Antibodies to receptors and ion channels are no known to cause neurological diseases
of the periphery (eg myasthenia gravis) and the central nervous system (eg. Limbic
encephalitis). In addition, there are now a number of different antibodies that often
affect the autonomic nervous system (several that will be addressed by other speakers
here). Antibodies to voltage-gated calcium channels (VGCC) in Lambert Eaton myasthenic
syndrome cause weakness distinguished from myasthenia by dry mouth, constipation and
bladder problem; antibodies to components of the voltage-gated potassium channel complex
(VGKC-complex) cause fasciculations, muscle cramps and pain, often associated with
excessive sweating, constipation or other gastro-intestinal disturbance. These VGKC-complex
antibodies, principally binding to CASPR2, also associate with the CNS condition Morvan’s
syndrome in which the autonomic disturbance can be more severe and cardiac arrhythmia
common. Antibodies that exclusively act in the CNS can also cause autonomic instability
as in NMDAR-antibody encephalitis, respiratory and bladder disturbance in progressive
encephalomyelitis with rigidity and myoclonus with glycine receptor antibodies, and
sometimes cardiac disturbance in patients with LGI1 antibodies that bind the other
main VGKC-complex protein. Thus the autonomic system can be affected by autoantibodies
acting centrally as well as peripherally, and the autonomic effects of these diseases
need to be studied in more detail. In each case, the disease responds to immunotherapies
such as steroids, plasma exchange, intravenous immunoglobulins and more aggressive
immunosuppressive treatments. Thus these are all potentially reversible neurological
disorders.
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© 2015 Published by Elsevier Inc.