HY lecture notes:
Diabetic retinopathy
Leading cause of blindness ages 20-64.
Caused by non-enzymatic glycosylation of retinal microvessels –> vascular damage with degeneration of capillaries –> reduced retinal blood flow + ischemia + damage to neurons of inner retina.
Initially it is non-proliferative, meaning there is no neovascularization of the retina, and many patients won’t notice any visual changes.
As retinal ischemia progresses, neovascularization occurs; this is called proliferative diabetic retinopathy. The tiny new blood vessels are fragile and can easy rupture, causing blindness. In addition, they can also grow into the vitreous humor, eventually leading to vitreous hemorrhage.
Cotton wool spots may be seen on fundoscopy, which are axonoplasmic aggregates from neuronal degeneration. HTN is the other common cause of cotton wool spots.
Treatment for diabetic retinopathy is with injections of VEGF inhibitors or laser photocoagulation.
Optic neuritis
Optic neuritis literally means inflammation of the optic nerve –> classically seen in multiple sclerosis –> can present with a wide array of visual changes, e.g., blurry vision, loss of color vision, and central scotoma. Essentially in the vignette they’ll say a woman 20s to 30s who has an episode of blurry vision + urge incontinence + other sensory or motor dysfunction –> answer = MS with optic neuritis.
Optic neuritis causes a Marcus Gunn pupil, which is also known as a relative afferent pupillary defect (RAPD).
In RAPD, shining a light in the eyes and moving it side to side will make it appear as though the affected eye’s pupil dilates, rather than constricts, in response to light. In reality, it doesn’t dilate; it just doesn’t constrict as much as the unaffected side.
In order to understand this, you must first know that optic nerve (CN II) afferent input from either eye will cause a bilateral efferent response via the oculomotor nerve (CN III), causing both eyes to constrict.
When you shine a light into one eye, the resultant constriction of that eye’s pupil is called a direct response. The constriction of the contralateral pupil is called the consensual response.
When CN II from one eye receives a light stimulus, that is transmitted in the form of an afferent signal to the Edinger-Wesphal nucleus of the midbrain, which will then relay an efferent signal back to both eyes via CN III, yielding both a direct and consensual response.
If CN II of the left eye is affected by optic neuritis, the left CN II is essentially communicating, “we don’t need to constrict either pupil that much because there’s not much light here; let’s constrict both pupils just a little.” So the result is, the direct and consensual constrictive response is weak. However, the right eye is normal, so if you shine the same light into it, the afferent signal will be much stronger, so the degree of constriction, as received via the efferent response, will also be stronger bilaterally.
Therefore, when you go back to the affected side with the light, the lesser degree of direct response will make it appear as though the pupil is dilating, when in reality it’s just constricting less relative to the robust level of constriction from the previous consensual response.
For instance, if we have a Marcus Gunn pupil in the right eye (left side of following diagram), this is what we’d see:
You’re probably like, “Oh wow fuck yeah. That diagram is actually crazy helpful. I don’t even think I totally understood MG pupil until now truthfully.” Yeah, I know. You like that.
Internuclear ophthalmoplegia
In MS, although optic neuritis is common, it is non-specific, and can be caused by other pathologies (e.g., sarcoidosis) and drugs (e.g., ethambutol). In contrast, internuclear ophthalmoplegia (INO), aka medial longitudinal fasciculus syndrome (MLF syndrome) is pathognomonic of MS (i.e., you only see it in MS).
In INO, when one eye abducts via abducens nerve (CN VI), the contralateral eye cannot adduct via CN III because of inflammation of the MLF.
The side that cannot adduct is the side whose MLF is affected. The normal side’s eye will demonstrate nystagmus.
It must also be stated that although the affected side cannot adduct, there is no CN III lesion, as evidenced by the patient being able to converge the eyes normally.
So if the left MLF is affected:
Right eye abducts (CN VI) –> left eye tries to adduct (CN III) but cannot, so there is nystagmus in the right to attempt to bring the eyes together in the midline. However patient can converge normally (CN III therefore intact on left, so Dx = INO).
Weber syndrome –> midbrain infarct characterized by ipsilateral CN III defect + contralateral hemiparesis/hemiplegia.
Lateral pontine syndrome –> (in FACIAL spelled backward –> AICA) –> AICA infarct + ipsilateral Bell palsy (facial); ipsilateral hearing loss (central deafness) + loss of pain/temperature sensation to ipsilateral face (facial hemianesthesia) + contralateral body.
Lateral medullary syndrome (Wallenberg syndrome) –> PICAchew (Pikachu) –> PICA infarct + dysphagia +/- ipsilateral Horner syndrome + ipsilateral facial sensory deficit. Horner syndrome is classically caused by pancoast tumor of the lung, but knowing it is caused by lateral medullary syndrome is really HY in terms of being able to differentiate these stroke syndromes!
Medial medullary syndrome –> infarct of paramedian branch of anterior spinal artery –> ipsilateral tongue deviation (CN XII) + contralateral hemiparesis/hemiplegia.
CN III palsy –> down and out –> can classically occur due to impingement from a posterior communicating artery (PCom) aneurysm.
CN IV palsy –> slightly elevated pupil in the midline –> worsens when head is tilted toward ipsilateral shoulder –> due to weakness of superior oblique (moves pupil inferomedially).
CN VI palsy –> medially-directed pupil.
Central pontine myelinolysis (CPM) –> causes locked-in syndrome –> caused by corrected hyponatremia (<135 mEq/L) too quickly with hypertonic (3%) saline. Na should be corrected no more than 6 to 12 mEq/L in the first 24 hours, and no more than 18 mEq/L in the first 48 hours. If hyponatremia is severe, a 100-150-mL bolus of hypertonic (3%) saline is acceptable. In contrast, if hypernatremia is corrected too quickly with hypotonic saline, cerebral edema will ensue.
The header image for this lesson is CPM.
