Ptosis is drooping of the upper lid margin in primary gaze, which can be broadly classified as congenital and acquired. Acquired ptosis is further classified as myogenic, aponeurotic, neurological, mechanical, and traumatic. Ptosis secondary to trauma is caused by heterogeneous mechanisms. It is usually associated with distorted anatomy, making the management challenging and outcomes unpredictable. We present the case of a 46-year-old male patient, diagnosed with right eye complete post-traumatic aponeurotic ptosis with fair Bell's and poor levator palpebrae superioris action, vertical dystopia, upgaze limitation, and upper lid scarring. He had difficulty in pursuing his occupation and maintaining a livelihood as complete ptosis led to the loss of binocularity and depth perception, which also led him to a high risk of occupational hazards. Therefore, we planned the patient's frontalis suspension procedure using autogenous fascia lata and the Crawford technique based on the risks and possible outcomes explained. Postoperatively, the patient's marginal reflex distance 1 (MRD 1) was 2 mm. The patient did not have any diplopia, achieved binocularity, and was satisfied with the results. He is managing well his day-to-day activities without any difficulty with depth perception.

Chronic Progressive External Ophthalmoplegia (CPEO) is a primary mitochondrial disorder (PMD) caused by mutations in nuclear genes encoding mitochondrial DNA (mtDNA) maintenance proteins. CPEO is characterized by mtDNA depletion and deletions, and patients primarily present with ocular and muscular features (isolated CPEO). However, additional encephalomyopathy, neurological complications, and Parkinsonism can drive a more severe disease form, CPEO-plus. The evolution from isolated CPEO to CPEO-plus remains poorly understood. Inflammatory and innate immune processes are emerging as strong disease modifiers and may underlie this heterogeneity. Instability of mitochondrial DNA is a major driver of organellar stress and release of mitochondrial contents into the cytosol. Mutations in several genes involved in mtDNA replication and maintenance have been implicated in triggering the escape of mitochondrial nucleic acids from the mitochondrial matrix. Once exposed to cytosolic innate immune sensors, mtDNA and mitochondrial double-stranded RNA (mt-dsRNA) act as potent immunogens, with more than 10 innate immune sensors capable of recognizing them. Therefore, mtDNA and mt-dsRNA release are likely pathological mechanisms in CPEO, yet the list of CPEO-related genes that can trigger inflammatory processes is far from complete. Here, we use patient-derived fibroblasts from individuals with CPEO carrying mutations in RNASEH1 and Twinkle, and provide - for the first time - evidence that their mutations drive innate immune activation through the release of different mitochondrial nucleic acids. RNASEH1 mutations lead to the accumulation and subsequent release of mt-dsRNA, while mtDNA remains protected. On the other hand, mutations in Twinkle cause the release of mtDNA without triggering mt-dsRNA production, or leakage. Supporting this notion, the POLRMT inhibitor IMT-1, and the STING inhibitor H-151, reduced interferon stimulated genes expression downstream of RNASEH1 and Twinkle mutations, respectively. Further, when we analyzed a unique compound patient line carrying mutations in both genes simultaneously, we detect both species of nucleic acids in its cytosol, indicating that both pathways can be engaged simultaneously in the same cell. Lastly, we show that cytosolic sensing triggers paracrine signaling to activate bystander microglia - the resident macrophages of the retina and brain - with potential implications to the neurological progression of CPEO. Overall, our findings reveal a new role for RNASEH1 and Twinkle in driving aberrant innate immunity and paracrine inflammation in CPEO. Our data support a model in which innate immunity is a universal feature of mutations causing mtDNA instability; yet different mutations engage distinct sensing pathways, and in complex scenarios multiple pathways can be triggered at the same time. Given the clinical heterogeneity observed in patients with PMDs, our findings that different signaling pathways are triggered in patient-specific manners might have direct implications for precision medicine approaches aimed at targeting specific innate immunity.

