Le mardi 11 février 2025, Madame Anne-Catherine CHAPELLE, titulaire d’un diplôme de médecin et d’un Certificat de formation à la recherche en sciences médicales, présentera l'examen en vue de l'obtention du grade de Doctorat en sciences médicales, sous la direction de Monsieur Jean-Marie RAKIC et de Monsieur Gordon Terence PLANT (University College of London)

Cette épreuve consistera en la défense publique d'une thèse intitulée : «Evaluation of ganglion cells in ischaemic optic neuropathies» . 

Le jury sera composé de :

Félic SCHOLTES (Président), Dominique DIVE (Secrétaire), Nathalie COLLIGNON (CHU), Julie DE ZAEYTIJD (UGent), Gordon PLANT(University College of London), Jean-Marie RAKIC, Matthieu ROBERT (Hôpital Necker).

Résumé de la thèse

This retrospective study included thirty-two patients with non-arteritic anterior ischemic optic neuropathy (NAAION) referred to our Neuro-ophthalmology Department at the University Hospital of Liège, Belgium in order to assess the ganglion cell layer thinning after an episode.

First, we have revealed two causes of inner nuclear layer cystic change in the same patients experiencing NA-AION, one reversible and the other likely permanent. This finding highlights the distinction between genuine edema related to transudation of fluid (in this case secondary to ischemic optic disc swelling) and the phenomenon observed in retrograde maculopathy that is related to the degree of retinal nerve fiber layer/ganglion cell complex thinning. Cystic change in the INL is associated with severe optic atrophy and have permitted to assess an inferior ganglion cell threshold where no visual function is observed.

Moreover, subretinal fluid is found in a high proportion of cases of NAAION. Visual function remained largely stable from presentation in this cohort. Corticosteroid intake at presentation did not influence visual recovery or timing of the resorption of tissue edema. With regard to pathogenesis, we proposed that the volume of transudate generated at the optic disc is the critical factor rather than dysfunction of retinal mechanisms subserving reabsorption.