Browsing by Subject "Sciatic nerve"

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    A Highly Miniaturized, Chronically Implanted ASIC for Electrical Nerve Stimulation
    (IEEE, 2022) Shah, Jay V.; Quinkert, Christopher J.; Collar, Brett J.; Williams, Michael T.; Biggs, Ethan N.; Irazoqui, Pedro P.; Electrical and Computer Engineering, School of Engineering and Technology
    We present a wireless, fully implantable device for electrical stimulation of peripheral nerves consisting of a powering coil, a tuning network, a Zener diode, selectable stimulation parameters, and a stimulator IC, all encapsulated in biocompatible silicone. A wireless RF signal at 13.56 MHz powers the implant through the on-chip rectifier. The ASIC, designed in TSMC’s 180 nm MS RF G process, occupies an area of less than 1.2 mm2. The IC enables externally selectable current-controlled stimulation through an on-chip read-only memory with a wide range of 32 stimulation parameters (90 – 750 μA amplitude, 100 μs or 1 ms pulse width, 15 or 50 Hz frequency). The IC generates the constant current waveform using an 8-bit binary weighted DAC and an H-Bridge. At the most power-hungry stimulation parameter, the average power consumption during a stimulus pulse is 2.6 mW with a power transfer efficiency of ~5.2%. In addition to benchtop and acute testing, we chronically implanted two versions of the device (a design with leads and a leadless design) on two rats’ sciatic nerves to verify the long-term efficacy of the IC and the full system. The leadless device had the following dimensions: height of 0.45 cm, major axis of 1.85 cm, and minor axis of 1.34 cm, with similar dimensions for the device with leads. Both devices were implanted and worked for experiments lasting from 21–90 days. To the best of our knowledge, the fabricated IC is the smallest constant-current stimulator that has been tested chronically.
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    The importance of nerve microenvironment for schwannoma development
    (Springer-Verlag, 2016-08) Schulz, Alexander; Büttner, Robert; Hagel, Christian; Baader, Stephan L.; Kluwe, Lan; Salamon, Johannes; Mautner, Victor-Felix; Mindos, Thomas; Parkinson, David B.; Gehlhausen, Jeffrey R.; Clapp, D. Wade; Morrison, Helen; Department of Pediatrics, IU School of Medicine
    Schwannomas are predominantly benign nerve sheath neoplasms caused by Nf2 gene inactivation. Presently, treatment options are mainly limited to surgical tumor resection due to the lack of effective pharmacological drugs. Although the mechanistic understanding of Nf2 gene function has advanced, it has so far been primarily restricted to Schwann cell-intrinsic events. Extracellular cues determining Schwann cell behavior with regard to schwannoma development remain unknown. Here we show pro-tumourigenic microenvironmental effects on Schwann cells where an altered axonal microenvironment in cooperation with injury signals contribute to a persistent regenerative Schwann cell response promoting schwannoma development. Specifically in genetically engineered mice following crush injuries on sciatic nerves, we found macroscopic nerve swellings in mice with homozygous nf2 gene deletion in Schwann cells and in animals with heterozygous nf2 knockout in both Schwann cells and axons. However, patient-mimicking schwannomas could only be provoked in animals with combined heterozygous nf2 knockout in Schwann cells and axons. We identified a severe re-myelination defect and sustained macrophage presence in the tumor tissue as major abnormalities. Strikingly, treatment of tumor-developing mice after nerve crush injury with medium-dose aspirin significantly decreased schwannoma progression in this disease model. Our results suggest a multifactorial concept for schwannoma formation-emphasizing axonal factors and mechanical nerve irritation as predilection site for schwannoma development. Furthermore, we provide evidence supporting the potential efficacy of anti-inflammatory drugs in the treatment of schwannomas.