Flashcards in Ophthalmology - Pupils Deck (14):
What is the pathway responsible for the light reflex?
The pupil constricts in bright light. Light detection by the retina is passed via the optic nerve (afferent pathway) to the midbrain (superior colliculus). 2nd order fibres pass to the Erdinger-Westphal nucleus (part of CN 3 nucleus) through the same and opposite sides (via the posterior commissure). Efferent fibres leave in the occulomotor nerve to the ciliary ganglion and after via the short ciliary nerve to the constrictor fibres of the sphincter pupillae (iris). The cerebral cortex is NOT involved. The light reflex is mediated by the parasympathetic system.
How do defects in the afferent pathway of the light reflex manifest?
Afferent defects are where there is an absent direct response. The pupil won't respond to light (i.e. remains dilated), but constricts to a beam in the other eye (consensual response). Constriction to accommodation still occurs.The pupils are the same size (consensual response unaffected).
It is important to distinguish a dilated pupil caused by a 2nd nerve lesion, from a dilated pupil caused by a 3rd nerve lesion. Lesion of the optic nerve will abolish pupillary response to light in the same and contralateral (normal) eye when light is shone into the affected one. When light is shone into the normal eye, it AND the contralateral pupil will constrict. The consensual reflex is preserved. Pupils tend to be less dilated in an afferent pathway lesion cf. an efferent one.
What causes afferent pupillary defects?
What is the Macrus-Gunn reflex?
On beaming light to the normal eye, both pupils constrict (direct and consensual reaction). If on swinging the light to the affected eye, the pupil dilates it is a Marcus-Gunn pupil. It happens because, when afferent transmission in the optic nerve is impaired, the waxing and waning of the consensual reflex (called "escape" becomes more exaggerated. It tests for a relative afferent pupillary defect.
What is an efferent pupillary defects?
Parasympathetic supply to the eye mediating constriction in bright light, is transmitted via the 3rd cranial nerve. If there is interruption to the parasympathetic supply the pupil will not constrict and remains dilated. With complete palsy of the 3rd nerve there is complete ptosis, a fixed dilated pupil, and the eye looks down and out (superior oblique and lateral rectus still acting).
Light is perceived by the affected eye but the pupil cannot respond. The other pupil constricts consensually. When the torch shines in the unaffected eye there is direct pupillary constriction but no consensual response from the affected eye.
What is the cause of efferent pupillary defects?
Cavernous sinus lesion
Superior orbital fissure syndrome
Posterior communicating artery aneurysm
Increased ICP --> transtentorial herniation*
Drugs - anticholinergics, TCAs, oral contraceptives, NSAIDS, antihistamines, mydriatics (e.g. topicamide)
*If the patient is comatose, pupil dilation and failure to react to light is the simplest way of detecting a 3rd nerve lesion. This is an important sign of transtentorial herniation.
What is a Holmes-Adie pupil?
Another cause of dilated (mydriatic) pupils. This is a benign condition usually affecting young women. The onset is usually acute and unilateral (80%). The pupils constrict sluggishly to light. Classically, a young women presents with sudden blurring of near vision, and a dilated pupil with slow responses to accommodation and especially to light - i.e. a tonic pupil.
If only the pupils are affected it is referred to as a Holmes-Adie pupil (sometimes Adie's pupil). If is is associated with absent tendon reflexes and decreased BP it is Holmes-Adie syndrome. It can be diagnosed with the pupillary response to pilocarpine (parasympathomimetic) - the tonic pupil will constrict, normal eye is not affected.
What is Horner's syndrome?
This occurs on disrupting sympathetic fibres so the pupil is miotic (smaller). The triad of Horner's syndrome is (i) ptosis, (ii) miosis and (iii) anhydrosis. These are unilateral, and enophthalmos may also be present.
It is caused by lesions to the sympathetic supply to the eye. These fibres descend from the ipsilateral hypothalamus through the lateral aspect of the brainstem into the spinal cord. Pupillary fibres pass out in the anterior roots of C8 and T1 and enter the sympathetic chain. Here they give rise to post ganglionic fibres in the superior cervical ganglion which ascend on the wall of the internal carotid artery to enter the skull.
Fibres can either:
- pass directly through the ciliary ganlgion to the iris, or
- join CNs 3, 4, 5 and 6 running to the eye and iris
What causes Horner's syndrome?
Interruption to the sympathetic supply at any point from its origin in the hypothalamus to the iris can cause Horner's syndrome.
- intrinsic tumour
- vascular lesion - e.g. posterior inferior cerebellar artery or basilar artery occlusion
- intrinsic tumour - e.g. glioma
Anterior roots, C8-T1:
- tumour - e.g. neurofibroma
- lower brachial plexus palsy - e.g. Klumpke's palsy
Cervical sympathetic chain:
- carcinoma of the apex of the lung (Pancoast syndrome)
Internal carotid artery:
- trauma and occlusion/ dissection
- tumour, granuloma
Why is the presence of anhydrosis in Horner's syndrome are useful localising feature?
Unilateral facial anhydrosis may indicate a lesion proximal to the carotid plexus - if distal, the sudomotor fibres will have separated, so sweating is intact.
What is congenital Horner's syndrome associated with?
Iris heterochromia. Here, there are fibre separations in the strone. It is also associated with Wilm's tumour, cerebral gigantism, and congenital rubella.
What is an Argyll-Robertson pupil?
This occurs in neurosyphilis and diabetes. There is bilateral miosis, pupil irregularity and no response to light, but there is response to accomodation (Prostitutes pupil - accomodates but does not react!). The iris is spongy, the pupils dilate poorly and there may be ptosis.
Argyll Robertson and Holmes-Adie pupils are examples of light near dissociation. Define this and give some other causes.
LND is where the eyes fail to react to light, but react to accomodation. Parinaud syndrome, meningitis, alcoholism, tectal lesions and mesencephalic lesions are all examples of causes of LNDs.