Case report: OCT aids in diagnosis of band optic atrophy
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Band optic atrophy is described as a horizontal band of optic disc pallor, often associated with a contralateral optic tract lesion and bilateral hemianopic visual field defects.
Relative afferent pupillary defect of the eye with the temporal visual field defect helps localize the lesion to the contralateral optic tract. Band optic atrophy (BOA) has several known causes: ischemia, demyelination, arteriovenous malformation, tumor, trauma, iatrogenic and idiopathic.
OCT previously has been used to document retrograde axonal loss of retinal nerve fiber layer (RNFL) thickness secondary to BOA. Further BOA OCT studies have expanded to document retrograde macular and retinal ganglion cell layer (GCL) thinning (Costa-Cunha et al., Nakamura et al., Monteiro et al., Zehnder et al.).
A case of BOA retrograde axonal degeneration, documented with OCT, with RNFL and GCL loss follows.
A 56-year-old Black man presented for a diabetic eye examination. He reported a history of diabetes mellitus, hypertension and an ischemic stroke 4 years earlier. Visual acuity was 6/6 OD and 6/6 OS. Pupils were equal, round and reactive to light with a 1+ afferent pupil defect of the left pupil. Extraocular motilities were within normal limits.
Confrontation visual fields suggested left-sided hemianopic visual field defects, which were confirmed with threshold perimetry testing. IOPs were within normal limits. Dilated fundus examination revealed mild superior temporal and inferior temporal atrophy of the right optic nerve and mild BOA of the left optic nerve. OCT testing confirmed RNFL thinning of both optic nerves consistent with the clinical examination, and GCL thickness showed bilateral hemi-atrophy secondary to retrograde degeneration correlating perfectly to the patient’s bilateral visual field defects. Review of the patient’s magnetic resonance imaging confirmed a right optic tract lesion.
Because the nasal retinal fibers serve the temporal visual field and cross in the chiasm to the contralateral optic tract, a contralateral optic tract lesion can produce an afferent pupillary defect in the eye with the temporal visual field defect in patients with hemianopic visual field defects due to the nasal-temporal visual field size difference. This is because the temporal visual field is approximately 60% to 70% larger than the nasal field (Newman et al., Galvez-Ruiz et al.)
Optic tract lesions can also cause retrograde degeneration of the nasal and temporal RNFL in the contralateral eye due to the same nasal retinal fibers crossing at the optic chiasm into the contralateral optic tract. Interestingly, this same optic tract lesion could also cause superior and inferior RNFL loss in the ipsilateral eye resulting from temporal retinal fibers remaining ipsilateral through the optic chiasm into the optic tract. This results in the predominantly nasal and temporal atrophy (ie, BOA) noted in the contralateral optic nerve and predominantly superior and inferior atrophy in the ipsilateral optic nerve owing to retrograde degeneration, which can be measured with OCT after approximately 6 weeks.
Thinning of RNFL and GCL can correlate well with the homonymous hemianopic visual field defects found in patients with optic tract lesions. This case shows the usefulness of OCT technology in helping to identify and pinpoint the likely location of visual pathway lesions when used in conjunction with clinical findings and correlating with other diagnostic testing.
References:
- Costa-Cunha LVF, et al. Am J Ophthalmol. 2009;doi:10.1016/j.ajo.2008.07.020.
- Galvez-Ruiz A, et al. Saudi J Ophthalmol. 2013;doi:10.1016/j.sjopt.2012.12.001.
- Kanamori A, et al. Ophthalmology. 2004;doi:10.1016/j.ophtha.2004.05.035.
- Monteiro MLR, et al. Am J Ophthalmol. 2007;doi:10.1016/j.ajo.2006.11.054.
- Monteiro MLR, et al. Eye (Lond). 2007;doi:10.1038/sj.eye.6702182.
- Monteiro MLR, et al. Invest Ophthalmol Vis Sci. 2014;doi:10.1167/iovs.14-14118.
- Nakamura M, et al. Graefes Arch Clin Exp Ophthalmol. 2012;doi:10.1007/s00417-012-2095-4.
- Newman SA, et al. Arch Ophthalmol. 1983;doi:10.1001/archopht.1983.01040020243018.
- Zehnder S, et al. J Neuroophthalmol. 2018;doi:10.1097/WNO.0000000000000589.
For more information:
Christopher J. Borgman, OD, FAAO, practices in the Advanced Care Ocular Disease Service at the Southern College of Optometry in Memphis, Tenn. He can be reached at cborgman@sco.edu.
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