Neuro-oftalmologia Flashcards
Como é o exame da aferencia visual?
(1) Acuity: Check w/ correction (>40 yo require near correction). Pinhole occluder (or paper w/ pinhole) to exclude refractive error. (2) Color vision (color plates, red desaturation). (3) Pupillary response to light & near; look for APD (detectable w/ dim stimulus). (4) Visual fi elds, each eye separately—laser pointer a great bedside test; have pt fi xate central target, move/fl ash red stim in areas of interest. (5) Funduscopy: Use dilating drops; if not possible, try small light at dimmest setting to ↓ glare; examine right eye w/ your right eye & left eye w/ your left eye: color & quality of optic disc & neuroretinal rim, degree of cupping, arteries & veins, venous pulsations at edge of optic cup, quality of nerve fi ber layer (NFL) (best seen w/ green light), peripapillary changes (hemorrhage, swelling, infi ltrates), & macula.
Descreva a anatomia da via visual aferente?
Optic nerve (ON): Where retinal NFL axons converge. Axons become myelinated post. to lamina cribrosa. Four portions: intraocular, intraorbital, intracancicular, intracranial. Blood supply: (1) anterior nerve & disc—post. ciliary arteries via ophthalmic artery; (2) post. nerve—pial circulation & central retinal/ophthalmic artery. Topographic representation of retina is preserved in ON. Exits orbit through optic canal (w/ ophth. artery & oculosympathetics). Subarachnoid space surrounds ON (anterior limit is lamina cribrosa). Field defects 2/2 ON dz can be global or regional; divided by affected area: (1) temporal retina—horizontal altitudinal, arcuate, central, & centrocecal; (2) nasal retina—step-like; enlarged blind spots occur when optic disc swells, displaces adjacent photoreceptors.
Retina: Photoreceptors (outer-) → retinal ganglion cells (inner-) → unmyelinated NFL (innermost retina); NFL axons travel to optic disc. Retinal projections: mainly lateral geniculate nucleus (LGN), also pretectal nucleus (pupillary light refl ex pathway), superior colliculus (fi xation, saccades, vergence, smooth pursuit), & hypothalamic suprachiasmatic nucleus (circadian rhythms). NFL axon paths: Foveal NFL → to optic disc (maculopapillary bundle); temporal retina NFL above & below fovea → disc in arced path (as arcuate bundles), respects horiz. meridian; nasal retina NFL axons → directly to disc. Arterial supply: Ophthalmic a. (ICA branch) travels w/ ON in optic canal, branches into central retinal artery (travels in ON to supply inner retina) & long & short post. ciliary arteries (supply ON head, ciliary body, choroid, outer retina); 1/3 people have cilioretinal artery (from post ciliary circulation) to supply central macula. Venous drainage: Veins follow retinal & ophthalmic a., exiting orbit through sup & inf orbital fi ssures → cav. sinus & pterygoid plexus. Field defects: dzs of temporal retinal NFL & optic disc & retinal arterial supply may respect horiz. meridian; primary retinal d/o’s do not. (Prechiasmal dzs respect vertical meridian).
Optic chiasm (OC): Produces crossed fi bers from nasal- & uncrossed fi bers from temporal-retina. Blood supply: Hypophyseal artery branches inferiorly (via ICA) & ACA branches superiorly. Located above pituitary/sella. Field defects: Divided by affected area of OC: (1) midsagittal region—inf, sup, or full bitemporal hemianopia (fi eld defect begins near vertical midline, not peripherally); (2) anterior chiasm—junctional scotomas w/ i/l ON-type defect (e.g., central scotomas) & c/l chiasm-type defect (e.g., superotemporal defect).
Optic tract: Info from c/l nasal- & i/l temporal-retina. Blood supply: Ant choroidal a. (via ICA) & PComm. lesion → c/l incongruous homonymous hemianopia (w/o central sparing).
LGN: 6-Layered thalamic nucleus; gets input from optic tract. Blood supply: Ant choroidal artery (ICA branch) → med & lat LGN; post choroidal artery (PCA branch) → hilum of LGN. Field defects (in stroke): c/l incongruous hemianopia, sectoranopia (postchoroidal stroke); quadruple sectoranopia (ant choroidal stroke).
