Neuro-opthalmology diseases

Question 1

Anatomy of sympathetic pathway

Answer 1

1st Order Neuron in posterolateral hypothalamus –> Ciliospinal centre of bulge (C8 - T1) –> 2nd Order Neuron (C8 - T1) –> Superior Cervical Ganglion –> 3rd Order Neuron (Superior Cervical Ganglion - carotid plexus) –> Eye

Question 2

Anatomy of parasympathetic pathway

Answer 2

Sensory in retina –> pretectal nucleus –> Dually innervates to other pretectal nucleus + Edinger Westphal nucleus –> Ciliary ganglion –> Eye.

Question 3

Components inside the cavernous sinus

Answer 3

1. CN 3, 4, V1, V2, VI

2. Internal carotid Artery

Question 4

PCA Stroke

Answer 4

A PCA stroke can cause isolated visual field loss without any other deficits (e.g. weakness, sensory loss, speech difficulties).

Question 5

Draw out the pathway for Internuclear Ophthalmoplegia

Answer 5

Lesions that localize to the medial longitudinal fascicles on the side o the adduction palsy (i.e. L eye does not adduct = L MLF lesion)

Question 6

Binocular diplopia

Answer 6

1. Goes away after covering one eye

2. Caused by eye misalignment (i.e. neurological causes)

Question 7

Monocular diplopia

Answer 7

1. Does not go away after covering one eye

2. Ocular causes or psychogenic

Question 8

Surgical CN III Palsy

Answer 8

Compressive lesions can damage the pupillary fibres located superomedially by direct compression (i.e. Posterior Communicating Artery aneurysm or tumour).

Question 9

Medical CN III Palsy

Answer 9

Ischemic cause - vascular risk factors (e.g. diabetes, hypertension) affect vasa nervorum –> ischemic damage to oculomotor nerve axons w/ preservation of pupillary fibres. Pupil-sparing III nerve palsy.

Question 10

Giant Cell Arteritis

Answer 10

Arteritic anterior ischemic optic neuropathy (AION) caused by GCA. GCA: A systemic vasculitis affecting medium-sized & large arteries; tends to occur in patients >60 years old. Preferential involvement of posterior ciliary artery, major source of blood supply to optic nerve head. Antecedent episodes of transient diplopia, monocular visual loss is common. Inflammatory markers (ESR, CRP) significantly elevated. Temporal artery biopsy to confirm diagnosis. Treat w/ strong corticosteroids to prevent other eye from being blind.

Question 11

Describe the aqueous pathway

Answer 11

Aqueous is the fluid that fills the front part of the eye, and it is important for maintaining the shape of the eye and providing nourishment for the avascular lens and cornea.

1. Aqueous is produced by the ciliary bodies (a band of muscles that lie behind the iris).
2. Travels through the posterior chamber (space between iris & lens). Enters anterior chamber through the pupil.
3. Drains through the angle (between iris & cornea) into the trabecular meshwork & canal of schlemm blood vessels)

Question 12

Glaucoma

Answer 12

Gradual death of the optic nerve, often associated with high intraocular pressure.

Question 13

Diabetic retinopathy

Answer 13

High amounts of glucose coursing through the blood vessels –> high glycosylation –> denaturing of collagen proteins in the walls of the vessels –> capillary thickening & wall breakdown. Observed with aneurysms. Dot-blot hemorrhages.

Question 14

Non-proliferative Diabetic Retinopathy

Answer 14

No proliferation.

Question 15

Proliferative Diabetic Retinopathy

Answer 15

On-going damage to the retinal vasculature –> decreased blood supply to the retina –> ischemic retina sends out chemicals to stimulate the growth of new vessels (VEGF) –> but new blood vessels are friable & prone to breaking & grow in wrong places. Can grow off the retina, onto the vitreous fluid. Traction of the vitreous humour –> retinal detachment & hemorrhage.

Question 16

Macular Edema

Answer 16

Despite the neovascularization phenomenon and its potential for detachments and hemorrhage, the most common cause of blindness in diabetic patients is from macular edema. This occurs when diffuse capillary and microaneurysm leakage at the macula causes the macular retina to swell with fluid. Macular edema occurs in about 10% of patients with diabetic retinopathy and is more common with severe retinopathy. On exam the macula looks cloudy and mildly elevated, and you can see past evidence of edema in the form of yellow-colored “hard exudates”. These exudates are fatty lipids that are left behind after past macular swelling subsides, similar to a dirt ring in a bathtub.

Question 17

Retinal detachment

Answer 17

Detachment between the sensory retina and the underlying retinal pigment epithelium & choroid plexus.

Question 18

Age Related Macular Degeneration

Answer 18

Extracellular deposits called “drusen” form deep in Bruch’s membrane (b/w choroid & retina to prevent nutrients from choroid & waste products from retina to reach the other membranes).

Question 19

“Wet” Age Related Macular Degeneration

Answer 19

A break in Bruch’s membrane will cause blood vessels to grow out from the choroidal circulation up into the retina. This neovascularization can bleed, create edema, and vision loss. Treat with anti-VEGF.

Question 20

Anatomy of the cornea

Answer 20

1. A - Anterior Epithelium
2. B - Bowman’s membrane
3. C - Corneal stroma
4. D - Descement’s membrane
5. E - Endothelium

Question 21

Accommodation

Answer 21

1. Constriction of pupils
2. Lens become rounder, more powerful to focus objects onto the retina.
3. Caused by contraction of the ciliary body & relaxation of the zonules (contraction of the ciliary bodies towards the lens). As we get older, the lens become stiffer & accommodative capacity diminishes (presbyopia).

Question 22

Myopia

Answer 22

Large, long, powerful eyeball that focuses image in front of the retina. Nearsightedness. Treated with a minus lens (convex) to weaken the overall refractive power of the eye and allows images to focus properly on the retina.

Question 23

Hyperopia

Answer 23

Small eye such that images fall behind the eye. Treated with a plus (concave) lens to allow images to fall on the retina. Cornea has a refractive index of 2/3. Lens has a refractive index of 1/3.