scholarly journals Relapse of Neuromyelitis Optica Spectrum Disorder Associated with Intravenous Lidocaine

2011 ◽  
Vol 2011 ◽  
pp. 1-3 ◽  
Author(s):  
Akiyuki Uzawa ◽  
Masahiro Mori ◽  
Saeko Masuda ◽  
Kazuhiko Aoe ◽  
Satoshi Kuwabara
Keyword(s):  
Neuromyelitis Optica ◽  
Japanese Woman ◽  
Spectrum Disorder ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
Transient Effects ◽  
Intravenous Lidocaine ◽  
Old Japanese ◽  
Lidocaine Injection ◽  
Lidocaine Administration ◽  
Multiple Sclerosis Patients

Lidocaine unmasks silent symptoms and eases neuropathic pain in multiple sclerosis patients; however, the effects of lidocaine in neuromyelitis optica have never been reported. We describe the case of a 59-year-old Japanese woman with neuromyelitis optica spectrum disorder who developed optic neuritis 1 day after intravenous lidocaine injection for treating allodynia. Her symptom seemed to result from a relapse of neuromyelitis optica induced by lidocaine administration, and not because of the transient effects of intravenous lidocaine administration. The possibility that lidocaine administration results in relapse of neuromyelitis optica due to its immunomodulating effects cannot be ruled out.

Neuromyelitis optica spectrum disorder presenting with repeated hypersomnia due to involvement of the hypothalamus and hypothalamus-amygdala linkage

2015 ◽  
Vol 21 (7) ◽  
pp. 960-962 ◽  
Author(s):  
Kodai Kume ◽  
Kazushi Deguchi ◽  
Kazuyo Ikeda ◽  
Tadayuki Takata ◽  
Yohei Kokudo ◽  
...  
Keyword(s):  
Neuromyelitis Optica ◽  
Japanese Woman ◽  
Spectrum Disorder ◽  
First Episode ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
Impaired Memory ◽  
Pituitary Dysfunction ◽  
Secondary Damage ◽  
Old Japanese ◽  
Temporal Lesion

We report the case of a 46-year-old Japanese woman with neuromyelitis optica spectrum disorder presenting with repeated hypersomnia accompanied by decreased CSF orexin level. First episode associated with hypothalamic-pituitary dysfunction showed bilateral hypothalamic lesions that can cause secondary damage to the orexin neurons. The second episode associated with impaired memory showed a left temporal lesion involving the amygdala. The mechanism remains unknown, but the reduced blood flow in the hypothalamus ipsilateral to the amygdala lesion suggested trans-synaptic hypothalamic dysfunction secondary to the impaired amygdala. A temporal lesion involving the amygdala and hypothalamus could be responsible for hypersomnia due to neuromyelitis optica spectrum disorder.

scholarly journals Dysregulated B cell differentiation towards antibody-secreting cells in neuromyelitis optica spectrum disorder

2022 ◽  
Vol 19 (1) ◽  
Author(s):  
Yasunobu Hoshino ◽  
Daisuke Noto ◽  
Shuhei Sano ◽  
Yuji Tomizawa ◽  
Kazumasa Yokoyama ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Neuromyelitis Optica ◽  
Transcriptome Analysis ◽  
Spectrum Disorder ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
B Cell Differentiation ◽  
B Cell Subsets ◽  
Multiple Sclerosis Patients ◽  
Antibody Secreting Cells

