Chorioretinopathies of Unknown Etiology (WhiteDots)
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Reported 2015, my last report in UVEA; based on AAO--With the help of Dr, Daniel Baskin and Dr, Pia Galvante
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Chorioretinopathies of Unknown Etiology (WhiteDots)
- 1. WHITE DOT SYNDROMES Leo Francis Pacquing Resident-in-Training Year3 DOH EYE CENTER Mon, APRIL 27, 2015
- 2. WHITE DOT SYNDROME DIFFERENTIAL • Syphilis • Diffuse Unilateral Subacute Neuroretinitis • Ocular Histoplasmosis Syndrome • Tuberculosis • Sarcoidosis • Sympathetic Ophthalmia • VKH • Intraocular Lymphoma • Pneumocystis Choroidopathy • Candidiasis
- 3. WHITE DOT SYNDROMES • Birdshot • APMPPE • Serpiginous Choroiditis • MCP • PIC • SFU • MEWDS • ARPE • AZOOR
- 8. WHITE DOT SYNDROMES in general… • Bilateral Involvement although asymmetrical (except MEWDS) is a RULE • Majority of patients are younger than 50 y/0 (except Birdshot Retinochoroidopathy & Serpiginous Choroiditis • Female Preponderance in Birdshot choroidopathy, PIC, MCP, AZOOR &MEWDS
- 9. WHITE DOT SYNDROMES etiology • Unknown – Infectious – Autoimmune/ Inflammatory • May be inherited Immune dysregulation that predisposes to Autoimmunity
- 10. WHITE DOT SYNDROMES Acute Zonal Occult Outer Retinopathy (AZOOR) Multifocal Choroiditis and Panuveitis (MCP) Multiple Evanescent White Dot Syndrome (MEWDS) Acute Annular Outer Retinopathy (AAOR) Punctate Inner Choroidopathy( PIC) Acute Idiopathic Blind Spot Enlargement Syndrome (AIBES) AZOOR-Complex Diseases Acute Posterior Multifocal Placoid Pigment Epitheliopathy (APMPPE) Serpigenous Choroidopathy Birdshot Retinochoidopathy *duh” doesn’t have white dots on them * * *
- 12. BIRDSHOT RetinoChoroidopathy HLA-A29 is 96% Sensitive Multifocal, Hypopigmented Ovoid Cream lesions (50-1500 um) Symptoms? BOV, floaters, Nyctalopia Confirmatory and not Diagnostic Vitritis? Common but variable severity CNV? Rare Vitiliginous ChorioRetinitis Fundoscopy Choroid and RPE
- 14. FA Findings Doesn't’t typically highlight spots ICGA Findings Shows spots- More numerous on exam ERG AF Findings Delayed 30 Hz Flicker Implicit Time Diminished scotopic B wave amplitudes Hypoautofluorescence (meh) Treatment: Initially-Systemic Cortecosteroids YES!!IMT:
- 16. •SUDDEN Onset of Bilateral, Asymmetric Visual loss associated with scotoma
- 17. Acute Posterior Multifocal Placoid Pigment Epitheliopathy (APMPPE) 50% have prodromal illness Symptoms: BOV, Scotomata, Photopsias Vitritis: Mild to moderate in 50% CNV: Rare APMPPE Fundoscopy: Multiple large flat,yellow-white placoid lesions at the level of RPE
- 18. A P M P P E Associations Non-Infetious • Erythema Nodosum • Wegener’s Granulomatosis • Polyarthritis Nodosa • Cerebral Vasculitis • Scleritis & Episcleritis • Ulcerative Colitis Infectious • Group A Streptococcus • Adenovirus Type 5 • TB • Lyme Disease • Mumps • Hepatitis B vaccination
- 19. APMPPE FA Findings Blocks early, Stains Late Blocks early ICGA Findings Hypofluorescent Spots= No. in FA AF Findings HypoAF lesions IMT? NO
- 20. APMPPE PROGNOSIS RISK FACTORS FOR VISION LOSS FOVEAL Involvement Older Age Unilateral Disease Longer interval of the initial and fellow eye involvement Recurrence
