Editing Morvan's syndrome (section)

==Mechanism==
Antibodies against [[voltage-gated potassium channels]] (VGKC), which are detectable in about 40% of patients with acquired neuromytonia, have been implicated in Morvan's [[pathophysiology]].  Raised serum levels of antibodies to VGKCs have been reported in three patients with Morvan's Syndrome.  Binding of [[blood serum|serum]] from a patient with Morvan's Syndrome to the [[hippocampus]] in a similar pattern of antibodies to known VGKC suggest that these antibodies can also cause CNS dysfunction.  Additional antibodies against [[neuromuscular junction]] channels and receptors have also been described.  Experimental evidence exists that these anti-VGKC antibodies cause nerve hyperexcitability by suppression of voltage gated K+ outward currents, whereas other, yet undefined humoral factors have been implicated in anti-VGKC antibody negative neuromyotonia.<ref name=clinical/> It is believed that antibodies to the Shaker-type K+ channels (the Kv1 family) are the type of potassium channel most strongly associated with acquired neuromyotonia and Morvan's Syndrome.<ref>{{cite journal|title=Neuromyotonia and limbic encephalitis sera target mature Shaker-type K+ channels: subunit specificity correlates with clinical manifestations |journal=Brain|date=2006-03-13|first=Kleopas A.|last=Kleopa |author2=Lauren B. Elman |author3=Bethan Lang|volume=129|issue=Pt 6|pages=1570–1584|doi=10.1093/brain/awl084|pmid=16613892 |display-authors=etal|doi-access=free}}</ref>

Whether VGKC antibodies play a pathogenic role in the [[encephalopathy]] as they do in the [[peripheral nervous system]] is as yet unclear.  It has been suggested that the VGKC antibodies may cross the [[blood–brain barrier]] and act centrally, binding predominantly to thalamic and [[striatum|striatal]] neurons causing encephalopathic and autonomic features.<ref name=sub-acute/>