TREATING THE PAIN IS CHASING THE TAIL. Part III: Therapist’s First Enemy – Hyperirritability of Peripheral Receptors
Dr. Ross Turchaninov
Phoenix, AZ
We continue our important discussion about the pain-analyzing system, its activation by somatic abnormalities, and its control during Medical Massage sessions. In Part I, Medical Massage Courses & Certification | Science of Massage Institute » TREATING THE PAIN IS CHASING THE TAIL. PART I, we discussed the function of peripheral receptors in healthy and pathologically affected soft tissues.
Part II Medical Massage Courses & Certification | Science of Massage Institute » TREATING THE PAIN IS CHASING THE TAIL. Part II: Nociceptors a.k.a. Pain Receptors was specifically dedicated to the function of nociceptors (a.k.a. pain receptors).
In Part III, we will cover a critically important subject for every therapist: Phenomenon of Hyperirritability.
PHENOMENON OF HYPERIRRITABILITY (PH)
PH is the first enemy a therapist encounters when working with a new patient. Understanding and controlling PH equals stable clinical results. Disregarding PH means treatment results will be only partial, and symptoms will sooner or later return with the same—or even greater—intensity.
Therapists in the treatment room must follow the strict rules established by the patient’s Central Nervous System (CNS). By respecting these rules, the brain will fully cooperate with the therapist’s hands as they attempt to help the patient. This brings us to the first major obstacle: PH.
Peripheral Receptors and Their Normal Functions
Let us first define PH first. As you read in Parts I and II of this article, the first critical element in the CNS’s control over normal tissue and organ function is the activity of different families of peripheral receptors. These receptors constantly inform the CNS about changes in the internal environment (e.g., a drop in blood oxygen level activates chemoreceptors, causing the CNS to increase cardiac and respiratory rates) and external environment (e.g., exposure to low temperatures activates temperature receptors in the soft tissues, triggering reflex vasoconstriction to prevent heat loss).
Thus, the CNS’s control over body functions depends entirely on data from peripheral receptors. While receptors are the main source of sensory information, the CNS does not want to overreact to every mild fluctuation in the internal or external environment. To avoid unnecessary overstimulation, the brain assigns each receptor family its own activation threshold.
Let us illustrate this concept with a simple experiment you may conduct on your own forearm.
Lightly touch the skin of your forearm with the thumb of your opposite hand. At the moment of contact, you feel a sense of touch. This sensation is generated by the brain after touch receptors in the skin are activated.
Now slowly increase the pressure. The sensation of touch changes into a sensation of pressure. This means you have activated a different family of peripheral receptors responsible for pressure sensation.
Continue increasing the compression intensity, and eventually you will begin to feel mild pain. As compression increases, the pain becomes more intense. At that moment, the compression force has deformed the nociceptors (a.k.a., pain receptor) activation threshold, and they begin firing signals to the CNS, which forms the perception of pain.
Everything in the human body is extremely logical. You did not change the stimulus—it was still the same finger pressing on the same area of the forearm—yet different degrees of compression triggered completely different sensations within the CNS.
This demonstrates that touch receptors (Merkel’s disks, Meissner corpuscles and Root Hair Plexi) possess the lowest activation threshold. Even a light breeze felt on the seashore activates touch receptors. Pressure receptors (Ruffini endings) have a higher threshold of activation. Finally, when tissue compression reaches a potentially dangerous level, nociceptors called free nerve endings are activated, and the CNS forms the perception of pain.
This simple experiment perfectly illustrates how the CNS selectively processes data from different families of peripheral receptors in order to respond appropriately while avoiding overstimulation.
Peripheral Receptors and Somatic Dysfunction
Let us now examine the behavior of peripheral receptors during somatic or visceral abnormalities. As an example, consider the Jump Test therapists use to locate an active trigger point (TP) in skeletal muscle according to trigger point maps.
In the case of a latent (“sleeping”) TP, the patient typically complains of tension in the affected muscle without pinpointed pain. During examination, the therapist applies slow compression over the suspected TP area, and the patient reacts with a withdrawal response, indicating the presence of the latent TP.
A logical question arises: Why does the same pressure applied over the TP trigger withdrawal, while identical pressure applied to neighboring areas of the same muscle does not?
The answer is the Phenomenon of Hyperirritability of nociceptors within the TP area.
Due to local vasoconstriction, the pH within the affected myofibrils changes, causing the activation threshold of nociceptors to drop slightly. In other words, the nociceptors begin firing to the CNS earlier than they normally would in healthy tissue.
During the early stages of a latent TP, the patient experiences only muscular tension because vasoconstriction has not yet reached a critical level. Without proper soft tissue therapy, vasoconstriction increases and triggers additional biochemical changes in the local tissues. At this point, the activation threshold of nociceptors drops significantly, and the patient develops acute pain, muscle spasm, and substantial loss of function.