- 21. Serpiginous Choroiditis Asymmetric Gray White lesions at the level of the RPE in a Pseudopodial /Geographic manner from the Optic Nerve Symptoms: Vitritis? CNV? BOV, Scotomas , Minimal 25% Helicoid Choroidopathy Fundoscopy
- 22. Serpiginous Choroiditis FA Findings: Blocks early, Stains Late (*plus the CNV findings if Present) ICG Findings: Hypofluorescent lesions throughout FAF : Active lesions are HyperAF; inactive Lesions are HypoAF IMT? YES!!! AAO: FAF is "Exquisitely Sensitive”
- 23. FUNDOSCOPY FAF Serpiginous Choroiditis SOURCE: AAO 2013-2015
- 24. Serpiginous Choroiditis FUNDOSCOPY FAF SOURCE: AAO 2013-2015
- 25. WHITE DOT SYNDROMES Acute Zonal Occult Outer Retinopathy (AZOOR) Multifocal Choroiditis and Panuveitis (MCP) Multiple Evanescent White Dot Syndrome (MEWDS) Acute Annular Outer Retinopathy (AAOR) Punctate Inner Choroidopathy( PIC) Acute Idiopathic Blind Spot Enlargement Syndrome (AIBES) AZOOR-Complex Diseases Acute Posterior Multifocal Placoid Pigment Epitheliopathy (APMPPE) Serpigenous Choroidopathy Birdshot Retinochoidopathy *duh” doesn’t have white dots on them * * * Ampiginous Choroiditis (Aka, Relentless Placoid Chorioretinitis)
- 26. • Features of Both APMPPE and Serpiginous • lesions are similar both clinically and angiographically, but the clinical course is atypical for both entities. • Posterior and peripheral lesions simultaneously with macular involvement. Relentless Placoid Chorioretinopathy
- 28. New lesions and recurrent attacks are typical, with up to 38% of patients Reaching final VA of 20/200 &CF
- 29. The addition of SYSTEMIC IMT at the outset has been suggested as CORTICOSTEROIDS ALONE ARE INEFFECTIVE Cyclosporine (Monotherapy) Prednisone, cyclosporine, Azathioprine (Triple Therapy) –RAPID REMMISION OF ACUTE DSE PROLONGED THERAPY—SINCE RECURRENCE is Frequently Observed. Anti-VEGF and FOCAL laser photocoagulation for CNV
- 30. Tb-SLC
- 31. Ocular Histoplasmosis Syndrome Multiple white atrophic chorioretinal scar (“spots”) Peripapillary Pigment changes CNV Maculopathy NO VITRITIS (vit cells) WHITE DOT?
- 32. Young Myopic Female 1/3 Symptoms: Vitritis: CNV: Photopsia, enlarged blind spot, BV Yes Yes, 28% at presentation Multifocal Choroiditis and Panuveitis
- 33. FA findings : Blocks Early, stains Late for active lesions ICGA findings: Hypofluorescent Spots are more numerous than FA FAF: Active lesions are HyperAF; Inactive lesions HypoAF IMT helpful? Yes
- 39. RESOLVING VKH
- 40. Punctate Inner Choroidopathy (PIC) Young Myopic Female 2/3 Symptoms: Photopsia, Metamophopsia, BV Vitritis CNV YES!; 79% At Presentation
- 41. FA Findings: Early Hyperfluorescence, late staining ICGA Findings: Hypofluorescent spont = FA FAF Meh IMT: NO TREATMENT Steroids (P) (S) Anti VEGF Laser Photocoag PDT
- 42. SARCOIDOSIS Characteristic Ocular Findings Granulomatous Anterior Uveitis • Vitreous Inflammation (Diffuse Inflammation Snowballs or string of pearls • Periphlebitis • Candlewax drippings (nodular granulomas along venules) • Yellow White Choroidal exudates • CME • Occlusive Retinal Vasculature • ON edema • Retinal, Choroidal, Optic Nerve Granuloma
- 43. MULTIPLE EVANESCENT WHITE DOT SYNDROME (MEWDS) Young Myopic Female 3/3 Symptoms: ACUTE UNILATERAL Photopsias, Enlarged blind spot, BV AIBES VITRITIS: Variable CNV Rarely FUNDOSCOPY: ACUTE PHASE Multiple discrete white to orange Spots (100-200um) at the level of the RPE or Deep retina typically In a PERIFOVEAL location “EVANESCENT” Because those spots are TRANSITORY and frequently MISSED GRANULAR PIGMETARY CHANGE
