Tracking Down the Origin of Trigger Points for Functional Improvement

Far from Pain Free

Americans consume over 80% of the prescription opioids in the world with only 4.6% of the world’s population. The cost of treating chronic pain was upwards of $635 billion in 2010 and increasing 9% annually. Chronic pain shared the top reasons for primary care visits with musculoskeletal pain affecting 1 in 3 persons in 2014. Excluding pain medication addiction, the cost of treating chronic pain was approximately 1 trillion dollars in 2016.

Joints of the Spine

The human body contains more than 200 joints or areas where 2 or more bones come together. Joints provide skeletal movement and stability. The body has 5 joints between the pelvis and the ankle that do not directly affect nerves. In roughly the same length, we have 75 joints (facets and discs) within the spine that convey 99% of the nerves to and from the body. Eighty-five percent of those nerve pathways carry sensory information to the brain while only 15% are necessary to operate the muscles and organs. The 3 different types of joints include fibrous, cartilaginous and synovial. Synovial joints allow the greatest degree of movement while both maintaining dynamic stability throughout their range of motion, and limiting excessive motion that can compromise the joints integrity. A spinal facet joint is a synovial joint and it consists of bone, cartilage and a capsular ligament, or wall of connective tissue that encloses a cavity containing synovial fluid. Facet joints are paired right and left and are technically synovial, plane joints between two adjacent vertebrae. There are a total of 56, or 28 pairs of facet joints in the spine and each is innervated by the recurrent meningeal nerves.

Part of the Problem

Nerve, muscle and skeletal (NMS) pain and dysfunction is presumed to originate from local tissue stress or trauma; i.e. it hurts where I strained muscle, sprained tendons, tore ligaments or my poor habits resulted in tissue failure. However, the greatest percentage of NMS pain originates from the sclerotomal structures of the spine. Sclerotomes are embryological spinal structures developed during pregnancy that include bone and spinal facet joints, cartilage and ligaments. Facet joint dysfunction is a more recent factor in the development of trigger point pain and dysfunction and plays a  prevalent role NMS pain.

Facet Dysfunction, Spasms and Pain

If the knee is weak, overstretched or torn, would it be stable throughout its range of motion? No. Would the knee affect the nerves that control other areas of your body? No. If the spine is weak, overstretched or torn, would it be unstable and affect the nerves entering and exiting it at different levels? Yes. Facet instability creates periarticular (around the joint) and intraarticular (inside the joint) inflammation. Facet joint inflammation is directly associated with joint trauma, abnormal joint loading, joint tracking error, ligament laxity, muscle overstretch and muscle spasms. Traumatic facet injury is frequently front and center in current literature, however non-traumatic facet overstretch due to lack of paraspinal muscle development, poor posture, detrimental ergonomics and lifestyle choices are driving the rapid need for intervention and effective pain management strategies. In other words, poor back strength exacerbates a complex evolutionary crisis in which paraspinal muscle mass does not support the length of the modern spine as a central lever in all motion. The mass to length ratio is falling precipitously as we are now the weakest generation in the history of humanity. Learning to identify and address facet joint dysfunction will drive the massage profession forward. Therapeutically, this novel approach to treating the muscles involved in managing facet dysfunction is both specialized and highly rewarding. 

We Missed the Problem

Have we missed the potential benefits in identifying facet instability? YES. Overstretch or trauma to the facet capsular ligament’s slow stretch mechanoreceptors (SSM) result in ligament laxity, sclerotome pain, and spondylogenic reflex syndromes (SRS). Innervated through a single spinal nerve or its branches, the SRS was discovered by Kelligren6 and researched by numerous authors over the past 75 years. The term “SRS” was originally coined by Sutter9 and ongoing research into the underlying pathophysiology of facet joints was published as recently as 2014.

