The results suggest that, using a transcranial multipulse stimulation, monitoring of motor-evoked potentials from the external anal sphincter is feasible during ketamine- and propofol-based anesthesia. However, further improvement of techniques would be required for intraoperative elicitation of motor-evoked potentials from the external anal sphincter.

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Various anodic substitution reactions such as fluorination, methoxylation, acetoxylation, and cyanation of heteroatom compounds containing a sulfur or nitrogen atom were comparatively studied using boron‐doped diamond (BDD), Pt, and glassy carbon (GC) anodes. It was found that BDD anode is highly effective for these anodic substitution reactions similarly to Pt anode although both BDD and GC electrodes are carbon‐based materials.

Neuronal excitability in the trigeminal sensory nuclei (TSN) changes after nerve transection. We examined the effects of chronic transection of the trigeminal nerve on the c-Fos-immunoreactivity in the TSN induced 2 h after 10 min of electrical stimulation of the trigeminal ganglion (TG) at C-fiber activating condition (1.0 mA, 5 ms, 5 Hz) in urethane-anesthetized rats. In the non-transected control rats, stimulation of the TG induced c-Fos-immunoreactive cells (c-Fos-IR cells) mostly in superficial layers (VcI/II) of the nucleus caudalis (Vc) in its full extent along the dorsomedial-ventrolateral axis, but modestly in the rostral TSN above the obex, the principal, oral, and interpolar nuclei. Three days, 1, 2, or 3 weeks after transection of the inferior alveolar (IAN), infraorbital, or masseteric nerves, the stimulation of the TG induced c-Fos-IR cells in the central terminal fields of the transected nerve in the rostral TSN and magnocellular zone of the Vc. However, the number of c-Fos-IR cells in the VcI/II decreased inside the central terminal fields of the transected nerve and increased outside the fields. These results indicate that transection of the trigeminal nerve increases the excitability of TSN neurons that receive inputs from injured mechanoreceptors and uninjured nociceptors, but decreases it from injured nociceptors. The altered c-Fos responses may imply mechanisms of neuropathic pain seen after nerve injury.

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