Quiz #5 Flashcards
Vertigo
Sensation of spinning while actually stationary.
Subtype of “dizziness,” but distinct from “lightheadedness.”
Peripheral vertigo
More common.
Inner ear etiology (eg, semicircular canal debris, vestibular nerve infection, Ménière disease [triad: sensorineural hearing loss, vertigo, tinnitus], benign paroxysmal positional vertigo [BPPV]).
Treatment: antihistamines, anticholinergics, antiemetics (symptomatic relief); low-salt diet ± diuretics (Ménière disease); Epley maneuver (BPPV).
Central vertigo
Brain stem or cerebellar lesion (eg, stroke affecting vestibular nuclei or posterior fossa tumor).
Findings: directional or purely vertical nystagmus, skew deviation, diplopia, dysmetria. Focal neurologic findings.
Glaucoma
Optic disc atrophy with characteristic cupping (thinning of outer rim of optic nerve head B versus normal A), usually with elevated intraocular pressure (IOP) and progressive peripheral visual field loss if untreated. Treatment is through pharmacologic or surgical lowering of IOP.
Open-angle glaucoma
Associated with older age, African-American race, family history.
Painless, more common in US.
Primary—cause unclear.
Secondary—blocked trabecular meshwork from WBCs (eg, uveitis), RBCs (eg, vitreous hemorrhage), retinal elements (eg, retinal detachment).
Closed- or narrowangle glaucoma
Primary—enlargement or anterior movement of lens against central iris (pupil margin) –> obstruction of normal aqueous flow through pupil –> fluid builds up behind iris, pushing peripheral iris against cornea and impeding flow through trabecular meshwork.
Secondary—hypoxia from retinal disease (eg, diabetes mellitus, vein occlusion) induces vasoproliferation in iris that contracts angle.
Chronic closure—often asymptomatic with damage to optic nerve and peripheral vision.
Acute closure—true ophthalmic emergency.
increased IOP pushes iris forward –> angle closes abruptly. Very painful, red eye, sudden vision loss, halos around lights, frontal headache, fixed and mid-dilated pupil. Mydriatic agents contraindicated.
macular degeneration
Degeneration of macula (central area of retina). Causes distortion (metamorphopsia) and eventual loss of central vision (scotomas).
Dry (nonexudative, > 80%)—Deposition of yellowish extracellular material in between Bruch membrane and retinal pigment epithelium (“Drusen”) with gradual decrease in vision. Prevent progression with multivitamin and antioxidant supplements.
Wet (exudative, 10–15%)—rapid loss of vision due to bleeding 2° to choroidal neovascularization. Treat with anti-VEGF (vascular endothelial growth factor) injections (eg,bevacizumab, ranibizumab).
diabetic retinopathy
Retinal damage due to chronic hyperglycemia. Two types:
Nonproliferative—damaged capillaries leak blood –> lipids and fluid seep into retina –>hemorrhages (arrows in A) and macular edema. Treatment: blood sugar control.
Proliferative—chronic hypoxia results in new blood vessel formation with resultant traction on retina. Treatment: peripheral retinal photocoagulation, surgery, anti-VEGF.
pupillary control
Miosis
Constriction, parasympathetic:
1st neuron: Edinger-Westphal nucleus to ciliary ganglion via CN III
2nd neuron: short ciliary nerves to sphincter pupillae muscles Short ciliary nerves shorten the pupil diameter.
Pupillary light reflex Light in either retina sends a signal via CN II to pretectal nuclei in midbrain that activates bilateral EdingerWestphal nuclei; pupils constrict bilaterally (direct and consensual reflex).
Result: illumination of 1 eye results in bilateral pupillary constriction.
Mydriasis
Dilation, sympathetic:
1st neuron: hypothalamus to ciliospinal center of Budge (C8–T2)
2nd neuron: exit at T1 to superior cervical ganglion (travels along cervical sympathetic chain near lung apex, subclavian vessels)
3rd neuron: plexus along internal carotid, through cavernous sinus; enters orbit as long ciliary nerve to pupillary dilator muscles. Sympathetic fibers also innervate smooth muscle of eyelids (minor retractors) and sweat glands of forehead and face. Long ciliary nerves make the pupil diameter longer.
Marcus Gunn pupil
When the light shines into a normal eye, constriction of the ipsilateral (direct reflex) and contralateral eye (consensual reflex) is observed. When the light is then swung to the affected eye, both pupils dilate instead of constrict due to impaired conduction of light signal along the injured optic nerve.
eye movements
CN VI innervates the Lateral Rectus.
CN IV innervates the Superior Oblique.
CN III innervates the Rest.
The “chemical formula” LR6SO4R3.
The strongest action of the superior oblique is depression when the eye is adducted. The further the eye is abducted, the more the superior oblique acts to intort the eye toward the nose.
Obliques go Opposite (left SO and IO tested with patient looking right). IOU: IO tested looking Up.
Cranial Nerve 3,4 and 6 palsies
CN III damage
CN III has both motor (central) and parasympathetic (peripheral) components.
Common causes include:
Ischemia –>pupil sparing
Uncal herniation –>coma
PCA aneurysm –> sudden-onset headache
Cavernous sinus thrombosis –>proptosis, involvement of CNs IV, V1/V2, VI
Midbrain stroke –> contralateral hemiplegia
Motor output to extraocular muscles—affected primarily by vascular disease (eg, diabetes mellitus: glucose –> sorbitol) due to decreased diffusion of oxygen and nutrients to the interior fibers from compromised vasculature that resides on outside of nerve.
Signs: ptosis, “down and out” gaze.
