Acquired Neuromyotonia Precipitated by Thyroid Surgery and Associated with Antiacetylcholine Receptor Antibodies

Case Report The thyroid gland of a 62-year-old man was subtotally removed because of nodosal enlargement. Hyperthyroidosis was indicated by elevated free triiodothyromine, free thyroxine and decreased thyroidstimulating hormone levels. Histology did not show any inflammation or tumor tissue, and he has been successfully treated with L-thyroxine. Two weeks after surgery, he realized that he could not relax his grip, and had generalized muscle stiffness. On neurological examination, signs of clinical pseudomyotonia with delayed relaxation were observed without any indication of neuropathy, myopathy or involvement of the central nervous system. No clinical symptoms and signs of MG were observed. Simultaneous concentric needle electromyography on superficial digital flexor, deltoid and abductor pollicis brevis muscles showed continuous spontaneous motor unit activity at rest with reDear Sir, Receptors and ion channels of the neuromuscular junction are targets of several acquired immune-mediated diseases. Antibodies generated against acetylcholine receptors (AchR) result in myasthenia gravis (MG), while antivoltage-gated calcium channels are pathogenic in Lambert-Eaton myasthenic syndrome [1] . Since the description of Isaacs’ syndrome in 1961, several phenotypic variants of acquired peripheral nerve hyperexcitability syndromes have been described [2] . In neuromyotonia, failure to relax voluntary muscle contraction (‘pseudomyotonia’) occurs together with muscle twitching or cramps. Muscle stiffness, increased sweating and hypertrophic calf muscles can be detected in some patients [2] . The association with other autoimmune diseases, especially MG, and the paraneoplastic origin in some cases, e.g. presence of thymoma, suggests an autoimmune origin. Indeed, plasma exchange alleviates the symptoms and the IgG of patients can transfer the disease. Antibodies against voltage-gated potassium channels (VGKC) can be detected in the peripheral blood of the majority of patients [3–5] . Interestingly, antibodies generated against Received: January 25, 2006 Accepted: March 24, 2006 Published online: June 14, 2006