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Four P'sPossibleProbablePrognosticPragmaticArteritic Anterior Ischemic Optic Neuropathy (A-AION)Giant Cell Arteritis (GCA) is an Immune-Mediated VasculitisAffects Medium and Large ArteriesIn eye mostly Posterior Ciliary Artery (PCA), then Central Retinal Artery (CRA), rarely Ophthalmic Artery (OA)Explain why GCA affects eyesCalled GCA because of granulomatous inflammation. Arteries lined with multinucleated giant cells: macrophages, lymphocytes, and fibroblastsIncidence of 2.3/100,000 in 6th decade. Increases with Age.Happens mostly to those > 50 years oldAge rangePredilection for North European, Scandinavian descent. Typically Caucasian though can happen in other racesWhy is it important?Profound vision lossCauses A-AIONCan become bilateral in 14 days in 1/3 if untreatedTreatableCRAO and Cilioretinal artery occlusion can occurCRAO occurs 5-10%A-AIONSudden painless vision lossUnilateral Optic Disc Edema1/10 patients (> 50 years old) with optic disc edema are A-AION. Other 9/10 NA-AIONSystemic SymptomsJaw Claudication (Odds Ratio 9.0)Neck Pain (Odds Ratio 3.4)AnorexiaLess predictable symptomsHeadacheFeverScalp TendernessMalaiseAverage number of symptoms = 3Visual Symptoms/SignsSudden, painless vision loss31% had amaurosis fugax 1-2 weeks beforeThis can be misleading. Not saying 31% of patients with Amaurosis Fugax have GCA6% diplopia8% ocular painOptic Disc Edema “chalky white pallor”Lab TestingESR – 86% sensitiveCRP – 100% sensitive, 82% specificCombined ESR and CRP – 99% sensitive, 97% specificCBC with differential looking for disease that can affect Red Blood Cells (i.e. Anemia, Polycythemia Vera)Look at plateletsOver 400,000 is indicative of GCAOther Diagnostic TestingFluorescein Angiography (FA) – characteristic late filling of choroid in the 2 weeks after Optic Disc Edema startsUltrasound, PET, MRI of limited benefitTemporal Artery Biopsy – especially indicated if clinical symptoms highly suggestive but either ESR or CRP are inconclusiveThis is a diagnosis that can be made by Optometrist or Ophthalmologist with use of ocular signs and symptoms combined with systemic symptoms and lab testing. Additional testing often not needed.Contralateral optic nerve can give us clues to A-AION vs. NA-AIONGo through Bayesian analysisIf C/D is > 0.4 1/5 have A-AIONIf C/D is < 0.3 1/15 have A-AIONSome advocate American College of Rheumatology criteriaNeed 3 of the following 5 criteriaOver 50 years of ageNew onset of HeadacheScalp tenderness or decreased temporal artery pulseESR > 50 mm/h(+) Temporal Artery BiopsyHaving 3 of these 5 gives 94% sensitivity and 91% specificity (not good enough)TreatmentMost studied and likely still most effective is oral steroid80-100 mg/day until labs normalizeDoes not typically improve vision (only 4% improve)Then taper for VERY long (years!)Evidence still lacks because not ethical to have a placebo groupNo evidence that IV steroid in mega dose any more effectiveLimited evidence for TNF blockers, Methotrexate and other immune modulatorsClinical PictureUnilateral Optic Nerve EdemaSystemic SymptomsPossible Visual SymptomsLab ResultsESR > 47 mm/hCRP > 2.45 mg/dlOptic Nerve in other eye > 0.4Positive Temporal Artery BiopsyNA-AIONNA-AION is due to acute ischemia of ONHPrimarily ischemia of PCANot ThromboembolicProven by FA and transcranial DopplerCharacterized by sudden, painless, unilateral vision loss75% wake up with vision lossHappens to age 49-64Incidence of 2.3-10.2 per 100,000Systemic risk factorsHypertensionDiabetes MellitusNocturnal hypotensionHyperlipidemiaAtherosclerosisAcuity is 20/20 in 1/3 of NA-AION. > 20/40 in 50%. < 20/200 in 20%No typically first visual field lossMore common in small optic cup< 0.15 in 33%< 0.3 in 75%However, not all small cups are at risk. Incidence only 10.2 per 100,000 at most. Average cup 0.3-0.4. So, 66% of population has 0.3-0.4. Not all of them will get NA-AION.Small cup exacerbates NA-AION form but not primary factorONH ischemia leads to axoplasmic flow stasis. In a small, crowded ONH this compresses surrounding tissue. This incites further swelling.Nocturnal hypotension is likely inciting factor in most casesFellow eye25% in 3 years17% in 5 yearsTreatment40% spontaneously resolveONH Decompression Trial24% progressed with Decompression12% progressed