- 44. FA FINDINGS : Punctate HYPER fluorescent spots that surrounds the fovea in a wreath-like configuration ICGA FINDINGS: Shows spots that are more numerous than FA/Examination ERG FINDINGS: Diminished A-Wave & Early Receptor Potential AF IMT Helpful: No …
- 46. Shows spots that are more numerous than FA/Examination ICGA FINDINGS: MULTIPLE EVANESCENT WHITE DOT SYNDROME
- 47. MEWDS
- 50. SYMPATHETIC OPHTHALMIA 1st one to raise his/hand 3 clues CLUE1: NOT a white dot Syndrome CLUE 2 Diffuse non Necrotizing Granulomatous PANUVEITIS CLUE 3 PHOTOPHOBIA 67% Decrease in accomodation (13%) DALEN FUCHS SPOTS
- 52. ARN
- 53. SLE
- 54. WHITE-YELLOW LESIONS (50-500 flm) located in the posterior pole to midperiphery at the level of the RPE Significant anterior segment inflammation and mild to moderate VITRITIS are typically present BILATERALLY
- 55. Difficult DX.. CALLED OCCULT FOR A REASON Acute zonal occult outer retinopathy (AZOOR) Symptoms: Unilateral Photopsias, Variable Scotomata VITRITIS? Mild CNV? RARELY ERG: Delayed 30 Hz Flicker CR-ATROPHY Lipofufucin laden cells
- 56. WHITE DOT SYNDROMES Acute Zonal Occult Outer Retinopathy (AZOOR) Multifocal Choroiditis and Panuveitis (MCP) Multiple Evanescent White Dot Syndrome (MEWDS) Acute Annular Outer Retinopathy (AAOR) Punctate Inner Choroidopathy( PIC) Acute Idiopathic Blind Spot Enlargement Syndrome (AIBES) AZOOR-Complex Diseases Acute Posterior Multifocal Placoid Pigment Epitheliopathy (APMPPE) Serpigenous Choroidopathy Birdshot Retinochoidopathy Ampiginous Choroiditis (Aka, Relentless Placoid Chorioretinitis)
- 57. MCP PIC OLDER AGE? SMALLER SPOTS VITRITIS CNV AT PRESENTATION 28% 79% WORSE VA prognosis
- 58. APMME SERPIGINOUS VIRAL PRODROME PAPILLITIS VITRITIS CNV AT PRESENTATION NO 25% WORSE VA prognosis 50% NO POSSIBLE NO Mild to Mod Minimal
- 59. BIRDSHOT APMPPE SERPIGINOUS MCP PIC MEWDS BLOCKS EARLY STAINS LATE yes yes yes yes no no ICGA SPOTS more Numerous on FA Yes No Yes Yes NO YES IMT yes no yes yes no no
- 60. GOOD MORNING
Editor's Notes
- INTRO: through the past years I really never got to absorb much “IN me” the white dot syndromes. It is Very heterogenous group of dse. I told myself twice on the previous reports on the previous years; “im gonna study the white dots” ----BUT when we actually see the patient, they don’t usually say “I have white dot syndrome” and if they do..we might get them wrong in a way. So its important for us to think about the differentilas of WHITe dots, this infectious and non infectious dse entities must be ruled out because they do bother you with the similar findings on clinical examinations.
- There are mouthful of them. And what is a white dot syndrome? Its non infectious dse entitities as far as we know. The inflammatory chorioretinopathies, or white dot syndromes, are a heterogeneous group of inflammatory disorders with overlapping clinical features that share in common the presence of discrete, multiple, well-circumscribed, yellow-white lesions at the level of the retina, outer retina, RPE, choriocapillaris, and choroid during some phase of their course.
