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.

Intraocular tuberculosis often evades diagnosis owing to its nonspecific clinical features and frequent absence of systemic signs. We describe a rare case of primary tubercular chorioretinitis in an immunocompetent woman in her early 20s who presented with acute vision loss, ocular pain, and redness in the left eye. Multimodal imaging demonstrated active inflammation arising within-not at the margin of-pre-existing focal chorioretinal atrophy, accompanied by retinal vasculitis and choroidal hypoperfusion. Systemic workup revealed no extrapulmonary involvement; however, interferon-gamma release assay was strongly positive. Following initiation of standard four-drug antitubercular therapy, adjunctive oral corticosteroids were administered, achieving complete resolution of intraocular inflammation and marked visual recovery, with no recurrence during long-term follow-up. This case highlights intralesional reactivation within chorioretinal atrophy as a distinctive imaging hallmark suggestive of tubercular etiology. Recognition of this pattern may facilitate earlier diagnosis of intraocular tuberculosis, particularly in endemic regions or in patients lacking overt systemic disease. Given the potential for irreversible vision loss, timely initiation of antitubercular therapy-guided by multimodal imaging and immunologic testing-is critical. Our findings underscore the need to consider ocular tuberculosis in the differential diagnosis of posterior uveitis, even in immunocompetent individuals with isolated ocular symptoms, and advocate for heightened awareness of this subtle yet pathognomonic feature to improve diagnostic precision and clinical outcomes.

A man in his late 60s with a history of arterial hypertension, dyslipidaemia and a cerebrovascular accident 20 years ago presented to the emergency department with sudden-onset blurred vision in his right eye, accompanied by pain, dizziness, sweating and high blood pressure (160/110 mmHg). Ophthalmic examination revealed a decreased visual acuity in the right eye (less than 6/60), with best corrected visual acuity of 6/7.5. Fundoscopy showed retinal cholesterol emboli and ischaemic changes. Carotid duplex ultrasound indicated possible stenosis of the internal carotid artery. The patient was started on antiplatelet therapy with acetylsalicylic acid and 24-hour cardiac telemetry monitoring. A brain MRI performed 2 days later showed acute ischaemic infarcts in the right frontal and periventricular regions. Intracranial and cervical magnetic resonance angiography confirmed internal carotid artery occlusion with no flow in the intracranial portion.

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.

Chronic relapsing inflammatory optic neuropathy (CRION) is a rare cause of recurrent optic neuritis characterized by steroid responsiveness and relapse upon treatment withdrawal. Because no definitive diagnostic test exists, the diagnosis is clinical and requires exclusion of more common demyelinating and antibody-mediated disorders. We describe a 45 year-old woman with a history of psoriasis, photodermatitis, and Hashimoto thyroiditis who presented with four episodes of severe left retro-orbital pain and progressive visual blurring over a three-year period, with the right eye remaining unaffected throughout. Each episode demonstrated left optic nerve enhancement on magnetic resonance imaging and responded promptly to intravenous corticosteroids. Extensive evaluation for multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and myelin oligodendrocyte glycoprotein (MOG) antibody disease was consistently negative. A diagnosis of seronegative CRION was established based on the recurrent steroid-responsive clinical pattern. Long-term immunosuppressive therapy with mycophenolate mofetil, later transitioned to mycophenolic acid due to gastrointestinal intolerance, resulted in clinical stability during follow-up. One additional relapse occurred following a brief three-day interruption of mycophenolate for treatment of cellulitis. CRION should be considered in patients with recurrent optic neuritis when workup for demyelinating and antibody-mediated conditions is negative. Early recognition and initiation of long-term immunosuppressive therapy are important to reduce relapse frequency and prevent cumulative optic nerve damage.