Wednesday, 29 May 2013

Retinal ganglion cell loss in CIS

Early loss of retinal ganglion cells in CIS; is due to focal inflammation or diffuse neurodegeneration? #MSBlog #MSResearch

EpubOberwahrenbrock et al. Retinal ganglion cell and inner plexiform layer thinning in clinically isolated syndrome. Mult Scler. 2013 May 23.

BACKGROUND: Axonal and neuronal damage are widely accepted as key events in the disease course of MS. 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.

OBJECTIVE: To characterize inner retinal layer changes in people with clinically isolated syndrome (CISers).

METHOD: 45 CISers and age- and sex-matched healthy controls were investigated using spectral domain optical coherence tomography (OCT). CISers' 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 >115ms and eyes unaffected by ON (CIS-NON).

RESULTS: 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.

CONCLUSION: 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.


"Are you surprised with this result? This is another example of neuroaxonal pathology occurring early in the course of the disease. The question is whether or not this is being driven by sub-clinical inflammatory lesions or is part of a more widespread neurodegenerative process. I suspect it is the former. This hypothesis is currently being tested with early aggressive therapy that should prevent ongoing neuronal and axonal loss in early MS."

1 comment:

  1. The retinal nerve fibre cell loss in MS is a true conundrum. The retinal nerve fibres have no myelin, but we are (I hope) all past the concept that MS is caused by an attack by the immune system on myelin or myelin producing cells.

    We know that 99% of MS patients exhibit optic nerve lesions in post mortem examination, so perhaps the retina and its structures are damaged during this inflammation. A brief perusal of the academic literature suggests that those with NMO also have significant and widespread retinal system abnormalities. If this is indeed the case then I would consider the case closed. MD/MD2, interested in commenting on this?

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