Abstract
Leber’s hereditary optic neuropathy (LHON) is typically characterized by vascular alterations in the acute phase. The aim of this study was to evaluate choroidal changes occurring in asymptomatic, acute and chronic stages of LHON. We enrolled 49 patients with LHON, 19 with Dominant Optic Atrophy (DOA) and 22 healthy controls. Spectral Domain-Optical Coherence Tomography (SD-OCT) scans of macular and peripapillary regions were performed in all subjects, to evaluate macular and peripapillary choroidal thickness, and retinal nerve fiber layer (RNFL) thicknes. Macular and peripapillary choroidal thicknesses were significantly increased in the acute LHON stage. On the contrary, macular choroidal thickness was significantly reduced in the chronic stage. Furthermore, peripapillary choroidal thickness was decreased in chronic LHON and in DOA. Both RNFL and choroid had the same trend (increased thickness, followed by thinning), but RNFL changes preceded those affecting the choroid. In conclusion, our study quantitatively demonstrated the involvement of the choroid in LHON pathology. The increase in choroidal thickness is a feature of the LHON acute stage, which follows the thickening of RNFL. Conversely, thinning of the choroid is the common outcome in chronic LHON and in DOA.
Highlights
Leber’s hereditary optic neuropathy (LHON) is typically characterized by vascular alterations in the acute phase
Leber’s Hereditary Optic Neuropathy (LHON) and Dominant Optic Atrophy (DOA) are both caused by mitochondrial dysfunction and are characterized by tissue selectivity, usually limited to damaging the retinal ganglion cells (RGCs) and their axons in the optic nerve[1,2,3,4]
We evaluated macular and peripapillary choroidal thickness in LHON patients
Summary
Leber’s hereditary optic neuropathy (LHON) is typically characterized by vascular alterations in the acute phase. The aim of this study was to evaluate choroidal changes occurring in asymptomatic, acute and chronic stages of LHON. Macular and peripapillary choroidal thicknesses were significantly increased in the acute LHON stage. Peripapillary choroidal thickness was decreased in chronic LHON and in DOA Both RNFL and choroid had the same trend (increased thickness, followed by thinning), but RNFL changes preceded those affecting the choroid. The increase in choroidal thickness is a feature of the LHON acute stage, which follows the thickening of RNFL. Leber’s Hereditary Optic Neuropathy (LHON) and Dominant Optic Atrophy (DOA) are both caused by mitochondrial dysfunction and are characterized by tissue selectivity, usually limited to damaging the retinal ganglion cells (RGCs) and their axons in the optic nerve[1,2,3,4]. The question arises, is there a primary micro-vascular disorder in LHON?
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