Portal de Periódicos da CAPES

Retinal ganglion cell loss in neuromyelitis optica: a longitudinal study

2018; BMJ; Volume: 89; Issue: 12 Linguagem: Inglês

10.1136/jnnp-2018-318382

1468-330X

Frederike Cosima Oertel, Joachim Havla, Adriana Roca‐Fernández, Nathaniel Lizak, Hanna Zimmermann, Seyedamirhosein Motamedi, Nadja Borisow, Owen White, Judith Bellmann‐Strobl, Philipp Albrecht, Klemens Ruprecht, Sven Jarius, Jacqueline Palace, Maria Isabel Leite, Tania Kuempfel, Friedemann Paul, Alexander U. Brandt,

Ocular Diseases and Behçet’s Syndrome

Objectives Neuromyelitis optica spectrum disorders (NMOSD) are inflammatory conditions of the central nervous system and an important differential diagnosis of multiple sclerosis (MS). Unlike MS, the course is usually relapsing, and it is unclear, if progressive neurodegeneration contributes to disability. Therefore, we aimed to investigate if progressive retinal neuroaxonal damage occurs in aquaporin4-antibody-seropositive NMOSD. Methods Out of 157 patients with NMOSD screened, 94 eyes of 51 patients without optic neuritis (ON) during follow-up (F/U) and 56 eyes of 28 age-matched and sex-matched healthy controls (HC) were included (median F/U 2.3 years). The NMOSD cohort included 60 eyes without (Eye ON − ) and 34 eyes with a history of ON prior to enrolment (Eye ON+ ). Peripapillary retinal nerve fibre layer thickness (pRNFL), fovea thickness (FT), volumes of the combined ganglion cell and inner plexiform layer (GCIP) and the inner nuclear layer (INL) and total macular volume (TMV) were acquired by optical coherence tomography (OCT). Results At baseline, GCIP, FT and TMV were reduced in Eye ON+ (GCIP p<2e −16 ; FT p=3.7e −4 ; TMV p=3.7e −12 ) and in Eye ON − (GCIP p=0.002; FT p=0.040; TMV p=6.1e −6 ) compared with HC. Longitudinally, we observed GCIP thinning in Eye ON− (p=0.044) but not in Eye ON+ . Seven patients had attacks during F/U; they presented pRNFL thickening compared with patients without attacks (p=0.003). Conclusion This study clearly shows GCIP loss independent of ON attacks in aquaporin4-antibody-seropositive NMOSD. Potential explanations for progressive GCIP thinning include primary retinopathy, drug-induced neurodegeneration and retrograde neuroaxonal degeneration from lesions or optic neuropathy. pRNFL thickening in the patients presenting with attacks during F/U might be indicative of pRNFL susceptibility to inflammation.