Abstract 99. Jahrestagung der DOG, 29. 9. - 2. 10. 01 im ICC, Berlin

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Impressum



Retrobulbar Optic Neuritis with Atypical Visual Field Defect

Juvan V., Juhn-Juvan I.

Eye Department, General Hospital, Meštroviceva b.b., HR 42000 Varaždin, Croatia

Introduction: A case of retrobulbar optic neuritis with slight reduction of visual acuity and monocular, predominantly nasal hemianopsia is described. The visual field defect has gradually improved during the course of the disease on corticosteroid therapy up to complete recovery, as documented by perimetry. Pattern VEP exhibited prolonged P1 latency, thus speaking in favour of MS pathology. To our knowledge such a visual field defect is atypical and rare in retrobulbar optic neuritis.
Case report: The patient complained about a nasal half-field visual defect and visual acuity reduction in the left eye. Right eye had no symptoms. Slight visual acuity reduction to 0,7 in the left eye was found, fundi and IOP were normal bilaterally. On automated perimetry (Octopus 1-2-3, G1) arcuate visual field defects in the left eye were found which were nasally much more pronounced, up to absolute scotoma, with rather clear vertical demarcation towards the rest of the visual field. Perimetry of the other eye showed only few small relative scotomas. Echography showed double countured affected optic nerve on B-scan, biometry did not exhibit any significant interocular difference. Pattern VEP, performed during therapy, exhibited bilaterally significant prolongation of P1 latency (RE 115,2 ms, LE 120,0 ms) and reduced amplitudes in the left eye. On administration of high doses of corticosteroids an improvement up to complete normalisation of visual field was achieved. NMR examination confirmed the hypothesis about MS being the cause of the disease.
Discussion: It is known that visual field defects in retrobulbar neuritis are mostly central, centrocecal, occasionally with peripheral constriction, rerely arcuate and exceptionally hemianoptic. Finally differential diagnosis with respect to ischemic, compressive and toxic opticoneuropathies is briefly discussed.



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