Study integrating ophthalmology and neurology Disorders affecting parts of CNS devoted to vision or eye Afferent system visual pathway incl ID: 1031986
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1. Neuro-ophthalmology
2. Neuro-ophthalmologyStudy integrating ophthalmology and neurologyDisorders affecting parts of CNS devoted to vision or eye:Afferent system (visual pathway, incl. optic nerve)Efferent system (ocular motor control, pupillary function)
3. Part INeuro-ophthalmologic Examination
4. ExaminationHistoryEye examination (visual acuity, tonometry, anterior segment examination, funduscopic examination)PerimetryColor vision, contrast sensitivity, electrophysiology (ERG, VEP)MRI of brain, Neurologic examination
5. Visual acuityEach eye separatelyDistance and near visionUsing of corrective lenses, pinholeUsing Snellen chart (20 feet) – normal 20/20Count fingers, hand motion, light perception, no light perception
6. Color visionEach eye separatelyComparison between eyesExamination:pseudoisochromatic plates (Ishihara)100 Hue test (Farnsworth-Munsell)
7. Farnsworth-Munsell 100 Hue testOrdering the color tiles as patient sees it
8. Contrast sensitivityExamining spatial frequencyDecreased in some optic nerve disorders (typically optic neuritis)
9. PerimetryTo assess the quality of visual fieldCharacteristic visual field defect =location of possible intracranial lesions
10. PerimetryAutomated static perimetry
11. PerimetryGoldmann kinetic perimetry
12. Electrophysiologic examinationERG = ElectroretinographyAccess possible functional pathology of retina (scotopic, photopic and central part)Flash ERG (activity of bipolar cells as an answer to stimation of photosensitive cells – rods, cones)Pattern ERG (activity of gaglionar cell as a response to stimulation of cones in macula)VEP = Visual evoked potentials (responses)Access the capability of anterior visual pathways –optic nerveMajor use: diagnosis/confirm of optic neuritis
13. Electrophysiologic examination
14. Electroretinography
15. Visual evoked potentials
16. Multifocal ERG, Multifocal VEPMostly experimental use, not standard in clinical medical practice here
17. Part IIPathology of Afferent system
18. Afferent systemRetina (cones, rods, bipolar and ganglion cells)Optic nerveOptic chiasmOptic tractLateral geniculate bodyOptic radiationVisual cortex (V1 = Brodmann area 17)
19. Pathologies of Afferent Visual System PapilledemaOptic NeuritisOptic NeuropathyOptic Atrophy
20. PapilledemaNot a disease - sing secondary due to elevated intracranial pressure (ICP)Unspecific signRequire immediate diagnosis = increased ICP is a life-threatening situation!!!60% of cases = increased ICP caused by intracranial tumor!!!Other possible causes: hydrocephalus, meningitis, encephalitis, brain abscess...
21. PapilledemaClinical pictureEarlyMargins are obscuredOptic cup initially preservedHyperemic discAcuteElevation of discRadial hemorrhagesGrayish-white exudatesChronicDisc edemaObiterated optic cup
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23. Optic neuritisInflammation of the optic nerveIntraocular – within the globeRetrobulbar – posteriot to the globeUsually unilateralTendency to repeatEtiologyOften associated with multiple sclerosis (MS) = demyelinating optic neuritis (20% = first sign of MS)Other possible inflammatory causes: Lyme disease, syphilis, inflammation from orbit, paranasal sinuses...
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25. Optic neuritisSymptomsSudden vision loss within several hours (mild blurring/light perception)Central, paracentral scotomaRetrobulbar/parabulbar painPresent afferent pupillary defectPrognosisdepends on underlying disordersMS = usually good – significant spontaneous improvement (several weeks)Some permanent disturbances of vision are possible (color vision decreasing, scotoma)
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28. Anterior Ischemic Optic NeuropathyEtiologyAcute disruption of blood supply (due to vascular changes, infarction)SymptomsSudden unilateral loss of visionAltitudinal or wedge-shaped visual field defectPresent afferent pupillary defectClinical pictureEdema of optic discSegmental obscuration of margins (correlation with visual field defect)
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30. Anterior ischemic optic neuropathy 2 formsBenign: Nonarteritic AIONMalign: Arteritic AIONArteritic AIONAssociation with systemic vasculitis (giant cell arteritis)Diagnosis: sedimentation rate, biopsy of temporal arteryHigh risk of affection of contralateral (fellow) eye within days/ weeks!!!Need for immediate therapy with high dose intravenous corticoids!!!
31. AION formsArteritic formNon-arteritic form% of cases AION10 %90%age70 years60 yearsSexFemale > maleFemale = maleSystemic disease associationGiant cell arteritis (Horton disease)idiopathicPrognosisVery raremildFellow eye affectionoften (50-90%)rare(10-20%)Diagnostics:Sedimentation (FW)Very highnormaltreatmentHigh dosage of systemic corticoidsNot available
32. Optic AtrophyIrreversible loss of axons as a result to damage of optic nerveEtiologyPrimary due to trauma, direct pressure by tumorSecondary due to affection of optic nerve (optic neuritis...)Glaucomatous due to glaucomatic damagePathogenesisAscending - lesion located anterior to the lamina cribrosaDescending – lesion located posteriot to the lamina cribrosa
33. Optic AtrophyClinical pictureTotal/partial pale optic discWell defined / blurred marginsConstricted / reduced retinal vesselsEtiologyVascular (AION, RAO)Inflammation (optic neuritis, neuroinfections)Compressive (orbital/intracranial mass)Traumatic (avulsion, bone fracture)Toxic (methyl alcohol, various poisons, cytostatics)Congenital/hereditary (LHON, Kjer atrophy)Systemic (hematooncological diseases)
34. Part IIIPathology of Efferent system
35. Efferent system1) Cranial neuropathies (III, IV, VI)2) Pupillary abnormalities
36. Eye movementOcular motility – produced by extraocular muscles4 rectus muscles (lateral, medial, superior, inferior)2 oblique muscles (superior, inferior)
37. Cranial neuropathiesSignsOculomotor nerve palsy DiplopiaMultiple muscle paralysisPtosis AnisocoriaTrochlear nerve palsyVertical diplopiaAbnormal head tiltAbducens nerve palsyHorizontal diplopia in the gaze palsy
38. Cranial neuropathiesEtiologyIschemic (diabetes, hypertension, hyperlipidemia)Demyelinating disease (MS)Compressive (tumor, aneurysm)Elevated ICPMultiple cranial neuropathies = suspect lesion in the posterior orbit or cavenrous sinus region
39. PupilMiosis – parasympathetic nervous systemMydriasis – sympathetic nervous system
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41. Sympathetic pathway
42. Pupillary abnormalitiesAnisocoria inequality of pupil sizeMay be physiologicPossible accidental discoveryMay be isolated / associated with eyelid or ocular motility abnormalitiesDiagnosisDirect shine at pupilTest near response (miosis with accomodation)Pupil sizes in light and dark
43. Horner’s SyndromeSignsMiosis (pupil does not dilate in dark)PtosisPseudo-enophthalmusAnhidrosis (diminished sweating)Heterochromia (if congenital)EtiologyTrauma, internal carotid artery dissection, brain stem strokes, MS, brain tumor, syringomyelia, apical lung tumor, goiter, thyroid carcinoma...
44. Adie’s PupilSignsNo present / slow miosis to lightPresent miosis to accomodationPupil is larger with light/near dissociationEtiologyInflammation (viral or bacterial infection)TherapyPilocarpine drops, thoracic sympathectomy
45. Thank you for your attention!