- There is this good grouping I saw on the internet and I think its legit as far as when I was doing the report. And at the back of the section of the book---the last page indeed..when I was reconciling—yes this GROUPING is LEGIT. SO this is how we are going to atack the white dots in this report…
- RetinoVitreal Lymphoma; Intraocular lymphoma PIOL
- Birdshot is rare dse, common among white woman past 40 y/o (book) While there is no systemic association of this dse, HLA-A29 haplotype correlation is very high. Its called BIRDSHOT because it is viewed wherein the lesions appear as the birds that went off from the stems as soon as the gun fire was shot. Funduscopy reveals characteristic multifocal, hypopigmented, ovoid, cream-colored lesions (50-1500 flm) at the level of the choroid and RPE in the postequatorial fundus; typically these show a nasal and radial distribution, emanating from the optic nerve, and frequently they follow the underlying choroidal vessels Vitritis is common but with variable severity and this patients rarely get CNV.
- Typically these show a nasal and radial distribuion, emanating from the optic nerve, and frequently they follow the underlying choroidal vessels .And it’s a slam dunk to see the infero nasal distribution of the this hypopigmented creamy ovoid lesions. Since Vitritis is common with variable severity, we expect the development of complications related to Vitritis Sequela. That is why in white dot syndromes we already know among them whom are treated aggressively when they are known to be relentless of having vitritis.
- Al though early birdshot lesions may show initial hypofluorescence with subtle late staining, in general, FA does not typically highlight the birdshot lesions themselves but rather is useful in identifying more subtle indices of active inflammation such as retinal vasculitis, CME, and optic nerve head leakage Indocyanine green (ICG) angiography discloses multiple hypofluores- cent spots, which are typically more numerous than those seen on clinical examination or on FA In previous studies they have found out that patients with birdshot develops Progressive visual field loss and (‘researchers in the start even documented) an abnormal electroretinogram (ERG) results seen with extended follow-up, suggesting that a more diffuse retinal dysfunction not fully explained by the presence of CME or other structural abnormalities contributes to visual loss. Fundus autofluorescence (FAF) imaging reveals hypoautofluorescence in areas of RPE atrophy that are more numerous and not uniformly correspondent with the birdshot lesions, suggesting that the choroid and RPE may be affected independently. Treatment consists of the initial administration of systemic corticosteroids, with early introduction of corticosteroid-sparing IMT, because birdshot retinochoroidopathy is typically incompletely responsive to corticosteroids alone and extended treatment is anticipated in most patients. Those who cannot handle systemic corticosteroids, some have tried using retisert or the Intravit injection of Fluocinolone Acetonide, BUT of course the effects are notorious later for patients since they developed cataract.
- uncommon condition presenting in otherwise healthy young adults, typically occurs with an influenza-like illness (50%) Asociated with central and paracentral scotoma with the fellow eye being involved within days to weeks. A genetic Predispostition may be present in association with some HLA in the development of this entity.
- SERET? ITS APMPPE Patients will typically present with a sudden onset of bilateral, asymmetric visual loss associated with central and paracentral scotomata, with the fellow eye becoming involved within days to weeks. There is minimal anterior segment inflammation, but vitritis of a mild to moderate degree is present in 50% of patients. Funduscopic findings include multiple, large, flat, yellow-white placoid lesions at the level of the RPE, varying in size from 1 to 2 disc areas, located throughout the posterior pole to the equator. CNV although rare may happen.
- A number of noninfectious systemic conditions have been reported in con- nection with APMPPE; its not recommended for us to memorize all these associations but if recurrence in patients being diagnosed with APMPPE occurs, its quite helpful for us to work up our patients of such entitities.
- The diagnosis of APMPPE is based on the characteristic clinical presentation and FA findings during the acute phase of the disease. early hypofluorescence (blockage) lesions and late hyperfluorescent staining. ICG angiography reveals choroidal hypofluorescence with hypervisualization of the underlying choroidal vessels while FAF will show HYPO-AF ;taken together, the FA, ICG, and FAF imaging findings suggest that affectation is in the level of the choroid.
