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Neuro/Behavior I > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Danger space

A

Retropharyngeal space

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2
Q

All constrictor muscles are innervated by

A

CN 10, vagus

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3
Q

Superior laryngeal inteenal nerve punches through:

A

The thyrohyoid membrane

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4
Q

Pharyngeal plexus is composed of

A

Glossopharyngeal nerve (CN9), and Vagus nerve (CN10)

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5
Q

What divides anterior 2/3 tongue from posterior 1/3?

A

Foramen cecum which is now just a depression

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6
Q

Hypoglossal nerve innervates any muscle with “glossus” EXCEPT:

A

palatoglossus which is vagus nerve (CN10)

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7
Q

Vagus nerve innervates any muscle with “palate” except:

A

tensor veli palantini which is trigeminal (CN5)

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8
Q

Contents of the pterygopalatine fossa

A
  1. maxillary artery
  2. sphenopalatine artery
  3. descending palatine artery
  4. pterygopalantine ganglion (dropping off V2)
  5. nerve of pterygoid canal
  6. greater palatine nerve
  7. lesser palatine nerve
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9
Q

intrinsic muscle of the tongue

A

1.) Superior longitudinal
2.) vertical and transverse
3.) inferior longitudinal

– all innervated by CN12 hypoglossal

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10
Q

True vocal cords

A

cricothyroid ligament

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11
Q

False vocal cords

A

Vestibular ligament

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12
Q

What muscle abducts vocal cords?

A

Posterior cricoarytenoid

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13
Q

You have hoarseness when this nerve is damaged

A

Recurrent laryngeal of CN10 (Vagus nerve)

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14
Q

Cataracts symptoms

A
  • painless
  • progressive decline in vision
  • watch for impairment in activities of daily living (surgery candidate)
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15
Q

Cataract findings

A
  • gross exam or slit lamp exam reveals opacification of the lens
  • Types of cataracts seen: Cortical, nuclear, posterior, subcapsular
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16
Q

Acquired risk factors for cataracts

A
  • increased age
  • smoking
  • excessive alcohol
  • excessive sunlight exposure
  • prolonged corticosteroid use
  • diabetes mellitus
  • trauma
  • infection
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17
Q

Congenital risk factors for cataracts

A
  • classic galactosemia
  • galactokinase deficiency
  • Trisomy 13, 18, 21
  • ToRCHeS infections (rubella)
  • Marfan syndrome
  • alport syndrome
  • myotonic dystrophy
  • NF2
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18
Q

Macular degeneration

A
  • age-related, any time after age 50, usually >70 is common
  • causes decreased central vision and scotomas and distorted vision
  • Risk factors: family history, smoking, poor nutrition
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19
Q

Metamorphopsia

A

distorted vision

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20
Q

Dry atrophic nonexudative macular degeneration

A
  • 80% of cases
  • Drusen develop between Bruch’s membrane and RPE
  • atrophy of RPE
  • prevention: antioxidant rich diet and supplements, smoking cessation
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21
Q

wet exudative macular degeneration

A
  • 10-15% of cases
  • abnormal choroidal blood vessel growth in the subretinal space causes leakage and bleeding –> scars
  • Diagnose: fluoresceine angiography and OCT testing
  • Treatment: anti-vegf injections
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22
Q

Anti-VegF

A

prevents vascular endothelial growth factor
- ranibizumab, aflibercept, pegaptanib, and bevacizumab

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23
Q

Vitamins to help macular degeneration

A

Vitamin A, C, E, Zinc, copper, lutein/xeaxanthin

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24
Q

Glaucoma

A

optic disc atrophy with characteristic cupping (thinning of the outer rim of the optic nerve head), usually due to intraocular pressure

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25
Q

open angle glaucoma risk factors

A

increased age, african american race, family history, ocular trauma

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26
Q

open glaucoma symptoms

A

usually no symptoms until very advanced, progressive peripheral visual field loss if untreated

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27
Q

Primary vs secondary open angle glaucoma

A

primary: age, genetics, etc
secondary: TM blockage by WBCs, RBCs, pigment from iris, scarring, scarring, retinal/other elements

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28
Q

Glaucoma testing

A
  • optical coherence tomography (OCT) of the optic nerve to measure neuroretinal rim
  • peripheral visual field testing
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29
Q

Glaucoma drugs acting on uveoscleral outflow

A

prostaglandin agonists (teal top)

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30
Q

Glaucoma drugs acting on trabecular outflow

A

muscarinic agonists

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31
Q

Glaucoma drugs acting on aqueous humor inflow

A

beta-blockers, alpha2 agonists, CAIs

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32
Q

Narrow/closed angle glaucoma risk factors

A
  • family history
  • small/short eye (usually hyperopic)
  • increased age
  • poorly controlled diabetes and hypertension, vascular disease
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33
Q

Primary vs secondary narrow/closed angle glaucoma

A

Primary: Small/crowded eye, enlarged lens or forward movement of lens against iris/pupil causing obstruction of aq. flow through pupil–> fluid builds up behind iris–> peripheral iris pushes against cornea–> further impedes flow through TM

Secondary: hypoxia from retinal disease–> vasoproliferation or the iris/angle which scars/contracts/blocks angle

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34
Q

Acute angle closure glaucoma

A

abrupt angle closure: true ophthalmic emergency

Symptoms: painful red eye, frontal/periocular HA, rock-hard eye, nausea/vomiting, vision loss, halos, prism/colors around lights, cloudy cornea, mid-dilated pupil

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35
Q

Assessing AC depth

A

oblique flashlight test, shadow on nasal side of iris shows shallow anterior chamber

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36
Q

Acute glaucoma treatment

A
  • Pilocarpine 2% q 15
  • Acetazolamide
  • oral glycerine or isosorbide
  • laser peripheral iridotomy
  • DO NOT GIVE EPINEPHRINE OR ANY DILATING DROPS (mydriasis worsens acute angle closure)
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37
Q

Ocular manifestations of systemic disease

A
  • diabetes
  • hypertension
  • vascular disease
  • thyroid disease
  • inflammatory conditions/arthritis
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38
Q

Diabetic retinopathy

A

slowly progressive, can rarely cause total blindness

  • treatment: preventable with blood sugar management, laser therapy, surgical-vitrectomy, AntiVEGF drugs
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39
Q

Nonproliferative diabetic retinopathy

A
  • elevated blood sugars damage capillaries–> dilate and leak blood into the retina–> dot/blot hemorrhages and microaneurysms
  • lipids and fluid also seep into the retina causing exudates, macular edema, and decreased vision
  • Treatment: blood sugar control, antiVEGF drugs, laser treatment, management of HTN and lipids
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40
Q

