Neuro VIII Flashcards
What happens with CN V motor lesion?
Jaw deviates TOWARD side of lesion due to unopposed opposite pterygoid
What happens with CN X lesion?
1) uvula deviates AWAY from side of lesion (SCM)
Weak side collapses and uvula points away
What happens with CN XII lesion?
Tongue deviates TOWARD side of lesion (“lick your wounds”) due to weakened tongue muscles on affected side.
What happens with facial nerve UMN lesion?
Contralateral paralysis of lower muscles of facial expression, sparing forehead due to bilateral UMN innervation
Presentation of facial nerve LMN lesion?
1) ipsilateral paralysis of upper and lower muscles of facial expression.
2) hyperacusis + loss of taste sensation to anterior tongue.
most common facial nerve palsy?
Idiopathic (aka Bell palsy)
other causes of facial nerve palsy?
1) lyme disease
2) HSV
3) herpes zoster (Ramsay hunt syndrome)
4) sarcoidosis
5) tumors
6) DM
path of venous drainage from eye and superficial cortex
eye and superficial cortex –> cavernous sinus –> internal jugular vein.
Cavernous sinus syndrome presentation
1) Variable ophthalmoplegia
2) decreased corneal sensation 3) Horner syndrome
4) occasional deceased maxillary sensation
CN most susceptible to injury with cavernous sinus syndrome
CN VI
Causes of cavernous sinus syndrome
1) mass effect from tumor
2) carotid-cavernous fistula
3) cavernous sinus thrombosis related to infection
tonotopy concept
Each frequency of vibration of hair cells leads to vibration at specific location on basilar membrane.
Where are frequencies heard in cochlea?
1) Low frequency heard at apex near helicotrema (wide and flexible).
2) High frequency heard base at base of cochlea (thin and rigid).
Rinne test findings with conductive hearing loss
Abnormal (bone greater than air)
Rinne test findings with sensorineural hearing loss
Normal (air greater than bone)
weber test results
Localizes to affected ear with conductive, and normal ear with sensorineural.
How do sudden extremely loud noises produce hearing loss?
Due to tympanic membrane rupture.
Where do cholesteatomas occur?
middle ear
What is a cholesteatoma?
overgrowth of desquamated keratin debris
Sequela of cholesteatoma?
Can erode ossicles and mastoid air cells causing conductive hearing loss.
Inner to outer layers of eye
Retina –> choroid –> sclera
what inhibits aqueous humor production?
1) beta blockers
2) A2 agonists
3) carbonic anhydrase inhibitors
Receptors on Iris dilator muscle?
alpha2
Receptors on iris sphincter muscle?
M3
Aqueous humor pathway
produced in ciliary body –> flows through posterior chamber up and over lens –> flows above iris –> then flows through trabecular meshwork and into canal of scheme and into episcleral vasculature (90% OR drains into urea and sclera (uveoscleral outflow)
With do M3 agonists affect?
trabecular outflow.
What do prostaglandin agonists affect?
Uveoscleral outflow
Hyperopia pathophys
Eye too short for refractive power of cornea and lens –> light focused behind retina.
Myopia pathophys
Eye too long for refractive power of cornea and lens –> light focused in front of retina.
astigmatism etiology and sequela
Abnormal curvature of cornea leading to different refractive power at different axes.
What is presbyopia caused by?
Decreased lens elasticity
cataracts?
painless, often bilateral opacification of lens.
cataracts RFs
1) age
2) smoking
3) excessive alcohol use
4) excessive sunlight
5) chronic corticosteroid use
6) DM
7) trauma
8) infection
congenital RFs for cataracts
1) classic galactosemia
2) galactokinase deficiency
3) trisomies 13,18,21
4) rubella
5) Marfan
6) Alport syndrome
7) myotonic dystrophy
8) NF2
Glaucoma etiology?
Optic disc atrophy with cupping + elevated IOP usually
visual manifestation of glaucoma?
Progressive peripheral visual field loss
What is cupping?