- Although visual acuity returns to 20/40 or better within 6 months in the majority of patients with APMPPE, 20% are left with residual visual dysfunction. Risk factors for visual loss include foveal involvement at presentation, older age at presentation, unilateral disease, a longer interval between initial and fellow eye involvement, and recurrence.
- Serpiginous choroiditis, also known as geographic or helicoid choroidopathy, is an uncommon, chronic, progressive inflammatory condition affecting adult men and women equally in the second to seventh decades of life. Classically, funduscopy reveals asymmetric bilateral disease with characteristic gray-white lesions at the level of the RPE projecting in a pseudopodia! or geographic manner from the optic nerve in the posterior fundus Patients present with painless, unilateral, paracentral scotomata and decreased vision with minimal vitreous involvement and a quiet anterior chamber. CNV occurrence is 25% of the time. Important to take note is that Disease activity s typically confined to the leading edge of the advancing lesion and may be associated with shallow subretinal fluid.
- For the FA, it usually will BLOCK EARLY and STAINS LATE plus FINDINGS OF CNV IF PRESENT. ---SO tis just means there is a blockage of the choroidal flush in the early phase of the study and staining of the active edge of the lesion in the later stage of the angiogram FOR ICG is is useful because it distinguishes the new serpiginous lesions which are hypofluorescent if you compare it to an adjacent CNV (HYPERfluorescent lesion) But if ICG is useful, FAF is exquisitely sensitive modality in detecting damage to the RPE and in monitoring the clinical course of the patient with serpiginous with CHARACTERISTIC HupoAF corresponding closely to areas of regressed disease activity and hyperAF highlighting areas of ACTIVE disease.
- FOR EXAMPLE from the figure at the AAO Book, Fundus photograph showing inactive serpiginous choroiditis with peripapillary chorioretinal atrophy extending into the macula beneath fovea. B, Corresponding fundus auto- fluorescence (FAF) image showing hypoautofluorescence corresponding to the chorioretinal atrophy.
- While the same patient on follow up shows Fundus photograph depicting discoloration of retinal pigment epithelium during exacerbation of disease activity (arrow). D, Corresponding hyperautofluorescent signal on FAF
- It has both features of APMPPE and serpiginous; The acute retinal lesions are similar to those of APMPPE or serpiginous choroiditis both clinically and angiographically, but the clinical course is atypical for both entities. Patients have numerous posterior and peripheral lesions predating or occurring simultaneously with macular involvement. Acute lesions heal over a period of weeks with resultant chorioretinal atrophy.
- The disease course is marked by progressive centrifugal extension, with marked asymmetry between the 2 eyes. New lesions and recurrent attacks are typical, with up to 38% of patients reaching a final visual acuity of between 20/200 and counting fingers in the affected eye. Late findings include atrophy of the choriocapillaris, RPE, and retina, with extensive RPE hyperpigmentation and subretinal fibrosis, and CNV occur- ring at the border of the old scar in up to 25%
- The disease course is marked by progressive centrifugal extension, with marked asymmetry between the 2 eyes. New lesions and recurrent attacks are typical, with up to 38% of patients reaching a final visual acuity of between 20/200 and counting fingers in the affected eye. Late findings include atrophy of the choriocapillaris, RPE, and retina, with extensive RPE hyperpigmentation and subretinal fibrosis, and CNV occur- ring at the border of the old scar in up to 25%
- READ SCREEN
- (DON’T CLICK UNTIL U READ TB-like)This Is another case. It is geographical and somewhat like helicoidal too but THIS is not Serpiginous but looks very closely to it. And its an important differential of your serpiginous. The reason its not 1. You don’t see anything that is contiguouswith the disc, (sparing of the peripapillary area). This has vitreous cells which serpiginous often does not have, they have + PPD and patients coming from TB endemic countries like Philippines (LABAN MANNY)..IT IS our great TB.. And its called TB-SLC (tuberculous serpigious like choroidopathy. Its quite important to differatiate beciase we treat them differently.
