What PainTrace™ Measures
PainTrace™ measurements do not measure pain itself, but rather a distinctive response of the body to pain. Thousands of measurements of hundreds of individuals over the course of nine years has shown clearly that individuals in substantial pain produce a trace that is distinctly different from normal persons. Individuals suffering more than momentary pain tend to produce a trace that is below the neutral baseline, in what we call the negative region. Most other individuals produce a “positive” trace above the baseline. Traces right on the baseline are primarily associated with unconsciousness, whether due to sleep or general anesthesia.
Why should negative traces be linked with pain? It is important to bear in mind that PainTrace™ was more or less an accidental discovery, not a theory-led invention. In its original embodiment, referred to as the Charge Density Pulse (CDP) device, its ability to measure basic components of electrophysiology in multiple species has been well established. (Levengood, 1998). It has been demonstrated that the device can be used as an objective measure of pain.(Levengood and Gedye 2003), (D’Angelo, 2005), (D’Angelo, 2006) (Ngeow et al 2005). These differences in traces with respect to pain were noted long before we were able to answer the question of why this should be so. We now know that what is being displayed in measurements of mammals is the relative predominance at that moment of activity in the parasympathetic nervous system (PNS) as compared to activity in the sympathetic nervous system (SNS). The body’s autonomic nervous system is composed of two basic components. The sympathetic (SNS) produces the well known fight-or-flight responses like increased heart rate and blood pressure. The parasympathetic nervous system (PNS) provides a balance to such stimulation and works to calm the body down. This includes heart rate, which is more or less constantly being determined by a combination of influences from these two complementary sets of nerves. If the nerve delivering PNS signals to the heart were cut, our hearts would beat about 20 times per second faster than they do now. In fact, when emergency room physicians are faced with someone with tachycardia, a runaway fast pulse rate, they often stimulate the PNS to slow down the heart rate.
Immediately after a painful stimulus, the SNS raises heart rate and blood pressure. Thus, these have long been used as a physical measure of pain. If the pain continues for more than a few minutes however, the PNS increases activity, and heart rate and blood pressure then return to normal. In studies of pediatric surgery, all previously-used pain indicators (including heart rate, facial expression and body movements) were found to vanish before the children even left the recovery room, although they were clearly still suffering pain, based on the nature of their surgeries (Beyer et al 1990) (O’Hara 1987).
The primary nerves that carry the PNS are the vagal nerves. They appear on both sides of the body but do not act symmetrically. It is the right vagal nerve that has the most effect on the heart (Warwick and Williams 1975) (Porges, 1995). It is this same right vagal nerve that is of interest to us because it has been shown to influence far more than heart rate and blood pressure. The right vagal nerve also acts to counter pain within our bodies by triggering production of our own natural opiates (or endorphins), as shown in humans (Ness 2000) and rats (Thurston ansd Radich 1992).and numerous species of other mammals (Maixner 1982, 1984). In fact electrical stimulation of the vagal nerve has provided partial pain relief in rats (Randich And Aicher 1988), in cats (Bossut 1992), monkeys (Randich 1992), and humans (Bossut and Maixner 1996).
On its way from the brain stem to the right side of the heart, the right vagal nerve also innervates or affects other tissue and organs including the skin, as measured in several mammalian species (Kaji et al, 1988), (Gibbins, 1990) (Morris and Gibbins), 1997), Since the effect of the vagal nerves is to slow physiological functioning, we see reduced physiological activity when the vagal nerves become more active
It is our own physiology that produces the natural electric charge that is always present on the skin. Technically referred to as skin potential, or SP, this has also been called the Tarchinoff effect in the field of electrophysiology, and it is this that PainTrace™ measures. Acceleration of a subject’s physiology in an adrenaline-producing activity increases this charge (de Erausquin, 1989) and, conversely, slowing of the physiology can reduce this charge (Cronin and Kirsner, 1982). This is depicted in the attached figures. Any time that SP on the right side of the body is reduced more than on the left, a negative trace is produced on the PainTrace™ readout. So this can be expected to occur when the right vagal nerve is stimulated, because it lowers the rate of physiological functions on that side. We have performed numerous experiments with known, natural triggers of the vagal nerves that have produced a corresponding trace on the PainTrace™ unit.
In humans these vagal/PNS mediated activities have included: blood pressure changes triggered by changes in posture (the ortho-clinostatic reflex), calming meditation, exhalation (vs. inhalation), cough suppression.. When these activities are performed by an experimental subject, their trace moves in the appropriate, negative direction that is associated with PNS. In cats, PainTrace™ changes that are consistent with increases in vagal activity have been measured during “orienting” (Porges, 1995, p. 303). Conversely, a rise in the trace occurs with control activities known to trigger SNS in humans: caffeine use, fear, anger, general emotional stimulation. In humans, cats, mice, and horses, the startle response (known to involve a spike in SNS activity) has produced appropriate rises in the traces of all species. Thus there is little doubt that that what PainTrace™ measures is a change in the ratio of electric skin potential on the right vs. left sides of the body, as triggered by activity within the right vagal nerve.