Abstract Background Anti-aquaporin 4 (AQP4) antibody (AQP4-Ab) is involved in the pathogenesis of neuromyelitis optica spectrum disorder (NMOSD). However, the mechanism involved in AQP4-Ab production remains unclear. Methods We analyzed the immunophenotypes of patients with NMOSD and other neuroinflammatory diseases as well as healthy controls (HC) using flow cytometry. Transcriptome analysis of B cell subsets obtained from NMOSD patients and HCs was performed. The differentiation capacity of B cell subsets into antibody-secreting cells was analyzed. Results The frequencies of switched memory B (SMB) cells and plasmablasts were increased and that of naïve B cells was decreased in NMOSD patients compared with relapsing–remitting multiple sclerosis patients and HC. SMB cells from NMOSD patients had an enhanced potential to differentiate into antibody-secreting cells when cocultured with T peripheral helper cells. Transcriptome analysis revealed that the profiles of B cell lineage transcription factors in NMOSD were skewed towards antibody-secreting cells and that IL-2 signaling was upregulated, particularly in naïve B cells. Naïve B cells expressing CD25, a receptor of IL-2, were increased in NMOSD patients and had a higher potential to differentiate into antibody-secreting cells, suggesting CD25+ naïve B cells are committed to differentiate into antibody-secreting cells. Conclusions To the best of our knowledge, this is the first study to demonstrate that B cells in NMOSD patients are abnormally skewed towards antibody-secreting cells at the transcriptome level during the early differentiation phase, and that IL-2 might participate in this pathogenic process. Our study indicates that CD25+ naïve B cells are a novel candidate precursor of antibody-secreting cells in autoimmune diseases.

scholarly journals Neuromyelitis optica spectrum disorder with deafness and an extensive brainstem lesion

Heliyon ◽  
2021 ◽  
Vol 7 (1) ◽  
pp. e06106
Author(s):  
Asako Onda ◽  
Mikihiro Yamazaki ◽  
Takashi Shimoyama ◽  
Hiroshi Yaguchi
Keyword(s):  
Neuromyelitis Optica ◽  
Spectrum Disorder ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
Brainstem Lesion

Sleep disorders as a possible predisposing attack factor in neuromyelitis optica spectrum disorder (NMOSD): A case-control study

2021 ◽  
Vol 204 ◽  
pp. 106606
Author(s):  
Samaneh Haji Molla Rabi ◽  
Shaghayegh Shahmirzaei ◽  
Mohammad Ali Sahraian ◽  
Razieh Sadat Kazemi Mozdabadi ◽  
Hossein Rezaei Aliabadi ◽  
...  
Keyword(s):  
Sleep Disorders ◽  
Neuromyelitis Optica ◽  
Case Control Study ◽  
Case Control ◽  
Spectrum Disorder ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
Control Study

scholarly journals The possible role of Interleukin-6 as a regulator of insulin sensitivity in patients with neuromyelitis optica spectrum disorder

BMC Neurology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Zhila Maghbooli ◽  
Abdorreza Naser Moghadasi ◽  
Nasim Rezaeimanesh ◽  
Abolfazl Omidifar ◽  
Tarlan Varzandi ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Neuromyelitis Optica ◽  
Serum Levels ◽  
Spectrum Disorder ◽  
Control Group ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
Downstream Signaling ◽  
Reduce Insulin Sensitivity ◽  
Circulating Levels

Abstract Background Neuromyelitis optica spectrum disorder (NMOSD) is associated with inflammatory mediators that may also trigger downstream signaling pathways leading to reduce insulin sensitivity. Methods We aimed to determine the risk association of hyperinsulinemia in NMOSD patients with seropositive AQP4-IgG and the serum levels of interleukin (IL)-6 and IL-17A compared with the control group. Serum levels of metabolic (Insulin, Fasting Blood Sugar (FBS), lipid profile) and inflammatory (IL-6 and IL-17) markers were assessed in 56 NMOSD patients and 100 controls. Results Hyperinsulinemia was more prevalent in NMOSD patients independent of age, sex and body mass index (BMI) (48.2% vs. 26%, p = 0.005) compared to control group. After adjusting age, sex and BMI, there was significant association between lower insulin sensitivity (IS) and NMOSD risk (95% CI: Beta = 0.73, 0.62 to 0.86, p = 0.0001). Circulating levels of IL-6 and IL-17 were higher in NMOSD patients, and only IL-6 had an effect modifier for the association between lower insulin sensitivity and NMOSD risk. Conclusions Our data suggests that inflammatory pathogenesis of NMOSD leads to hyperinsulinemia and increases the risk of insulin resistance.

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