Proliferative diabetic retinopathy

A
  • damaged vasculature leads to hypoxia and thus VEGF production in the retina–> abnormal blood vessel proliferation–> causes fragile vessels–> vitreous hemorrhage
  • treatment: AntiVEGF injections, surgery, panretinal photocoagulation (laser)
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41
Q

hypertensive retinopathy

A
  • narrowing and sclerosis of arterioles (copper wiring/silver wiring)
  • arteriovenous crossing changes (AV nicking, tapering, banking)
  • Flame hemorrhages
  • Cotton wool spots
  • optic disc edema in severe cases
    – Treatment is to control blood pressure
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42
Q

Retinal arterial occlusion

A

Sudden severe loss of vision in one eye, painless, vision loss usually permanent but may recover if treated rapidly. Cherry red spots

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43
Q

Cherry red spots

A

acute central retinal artery occlusion

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44
Q

Medical evaluation for embolic sources

A

1.) Carotid US looking for atherosclerosis
2.) Cardiac US looking for cardiac vegetations or patent foramen ovale
3.) Systemic evaluation looking for vasculitis, systemic vascular disease or hyper coagulability disease

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45
Q

Acute arterial occlusion management

A
  1. rebreathing CO2
  2. timolol or levobunolol to lower ocular pressure
  3. IV acetazolamide to lower ocular pressure
  4. massaging of globe with lids closed
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46
Q

Retinal vein occlusion

A

Blockage of central or branch of retinal vein. More common w hypertension of diabetes
- vein is compressed by overlying atherosclerotic arteriole–> turbulent flow –> clotting

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47
Q

Thyroid ophthalmopathy

A
  • Dry eyes (keratitis sicca)
  • Proptosis (protrusion of the eyes)
  • Ocular injection
  • Chemosis (swelling of conjunctiva)
  • Lid retraction and lid lag
  • Ocular muscle restriction (diplopia)
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48
Q

Treatment of Thyroid ophthalmopathy

A

1.) tear substitutes
2.) monitor/control thyroid hormone levels
3.) tepezza (med)
4.) corticosteroids
5.) orbital irradiation or surgical decompression
6.) sometimes requires extensive surgery (orbital, muscle, lid)

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49
Q

Uveitis

A
  • Inflammation of the uveal tract
  • Iritis/anterior uveitis
  • Pars planitis/intermediate uveitis
  • Choroiditis/ posterior uveitis
  • Retinitis/ posterior uveitis
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50
Q

Anterior Uvetitis Symptoms/findings

A
  • photophobia
  • pain
  • conjunctival injections
  • cell and flare in the anterior chamber aqueous
  • keratic precipitates
  • hypopyon
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51
Q

Uveitis treatment

A
  • Topical/systemic steroids, NSAIDs
  • System immunomodulating drugs for chronic cases
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52
Q

Retinitis

A
  • retinal inflammation, hemorrhage, edema, and often necrosis
  • often results in severe retinal scarring, retinal detachment, and vision loss
  • must diagnose and treat the underlying disease
  • typically from infections (CMV, HSV, VZV, bacterial, parasitic, more frequent in immunosuppressed individuals)
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53
Q

Retinitis pigmentosa

A
  • very characteristic bone spicule pigment deposition outside of the macula
  • inherited retinal degeneration
  • painless, progressive vision loss
  • begins with night blindness because rods are affected first
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54
Q

Papilledema

A
  • Optic disc swelling, usually bilateral
  • patient may be asymptomatic or may notice diminished vision or scotoma
  • enlarged blind spot on visual field tests
  • etiology: increased ICP–> medical emergency
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55
Q

Retinal detachment

A
  • sudden partial vision loss in one eye
  • painless, progressive, always sustained
  • Floaters and photopsias (flashes)
  • Risk factors: high myopia (longer axial length), prior trauma, proliferative diabetic retinopathy, vitreous aging and detachment
  • Scleral buckling procedure used to treat this
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56
Q

ANS contributions to eye fxn

A

1.) eyelid position (superior tarsal m) – NE alpha1
2.) Pupil size – NE alpha1 causing mydriasis (dilator) and ACh M3 causing miosis (constrictor)
3.) Accommodation (ciliary m) – Relax=distant vision, Constriction=near vision
4.) Aqueous humor

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57
Q

Sympathetic cell body locations

A

Pre: T1-L2 intermediolateral cell column (lateral horn)
Post: superior cervical ganglion (carotid plexus–> long ciliary)

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58
Q

Parasympathetic cell body locations for the eyes

A

Pre: Edinger-Westphal nucleus, CN3–> short ciliary
Post: Ciliary ganglion

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59
Q

Direct sympathomimetics

A
  • Norepinephrine
  • Epinephrine
  • Phenylephrine
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60
Q

Indirect pre-synaptic sympathomimetics

A
  • block reuptake and promote release
  • Amphetamine, cocaine
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61
Q

Alpha-1 causes

A

pupillary dilation

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62
Q

Alpha-2 causes

A

Decreased aqueous humor production and pupillary constriction

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63
Q

Two functions of the ciliary body

A

1.) accommodation via the ciliary muscle
2.) generation of aqueous humor

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64
Q

Parasympathetic reactions of the ciliary body

A

1.) ACh—> M3—> contraction of pupillary sphincter—> miosis—> wider angle

2.) ACh—> M3—> contraction of ciliary muscle circular fibers—> relaxation of zonules—> rounded lens—> near vision

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65
Q

Sympathetic reactions of the ciliary body

A

1.) NE—> alpha1—> contraction of pupillary dilator—> mydriasis—> narrower angle

2.) NE—> alpha1—> contraction of ciliary longitudinal and radial fibers—> tightening of zonules—> flattened lens—> distance vision

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66
Q

Phenylephrine

A

• Mydriatic that dilated pupil without affecting ciliary muscle (lens)
• selective alpha1 agonist used in eyedrops to dilate the pupil
• reverses ptosis in Horner’s syndrome

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67
Q

Atropine, scopolamine, tropicamide

A

• nonselective, muscarinic antagonist
• cycloplegic used to dilate the pupil and flatten the lens (near vision, parasympathetic)

