Norrie disease is a rare, severe inherited neurodevelopmental disorder primarily affecting the eye. It was first described by the Danish ophthalmologist Gordon Norrie in 1927, and later, Dr. Mette Warburg established its X-linked recessive inheritance pattern in 1961. The condition is caused by mutations in the NDP gene located on chromosome Xp11.3, which encodes the protein norrin. Norrin is a secreted protein that acts as a ligand for the Wnt/β-catenin signalling pathway (binding to the Frizzled-4 receptor), playing a critical role in the vascular development of the retina and the stria vascularis of the cochlea.

Like many students, my early encounters with ophthalmology were limited to a handful of lectures and the occasional slit-lamp demonstration, which often felt more intimidating than enlightening. Formal ophthalmology exposure is not only short but also highly variable: many students receive only brief standalone attachments or integrated teaching alongside other specialties. In a national survey of UK medical schools, nearly two-thirds offered just one to two weeks of dedicated ophthalmology teaching, while almost a third integrated ophthalmology with other subjects rather than providing it as a distinct block (1). These factors lead many students in their final year to seek elective placements in ophthalmology, often overseas—a path I also chose to follow by organising my elective in Kyoto, Japan.

As vigabatrin was being used, it became associated with retinal toxicity causing constriction of the visual field. These visual field deficits reported in association with vigabatrin prompted a review of its place in the management of epilepsy, halting its use. However, in 2009, it was later approved by the United States Food and Drug Administration (FDA) for use as monotherapy in the treatment of infantile spasms in patients aged 1 month to 2 years, based on the benefits of the treatment outweighing the risks.

To the best of our knowledge, bilateral rhegmatogenous retinal detachment following uncomplicated phacoemulsification has not previously been reported. We reflect on the need for this condition review having been inspired by a case in which bilateral RRD followed what had appeared to be straightforward cataract surgery.

Conjunctival foreign bodies are a common ophthalmic presentation frequently encountered in routine clinical practice. However, the appearance of a worm-like conjunctival lesion can pose a diagnostic challenge, particularly in patients with a history of travel to regions endemic for parasitic infections. This report outlines the investigation, diagnostic work-up, and management of conjunctival foreign bodies, reflecting on a case of suspected Axenfeld nerve loops masquerading as a conjunctival foreign body. In such cases, careful clinical assessment and appropriate diagnostic evaluation are essential to establish an accurate diagnosis and guide optimal management.

Shahmeer Hamid Introduction Oculodermal melanocytosis, classically known as Nevus of Ota, is a congenital or acquired pigmentary disorder characterised by blue-grey hyperpigmentation of the skin and mucous membranes in the…

Ramsay Hunt syndrome (RHS), also known as herpes zoster oticus, is caused by reactivation of latent varicella–zoster virus (VZV) within the geniculate ganglion of the facial nerve. It represents an important and distinct cause of acute lower motor neurone facial nerve palsy and is associated with more severe disease and poorer recovery than idiopathic facial nerve palsy (Bell’s palsy). From an ophthalmic perspective, RHS is clinically significant due to its association with lagophthalmos, corneal exposure, and sight-threatening ocular surface disease. Early recognition is critical, as management differs from Bell’s palsy and requires prompt antiviral therapy.

Gradenigo syndrome is a rare but important complication of otitis media. It is classically described as a triad of persistent ear infection, abducens nerve (cranial nerve VI) palsy, and retro-orbital or facial pain along the trigeminal nerve (cranial nerve V) distribution. From an ophthalmologist’s perspective, the lateral rectus weakness and resulting diplopia are often the first symptoms that prompt referral. The syndrome arises when infection spreads to the petrous apex of the temporal bone, leading to osteomyelitis and subsequent cranial nerve dysfunction.

Choroideremia (CHM) is a rare, X-linked recessive chorioretinal dystrophy characterized by the progressive degeneration of the choriocapillaris, retinal pigment epithelium (RPE), and photoreceptors. The condition was first described by the Austrian ophthalmologist Ludwig Mauthner in 1872. The genetic basis was elucidated in 1990 when potential cloning identified the CHM gene located on chromosome Xq21.2.

Gyrate atrophy of the choroid and retina is a rare, autosomal recessive metabolic disorder affecting the chorioretinal tissues. The disease is caused by mutations in the OAT gene located on chromosome 10q26, which encodes the mitochondrial enzyme ornithine aminotransferase.