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image: Brian Weinshenker speaking at MS Frontiers 2007

Brian Weinshenker

What it was, is , isn't and might be.

An outstanding presentation was given by Brian Weinshenker, professor of neurology at the Mayo Clinic of Medicine in Minnesota in the US on his recent work on Neuromyelitis optica (NMO). NMO is an inflammatory demyelinating disorder of the central nervous system that most commonly targets the optic nerves and spinal cord selectively. Until recently it was a matter of debate whether NMO was a distinct disease or a peculiar variant of MS, however in recent years medical opinion has shifted due to a number of developments. An analysis of the disease course and features of patients with severe optic neuritis and inflammation of the spinal column revealed that, unlike MS, NMO involves severe attacks of optic neuritis and inflammation effecting three or more segments of the spine. Studies have also revealed distinctive immune changes characteristic of NMO which invokes B cell participation in the disease process.

Finally there was the discovery of a specific antibody (NMO-IgG) in patients with NMO, but not in patients with MS. The recent discovery that NMO-IgG reacts with aquaporin 4 has opened new avenues for understanding the pathogenesis of NMO as this is the first instance in which a specific target for an immune reaction resulting in an inflammatory demyelinating disease in humans has been identified. Aquaporin 4 is a mercurial-insensitive water channel protein which is the dominant water channel within the CNS. They provide a pathway for water transport through cell membranes. It is speculated that an unknown stimulus leads to production of circulating NMO-IgG, which in turn leads to a disruption of the cellular water transport mechanisms which might contribute to some of the lesions that occur in NMO. NMO-IgG is now used as a clinical test for NMO and will hopefully provide considerable insight into the pathogenesis of the condition.

 

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Page last updated on 15 Oct 07 by Christopher Carr. Page next due for review on 25 Dec 07
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