Hello, everyone. My name is Henry Ortiz, and I am a second-year osteopathic medical student at the University of New England. Today, I will discuss our findings on the parasympathetic nervous system's influence on hypoalgesia induced by noxious electrical stimulation, otherwise known as NXES. You may have heard of transcutaneous electrical nerve stimulation, or TENS, which is used to treat pain. TENS involves the application of electrical current through the skin, and it feels like a strong but comfortable tingling or buzzing sensation. This study involves a different type of stimulation that is increased to the maximum level of pain that is still tolerable. This should activate the natural pain inhibition system inherent in our nervous systems that is referred to as DNIC in animal models and CPM in humans. Noxious electrical stimulation has been shown to produce long-term hypoalgesia in both healthy and clinical populations. However, not all patients experience pain relief. This study is designed to examine the influence of the autonomic nervous system on pain inhibition in young healthy adults. The parasympathetic activation is assessed using heart rate variability, or HRV, of the respiratory sinus arrhythmia, which is shown in the lower figure here. The red signal is heart rate, and the blue signal indicates respiratory inhalation and exhalation. When heart rate increases during inhalation and decreases during exhalation. When an individual is in a heightened state of fight or flight or freeze, heart rate variability is low. When they return to a state of rest and digest, heart rate variability increases. The fluctuations are based on a complex interaction between the intrinsic cardiac nervous system, the autonomic nervous system, and baroceptor reflexes, which I'll explain in another slide. First, I'd like to shift our attention over to the portion of the research protocol that encompasses our findings. The session starts with a collection of baseline pressure pain threshold and heat temporal summation, followed by 10 minutes of resting ECG, before applying 20 minutes of noxious electrical stimulation. Heat temporal summation, as seen here in figure 1, is measured of pain facilitation. 10 mildly painful heat pulses are applied to the knee every 1.5 seconds. Participants rate the pain on a visual analog scale, and the differences between the highest pain rating and the first is used in the analysis. We also use pressure pain thresholds, shown here in figures 2 and 4, to assess pain inhibition. Pressure is applied at the knee, and the person indicates when the sensation changes from pressure to pain. This is measured twice, and the averages are used in the analysis. The noxious electrical stimulation is applied to the knee, as shown here in figure 3. The parameters are shown in the slide here in the corner, and the stimulation is increased to the highest tolerated level. The amplitude is adjusted throughout the 20 minutes to maintain a constant dose of NXES. As shown here in figure 5, an increase in PPT after NXES indicates pain inhibition because it takes more pressure for the person to perceive pain. This slide describes the heart rate variability measures in more detail. Heart rate is measured for the 10 minutes during resting, and the 20 minutes of noxious electrical stimulation. Figure 6 here on the top shows the R waves of the ECG signal that are identified. The times between successive R waves are calculated and saved in a time series shown at the bottom here of figure 6. The RR interval time series is analyzed in the time domain to obtain the root mean square of the squared differences of RR intervals, which is known as RMSSD, and PNN50, which is the percentage of successive RR interval pairs that differ by more than 50 milliseconds. The time series is then put through a fast Fourier transform shown here in figure 7 that identifies the frequencies and proportion of sine waves that make up the time series. The resulting power spectrum is shown here in figure 8. On the left, you can see the participants' HRV data at rest, which has a frequency power of about 64.7%. On the right, you can see the same participants' data, where they only had 18.6% high frequency power. This indicates that NXES stressed the nervous system and reduced parasympathetic input. Here we see the results from 9 male and 10 female young healthy participants. Figure 9 shows the inhibition of pressure pain in the blue bars and inhibition of temporal stimulation in the purple bars. Figure 10 shows the average reduction in high frequency power during noxious electrical stimulation, indicating that NXES was indeed stressful to the nervous system in the group as a whole. Figure 11 shows the individual differences in high frequency power that are quite variable and more detailed analysis of individual differences is warranted. In figure 12, we see no relationship observed between baseline HRV and changes in pain perception during heat temporal stimulation. However, the change in HRV during the NXES did relate to changes in heat temporal stimulation after the NXES. The first key finding was that NXES significantly inhibited pain, which is consistent with prior studies in our lab. Second, we found that baseline HRV had no influence on pain inhibition that was observed after noxious electrical stimulation. However, we observed a significant reduction in HRV as measured high frequency power, indicating that noxious electrical stimulation significantly stressed the nervous system, resulting in less parasympathetic activity. We also found that despite the appearance of large variability in the responses of individual participants, on average, the participants who did display an increase in parasympathetic activity measured by RMSSD had the largest inhibition of pain from heat temporal stimulation. In summary, our findings suggest that noxious electrical stimulation induces hypoalgesia through mechanisms that involve the autonomic nervous system. While these findings provide valuable insights, further research is needed to explore these relationships in individuals with chronic pain and to assess whether similar changes occur during functional activities. I'd like to give a special thanks to the University of New England College of Osteopathic Medicine, the Westbrook College of Health Professions, Department of Physical Therapy, and all the participants who made this research possible. I'd also like to give thanks to Kahn Family Research Fellowship for providing the funding necessary for this research. Please feel free to scan the QR code here in the bottom right hand corner of the slide to access the document containing the references for our research. Thank you for your time and attention, and I'd be happy to share any of the questions you guys might have.

parasympathetic nervous system

noxious electrical stimulation

hypoalgesia

heart rate variability

pain inhibition