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Figure 4 | Journal of Translational Medicine

Figure 4

From: Activation of axonal Kv7 channels in human peripheral nerve by flupirtine but not placebo - therapeutic potential for peripheral neuropathies: results of a randomised controlled trial

Figure 4

Effect of oral flupirtine and placebo on postischemic ectopic axonal discharge in motoneurones to abductor pollicis brevis in healthy subjects. Representative EMG activity recorded from APB in a single subject before during (grey shading) and after a period of ischemia of the lower arm before (A, Control) and after a single oral dose of flupirtine (200 mg, C). The 10 minute period of ischemia (grey) was produced by inflating a cuff around the upper arm at 200 mmHg for. The upper traces in panels A&D show raw EMG activity while the lower trace is a running power spectral density (PSD calculated from discrete 2048 point FFTs with 50% overlap and a Hamming window), with power indicated by colour. For comparisons, average PSDs during the 600s peri-ischemic (grey) and post-ischemic (black) periods are shown as absolute power (B&E) and normalised to total power (C&F). Under control conditions (A), in the post-ischemic period EMG activity comprises high frequency motor unit discharges (A, inset right) and this is reflected in the increased power in the frequency domain around 200 Hz (B&C). Two hours after a single oral dose (200 mg) of flupirtine (D) EMG activity in the peri-ischemic period is little affected, however EMG activity in the post-ischemic period is considerably reduced. The absolute reduction in post-ischemic EMG activity is reflected in the absolute PSD (E). Following flupirtine, high frequency motor unit discharges still occur post-ischemically but number of action potentials in these bursts is less (D, inset right) and this is reflected in the normalised PSD (F) with frequency components around 200 Hz being less prominent than before flupirtine (C)

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