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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 eatures and outcomes of patients with ocular neuromyotonia.
10 ls in a large series of patients with ocular neuromyotonia.
11 sms of cerebellar dysfunction and persistent neuromyotonia.
12 ravenous immunoglobulin, considering primary neuromyotonia.
14 adiation is the most common cause for ocular neuromyotonia, affecting the sixth cranial nerve most of
15 associated with a broad range of phenotypes: neuromyotonia alone or with seizures, EA1 with seizures,
16 on of voltage-gated K(+) channels (VGKCs) in neuromyotonia and demyelination in peripheral neuropathi
17 des of cerebellar dysfunction and persistent neuromyotonia and is associated with an increased incide
19 ied antibody-mediated mechanisms in acquired neuromyotonia, and began the molecular work that identif
20 roup of patients with undulating myokymia or neuromyotonia, and EMG doublet or multiplet ('myokymic')
21 s case highlights the overlap of myasthenia, neuromyotonia, and thymoma, emphasizing the importance o
22 mbert Eaton myasthenic syndrome and acquired neuromyotonia are caused by antibodies to voltage-gated
23 uch as Lambert-Eaton myasthenic syndrome and neuromyotonia are clearly mediated by autoantibodies.
24 mplex proteins.We present a case of acquired neuromyotonia as the heralding symptom of recurrent thym
26 ed protein, or glycine receptor antibodies), neuromyotonia (Caspr2 antibodies), and opsoclonus--myocl
29 se many terms including undulating myokymia, neuromyotonia, Isaacs' syndrome and Cramp-Fasciculation
31 ases of fetal arthrogryposis and in acquired neuromyotonia, Morvan's syndrome and Miller-Fisher syndr
32 tissue have been identified in patients with neuromyotonia, Morvan's syndrome, limbic encephalitis an
33 essed Shaker-type K+ channels cause acquired neuromyotonia, MoS and LE, and suggest that future assay
34 antibody with limbic encephalitis (n = 1) or neuromyotonia (n = 1), and collapsin response-mediator p
35 neural tissues with sera from patients with neuromyotonia (n = 10), MoS (n = 2) or LE (n = 5), compa
36 in several neurological syndromes, including neuromyotonia (NMT), Morvan syndrome (MoS), and limbic e
37 tactin-associated protein-antibody-2, 10 had neuromyotonia or Morvan's syndrome, compared with only 3
40 .1 subunits more prominently than did MoS or neuromyotonia sera, suggesting an association between hi
42 ility is the chief manifestation of acquired neuromyotonia; the combination of neuromyotonia with aut
44 patients with an observed episode of ocular neuromyotonia were included and the medical records were
47 f acquired neuromyotonia; the combination of neuromyotonia with autonomic and CNS involvement is call