The retinal nerve fibre layer in patients with multiple sclerosis

There are two main disease courses in Multiple Sclerosis (MS): (1) a
relapsing-remitting subtype (relapsing-remitting MS, RRMS) and (2) a chronic
progressive disease course. In most patients, the disease begins with a
relapsing-remitting course, which later converts to chronic progression
(secondary progressive MS, SPMS). A small group of MS patients remains largely
free of disease symptoms, even after very long disease duration. This disease
course is called benign MS (BMS). The largest part of disability appears during
the chronic progressive phase.

Recently, it has become clear, that tissue injury in MS is not only caused by
inflammation but for a part also through neurodegeneration that is independent
of inflammation. This degenerative process is called axonal degeneration.
Axonal degeneration is the most important underlying mechanism of chronic
progression in MS. The pathophysiology of axonal degeneration is unknown and
there is thus no treatment for it.

There is no simple method to measure axonal degeneration in vivo. The diameter
of the retinal nerve fibre layer can be measured with the ophthalmologic tool
optical coherence tomography (OCT). As the retina is a part of the brain, we
suspect that a decreased diameter of the retinal nerve fibre layer may be a
measure of axonal degeneration in the brain. I an earlier study it was shown
that the diametere of the retinal nerve fibre layer is significantly smaller in
MS patients than in healthy control persons, but the different disease courses
of MS were not considered in this previous study.

In this study we would like to investigate whether the diameter of the retinal
nerve fibre layer differs between healthy control persons and patients with
different disease courses of MS.

Explorative case control studie.

Minimal risk and burden:
(1) one neurologic examination (to measure the extend of disability)
(2) one VEP examination (non-invasive)
(3) one OCT examination (non-invasive)

If the examination of the retina with OCT should not be possible without the
use of pupil-dilating drugs, the patients will be treated once with
pupil-dilating eye-drops (tropicamide 0.5%). This treatment carries the risk of
an allergic reaction to tropicamide, the worsening of a narrow-angle-glaucoma,
and the inability to drive a motor vehicle safely. We reduce the risk of an
allergic reaction and glaucoma by excluding patients with allergy to
tropicamide and know narrow-angle glaucoma. The cost of transport that becomes
necessary after use of the pupil-dilating eye-drops will be paid for.