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Optic Atrophy and Altitudinal Visual Field Loss

Optic Atrophy and Altitudinal Visual Field Loss. Keith Tyhurst and Heather Weber University Eye Center Grand Rounds July 21, 2005. B.B. 69 year-old AA Female Presented to the EHMS clinic for her scheduled 6 month DFE and IOP check Also needed a HVF and an OCT. Some background information.

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Optic Atrophy and Altitudinal Visual Field Loss

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  1. Optic Atrophy and Altitudinal Visual Field Loss Keith Tyhurst and Heather Weber University Eye Center Grand Rounds July 21, 2005

  2. B.B. • 69 year-old AA Female • Presented to the EHMS clinic for her scheduled 6 month DFE and IOP check • Also needed a HVF and an OCT

  3. Some background information • Previous history of optic atrophy, chorioretinal scar, and perimacular drusen in the OD • Has been seen at the UEC since 1994 • Does not wear an Rx and uses OTC readers for reading

  4. Medical History • Significant for HTN and Arthritis • Takes Verapamil and Triamterene

  5. Ocular History • Possible ocular trauma from a car accident 17 years ago • B.B. reports that she received no medical attention after the accident • Does not remember hitting her head on either the seat and windshield • Cannot remember any other instances of ocular trauma

  6. Work-up • Visual acuity: OD 20/30-2 OS 20/25-2 • Refracted 2-16-05 and 3-1-05 • OD: +0.75 20/25 (saw 20/20 on 3/1 with the same lens) • OS: +1.25 -1.25 x 0 20/20 (balance found +1.50, no mention of VA through this lens • Confrontation: Constricted Inferior OD and OS with the OD>OS • Pupils: PERRL OD, OS with (-)APD • Pachymetry: 545 OD, 552 OS

  7. Slit Lamp Exam • Findings unremarkable OU • Anterior Chamber Deep and Quiet OU • NS cataract 1+ OU • IOP 18 OU at 8:43 A.M. • Gonioscopy (2-16-04): Steep insertion, CB visible with mild pigmentation temporally and significant pigment in all other quadrants OU

  8. OS OS

  9. Dilation OS • ONH: 0.4/0.4 (s 0.3, i 0.3) Good color and distinct margins • No change from previous ONH photos (11/05/03) • Macula: normal • Periphery: not assessed • Previous artery attenuation and venustortuositynoted

  10. Chorioretinal scar OD

  11. Fundus Photos From XX/XX/XXOD OD

  12. Dilation OD • ONH: 0.7/0.7 (s 0.3, i 0.1) with superior temporal rim pallor and peripapillary atrophy temporally • No hemorrhages at or around the disk • No change from previous ONH photos (11/05/03) • Macula: 3 perimacular hard drusen normal • Old circumferential linear chorioretinal scar with no CNV and no change from previous photos • Periphery: not assessed

  13. Flow Sheet for OD and OS

  14. 10-21-03

  15. 12-01-03

  16. 7-6-05

  17. 7-6-05

  18. OCT 7-6-05

  19. NFL

  20. The plot thickens….. • What explains the appearance of the OD optic nerve? • Cupping • Pallor of the cup and rim • Peripapillary atrophy • What makes up our DDx?

  21. Glaucoma Anterior ION Posterior ION Traumatic optic neuropathy Cataract Space occupying lesion in anterior visual pathway Hereditary optic neuropathies (Leber’s and autosomal dominant) Congenital optic disc anomalies: coloboma, pits, hypoplasia Compression from fusiform aneurysms of the intracranial carotid arteries Syphilis Methanol Poisoning Radiation Optic Neuropathy Audience Participation Time:Our comprehensive DDx list

  22. Ruling out DDx • Most can be ruled out via a good history • So, are the cataracts causing the VF defects? • No, VF would show depressed pattern deviation • What about a space occupying lesion? • No,VF defect has never progressed over the last 2 years so the chance of a non growing lesion is very remote • Since VF has not changed, should we order an MRI or CT? • No, not cost effective for B.B.

