Contemporary Medical Acupuncture Program

Neurofunctional Treatment of Pain with Movement Disorders

Common sources of neurological amplification – part 2/3: Common Complexities

By Dr. Alejandro Elorriaga Claraco
October 1, 2019

In the last issue, a general introduction to the complex topic of “pain with movement” disorders was provided with a detailed discussion of the first contributor to a pain syndrome, i.e. the activity of local nociceptors with receptor fields on dermatomal, myotomal and sclerotomal tissues. An important caveat was provided associated with this idea – the well-known neurofunctional fact that activity of local nociceptors does not necessarily require tissue damage. This is one of the most frustrating facts associated to pain syndromes, as in our clinical search for reasons to explain pain symptoms, we tend to naturally believe that some sort of tissue damage has to be present, forgetting that pain is ultimately a brain event and that even at the tissue level, the main contributors to any nociceptive activity have to be either purely neurological (i.e. neuropathic behavior of peripheral nerves) or have an effect on the activity of the nociceptive fibres and/or their receptor fields (e.g. biochemical changes in the perineural space). Let’s briefly discuss the next five (of 10) most important contributors to pain syndromes.

Referred pain from trigger points (TPs), mostly in muscles and fascia, but also in ligaments and capsules, are neurofunctional clinical entities responsible for the famous Travell and Simons’ myofascial pain syndromes. In the example provided at right (an elbow pain syndrome), number two corresponds to a supraspinatus muscle trigger point that is referring pain to the elbow, something I’ve encountered numerous times over the years.

Common complexities. Common sources of neurological amplification: Part 2

The fascinating phenomena of trigger points and referred pain have revolutionized the way we deal with common pain syndromes where a structural problem cannot be found, despite the often-surprising intensity of the pain experienced by the patient. Several decades ago, in their seminal two-volume work Myofascial Pain and Dysfunction, the Trigger Point Manual, Janet Travell and David Simons presented to the medical community the foundation for the understanding and effective treatment of many common pain syndromes that were previously a mystery for most health care practitioners. Some important clinical facts associated to TPs:

• Muscles harboring TPs have painfully restricted full range of motion and localized tenderness on palpation. TPs are more common on girdle muscles (shoulder and hip regions, neck and lower back) and mastication muscles. They affect about 30 percent of the population.

• TPs can be active or latent. When active, these TPs can cause a pain syndrome perceived elsewhere. The territories where pain is perceived by the patient show marked individual variations within a typical referred pain pattern for a given muscle.

• It appears that both peripheral and central mechanisms are involved in the contribution to the phenomena of referred pain from muscles and fascia, and that myelinated fibres are involved in the peripheral component.

Obviously a full discussion of this rather large subject is beyond the scope of this article, but I’d like to encourage clinicians to always look for these proximal and distal contributors to the pain experience, even in acute injuries, as an acute event may elicit the activation of previously dormant trigger points, making the clinical picture more difficult to understand. There could be inconsistencies in the symptoms relative to the structural extent of the acute injury that can only be explained by the activation of those pre-existing TPs. Functional “deactivation” of TPs using needling techniques such as neurofunctional electroacupuncture or dry needling is the current gold standard for dealing with these important contributors to pain syndromes. However, other therapeutic approaches using miscellaneous manual techniques have also proven valuable in the management of these syndromes.

Visceral trigger points (VTPs) are the equivalent to the myofascial TPs discussed above, and curiously, they were known long before Travell and Simons published their books. For instance, in the last half of the 19th century, Dr. Henry Head, later the editor of the journal Brain, published a number of articles, with beautiful drawings, presenting the many clinical observations he had gathered from patients with visceral disease that manifested pain on the trunk and girdles. The beautiful image(s) provided on page 20 is from Dr. Head’s article “On Disturbances of Sensation with Especial Reference to the Pain of Visceral Disease. Parts I and II” published on the journal Brain in 1893!

Some insight into pain from visceral origin:

• A number of nerve fibres are involved in this phenomenon, such as C and A-delta fibres: intensity coding receptors, high threshold receptors, and silent nociceptors.

• Multiple causative factors could be involved in the activation of the above-mentioned fibers: distension, necrosis, inflammation, and ischemia.

• Clinically, pain of visceral origin is usually poorly localized, and most of the time is accompanied by reflex autonomic manifestations such as nausea, vomiting, diffuse sweating, anxiety, and unpleasantness. Visceral pain frequently refers to somatic structures that are innervated by fibres in the same spinal segments as the innervation of the diseased visceral organ; these can produce referred muscle hyperalgesia and increased contractions in that territory. Another common examples of this phenomenon include shoulder pain from gall bladder or liver disease, or problems in the ureter felt on the lumbar musculature.

• A clinical finding from heart disease: angina pectoris pain may refer pain to the neck and jaw. Interestingly, sympathectomy reduces angina pain but not the neck and jaw pain, making very likely that vagal afferents contribute to the expression of this particular referred pain pattern.

