COMMUNITYVOTES WINDSOR 2023 PLATINUM WINNER

You may have met Jordyn while she was working reception while awaiting the birth of her son Theodore.  What you may not know, is that Jordyn is Spencer’s wife.

I couldn’t be happier to reintroduce Jordyn to our clinic – this time as our Registered Massage Therapist. Although being Jordyn’s husband may make me slightly biased, I can say that I completely trust my own physical health with her therapy.  Watching her complete her studies has brought a new light towards the profession of Massage Therapy.  The educational material is quite in-depth and when applied correctly it can make a profound positive impact on the patient’s health.  Having Jordyn as part of my patient’s healthcare team, will significantly benefit their treatment plans and above all else – their quality of life.  Please join me in welcoming Jordyn to our clinical team.

– Spencer Jean, DO, DO(MP), MBA

You may have had TENs as a form of treatment in your past, heard of the treatment or even have a TENs machine at home to use for your condition.

BUT, do you know what a TENs Machine actually does?  How it works? Are you getting the most benefits out of the treatment? In this article, I’ll explain everything you as a patient need to know about TENs Treatment so you are confident in knowing how to properly use the machine at home (if you have one) or you are educated on how it can help you and your condition clinically.

TENS (Transcutaneous Electrical Nerve Stimulation) is a method of electrical stimulation which primarily aims to provide a degree of symptomatic pain relief by exciting sensory nerves and thereby stimulating either the pain gate mechanism and/or the opioid system.

FREQUENCY (B): The machine will deliver discrete ‘pulses’ of electrical energy, and the rate of delivery of these pulses (the PULSE RATE or FREQUENCY (B) will normally be variable from about 1 or 2 pulses per second (pps) up to 200 or 250 pps (sometimes the term Hertz or Hz is used here). To be clinically effective, it is suggested that the TENS machine should cover a range from about 2 – 150 pps (or Hz).

DURATION (C):  In addition to the stimulation rate, the DURATION (OR WIDTH) OF EACH PULSE (C) may be varied from about 40 to 250 micro seconds. (a micro second is a millionth of a second). Recent evidence would suggest that this is possibly a less important control that the intensity or the frequency and the most effective setting in the clinical environment is probably around 200’s.  The reason that such short duration pulses can be used to achieve these effects is that the targets are the sensory nerves which tend to have relatively low thresholds ( i.e. they are quite easy to excite) and that they will respond to a rapid change of electrical state. There is generally no need to apply a prolonged pulse in order to force a sensory nerve to depolarise, therefore stimulation for less than a millisecond is sufficient.

BURST MODE (D):  In addition, most modern machines will offer a BURST MODE (D) in which the pulses will be allowed out in bursts or ‘trains’, usually at a rate of 2 – 3 bursts per second.

MODULATION MODE (E): may be available which employs a method of making the pulse output less regular and therefore minimizing the accommodation effects which are often encountered with this type of stimulation. Both the burst and modulation modes will be discussed in more detail in the following sections.

MECHANISM OF ACTION

The type of stimulation delivered by the TENS unit aims to excite (stimulate) the sensory nerves, and by so doing, activate specific natural pain relief mechanisms. For convenience, if one considers that there are two primary pain relief mechanisms which can be activated :

The Pain Gate Mechanism and the Endogenous Opioid System, the variation in stimulation parameters used to activate these two systems will be briefly considered.

Pain relief by means of the pain gate mechanism involves activation (excitation) of the A beta (A?) sensory fibres, and by doing so, reduces the transmission of the noxious stimulus from the ‘c’ fibres, through the spinal cord and hence on to the higher centres. The A? fibres appear to appreciate being stimulated at a relatively high rate (in the order of 80 – 130 Hz or pps).

An alternative approach is to stimulate the A delta (A?) fibres which respond preferentially to a much lower rate of stimulation (in the order of 2 – 5 Hz, though some authors consider a wider range of 2 – 10Hz), which will activate the opioid mechanisms, and provide pain relief by causing the release of an endogenous opiate (encephalin) in the spinal cord which will reduce the activation of the noxious sensory pathways.

A third possibility is to stimulate both nerve types at the same time by employing a burst mode stimulation. In this instance, the higher frequency stimulation output (typically at about 100Hz) is interrupted (or burst) at the rate of about 2 – 3 bursts per second. When the machine is ‘on’, it will deliver pulses at the 100Hz rate, thereby activating the A? fibres and the pain gate mechanism,

For some patients this is by far the most effective approach to pain relief, though as a sensation, numerous patients find it less acceptable than some other forms of TENS as there is more of a ‘grabbing’, ‘clawing’ type sensation and usually more by way of muscle twitching than with the high or low frequency modes.

Usually uses stimulation at a relatively high frequency (80 – 130Hz) and employ a relatively narrow (short duration) pulses though as mentioned above, there is less support for manipulation of the pulse width in the current research literature.