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68
Q

Duration of action of dilator drugs

A

1.) tropicamide: onset, 20-25 minutes. Duration 15-20 minutes

2.) phenylephrine: onset, 30 minutes duration 2-3 hours

3.) scopolamine (alpha1 agonist): onset, 30-40 minutes. Duration 36-48 hours

4.) atropine: onset, 30-40 minutes. Duration 2 days

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69
Q

Anisocoria

A

Different size pupils

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70
Q

Anisocoria problem with dilated eye

A

1.) decreased parasympathetic constrictor

2.) increased sympathetic dilator

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71
Q

Anisocoria problem with constricted eye

A

1.) increased parasympathetic constrictor

2.) decreased sympathetic dilator

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72
Q

Apraclonidine

A

• alpha2 > alpha1 agonist
• normal eye: drug works on alpha-2 receptor on postganglionic cell (constrict)
• abnormal eye: drug works on alpha one on the actual eye (dilation)
• net result is reversed anisocoria

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73
Q

Ways to modulate, intraocular pressure

A

decrease inflow/production:
1.) alpha2 agonist (apraclonidine)
2.) beta1 antagonist (timolol)
3.) carbonic anhydride antagonist (acetazolamide)

Increase efflux:
4.) prostaglandins (latanoprost)
5.) cholinergic agonist (pilocarpine)

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74
Q

Prostaglandins

A

• most effective at reducing intraocular pressure
• increase uvealscleral outflow
• long duration of action
• side effects: hyperemia (red eye), eye irritation, increased lashes, changes in iris and lash pigmentation

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75
Q

Beta blockers

A

• nonselective, competitive beta receptor antagonists that reduce aqueous humor production
• side effects: bronchoconstriction, bradycardia, depression, confusion, fatigue

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76
Q

Treatment of a cute closed angle glaucoma

A

1.) Timolol: beta blocker.
2.) apraclonidine: alpha-2 agonist
3.) pilocarpine: nonspecific muscarinic, agonist
4.) Acetazolamide: carbonic anhydrase, inhibitor

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77
Q

Osseous, bony labyrinth

A

• connected series of canals (vestibule, cochlear, semicircular canals, carved out of temporal bone)
• contains perilymph (high Na, low K extracellular fluid)

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78
Q

Membranous labyrinth

A

• tube suspended with an osseous labyrinth
• contains endolymph (high K, low Na extracellular fluid)

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79
Q

Where are receptor hair cells found?

A

• the junction of Bony and membranous labyrinth
• stereocilia in endolymph, cell bodies in perilymph
• gelatinous, matrix overlays apical surface

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80
Q

Receptive areas of the inner ear

A

• 3 cristae ampullaris (one per semicircular canal)
• 2 maculae (one in the utricle, and one in the saccule within the vestibule)
• 1 organ of Corti (cochlea)

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81
Q

Type one stereocilia

A

• true sensory receptors
• piriform flask shape, globular base with nucleus
• inner hair cells

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82
Q

Type two stereocilia

A

• biological amplifiers— motor
• cylindrical with central nucleus
• outer hair cells

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83
Q

Structure and function of hair cells

A

• Mechanoreceptors
• generate receptor potential and release neurotransmitter
• stair-like arrangement with directionality
• kinocilium: near the longest hair

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84
Q

Conductive hearing loss

A

External or middle ear problem

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85
Q

Sensorineural hearing loss

A

Cochlea or auditory nerve problem

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86
Q

Central processing disorders

A

Brain problem (cocktail party effect)

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87
Q

Tympanic membrane

A

• separates external from middle ear
• oval membrane connected to annulus (bony ring)
• appearance pearly, white, reflective with a cone of light

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88
Q

Pars flaccida

A

Region above the malleus that does not vibrate

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89
Q

Pars tensa

A

Movable part of the tympanic membrane that transmits sounds to ossicles

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90
Q

Auditory eustachian tube

A

Middle ear is vented by auditory tube that connects to the pharynx. The purpose is to keep air pressure in the tympanic cavity, equal to the pressure in the external ear canal to allow unobstructed vibration of ossicles.
• shorter and less steep slant in children causes more infections

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91
Q

Modiolus

A

Bony core that defines medial direction of the cochlea. Auditory nerve fibers run down the center

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92
Q

Three sections of the cochlea

A

• scala tympani and scala vestibule contain perilymph
• scala media contains endolymph
• basilar membrane: separates scala tympani from scala media
• vestibular membrane: separates scala vestibuli from scala media

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93
Q

Where does the round window terminate?

A

Scala tympani

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94
Q

Spiral ganglion

A

• cell bodies found in the modiolus
• fibers that run to the brain stem—> cortex, tonotopic map

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95
Q

What produces endolymph and is responsible for the endocochlear potential?

A

Stria vascularis

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96
Q

The most common inherited cause of hearing loss

A

Defects in the gene that codes for the connexin protein that normally forms gap junctions in the potassium recycling system

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97
Q

Where are high frequencies in the cochlea?

A

At the base. Low frequencies are at the Apex. This is called place principle.

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98
Q

Outer hair cell function

A

Sound—> basilar membrane displacement—> stereocilia deflection—> receptor potential’s generated on inner and outer hair cells—> outer hair cells contract and amplify the sound potential for the inner hair cells

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99
Q

Functional auditory pathway

A

Hair cells in the cochlea— auditory nerve—> cochlear nuclei— trapezoid body—> superior olivary complex—> inferior colliculi— brachium of IC—> medial geniculate nucleus—IC—> primary auditory cortex in the superior temporal gyrus

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100
Q

All central projections are bilateral starting after the:

A

Trapezoid body

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101
Q

Descending pathways for vestibulocochlear fxn:

A

1.) suppress hair cell function
2.) contract middle ear muscles (stapedius)

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102
Q

The only way to have an ipsilateral hearing loss from a single lesion is to have a defect where?

A

Peripheral to the superior olivary nucleus

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103
Q

Superior olivary nuclei receive:

A

Bilateral input from cochlear nucleus
• sounds are localized because higher frequency stimuli are louder in one ear and lower frequency stimuli reach one ear first

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104
Q

The cocktail party effect indicates damage to where?

A

The inferior colliculus (or internal capsule)
• cannot decide what is important

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105
Q

Three fundamental functions of the vestibular system

A

1.) balance, and posture.
2.) coordination of head and body movements.
3.) fixating the visual image on the fovea ( vestibuloocular reflex)

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106
Q

Semicircular canals

A

• motion detectors
• hair cells are found in the ampulla
• lesions induce the sensation of spinning— vertigo

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107
Q

Otolith organs

A

• gravity detectors
• hair cells found in 2 macula
• lesion induces the sensation of tilt

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108
Q

Ampullary crest

A

Piece of bone that protrudes into the ampulla where the hair cells can be found

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109
Q

Kinocilium

A

Basal body, gives directionality to the hair bundle— next to the tallest stereocilia, but not connected

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110
Q

Cupula

A

Stereocilia are embedded in this gelatinous matrix

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111
Q

Deflection of the stereocilia toward what causes depolarization?