A great deal of scientific literature in peer reviewed journals supports the model discussed here of PNS and the body’s response to pain. As early as 1992, Randich and Gilbert published a 22 page review article on this subject with 110 references. When pain is experienced, the body’s first response is to activate the SNS-driven fight-or-flight response, with increased pulse, blood pressure, and breathing rate. This then draws a counter-response from PNS to calm the body, by increasing activity of the vagal nerves to lower pulse, blood pressure, and respiratory rate, as well as provide some pain relief (Herrero 1996). In the past two decades a great deal of research has revealed that this PNS activity can, in fact, partially protect the body from pain.
In 1981, involvement of the parasympathetic nervous system (PNS), as mediated by vagal afferent nerve fibers, was first noted in natural pain control in rats. (Maixner et al, 1982) Increased PNS activity produces a negative trace and has often shown pain-fighting properties, which appear to be mediated through the body’s natural opiates. (Ren et al. 1988). The PNS-produced pain-relief was reversed with nalaxone (which counteracts the effect of any opiates), thus confirming the connection between enhanced vagal activity, endorphins, and pain relief.
Much of the literature on this subject involves vagal afferent stimulation (VAS), and has shown an involvement with the baroreceptors that sense the changes in our blood pressure and seek to counter them. Artificial electrical stimulation of vagal nerve fibers increases tail flick latency in rats (i.e. it raises their pain threshold. (Ren et al, 1988). Chronic genetic hypertension, which is associated with enhanced resting cardiopulmonary vagal activity, also suppresses pain behaviors in the rat. (Maixner et al. 1982). This response is produced by increased activity in the vagal nerves (or PNS). Conversely, humans with low blood pressure (and therefore low PNS activity) demonstrate increased sensitivity to pain, while hypertensive humans are more pain tolerant.
Work with cats has shown that stimulating the right side vagal nerves affects responses to pain (Bossut and Maixner, 1996). Work with humans has also found that electrical stimulation of vagal nerves produces partial pain relief (Ness, et al, 2000). Vagal stimulation in rats has consistently reduced pain (Thurston and Randich, 1992). This effect is eliminated if the right vagal nerve is cut (Maixner and Randich, 1984).
The only other non-invasive method for measuring vagal activity is heart rate variability (HRV) analysis. This requires using an electrocardiogram to measure the heart rate of an individual who is usually breathing in time to a metronome set to 6 breaths per minute. The data is then fed through sophisticated computer programs involving Fourier transforms and power law analysis. Consistency, between readings minutes apart on the same subject can vary widely: from 47% to 170%. While these readings have been shown to equate to vagal activity in some instances, their ability to do so when baroreceptors are stimulated has been questioned (Goldberger et al, 1994, 1996, 2001) (Deschamps, 2005) (Sucharita, 2002) . This is crucial because it is the baroreceptors that trigger the vagal response to pain. Other disadvantages of the HRV method are the need of several minutes for measurement, results only available afterwards following computer analysis. Finally HRV is unable to follow rapid changes since it is a method of averaging, which limits its ability to record changes lasting less than five minutes . PainTraceÔ by comparison creates an easily understood graph that unfolds in real time and can track changes as short as one second.
In summary, over 20 years of peer-reviewed research has established the action of the same neural pathways that PainTrace™ has been shown to measure. Researchers have confirmed that these pathways are involved in the body’s response to pain.
Others before us have proposed using vagal tone as an index of pain in humans (Porter, 1993) and horses (Reitmann, 2004). The traditional practice of twitching horses may likely work by increasing vagal tone. A study of 74 horses found that twitching increases behavioral pain threshold, makes the horses groggy, and the effects are cancelled when endorphins are chemically blocked with nalaxone (Lagerweij, 1984), just as is true for the pain relief provided by increased vagal tone in other mammalian species (Maixner, et al, 1982), (Ren ET al, 1988). Twitching has also been found to produce an immediate rise in beta-endorphin levels in the blood upon application if the twitch, and a drop immediately after the removal of the twitch, paralleling a respective rise and fall in pain thresholds (Schelp, 2000).
Biographs, Inc. has demonstrated consistently how the pattern of PainTrace™ recordings occurring during controlled activation of these pathways are the same pattern of traces produced by people undergoing any kind of prolonged pain. We have also demonstrated that the opposite, a rise in the trace consistent with less vagal PNS activity, occurs when effective pain relief is provided -- regardless of the kind of pain therapy involved. This allows an opportunity for the pain therapist to obtain objective confirmation of the patient’s pain as well as the effectiveness of the therapy provided.
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