Most patients seem to find best effect at around 200s. The stimulation is delivered at ‘normal’ intensity – definitely there but not uncomfortable. 30 minutes is probably the minimal effective time, but it can be delivered for as long as needed. The main pain relief is achieved during the stimulation, with a limited ‘carry over’ effect – i.e. pain relief after the machine has been switched off.

FREQUENCY SELECTION : with all of the above mode guides, it is probably inappropriate to identify very specific frequencies that need to be applied to achieve a particular effect. If there was a single frequency that worked for everybody, it would be much easier, but the research does not support this concept.  Patients (or the therapist) need to identify the most effective frequency for their pain, and manipulation of the stimulation frequency dial or button is the best way to achieve this.

• • • Acute pain is usually most effective between 80 and 120 Hz.
    • Chronic pain can also benefit from lower settings 2 to 10Hz that stimulates an endorphin release.
    • A setting between 35 and 50Hz is commonly used to stimulate muscles for strengthening or even relaxation.

STIMULATION INTENSITY : As identified above, it is not possible to describe treatment current strength in terms of how many microamps. The most effective intensity management appears to be related to what the patient feels during the stimulation, and this may vary from session to session.

As a general guide, it appears to be effective to go for a ‘definitely there but not painful’ level for the normal (high) TENS. There is a growing body of evidence that suggests that a ‘strong’ sensation, whichever mode is being used, might achieve better clinical effects.

ELECTRODE PLACEMENT :  In order to get the maximal benefit from the modality, target the stimulus at the appropriate spinal cord level (appropriate to the pain). Placing the electrodes either side of the lesion – or pain areas, is the most common mechanism employed to achieve this. There are many alternatives that have been researched and found to be effective – most of which are based on the appropriate nerve root level :

• • • Stimulation of appropriate nerve root(s)
    • Stimulate the peripheral nerve (best if proximal to the pain area)
    • Stimulate motor point (innervated by the same root level)
    • No Sensation
    • Just Sensation
    • Definite Sensation
    • Strong Sensation
    • Painful
    • Stimulate trigger point(s) or acupuncture point(s)
    • Stimulate the appropriate dermatome, myotome or sclerotome

TENs is a great modality to incorporate to achieve pain relief for both acute and chronic conditions – When used appropriately.  Although the primary goal of the treatment itself is not to cure or fix the condition, it’s mechanism of action to achieve pain relief will indirectly help you manage your condition or aid in the correction causing the painful stimuli.  When there is less pain – you will be able to do more of your exercises and enjoy your daily routine better.

For chronic pain, there is a strong correlation in how the brain perceives the painful area.  A lot of the time, the brain believes there is still an issue going on in the area and sends a painful response – even if the initial injury has resolved.  Using a TENs at home is a great way to help retrain the psychosomatic system of the brain to help it shut off the painful sensory receptors.

If you are unsure if your TENs Machine is set up appropriately for your condition to achieve the maximum benefit, please let us know and we would be glad to set it up correctly for you.

If you do not have a TENs Machine for home use and you believe it may help you and your condition(s) please let us know!  We would be happy to have that discussion with you and let you know if we believe a TENs Machine would be a great option for you and your condition.  If you have extended health insurance and we believe a TENs should be used at home for your condition, we will help/ guide you through the entire process of getting reimbursed.

Chances are very good that if you have pain or discomfort, inflammation is to blame; if not wholly, then at least in large part.

Inflammation is directly involved in the pain conditions ranging from sciatica to arthritis, whiplash to tennis elbow, and from migraines to postexercise muscle soreness. So how exactly does inflammation trigger pain?

Pain (like inflammation itself) is biologically and behaviorally necessary. Pain protects against tissue damage by shaping our behavior, while inflammation protects against tissue damage by mobilizing our immune system’s physiological safeguarding and repair functions. Both of these kinds of protection—behavioral and immunological—make sense when danger or damage are actually present; but both pain and inflammation can become problematic when they chronically persist after the threat is no longer around.

Also, keep in mind that pain and nociception are not the same thing. Nociception is a nerve signal indicating potential mechanical, thermal, or chemical threat to tissues; pain is the experience the nervous system generates in response.

Many times, when your pain is prolonged, it can be because there is continued nociceptive input (for example, from ongoing mechanical or inflammatory irritation). But pain can persist even with little or no tissue damage; or, even when there is obvious damage or degeneration, there can be little or no pain experience at all. And while your pain may not be as related to physical tissue damage as we might have thought, there turns out to be a strong relationship between pain and expectations, fears, context, memory, and social influences.

These psychosocial factors play a role in inflammation, as well as in pain. For example, high hostility scores have been correlated with increased inflammation, while openness (hostility’s flip-side) has been associated with decreased inflammatory markers. But the relationship between pain, inflammation, and psychosocial factors is nuanced and complex: while depressed people often have stronger inflammatory responses, turning down inflammation with immunosuppressive drugs can also trigger depressive mood changes. So even though pain, inflammation, and reactive emotions are deeply interconnected, they don’t move in lockstep with one another. Instead, they could be thought of as different modes of physical, psychological, and behavioral adaptation that we use in varying ways in the face of perceived threat.

