Cervical Muscles and Postural Balance

By Marc Heller, DC

To complete our series on the cervical spine, let's talk about the musculature. Helping chronic neck problems requires a normalization of posture, which in turn requires normal muscle tone.

The key to getting your adjustments to "hold" is retraining the patient's postural patterns. This is not always easy, but usually worth the effort. Remember, a 10-percent change in the posture may make a 99-percent change in symptoms and function. Your patients' posture may not end up looking perfect, but if they can improve it to some degree, they will function much better.

We love to adjust the spine. Teaching rehabilitation is a bit less glamorous and inherently slower. We move from the "Fix me, Doc" model to patients taking on their own healing. If patients take the responsibility to do the work, they can reap lifelong benefits. An excellent article on this topic by Craig Liebenson is in the January 2 edition of the Journal of Bodywork and Movement Therapy. Dr. Liebenson does an excellent job with the material that we discuss here, with great literature references, and a more detailed progressive version of how to reactivate the deep neck flexors.

The major postural neck pattern is the "chin-poke," what Janda calls the "upper-crossed syndrome." These patients lead with their chins, which is especially obvious when they are sitting or getting out of a chair. Sitting at a computer all day is especially hazardous to these folks.

Instead of a gentle cervical lordosis, the upper cervical spine is hyperextended, leading to suboccipital tension, potential headaches or other upper cervical problems. The rest of the cervical curve will be absent, with the whole of the lower cervical jutting forward. This predisposes one to the anterior, lower cervical subluxation and fascial patterns, which I outlined in two previous articles (www.ChiroWeb.com/archives/20/08/06.html, and atwww.ChiroWeb.com/archives/20/11/10.html).

The muscles pulling the neck forward are primarily the scalenes and SCM, which will be hypertonic and tight. These muscles are unopposed by the deep neck flexors, the longus colliand longus capitus, which are inhibited and weak.

Neck posture does not begin in the neck. People who slump when they sit inevitably jut their necks forward. The pattern begins in the low back, with a lack of spinal stabilization muscle activity; continues into the lower thoracics with an excessive kyphosis and the apex inferior to T7; and shows up in the upper thoracics as a flattening, with loss of activity of the scapular stabilizers.

I am going to give you three practical, key exercises. I've found that the principles that we apply in "framework low-force adjusting" also apply to appropriate rehab. The principle of working at the soft edge of the barrier is applied to stretching (for much improved results), and to decrease the risk of patients injuring themselves. Effective stretching is gentle and stops at the first resistance or barrier, then is held until the body "lets go." Overstretching just activates the stretch reflex and tightens the muscles. Accuracy is also critical here. Often the bigger muscles are overactive, and the smaller tonic muscles are inhibited. Our goal is a subtle retraining on a subcortical level.

Deep Neck Flexor Strengthening

One can strengthen and tone the deep neck flexors with a deceptively simple exercise. This is a difficult muscle to assess; the posture of chin poke tells you the patient needs this.

1. Start with both of your hands under the patient's chin.


2. With the fist of one hand, provide resistance to the patient pushing the chin inferior. This motion is not quite isometric, but has a very limited range. The patient will use this fist as a fulcrum to simultaneously lift the sternum and tuck the chin, both done gently.


3. The other hand wraps around the front of the neck, and the patient can use the fingers and thumb to monitor the more superficial sternocleidomastoid (SCM) and scalenes. If these fire or tighten, they are using the wrong muscles to flex the neck.


4. Hold this gentle contraction for 15-30 seconds, and repeat several times per day.

The sensation is that of lifting. Sometimes I have the patient imagine two balloons: one lifting the sternum; the other lifting the crown. This is a strengthening exercise, but is not done maximally. We are attempting to activate the deep neck flexors, tonic muscles designed to work for long periods. The level of activation is 10-25 percent of the maximum, just enough to posturally lift without activating the overactive synergists of the SCM and scalenes.

Neck Stretches

We also usually need to stretch the SCM and scalenes. I assess these with palpation. Are they tight and tender? I have seen many versions of these stretches, and have not been satisfied that they are effective. These are my own variations. The key is using the lower hand as a fulcrum, or to tether the muscle to allow an effective stretch without excessive range of motion. (You can download handouts with pictures of the SCM stretch from my website atwww.drmarcheller.com/scm_stretch.htm. You really need to make sure you understand these stretches yourself before you teach them to your patients. If not done correctly, stretches are useless.)

The following four-step, self-stretch exercise is a bit complicated. I wish it were simpler, but once the patient understands it, it works great.

