Acute visual disturbance 4 - anisocoria Flashcards
anisocoria means
unequal pupils
relatively common
how different do the pupils have to be
difference in pupil size >1mm
anisocoria may be due to
impaired dilation (sympathetic)
or impaired constriction (parasympathetic)
causes range from benign to life threatening
how do you know which is the problem eye
what should you do if the anisocoria gets worse under bright light
third nerve palsies cause problems with ocular motility, the eye turns down and out and there is ptosis
if this features are not present there may be a different condition called Adie’s tonic pupil
what are you concerned about if the anisocoria gets worse under dim light
constriction is
parasympathetic
dilatation is
sympathetic
sympathetic pathway
three order neutron pathway
1. hypothalamus -> ciliospinal centre of budge (C8 - T2)
2. -> lung apex & ICA -> superior cervical ganglion (carotid bifurcation)
3. ICA & cavernous sinus -> nasociliary nerve (CN V) -> dilator muscle, Muller muscle and lower eyelid smooth muscle
parasympathetic pathway
four-order neutron pathway
1. retinal ganglion cells -> optic nerve, chiasma, tract -> bilateral pretectal nuclei (dorsal midbrain)
2. -> bilateral EW nuclei
3. -> CN III -> cavernous sinus, superior orbital fissure & ipsilateral cilliary ganglion
4. -> post ganglionic short ciliary nerves -> pupil sphincter and ciliary muscles
HxPC of anisocoria
may be asymptomatic
there may be glare (if one pupil is dilated), impaired accomodation
may be chronic or sudden onset
associated symptoms may include headache, ptosis, diplopia, neck pain, focal nuerology, pulsatile tinnitus
POHx (past ocular history)
uveitis (can cause abnormal pupil, but this is not likely to be affected by dim or bright light)
ocular or head/neck surgery
medication Hx
atropine or pilocarpine eye drops
sublingual atropine, nasal decongestants
what examinations should you do
- visual Acuity
- visual Fields
- pupil Reflexes
- Opthalmoscopy
- Colour vision
AFROC
ptosis and strabismus indicates
third nerve palsy
proptosis indicates
orbital tumour
if there is anterior chamber cells, and posterior synechiae
uveitis
if theree is sectoral palsy and vermiform movements
adie’s
heterochromia may indicate
congenital horner’s
what are some things you might see on a list lamp
structural defects, anterior chamber cells, posterior synechiae
sectoral palsy and vermiform movements
heterochromia
anisocoria greater in the dark
sympathetic lesion, may be Horner;s syndrome, uveitis, mechanical
how do you confirm if it is Horner’ syndrome
use apraclonidine
this will cause dilatation in Horner’e due to denervation sensitivity (alpha-1 effect predominates over alpha-2)
anisocoria greater in the light
parasympathetic defect
may be caused by third nerve palsy, adie’s trauma, pharmacological
how do you confirm Adie’s
low dose pilocarpine (0.1%) causes constriction in Adie’s pupil from hypersensitivity due to up regulation of cholinergic receptors
how to figure out the cause of a anisworia greater in light
physiological unequal pupil sizes
up to 20% of the population have uneven pupil sizes <1mm difference
the inequality will persist in light and dark
may be intermittent, persistent or self resolving
oculomotor nerve palsy
third nerve palsy
depressed and out turned eye
a third nerve palsy does not always have pupil involvement
pupil involvement indicates that there may be an aneurysm of the posterior communicating artery causing the third nerve palsy
why does pupil involvement in a third nerve palsy call for concern
a third nerve palsy does not always have pupil involvement
pupil involvement indicates that there may be an aneurysm of the posterior communicating artery causing the third nerve palsy
requires prompt imaging
aetiology of oculomotor palsy
microvascular, aneurysm, tumour, trauma, infiltrative (e.g. leukaemia)
most cases without pupil involvement are ischameic (hypertension, diabetes etc.)
presentation of occulomotor nerve palsy
diplopia, ptosis, pain, pupil involvement
eye turned down and out
unable to adduct, infraduct, supraduct
DDx for oculomotor nerve palsy
myasthenia gravis
thyroid orbitopathy
giant cell arteritis
prognosis of oculomotor nerve palsy
ischameic cases often resolve within 3 months
aetiology Horner’s syndrome
central (first order): CVA, demyelination, tumour
preganglionic (second order): apical lung CA, mediastinal aneurysm, neck/thoracic surgery
postganglionic (third order): ICA dissection, cavernous sinus lesions (thrombosis, tumour etc.)
presentation of Horner’s syndrome
ptosis, mitosis, anhidrosis, ocular redness, asymmetric facial flushing
systemic neurological signs and symptoms
DDx of Horner’s syndrome
physiological anisocoria, involutional ptosis, CN III palsy, chronic Adie pupil
management of Horner’s syndrome
clinical diagnosis confirmed with apraclonidine
acute painful Horner’s (ICA dissection) = emergency
other management based on aetiology
what do you do for acute painful Horner’s
ICA dissection
emergency
CTA/MRA and anticoagulation
prognosis of Horner’s syndrome
this depends on the aetiology
aetiology of Adie’s tonic pupil
- ciliary ganglion damage -> postganglionic parasympathetic denervation -> mydriasis worse in light (sluggish light reflex)
- idiopathic, post-viral, trauma including surgery, migraine, tumour, VZV, EtOH
presentation of Adie tonic pupil
mainly unilateral, F>M, approx 30 yo, photophobia, slow dark adaptation, blurriness
light near dissociation
can happen post virl
generally benign