A

The utricle

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112
Q

Functional vestibular pathway

A

Hair cell in semi circle canals or otolith organ—> vestibular nerve—> vestibular nuclei—> medial lemniscus—> ventroposterior nucleus in thalamus—> internal capsule—> vestibular cortex

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113
Q

Lateral vestibulospinal reflex

A

Compensates for tilt and movement of the body, by adjusting actions of neurons and innervating, ipsilateral limbs, and trunk muscles

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114
Q

Medial vestibulospinal reflex

A

Stabilizes head position during walking by acting on neurons, innervating ipsilateral and contralateral neck muscles

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115
Q

Vestíbulo ocular reflex

A

• to adjust I position to compensate for head movements in order to keep the visual image focused on the fovea
• rotation of head, and One Direction results and contradiction of extraocular muscles to slowly rotate the eyes in the opposite direction

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116
Q

VOR pathway

A

Head turns left—> depolarization of left hair cell, hyperpolarization of right hair cell—> excitation left vestibular nuclei, inhibition right vestibular nuclei—> contraction left medial rectus, and right lateral rectus—> relaxation right medial rectus, and left lateral rectus—> eyes turn to the right

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117
Q

Snellen chart

A

X/Y: (20/20, 20/40, etc)
X= distance of patient from chart
Y= distance at which a normal I can read the line of letters

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118
Q

Ishihara plates

A

Test color vision and color blindness

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119
Q

Special testing when examining eye

A

1: visual acuity
2: visual fields
2/3: pupillary reflexes
2/4/6: extraocular motion
7: eyebrows

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120
Q

Sudden, painless, unilateral, vision loss, differential diagnosis

A

1.) vitreous hemorrhage (diabetes/trauma)
2.) retinal detachment
3.) retinal vein occlusion
4.) central retinal artery occlusion

121
Q

Sudden painful, unilateral vision loss, differential diagnosis

A

1.) corneal abrasion/ulceration (traumatic, or infectious)
2.) uveitis
3.) traumatic hyphema
4.) acute glaucoma

— also consider optic neuritis from MS patients

122
Q

Dendritic ulcerations of the eye come from:

A

HSV keratitis: no facial rash
VZV: dermatomal facial rash

123
Q

Anterior uveitis symptoms

A

Deep eye pain, photophobia, conjunctiva vessel dilation, ciliary flush, small pupil/irregular pupil, cornea clear or slightly cloudy

124
Q

Hyphema

A

• Filling of the anterior chamber
• trauma, ciliary body problem, tumor
• refer to ophthalmology

125
Q

Sudden painless, bilateral vision loss

A

• medication’s such as anti-cholinergics, cholinergics, and steroids

126
Q

Sudden painful bilateral vision loss

A

Chemicals or toxins, or radiation exposure, etc

127
Q

Central vision loss with:

A
  1. Macular degeneration
  2. Cataracts
128
Q

Peripheral vision loss with:

A

Open angle glaucoma

129
Q

Specs or floaters that are moving indicates:

A

Vitreous floaters

130
Q

Fixed defects (scotomas) suggest

A

Lesions of retina or visual pathway

131
Q

Unilateral diplopia is seen with

A

Cornea or lens problems

132
Q

Bilateral diplopia is seen with

A
  1. CN3,4,6 lesions
  2. Extraocular muscles problems.
133
Q

Five signs and symptoms associated with red eye that should prompt ophthalmologist consultation

A

1.) globe pain: iritis, uveitis, glaucoma
2.) decreased visual acuity: risk for permanent vision loss
3.) sluggish pupillary reflex: concern for retinal, or CNS disease
4.) dendritic corneal: HSV keratisis
5.) vesicular lesion around the eye: concern for herpes zoster

134
Q

Pinguecula

A

• thickening of the conjunctiva
• no other symptoms, typically exposed to aggressive weather (surfers eye)

135
Q

Pterygium

A

• hyperplasia of normal tissue
• comes from chronic dry eye
• foreign body feeling

136
Q

Arcus senilis, corneal arcus

A

Everyone develops this as they age— gray surrounding outer iris

137
Q

Hordeolum

A

Stye — infection of the glands of the eyelid (typically staph). Is painful

138
Q

Chalazion

A

Sterile chronic inflammation that results from a blocked gland in the eyelid, typically painless

139
Q

Peri orbital cellulitis

A

Superficial skin cellulitis— preseptal, does not involve the orbit

140
Q

Orbital cellulitis

A
  • Refer to ophthalmology
  • Involves infection in the orbit, pushes the eye out
141
Q

Otitis externa

A

• caused by an overgrowth of the microbial microbiota of the external ear
• pseudomonas aeruginosa is a frequent cause of swimmers, ear, and malignant otitis externa
• inflammation of ear canal, pain, itching, and purulent ear drainage

142
Q

Risk factors of otitis externa

A

Trauma, foreign bodies, excessive moisture, extension of middle ear infection, diabetes

143
Q

Cerumen

A

(Ear wax) contains lysozyme. It is slightly acidic: deterring microbial growth

144
Q

Acute localized otitis externa

A

Most often staphylococcus pustule, or furuncle associated with hair follicle

145
Q

Acute diffuse otitis externa

A

Cost from Pseudomonas aeruginosa, itchy, red canal, and painful

146
Q

Malignant otitis externa

A

Caused by pseudomonas aeruginosa, invasion of adjacent bone and cartilage which can progress to cranial, nerve palsy and death.
• more common in elderly, poorly controlled diabetes, and immunocompromised

147
Q

Treatment of otitis externa

A

1.) NSAIDs
2.) ciprofloxacin + steroid (ear drops)
3.) neomycin + polymyxin + hydrocortisone (ear drops)

• avoid flushing the year, unless tympanic membrane is intact
• cleansing with a topical solution that has a low pH

148
Q

Causes of otitis media

A

1.) Streptococcus pneumoniae
2.) non-typeable Haemophilus influenzae
3.) respiratory viruses
3.) less common, Moraxella catarrhalis, group A strep, and staphylococcus aureus

149
Q

Acute otitis media (AOM)

A

Bacterial or viral otalgia, red eardrums, puss, and fever

150
Q

Otitis media with effusion

A

Buildup of fluid and eustachian tube

151
Q

Viruses causing a cute otitis media

A

RSV, influenza, enterovirus, coronavirus, rhinovirus are most common in the middle ear fluids

