ABSTRACT
INTRODUCTION: To visualize peripheral nerves in patients with chronic inflammatory demyelinating polyneuropathy (CIDP), we used MR imaging. We also quantified the volumes of the brachial and lumbar plexus and their nerve roots. METHODS: Thirteen patients with CIDP and 12 healthy volunteers were enrolled. Whole-body MR neurography based on diffusion-weighted whole-body imaging with background body signal suppression (DWIBS) was performed. Peripheral nerve volumes were calculated from serial axial MR images. RESULTS: The peripheral nervous system was visualized with 3-dimensional reconstruction. Volumes ranged from 8.7 to 49.5 cm3 /m2 in the brachial plexus and nerve roots and from 10.2 to 53.5 cm3 /m2 in the lumbar plexus and nerve roots. Patients with CIDP had significantly larger volumes than controls (P < 0.05), and volume was positively correlated with disease duration. CONCLUSIONS: MR neurography and the measurement of peripheral nerve volume are useful for diagnosing and assessing CIDP. Muscle Nerve 55: 483-489, 2017.
Subject(s)
Magnetic Resonance Imaging/methods , Peripheral Nervous System/diagnostic imaging , Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/diagnostic imaging , Adult , Aged , Aged, 80 and over , Case-Control Studies , Female , Humans , Imaging, Three-Dimensional , Lumbosacral Plexus/diagnostic imaging , Male , Middle Aged , Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/physiopathology , Statistics as TopicABSTRACT
Clioquinol is considered to be a causative agent of subacute myelo-optico neuropathy (SMON), although the pathogenesis of SMON is yet to be elucidated. We have previously shown that clioquinol inhibits nerve growth factor (NGF)-induced Trk autophosphorylation in PC12 cells transformed with human Trk cDNA. To explore the further mechanism of neuronal damage by clioquinol, we evaluated the acetylation status of histones in PC12 cells. Clioquinol reduced the level of histone acetylation, and the histone deacetylase (HDAC) inhibitor Trichostatin A upregulated acetylated histones and prevented the neuronal cell damage caused by clioquinol. In addition, treatment with HDAC inhibitor decreased neurite retraction and restored the inhibition of NGF-induced Trk autophosphorylation by clioquinol. Thus, clioquinol induced neuronal cell death via deacetylation of histones, and HDAC inhibitor alleviates the neurotoxicity of clioquinol. Clioquinol is now used as a potential medicine for malignancies and neurodegenerative diseases. Therefore, HDAC inhibitors can be used as a candidate medicine for the prevention of its side effects on neuronal cells.
