Herpes simplex virus is responsible for numerous ocular diseases, the most common of which is herpetic stromal keratitis. This is a recurrent infection of the cornea that typically begins with a subclinical infection of the cornea that establishes a latent infection of sensory ganglia, most often the trigeminal ganglia. Recurring infections occur when the virus is reactivated from latency and travels back to the cornea, where it restimulates an inflammatory response. This inflammatory response can lead to decreased corneal sensation, scarring, and blindness. The diagnosis of these lesions as the result of a recurrent herpes simplex virus infection can at times be problematic. Currently, herpetic stromal keratitis is diagnosed by its clinical presentation on the slit-lamp examination, but the literature does not always support the accuracy of these clinical findings. Other diagnostic tests such as polymerase chain reaction assay, enzyme-linked immunosorbent assay, immunofluorescent antibody, and viral cultures have provided more definitive diagnosis, but also have some limitations. That said, accurate diagnosis is necessary for proper treatment, in order to prevent serious consequences. Current treatment reduces the severity of lesions and controls further viral spread, but does not provide a cure.

Background: Optic neuritis (ON) is often the presenting symptom in inflammatory central nervous system demyelinating disorders. Objective: To compare the frequency and pattern of optic chiasm involvement in patients with aquaporin-4-immunoglobulin G (AQP4-IgG)-associated ON to patients with myelin oligodendrocyte glycoprotein-immunoglobulin G (MOG-IgG)-associated ON. Methods: Retrospective review of all patients evaluated at Mayo Clinic, Stanford University and Ramathibodi Hospital who were found to have: (1) ON, (2) either MOG-IgG or AQP4-IgG by cell-based assay, and (3) magnetic resonance imaging (MRI) at the time of ON. MRI was reviewed for contrast enhancement of the optic chiasm and the pattern of involvement. Results: One hundred and fifty-four patients (74 AQP4-IgG and 80 MOG-IgG) were included. Among patients with AQP4-IgG-ON, 20% had chiasmal involvement, compared with 16% of patients with MOG-IgG-ON ( p = 0.66). In patients with chiasmal involvement, longitudinally extensive optic nerve enhancement (from orbit extending to chiasm) was identified in 54% of MOG-IgG-ON patients, compared with 7% of AQP4-IgG-ON patients ( p = 0.01). Conclusion: Chiasmal involvement of MOG-IgG-ON and AQP4-IgG-ON occur at more similar frequencies than previously reported. Furthermore, MOG-IgG-ON chiasmal involvement is more likely to be part of a longitudinally extensive optic nerve lesion.

No abstract

Background and Objectives:Asymptomatic or persistent optic nerve enhancement in aquaporin (AQP)-4-immunoglobulin G (IgG) positive neuromyelitis optica spectrum disorder (NMOSD) is thought to be rare. Improved understanding may have important implications for assessment of treatment efficacy in clinical trials and in clinical practice. Our objective was to characterize NMOSD inter-attack optic nerve enhancement.Methods:This was a retrospective cohort study performed between 2000-2019 (median follow-up 5.5 [range 1-35] years) of AQP4-IgG positive optic neuritis (ON) patients evaluated at Mayo Clinic. MRI orbits were reviewed by a neuro-radiologist, neuro-ophthalmologist and neuroimmunologist blinded to clinical history. Inter-attack optic nerve enhancement (>30 days after attack) was measured. The correlation between inter-attack enhancement and Snellen visual acuity converted to Logarithm of the Minimum Angle of Resolution (LogMAR) at attack and at follow-up were assessed.Results:198 MRI scans in 100 AQP4-IgG+ NMOSD patients were identified, with 107 inter-attack MRIs from 78 unique patients reviewed. Seven scans were done prior to any ON median 61 days before attack [range 21-271 days]) and 100 after ON (median 400 days after attack [33-4623 days]).Optic nerve enhancement was present on 18/107 (16.8%) inter-attack scans (median 192.5 days from attack [33-2943]) of patients with preceding ON. On 15 scans, enhancement occurred at the site of prior attacks; the lesion location was unchanged, but the lesion length was shorter. Two scans (1.8%) demonstrated new asymptomatic lesions (prior scan demonstrated no enhancement). In a third patient with subjective blurry vision, MRI showed enhancement preceding detectable eye abnormalities on examination noted 15 days later. There was no difference in visual acuity at preceding attack nadir (LogMAR VA 1.7 versus 2.1; p=0.79) or long-term visual acuity (LogMAR VA 0.4 versus 0.2, p=0.56) between those with and without inter-attack optic nerve enhancement.Discussion:Asymptomatic optic nerve enhancement occurred in 17% of NMOSD patients at the site of prior ON attacks and may represent intermittent blood-brain-barrier breakdown or subclinical ON. New asymptomatic enhancement was only seen in 2% of patients. Therapeutic clinical trials for NMOSD require blinded relapse adjudication when assessing treatment efficacy and it is important to recognize that asymptomatic optic nerve enhancement can occur in ON patients.