Background: Orbital metastases are rare in breast cancer, representing only 3-10% of ocular metastases. This report highlights a case where orbital involvement was the first indicator of systemic metastatic spread. Case Presentation: A 72-year-old woman with a history of Estrogen Receptor (ER)-positive (5%), Progesterone Receptor (PR)-negative, Human epidermal growth factor receptor-2 (HER2)-negative breast cancer (diagnosed 3 years prior) presented with right orbital pain, diplopia, and periorbital swelling. Imaging revealed multiple myositis of the extraocular muscles, compressive displacement of the optic nerve, and right periorbital edema. Bone scintigraphy identified multifocal skeletal metastases. A navigation-assisted biopsy confirmed metastatic invasive ductal carcinoma, immunohistochemically consistent with the primary tumor (ER/PR-negative, HER2-negative). A systematic analysis using next-generation sequencing indicated aberrant activation of the phosphoinositide 3 kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway. Chemotherapy, targeted therapy and bisphosphonate therapy were initiated, with planned radiotherapy for symptomatic progression. Conclusion: Orbital symptoms in breast cancer survivors, even subtle ones, necessitate prompt evaluation for metastatic disease. Multimodal imaging (e.g., Computed Tomography (CT)/Magnetic Resonance Imaging (MRI)) combined with image-guided biopsy is critical for diagnosis. Early detection enables multidisciplinary palliative strategies to optimize quality of life while addressing systemic dissemination.

Functional endoscopic sinus surgery (FESS) is a widely used procedure for chronic sinusitis. Although it is generally considered a safe procedure, serious ophthalmic complications might occur. In this report, we discuss the results of Foster augmented full tendon vertical muscle transposition (VRT) with and without resection for two cases presented with iatrogenic complete medial rectus transection following FESS.

The lacrimal gland produces the aqueous component of the tear film, and its disease can cause dry eye, pain, proptosis, or diplopia. Lacrimal gland lesions are diverse: roughly half inflammatory, a quarter lymphoproliferative, and a quarter epithelial tumor, with substantial overlap in imaging features. Consequently, tissue sampling remains essential for accurate diagnosis and management. Conventional CT and MR imaging aid in diagnosis and define anatomic extent; correlating imaging with clinical history and examination is vital. Advanced MR techniques may offer tissue-specific information. The lacrimal sac and extra-orbital sites should also be considered in formulating differential diagnoses and treatment strategies.

Background Differentiating progressive supranuclear palsy (PSP) from Parkinson disease and other parkinsonisms is challenging. MRI measures have been investigated, but most studies included small samples, limiting result reliability. Purpose To compare the performance of planimetric and linear MRI measurements in differentiating PSP from other parkinsonisms and identify an optimized linear marker. Materials and Methods Participants with PSP and non-PSP parkinsonisms and controls were included in this secondary analysis of multiple international prospective studies (enrollment: 2006-2024). The previously established midbrain line, midbrain area, pons to midbrain area ratio, and MR parkinsonism index were compared with a new simple linear marker based on two midbrain measures performed on midsagittal T1-weighted sections (dual-line midbrain PSP index [DMPI]). Logistic regression including DMPI, age, and sex was used to differentiate participants with PSP (PSP-Richardson syndrome, PSP variants) from those with non-PSP parkinsonisms and controls in two large independent cohorts and in a small cohort of participants with pathologically proven diagnoses. Results A total of 2111 participants (mean age, 67.8 years ± 8.4 [SD]; 54% male) were included (Italian: 136 PSP, 238 non-PSP, 85 controls; international: 520 PSP, 564 non-PSP, 525 controls). All markers were compared in a subcohort (PSP [n = 161]; non-PSP parkinsonisms [n = 203]) representative of the overall cohort. All measures showed area under the receiver operating characteristic curve (AUC) values over 0.90 for differentiating PSP from non-PSP parkinsonisms, with the DMPI and midbrain area performing best (AUCs, 0.97 [95% CI: 0.95, 0.98] and 0.95 [95% CI: 0.93, 0.97], respectively) and the DMPI showing the smallest percentage of uncertain cases (gray zone, 29 of 364 participants [7.97%]). In the entire Italian and international cohorts, the DMPI distinguished participants with PSP from those with non-PSP, with AUCs of 0.97 (95% CI: 0.97, 0.98) and 0.96 (95% CI: 0.95, 0.97), respectively. Excellent DMPI performance was also observed in participants with early-stage disease (AUC, 0.97 [95% CI: 0.95, 0.99]) and those with pathologically confirmed diagnoses (n = 43) (AUC, 0.94 [95% CI: 0.86, 1.00]). Conclusion The DMPI and midbrain area performed well for differentiating PSP from other neurodegenerative parkinsonisms. Clinical trial registration nos. NCT03068468, NCT01110720, NCT01049399, NCT01804452 © The Author(s) 2026. Published by the Radiological Society of North America under a CC BY 4.0 license. Supplemental material is available for this article.

