What is the pathway for autonomic innervation causing Dilation?
Dilation = Hypothalamus to T1-L2; from there to Supererior Cervical Ganglion; from there to Pupil Dilator (3 neurons)
Constriction = Cortex/midbrain to Edinger-WEstphal Nucleus of CN3; from there to Ciliary Ganglion; from there to Pupil Constrictor (3 neurons)
(Somatic pathways have 2 neurons - upper and lower motor neurons!)
What drugs would you use to pharmacologically dilate the eye?
Alpha-1 Adrenergic Agonist = Phenylephrine
Cholinergic Antagonist = Tropicamide (best for short term); Atropene, Scopolamine, Cyclopentolate
What drug can you give (but we dont in US) to reverse Mydriasis?
Dapiprazole - Topical alpha blocker but causes headaches
What are the two types of glaucoma and what happens there?
Open Angle = (MORE in African Americans over 75) High IOP even though drainage open and iridiocorneal angle is normal - need to treat by lowering IOP
Closed Angle = angle between iris and cornea is small and less room to drain aqueous humor through trabecular meshwork so build-up IOP - DO NOT DILATE THESE EYES! Kicks narrow angle into closure (more common in East Asians)
What are the clinical characteristics of Acute Angle Closure?
Red Painful eye
Nausea and Vomiting
Fixed Mid-dilated pupul
Vision not working at high pressures
Tx = Iridotomy
Treatments for Gluacoma?
Need to lower IOP so best to use Prostaglandins like Latanoprost to induce low levels of inflammation to lower IOP
ALSO can use:
- Beta Antagonists = Betaxolol or Timolol for Beta-1 block to stop production of Aq Humor from ciliary body (Systemic side effects!)
- Alpha 2 Agonists = Brimonidine and Apraclonidine to decrease inflow of Aq humor from ciliary body
- Cholinergic Agonists = Pilocarpine and Carbamylcholine muscarinic cholinergic agonists to constrict and open up the angle
What should you NEVER do with Glaucoma patients?
NEVER use Anti-cholinergics bc can precipitate pupillary dilation causing acute angle closure which is medical emergency
Do not use Benedryl, Anti-psychotics etc
Diagnosing Horner’s Syndrome -Step 1: Which Pupil is Affected?
Note Aniscoria (3 mm or more difference in pupils) and ptosis
Then add light (pupils should constrict) and if situation is worse then DILATED one is bad one
Then add dark (pupils should dilate) and one stays CONSTRICTED is bad one
Diagnosing Horner’s Syndrome: Step 2 - Confirming Horner’s
Use Cocaine (blocks reuptake of NE so normally causes pupillary dilation) to see if with time the pupil STILL DOES NOT DILATE
Conclusion - problem with nerve terminal NE release to confirm Horner’s
Diagnosing Horner’s Syndrome: Step 3 - Discerning where neurological block is
Add Hydroxyamphetamine (indirect adrenergic agonist to act on post-ganglionic neuron to stimulate presynaptic release of NE)
If add and get dilation - 3rd order neuron intact and problem is more 1st or 2nd
If doesn’t Dilate then damaged 3rd order and no NE release
What is a weird common-ish cause of Horner’s syndrome?
Apical Lung Tumor = Pancoast
lesion in apex of lung compressing brachial plexus and results in SEcond-Order horner syndrome bc impringing on sympathetic pathway
So like…it’s hard to get cocaine, right? What could you use instead to Dx Horner’s Syndrome?
Apraclonidine - A2 agonist with minor A1 component*
weak A1 activity BUT in Horner’s syndrome the denervated pupil would upregulate receptors and be HYPERSENSITIVE to any NE onto A1 effect and so a small A1 agonist would cause dilation in Horner’s and no effect in normal person
Also in Horner’s A2 agonist has no change in NE release …duhhh