Journal of the peripheral nervous system : JPNS
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J. Peripher. Nerv. Syst. · Sep 2013
Correlation of nerve ultrasound, electrophysiological, and clinical findings in post Guillain-Barré syndrome.
We aimed to correlate functional disability, electrophysiology, and nerve ultrasound in patients after Guillain-Barré syndrome (GBS). Seventy-five healthy controls and 41 post-GBS patients (mean 3.4 years, SD ± 2.91 years after onset) underwent clinical, sonographic, and electrophysiological evaluation. Compared to healthy controls, the post-GBS patients showed: (1) a mean Rasch-built Overall Disability Scale score of 31.8 (SD ± 11.6), modified Rasch-built fatigue severity scale score of 15.6 (SD ± 3.2), Medical Research Council sum score of 22 (SD ± 5.6); (2) electrophysiological signs of permanent axonal loss in the majority of the peripheral nerves; (3) sonographical evidence of higher cross-sectional area values (CSA) of the ulnar (elbow, p < 0.001), radial (spiral groove, p < 0.001), tibial nerve (popliteal fossa, p < 0.001) and brachial plexus (supraclavicular space, p < 0.001). ⋯ Neither nerve ultrasound nor electrophysiology correlated with muscle strength, overall disability, and fatigue scale. Compared to healthy controls, post-GBS patients had significant functional disability. Despite significant abnormalities in both electrophysiology and ultrasound compared to healthy controls, neither electrophysiology nor nerve ultrasound correlated with functional disability of these patients.
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Alterations in peripheral nervous system (PNS) insulin support may contribute to diabetic neuropathy (DN); yet, PNS insulin signaling is not fully defined. Here, we investigated in vivo insulin signaling in the PNS and compared the insulin responsiveness to that of muscle, liver, and adipose. Non-diabetic mice were administered increasing doses of insulin to define a dose-response relationship between insulin and Akt activation in the dorsal root ganglion (DRG) and sciatic nerve. ⋯ At a therapeutically relevant dose, Akt was activated in the muscle, liver, and adipose at 30 min, correlating with the changes in blood glucose levels. Interestingly, the sciatic nerve showed a similar signaling profile as insulin-sensitive tissues; however, there was not a comparable activation in the DRG or spinal cord. These results present new evidence regarding PNS insulin signaling pathways in vivo and provide a baseline for studies investigating the contribution of disrupted PNS insulin signaling to DN pathogenesis.