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Abstract #46316 Published in IGR 13-2
Glaucoma and blindness, an early axonal diagnosis and prevention by MRI
Iba-Zizen M-T; Cabanis EA; Istoc A; Yoshida MNeuroradiology Journal 2010; 23: 276
Aim: New concepts in glaucoma (70 million people in the world), born from a MRI neuro-ophthalmological research undertaken for 16 years, are presented. The modern experimental research is gradually (4 yrs) validating these new horizons(1,2). Material and Methods: Since 1994, 850 adults, male and female, had been addressed at the MR neuroimaging dept of the CHNO des XV-XX first and then (Sept. 2008) at the CIMN, with 1,5 T then 3T GEHC systems since 2006. The functional visual deficit measurements (tonometry, refracto-metry, central and peripheral campimetry, manual and automated...) were usually completed by an optic discs and retinal imaging (SLO, OCT....). MR cephalic sequences and planes (axial NOP, oblique vertical TONOP, NOP perpendicular coronal, sagittal) allow a precise visualization of the 2(nd) (intradural) and 3(rd) visual neuronal tracts, exploring the visual pathways nullfrom the optic nerve head to the calcarian fissurenull without partial volume effect. 3T (f)MRI and (DT)MRI were added Results: A T2 hypersignal inside the orbital or cisternal portions of the optic nerve translates the axonal suffering, announcing the axonal death and, consequently, the rarefaction of the tract, a progressive atrophy of the former optical way, detected in IRM. This atrophy begins always behind, in the intracranial portion of the million and half of deutoneurons (from geniculate bodies to the optical tract and chiasma), respecting the 1st intraocular part of the two optical nerves, their 1 millimeter long nullheadnull. It is situated behind the optic disk (papilla), classically visible only with direct ophthalmoscopy. The atrophy is always bilateral, asymmetric, even with a unilateral deficit. In case of acute optical neuropathy with fast visual deterioration (AV, CV) confirm that fact. Discussion: 1. These results, pathognomonic for us and never denied, lead to discuss the primary role of the intraocular hypertonicity, since the degeneration of the optical way is demonstrated as nullretrogradenull, from back ahead (distal to proximal), and not nullanterogradenull, from the eyeball (papilla) towards the geniculate bodies as in retinal pathologies. 2. Now some axonal transport experiments (mices glaucoma) confirm these facts. 3. It may be supposed that glaucoma belongs to encephalic neuro-degenerative pathologies, as well as Parkinson's or Alzheimer's diseases(4) Conclusion: The possibly long period (several years) between a preliminary MRI diagnosis of nullglaucomatous axonopathynull and the late evolutive stage (blindness) imposes an evolution to the ophthalmological clinical practice. Trusting in this new axonal MRI diagnosis, the patient and physicians could gain from the most recent neuro-protective therapeutics pushing back the blindness.
M.-T. Iba-Zizen. Centre d'Imagerie Neurologique et Neuro-Ophtalmologique (CINNO), Centre Hospitaller National d'Ophtalmologle des XV-XX, Paris, France.
Classification:
1.5 Glaucomas as cause of blindness (Part of: 1 General aspects)