Refers to neurological activity originating in the spinal cord segments that provide innervation to the clinically affected dermatome, myotome and/or sclerotome. The most common reason for this abnormal neurological activity is a “neurofunctional disturbance” in the spinal segment, which triggers some sort of irritation of the afferent sensory neurons whose cell bodies are located in the dorsal root ganglia of the spinal nerves. In turn, this irritation causes the neurons to secrete numerous vasoactive, pro-algic and proinflammatory substances such as substance P, CGRP (calcitonin generelated peptide), neurokinin A, endothelin-3, VIP (vasoactive intestinal polypeptide), 5-HT (serotonin), nitrix oxide, and inflammatory cytokines like IL-1 and IL-6 (interleukines) and tumor necrosis factor alpha, in their own receptor fields (both at the periphery and at the spinal cord). These substances are immune-active and vasoactive and cause leaking of the small vessels with accumulation of liquid and solid materials from the plasma extravasation that eventually leads to a “sensitization” of the receptor field of the neuron both in the periphery of the body and at the dorsal horn in the spinal cord. In a nutshell, the process of neurogenic inflammation that may take place in a very short time after an injury or from exposure to an allergenic substance or an immune system threat, but that usually develops over longer periods of time (months and years) due to non-specific segmental dysfunction. Neurogenic inflammation results in, and is the result of, what has been called Spinal Segmental Sensitization Syndrome, a physiopathological state that clinically presents with one or several of the following: segmental hyperalgesia with allodynia and hyperalgesia in the associated dermatome, hyperalgesia in the corresponding myotome (with trigger points), hyperalgesia in the associated sclerotome (with or without structural enthesopathy), and sympathetic hyperactivity (with tissular microedema and/or visceral dysfunction) in the territories supply by the preganglionic sympathetic neurons associated to the involved spinal segments.


In the past, clinical syndromes associated with spinal segmental sensitization and associated intervertebral dysfunction, have been explained clinically by mechanistic concepts that are no longer sustainable, such as the osteopathic lesion or the chiropractic subluxation complex. To me, these mechanistic concepts need to be replaced by the physiologically sound (and evidence-based) Spinal Segmental Sensitization Syndrome briefly described above. Based on research, we know that is associated with complex biochemical, neurological and immune reactions, all functionally related to the peripheral nervous system active role in modulating innate and adaptive immunity, as well as its role in the integrative protective function in host defense and the response to tissue injury.

Although most studies emphasize the contribution of the primary afferent C fibres to neurogenic inflammation as discussed in #4, there is also evidence for a contribution of sympathetic postganglionic terminals, which are in direct contact with spinal sympathetic neurons, which in turn are connected with spinal somatic neurons at the same levels. It is well established that the sympathetic nervous system is involved in a host of physiological responses evoked by noxious stimulation, including changes in blood flow to muscle and skin, changes in blood pressure, heart rate, sweat glands secretion, and pupil diameter.

Studies in cats have shown that noxious stimulation of the skin caused inhibition of skin sympathetic neurons while most muscle vasoconstrictor neurons in that territory were excited. This occurred in both anesthetized and spinalized cats, suggesting the involvement of a spinal reflex similar to the one on the brain stem. In people with spinal cord injury, it’s known that episodes of sudden increases in blood pressure are due to a spinally mediated reflex activation of sympathetic vasoconstrictor neurons supplying skeletal muscle and the gut. In my opinion, the net effect of the spinal segmental sympathetic contribution to pain problems is the lack of proper modulation of the vasomotor activity in the arterial system supplying the somatic tissues associated to those segments, and that results in suboptimal perfusion of those tissues, with a whole array of physiological negative consequences.


As already stated in #5, sympathetic neurons also play a role in neurogenic inflammation, as well as contribute to peripheral vasomotor dysfunction, and have an influence on the vitality of the joints and other tissues. Clinicians cannot access postganglionic sympathetic neurons; however, it is possible to indirectly neuromodulate these neurons using painless neurofunctional acupuncture and some gentle manual techniques over the sternocleidomastoid muscle (for a case of elbow pain as in the example provided).

In my opinion, segmental somatic and sympathetic contributions to pain syndromes are likely the most relevant (and common) neurofunctional factors in the variable prognosis of these complex clinical problems, and probably the most common reasons behind the variable clinical evolution among apparently similar pain problems. The neurofunctional state of the body prior to an injury or pain problem seems more important for the long-term improvement of that condition than the particular structural factors associated to it. In other words, a sprain is not just a ligament problem (or a low back pain episode is not just a disk/facet joint/muscle problem), but it is best viewed as a complex neurodysfunction of segmental origin associated to peripheral nociceptive activity caused by a combination of neurogenic inflammation and the phys i ol o g ical act ivat ion of miscellaneous nociceptors triggered by the particular injury.

In conclusion, in every clinical pain syndrome, a thorough neurofunctional examination of spinal segments is mandatory in order to identify any sensitized segments associated with the problem; this examination should take place on the territory innervated by the posterior primary rami, and on the corresponding dermatome, myotome and sclerotome supplied by the corresponding nerves from anterior rami of the same spinal origin.

A third and last article of this series will discuss the remaining four important contributors to pain syndromes, and provide advice, from my clinical experience, on how to approach the examination of these complex patients.

This article was originally posted in the Canadian Chiropractor Magazine on May 2019.