Pain Referral Patterns

Volume: 4
Issue: 3
March 15, 2009
Pain Referral Patterns

Dear Colleagues: 
 
I wonder if you find pain patterns as interesting as I do?  This is a subject that first drew me to orthopaedic medicine, the late James Cyriax’s system of identifying the precise anatomical locations generating musculoskeletal pain.  In addition to his method of “systematic examination of the moving parts by selective tension” he also showed that musculoskeletal pain refers from specific structures in predictable patterns. 
 
A knowledge of anatomy was the key.  For example, pain referring down from the shoulder joint, i.e. in a C5 dermatomal pattern would have to be coming from a gleno-humeral structure – joint, bursa or tendon.  On the other hand, pain referring upward, to the upper shoulder or lower lateral neck would have to be coming from the acromio-clavicular joint as it receives C4 innervation. 
 
The systematic study of referred pain began long ago – in the 1800s.  Surgeons already knew that pain could be referred from inflamed organs. Then in the late 1800s British neurologist Sir Henry Head demonstrated that referred pain from organs followed the body’s ontogenetic segments in a systematic way.  To this day these patterns are called “Head zones”.
 
Kjellgren’s experiments in the 1930s, using injections of hypertonic solutions into muscles, ligaments and perisoteum demonstrated referral of pain from somatic structures.  Janet Travel refined this work by studying muscle trigger points.  Using injections of local anesthetic, she showed that myofascial pain syndromes could be diagnosed and treated by identifying and injecting the corresponding trigger points.  Her two-volume textbook Myofascial pain and dysfunction: The trigger point manual (now revised and updated by David Simons) remains the standard reference on this subject.  
 
George Hackett, a Cleveland trauma surgeon, did similar work in the 1940s and 50s on ligament trigger points.  He demonstrated that ligaments stabilizing the pelvic ring and lumbar spine were common generators of referred pain (in consistent patterns for each ligament) into the groin, hip and/or down the leg.  Hackett went on to become one of the pioneers of prolotherapy (or sclerotherapy), a method of treating ligament “laxity” and pain by injecting “proliferating” solutions such as dextrose into fibro-osseous junctions.  
 
Pain referral patterns overlap from muscle trigger points, ligament trigger points, and no doubt from injured periosteum.  It is interesting how pain from adjacent or related  somatic structures can refer in similar ways.  Notice the similar referral patterns of two phylogenetically related structures: the ilio-lumbar ligament and the inferior quadratus lumborum muscle. 
 

How can knowledge of these patterns help the neural therapist?  A recent case presenting in my office shows how: 
 
An otherwise healthy 55 year-old operating room nurse presented with right inferior heel pain of 6 months duration.  This pain had developed during recovery from a fracture of her ipsilateral posterior ramus of the ischium.  It was similar to a chronic pain in the heel she had experienced for a few years 25 years earlier.  In the previous episode the heel pain had settled with the help of foot orthotics. 
 
With the help of autonomic response testing, an interference field was detected at the site of the pelvic fracture.  However neural therapy (with the Tenscam) produced no lasting benefit.  Because of the history of a similar heel pain 25 years previously, the foot region was also searched for interference fields.  One was found over a two-inch portion of the distal Achilles tendon.  Neural therapy of this spot produced pain relief lasting a few days.  However repeat neural therapy of not only the Achilles tendon but also the pelvic fracture site was needed for a cure of the chronic heel pain.
 
As so often happens in office-based clinical medicine, one can only speculate as to the mechanisms of these pain patterns.  Here is my theory: 
 
A sub-threshold memory of the 25 years old pain i.e. “tissue memory” was present (in the tissues or in the central nervous system).   The pelvic fracture was anatomically very close to the part of the ischium to which the sacro-tuberous ligament attaches.  Hackett’s work showed that sacrotuberous ligament pain refers to the inferior aspect of the heel.  Presumably adjacent periosteum refers in a similar way. 
 
I suspect that this woman’s heel pain was a result of summation of two sub-threshold pain experiences, leading to an element of neurogenic inflammation.  If summation were the only process in play, treatment of the pelvic fracture interference field should have reduced the afferent neurological input to below threshold level again, thus eliminating the pain.  However, it did not, and neural therapy of both interference fields was necessary to achieve lasting pain relief. 
 
In my experience pain referral patterns frequently do not follow the classical patterns described in the textbooks.  This is because so often more than one “pain generator” is present.  Understanding this concept is invaluable in successfully treating our patients with neural therapy. 

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