and synapse in the sphenopalatine ganglion.

Postganglionic fibers travel with the lacrimal nerve to reach the lacrimal gland and cause reflex tearing. Ophthalmologic considerations: Abnormalities in this pathway may cause hypolacrimation, hyperlacrimation, or inappropriate lacrimation [4]. Hypolacrimation may be secondary to deafferentation of the tear reflex on one side, which can be due to severe trigeminal neuropathy, or damage to the parasympathetic lacrimal fibers in the efferent limb of the reflex [4]. Lesions may affect the nervus intermedius, greater superficial petrosal nerve, sphenopalatine ganglion, or zygomaticotemporal nerve.

Hyperlacrimation may be due to excessive triggers of the tear reflex arc or from efferent parasympathetic fiber overstimulation. Inappropriate lacrimation can occur with the gustolacrimal reflex, described below. The reflex describes unilateral lacrimation when a person eats or drinks [14]. The nerves may redirect themselves through the greater superficial petrosal nerve to reach the lacrimal gland, causing ipsilateral tearing when the patient eats.

The reflex is classically tested with an optokinetic drum or tape with alternating stripes of varying spatial frequencies.