Parasympathetic output—fibers on the periphery are first affected by compression (eg, PCom aneurysm, uncal herniation).
Signs: diminished or absent pupillary light reflex, “blown pupil” often with “down-and-out” gaze.
CN IV damage
Eye moves upward, particularly with contralateral gaze B (–>going down stairs, head may tilt in the opposite direction to compensate). Can’t see the floor with CN IV damage.
CN VI damage Affected eye unable to abduct and is displaced medially in primary position of gaze.
Visual Field Defects
- Right anopia - cutting optic nerve (same side)
- Bitemporal hemianopia (pituitary lesion, chiasm)
- Left homonymous hemianopia (optic tract)
- Left upper quadrantanopia (right temporal lesion, MCA) - Meyer Loop - temporal lobe
- Left lower quadrantanopia (right parietal lesion, MCA) - dorsal optic radiation - parietal lobe
- Left hemianopia with macular sparing (PCA infarct)
- Central scotoma (eg, macular degeneration)
Internuclear ophthalmoplegia
Medial longitudinal fasciculus (MLF): pair of tracts that allows for crosstalk between CNVI and CN III nuclei. Coordinates both eyes to move in same horizontal direction. Highly myelinated (must communicate quickly so eyes move at same time). Lesions may be unilateral or bilateral (latter classically seen in multiple sclerosis).
Lesion in MLF = internuclear ophthalmoplegia (INO), a conjugate horizontal gaze palsy. Lack of communication such that when CNVI nucleus activates ipsilateral lateral rectus, contralateral CN III nucleus does not stimulate medial rectus to contract. Abducting eye gets nystagmus (CN VI overfires to stimulate CNIII). Convergence normal.
MLF in MS. When looking left, the left nucleus of CN VI fires, which contracts the left lateral rectus and stimulates the contralateral (right) nucleus of CN III via the right MLF to contract the right medial rectus. Directional term (eg, right INO, left INO) refers to which eye is paralyzed. INO = Ipsilateral adduction failure, Nystagmus Opposite.
Glaucoma Drugs
β-blockers
- –Timolol, betaxolol, carteolol
- decreasedaqueous humor synthesis
- –No pupillary or vision changes
α-agonists
—Epinephrine (α1), apraclonidine, brimonidine (α2)
—decreasedaqueous humor synthesis via vasoconstriction (epinephrine)
—decreased aqueous humor synthesis (apraclonidine, brimonidine)
Adverse Effects:
–Mydriasis (α1); do not use in closed-angle glaucoma
–Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritus
Diuretics
—Acetazolamide
— decreasedaqueous humor synthesis via inhibition of carbonic anhydrase
No pupillary or vision changes
Prostaglandins
- –Bimatoprost, latanoprost (PGF2α)
- – increasedoutflow of aqueous humor via decreased resistance of flow through uveoscleral pathway
- –SEs: Darkens color of iris (browning), eyelash growth
Cholinomimetics (M3)
—Direct: pilocarpine, carbachol
—Indirect: physostigmine, echothiophate
—increasedoutflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
Use pilocarpine in acute angle closure glaucoma—very effective at opening meshwork into canal of Schlemm
—SEs: Miosis (contraction of pupillary sphincter muscles) and cyclospasm (contraction of ciliary muscle)
Personality disorders
Inflexible, maladaptive, and rigidly pervasive pattern of behavior causing subjective distress and/or impaired functioning; person is usually not aware of problem (ego-syntonic). Usually presents by early adulthood. Three clusters: A, B, C; remember as Weird, Wild, and Worried, respectively, based on symptoms.
Cluster A personality disorders
Odd or eccentric; inability to develop meaningful social relationships. No psychosis; genetic association with schizophrenia.
“Weird.”
Cluster A: Accusatory, Aloof, Awkward.
—Paranoid: Pervasive distrust (Accusatory) and suspiciousness of others and a profoundly cynical view of the world.
—Schizoid: Voluntary social withdrawal (Aloof), limited emotional expression, content with social isolation (vs avoidant).
—Schizotypal: Eccentric appearance, odd beliefs or magical thinking, interpersonal Awkwardness.
Pronounce schizo-type-al: odd-type thoughts
Cluster B personality disorders
Dramatic, emotional, or erratic; genetic association with mood disorders and substance abuse.
“Wild.”
Cluster B: Bad, Borderline, flamBoyant, must be the Best
—Antisocial: Disregard for and violation of rights of others with lack of remorse, criminality, impulsivity; males > females; must be ≥ 18 years old and have history of conduct disorder before age 15. Conduct disorder if males; splitting is a major defense mechanism.
Treatment: dialectical behavior therapy.
—Histrionic: Excessive emotionality and excitability, attention seeking, sexually provocative, overly concerned with appearance.
FlamBoyant.
—Narcissistic: Grandiosity, sense of entitlement; lacks empathy and requires excessive admiration; often demands the “best” and reacts to criticism with rage.
Must be the Best.
Cluster C personality disorders
Anxious or fearful; genetic association with anxiety disorders.
“Worried.” Cluster C: Cowardly, obsessive-Compulsive, Clingy.
- –Avoidant: Hypersensitive to rejection, socially inhibited, timid, feelings of inadequacy, desires relationships with others (vs schizoid). Cowardly.
- –Obsessive Compulsive: Preoccupation with order, perfectionism, and control; ego-syntonic: behavior consistent with one’s own beliefs and attitudes (vs OCD). —Dependent: Excessive need for support, low selfconfidence. Patients often get stuck in abusive relationships. Submissive and Clingy.