Primary visual cortex (striate cortex): Target of optic radiations. Blood supply: OL: PCA, occipital pole: PCA, MCA (dual supply). Lesions → c/l congruent homon. hemianopsia; rare ant. mesial OL lesion → c/l monocular peripheral crescent-shaped fi eld defect. Macula represented at occipital pole → lesions ant. to pole spare macular vision.
Visual association cortex: “Where” visual stream is superior (OL/PL). Lesions yield visuospatial defi cits (e.g., visual attention, spatial organization). “What” visual stream is inferior (OL/TL). Lesions → semantic defi cits (e.g., object recognition, color). Blood supply: OL/PL regions via superior MCA branches; OL/TL regions via PCA & inferior MCA branches.
Qual a definição de papiledema?
Def: Papilledema refers specifi cally to optic disc swelling from ↑ ICP. Disc swelling occurs 2/2 impaired axoplasmic fl ow; develops over days from onset of ↑ ICP. Causes of ↑ ICP include: Neoplasia, infxn, immune-mediated infl ammation, diffuse central demyelination, cerebral VST, inborn & acquired errors of metabolism & toxins, cranial abnlities, spinal block, & marked systemic HTN. No cause identifi able: dx idiopathic intracranial HTN (IIH) (aka pseudotumor cerebri); involves ↓ CSF absorption
Qual a epidemiologia do papiledema?
Epid: ↑ ICP: Any age group, has myriad causes. IIH: Mainly in overweight women aged 20s–30s; also a/w tetracycline exposure & corticosteroid withdrawal; rare familial IIH.
Quais as manifestações clinicas do papiledema?
P/w: scant visual sx early (e.g., mild blurring); visual loss w/ severe papilledema (when central vision affected); vitamin A toxicity; transient visual obscurations (often w/ bending forward), positional HA (worse from standing to sitting, prolonged supine), horizontal diplopia, whooshing sounds, “pulsatile tinnitus,” neck stiffness, n/v
Como faço o diagnostico do papiledema?
(1) Funduscopy: Optic disc swelling (begins superiorly & inferiorly) w/ splinter peripapillary hemorrhages (best seen w/ green light), subhyaloid or vitreal hemorrhage (w/ rapid rise of ICP), obscuration of vessels at disc margins (from swollen NFL), loss of optic cup (late), variable cotton wool spots, chorioretinal folds (if severe), & loss of venous pulsations (only implies nl ICP at that moment, as ICP can fl uctuate).
(2) Visual fi elds: Enlarged blind spots (2/2 displacement or compression of photoreceptors adjacent to disc); prolonged ↑ ICP → visual fi eld constriction (begins inferonasally; central fi eld affected last); serial visual fi elds recommended.
(3) U/l or b/l abducens defi cit/s.
(4) Check blood pressure.
(5) MRI & MRV brain to r/o mass lesions & venous sinus thrombosis.
(6) LP to confirm high ICP.
Qual o tratamento do papiledema?
(1) ↑ ICP: treat underlying cause.
(2) IIH: Acetazolamide long-acting capsules 500 mg PO Bid (up to 2,000 mg/day); warn of common (often transient) SEs to ensure compliance (dysguesia, tingling). Furosemide if acetazolamide (sulfa) allergic or refractory. Severe visual loss or refractory to meds: CSF shunting, ON sheath fenestration. HAs refractory: consider other common primary HA d/o’s (e.g., migraine) & Rx. Treat systemic HTN (untreated may increase risk of visual loss). Weight loss, nutrition counseling for IIH. (3) ICP lowering medicines & shunting also considered in nonIIH causes of papilledema when HA & visual loss require Rx; serial LP not routinely recommended.
Qual o prognóstico da hipertensão intracraniana idiopática (pseudotumor)?
(1) IIH: Most improve, can be tapered off meds in 8–12 mo; high ICP may remain despite resolution of si/sx; delayed recurrences w/ visual loss occur (Corbett, 1982). Poorer prognosis w/ initial severe visual loss (loss of central acuity or marked visual field loss); usu. treated more aggressively.
