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Neurology. 2014 Jul 1;83(1):73-7. doi: 10.1212/WNL.0000000000000545. Epub 2014 May 23.

Dynamic formation of macular microcysts independent of vitreous traction changes.

Author information

1
From the NeuroCure Clinical Research Center (A.U.B., T.O., E.M.K., F.P.), and Clinical and Experimental Multiple Sclerosis Research Center, Department of Neurology (F.P.), Charité-Universitätsmedizin Berlin; and University Eye Hospital Freiburg (W.A.L.), Germany. alexander.brandt@charite.de.
2
From the NeuroCure Clinical Research Center (A.U.B., T.O., E.M.K., F.P.), and Clinical and Experimental Multiple Sclerosis Research Center, Department of Neurology (F.P.), Charité-Universitätsmedizin Berlin; and University Eye Hospital Freiburg (W.A.L.), Germany.

Abstract

OBJECTIVE:

To test the assumption of vitreous traction as a cause of macular microcysts in neuroinflammatory diseases and to establish a testable model to quantify vitreous traction changes.

METHODS:

Retrospective cohort study including 9 patients with neuroinflammatory diseases and macular microcysts that were longitudinally analyzed using optical coherence tomography. A mechanical model was developed to test the theory of vitreous traction vs macular swelling. This model was applied to one case presenting with dynamic microcyst evolution over 2 years with 4 visits.

RESULTS:

None of the patients' eyes with microcysts showed any signs of vitreous traction upon qualitative meticulous optical coherence tomographic analysis. The longitudinal changes analyzed in one patient were in the opposite direction as predicted by the mechanical model involving vitreous traction.

CONCLUSIONS:

Vitreous traction does not appear to be a causative factor in macular microcyst formation. Quantitative analysis in one case shows even a reduced traction caused by an increase in macular thickness leading to vitreous impingement by the macular wall. The presented model might also serve as a quantification approach in other studies investigating macular microcysts.

PMID:
24857925
DOI:
10.1212/WNL.0000000000000545
[Indexed for MEDLINE]

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