152
Q

Streptococcus pneumoniae, virulence factors

A

1.) drug resistance due to changes in the penicillin binding protein
2.) capsule blocks phagocytosis by interfering with a deposition of compliment on surface of organism
3.) neuraminidases cleave host mucins
4.) pneumolysin performing toxin, binds cholesterol and disrupts cilia of the cochlea

153
Q

Haemophilus influenzae

A

• nonmotile, biofilms, facultative anaerobe
• grows with NAD (V) and hematin (X) in chocolate agar
• non-typeable non-encapsulated (NTHi) colonize nasopharynx, and 80% of people and spreads to eustachian tube
• express many beta-lactamases

154
Q

Moraxella catarrhalis

A

• colonization of upper respiratory tract in infants
• produce beta-lactamases
• hockey puck test- easily slides across the agar
• G (-), dipplococci, oxidase (+)

155
Q

AOM treatment

A

• 6-24mo: oral amoxicillin, if no improvement switch to amoxicillin-clavulanate (Augmentin)
• ear tube for recurrent infection

156
Q

Complications of recurrent AOM

A

1.) conductive, hearing loss and delayed speech
2.) cholesteatoma: cyst of epithelial cells
3.) infection spreads to mastoid, inner ear, temporal bone, meninges, and brain

157
Q

Normal biota of the eyes

A

Staphylococcus epidermidis, micrococcus, Streptococcus, Corynebacterium

Defense: high IgA, mucus, lysozymes

158
Q

Blepharitis

A

Inflammation of the eyelid/ stye
- staphylococcus epidermidis, G(+), cocci, catalase(+), coagulase(-)

  • treatment: erythromycin
159
Q

Conjunctivitis

A

Pink eye, conjunctivitis blood vessels from conjunctiva creating red eye. Risk factors include contact, lens, wearers, swimming pools, etc.

160
Q

Keratitis

A

Cornea infection (HSV1, VZV)

161
Q

Endophthalmitis

A

Anterior chamber infection of aqueous humor

162
Q

Periorbital infection

A

Soft tissue and bone surrounding the eye getting infection

163
Q

Allergic conjunctivitis

A

• Type one hypersensitivity to airborne allergens mediated by IgE.
• managed with anti-histamines, NSAIDs, and antigen avoidance

164
Q

Adenovirus conjunctivitis

A

• non-enveloped, double stranded, DNA virus (class 1)
• lytic an epithelial cells and latent in lymphoid cells
• infects, epithelial cells of respiratory tract (4,7), conjunctiva (invasive, 19,37), and enteric organs (40,41,42)

165
Q

What determines the specificity of adenovirus conjunctivitis binding?

A

Penton fibers on the surface of cells

166
Q

Acute bacterial conjunctivitis

A

• children: staphylococcus aureus, Streptococcus pneumonia, Haemophilus influenzae
• adults: staphylococcus aureus
• treatment: trimethoprim, polymyxin, ophthalmic drops, moxifloxacin (fluoroquinolone) drops

167
Q

Hyperacute bacterial conjunctivitis

A

• Neisseria gonorrhea
• copious, yellow, green discharge
• preauricular adenopathy
• gram-negative, intracellular, diplococci and grows on Thayer Martin media
• treatment: systemic ceftriaxone, topical antibiotics, and irrigation

168
Q

Inclusion conjunctivitis and trachoma: chlamydia trachomatis

A

• inclusion conjunctivitis (serotypes D-K)
• trachoma (serotypes A-C) leading cause of blindness due to multiple infections
Treatment: systemic, azithromycin, and improve hygiene

169
Q

Chlamydia trachomatis

A

Elementary body enters epithelial cells, converts to reticulate body, and then replicates using binary vision

170
Q

HSV1- keratoconjunctivitis

A

• similar presentation to adenovirus all the lesions can be painful, especially of scarring on the cornea occurs
• avoid corticosteroids since I can facilitate corneal penetration
• if corneal involvement treat with topical trifluridine and systemic acyclovir, and prophylactic erythromycin

171
Q

Trifluridine

A

A permitting analog affective against acyclovir resistant viruses, because it can be phosphorylated by host kinases
— much more toxic, use topically

172
Q

Acanthamoeba keratitis

A

Rare, parasitic infection of the cornea the primarily occurs in contact lens wearers
• infection initiated at the epithelium and moves to include the stroma which results in a partial or complete paracentral ring infiltrate

173
Q

Chorioretinitis

A

• Blurred vision and visual field defects
• blood-borne route via retinal arteries, frequently manifestation of systemic disease
• toxoplasma gondii and CMV in HIV, positive individuals in units

174
Q

Toxocara canis and onchocerca volvulus

A

Cause chorioretinitis eye infections, the latter from blackflies causing river blindness

175
Q

Neonate toxoplasma gondii

A

• ToRCHeS infection
• presents with chorioretinitis and intracranial calcifications
• transmits transplacentally during gestation from cat feces, or ingestion of contaminated meat
• triad of congenital toxoplasmosis: Chorioretinitis, hydrocephalus, and intracranial classifications
• treatment: pyrimethamine, sulfadiazine, and folate

176
Q

Adult toxoplasma gondii (toxoplasmosis)

A

• new onset, seizures and decrease visual acuity
• more common in HIV patients with CD4+ T cells below 100
• MRI of the head shows a ring, enhancing lesion with surrounding edema in Mass Effect
• can also lead to chorioretinitis

177
Q

Measurements of hearing loss

A
  • observation
  • whisper test
  • tuning fork exam
  • pure tone audiometry
  • speech audiometry
  • otoacoustic emissions (OAE)
  • auditory brainstem response (ABR)
178
Q

Rinne

A

AC > BC (normal)
BC > AC (CHL)
Weber abnl but Rinne normal: sensorineural hearing loss

179
Q

Weber

A

Midline bilateral hearing: normal
Lateralizes to CHL or better ear: abnl

180
Q

Audiogram can be used for

A
  • Frequency (Hz)
  • intensity in dB
  • pure tone avg
  • air/bone conduction
  • speech reception threshold (SRT)
  • speech discrimination score
181
Q

Hearing Threshold Level

A

<25 dB: Normal
26-40 dB: mild hearing loss
41-55 dB: moderate hearing loss
56-70 dB: moderately severe hearing loss
71-90 dB: severe hearing loss
> 90 dB: profound hearing loss

182
Q

Otoacoustic emission testing

A
  • outer hair cells emit low intensity sound following acoustic stimulation
  • part of the newborn screening test
183
Q