  23. What about glaucoma in the OD, OS, or both? • Thoughts? • Not such any easy decision as the others • Hold on for our opinion

  24. Glaucoma • Mark Kahrhoff had an excellent talk on glaucoma at the June Grand Rounds • Consequently, I’ll try not to repeat much of what he previously discussed

  25. Glaucoma • Glaucoma essentially begins with sectoral NFL loss that is revealed by nerve fiber analyzer and later by a VF machine. • Over time, the glaucoma begins to cause: • A vertical or concentric enlargement of the cup • A focal notch • Deepening of the cup along the z axis

  26. NFL Anatomy

  27. 7-6-05

  28. 7-6-05

  29. Useful Glaucoma Tips • Always establish the rate of progression of field loss • The faster the change, the more urgent need for treatment • Progression of peripapillary atrophy is a red flag for glaucoma • Indicates progressive RPE loss and optic atrophy

  30. Why might B.B. have glaucoma? • Asymmetric cups • 0.7 to 0.4 • Increasing CD’s since 1994 • Used to be 0.25(?) now 0.7 • Possible IOP increase over the last year • History of trauma might have damaged the nerve and increased susceptibility to glaucomatous change • Possible nasal step in the left eye • Peripapillary atrophy

  31. Why might B.B. not have glaucoma? • No progression on VF over the last 2 years • The ONH appearance matches the fundus photos from 11/05/03 • Change analysis shows slight improvement in the PSD OU • Changes might be consistent with previous ION

  32. Ischemic Optic Neuropathy (ION) • Optic nerve disease of sudden onset • Results in variable vision and visual field loss • Classified into two types: • Nonarteritic ION • Arteritic ION

  33. Nonarteritic ION Age = 45-65 Min. to severe visual loss Swollen disc that is often segmental MHx of Hypertension in ~50% ESR up to 40 No response to steroids Arteritic ION Age = 65+ Severe visual dysfunction Swollen disc, normal disc, or central artery occlusion MHx = malaise, weight loss, fever, polymyalgia, head pain ESR = 50-120 Return of vision with use of steroids NAION vs. AION

  34. Nonarteritic ION • Infarction of the anterior portion of the optic nerve • Affects the prelaminar portion of the optic disc and creates an imbalance in the pressure-perfusion ratio • Occlusion or partial occlusion of the short posterior ciliary arteries is confirmed by FA • Optic nerve is normally protected from vascular non-perfusion by watershed zones • Some gaps exist in the boundaries of the zones, which explains sectoral disc involvement

  35. Nonarteritic ION • Disc signs: • Isolated sectoral edema to entire disc edema • Linear flame-shaped hemorrhages can occur on the disc margin but disappear in 3-5 weeks • After acute activity subsides optic atrophy will appear in about 3 months

  36. NAION vs. Glaucoma • Glaucoma also has a pressure-perfusion ratio alteration, but over a long period of time • Any patient with chronically lowered pressure-perfusion ratio is at greater risk for developing ION • However, it’s hard to determine if there was a mild glaucoma already present before the ION occurred • Both are characterized by loss of retinal ganglion cells and their axons • RGCs die by apoptosis in both cases

  37. NAION vs. Glaucoma • Distinguishing features: • Onset (NAION = fast onset of vision loss, usually upon awakening) • Intensity: NAION is a more intense, acute onset ischemic event • Duration of damage: field loss usually occurs within 2-3 days of the ION

  38. Cupping and ION • Infarction destroys neural tissue and connective tissue which may lessen support for the disc • Retrolaminar optic nerve can infarct and become fibrotic • This can lead to backward traction on the lamina cribrosa and maximal cupping at 4 months post-AION • Loss of neural tissue and ischemic insults to the lamina may contribute to its weakening

