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Year : 2022  |  Volume : 2  |  Issue : 2  |  Page : 472

Commentary: Enigma of foveolar hyper-reflective track in photic retinopathy

Department of Vitreo Retina, Netralaya Super Speciality Eye Hospital, Ahmedabad, Gujarat, India

Date of Web Publication13-Apr-2022

Correspondence Address:
Kushal Delhiwala
Netralaya Superspeciality Eye Hospital, KD House, 1st Floor, Above Andhra Bank, Parimal Cross Roads, Ellisbridge, Ahmedabad - 380 006, Gujarat
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijo.IJO_3134_21

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How to cite this article:
Delhiwala K, Khamar B. Commentary: Enigma of foveolar hyper-reflective track in photic retinopathy. Indian J Ophthalmol Case Rep 2022;2:472

How to cite this URL:
Delhiwala K, Khamar B. Commentary: Enigma of foveolar hyper-reflective track in photic retinopathy. Indian J Ophthalmol Case Rep [serial online] 2022 [cited 2022 May 18];2:472. Available from: https://www.ijoreports.in/text.asp?2022/2/2/472/342992

Photic retinopathy is known to be associated with unprotected and extended exposure to light from solar radiation, gas arc welding, lasers, and even medical imaging devices of the retina. Wavelengths of light from these sources vary from near-infrared to ultraviolet spectrum (UV-B). It is more often seen in children and young adults as a clear lens allows unfiltered passage of this light spectrum toward the retina. Photic retinopathy predominantly results from photochemical damage in the outer retina at the level of the retinal pigment epithelium (RPE) and photoreceptors (PR) with minor contributions from thermal and mechanical damage. Optical coherence tomography (OCT) in eyes with photic retinopathy generally shows subfoveal interruption in hyperreflective bands of the outer retina corresponding to ellipsoid zone (EZ) and an external limiting membrane (ELM). En-face OCT imaging also demonstrates an area of EZ alteration following photic injury and serial changes associated with its regeneration during healing.[1] Authors in the current issue of the Indian Journal of Ophthalmology - Case Reportsy (IJO) have described a vertical hyperreflective track (HRT) extending from outer to inner retinal layers at the center of fovea as an OCT biomarker in eyes with acute photic retinopathy which resolved with treatment and was associated with clinical improvement.[2] This unique finding has been reported previously, which also showed resolution and improved visual acuity.[1],[3] This finding so far has been attributed to 1) inflammatory cell accumulation secondary to chemokine upregulation following light exposure and breakdown of the blood–retinal barrier;[3] 2) possible early edema of Henle fibers as hyperreflective bands reported to follow Henle fibers' arrangement;[2] and 3) light-induced photocoagulation of retinal proteins.[3] Authors in the current issue of IJO postulate that HRT can be due to a sudden increased concentration of energy at the level of RPE and PR leading to conduction of high-intensity microcurrents through the retinal layers at the fovea.[2]

Precise location and configuration of described HRT correspond to foveola which contains only densely packed cone photoreceptors interleaved with vertically oriented Muller cells, which form inverted cone-shaped zone in the inner third of foveola (MCC).[4] Muller cells have been suggested to have optical fiber characteristics, guiding the light toward the photoreceptors.[5] They also provide structural stabilization to retinal tissue, with MCC keeping cone cells together at foveola. Muller cells also play a role in fluid homeostasis and modulation of the inflammatory response following retinal injury.[5]

The probable explanation for HRT appearance and its subsequent resolution may be attributed to

  1. Disturbed arrangement of Muller cells as a sequela to photic injury and its rearrangement over time.
  2. Extension of inflammation to Muller cells following photic damage to photoreceptor and RPE and its resolution over time. Muller cell stimulation leads to the upregulation of inflammatory mediators along with activation of macrophages and other microglia at the site of injury.
  3. Reactive gliosis following photic injury to protect the retinal tissue and promote repair and remodeling followed by reorganization. This is associated with upregulation and increased expression of intermediate filaments in Muller cells.
  4. Loss of focal RPE pump function leading to disturbed fluid homeostasis and accumulation of metabolic waste locally, which recovers over time.

Intraretinal changes associated with the aforementioned possible pathomechanisms show hyperreflectivity on OCT scans in various other retinal diseases as well.

Though various possible explanations are enumerated above, photochemical damage to Muller cells in the region of foveola seems to be more likely as foveola contains only cones and Muller cells. Muller cells are known to be associated with regenerative responses.

Moreover, serial en-face OCT imaging within the area of HRT at frequent intervals, particularly in the acute stage of photic retinopathy, may also provide better insight into its natural course and pathomechanisms.

  References Top

Gunzinger JM, Fasler K, Barthelmes D, Maloca P, Hasler PW, Böni C, et al. En face optical coherence tomography imaging ellipsoid zone regeneration in laser-induced and solar maculopathies. Case Rep Ophthalmol Med 2019;2019:3849871. doi: 10.1155/2019/3849871.  Back to cited text no. 1
Sindal MD, Ratna B, Jose K. Hyper-reflective track as an imaging biomarker for clinical improvement in photic retinopathy. Indian J Ophthalmol Case Rep 2022;2:469-71.  Back to cited text no. 2
  [Full text]  
Bruè C, Mariotti C, De Franco E, Fisher Y, Guidotti JM, Giovannini A. Solar retinopathy: A multimodal analysis. Case Rep Ophthalmol Med 2013;2013:906920. doi: 10.1155/2013/906920.  Back to cited text no. 3
Tschulakow AV, Oltrup T, Bende T, Schmelzle S, Schraermeyer U. The anatomy of the foveola reinvestigated. PeerJ 2018;6:e4482. doi: 10.7717/peerj. 4482.  Back to cited text no. 4
Bringmann A, Wiedemann P. Müller glial cells in retinal disease. Ophthalmologica 2012;227:1-19. doi: 10.1159/000328979.  Back to cited text no. 5


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