Etiology of sensorineural hearing loss

A
  • Presbycusis
  • infection
  • trauma
  • ototoxic drugs
  • autoimmune
  • sudden SNHL
  • congenital/hereditary
  • neurologic
  • neoplastic
  • Meniere’s disease
184
Q

Etiology of conductive hearing loss

A
  • ear wax impaction
  • otitis media
  • tympanic perforation
  • cholesteatoma
  • tympanosclerosis
  • ossicular erosion
  • otosclerosis
  • congenital absence of external or middle ear structures
185
Q

Otosclerosis

A
  • autosomal dominant, incomplete penetrance
  • 60% have family history
  • fluoride prevents
  • Rx: hearing aids or stapedectomy with prosthetic
186
Q

Temporal bone fx

A
  • head trauma
  • Symptoms: HA, vertigo, SNHL, CHL, CN7 paralysis, CSF leak via ear canal or nose
  • Rx: Neurosurg obs, lumbar drain, ossicular reconstruction
187
Q

Acoustic Neuroma

A
  • not common (aka vestibular schwannoma)
  • Symptoms: asymmetric SNHL, CN7 paralysis, aural fullness, CN5 numbness, diplopia
  • diagnose with: MRI, IACs with contrast
    -Rx: obs, surgery, imaging
188
Q

Vertigo

A

a symptoms where a person feels as if they or the objects around them are moving when they are not. Often it feels like a spinning or swaying movemnet

189
Q

Disequilibrium

A

Sensation of impending fall or of the need to obtain external assistance for proper locomotion. It is sometimes described as a feeling of improper tilt of the floor, or as a sense of floating

190
Q

Imbalance

A

implies orthopedic or neuro problem

191
Q

Dizziness

A

all-encompassing term (light-headed, orthostatic, hypoglycemia, inability to concentrate)

192
Q

Vestibular work-up

A
  • H & P
  • radiology: MRI or CT
  • electronystagmography: oculomotor, positional, and caloric testing
  • Rotary chair
  • computerized dynamic posturography
  • vestibular evoked myogenic potentials
193
Q

Benign Paroxysmal Positional Vertigo

A
  • most common peripheral vertigo
  • caused by: post-trauma, post viral infection
  • symptoms: recurrent brief positional vertigo, latency, fatigability
  • Diagnose by: Hx, Dix-hallpike
194
Q

Canalithiasis

A

Occurs when otoconia are moving within the semicircular canal, causing vertigo and nystagmus that resolves within 60 seconds. Very common

195
Q

Meniere’s disease

A

Symptoms:
- fluctuating SNHL
- tinnitus
- episodic vertigo
- aural fullness
- 25-30% bilateral
- progressive
- often asymptomatic between spells

Management: R/O stroke, tumor, infection, trauma, hypothyroid, salt restriction, evenly spaced meals and water, diuretics, steroids, vestibular suppressants, allergy rx, surgery

196
Q

Vestibular suppressants

A
  1. Meclizine
  2. Benzos
  3. scopolamine
197
Q

Vestibular neuronitis

A
  • viral infection of the vestibular nerve. Very sick patients
  • symptoms: vertigo lasts hours to days, no hearing loss
  • prodromal viral URI
  • may last weeks to months
  • Rx: meclizine, benzos, antiemetics
198
Q

Labyrinthitis

A
  • bacterial or viral
  • Sudden hearing loss and vertigo, tinnitis
  • infection spreads from middle ear through round window or oval window
  • diagnose with H&P, audiogram (SNHL)
  • Rx: IV abx, vestibular suppressants, surgical management of middle ear infection, steroids
199
Q

Anotia

A

Complete lack of ear
- 10% are syndromic, 30% are bilateral
- associated with ear canal atresia and middle ear abnormalities
- reconstruction or prosthetics, bone anchored hearing aid

200
Q

Microtia Grade I

A
  • ear is slightly smaller than normal
  • conchal bowl is cupped
  • all subunits are present
  • surgery not usually needed
201
Q

Microtia Grade II

A
  • auricle is half sized
  • all structures are present
  • soft tissues are deficient
  • surgery is occasionally beneficial
202
Q

Microtia Grade III

A
  • small cartilage piece in superior remnant
  • anterior deflected lobule
  • surgical repair at age 5-6 years old
  • protheses works well
203
Q

Lop ear

A
  • most common external anomaly: absence of the antihelical fold
  • fixed with ear molding in neonates, surgery can be offered
204
Q

preauricular pits and fistulas

A
  • frequently get infected
  • Rx with abx and incision and drainage
  • frequently bilateral, can affect any part of the auricle
205
Q

Auricular appendages

A
  • arrested development of fusion of the hillocks of His, creates tiny “ears” made of cartilage and skin
  • excision is optional, dangerous with facial nerve being superficial in infants
206
Q

Relapsing polychondritis

A
  • autoimmune, episodic, progressive
  • involves nose, joints, airway, heart valves- cartilage only on the ear, lobe not involved. Looks like cellulitis
  • ESR and IgG elevation
  • Rx: steroids and NSAIDs
207
Q

Nodularis chronicus helicus

A
  • very painful nodule in the helix that looks like skin cancer, benign
  • caused by prolonged pressure
  • excision biopsy
208
Q

Auricular hematoma

A
  • caused by trauma, treat with incision and drainage then abolster
  • untreated results in cauliflower ear
209
Q

Cellulitis of the pinna

A
  • symptoms include pain, swelling, redness, and fever
  • caused by staph, strep, and pseudomonas
  • Rx: antibiotics and pain relief
  • Risk factors: diabetes, foreign bodies, piercings, trauma
210
Q

Ear canal osteomas and exostosis

A
  • benign projections in canal
  • caused by significant cold water experience
211
Q

Carcinoma of ear canal

A
  • painful, bleeding, soft tissue mass in the canal
  • needs a biopsy, excision, and radiation therapy
  • can metastasize and be fatal
212
Q

Otitis externa

A
  • very painful red swollen canal with purulence
  • seen in swimmers, Q tip users, diabetics, immunosuppression
  • Rx: abx drops and systemic abx
  • topical suction and debridement
  • caused by: pseudomonas, e. coli, staph corynebacter
  • affected hearing
213
Q

Herpes zoster oticus

A
  • purulent ulcers in and around ear
  • decreased hearing and severe pain, CN7 paralysis, antiviral rx and pain relief
  • risk to immunocompromised
214
Q

