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1 ial dystonic seizures, Morvan's syndrome and neuromyotonia.
2 toms, electrophysiologically confirmed to be neuromyotonia.
3 s sampled, which suggests the possibility of neuromyotonia.
4 had a history of episodic ataxia and 19 had neuromyotonia.
5 halitis and seizures, Morvan's syndrome, and neuromyotonia.
6 current trains of axonal firing described in neuromyotonia.
7 re similar to the clinical manifestations of neuromyotonia.
8 encephalitis, Morvan's syndrome and acquired neuromyotonia.
9 sms of cerebellar dysfunction and persistent neuromyotonia.
10 ravenous immunoglobulin, considering primary neuromyotonia.
12 associated with a broad range of phenotypes: neuromyotonia alone or with seizures, EA1 with seizures,
13 on of voltage-gated K(+) channels (VGKCs) in neuromyotonia and demyelination in peripheral neuropathi
14 des of cerebellar dysfunction and persistent neuromyotonia and is associated with an increased incide
16 ied antibody-mediated mechanisms in acquired neuromyotonia, and began the molecular work that identif
17 roup of patients with undulating myokymia or neuromyotonia, and EMG doublet or multiplet ('myokymic')
18 s case highlights the overlap of myasthenia, neuromyotonia, and thymoma, emphasizing the importance o
19 mbert Eaton myasthenic syndrome and acquired neuromyotonia are caused by antibodies to voltage-gated
20 uch as Lambert-Eaton myasthenic syndrome and neuromyotonia are clearly mediated by autoantibodies.
21 mplex proteins.We present a case of acquired neuromyotonia as the heralding symptom of recurrent thym
23 ed protein, or glycine receptor antibodies), neuromyotonia (Caspr2 antibodies), and opsoclonus--myocl
25 se many terms including undulating myokymia, neuromyotonia, Isaacs' syndrome and Cramp-Fasciculation
27 ases of fetal arthrogryposis and in acquired neuromyotonia, Morvan's syndrome and Miller-Fisher syndr
28 tissue have been identified in patients with neuromyotonia, Morvan's syndrome, limbic encephalitis an
29 essed Shaker-type K+ channels cause acquired neuromyotonia, MoS and LE, and suggest that future assay
30 antibody with limbic encephalitis (n = 1) or neuromyotonia (n = 1), and collapsin response-mediator p
31 neural tissues with sera from patients with neuromyotonia (n = 10), MoS (n = 2) or LE (n = 5), compa
32 in several neurological syndromes, including neuromyotonia (NMT), Morvan syndrome (MoS), and limbic e
33 tactin-associated protein-antibody-2, 10 had neuromyotonia or Morvan's syndrome, compared with only 3
36 .1 subunits more prominently than did MoS or neuromyotonia sera, suggesting an association between hi
38 ility is the chief manifestation of acquired neuromyotonia; the combination of neuromyotonia with aut
40 f acquired neuromyotonia; the combination of neuromyotonia with autonomic and CNS involvement is call
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