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Arm Cortex S3C2440 Microcontroller Application for Transcranial Magnetic Stimulation's Pulse Forming on Bax Reactive Cells and Cell Death in Ischemia Induced Rats

  • Tac, Han-Ho (Department of Electrical Engineering, Gyeongnam National University of Science and Technology) ;
  • Kim, Whi-Young (Department of Biomedical Engineering, Dongju College)
  • Received : 2016.01.21
  • Accepted : 2016.03.24
  • Published : 2016.06.30

Abstract

Transcranial magnetic stimulation devices has been used mainly for diagnostic purposes by measuring the functions of the nervous system rather than for treatment purposes, and has a problem of considerable energy fluctuations per repeated pulse. The majority of strokes are caused by ischemia and result in brain tissue damage, leading to problems of the central nervous system including hemiparesis, dysfunction of language and consciousness, and dysfunction of perception. Control is difficult and the size is large due to the difficulty of digitalizing the energy stored in a capacitor, and there are many heavy devices. In addition, there are many constraints when it is used for a range of purposes such as head and neck diagnosis, treatment and rehabilitation of nerve palsy, muscle strengthening, treatment of urinary incontinence etc. Output stabilization and minimization of the energy variation rate are required as the level of the transcranial magnetic stimulation device is dramatically improved and the demand for therapeutic purposes increases. This study developed a compact, low cost transcranial magnetic stimulation device with minimal energy variation of a high repeated pulse and output stabilization using a real time capacitor charge discharge voltage. Ischemia was induced in male SD rats by closing off the common carotid artery for 5 minutes, after which the blood was re-perfused. In the cerebrum, the number of PARP reactive cells after 24 hours significantly decreased (p < 0.05) in the TMS group compared to the GI group. As a result, TMS showed the greatest effect on necrosis-related PARP immuno-reactive cells 24 hours after ischemia, indicating necrosis inhibition, blocking of neural cell death, and protection of neural cells.

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References

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