Pupillary light reflex

The pupillary reflex mediates pupil contraction in response to light. Afferent signals from CN II fibres are passed to the pretectal area of the brainstem and lead to stimulation of the Edinger-westphal nucleus. Consequently, parasympathetic CN III efferent fibres mediate constriction of the pupil via sphincter pupillae. Since afferent signals split bilaterally at the optic chiasm, the reflex is consensual where shining light into either eye should make both pupils constrict. By testing both eyes, problems in the circuit may be localised. The reflex provides a quick assessment of brain function even in the unconscious patient, especially as the oculomotor nerve is vulnerable to stretch by raised intracranial pressure e.g. in cerebral haemorrhage.

Pupil dilation

Pupil dilatation is mediated by the dilator pupillae, innervated by the sympathetic tract. The sympathetic pathway originates in the hypothalamus: first-order neurons pass to the lateral grey column of the thoracic spinal cord (the ciliospinal column of Budge), second-order neurons travel from C8-T1 to the superior cervical ganglion and third-order neurons hitchhike with the internal carotid artery to join CN Va, entering the orbit and passing through the ciliary ganglion on to the pupil (whilst innervating eye blood vessels). Sympathetic fibres also contribute to the superior tarsal (Müller’s) muscle which raises the upper eyelid with the levator palpebrae superioris.

CLINICAL CORNER

Horner’s syndrome results from damage to the sympathetic autonomic nervous pathway in the head, including trauma to the superior cervical ganglion. Primary symptoms (occurring ipsilateral to damage) include ptosis (drooping of the eyelids), miosis constriction of the pupil and anhydrosis (no sweating) of the cheek.

Corneal reflex

The corneal reflex induces a blink to protect the eye in the presence of a foreign body. Afferent signals via CN Va to the pons induce contraction of the orbicularis oculi via CN VII.