if left aloneASA is no helpCorticosteroids may benefit1 trial showed 70% in Tx group acuity improved compared to 40% ControlVF improved 40% in Tx group vs. 25% ControlIntravitreal Kenalog, Avastin – no evidence of benefit. Could exacerbate by increasing IOPAmiodorone – no evidence that it causesUsed to treat patients who likely have HTN, DM, and nocturnal hypotensionViagra etcIncipient NA-AIONNot all eyes have poor acuity at onsetFrequently misdiagnosed as diabetic papillopathyClinical PictureUnilateral Optic Nerve EdemaAge > 50No systemic symptomsTypically Diabetic and/or HypertensiveOptic Nerve in other eye < 0.3Ophthalmic SourcesDrusen –B-Scan helps differentiateCRVOHypotonyCRVO and Hypotony will be obvious upon examination. On the list to remind us that we don’t need to search for other causes if these are present Inflammatory (Can be infectious or non-infectious)SyphillisTBLymeSarcoidUveitisOptic Neuritis (this is a subset of Inflammatory)Acute inflammatory optic neuropathyResult of demylenating processIncidence between 1-5 per 100,000Age: Majority between 18-46 (95%)? Women. 85% WhiteSymptomsSudden unilateral vision loss (anywhere from 20/20 to NLP)In ONTT, 2/3 of contralateral eyes had some visual function lossPain – worse with eye movements92% of patients in ONTT had eye painVision loss lasts up to 4 weeks days before recoveryMay not recover full functionEven if 20/20, patients say vision not as good as beforeSigns1/3 of patients manifest with swollen optic nerve (papillitis)2/3 retrobulbar – no swollen nerve+APDWide variety of VF defects – none distinguish Optic Neuritis from other Optic NeuropathiesOften impaired contrast sensitivity and/or color visionONTT – 94% had color defects in acute phaseONTT – 40% had residual color vision defectsCannot help us differentiate between other optic neuropathiesSystemic AssociationsMultiple Sclerosis (MS)Optic neuritis occurs in ? of patients with MSIs initial event in ? patients with MSSymptomsNumbness, tingling, weaknessBalance and gait disturbanceBladder dysfunctionUhthoff’s phenomenon – heat L’hermitte symptomSignsOculomotor: nystagmus, INO, 6th nerve palsyOptic NeuritisAdditional TestingLab tests, MRI not needed for Dx of Optic Neuritis. MRI aids in prognosis and diagnosing MSOptic Neuritis Treatment Trial (ONTT)Evaluated use of steroids in treating acute optic neuritis457 patients with unilateral optic neuritisRandomized to one of three groupsOral pred (1mg/kg/day) x 14 daysIV Methylprednisolone x 3 days then oral prednisone x 11 daysOral placebo x 14 days93% of all patients recovered to at least 20/40 at 1 yearIV steroid followed by oral steroid speeded recovery (4 days compared to 15 days) and reduced recurrence of developing Clinically Significant Multiple Sclerosis (CDMS) by 2 yearsAbout 1/3 overall had recurrence. In Oral Pred group, 44% recurrenceMS patients had more recurrence than non-MS patientsOral steroid did not improve visual outcome and increased rate of new attack of optic neuritisAt 10 years:91% were 20/40 or betterOverall rate of developing MS was 38%If no lesions on MRI, risk of MS was 20% at 10 yearsIf 1 or more lesion, 56%Clinical PictureUnilateral Optic Nerve EdemaTypically 18-45 years of ageSystemic SymptomsPossible L’Hermitte, UthoffNumbness, tinglingVarying acuities+APD, reduced field, wide rage of acuity, reduced color, reduced contrastCompressiveUncommonMost likely from Pituitary TumorCan push forward and press on optic nerveJunctional ScotomaCan be from Graves’ disease and EOM/Orbital fat compressionMain Points:Mnemonic VOICGCA is a diagnosis that Optometrist can make. No expensive testingVery Serious! Use Age Use Symptoms Use Other EyeC/DBilateral ODE is differentReferencesHayreh S S. Ischemic Optic Neuropathy. Progress in Retinal and Eye Research. 2009;28:34-62Rahman W, Rahman F. Giant Cell (Temporal) Arteritis: An Overview and Update. Survey of Ophthalmol. 