 Spondylogenic Reflex Pain

Acute or chronic facet ligament laxity, mechanoreceptor signaling, reflexive effector target tissue facilitation and progressive pain signaling via neuronal excitability, glutamate signaling, nerve growth factor and peptidergic joint afferents form a complicated relationship between function, dysfunction and pain. As a comprehensive pathological entity, we can further define the SRS process.

Trigger Points Originate Here

All pain aside, the hallmark of an active SRS is persistent multi-muscle over facilitation. Over-facilitation leads to metabolic fatigue and subsequent trigger point development. Inadequate nutrition, overload strain, poor posture, poor ergonomics and lower than normal core body temperature can further exacerbate existing trigger point activation.

Low Core Temperature

Core temperature (CT°) or the internal metabolic temperature of the body, is the result of an average set of metabolic processes. For humans, average CT° is 98.6 F° orally and 99.4 F° auricular. CT° allows for efficient circulation, enzyme activity, protein synthesis, nerve and muscle fibril activity, cellular detoxification and lymphatic drainage; all critical factors in muscle efficiency and recovery. If CT° approaches 104 F°, muscle metabolism will cease functioning and loose its contractile ability. In comparison, most mammals lose muscle efficiency at approximately 102 F°. If the core is too low (.8 F° or more below normal), muscle will proportionally fail to clear metabolic waist and will  lose its ability to relax or lengthen. Muscle will also contract or spasm more readily in response to cold air (chill reflex) and will struggle to return to its resting phase after contracting. A good example of this involves muscle shortening and spasms when subjected to prolonged periods of cold air, i.e. as with an air conditioner blowing on your neck.

 Core Temperature and TrP Pain

Trigger points are products of prolonged muscle facilitation or muscle overload generating metabolic waste, hypoxia and restricted nutrient supply faster than lymphatics and venous circulation can clear. Low CT° further compounds this process by allowing a prolonged contraction phase while inhibiting the relaxation phase. When the belly of the muscle cannot eliminate metabolic byproducts through normal clearing channels, they will migrate and concentrate at the muscle/fascia interface. The fascia, not the muscle belly contains nociceptors; accumulated waste will activate fascial pain fibers and generate myofascial trigger point pain referral. This becomes the palpable location of the trigger point.

Spondylogenic Reflex Meets TrP

Facet capsular ligament overstretch will persistently fire slow stretch mechanoreceptors and in turn activate the SRS. The SRS will always activate or facilitate predefined effector target tissues to include partial or whole muscles in the head, neck, torso, pelvis and all extremities.

Once activated, the SRS becomes a cascade of reflexive facilitation of extraneous muscles that create a specific, yet broad subset of dysfunction. As defined in the following, the potential for pain can occur at every step. This subset is definitive and includes:

(A) Chronic muscle shortening and contractures along the spine.

(B) Inflammatory nerve root compression syndromes.

(C) Myotome activation at multiple levels of the spine and body.

(D) Specific muscle over facilitation with agonist/antagonist reciprocal inhibition. (E) Muscle metabolic fatigue with muscle weakness.

(F) Muscle compartment imbalances with joint tracking error.

(G) Attachment tendonitis in over facilitated muscles.

(H) Myofascial trigger point development in the below normal CT° client. (I) Local pain from the histological stress associated with any number of the above stated reactions.

Awareness of the facet joint as a prevalent source of NMS pain and Trp activation is rapidly surpassing years of emphasis on the spinal disc as primary players.  If it sounds complicated, it is and yet, it is not. When viewed as a definitive pathological entity, the SRS quickly illustrates how a simple, yet little known reflex originating from the facet joint capsular ligament can become a powerful source of pain and chaos.

Deriving an SRS Assessment

Deriving an SRS assessment involves a quick and effective small set of tools necessary for identification and the requisite knowledge on how to effectively treat this problem. There is much to learn about the topic and an article can only be an introduction. Combined with the above information, the included case studies illustrate the practical outcomes of SRS management and how science can take Massage and Physical Therapy into a new era of predictable, dependable, reproducible and immediate objective improvements. These illustrations include case study examples using SRT and/or complimentary SRA procedures to generate an immediate therapeutic change in facet status.

