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Hello. I would like to introduce myself. I am Friedemann Paul, a clinical neurologist and Professor of Clinical Neuroimmunology at Charité University Medicine Berlin in Berlin, Germany. I am head of the clinical department for multiple sclerosis research.

Today I would like to give a presentation on diagnosis and differential diagnosis of multiple sclerosis using a new diagnostic tool called optical coherence tomography (OCT).

You are probably familiar with the diagnosis of multiple sclerosis that stems from a clinical presentation of the patient that is made by means of MRI of the brain and spinal cord, and the analysis of the cerebrospinal fluid with the detection of oligoclonal bands.

The problem is that we have no highly specific diagnostic marker for multiple sclerosis. That means that any of these markers, such as cerebrospinal fluid or MRI, has numerous differential diagnoses that have to be considered in making a diagnosis of multiple sclerosis. There is still a long delay between the patient's first symptoms and the establishment of a correct diagnosis, and there are unfortunately still a high number of false diagnoses. We may have a new tool in OCT, but I would like to say a few words on conventional MRI.

On the T2-weighted images -- the classic MRI applied to patients with suspicion of multiple sclerosis -- we typically see T2 hyperintense lesions in the periventricular regions. The problem is that although this technique is highly sensitive, it is not very specific.

A T2 hyperintense lesion can be caused by edema, demyelination, axonal loss, or a combination of these, or it can have another cause that is not necessarily inflammatory in origin, so we have a problem with diagnostic specificity of T2-weighted MRI.

A new diagnostic tool has emerged. It is OCT, which the neurologists have adapted from the ophthalmologists. The principle is near-infrared backscattered light that provides pseudohistologic images of the retina, which can depict and quantify the various retinal layers.

What is so nice about this tool is that it is highly accepted by patients. It's not painful, it's not invasive, and it takes just about 10-15 minutes to get some very nice scans of the retina.

Here is an example. On the right, in the middle row, is a peripapillary retinal nerve fiber layer ring scan from a healthy eye. All of the measures are in green. On the left is the peripapillary ring scan from a patient who has experienced optic neuritis, and there is a substantial reduction of the retinal nerve fiber layer in some of the sectors.

With the newer techniques we are able to segment the various retinal layers and to quantify damage to the ganglion cell layer, the inner nuclear layer, or even the deeper layers of the retina. This is very helpful for our understanding of disease pathogenesis in multiple sclerosis.

This slide summarizes studies from all over the world that have investigated multiple sclerosis patients with and without optic neuritis. Here are data from eyes that have experienced optic neuritis. Many studies have consistently shown a substantial reduction of the retinal nerve fiber layer thickness following optic neuritis. This is not surprising if you imagine that an inflammatory demyelinating event to the optic nerve causes axonal damage, which then is detectable in a reduction of the retinal nerve fiber layer by OCT.

Maybe more surprising is this slide. The same studies reported a significant reduction of the retinal nerve fiber layer in eyes without history of optic neuritis. The extent of damage is less than with optic neuritis. According to the scale, it is about 10 µ vs 25-30 µ in optic neuritis, still a significant reduction. The question emerges as to whether this indicates subclinical optic neuritis in these eyes or an underlying continuous neurodegeneration that is prevalent in multiple sclerosis.

Why are these findings clinically relevant for our patients?

Work from the United States has nicely shown that there is a strong association between structural retinal damage detectable by OCT and functional impairment of vision (eg, visual quality of life and contrast acuity).

The lower graph shows that the higher the reduction of the ganglion cell layer, the poorer the performance on a contrast sensitivity test (the Sloan charts) and the poorer the visual quality of life. Therefore, structural damage to the retina detectable by OCT has a substantial impact on the patient's quality of life and visual functioning.

Another area of interest for OCT is its utility for differential diagnosis.

This graph shows 3 eyes, 1 from a patient with multiple sclerosis after optic neuritis and 2 from patients with neuromyelitis optica -- optic neuritis with and without macular cyst.

In the left column is a typical OCT ring scan from a patient with multiple sclerosis following an optic neuritis: a temporal preponderance of the retinal damage, as compared with the 2 eyes from patients with neuromyelitis optica, where you see a more even distribution of the retinal damage. Looking at the estimates of the measures of OCT damage in microns, the damage in eyes with neuromyelitis optica is more pronounced than in multiple sclerosis eyes, which is also in line with the clinical experience that optic neuritis in multiple sclerosis is usually less severe than in neuromyelitis optica.

To sum up, OCT may become a new and valuable tool in the differential diagnosis of a chronic central nervous system inflammation affecting the visual symptoms, such as multiple sclerosis, neuromyelitis optica, Susac syndrome, and others. My personal conviction is that OCT will enter the diagnostic routine in daily clinical practice within the next few years.

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