- Is this a White Dot Sydrome? NO ITS not, its an entity know to have PERIPAPILLARY PIGMENT CHANGES, CNV MACULOPATHY, NO VITRITIS; OHS which is differentiated from THIS (NEXT SLIDE)
- (which is differentiated to this having the presence of PUNCH OUT YELLOW WHITE DOTS in a peripapillary, mid peripheral and anterior Equatorial distribution. MCP although classified as panuveites, is presented here as white dot syndrome given the fundocopic appearance and predominance of posterior pole involvement. it is disorder of unknown etiology affecting the choroid, retina and vitreous that presents asymmetrically most often in the YMF with symptoms of photopsias, blind spot enlargement, and BV Vitritis? Yes. And again this is your triad!
- FA Findings: Blocks early and stains late for the acute active lesions while the inactive lesions will appaer as transmission defects ( transmission deffects) meaning problem in the RPE, where they will appear as HYPER fluorescent lesions that FADES in the late phases of the angiogram) FOR ICGA: just like your birdshot showing HYPO fluorescent lesions compatible with active CHOROIDITIS that ARE MORE numerous than those seen on FA or Clinical Exam clustered around the optic neve---explaining those enlarged blind spots. And its being correlated by requesting your FAF that is going to show you HYPER if active HYPO if its inactive. –So helpful siya sa Monitoring of these lesions, or in evaluating your treatment.
- FAF ulet, a case of 36 y/o F showing us A. Area of CNV (ARROW Head ) that was treated with PDT 3 years earlier. FAF of the same photo shows the multiple hyPO AF spots (arrow heads) that did not correspond to the fundus exam. Then 3 years later—the PHOTO in 2012 alrrady shows you those HYpoAF before and the FAF of the same year shows us the slightly enlarged HYpoAF—signifying INACTIVE lesions.
- MCP parin toh, showing us the lesions are smaller than those seen in birdshot, or APMPPE and evolve into ATROPHIC SCARS w varying degreed of hyperpigmentation.
- 2 years later.
- FAF with the Hypo AF
- This is a spectralis OCT showing us the PUNCH OUT LESIONS giving the hyper reflectivity of the choroid because something just like your MCP just made a whole punch through it. Right?
- Here is a patient with liitle white dots on it with complains flu like symptoms, headache, of scalp tenderness, hearing defects---of course this is your VKH That’s the sunset glow fundus-right? Depigmentation of the RPE level and Choroid, seen most commonly among chronic VKH---That’s at the CONVALESCENT STAGE!!! Where the process of Autoimmunitity as we all know is directed against the stromal choroidal melanocytes.
- IS this a white dot?! Yes it is! PIC is an idiopathic inflammatory disorder that, like MCP, occurs in otherwise healthy myopic white women, but it presents at a younger median age (29 vs 45 years, respectively). I don’t know y MCP was tagged as YOUNG.. (Joke) SYMPTOMS: SCREEN VITRITIS….NO NEVER! BUT… FOR CNV??????---- IT’S A BIG YES!!!! For which 79% of them have at presentation, so f there is one WHITE DOT asked in the EXAM asking CNV at presentation---the answer is PIC
- This is a picture of PIC with an associated CNV. A, Fluorescein angiogram showing early hyperfluores- cence of the PIC lesions, w ith lacey hyperfluorescence of CNV. B, Late hyperfluorescence and staining of PIC lesions and leakage due to CNV. May SMILEY diayan ksi this is unique among the others that has just been discussed… EARLY HYPERFLUORESCENCE SIYA. ICGA---READ SCREEN FAF----MEH IMT…NOT Really…Since notorious for having CNV at presentation: we usually treat them with anti VEGF due to the hign incidence of CNV. And the visual prognosis of PIC is FAVORABLE in eyes W/O CNV Treatment options are as ff: Periorcular and systemic steroids, Anti VEGF, Laser, and PDT due to the CNV once again.
