Wolfram syndrome (WFS) is an uncommon autosomal recessive neurodegenerative disorder characterized by diabetes mellitus, diabetes insipidus, optic nerve degeneration, hearing impairment, and other abnormalities. Additionally, a portion of individuals experience neurological, endocrine, behavioral, and urinary tract disorders that make management more challenging. Here, we present a 22-year-old male who was diagnosed with type 1 diabetes at the age of 4 and received treatment with basal-bolus insulin therapy. He had blurring of vision and hearing loss at 13 years of age, and our evaluation revealed optic atrophy and sensorineural hearing loss. He had polydipsia and polyuria (intake/output of 5-6 L/day) despite a fairly controlled blood glucose level. Serum anti-diuretic hormone (ADH) was done, which confirmed the diagnosis of central diabetes insipidus. His sonogram and urinary flow studies revealed bilateral hydroureteronephrosis with reflux uropathy. We diagnosed him with neurogenic bladder disorder with detrusor sphincter dyssynergia. This patient had an early onset urological disorder with involvement of eyes and ears, with diabetes mellitus and diabetes insipidus, which satisfied the criteria of WFS. The genetic test confirmed the diagnosis. He is currently being managed with insulin and desmopressin.

Various forms of cancer and chemotherapeutics are associated with optic neuropathy. Cisplatin is a platinum analogue chemotherapeutic commonly associated with ocular toxicity among many other serious adverse effects. Carboplatin is a more chemically stable platinum analogue that is generally better tolerated with a comparatively favorable side effect profile. There are very few reports of carboplatin precipitating optic neuropathy. This case report describes a rare occurrence of carboplatin-induced blinding optic neuropathy. We treated a patient receiving carboplatin for neuroendocrine bladder cancer who developed rapidly progressive bilateral optic neuropathy over the course of three days. Upon evaluation at our clinic, his visual acuity had declined to light perception only and 20/60 in his left and right eye, respectively. Carboplatin therapy was immediately held and steroids were initiated. Despite the intervention, the patient\'s visual deficits have not improved at the one-year follow-up. Although the mechanism by which carboplatin causes ocular toxicity remains speculative, arterial ischemia appears to be the likely mechanism given the irreversible nature of visual decline. As demonstrated by our patient\'s course, irreversible vision loss despite high-dose steroid intervention necessitates expeditious recognition and management of this rare adverse effect. ​​​​​.

We present a case of Non-Arteritic Anterior Ischemic Optic Neuropathy (NA-AION) with uncertain etiology but a good recovery with a total gain of central visual acuity.