2005;50:415-28Cullen J F. Temporal Arteritis 50 years on. Br J Ophthalmol 2009;93:833-834Hayreh S S, et al. Ocular Manifestations of Giant Cell Arteritis. Am J Ophthalmol 1998;125:509-520Liu G T, et al. Visual Morbidity in Giant Cell Arteritis. Ophthalmology 1994;101:1779-1785Hayreh SS, et al. Giant Cell Arteritis: Validity and Reliability of Various Diagnostic Criteria. Am J Ophthalmol 1997;123:285-96Bhatti M T, Tabandeh H. Giant Cell Arteritis: Diagnosis and Management. Curr Opin Ophthalmol 2001;12:393-399Niederkohr, R D, Levin L A. Management of the Patient with Suspected Temporal Arteritis: A Decision-Analytic Approach. Ophthalmology 2005;112:744-756Wang X, et al. Giant Cell Arteritis. Rheumatol Int 2008;29:1-7Mitchell E B, Cestari D M. Giant Cell Arteritis and Angiogenesis: A Review. Seminars in Ophthalmology 2009;24:190-193Hayreh S S, et al. Visual Improvement with Corticosteroid Therapy in Giant Cell Arteritis. Report of a Large Study and Review of Literature. Acta Ophthalmol Scand 2002;80:353-367Danesh-Meyer H V, et al. The Prevalence of Cupping in End-stage Arteritic and Nonarteritic Anterior Ischemic Optic Neuropathy. Ophthalmology 2001;108:593-598Parikh M, et al. Prevalence of a Normal C-Reactive Protein with an Elevated Erythrocyte Sedimentation Rate in Biopsy-Proven Giant Cell Arteritis. Ophthalmology 2006;113:1842-1845 Tehrani R, et al. Giant Cell Arteritis. Seminars in Ophthalmology 2008;23:99-110Hall J K. Giant Cell Arteritis. Curr Opin Ophthalmol 2008;19:454-460Danesh-Meyer H, et al. Comparison of Arteritis and Nonarteritic Anterior Ischemic Optic Neuropathies with Heidelberg Retina Tomograph. Ophthalmology 2005;112:1104-1112Danesh-Meyer, et al. Poor Prognosis of Visual Outcome after Visual Loss from Giant Cell Arteritis. Ophthalmology 2005;112:1098-1103Foroozan R, et al. Recovery of Visual Function in Patients with Biopsy-proven Giant Cell Arteritis. Ophthalmology 2003;110:539-542Hall J K, et al. The Role of Unilateral Temporal Artery Biopsy. Ophthalmology 2003;110:543-548Pineless S L, Arnold A C. Giant Cell Arteritis. Int Ophthalmol Clin 2007;47:105-119Hayreh S S, et al. Occult Giant Cell Arteritis: Ocular Manifestations. Am J Ophthalmol 1998;125:521-526Hayreh S S, Zimmerman M B. Nonarteritic Anterior Ischemic Optic Neuropathy: Refractive Error and Its Relationship to Cup/Disc Ratio. Ophthalmology 2008;115:2275-81Beck RW, Cleary P, Optic Neuritis Study Group: Optic Neuritis Treatment Trial: One-year Follow-up Results. Arch Ophthalmol 111: 773-775, 1993.Beck RW, Cleary PA, Backlund JC, Optic Neuritis Study Group: The course of visual recovery after optic neuritis. Experience of the Optic Neuritis Treatment Trial. Ophthalmology 101: 1771-1778, 1994Beck RW, Optic Neuritis Study Group: Corticosteroid Treatment of Optic Neuritis: A need to change treatment practices. Neurology 42: 1133-1134, 1992. Beck RW, Trobe JD, Optic Neuritis Study Group: What we have learned from the Optic Neuritis Treatment Trial. Ophthalmol 102: 1504-1508, 1995. Beck RW. The Optic Neuritis Treatment Trial. Editorial Arc Ophthalmol 106: 1051-1052, 1998.CHAMPS Study Group: Interferon β-1a for Optic Neuritis Patients at High Risk for Multiple Sclerosis. Am J Ophthalmol 132(4): 463-471, 2001.Harkins T. A summary of the optic neuritis treatment trial. Clin Eye Vis Care 6 (1): 33-36, 1994Harkins T. Treating Multiple Sclerosis. Clin Eye Vis Care 6 (3): 133-136, 1994Optic Neuritis Study Group: High- and Low- Risk Profiles for the Development of Multiple Sclerosis within 10 years After Optic Neuritis. Arch Ophthalmol 121: 944-949, 2003.Lepore FE. The Origin of Pain in Optic Neuritis: Determinants of Pain in 101 Eyes with Optic Neuritis. Arch Neurol?48(7):748-749, 1991.Optic Neuritis Study Group: Visual function 5 years after Optic Neuritis: Experience of the Optic Neuritis Treatment Trial. Arch Ophthalmol 115(12): 1545-1552, 1997.Optic Neuritis Study Group: Visual Function more than 10 years after Optic Neuritis: Experience of the Optic Neuritis Treatment Trial. Am J Ophthalmol 137(1): 77-83, 2004.Optic Neuritis Study Group: Visual Function 15 years after Optic Neuritis: A Final Follow-up Report from the Optic Neuritis Treatment Trial. Ophthalmology 115(6): 1079-1082, 2008.Sergott RC, Brown MJ. Current concepts of the pathogenesis of optic neuritis associated with multiple sclerosis. Surv Ophthalmol 33(2): 108-116, 1988.Trobe JD, Sieving PC, Guire KE, Fendrick AM. The impact of the optic neuritis treatment trial on the practices of ophthalmologists and neurologists. Ophthalmology 106(11): 2047-2053, 1999.Optic Neuritis Study Group: Multiple Sclerosis Risk after Optic Neuritis. Arch Neurol 2008;65:727-732 ................
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