Graves' orbitopathy (GO) is a progressive autoimmune disorder of visual organ, mostly associated with Graves' disease (GD). Although rituximab has been used as an off-label therapy for steroid-resistant GO, paradoxical immune reactivation has also been reported. We present a rare case of GO that developed after bendamustine-rituximab (BR) therapy for chronic lymphocytic leukemia (CLL). A 73-year-old male with a 3-year history of GD, presented with new onset of bilateral proptosis, diplopia, and decreased visual acuity, that happened two weeks after his second BR cycle for CLL. The anamnesis was negative for both smoking, and radioiodine therapy. Laboratory studies showed persistently elevated thyrotropin receptor antibodies levels in plasma, and extraocular muscle enlargement on orbital MRI. The active phase (CAS 6/6) of moderate-to-severe (EUGOGO) GO was diagnosed. Despite two courses of intravenous methylprednisolone (cumulative dose - 12.2 g) and 10 retrobulbar dexamethasone injections, the patient progressed to dysthyroid optic neuropathy. Although the patient had a predisposing autoimmune background, the close temporal association with BR therapy, progressive disease course, and glucocorticoid resistance suggest that chemotherapy-induced immune dysregulation played a critical role in triggering GO. Rituximab-related B-cell depletion and cytokine release syndrome may have facilitated T-cell-mediated orbital inflammation, while bendamustine-induced lymphopenia further disrupted immune tolerance. This case illustrates the potential for paradoxical autoimmune activation following BR therapy in a predisposed patient. Clinicians should monitor for GO signs, and symptoms before, during, and after BR therapy in patients with underlying thyroid autoimmunity. Further clinical trials are needed to verify this phenomenon.

Post-dural puncture headache (PDPH) is a common complication of neuraxial anesthesia, particularly in the obstetric population, where its incidence is higher due to the frequent use of epidural techniques and the occurrence of accidental dural puncture. The condition arises from cerebrospinal fluid leakage following disruption of the dura mater, leading to intracranial hypotension, compensatory cerebral vasodilation, and traction of pain-sensitive structures, which collectively explain its characteristic orthostatic presentation. Pregnancy-related physiological changes, including increased intra-abdominal pressure and epidural venous engorgement, further contribute to its development and severity. Clinically, PDPH presents as a positional headache that worsens in the upright position and improves with recumbency, often accompanied by nausea, photophobia, diplopia, and auditory symptoms. Diagnosis is primarily clinical and relies on a history of recent neuraxial procedures and the absence of red flag neurological signs. However, careful evaluation is necessary to exclude other serious postpartum conditions such as preeclampsia, cerebral venous sinus thrombosis, and intracranial hemorrhage. Prevention focuses on optimizing procedural techniques, including the use of small-gauge atraumatic needles, minimizing puncture attempts, and ensuring proper training. Management strategies depend on symptom severity and range from conservative measures, such as hydration, analgesics, and caffeine, to pharmacological interventions. In moderate-to-severe cases, the epidural blood patch remains the gold standard treatment, offering high success rates. Given its potential impact on maternal function, breastfeeding, and mental health, a multidisciplinary and patient-centered approach is essential to improve outcomes and reduce long-term complications.