1-17,18 Pupils Flashcards
Describe the parasympathetic pathway for pupillary reflexes
Parasympathetic (afferent)
- Retina -> Optic nerve -> chiasm -> tract -> midbrain at level of superior colliculus
Parasympathetic (interneuron)
- Pretectal nuclei of SC -> Edinger-Westphal nuclei
Parasympathetic (efferent)
- EW –(Ocular motor, CN3)–> Ciliary ganglion -> Sphincter pupillae + cilliary muscle.
Note: Near ref;ex starts at different centre, synapses at E-W nuclei (slightly in front of where the pupils pathway synapses), and follows same pathyway as pupils afterwards.
Describe sympathetic (efferent) pathway
- Posterior hypothalamus at brainstem to Ciliospinal centre of budge (C8 – T2 near neck)
- Past/near lung apex, to Superior cervical ganglion
- Surround ICA, past cavernous sinus, becomes ophthalmic division of CNV
- Innervates dilator pupillae
Describe Horner’s syndrome
- What is it?
- Causes?
- Characteristics?
- Pupil reflexes?
Sympathetic supply is interrupted to iris dilator. This means pupil is smaller than normal.
- Either congenital or iatrogenic (caused by medical procedure of some kind)
Characterised by:
- Miosis
- Ptosis (muller’s muscle innervated by symp. Can apear as pseudo-enophthalmos meaning eye appears sunken in on one side)
- Anhidrosis (skin supplied by symp so little/no sweat on one side)
- Only aniscoria much larger in dark.
Describe gold standard for diagnosing Horner’s.
- What drug, concentration, drops?
- How it works?
4% Cocaine 1gtt OU
At the sympathetic synapse, cocaine will block NA reuptake.
- In a normal pupil, this means NA concentrations increase so dilator is more innervated thus pupil dilation.
- In the horner’s affected eye, NA isn’t being released to begin with. This means blocking uptake has no effect as there’s no NA at the synapse anyway. Dilator remains unchanged so pupil is unchanged.
Describe the other (non-gold standard) way of diagnosing Horner’s
- What drug, concentration, drops?
- How it works?
- Why not gold standard?
1% Apraclonidine 1gtt OU
Iris uses alpha-1 adrenergic receptors. Apraclonidine is a weak alpha-1 agonist (but strong for alpha-2).
- In a normal pupil, the apraclonidine is too weak to bind to the alpha-1 receptors at the iris dilator. No pupil changes.
- In a horner’s pupil, the lack of alpha-1 action over time makes it subjected to denervation supersensitivity. This means it upregulates alpha-1 recetors so there’s much more of it. As a result, even a weak alpha-1 agonist like apraclonidine is able to induce a response in the dilators thus pupil dilation.
- This isn’t gold standard since it relies on denervation supersensitivity which no one knows when it occurs. If Horner’s was recent, it’s likely it hasn’t undergone this process yet so false negative when diagnosed w/ apraclonidine.
How to localise Horner’s using least common method?
- What drug, concentration, drops?
- How it works?
1% hydroxyamphetamine 2gtt OU
It causes N3 (3rd order neuron of sympathetic efferent pathway) to release it’s NA
- In a horner’s N1 or N2 problem, The N3 synapse is not damaged, it’s just that it’s not being stimulated by N2 because either N1 or N2 is damaged. So when hydroxyamphetamine comes, it can release the N3 NA it’s been storing this whole time and thus act on dilators to cause pupil dilation.
- In a horner’s N3 problem, N3 doesn’t have any NA since it’s damaged. When hydroxyamphetamine comes, it has no effect since no NA can be released at N3 thus pupil unchanged.
More common method of localising Horner’s?
- What drug, concentration, drops?
- How it works?
0.1% Adrenaline or 1% Phenylephrine 1ggt OU
Acts as low concentration weak neurotransmitter for sympathetic nervous system. In a functioning SNS, Monoamine Oxidases (MAO) are produced at N3 which break down neurotransmitters.
- In an N1 or N2 problem, MAO is still being produced by N3 so when stimulated, the neurotransmitters released by N3 will be broken down thus pupil unchanged.
- In an N3 problem, MAO is not being made since N3 is broken. This means a small amount of neutrotransmitter is able to elicit a response in the dilators thus pupil dilation.
