Infection-Associated Peripheral Nerve Hyperexcitability: An Under-Recognized Entity

Peripheral nerve hyperexcitability (PNH) and neuromyotonia have been mainly attributed to antibodies against voltage-gated potassium channels (VGKC). Concurrent autoimmune disorders, malignancies, and heavy metal toxicity have also been implicated. There is scarce mention about infection as a triggering factor for PNH. There are no reports of methicillin-resistant Staphylococcus aureus (MRSA) infection being a possible precipitating factor for development of PNH.

Case series and literature review.

Four subjects were diagnosed to have features of PNH based on clinical and electrophysiological assessment. All the subjects had concurrent evidence of cutaneous abscesses requiring surgical intervention and antibiotic therapy. The cultures in all of them revealed growth of Staphylococcus aureus with three of them being MRSA isolates. Two subjects tested positive for anti-VGKC antibodies. There was remarkable resolution in neuromyotonia after antibiotics in three subjects. One subject succumbed to fulminant MRSA septicemia.

There appears to be a definitive link between staphylococcal infection (MRSA in particular) and development of PNH. The temporal evolution of PNH associated with the infection and resolution following treatment of the infection does support a causal association. The enterotoxins produced by staphylococci act as superantigens and could trigger an inflammatory cascade along with development of cross reacting antibodies against VGKC in peripheral nerves. Future studies with animal models could provide more directions in this regard.