Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Autoimmunity has been demonstrated in a diverse range of peripheral neurological disorders, such as myasthenia gravis and acquired neuromyotonia. Serum antibodies found in these conditions are directed against ion channels and receptors situated on the cell surface and have been shown to produce pathogenic effects. The symptoms of these peripheral disorders have been transferred to animals by passive or active immunisation and, in humans, treated successfully with immunomodulatory therapy. Recently, a number of central nervous system disorders (CNS), such as limbic encephalitis, certain forms of epilepsy, neuromyelitis optica and cerebellar ataxia, have been hypothesised to associate with specific serum autoantibodies. In this article we consider this rapidly expanding field of CNS disorders, discuss evidence for their proposed autoimmune aetiology and review whether the antibodies detected have been shown to be pathogenic or if they are secondary to preceding neuronal damage.

Original publication

DOI

10.1080/08916930701619490

Type

Journal article

Journal

Autoimmunity

Publication Date

02/2008

Volume

41

Pages

55 - 65

Keywords

Aquaporin 4, Autoantibodies, Autoantigens, Autoimmune Diseases, Autoimmune Diseases of the Nervous System, Calcium Channels, Central Nervous System Diseases, Cerebellar Ataxia, Glutamate Decarboxylase, Humans, Neuromyelitis Optica