Otorrhea

A

ear drainage seen in AOM, otitis externa, allergy, trauma, CSF leakage

215
Q

Otomycosis

A
  • itchy, painful ear with drainage and decreased hearing caused by fungal infection
  • antifungal drops and pain relief
  • alcohol, vinegar, and water lavage or debridement
216
Q

Tympanic membrane perforation

A
  • hearing loss, otorrhea, tinnitis
  • Rx: keep dry, tympanoplasty for a persistent perf for CHL, or to protect middle ear and inner ear
  • often heals with time
217
Q

Bullous myringitis

A
  • inflamed tympanic membrane with serous bullae associated with virus or mycoplasma p URI
  • symptoms: otalgia, otorrhea, hearing loss
  • Rx: analgesia, antibiotics, decompression of painful vesicles and steroids for SNHL
218
Q

Tympanosclerosis

A

white plaques on the tympanic membrane from hyalin or calcium deposition
- if middle ear is involved there may be CHL, otherwise benign

219
Q

Cholesteatome

A
  • otorrhea, hearing loss, inner ear problems
  • soft ball of keratin involving the skin and causes bony erosions
  • Surgery almost always indicated to prevent ear destruction
220
Q

Middle ear cholesteatoma

A
  • squamous epithelium in middle ear causing bone and soft tissue destruction of ear structures. Pressure necrosis and secondary infection and proteolytic enzyme release by cholesteatoma
  • looks like: pearly mass aural fullness, hearing loss, vertigo, chronic otorrhea
  • Rx: surgical removal via tympanomastoidectomy
221
Q

acute otitis media (AOM)

A
  • acute middle ear infection, second most common disease in children. Eustachian tube dysfunction causes negative middle ear pressure, results in transudative fluid collection in middle ear space and subsequent infection
  • symptoms: otalgia, aural fullness, hearing loss, tinnitis, fever, red or creamy tympanic membrane
222
Q

What pathogens cause AOM?

A

S. pneumoniae, H. influenza, Mor. Catarrhalis

223
Q

Surgical management of AOM

A
  • myringotomy and tubes (PE)
  • adenoidectomy
  • mastoidectomy
224
Q

Most common diseases of olfaction

A
  • obstructive nasal and sinus disease
  • URI
  • head trauma
225
Q

Dermoid cyst

A

cyst of squamous cell epithelium containing epidermal appendages, where epidermal elements are displaced during intramembranous growth phase of nasal bones
- location: frontotemporal region, ortibal region, nasoglabellar region

226
Q

Nasal glioma

A

Outside of face, no intracranial involvement. Develops from extracranial rests of glial tissue

227
Q

Nasal encephalocele

A
  • extracranial protrusions of meninges, CSF fluid, and neural tissue, requires neurosurgery
228
Q

The retina, posterior layers of the iris, and optic nerve are derived from

A

the neuroectoderm of the forebrain

229
Q

The Lens and corneal epithelium are derived from

A

The surface ectoderm of the head

230
Q

the fibrous and vascular coats of the eye are derived from

A

Mesoderm

231
Q

the choroid, sclera, and corneal epithelium are derived from

A

neural crest cells

232
Q

Development of the eyes

A

Diencephalon–> Optic grooves on cranial end of the embryo–> forms hollow pouches, optic vesicles (which are continuous with the forebrain cavity)–> connection forms optic stalks–> Vesicles become lens placode–> lens pit–> lens vesicles–> double walled optic cups–> retinal fissures develop on the ventral surface of the cups–> deepest part of cup becomes the optic disc and the neural retina continues with the optic stalk

233
Q

Vasculature of the eye

A

hyaloid artery/vein develops into the central artery/vein. This supplies the inner layer of the optic cup, the lens vesicle, and the mesenchyme in the cavity of the optic cup

234
Q

Retinal development

A

walls of the optic cup –>
1.) outer layer: thin, becomes the pigment layer of the retina
2.) inner layer: thick, becomes the neural retina

  • during development the two retinal layers are separated by an intraretinal space
235
Q

Inner cup thick retinal layer

A

becomes the neural retina
- light sensitive
- contains photoreceptors
- contains cell bodies of neurons
- differentiation regulated by FGF

236
Q

Optic nerve sheaths

A

1.) outer dural
2.) intermediate sheath continuous with arachnoid mater
3.) inner sheath continuous with the pia mater

237
Q

Coloboma

A
  • incomplete closure of retinal fissure
  • present anywhere between the cornea and optic nerve
238
Q

Retinochoroidal coloboma

A

gap in the retina

239
Q

Coloboma of the iris

A
  • leads to a keyhole appearance of the pupil
  • looks like a melted pupil
240
Q

Detachment of the retina

A
  • failure of the inner and outer layers of the optic cup to fuse
  • can also result from unequal growth between the two layers
  • intraretinal space persists
  • lack of fusion or trauma causes
    -co-occurs with down syndrome and Marfan syndrome
241
Q

Cyclopia

A

-eyes are partially or completely fused, referring to a singular median eye
- occurs in holoprosencephaly

242
Q

Synophthalmia

A

-fused eyes, two separate structures
- occurs in holoprosencephaly

243
Q

Microphthalmia

A
  • underdeveloped eyes, varies in severity
  • inherited or caused by infectious agents (rubella, toxoplasma gondii, HSV)
244
Q

maldevelopment shortly after the optic vesicles form:

A

Lens does not form

245
Q

Maldevelopment occurring before the retinal fissure closes:

A

eye is almost a typical size but has gross ocular defects

246
Q

Maldevelopment later in development

A

Eyes are smaller, with minor abnormalities

247
Q

Anophthalmia

A

-absence of eye, rare
- eyelids still form, orbital defects

248
Q

Primary anophthalmos

A
  • eye is cause
  • eye development is arrested early in the fourth week
  • failure of the optic vesicle to form
249
Q

Secondary anophthalmos

A
  • Forebrain is the cause
  • development of the forebrain is suppressed
  • absence of the eye or eyes (among other defects)
250
Q

Ciliary body

A
  • wedge shaped extension of the choroid and projects to the lens
  • connects to the lens via the ciliary process
  • ciliary muscle focuses the lens
251
Q

Lens development

A

Mesenchyme–> edge of optic cup–> lens

252
Q

Iris

A

develops from the rim of the optic cup. Grows inward to partially cover the lens
- Derived from neural crest cells that migrate into the iris

253
Q

Dilator and sphincter pupillae

A

muscles of the iris developed from neuroectoderm of the optic cup

254
Q

Iris color is determined by

A

Chromatophores in the loose vascular connective tissue of the iris

255
Q

Blue iris

A

melanin pigment is confined to the pigmented epithelium on the posterior surface of the iris

