The pupil Done by Nebras abu abed

Pupillary responses

Responeses :

1) response to light

2)accommodation for near vision (near response )

These reactions are performed by reflex arcs with afferent and efferent

limbs :

1)Afferent : simply by the optic nerve

2)Efferent : by sympathetic and parasympathetic

More light through optic nervepretectal nucleusedinger-westphal

nucleus preganglionic parasympathetic fibres carried by oculomotor

nerve ciliary ganglion postganglionic parasympathetic fibres (short

ciliary nerves ) to pupilloconstrictor smooth muscle fibres miosis .

Less light through optic nerveoptic tract pretectal nucleusedinger-

westphal nucleus to hypothalamus to ciliospinal centre in C8, T1 & T2

Preganglionic sympathetic fibres to superior cervical ganglionpost

ganglionic fibres around ICA trigeminal nerve ophthalmic

nervenasociliary nerve long ciliary pupillodilator muscle mydriasis .

Disorders of pupillary function

May result from :

1)Ocular disease

2)Disorders of afferent and efferent controlling pathways

3)Drugs !!!

1)Ocular diseases

Anterior uveitis if it caused post synechiae…it will give the pupil an irregular

appearance .

Can result from intraocular surgery

Blunt trauma to eye

In acute close angle glaucoma

2)Controlling pathways

Lesions of pupillary pathways can be broadly classified into afferent and

efferent defects .

Affernet defects can be either complete or incomplete(hence the name

relative afferent pupillary defect )

Efferent(c,d) and complete afferent(a,b)

defects

Relative afferent pupillary defect

Best detected by swinging light torch : light is repeatedly shone into the

affected eye alternating with the good side . When the light is shining on

the unaffected eye , both pupils constrict . When it’s transferred to the

diseased side , there is bilateral pupillary dilation .

Seen in optic nerve lesions such as optic neuritis and may be seen in very

severe disease of retina but not with opacities of the cornea or lens .

https://www.youtube.com/watch?v=HSYo7LhfV3A

Horner syndrome

It arises from lesions affecting the sympathetic efferent pathway which will

cause :

1)Miosis : results form loss of dilator function

2)Ptosis : muller muscle is affected

3)Enophthalmus : the reduced palpebral aperture size gives an impression of

recession .

4)Anhydrosis , if the sympathetic pathway is affected proximal to the base of

skull .

Because of its extended course , the sympathetic pathway may be

affected by multiple pathologies , examples :

1) Syringomyelia , an expanding cavity within the spinal cord, sometimes

extending into the medulla (syringobulbia), which compresses the

pathway. Typically, it also causes wasting of the hand muscles and loss of

sensation.

2) Small-cell carcinoma at the lung apex which catches the cervical

sympathetic chain. Involvement of the brachial plexus gives rise to pain

and to T1 wasting of the small muscles of the hand in Pancoast’s syndrome.

3) Neck injury , disease or surgery .

4) Cavernous sinus disease , it affects the sympathetic plexus around ICA

Light-near dissociation

Impaired reaction of pupils to light , while the near response to

accommodation is retained . Seen in :

1)Argyll roberston pupil .

2)Midbrain pupil .

3)DM & multiple sclerosis .

1)Argyll Roberston pupil

The pupils are bilaterally small and irregular .

Accommodate but don’t react to light at all .

Classically seen in neurosyphilis , it’s suggested that a periaqueductal lesion

on dorsal aspect of edinger-westphal nucleus involves fibres associated

with response to light but spares those associated with near response .

Adie’s tonic pupil

It’s due to ciliary gangilionitis which results in partial parasympathetic denervation of iris with resultant upregulation of its muscarinic receptors…

The consequences are

1)Unilateral enlarged pupil that can become bilateral overtime .

2)Poor reaction to light with characteristic slow , worm-like(vermiform) contraction of iris .(sectoral paresis)

3) Slow sustained miosis on accommodation(hence the name tonic) , results from muscarinic supersenitivity .

4)Constricts to dilute pilocarpine (0.1%),unlike the normal pupil .

5) Can be part of bigger syndromeadie-holmes syndromeAreflexia .

The ciliary body is nine times more innervated than iris so it isn’t affected as the iris .

Adie’s Argyll

unilateral bilateral

ciliary ganglionitis periaquidectal lesion

mydriasis & regular miosis & irregular

slow & sluggish light reflex absent light reflex

Tonic miosis on accommodation normal accomodation

2)Midbrain pupil

Arises from lesions affecting the pretectal nuclear complex in dorsal region of midbrain produces mydriasis and light near dissociation .

Causes include demyelination , infarction , enlargement of 3rd ventricle and

space occupying tumors such as pineloma .

3)Drugs

Other causes of pupillary abnormalities

In coma, both pupils may become miosed with preservation of the light

reflex if a pontine lesion is present, but remember that patients taking

pilocarpine for glaucoma or receiving morphine also show bilateral miosis.

Midbrain lesions cause loss of the light reflex with mid-point pupils. Coma

associated with a unilateral expanding supratentorial mass, e.g. a

haematoma, results in pressure on the third nerve and dilation of the pupil.

Intrinsic third nerve (Parasympathatic) lesions also cause a dilated pupil.

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