Thinning Of Inner Nuclear Layer Research Articles

PARACENTRAL ACUTE MIDDLE MACULOPATHY AND HENLE FIBER LAYER HEMORRHAGE IN DENGUE FEVER: MULTIMODAL IMAGING AND REVIEW OF THE LITERATURE.

To use multimodal imaging to report a case of dengue fever presenting with Henle fiber layer hemorrhage (HH) and acute paracentral acute middle maculopathy (PAMM). Fundus photography and autofluorescence, fluorescein angiography, and optical coherence tomography (OCT) were acquired over a month, and a literature review of dengue fever-associated maculopathy was performed. A 19-year-old man presented with a sudden loss of vision in both eyes 12 days after experiencing initial systemic symptoms suggestive of dengue fever. His best-corrected visual acuity (BCVA) was counting fingers in the right eye (OD) and 20/200 in the left eye (OS). Pupillary light reflex was reduced in both eyes (OU). Dilated fundoscopic examination revealed optic disc swelling and a small deep hemorrhage near the fovea in OU. OCT revealed a petaloid shape hyperreflectivity involving both outer nuclear and plexiform layers in OU and a subtle hyperreflectivity thinning the inner nuclear layer (INL) in OS, findings compatible with HH and PAMM, respectively. Immunoglobin M was positive for dengue fever. Thus, a diagnosis of dengue fever-associated maculopathy was performed and oral steroids were started. After a month, the final BCVA reached 20/25 (OD) and 20/20 (OS), the HH reabsorbed utterly, and a INL thinning in the area of the PAAM was observed. Dengue fever-associated maculopathy can present with PAAM and HH. Multimodal imaging is helpful to characterize the extension of the changes in the retina and to monitor its recovery. In such cases, structural and functional damage may occur despite treatment with oral steroids.

Altered Elastin Turnover, Immune Response, and Age-Related Retinal Thinning in a Transgenic Mouse Model With RPE-Specific HTRA1 Overexpression.

A single-nucleotide polymorphism in HTRA1 has been linked to age-related macular degeneration (AMD). Here we investigated the potential links between age-related retinal changes, elastin turnover, elastin autoantibody production, and complement C3 deposition in a mouse model with RPE-specific human HTRA1 overexpression. HTRA1 transgenic mice and age-matched CD1 wild-type mice were analyzed at 6 weeks and 4, 6, and 12 to 14months of age using in vivo retinal imaging by optical coherence tomography (OCT) and fundus photography, as well as molecular readouts, focusing on elastin and elastin-derived peptide quantification, antielastin autoantibody, and total Ig antibody measurements and immunohistochemistry to examine elastin, IgG, and C3 protein levels in retinal sections. OCT imaging indicated thinning of inner nuclear layer as an early phenotype in HTRA1 mice, followed by age and age/genotype-related thinning of the photoreceptor layer, RPE, and total retina. HTRA1 mice exhibited reduced elastin protein levels in the RPE/choroid and increased elastin breakdown products in the retina and serum. A corresponding age-dependent increase of serum antielastin IgG and IgM autoantibodies and total Ig antibody levels was observed. In the RPE/choroid, these changes were associated with an age-related increase of IgG and C3 deposition. Our results confirm that RPE-specific overexpression of human HTRA1 induces certain AMD-like phenotypes in mice. This includes altered elastin turnover, immune response, and complement deposition in the RPE/choroid in addition to age-related outer retinal and photoreceptor layer thinning. The identification of elastin-derived peptides and corresponding antielastin autoantibodies, together with increased C3 deposition in the RPE/choroid, provides a rationale for an overactive complement system in AMD irrespective of the underlying genetic risk.

Paracentral Acute Middle Maculopathy Mimicking Retrobulbar Optic Neuropathy

A 70-year-old woman presented with acute awareness of decreased color vision in her right eye. Fundus examination and a flash electroretinography (ERG) were both normal. A multifocal ERG (mfERG) however revealed foveal depression, and thinning of inner nuclear layer was noted on macular optical coherence tomography (OCT), and a diagnosis of resolved paracentral acute middle maculopathy was made. Clinicians should be aware of the complementary role of OCT and mfERG in unexplained acute central visual loss to distinguish retinal from neuro-ophthalmic etiologies. Structural ocular imaging with OCT shows features of inner, middle, and outer retinal localizations to the visual loss.

Longitudinal follow-up of two patients with isolated paracentral acute middle maculopathy.

Objective: To describe longitudinal retinal changes in two cases of isolated paracentral acute middle maculopathy (PAMM).Case series: We reported two cases (64 and 67-year-old men) with isolated PAMM, who were followed-up for over 5 and 2.5 years, respectively. Both cases exhibited similar clinical natural histories. The first examinations took place several days after onset, with funduscopy showing that both cases exhibited paracentral scotoma with good visual acuity and small gray lesions, while optical coherence tomography (OCT) showed the presence of a hyperreflective band that ranged from the inner plexiform layer to the outer plexiform layer (OPL). The lesions became unremarkable within 1 month. The hyperreflective band also became unremarkable and was limited to the inner nuclear layer (INL) within 1 month, with the band disappearing within several months. Subsequently, OCT showed there was a thin and irregular INL and OPL, an excavated change of the inner retinal surface, along with outer nuclear layer (ONL) thickening. After several years, OCT angiography demonstrated normal flow of macular capillaries in the superficial capillary plexus, and decreased flow in the lesion with dilation of the capillaries around the area in the deep capillary plexus (DCP). Focal serous retinal detachment (SRD) occurred in one case after 4–5 years.Conclusion: Our findings indicated that long-term retinal changes in PAMM resulted in excavation of the inner retinal surface, INL thinning, ONL thickening and abnormal vasculature, especially in the DCP. Focal SRD may be a rare complication that can present at 4 years after onset.