Confirming SRS Activity through Infrared Imaging

For each case, note the area of complaint and the SRS facet being treated. The following sample reflects the impact of facet instability on remote and seemingly unrelated areas of pain and dysfunction.  Infrared (IR) Imaging is a perfect tool to compare pre and post SRT treatment outcomes. Note that white illustrates the highest temperature area within the image and blue the coolest. Spots 1-4 (SP1-4) emphasize a peak temperature within a given area of the low back, and the posterior thigh and right knee.

 Images 1-3

Images 1-3

C3/C4 SRS in Elite Athlete

Case Study: A seasoned 36-year-old female marathon and trail runner presents two weeks prior to the Imogene Pass Run unable to train. She developed progressive and debilitating right hamstring pain, spasms and trigger points over the previous year while training for this and other running events. Her complaint progressed into unrelenting right buttock pain, burning in the right posterior thigh and right hamstring muscle spasms. Her MRI/Medical diagnoses included tight hamstring muscle, moderate DJD and L4/5 Grade II spondylogenic spondylolisthesis (SS).

She was prescribed 3 months of physical therapy. The Initial steroid injection provided moderate relief while continued physical therapy spinal manipulation aggravated her condition. A second injection proved ineffective. Her initial SRA chiropractic evaluation revealed a spondylogenic reflex syndrome (SRS or primary unstable zygapophyseal joint) at the C4 right and C3 left levels. Specific soft tissue therapy (Spinal Reflex Therapy) to C3 and C4 paraspinal muscles only resulted in a significant reduction in reflexive psoas muscle contractures and trigger points aggravating her low back condition and lower extremity.

Summary

In essence, reducing SRS activity through Spinal Reflex Therapy resulted in a decrease in lumbar facet periarticular nerve compression at the L4/L5 innervation of the biceps femoris, gracilis and popliteus muscles. It further reduced metabolic fatigue, spasms, pain and causalgia in the target tissue and increased the patient’s muscle load capacity, endurance and power.

This study illustrates how the SRS soft tissue facilitation cascade limiting a client’s ability to perform and how mitigation can return function and performance. After 1.5 weeks of treatment, the client not only completed the 17.1 mile run over the 13,114 ft. mountain pass with marginal discomfort; she ranked 1st in her age group and achieved her best time to date.

 Image 4

Image 4

Images

IMAGE 1 Pre Treatment Low Back Focal Thermal Profile - Sp1 references a focal infrared inflammatory profile at the L4 level with a max temperature of 99.2 F°, well above the average 86-94 F° resting temperature of paraspinal muscle.

IMAGE 2 Pretreatment Posterior Thigh/Knee Inflammation - Sp2 for the right thigh is 98.0 F° compared to left Sp3 at 97.0 F°. Right hamstring metabolism is operating at 1.0 ‘F higher than the left. Sp4 illustrates posterior knee attachment tendonitis per popliteus facilitation at 97.2 F°.

IMAGE 3 IR Changes as of at 40 Minutes Post Treatment – SP2 reduction of 1.3 F° (95.7 F°), SP3 reduction of 1.6 F° (95.4 F°) and Sp4 reduction of 3.3 F° (93.9 F°) reflect a generalized reduction in inflammation associated with C3 and C4 SRS via a decrease in psoas and paraspinal muscle over facilitation. The GII SS diagnosis was not the determinant factor in performance impairment for this patient. Lumbar manipulation was contraindicated and appeared to destabilize her SS further.

IMAGE 4 SRS Correlate to HX and Physical Findings - The primary driving spondylogenic reflex (C4R) and reflexively facilitated core muscles are mapped. Note the C4R SRS (red), its psoas muscle facilitation relationship (muscle #11) and its potential for multiple levels of facet neurocompression.

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