Browsing by Subject "Electric stimulation"

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    Increased threshold of short-latency motor evoked potentials in transgenic mice expressing Channelrhodopsin-2
    (PLoS, 2017-05-31) Wu, Wei; Xiong, Wenhui; Zhang, Ping; Chen, Lifang; Fang, Jianqiao; Shields, Christopher; Xu, Xiao-Ming; Jin, Xiaoming; Neurological Surgery, School of Medicine
    Transgenic mice that express channelrhodopsin-2 or its variants provide a powerful tool for optogenetic study of the nervous system. Previous studies have established that introducing such exogenous genes usually does not alter anatomical, electrophysiological, and behavioral properties of neurons in these mice. However, in a line of Thy1-ChR2-YFP transgenic mice (line 9, Jackson lab), we found that short-latency motor evoked potentials (MEPs) induced by transcranial magnetic stimulation had a longer latency and much lower amplitude than that of wild type mice. MEPs evoked by transcranial electrical stimulation also had a much higher threshold in ChR2 mice, although similar amplitudes could be evoked in both wild and ChR2 mice at maximal stimulation. In contrast, long-latency MEPs evoked by electrically stimulating the motor cortex were similar in amplitude and latency between wild type and ChR2 mice. Whole-cell patch clamp recordings from layer V pyramidal neurons of the motor cortex in ChR2 mice revealed no significant differences in intrinsic membrane properties and action potential firing in response to current injection. These data suggest that corticospinal tract is not accountable for the observed abnormality. Motor behavioral assessments including BMS score, rotarod, and grid-walking test showed no significant differences between the two groups. Because short-latency MEPs are known to involve brainstem reticulospinal tract, while long-latency MEPs mainly involve primary motor cortex and dorsal corticospinal tract, we conclude that this line of ChR2 transgenic mice has normal function of motor cortex and dorsal corticospinal tract, but reduced excitability and responsiveness of reticulospinal tracts. This abnormality needs to be taken into account when using these mice for related optogenetic study.
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    Troubleshooting Interstim Sacral Neuromodulation Generators to Recover Function
    (Springer Nature, 2018-08-20) Powell, C.R.; Urology, School of Medicine
    PURPOSE OF REVIEW: Sacral neuromodulation (SNM) is being used to treat lower urinary tract symptoms (LUTS) with growing popularity among clinicians in multiple specialties. As this therapy becomes more common in the USA and Europe, urologists will encounter more patients implanted with SNM generators. RECENT FINDINGS: Over time, it has recently been understood that up to 53% will develop pain at the implant site as reported by Groen et al. (J Urol 186:954, 2011) and 3-38% will lose effective stimulation as reported by Al-zahrani et al. (J Urol 185:981, 2011) and White et al. (Urology 73:731, 2009). There is a paucity of troubleshooting methodology in the literature, apart from revision surgery, to salvage the SNM generator. In fact, it has been suggested that one contemporary series' failure rate is lower than some historic series because of the ability to reprogram devices as reported by Siegel et al. (J Urol 199:229, 2018). Standard algorithms for such reprogramming efforts are lacking in the literature and may salvage some patients otherwise destined for surgical revision or addition of multimodal therapy to achieve acceptable symptom control. It is possible to troubleshoot and thereby salvage many SNM generators, saving patients from surgical revision in many cases and increasing the number of patients with persistent benefit from SNM. The algorithms presented in this manuscript represent a systematic strategy for reprogramming and troubleshooting SNM generators.