Cotton-wool spots in patients with migraineCotton-wool spots (CWSs) refer to localized accumulations of axoplasmic debris in the retinal nerve fibre layer that result from interruption of ganglion cell axon organelle transport.1 The histologic hallmark is the cytoid body, which represents the terminal swelling of a disrupted ganglion cell axon that has expanded and accumulated mitochondria and other organelles and subcellular material.1 In an otherwise healthy person, even a single CWS is considered abnormal, and it is recommended that investigations for underlying systemic disease be initiated.
Severe optic neuropathy as the presenting sign of leptomeningeal carcinomatosis from pancreatic cancerPancreatic cancer is one of the deadliest cancers in North America with an overall 5-year survival rate of less than 10%.1 The majority of pancreatic solid tumours metastasize to other organs, mainly to the liver and other peritoneal organs.1 Leptomeningeal metastasis (LM) or carcinomatous meningitis is infiltration of cancer cells to the leptomeninges and cerebrospinal fluid and is extremely rare in the setting of pancreatic adenocarcinoma with only 19 English cases reported (Supplementary Table 1, available online).
Diffusion-weighted imaging hyperintensity and low apparent diffusion coefficient of the optic nerve in myelin oligodendrocyte glycoprotein–IgG optic neuritisMyelin oligodendrocyte glycoprotein (MOG)–IgG has emerged as a reproducible marker for patients with optic neuritis or those with an aquaporin-4 (AQP4)–IgG–negative neuromyelitis optica spectrum disorders (NMOSD) phenotype.1 MOG-IgG optic neuritis tends to have a more favourable prognosis compared with those with AQP4-IgG, but poor visual outcomes may occur in a minority of patients with this condition.2 Certain magnetic resonance imaging (MRI) features may suggest MOG-IgG disease—especially perineural enhancement and longitudinal involvement.
Pseudo-Foster Kennedy syndrome due to idiopathic intracranial hypertensionFoster Kennedy syndrome is characterized by optic atrophy in one eye and papilledema in the other caused by a frontal lobe mass ipsilateral to the atrophic optic nerve. It was first described by Foster Kennedy in 1911 in a case series of 6 patients with expanding frontal lobe lesions.1 Foster Kennedy syndrome is thought to be present in 1% to 2.5% of intracranial masses.2