Send to

Choose Destination
Mult Scler. 2013 Dec;19(14):1887-95. doi: 10.1177/1352458513489757. Epub 2013 May 23.

Retinal ganglion cell and inner plexiform layer thinning in clinically isolated syndrome.

Author information

NeuroCure Clinical Research Center and Experimental and Clinical Research Center, Charité University Medicine Berlin and Max Delbrück Center for Molecular Medicine, Berlin, Germany.



Axonal and neuronal damage are widely accepted as key events in the disease course of multiple sclerosis. However, it has been unclear to date at which stage in disease evolution neurodegeneration begins and whether neuronal damage can occur even in the absence of acute inflammatory attacks.


To characterize inner retinal layer changes in patients with clinically isolated syndrome (CIS).


45 patients with CIS and age- and sex-matched healthy controls were investigated using spectral domain optical coherence tomography. Patients' eyes were stratified into the following categories according to history of optic neuritis (ON): eyes with clinically-diagnosed ON (CIS-ON), eyes with suspected subclinical ON (CIS-SON) as indicated by a visual evoked potential latency of >115 ms and eyes unaffected by ON (CIS-NON).


CIS-NON eyes showed significant reduction of ganglion cell- and inner plexiform layer and a topography similar to that of CIS-ON eyes. Seven eyes were characterized as CIS-SON and likewise showed significant retinal layer thinning. The most pronounced thinning was present in CIS-ON eyes.


Our findings indicate that retinal pathology does occur already in CIS. Intraretinal layer segmentation may be an easily applicable, non-invasive method for early detection of retinal pathology in patients unaffected by ON.


Clinically isolated syndrome; optical coherence tomography; retinal ganglion cell layer; retinal nerve fiber layer

[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Atypon Icon for Zurich Open Access Repository and Archive
Loading ...
Support Center