256
Q

Brown iris

A

Melanin pigment distributed through the stroma of the iris

257
Q

Heterochromia

A

eyes are different colors

258
Q

Sectoral heterochromia

A

one eye has two different colors

259
Q

Congenital aniridia

A
  • Complete or partial absence of an iris
  • arrested development at the rim of the optic cup
  • associated with glaucoma, cataracts, other eye abnormalities
  • Familial, PAX6 gene
260
Q

Primary lens fibers

A
  • posterior wall of the lens
  • highly transparent, do not proliferate: must last a lifetime
261
Q

Secondary lens fibers

A
  • cells from the equatorial zone elongate
  • continue to form during adulthood, only fibers that grow
  • Helps the lens increase in diameter
262
Q

Tunica vasculosa lentis

A
  • surrounds developing lens- blood supply
  • anterior: anterior pupillary membrane derived from mesenchyme posterior to cornea
  • degenerates before birth
263
Q

Persistent pupillary membrane

A

• resembles web like strands of connective tissue over the pupil
• common in premature newborns
• tends to atrophy and rarely interferes with vision
• persists: congenital atresia of pupil, blocking vision- require surgery or laser treatment

264
Q

Persistent hyaloid artery

A

May appear as a freely moving nonfunctional vessel, may form a cyst

265
Q

Aphakia

A

Absence of a lens, results from failure of the lens placode to form or failed lens induction by the optic vesicle

266
Q

Congenital cataracts

A

Congenital opaque lenses, which can lead to blindness. Can be caused by teratogenic agents like rubella early and development.

267
Q

Vitreous body

A

• formed within the cavity of the optic cup, composed of vitreous humor
• primary vitreous humor derived from mesenchymal cells of neural crest origin
• secondary vitreous humor: gelatinous layer surrounding primary consisting of primitive hyalocytes, collagenous material, hyaluronic acid

268
Q

Anterior chamber

A

Develops from a cleft like space between the developing lens and cornea. Lens induces the surface ectoderm to become the conjunctiva and corneal epithelium to close off space

269
Q

Posterior chamber

A

Develops from a space that forms posterior to the developing Iris and anterior to the developing lens.

270
Q

Scalero venous sinus

A

Anterior and posterior chambers of the eye are able to communicate through this

271
Q

Cornea

A

• Transparent, multi layered, avascular
• induced by the lens vesicle to form

272
Q

Ectoderm and cornea

A

Gives rise to the external corneal epithelium

273
Q

Mesoderm and cornea

A

Gives rise to mesenchyme (central stroma layer)

274
Q

Neural crest cells and cornea

A

Migrate from optic up and give rise to the corneal endothelium

275
Q

Eyelid development

A

Neural crest cells—> Mesenchyme—> bulbar conjunctiva/palpebral conjunctiva

Surface ectoderm —> eyelashes, and glands

276
Q

Lacrimal glands

A

• develop from surface ectoderm
• superolateral angles of the orbits
• do not function until six weeks post birth

277
Q

Coloboma of the eyelid

A

• large defect of the eyelid
• usually a notch in the superior eyelid (like cleft lip) causes dryness

278
Q

Cryptophthalmos

A

Congenital absence of the eyelid (no slit for opening), rare
— skin still covers the eye, eyeball is usually small and nonfunctioning

279
Q

Internal ear development

A

• first part of the ear to develop
• otic placode—> otic pit—> otic vesicle—> diverticulum—> Endolymphatic, duct and sac

280
Q

Dorsal utriclar part

A

Becomes the small endolymphatic ducts, utricles, and semi circular ducts

281
Q

Ventral saccular part

A

Becomes the saccules and cochlear ducts

282
Q

The cells of the spiral ganglion are

A

Bipolar

283
Q

Perilymphatic space develops two divisions:

A

1.) scala tympani
2.) scala vestibuli

284
Q

Middle ear development

A

First pharyngeal pouch —> Tubotympanic recess—> proximal: auditory tube, distal: tympanic cavity

285
Q

Meckel’s cartilage (first arch)

A

Malleus, incus, tensor tympani muscle

286
Q

Reichart’s cartilage (second arch)

A

Stapes, stapedius muscle

287
Q

External ear development

A

First pharyngeal groove—> external acoustic meatus

Ectodermal cells —> meatal plug that degenerates

First pharyngeal membrane —> tympanic membrane

288
Q

The auricle (pinna) develops from

A

Mesenchymal proliferations in the first and second pharyngeal arches (auricular hillock)

289
Q

Auricle receives innervation from

A

CN5, 7, lesser occipital, auricular, and greater auricular nerves (sensory)

290
Q

Atresia of the external acoustic meatus

A

Failure of the Miedo plug to canalize. Most cases associated with first arch syndrome.

291
Q

Prominauris

A

Prominent ears, may be associated with other ear malformations. Can be corrected surgically, or with ear molding (during first week of life because of high estrogen levels)

292
Q

Ear tags

A

• mine are appendages or tags from supernumary hillocks
• first pharyngeal groove problem
• associate with hearing loss on ipsilateral side
• seen in Goldenhar and other syndromes

293
Q

Adie pupil

A

• secondary to bacterial/viral infection, causing inflammation/damage to the post ganglionic parasympathetic neurons innervating, the pupillary, sphincter and ciliary body
• dilated pupil that reacts minimally to light, but better to accommodation

294
Q

Holme-Adie syndrome

A

Impaired deep tendon reflexes and light pupillary reflex is due to a diffuse autonomic disease

295
Q

Argyle Robertson pupil

A

• small pupils in light and dark with no reaction to light
• accommodation miosis is briskly intact, and not tonic
• finding in neurosyphilis and diabetic neuropathy
• attributed to dorsal midbrain lesion (pretectal nuclei) that interrupts the pupillary light reflex pathway, but spares the ventral pupillary near reflex pathway

296
Q

Internuclear ophthalmoplegia

A

• involvement of MLF on one side results in ipsilateral INO
• INO is characterized by loss of adduction of the ipsilateral eye and contralateral nystagmus with opposite gaze

297
Q

Left one and a half syndrome

A

• ipsilateral, conjugate, horizontal, gaze palsy, and ipsilateral internuclear ophthalmoplegia
• caused by a lesion that affects the lateral gay center or the abducens nucleus and the ipsilateral MLF

298
Q

MLF

A

Medial longitudinal fasciculus— fiber, tract, responsible for transmitting information that is vital for the coordination of different eye movements

Neuro/Behavior I (3 decks)

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