Hyperirritability Is a Universal Phenomenon
The phenomenon of hyperirritability is a common feature of all peripheral receptors. For example:
- Patients with peripheral edema often complain of itching. This itch results from hyperirritability of touch receptors caused by compression from accumulated fluid in the dermis.
- A patient may report acute cervical pain after sitting under cold air from an air conditioner. Hyperirritability of temperature receptors in the neck and shoulder triggers massive sensory input to the CNS, falsely informing the brain that the tissues are exposed to dangerously low temperatures. However temperature receptors from neighboring parts of the body did not report any dangerous changes. As a result of confusion the brain overreacts by producing acute muscle spasm in the cervical muscles as a protective response.
- A patient with acute lower back pain may report feeling perfectly fine until twisting to get into a car seat, at which point severe pain suddenly appeared. During the twisting movement, muscle spindle receptors in the lumbar erectors entered a hyperirritable state and informed the CNS about a supposedly dangerous degree of overstretching. Other receptors in neighboring tissues did not report the same information, confusing the sensory cortex. The brain responded with its only immediate protective mechanism—acute muscle spasm—to immobilize the area and “protect” the spinal nerves from possible compression.
PHENOMENON OF HYPERIRRITABILITY and BRAIN’s COMPENSATORY REACTIONS
PH is a reduction in the normal activation threshold of peripheral receptors. When this occurs, compromised receptors generate excessive sensory input to the CNS.
This misleading sensory overload triggers compensatory reactions by the brain, designed to prevent further “damage,” even when no actual tissue damage exists.
A classic example is shoulder elevation and inability to turn the head in the presence of an active trigger point in the levator scapulae muscle. Another example is anterior pelvic rotation in patients with chronic TMJ dysfunction.
Thus, in virtually all cases of chronic somatic pain, the therapist deals not only with the original trigger but also with layers of compensatory reactions built on top of it.
The problem is that the symptoms produced by compensatory reactions are usually what dominate the patient’s attention at the time of the first clinical visit.
Two Major Groups of Patients
This brings us to another important topic: the nature of somatic dysfunction. Patients can generally be divided into two major groups.
Group 1: Trauma was the initial trigger of somatic pain and dysfunction.
The patient’s brain will always remember the traumatic event that started the problem, even years later. The longer the patient suffers from post-traumatic pain, the more secondary compensatory reactions the brain develops. These reactions further compromise tissue function, and the patient often complains about them first.
Group 2: The patient does not remember a traumatic episode.
Symptoms either appear suddenly as acute pain or gradually intensify over time. In these cases, the therapist is primarily dealing with compensatory reflex reactions formed secondarily in response to initial hyperirritability of peripheral receptors.
There is an important difference in the activation of the pain-analyzing system between these two groups.
For Group 1, the chain of events is relatively straightforward:
Trauma → immediate activation of the pain-analyzing system → development of compensatory reactions.
For Group 2, the process is far more complicated:
Soft tissue dysfunction develops slowly, and the patient’s brain may compensate for peripheral irritation or tension between myofibrils or in fascia for months or even years. Therefore, the moment pain appears is not the true beginning of the pathology. The dysfunction has already been developing for a long time.
At some point, however, peripheral receptors enter a state of hyperirritability, and only then do symptoms such as pain, burning, itching, numbness, cramps, or weakness emerge. In other words, these symptoms are not the problem itself—they are the brain’s cry for help.
PH and excessive sensory input eventually overwhelm the subconscious to compensate for dysfunction. At that moment, the “cry for help” reaches conscious awareness, and the patient finally seeks treatment because severe pain appeared suddenly or gradually became intolerable.
In chronic pain patients from either group, the first critical therapeutic step is the elimination of PH, restoration of normal receptor activation thresholds, and only afterward implementation of the full Medical Massage protocol.
Elimination of PH
- Under no circumstances should the therapist activate the patient’s pain-analyzing system at the beginning of therapy. The patient is already in pain, and the outdated “no pain, no gain” philosophy in clinical work must stop!
- The Inhibitory Regime of Massage Therapy is the first excellent tool for eliminating PH and resetting peripheral receptors.
In the affected area, apply massage strokes in inhibitory regime using a combination of drainage and kneading while attempting to control the entire tissue mass.
The therapist must work with strict consistency and repetitions:
- same speed of strokes,
- same pressure,
- same direction, along the drainage,
- same sequence of techniques (e.g., four effleurage strokes followed by two kneading strokes).
This introductory phase should continue until the patient reports a decrease in acute pain.
3. Apply steady electric vibration with a frequency of at least 60 Hz. Do not use vibration generated by percussion. Use only oscillatory vibration.
4. The patient should visit a swimming pool between sessions and engage in light repetitive muscle contractions. Elimination of gravitational load supports the therapist’s work by helping maintain proper peripheral receptor function.
ABOUT THE AUTHOR
For Dr. R. Turchaninov’s bio, please click here: Who is Dr. Ross Tourchaninov?
Category: Medical Massage
Tags: 2026 Issue #1
