Saturday, January 21, 2012

Myofascial Trigger Points and Applied Kinesiology: Dr. George J. Goodheart, Jr., and Dr. Janet Travell Converge


 In March of 1978, Dr. George J. Goodheart, Jr., was a speaker with Dr. Janet Travell at the Rowe-Smith Memorial Seminar in San Antonio Texas.
In the Rowe Smith seminar both Drs. Travell and Goodheart were presented with a patient suffering temporomandibular disorder (TMD). The patient could open their mouth on a very limited basis. Dr. Travell treated the patient with spray-and-stretch techniques and helped him with pain reduction and mouth-opening (to the width of two fingers, with the accepted normal being three fingers of the non-dominant hand), but the patient’s mouth was still somewhat painful on opening. Dr. Travell then curtsy’d to Dr. Goodheart as though to say, “your turn.” Dr. Goodheart then treated the patient; after his AK assessment and treatment, the patient could open their mouth to the normal three-finger width and without pain.
Drs. Travell and Goodheart were then given strong applause from the crowd after their ministrations, with Dr. Travell and Goodheart offering a curtsy in unison to the gathered assembly of dentists.
Dr. Travell told the audience (mostly dentists) that she understood that Dr. Goodheart had found another method for the diagnosis of muscular dysfunctions and myofascial trigger points using the applied kinesiology manual muscle test method.
Drs. Masters and Shockley (dentists who organized the San Antonio meeting) congratulated Dr. Goodheart on his presentation with Dr. Travell at this seminar.

Letter congratulating Dr. Goodheart on his
presentation with Dr. Janet Travell

Dr. Janet Travell with her patient in the White House 
President John F. Kennedy

Myofascial trigger point (MTrP) weakness occurs when a muscle cannot fully activate all of its contractile fibers because of the presence of a trigger point. The importance of this observation, that motor dysfunction and particularly muscle inhibition are present in muscles housing MTrPs cannot be over-estimated. The weakness results from reflex motor inhibition and may occur without atrophy of the affected muscle, emphasizing Travell’s insight that the MTrP is directly influenced by the CNS and vice versa. A few investigators have reported on the effects of MTrPs on muscle activity using newer online computer analysis of EMG amplitudes. These reports indicate that MTrPs not only influence the muscle in which they reside, but that their influence can be transmitted through the CNS to other muscles. (Simons et al., 1999) According to Simons et al. (1999), “the motor effects of MTrPs may be the most important influence they exert, because the motor dysfunction they produce may result in overload of other muscles and spread the MTrP problem from muscle to muscle.”
For instance accelerated fatigability and significantly decreased median power frequency of the trapezius muscle with MTrPs has been demonstrated, compared to the contralateral muscle that was pain-free. (Hagberg & Kvarnstrom, 1984)
The weakness and loss of work tolerance in muscles with MTrPs are often interpreted by doctors, therapists and their patients to be an indication for increased exercise to correct the muscle impairment. However Simons et al (1999) warn, “If this is attempted without inactivating the responsible MTrPs, the exercise is likely to encourage and further ingrain substitution by other muscles with further weakening and deconditioning of the involved muscle.” Headley and Simons report muscle inhibition during movement when trigger points are present. (Headley, 1993; Simons, 1993) Headley illustrated two examples of movement-specific inhibition in which the muscle functioned well during isometric strength testing but did not contract at all during the movement for which it would normally serve as prime or synergistic mover. A frequently seen example is an anterior deltoid muscle that is strongly inhibited during shoulder flexion but is recruited essentially normally during shoulder abduction. The normal functional pattern returned with inactivation of the MTrP in the infraspinatus muscle. (Simons, 1993)
Mense & Simons (Mense & Simons, 2001) remark that for muscles accessible to palpation (many are not), a MTrP is consistently found within a palpable taut band. However, “It is difficult to measure with accuracy, specificity, and reliability. Several studies indicate that palpable taut bands can be present in normal muscles without any other indication of abnormality, such as tenderness or pain.” However, an active trigger point will inhibit the function of the muscle in which it is housed as well as those which lie in its target zone of referral. (Simons et al., 1999; Headley, 1993; Simons, 1993) For instance active MTrPs in the quadratus lumborum muscle have been shown to inhibit the gluteal muscles. (Headley, 1993)



After the detection of the muscle stretch reaction, a clinical decision might be made to treat the active trigger points found in the muscle as the primary treatment strategy. However, as Travell & Simons point out, (Travell & Simons, 1999) other dysfunctional features may be at work. Joint imbalances, biochemical, hormonal, dietary, or emotional imbalances might be the primary factors producing trigger point activity.  After the successful treatment of a local joint dysfunction, the aberrant behavior of local trigger points might resolve. On the other hand, MTrP deactivation may be a requirement for that treatment process to succeed. Resolution of most (sometimes all) of the perpetuating factors may be required to effectively treat chronicity in MTrP disorders.
According to Simons et al., (1999) the basic reason why therapy provides only temporary relief for MTrPs is because perpetuating factors have not been adequately addressed. Systemic perpetuating factors for MTrP problems encompass many conditions that compromise muscle energy metabolism. Travell & Simons (Travell & Simons, 1999, 1983) presented these metabolic, structural, and psychosocial factors in both editions of their classic textbook. Each of these factors of dysfunction has been given specific AK treatment approaches, making the comprehensive treatment of these “perpetuating factors” of MTrPs especially amenable to treatment using AK.

