Compressive optic neuropathy with a structural abnormality detected prior to functional impairment: Photo essay

Compressive optic neuropathy (CON) is induced by any intrinsic or extrinsic compressive lesion affecting the optic nerve.[1,2] In CON, as conduction block caused by mass effect occurs earlier than retrograde degeneration, functional impairment generally precedes structural abnormalities.[1] Case Report Discussion A 10-year-old girl was referred to the ophthalmology department for vision-related examination. Magnetic resonance imaging (MRI) for a precocious puberty examination revealed a compressive brain tumor spreading across the optic chiasm and right optic tract [Fig. 1]. She had no subjective vision-related symptoms. Visual acuity was 20/16 in both eyes, and pupillary light reflexes appeared normal without relative afferent pupillary defects. Goldmann kinetic perimetry revealed neither decreased sensitivity nor scotoma in either eye [Fig. 2a and b]. Slit-lamp examination showed normal anterior and posterior segments in bilateral eyes [Fig. 3a and b]. The thinning pattern on optical coherence tomography (OCT) indicated preferential atrophy of the horizontal peripapillary retinal nerve fiber layer sectors in both eyes [Fig. 4a and b]. Conversely, diffuse thinning was evident in the macular ganglion cell complex layer of the nasal and temporal hemifield retinal regions in the right eye, and the hemi-nasal area was predominantly damaged in the left eye [Fig. 4c-f]. OCT observations were consistent with MRI findings affecting the optic chiasm and right optic tract; however, no obvious visual functional impairment were noted.[3,4] We plan to monitor her visual function regularly.Figure 1: Cranial MRI on the patient’s first visit. (a) T2-weighted non-enhancement MRI of the head (coronal view) reveals a high-intensity lesion in the optic chiasm, predominantly on the right side (white circle). (b) T2-weighted unenhanced MRI of the head (axial view) shows a high-intensity lesion in the right optic tract (white circle). MRI = magnetic resonance imaging.Figure 2: Visual field examination results on the patient’s first visit. (a and b) Results of Goldmann kinetic perimetry show neither decreased sensitivity nor scotoma in either eyeFigure 3: Fundus imaging on the patient’s first visit. (a and b) Fundus images show no abnormal findings in either eyeFigure 4: OCT of the optic nerve head circumference and macular area on the patient’s first visit. Temporal-superior-nasal-inferior-temporal graphs provide a profile of pRNFL thickness (a and b). The thinning pattern indicates preferential atrophy of the horizontal sectors of the pRNFL in both eyes (a and b; black arrows). Thickness maps show diffuse thinning of the mGCC in both eyes (c and d). In the deviation map, diffuse thinning is observed in both nasal and temporal hemifield retinas of the right eye, and the hemi-nasal area is predominantly damaged in the left eye (e and f; black circles). OCT = optical coherence tomography, pRNFL = peripapillary retinal nerve fiber layer, mGCC = macular ganglion cell complex layerConclusion Structural abnormality was detected prior to functional impairment, contrary to conventional theory. Although surviving axons and ganglion cells may compensate for the functional loss, the underlying mechanism has not been clarified.[2] Since postoperative prognosis is related to the degree of structural damage, early diagnosis is important for visual function.[5] When structural abnormalities are noted on OCT, ophthalmologists should consider CON, even without functional impairment. Authors’ contributions S.K. and T.M. participated in concepts, design, literature search, data acquisition, manuscript preparation, manuscript editing, and manuscript review. In addition, T.M. is the guarantor of this report. Y.K. and K.N. participated in design, manuscript editing, and manuscript review. All authors consented to their names being published in this report and insist on the intellectual honesty and validity of the data provided. All authors read and approved the final version of the paper. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship: Nil. Conflicts of interest: There are no conflicts of interest.