(2) Papilledema takes wks to resolve after ICP → nl. Some do not get full resolution; optic atrophy may ensue w/ blurred disc margins (“secondary atrophy”).
Qual a definição de quiasmopatias?
Dysfxn of optic chiasm, typically from external neoplastic compression, but nonneoplastic compression, intrinsic dz, & rarely, toxins may be culprit. DDx: Optic neuropathy that produces temporal visual fi eld defects: B12 defi ciency-related optic neuropathy, hereditary optic atrophy.
Qual a apresentação clínica das quiasmopatias?
Tríade: # Typically nonlocalizing visual complaints such as blurred vision; Photophobia; # HA; # pituitary or hypothalamic dysfxn (e.g., galactorrhea, acromegaly, precocious puberty, diencephalic syndrome); frontal lobe dysfxn.
Como faço diagnóstico das quiasmopatias?
# Temporal visual fi eld defects (superior or inferior; asymmetric): w/ compression from below or above, defects begin adjacent to vertical midline, not peripherally; even if only monocular temporal defect, still high concern for chiasmopathy. Junctional scotoma or fi eld defect: w/ lesion of anterior chiasm, an i/l ON-type defect (central or paracentral scotomas) & c/l superotemporal defect. Optic disc pallor. # Check brain & orbital MRI w/ gado. If MRI unrevealing check for B12 defi ciency & other causes of optic neuropathy
Qual o quadro clinico do adenoma de hipófise, principal causa de quiasmopatia?
P/w: Slow-onset visual loss (often unnoticed); hyperprolactinemia (galactorrhea, amenorrhea, ↓ libido), ↑ ↑ growth hormone (acromegaly, frontal bossing, thick skin) most common although those w/ visual dysfxn typically large & non-fxning
Exam: Superotemporal fi eld defects, CN III, IV, VI palsies if cavernous sinus invasion
Qual a diferença de tratamento dos adenomas de hipofise e dos craniofraingeomas? Qual o prognóstico?
Adenomas: Prolactinomas: First Rx medically (dopamine agonist), others monitored w/ exam (visual fields) & MRI; if visual compromise: resection (transphenoidal)
Prognóstico: Good if Rx early; can recur—must have serial exams/MRIs.
Craniofaringeomas:
Surgery, but complication rate»_space; for pituitary adenoma (endocrine Δs, iatrogenic visual loss).
Prog: Visual recovery can occur; recurrences w/ accumulation of cystic fl uid or growth of tumor. Must f/u w/ serial exam & MRI.
Quais as diferenças radiológicas entre adenomas e craniofaringeomas? (os dois principais tumores selares e supraselares)
No adenoma: MRI: Smooth, homogenously non-enhancing sellar mass w/in the normally enhancing pit gland compressing chiasm from below
No craniofaringeoma: MRI: Sellar region cystic mass w/ peripheral enhancement that compresses chiasm from above or below
Quais as causas de quiasmopatia que não adenoma ou craniofaringeoma?
Apoplexieia pituitaria, aneurisma, meningeoma, glioma, sarcidose, doenças desmielinizantes, pos-TR, etc.
RM de cranio é o exame de investiogação de quiasmopatias pois identifica os dois principais e já considera o diferencial.
Quais as sindromes visuais corticais?
- Hemianopsia homonima
- Negligencia visual
- Alexia sem agrafia
- Sd de Balint : simultaneognosia e apraxia optica
- Sd de Anton: Cegueira cortical
- Prosopagnosia e agnosia visual de objetos
- Discromatopsia central
Qual a propedeutica do sistema visual eferente?
Examine: Lid position, pupils in light & dark (& quality of constriction & dilation), eye mvmts of each eye independently (ductions) & eyes moving together (versions), saccades & pursuits, adventitious eye mvmts in primary & eccentric gaze. If strabismus (ocular misalignanament) not apparent w/ duction or version, do alternating cover testing while pt fi xates on target in primary, right-, left-, & upgaze as well as head tilts; w/ mild left abducens palsy, for example, only sign may be a subtle esotropia on left gaze (by alternate cover testing).