Thinning of outer rim of optic nerve head.
open-angle glaucoma RF’s
1) increased age
2) AA race
3) family history
Which glaucoma type is more common in US?
open-angle
Cause of secondary open-angle glaucoma
1) blocked trabecular meshwork from WBCs (uveitis), RBCs (vitreous hemorrhage), retinal elements (retinal detachment).
primary closed angle glaucoma pathophys
Enlargement or forward movement of lens against central iris (pupil margin) leads to obstruction of normal aqueous flow through pupil –> fluid builds up behind iris, pushing peripheral iris against cornea and impeding flow through trabecular meshwork.
Secodnary closed angle glaucoma pathophys
Hypoxia from retinal disease induces vasoproliferation in iris that contracts angle.
causes of secondary closed angle glaucoma
1) DM
2) vein occlusion
chronic closed angle closure glaucoma pathophys
often asymptomatic with damage to optic nerve and peripheral vision.
acute closure glaucoma pathophys
Increased IOP pushes iris forward –> angle closes abruptly.
acute closure glaucoma presentation
very painful, red eye, sudden vision loss + halos around light + rock-hard eye + frontal headache
Drug contraindicated with acute closure glaucoma
epinephrine (mydriatic effect)
How to differentiate allergic, bacterial, viral conjunctivitis?
Allergic –> itchy eyes and bilateral
Bacterial –> pus
Viral –> sparse mucous discharge, swollen pre auricular node.
most common cause of conjunctivitis?
viral (adenovirus)
anterior uveitis
iritis
intermediate uveitis
pars planitis inflammation
posterior uveitis
choroidits and/or retinitis
other findings in uveitis
1) hypopyon
2) conjunctival redness
hypopyon
accumulation of pus in anterior chamber
Uveitis associations
- systemic inflammatory disorders
1) sarcoidosis
2) RA
3) JRA
4) HLA-B27 associations
Visual effects of macular degeneration?
1) metamorphopsia
2) loss of central vision (scotomas)
metamorphopsia
distortion of vision
dry mac degeneration prophylaxis
multivitamin + antioxidants
more common type of macular degeneration?
Dry (over 80%)
where does drusen deposit with macular degeneration?
In and between Bruch membrane and retinal pigment epithelium.
difference in presentation between wet and dry macular degeneration?
Dry presents with gradual loss vision; wet with rapid loss of vision
cause of wet macular degeneration?
Bleeding secondary to choroidal neovascularization.
wet macular degeneration treatment
ranibizumab
non proliferative diabetic retinopathy pathophys..
Damaged capillaries leak blood –> lipids and fluid seep into retina –> hemorrhages and macular edema occur.
treatment for non proliferative diabetic retinopathy pathophys..
blood sugar control
proliferative diabetic retinopathy pathophys..
Chronic hypoxia results in new blood vessel formation with resultant traction on retina.
proliferative diabetic retinopathy treatment
1) peripheral retinal photocoagulation
2) surgery
3) anti-VEGF
Retinal vein occlusion pathophys
Blockage of central or branch retinal vein due to compression from nearby arterial atherosclerosis.
Retinal vein occlusion presentation on fundoscopy
Retinal hemorrhage and venous engorgment. Edema in affected area.
retinal detachment pathophys
Separation of neurosensory layer of retina (photoreceptor layer with rods and cones) from outermost pigmented epithelium –> degeneration of photoreceptors –> vision loss.
normal function of pigmented retinal epithelium
Shields retina from excess light and supports retina.
Causes of retinal detachment
1) retinal breaks
2) diabetic traction
3) inflammatory effusions
fundoscopy findings with retinal detachment?
1) Crinkling of retinal tissue
2) changes in vessel direction
Rss for retinal detachment
1) high myopia
2) history of head trauma
retinal detachment presentation
1) often preceded by posterior vitreous detachment (flashes and floaters)
2) eventual monocular vision loss like curtain drawn down.
CN XI lesion
1) Weakness turning head to contralateral side of lesion (SCM). Shoulder droop on side of lesion (trapezius).
2) Left SCM contracts to help turn the head to the right.
