Abstract Introduction Conjunctival melanoma is a rare but aggressive ocular surface malignancy associated with a high risk of local recurrence and metastasis. Adjuvant treatment may be required to improve local tumor control. In palpebral conjunctival tumors, stable fixation of a brachytherapy plaque can be technically challenging. Case Presentation We report a case of recurrent palpebral conjunctival melanoma in a 70-year-old man who presented with a painless palpable mass beneath the right upper eyelid at the site of the previously treated melanoma. In 2022, the patient had undergone surgical excision and adjuvant cryotherapy at another hospital. Clinical examination revealed a multilobulated lesion on the medial part of the right upper palpebral conjunctiva measuring approximately 1.5 cm. The tumor was treated with “no-touch” excision, adjuvant cryotherapy, amniotic membrane placement, and postoperative brachytherapy with a ruthenium-106 plaque. Stable plaque positioning was achieved using a sandwich technique to ensure adequate contact between the radioactive surface and the target tissue. The postoperative course was uneventful, and adjuvant topical treatment was prescribed. Conclusion This case highlights an organ-preserving multimodal approach in the management of recurrent palpebral conjunctival melanoma and introduces a distinctive sandwich fixation technique for ruthenium-106 plaque brachytherapy. The technique enabled stable plaque positioning and close contact with the target tissue while preserving eyelid anatomy and ocular surface integrity.
Background: Transient Smartphone Blindness (TSB) is a recently described phenomenon characterized by brief, monocular vision loss following unilateral smartphone use in a dark environment. It often mimics serious neurological and vascular emergencies, leading to extensive diagnostic investigations. Case Presentation: A 34-year-old female presented after two episodes of transient monocular vision loss and blurred vision in her right eye. The episodes occurred while she was lying on her side in bed, viewing her smartphone with one eye while the other was obscured. Initial neurological workup, including MRI, CT, and vascular imaging, was negative. She was initially prescribed aspirin for suspected amaurosis fugax. Subsequent ophthalmological evaluation and a detailed history confirmed a diagnosis of TSB. All clinical examinations, including OCT and visual field testing, were normal. Conclusions: TSB is a benign condition caused by asymmetric retinal light adaptation. This case highlights the importance of taking a detailed (postural) history in patients with transient monocular vision loss to avoid misdiagnosis.
Purpose: To report a 3-year ROI-based longitudinal follow-up of an nAMD-associated retinal pigment epithelium (RPE) tear using polarization-sensitive optical coherence tomography (PS-OCT)–derived polarimetric entropy (PE), with concurrent MP-3 microperimetry. Methods: A 75-year-old woman with an nAMD-related RPE tear was followed for 3 years. At baseline and follow-up visits, decimal best-corrected visual acuity (BCVA), structural OCT findings, en-face PE at the RPE level, and MP-3 retinal sensitivity were recorded. Two fixed regions of interest (ROIs; RPE tear ROI and RPE tear flap ROI) were defined at baseline and propagated across visits using image registration. Mean PE and mean MP-3 sensitivity (dB) were calculated within each ROI. Results: BCVA improved from 0.3 at baseline to 0.9 at 6 months and 1.0 at 1 year, then declined to 0.7 at 2 years and 0.6 at 3 years, when subretinal fluid (SRF) was present (anti-VEGF administered as needed). From baseline to 6 months, PE increased in both ROIs (RPE tear ROI: 0.085→0.193; RPE tear flap ROI: 0.413→0.543), and MP-3 sensitivity also increased (RPE tear ROI: 10.1→22.0 dB; RPE tear flap ROI: 14.0→19.7 dB). At 1 year, PE was 0.180/0.347 and MP-3 sensitivity was 22.2/17.2 dB in the RPE tear/RPE tear flap ROIs, respectively (BCVA 1.0). At the later SRF-positive visits, PE values were 0.182/0.350 at 2 years and 0.249/0.362 at 3 years, whereas MP-3 sensitivity decreased to 18.8/13.9 dB and 11.9/9.2 dB, respectively. Conclusion: PE increased during early follow-up and subsequently showed region-specific longitudinal changes within the RPE tear and RPE tear flap ROIs, while MP-3 sensitivity decreased at later visits associated with recurrent exudation. These findings suggest that PE may provide longitudinal structural information regarding RPE remodeling, with microperimetry providing complementary functional context.
Introduction We report a patient with type 1 diabetes in whom teprotumumab, an insulin-like growth factor-1 receptor (IGF-1R) inhibitor, produced a marked response in chorioretinal folds thought to be caused by active thyroid eye disease. Case Presentation The patient was a 73-year-old man. Although he improved after three courses of steroid pulse therapy at a previous hospital for active thyroid eye disease, which manifested as eyelid swelling and impaired ocular movement, the disease relapsed, with bilateral chorioretinal folds and decreased visual acuity in the left eye; therefore, teprotumumab was initiated. One week after treatment initiation, the chorioretinal folds in both eyes had resolved, and left-eye visual acuity had improved. Conclusion Although teprotumumab has been reported to be effective for proptosis and binocular diplopia caused by active thyroid eye disease, this case suggests that it may also be effective for active thyroid eye disease complicated by chorioretinal folds.
Background Optic nerve hypoplasia is a congenital developmental anomaly characterized by underdevelopment of the optic nerve and a reduced number of retinal ganglion cell axons. It may occur as an isolated ocular finding or within the septo-optic dysplasia spectrum. Although usually diagnosed in infancy or childhood, congenital optic nerve anomalies may remain undocumented until adulthood and can be difficult to distinguish from longstanding acquired optic atrophy. Case Presentation A 65-year-old man presented for ophthalmological evaluation during a medical disability board assessment. He reported poor vision in both eyes since early life, with subjective worsening over the previous 4–5 years. Best-corrected visual acuity was hand motions bilaterally. Intraocular pressure was 12 mmHg in both eyes, and no relative afferent pupillary defect was detected. Fundus examination showed bilateral pale, atrophic, and hypoplastic-appearing optic discs. The classic double-ring/double-edge sign was not clearly visible. The disc–macula distance/disc diameter ratio was 2.18 in the right eye and 2.00 in the left eye, values that were not clearly increased. Optical coherence tomography demonstrated bilateral retinal nerve fiber layer thinning, decreased foveal cup, and flattened umbo. No recordable response was obtained bilaterally during VEP testing. Cranial computed tomography showed empty sella. Endocrinological evaluation did not demonstrate pituitary hormone deficiency. Magnetic resonance imaging was not performed. Genetic testing for common primary Leber hereditary optic neuropathy mutations was negative; however, a homoplasmic mitochondrial cytochrome b region m.14896G>A variant was identified. Conclusion This case highlights the diagnostic difficulty of bilateral severe optic disc pallor with hypoplastic-atrophic appearance in an older adult. Although disc–macula ratios were not clearly increased, the lifelong history of poor vision, bilateral optic disc abnormalities, retinal nerve fiber layer thinning, abnormal foveal morphology, and absent VEP responses supported a severe bilateral optic pathway disorder with a possible congenital or developmental component. The absence of pituitary hormone deficiency and lack of documented midline brain malformation did not support definite septo-optic dysplasia. The mitochondrial cytochrome b m.14896G>A variant should be interpreted cautiously as an associated finding or variant of uncertain significance.
