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In their case report, Hines et al. reported spinal myoclonus as a novel neuromuscular manifestation of Caspr2 paraneoplastic disease. Caspr2 antibodies have been previously identified in conjunction with limbic encephalitis and neuromyotonia, but not in cases of spinal myoclonus. To make the diagnosis of spinal myoclonus, as Drs. Tipton, van Gerpen, and Chen appropriately acknowledge, there must be simultaneous and stereotypical activation from at least 4 muscle groups with contiguous spinal cord innervation. Given the novelty of the findings, alternative diagnoses—such as stiff-person syndrome (SPS) and the triple flexion response—must be definitively excluded. Hines et al. verify that the 2 most common SPS antibodies, GAD65 and amphiphysin, were absent from the serum, and that EMG confirmed 5 muscle groups were involved in this stereotypical response. In addition, treatment of the underlying malignancy led to resolution of motor symptoms, further implicating a pathogenic paraneoplastic process. Although the final electrographic diagnosis remains contested, this case highlights the clinical diversity of paraneoplastic disorders and the importance of accurate characterization of clinical and EMG findings in neurologic disease.
In their case report, Hines et al. reported spinal myoclonus as a novel neuromuscular manifestation of Caspr2 paraneoplastic disease. Caspr2 antibodies have been previously identified in conjunction with limbic encephalitis and neuromyotonia, but not in cases of spinal myoclonus.
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Author disclosures are available upon request (journal{at}neurology.org).
- © 2019 American Academy of Neurology
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