Drs. Goodheart and Travell’s
(AK and Myofascial Trigger Point)
Concepts Merge

Travell and Simons’ concepts regarding MTrPs have converged with applied kinesiology’s concept of the triad of health. The work of Raymond Nimmo, DC has worked in parallel with Travell and Goodheart in describing soft tissue changes that generate local and distant pain – myofascial trigger points. The evaluation of the multiplicity of factors that create and sustain MTrPs has been shown to be fundamental to successful treatment of this complex and widespread disorder. This convergence in many ways resembles the methods used in AK for spinal joint dysfunctions, neurolymphatic and neurovascular reflex stimulation, strain-counterstrain, fascial release, percussion, and nutritional evaluation and treatment. Possessed with a better understanding of the effect of MTrPs upon the function and strength of muscles, clinicians can expect that Travell and Simons’ approach will continue to influence AK methods and vice versa. 
With the complexity of the referred pain symptoms in the typical patient with MTrPs, as well as the complexity of the MTrP phenomena itself (central versus attachment MTrPs, active versus latent MTrPs, overlapping referred pain zones, etc.) the diagnosis of the presence and then the precise localization of the MTrP are expedited with the AK MMT. The MMT identifies the dysfunctional muscle housing the MTrP, and the process of therapy localization and/or challenge allows for the identification of the precise location of the trigger point that immediately improves the muscle stretch reaction and MMT finding.
After the detection of the muscle stretch reaction, a clinical decision might be made to treat the active trigger points found in the muscle as the primary treatment strategy. However, as Travell & Simons point out, (Travell & Simons, 1999) other dysfunctional features may be at work. Joint imbalances, biochemical, hormonal, dietary, or emotional imbalances might be the primary factors producing trigger point activity.  After the successful treatment of a local joint dysfunction, the aberrant behavior of local trigger points might resolve. On the other hand, MTrP deactivation may be a requirement for that treatment process to succeed. Resolution of most (sometimes all) of the perpetuating factors may be required to effectively treat chronicity in MTrP disorders.
According to Simons et al., (1999) the basic reason why therapy provides only temporary relief for MTrPs is because perpetuating factors have not been adequately addressed. Systemic perpetuating factors for MTrP problems encompass many conditions that compromise muscle energy metabolism. Travell & Simons (Travell & Simons, 1999, 1983) presented these metabolic, structural, and psychosocial factors in both editions of their classic textbook. Each of these factors of dysfunction has been given specific AK treatment approaches, making the comprehensive treatment of these “perpetuating factors” of MTrPs especially amenable to treatment using AK.





Travell and Simons’ concepts regarding MTrPs have converged with applied kinesiology’s concept of the triad of health. The evaluation of the multiplicity of factors that create and sustain MTrPs has been shown to be fundamental to successful treatment of this complex and widespread disorder. The respect and friendship between Drs. Goodheart and Travell will continue in the decades to come, with cooperative research and clinical patient care using the best-practices from both of these schools of thought for the evaluation and treatment of myofascial trigger points and muscle pain and dysfunction.

Dr. Travell's letter to Dr. Goodheart
Selected from three new textbooks on Applied Kinesiology, with 2nd Editions now in color!






Each of these books available in Europe at:
References:

·       Hagberg M, Kvarnström S. Muscular endurance and electromyographic fatigue in myofascial shoulder pain. Arch Phys Med Rehabil. 1984;65(9):522-5.

·       Headley BJ. Muscle inhibition. Physical Therapy Forum. 1993:24-26.

·       Mense S, Simons DG. Muscle Pain: Understanding Its Nature, Diagnosis, and Treatment. Lippincott Williams & Wilkins: Philadelphia; 2001.

·       Simons D, Travell J, Simons L. Myofascial pain and dysfunction: The trigger point manual, Vol. 1: Upper half of the body, 2nd Ed. Williams & Wilkins: Baltimore; 1999.

·       Simons DG. Referred phenomena of myofascial trigger points. In: New Trends in Referred Pain and Hyperalgesia, Eds.  Vecchiet L, Albe-Fessard D, Lindlom U. Elsevier: Amsterdam; 1993.




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