  39. Cupping and NAION • Excavation of the disc may occur secondary to NAION • Loss of rim tissue is diffuse (no notching or focal obliteration of the rim) • Cupping always occurs after the presentation of atrophy • In glaucoma, the cupping precedes the atrophy • Cupping as a result of end-stage AION has been reported more consistently than cupping due to NAION

  40. Cupping and NAION • Retrospective study by Helen, Danesh-Meyer, Savino, and Sergott: The Prevalance of Cupping in End-stage Arteritic and Nonarteritic Anterior Ischemic Optic Neuropathy Ophth. Vol. 108, Number 3, March 2001 • Only 3 of 113 eyes with NAION were shown to have cupping • Discs were typically described as having segmental or diffuse disc pallor • Cupping was identified in 85 of 92 eyes with AION

  41. Cupping and NAION • Orgul et al has reported one case with photos before and after the AION showing definite cupping afterwards • Quigley and Anderson found that 6 of 61 eyes diagnosed with NAION developed cupping similar to glaucoma • However, they raised the issue that some of those in the study (esp. with AIONs) may have had underlying glaucoma

  42. Cupping and Glaucoma • Loss of neuroretinal rim area • Often focal or notched loss of rim tissue • Increase in the absolute size of the optic cup and in the C/D ratio • Vertical elongation of the cup • Excavation of the lamina cribrosa • Enlarged Chorioretinal atrophy • Asymmetry of these findings between the two eyes • Peripapillary atrophy

  43. Pallor • Location and degree of pallor can be a very useful feature when trying to distinguish between glaucomatous cupping and ION cupping • Pallor of glaucomatous nerves usually does not extend beyond the area of the cup • Pallor of NAION nerves can extend into the neuroretinal rim • NAION nerve pallor is usually more profound than glaucomatous cups • Problems with pallor observation: • With advanced cupping, pallor can no longer be a differentiating sign • Rim pallor may be very subtle even when there is neuroretinal rim intact

  44. Fields -- NAION • Usually maximal at onset, but can deteriorate for 2-3 days • Often sudden onset of altitudinal defect • Consistent with the termination of the NFL at the horizontal raphe • Usually inferior • Improvement is distinctly rare

  45. Afferent Pupillary Defects • Relative APDs are caused by an incomplete optic nerve lesion or severe retinal disease • Normal afferent visual function may be evident even when pallor is present • No APD was found previously upon testing with a BIO http://www.mrcophth.com/eyeclipartchua/pupils.html

  46. Conclusions • B.B. remains a glaucoma suspect but does not yet appear to have glaucoma • Whether the cupping is due to the previous ION or due to glaucoma, she needs to be followed closely for changes • Continue to monitor IOP, VF, and ONH every 6 months

  47. References • Danesh-Meyer, H. et. al. (March 2001) The Prevalence of Cupping in End-stage Arteritis and Nonarteritic Anterior Ischemic Optic Neuropathy. Ophthalmology. Vol. 108(3): 593-597. • Duane, TD., ed. (1982). Clinical Ophthalmology. Vol. 2(26-31). Philadelphia: Harper & Row. • Jakobiec, F. and Y. Shiuey. (Winter 2001) Neuro-Ophthalmology: A Subspecialty Perspective. International Ophthalmology Clinics. Vol. 41(1): 139-146. • Kanski, J. Clinical Ophthalmology. Figure 9.24. Page 202.

  48. References (Con’t) • Quigley, H. and DR Anderson. (Sep-Oct. 1977) Cupping of the Optic Disc in Ischemic Optic Neuropathy. Trans Sect Ophthalmol American Academy of Ophthalmology and Otolaryngology. Vol. 83(5): 755-762. • Roodhooft, JMJ. (2003). Nonglaucomatous Optic Disc Atrophy and Excavation in the Elderly. Bull. Soc. Belge Ophthalmol. Vol 287: 45-49. • Sowka, J. and A. Kabat. (2000, Nov. 15). Six Signs to Tracing Visual Field Loss. Retrieved July 19, 2005, from http://www.revoptom.com.archive/FEATURES/RO1100f8sixsigns.htm

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