Descreva anatomia da via visual eferente
# Supranuclear control: Frontal eye fi elds (FEF; in premotor cortex) project to c/l paramedian pontine reticular formation (PPRF); PTO jxn also important for cortical eye mvmnt control. Damage to FEF → i/l gaze deviation. Damage to PPRF → c/l gaze deviation. #Brain stem: CN III nucleus (midbrain), CN IV nucleus (midbrain), CN VI nucleus (pons). CN III nucleus: Consists of medial oculomotor component (oculomotor nerve to superior rectus, medial rectus, inferior rectus, inferior oblique, levator palpebrae muscles), & paramedial parasympathetic component (Edinger-Westphal nucleus to iris sphincter & ciliary muscles). Nerve exits ventral midbrain after coursing through red nucleus, substantia nigra, & cerebral peduncle. CN IV nucleus: Consists of medial motor component (trochlear nerve to superior oblique muscle). Nerve fi bers cross to c/l side & exit dorsal midbrain. CN VI nucleus: Consists of medial motor component (abducens nerve to lateral rectus muscle). Nerve exits ventral caudal pons. PPRF: Controls horizontal conjugate gaze; internuclear communication through myelinated medial longitudinal fasciculus (MLF) Vertical conjugate gaze controlled by internuclear communication through rostral interstitial nucleus of MLF (riMLF) in dorsal midbrain.
Quais as principais síndromes de acometimento conjunto de pares cranianos?
# Internuclear ophthalmoplegia (INO) results from MLF dz. # Damage to MLF & adjacent PPRF → “one & a half” syndrome (INO + i/l gaze palsy) # Dorsal midbrain syndrome includes limitation of upgaze due to injury of riMLF. # Subarachnoid space/cisterns: Cranial nerves course anteriorly toward cavernous sinus. Can be affected by basilar meningitis or space-occupying lesions. # Cavernous sinus: Dura-lined venous plexus through which runs the ICA, postganglionic sympathetic nerves, CN III, CN IV, CN VI & CN V (V1 & V2 branches). CN VI is free fl oating, all other nerves are adherent to lateral dura. Lesions affecting cavernous sinus: Meningioma, lymphoma, pituitary adenoma, nasopharyngeal carcinoma, metastatic dz, intracavernous ICA aneurysm, carotid-cavernous fi stula (auscultate for orbital bruit), Tolosa Hunt, Wegener’s, other causes of pachymeningitis. # Orbital apex: Contains ON & ophthalmic artery in addition to CN III, CN IV, CN VI, & CN V1 (CN V2 exits through foramen rotundum). Lesions affecting orbital apex: Orbital pseudotumor, thyroidassociated eye dz, meningioma, lymphoma, nasopharyngeal carcinoma, metastatic dz, mucormycosis, aspergillosis, Tolosa-Hunt. Look for conjunctival injection, proptosis, chemosis. # Superior orbital fissure: Contains ophthalmic vein + CN III, CN IV, CN VI, & CN V1.
Quais são as vias simpáticas e parassimpaticas?
# Oculosympathetic pathway: Originates in hypothalamus, descends through brainstem & cervical cord (intermediolateral cell column) to C8–T2 (ciliospinal center of Budge), synapses & exits cord, ascends near cord to synapse on superior cervical ganglion (near lung apex), then ascends along carotid through cavernous sinus to end organs (Muller muscle, pupil dilator muscle). Damage to this pathway: Partial or complete Horner syndrome.
Oculoparasympathetic pathway: Input from retina projects to pretectal nucleus in dorsal midbrain, then projects ipsilaterally (through pretecto-oculomotor tract) & contralaterally (through posterior commissure) to Edinger-Westphal nuclei; signal then travels w/ both oculomotor nerves to both ciliary ganglia w/in orbit, then innervates iris sphincter muscle (pupillary constriction) & ciliary muscles (accommodation). Underlies consensual response to light as well as lens accommodation for near vision. Damage: Parinaud (aka dorsal midbrain) syndrome, Adie tonic pupil, Argyll Robertson pupils.