In inflammation, the nervous and immune systems work together. Tissue injury or irritation triggers the release of pro-inflammatory molecules into the surrounding interstitial environment (Image 1). Very quickly, the resulting “inflammatory soup” chemically excites and sensitizes nearby peripheral nerves, triggering behavior-altering soreness and pain (as well as initiating the cascade of the inflammatory progression, discussed in “Understanding Inflammation’s Progression”). Pain sensitization is a key link between the immune and nervous systems: sensitization amplifies the actual nociceptive signals (not just the experience of pain), either peripherally at the tissue receptors themselves, or centrally, within the spinal cord and brain.

Interestingly, inflammation-related sensitization isn’t limited to the directly injured areas. Inflammatory markers have also been found within related dorsal root ganglia along the spine (associated with processing chronic pain), neural pathways within the spinal cord, and perhaps most intriguingly, even in immune cells in parts of the brain associated with both sensation and movement of the painful area (glial cells in the sensorimotor cortex, Image 2). In the short term, this neural coinflammation protectively inhibits muscular activity related to a painful (and potentially injured) area. But if prolonged, inflammatory sensitization can lead to numerous neurological and myofascial changes, including muscle size reduction (within days), reduced fatigue resistance, contraction speed change, and infiltration of fibrous and fatty tissues (within weeks or months, Image 3).

Curiously, these inflammatory changes have been observed in muscles and fascia far from an injury, such as in spinal multifidus not adjacent to the site of a disk injury. In other words, inflammation doesn’t just affect the fascia and connective tissues of the locally painful area. Over time, local pain can also inflame:

• • Other myofascial structures far from the injury site;
  • The neurons that connect the injured areas with the brain;
  • And strangely, the ankle area of your brain’s body map.

As bad as this sounds, the body and brain have a tremendous capacity for adaptation. This means that all these things can also get better, and hands-on work has repeatedly been shown to help. There is a lot more to say about handson work’s relevance to the inflammation/ pain relationship before we get into actual techniques. Other important concepts include the ways local pain and inflammation are affected by systemic (whole-body) inflammation, the role of the vagus nerve and autonomics, stress, the controversies around ice, diet, and much more.

Musculoskeletal pain inflames both local tissues and the brain. In a recent study of sciatic pain (Loggia et al., 2015), inflammation wasn’t limited to the locally painful tissues of the low back and leg. Glial cells (inset), which play a key role in both immunity and chronic pain, also respond with inflammatory activation (orange) in the corresponding regions of the brain’s sensory and motor cortexes. This has implications for the use of both therapeutic sensation (such as produced by touch) and active client movement when working with musculoskeletal inflammation.

Tissue injury releases inflammatory molecules and cells into the surrounding interstitial environment. The resulting “inflammatory soup” chemically excites and sensitizes nearby sensory nerves, generating a nociceptive (pain-triggering) signal.

Over time, inflammation and pain can cause myofascial infiltration of fibrous and fatty tissues. A: Healthy skeletal muscle (rat tibialis anterior) with ~5 percent extracellular material. B: Fibrotic changes six months after inflammatory injury, showing extracellular increase to 20 percent of cross section. In another recent study (Bove et al., 2018), rats with repetitive strain injuries receiving modeled manual therapy (bilateral mobilization, skin rolling, and stretching) showed a reduction in nociceptor activity, neural inflammation, and fibrosis compared to unmassaged rats.

1. Girard et al., “Trait Hostility and Acute Infl ammatory Responses to Stress in the Laboratory,” PLoS One 11, no. 6 (2016); M. Luchetti et al., “Five-Factor Model Personality Traits and Infl ammatory Markers: New Data and a Meta-Analysis,” Psychoneuroendocrinology 50 (2014): 181–93.
2. L. Loggia et al., “Evidence for Brain Glial Activation in Chronic Pain Patients,” Brain 138, no. 3 (March 2015): 604–15.
3. James et al., “Dysregulation of the Infl ammatory Mediators in the Multifi dus Muscle After Spontaneous Intervertebral Disc Degeneration PARC-null Mice is Ameliorated by Physical Activity,” Spine 43, no. 20 (2018): E1,184–94. doi:10.1097/BRS.0000000000002656.
4. M. Bove et al., “Manual Therapy Prevents Onset of Nociceptor Activity, Sensorimotor Dysfunction, and Neural Fibrosis Induced by a Volitional Repetitive Task, Pain (November 16, 2018): doi: 10.1097/j.pain.0000000000001443 [Epub ahead of print].

If you have any questions or concerns about your inflammation or condition, please reach out to us at

519-735-7555.