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1 with GABAB encephalitis have presented with limbic encephalitis.
2 s, and a mixed movement disorder rather than limbic encephalitis.
3 he cognitive impairment associated with this limbic encephalitis.
4 age-gated potassium channel complex antibody limbic encephalitis.
5 dentify the real autoantigen associated with limbic encephalitis.
6 be the target of antibodies associated with limbic encephalitis.
7 patients (P < 0.0001), who predominantly had limbic encephalitis.
8 Only 26% had classical limbic encephalitis.
9 y been reported in three cases of reversible limbic encephalitis.
10 romyotonia (NMT), Morvan syndrome (MoS), and limbic encephalitis.
11 ented as classic paraneoplastic syndromes (5 limbic encephalitis, 1 paraneoplastic encephalomyelitis,
12 e neurological presentations (5 brainstem or limbic encephalitis, 3 cerebellar ataxia, 2 Lambert-Eato
13 reactivation is well established as causing limbic encephalitis after haematopoietic stem cell trans
14 seen with symptoms suggestive of autoimmune limbic encephalitis, although they can be paucisymptomat
15 whereas LGI1 autoantibodies are involved in limbic encephalitis, an acquired epileptic disorder asso
16 ients with neuromyotonia, Morvan's syndrome, limbic encephalitis and a few cases of adult-onset epile
18 We analysed sera and CSF of 57 patients with limbic encephalitis and antibodies attributed to voltage
20 with various clinical presentations, such as limbic encephalitis and complex and diffuse encephalopat
21 od B-cell populations from two patients with limbic encephalitis and faciobrachial dystonic seizures
22 vant, but not all patients had a 'classical' limbic encephalitis and some did not receive immunothera
23 re found in patients with different forms of limbic encephalitis, and in a few patients with epilepsy
24 h VGKC antibodies described in patients with limbic encephalitis, and the subsequent seminal paper de
25 re considered definitely autoimmune, 10 with limbic encephalitis (antibody specificity: 5 LGI1, 1 con
27 ated potassium channels should be changed to limbic encephalitis associated with LGI1 antibodies, and
28 ibodies, 79 had the presumptive diagnosis of limbic encephalitis, dementia, cognitive dysfunction, or
29 otein-2 (CASPR2), are found in patients with limbic encephalitis, faciobrachial dystonic seizures, Mo
30 otassium channel complex antibody-associated limbic encephalitis has recently been recognized as a fo
32 a single institution, who developed subacute limbic encephalitis initially considered of uncertain ae
38 -responsive clinical presentations including limbic encephalitis, Morvan's syndrome and acquired neur
39 onopathy (n = 7), K(+)-channel antibody with limbic encephalitis (n = 1) or neuromyotonia (n = 1), an
42 and two as stiff person syndrome; five had a limbic encephalitis or epileptic encephalopathy, two had
46 es showed that antibodies from patients with limbic encephalitis previously attributed to voltage-gat
49 ated 1, are associated with a common form of limbic encephalitis that presents with cognitive impairm
50 description of focal cortical dysplasia and limbic encephalitis, the pathology of status epilepticus
51 same period, only one paraneoplastic case of limbic encephalitis was identified between the two main
53 -treated LGI1 VGKC-complex antibody-mediated limbic encephalitis were investigated using in vivo ultr
55 ium channel (VGKC) complex antibody-mediated limbic encephalitis with generalized hippocampal atrophy
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