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"Ask Dr. Frank!"™

Dr. Frank Jarrell (Bio)

Question:
Please help. I'm interested in locating the EMG article which reports that C3 facet stimulation causes a quadriceps contraction.

Answer: Dr. Frank Jarrell
It is not quite that simple. There is no article indicating C3 affects/correlates w/ the quads. It is through the process of systems analysis, biomechanics, neurology, physiology, histology, clinical application and post therapeutic response that correlates are formed.

Currently, Axial Spinal Reflexes are reflexes mapped through needle EMG studies out of Germany in the late 1970s and they illustrate an unmapped neurological pathway that is not currently embraced by classical neurology.

On the other hand, neither are Myofascial pain pathways. It you perform Travel and Simmons, or later, Saint Johns Myofascial Therapy, or Trigger point therapy for referred pain conditions, you are performing a non-proven technique based on unsubstantiated neurological pathways per traditional science. This also applies to myotomal and sclerotomal pathways. Basic rule in classical neurology, if it isn’t traditional, it isn’t valid.

Clinically, we both know that there is significant data and experience to substantiate a probable relationship to client/patient response to care.

I will best describe this C3 relation as follows: Please understand that this is only one of a large number of ASR pathways affecting not only the knee, but other functional conditions including rotator cuff, plantar fascitis, hip, spine, etc.

The correlate essentially works like this: C3 ASR will induce various fiber contractions in multiple core muscles. These prolonged contractions will result in local biomechanical loading at pre-defined spinal segmental levels. Prolonged segmental stress will induce nerve root irritation (early and mid stage) with a facilitory effect on the motor units in question, i.e.: the rectus femoris in this case. The RF contracture will induce a patellar "squenching" with potential underlying meniscus abrasion, edema and restricted AROM, i.e.: chondromalacia patellar syndrome.

The typical PT/Ortho strategy will include site specific analysis of the problem with appropriate traditional intervention. This may or may not alleviate or correct the condition. The primary difference with SRA is to apply known strategies in diagnostics and treatment, in addition to identifying upstream neurology and biomechanics that may be the primary or aggravating factor in the condition.

If a site specific emphasis blinds the practitioner to other interactive factors, outcomes may be routinely compromised.

The ASR/condition correlate process is well beyond speculation at this point. The ASR is a proven reaction, the biomechanics are basic to the chiropractic and physical therapy fields, nerve root compression syndromes are fundamental to chiropractic and are well researched in neurophysiology over the last 20-25 years with vast amounts of literature on the subject, and the clinical application and repeatable outcomes of SRA are evident through my studies and practice with professional athletes in running, cycling and soccer, pre and post knee surgical intervention, and the patients I work with to resolve and avert knee surgeries from as far away as Germany and Norway.

A case in point is a 42 year old male in Germany with a history of professional soccer for 25 years who was scheduled for an osteotomy of the right tibia to reduce degenerative loading of the medial meniscus after failed therapy for 2 years. As of last June he could walk .5 blocks before severe pain would stop his activities. I have applied SRA protocols over five intensive sessions of 3-5 days at a time over the course of 10 months. He was able to run 2.5 km on mountain trails after his second session, and 2 consecutive days of 2 hours of walking, 4 runs up and down the steps of the Philly Museum of Art, and kick a soccer ball for 45 min. as of last March. He is relatively pain free and does not require surgery at this time. His primary regulatory ASRs where T4 and T1 with resulting in compression loading of the L3 and L4 segments resulting in hip and knee biomechanical dysfunction. This is a prime example of managing upstream neurology as a means to correct simple, but pathological joint mechanics.

Whether Tom Danielson, Lance Armstrong, Jose Azervedo, Gary Speed, or Joey O’Brian, or my seventy-seven year old sciatic patient with degenerative posterior stair-stepping of the lumbar spine, the SRA protocol is profoundly effective.

This aspect of ASR management is covered thoroughly in the Advanced levels of SRA training.

Ask Archives

What are migraines/ how does SRA address them?

C3 facet stimulation and quadriceps contraction

"Ask Dr. Frank!"™

Dr. Frank Jarrell (Bio)

Answer: Dr. Frank Jarrell
Migraines are frequently mis-diagnosed and many headache symptoms are arbitrarily classed as migraines when they are myofascial or ASR induced.

The classical definition as stated on MedicineNet.com is: A form of vascular headache. Migraine headache is caused by a combination of vasodilatation (enlargement of blood vessels) and the release of chemicals from nerve fibers that coil around the blood vessels. During a migraine attack, the temporal artery enlarges. (The temporal artery is an artery that lies on the outside of the skull just under the skin of the temple.) Enlargement of the temporal artery stretches the nerves that coil around the artery and causes the nerves to release chemicals. The chemicals cause inflammation, pain, and further enlargement of the artery. The increasing enlargement of the artery magnifies the pain.

Migraine attacks commonly activate the sympathetic nervous system in the body. The sympathetic nervous system is often thought of as the part of the nervous system that controls primitive responses to stress and pain, the so-called "fight or flight" response. The increased sympathetic nervous activity in the intestine causes nausea, vomiting, and diarrhea. Sympathetic activity also delays emptying of the stomach into the small intestine and thereby prevents oral medications from entering the intestine and being absorbed. The impaired absorption of oral medications is a common reason for the ineffectiveness of medications taken to treat migraine headaches. The increased sympathetic activity also decreases the circulation of blood, and this leads to pallor of the skin as well as cold hands and feet. The increased sympathetic activity also contributes to the sensitivity to light and sound sensitivity as well as blurred vision.

However, if you consult Travell and Simons Myofascial Pain and Dysfunction, you will find many CNS symptoms to include blurred, shimmering, and venation blind visual changes, nausea, vomiting, sweating, anxiety, photophobia and sensitivity to sound, as well as the headache pain distribution from SCMs, Traps, and TMJ musculature. Suspect migraines must be ruled out as myofascial first. ASRs are notorious for perpetuating myofascial reactions in muscle tissue. Therefore, ASR activity must be evaluated as a precipitating or causative factor as well. The final aspects of migraines that must be addressed include caffeine, tobacco, prescription and recreational drugs, glutamate (food spiking agent), dehydration, mineral deficiencies, food allergies and hypoglycemia as complicating factors.

The current migraine model cannot define whether temporal arterial vasodilatation is the cause or the result of the complex. My clinical experience is that true migraine headaches are more of a rarity and that the ASR/myofascial pathway (and above complicating factors) constitute the majority of this cases. SRA procedures can greatly reduce many of the migraine symptoms, but long term management must include management of aggravating and complicating factors.