Describe Argyll Robertson pupil
- Caused by?
- Damages the…
- Characterisitcs?
- Light reflexes?
Very specific sign of syphillus (Treponema pallidum infection of CSF)
- Midbrain lesions affects parasympathetic efferent pathway.
– Damages dorsal (back) EW (light reflex)
– Does NOT damage ventral (front) EW (near reflex)
Characterised by:
- Light-near dissociation
- Bilateral miotic pupils
- Slow difficult pupil dilation
(unsure as to why it causes miosis despite affecting parasymp but who knows).
- Room light = miotic
- No direct or consensual in BE
- Dim lights = slow difficult dilation
- Near reflex maintained
Describe Adie’s Tonic Pupil
- Damage where?
- Causes?
Describe the acute version
- Presentation?
- Symptoms/signs?
- Light reflexes?
Ciliary ganglion damage interrupts parasympathetic pathway.
- 5% affects sphincter, 95% affects ciliary muscle
- Mostly idiopathic
- Sometimes no deep tendon reflexes (hit knee w/ hammer) as concurrent denervation of dorsal root ganglia (“Holmes-Adie syndrome”)
- Most likely unilateral at start, can become bilateral.
- Dilated pupil w/ poor/slow light reflex. Causes:
– Glare, photophobia
– Accommodation issues - Bright room = anisocoria (affecetd = larger)
- Dim room = less noticeable aniscoria
How to test for acute Adie’s tonic pupil?
- Drug, concentration, drops?
- How does it work?
0.0625% - 0.125% pilocarpine 1gtt OU.
Pilocarpine normally stimulates acetylcholine release causing pupil constriction. However, at this low concentration, a normal pupil does not constrict whilst an Adie’s tonic pupil would’ve gone thorugh denervation supersensitivity so it will constrict.
Describe chronic Adie’s tonic pupil
- Pathogenesis?
- Characteritics?
Damaged fibres repaired after 2 months.
- Accommodation recovery far better than light reflex recovery.
- Aberrant regeneration where repairing fibres that are meant to go to ciliary muscle, ends up going to iris sphincter by accident. Aberrant regeneration starts segmental and slowly spreads. giving vermiform movevment).
Characteristic:
- Vermiform pupil margin movement (Some parts of iris constrict, some don’t)
- Light-near dissociation (near reflex good, light reflex bad)
Describe long-standing Adie’s tonic pupil
- Pathogenesis
- Characteristics
- Normal constant ciliary muscle stimulation (even in dark) -> aberrant fibres stimulate sphincter instead = small resting pupil size.
Characteristic “little old Adie’s pupil” - Affected pupil smaller than normal pupil
- Slow tonic near reflex
- Slow sustained relation back to distance.
CNIII palsy?
- Damage where?
- Affecfts what?
- Causes?
- Presentation?
CNIII damage meaning damaged innervation to:
- Outer parasympathetic efferent fibres e.g. Sphincter, ciliary.
- Inner somatic fibres = SR, IR, IO, MR, LPS
Causes:
- Idiopathic (25%)
- Microvascular infarction
- Compressive lesion (assume this until proven otherwise)
- Trauma
Either complete (both inner and outer) or partial
Complete:
- Limited adduction, elevation, depression
- Eye faces down + out -> strabismus + diplopia
- Profound to complete ptosis
- Accommodation issues
- Fixed dilated pupil
Partial:
- Variable EOM dysfunction and ptosis
- Pupil involving/sparing.
Describe partial CNIII palsy that’s pupil-involving
Describe light reflex seen
Outer parasympathetic fibres are compressed by lesion e.g. tumour. Inner fibres are spared. Outer fibres control sphincter and accommodation so it involves pupil. “Surgical” lesions since requires surgery to remove.
Can also have oculomotor synkinesis where aberrant regeneration of lid and pupil gaze.
Bright room = anisocoria (larger in affected)
Dim room = anisocoria smaller
No direct or consensual in affected eye (affected eye won’t change size)
Describe partial CNIII palsy w/ pupil sparing
This means only inner is damaged. If so, usually due to vasa vasorum blood supply is damaged meaning some medical issue thus “medical” lesions.
