Pupil margin is positioned more anteriorly than the iris root and gets support from the lens
Slightly off-centre: inferonasal
Varies in size from 1 to 8mm in diameter
Physiological anisocoria (less than 0.4mm difference) is present in 25% of the population and may change sides!
Physiological tremor in pupil known as hippus (or pupillary athetosis)
Mydriasis occurs in low light, excitement or fear
Miosis occurs in illumination, convergence/accommodation and sleep
The strength of constriction increases with light intensity up to 9 log units above the scotopic threshold and then levels off
The pupil cannot respond to stimuli of greater than 5Hz frequency
Pupillary dilatation:

Stiles-Crawford effect: light entering at the edge of the pupil is less effective at stimulating photoreceptors than light entering centrally because it meets the receptors obliquely rather than head on
Pupil size is associated with:

## Light reflexes

Only one functioning pupil is needed to test the anterior visual pathways
The latency of the pupil light reaction is 0.2 to 0.5s
Afferent impulses travel from the retina through the optic nerve, chiasma and tracts

Fibres leave the tract and synapse in the pretectal olivary nucleus near the superior colliculus
Each pretectal nucleus receives only an ipsilateral input
Axons of the pretectal nerve cells synapse with the parasympathetic nuclei (Edinger-Westphal nuclei) of the oculomotor nerve on BOTH sides of the midbrain
Preganglionic fibres travel with the oculomotor nerve ( through its inferior division to the inferior oblique) to the ciliary ganglion and synapse
Postganglionic fibres travel in the short ciliary nerves to the sphincter pupillae muscle and both pupils constrict
Since both Edinger-Westphal nuclei are innervated, an unilateral optic nerve lesion will not affect the indirect/consensual response in the ipsilateral eye

Pupillary reflexes originate in the brainstem and are therefore unaffected by cortical lesions
Causes of efferent pupillary defect (fixed dilated pupil)

Brain stem lesions at the level of the superior colliculus and red nucleus, typically accompanied by so-called long tract signs
Third nerve lesions, usually compressive (but 20% of microvascular palsies involve the pupil)

Ciliary ganglion or short ciliary nerve lesions
Iris damage due to surgery or grossly elevated IOP
Mydriatic drugs (pilocarpine will not constrict such a pupil but will constrict a pupil affected by a neurological lesion)

## Mydriasis

Contraction of the dilator pupillae (innervated by alpha-1-adrenergic{' '} receptors)
Stimulated by noradrenergic sympathetic nerves passing through the ciliary ganglion

## Miosis

Stimulation and contraction of sphincter pupillae
Stimulated by cholinergic postganglionic parasympathetic fibres from the ciliary ganglion

## Horner’s syndrome

Central brain stem lesions (ie. first-neurone: the descending reticulospinal fibres within the medulla oblongata eg. lateral medullary syndrome -see below)
Preganglionic lesions (second neurone: travels from T1 exit over apex of lung and around first rib up to carotid bifurcation)
Postganglionic lesions (third neurone: travels from superior cervical ganglion to eye along the internal carotid and within the cavernous sinus)

No anhidrosis since the postganglionic sympathetic fibres controlling facial sweating follow the external carotid artery rather than the internal. They separate from the fibres to the pupil approximately at the level of the carotid bifurcation

Anisocoria (especially in low light conditions) due to failure of normal dilation by the affected pupil

Classic drugs tests for Horner’s

Cocaine will not dilate a Horner’s pupil since increasing adrenergic activity by preventing reuptake has no effect on an interrupted neural pathway
Hydroxyamphetamine (increases adrenaline release from postganglionic nerve terminals) will dilate a first or second neurone Horner’s but not a third order neurone lesion (since there’s no noradrenaline to release)
Adrenaline, apraclonidine and phenylephrine will dilate a post-ganglionic Horner’s due to denervation hypersensitivity
Note: there is no test to distinguish a second from a first-order lesion

Lateral medullary syndrome

Cerebellum: ataxia
IX and X nuclei: swallowing difficulty
Descending sympathetic tracts: Horner’s syndrome
Spinothalamic tract: contralateral (due to decussation) sensory loss of pain and temperature
Trigeminal nerve (sometimes involved): ipsilateral facial sensory loss

## Light-near dissociation

Retinal lesions
Optic nerve lesions
Pineal lesions
Pretectal lesions eg. Sylvian aqueduct syndrome, Argyll-Robertson
Third nerve lesions: secondary to aberrant regeneration of neurones to the iris sphincter normally supplying medial rectus
Ciliary ganglion lesions (as above for third nerve lesions), eg. Adie’s

## Argyll-Robertson pupil

## Adie pupil

Sluggish light reaction: may present with blurred vision due to mydriasis
Strong near response (with light-near dissociation)
Supersensitive to cholinergics eg. pilocarpine, due to “post-denervation phenomenon”

Using dilute pilocarpine can aid the diagnosis of an Adie’s pupil