MRI signs of brachial plexus and median nerve inflammation and morphological changes in chronic whiplash associated disorder

Physiotherapy ◽  
2019 ◽  
Vol 105 ◽  
pp. e2
Author(s):  
J. Greening ◽  
K. Anantharaman ◽  
R. Young ◽  
A. Dilley
2021 ◽  
pp. 1-9
Author(s):  
Kyosuke Koide ◽  
Atsuhiko Sugiyama ◽  
Hajime Yokota ◽  
Hiroki Mukai ◽  
Jiaqi Wang ◽  
...  

<b><i>Introduction:</i></b> This study assessed the morphological changes and diffusion tensor imaging (DTI)-derived parameters of the brachial plexus using magnetic resonance neurography (MRN) in patients with anti-myelin-associated glycoprotein (anti-MAG) neuropathy. <b><i>Methods:</i></b> Eight patients with anti-MAG neuropathy underwent MRN of the brachial plexus with 3-dimensional (3D) short tau inversion recovery (STIR) and DTI sequences. Two neuroradiologists and a neurologist qualitatively assessed nerve hypertrophy on 3D STIR MRN. The cross-sectional area (CSA) of the nerve roots was measured. Quantitative analyses of fractional anisotropy (FA) and axial, radial, and mean diffusivity (AD, RD, and MD) were obtained after postprocessing on DTI and manual segmentation. <b><i>Results:</i></b> There was nerve hypertrophy in 37.5% of the patients with anti-MAG neuropathy. All patients with anti-MAG neuropathy with nerve hypertrophy were refractory to rituximab therapy. The CSA of the nerve roots was inversely correlated with FA and positively correlated with MD and RD. FA decreased in the nerve roots and inversely correlated with disease duration. <b><i>Conclusions:</i></b> Nerve hypertrophy appears in the proximal portion of peripheral nerves, such as the brachial plexus, in patients with anti-MAG neuropathy. Altered diffusion in the nerve roots might be associated with the loss of myelin integrity due to the demyelination process in anti-MAG neuropathy.


2019 ◽  
Vol 7 ◽  
pp. 2050313X1984297 ◽  
Author(s):  
Miyako Kishimoto ◽  
Masayuki Adachi ◽  
Koichi Takahashi ◽  
Kazushige Washizaki

In this study, we report a case of a 50-year-old Japanese man who had chronic whiplash-associated disorder, hyperlipidaemia, hyperuricacidaemia, and mild liver dysfunction due to excessive alcohol intake. Recently, he developed mild tremor in his left hand. Initiation of clonazepam (0.5 mg once daily before bedtime) helped to gradually ameliorate the tremor. However, 13 days after clonazepam initiation, his liver function and lipid profiles aggravated, and his postprandial glucose level increased to 400 mg/dL. Clonazepam was stopped promptly, and at 7 days after discontinuation, the abnormal triglyceride levels, liver dysfunction, and glycometabolism improved without any other medical intervention. This case may provide information on cautious use of clonazepam. When clonazepam is used for patients with existing hyperlipidaemia and liver dysfunction, it may cause abnormal lipid profile, aggravate liver dysfunction, and lead to remarkable glucose elevation.


2007 ◽  
Vol 20 (2) ◽  
pp. 150-156 ◽  
Author(s):  
S.K. Pandey ◽  
V.K. Shukla

2016 ◽  
Vol 46 (10) ◽  
pp. 902-910 ◽  
Author(s):  
Scott F. Farrell ◽  
Peter G. Osmotherly ◽  
Jon Cornwall ◽  
Peter Lau ◽  
Darren A. Rivett

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