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Retinal ganglion cell loss in neuromyelitis optica: a longitudinal study.

Frederike Cosima OertelJoachim HavlaAdriana Roca-FernándezNathaniel LizakHanna ZimmermannSeyedamirhosein MotamediNadja BorisowOwen B WhiteJudith Bellmann-StroblPhilipp AlbrechtKlemens RuprechtSven JariusJacqueline PalaceMaria Isabel LeiteTania KuempfelFriedemann PaulAlexander U Brandt
Published in: Journal of neurology, neurosurgery, and psychiatry (2018)
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.
Keyphrases
  • drug induced
  • liver injury
  • oxidative stress
  • multiple sclerosis
  • single cell
  • cell therapy
  • adverse drug
  • human health
  • electronic health record