- What white dot syndrome is this Looks like APMPPE Big work up---Chext xray Hilar Adenopathy
- Another case!!! Its Uncommon Idiopathic inflammatory condition THIS IS YOUR MEWDS.. And the E stands for Evanescent, Uncommon Idiopathic inflammatory condition of the retina that typically affects otherwise healthy YMF in the second to forth decade of life. This is the 3rd among the YMF (young myopic females) Symptoms, 1/3 of them have viral prodrome, and Patients present with Acute unilateral (80%) Blurred vision, photopsias and central or paracentral scotoma corresponding to the enlarged blind spot. THIS is the SISTER of AIBES because if you Have all this symptoms but DONT Have any White DOTS.then they might call your condition Acute Idiopathic Blind Spot Enlargement Syndrome (AIBES) FUNDOSCOPY during the ACUTE PHASE of the disease Multiple discrete white to orange Spots (100-200um) at the level of the RPE or Deep retina typically In a PERIFOVEAL location. THIS SPOTS are TRANSITORY and ARE FREQUENTLY MISSED they leave instead a GRANULAR PIGMENTARY CHANGE ----A PATHOGNOMONIC FINDING Vitritis…MAYBE CNV..NOT USUALLY but it can happen
- FA reveals characteristic punctate hyperfluorescent lesions in a wreathlike configuration surrounding the fovea that stain late (Fig 6-47). ICG angiography shows multiple hy- pofluorescent lesions that are more numerous than those seen on clinical examination or FA and that typically fade with resolution of the disease (Fig 6-48) . Visual field abnormalities are variable and include generalized depression, paracentral or peripheral scotomata, and enlargement of the blind spot. The ERG reveals diminished a-wave and early receptor potential (ERP) amplitudes, both of which are reversible. The multifocal ERG (mfERG) and electro-oculogram (EOG) localize the disease process to the RPE-photoreceptor complex rather than to the choroid. FAF;;;meh IMT not usually coz the course is usually benign. And they don’t get vitritis hence no CME, CATRACT, or ERM so the prognosis is excellent with visual recovery at 2-10 weeks without treatment. But residual symptoms may occur.
- Here is the xmas wreath pattern I was talking about
- ICG of Mewds
- The recent demonstration of abnormal photoreceptor inner outer segment junction reflectivity on Spectral-domain optical coherence tomogra- phy (SD-OCT) and its correspondence with hypofluorescent spots visualized on ICG angiography and changes in microperimetry sensitivity fFURTHER supports the localization of the disease process to the RPE-photoreceptor complex, as these abnormalities completely resolve during the course of the disease.
- CLUE1: NOT a white dot Syndrome CLUE 2 Diffuse non Necrotizing Granulomatous PANUVEITIS CLUE 3 PHOTOPHOBIA 67% Decrease in accomodation (13%) Dalen Fuchs
- Could be anything but the patient had VZV
- Subretinal fibrosis and uveitis syndrome is an EXTREMELY UNCOMMON panuveitis of unknown etiology affecting otherwise healthy myopic women between the ages of 14 and 34 years. But when it occurs, it is usually DEVASTATING.. With Serous neurosensory retinal detachment, CME, and CNV as Sequel.
- Acute zonal occult outer retinopathy (AZOOR) is typified by acute LOSS OF 1 OR MORE ZONES OF OUTER RETINAL FUNCTION associated with photopsia, MINIMAL funduscopic changes, and abnormal ERG findings; Patients are typically young, myopic women who present with acute unilateral visual disturbances with mild vitritis in 50% of the, APPARENTLY NORMAL FUNDOSCOPIC EXAM’N AND VA in 20/40 range and they rarely get CNV. ERG shows pattern of dysfunction to the Photoreceptor-RPE complex and inner retina HAVING DLAYED 30HZ Flicker ERG and reduction in EOG light rise. Results of Micro ERG shows decreased respose from the Blindspot and other VF defects with corresponding loss of INNER and OUTER segment on OCT. That is the picture on (D)w/c OCT shows defects in INNER/OUTER segment FA in this case is not helpful in DX since it shows HYPER, HYPO and window defects corresponding to zones of RPE derangements. FAF (PICTURE) MAYBE useful in observing patietns (HYPO-AF for the atrophied choriocapillary and HYPER-AF seen at the BORDER of the expanding lesion. MAJORITY of patients develop bilateral disease and recurrence in 1/3 of patients. VF dfects usually stabilizes in three-quarters of patients. Cancer associated Retinopathy and Retinitis Pigmentosa should be apart of the Differentials of AzooR. IT is unclear whether Corticosteroids or IMT alters the disease.