Stretching the Right SCM

1. Using your left hand, pinch the right SCM between your thumb and first two fingers, either just above the clavicle, or where it feels tightest. The SCM is a large diagonal muscle, about the width of your thumb, and is quite superficial.


2. Tuck the chin and lift the sternum. This is the same motion as in the neck flexor strengthener, described above.


3. Turn the head about 20 degrees toward the right.


4. Final step: While maintaining all of the other positions, tip the head toward the left. Pull down gently on the SCM with the pinching hand and keep the chin tucked. You should feel the stretch strongly under your pinching hand.

Hold the stretch for 30-60 seconds, with two repetitions, or gradually go in and out of the stretch position. Do two or more times per day.

The following is another exercise that can be self-applied and taught to your patients.

Stretching the Left Scalenes

1. Tip your head to the left to relax the muscle. Use your right hand: either the edge of your fingers or your thumb. Find the tight part of the muscle by sliding your hand up above and then behind the collar bone. Push down to tether or hold the muscle down.


2. Keep your chin tucked. Tip (side-bend) your head to the right. You can tip your head back a little if it helps. Try rotating your head toward or away from your hand, seeing which direction gets you a better stretch to the front of your neck and engages the tight fibers. Move only until you begin to feel the stretch in the front of your neck. You don't need to sidebend your neck very far.


3. Hold the stretch for 30-60 seconds. Repeat one to two times, or slowly go in and out of the stretch position, repeating three to 10 times. Do this stretch two or more times per day.


4. Gently stretch; don't overdo it.

There you have it - three basic exercises for the neck. You can download the handouts from my website and use them with your patients. When taught correctly, and understood and utilized by the patient, they can make a huge difference in posture and pain patterns.

References and Resources 

1. Liebenson C. Functional reactivation for neck pain patients. Journal of Bodywork and Movement Therapy 2002;6(1):63-68.
2. Janda. Evaluation of Muscular Imbalance, in Rehabilitation of the Spine. Williams and Wilkins, 1996.

The Iliopsoas: A Possible Cause of Acetabular Labrum Tear

By Warren Hammer, MS, DC, DABCO

An anatomic study that appeared recently in the American Journal of Sports Medicine¹identified - for the first time - the cross-sectional anatomy of the iliopsoas tendon at the level of the labrum.

Several authors have implicated iliopsoas impingement on the anterior labrum as a cause of labral tears. They have stated that a tight iliopsoas tendon could cause compression over the anterior capsulolabral complex, leading to labral lesions. Labral tears at the 2 o'clock to 3 o'clock position of the acetabulum (see image below) are directly under the iliopsoas tendon. This labral tear is considered an anterior tear, while most labral tears caused by trauma, femoroacetabular impingement, capsular laxity/hip mobility, dysplasia or degeneration  are usually found at the 11:30 to 1 o'clock position.

The hip labrum is important because it maintains joint congruity, acts as a sealant to the hip joint, and maintains negative intra-articular pressure that stabilizes the hip joint.^1-2 Surgeons have noted tight psoas tendons overlying and impinging on torn or inflamed anterior labrums.³ Ninety-two percent of labral lesions are in the anterior quadrant of the acetabulum and are related to degenerated hips.¹

Labral tears at the 2 o�clock to 3 o�clock position of the acetabulum are directly under the iliopsoas tendon.The above information is important since tightness of the iliopsoas should become a routine evaluation not only for hip patient complaints, but also as a preventative measure against hip pain and possible eventual degeneration. In a previous article,⁴ I discussed how a tight psoas can also be responsible for compressing the hip capsule. Tightness of the hip capsule can create an increase in the intra-articular pressure. High pressure within the hip capsule creates high intraosseous venous pressure due to blockage of flow in the periarticular veins, such that hemodynamic changes in the bone marrow aresecondary to high pressure within the capsule.⁵

The iliopsoas can be stretched by methods such as post-facilitation stretching, fascial release, and active isolated stretching⁶ (also discussed previously); friction massage or Graston Technique at the insertion on the lesser trochanter can also be beneficial. Treating the psoas also requires evaluation and treatment of hip mobility. Loss of hip motion can be directly related to restricted myofascia, and restricted fascia could be due to loss of joint motion. Both must be considered. Reflex inhibition of tight myofascia can be responsible for a tight hip capsule, rather than capsular contraction.

Ferguson⁷ states that to create absolute lengthening of the psoas, it is necessary to normalize femoral/acetabular dysfunction (F/A), just as normal F/A function will depend on a fully lengthened psoas. Hip joint-play dysfunction should be evaluated. There will never be normal joint function if myofascial dysfunction abnormally stresses the joint, nor can there be normal myofascial function if there is joint dysfunction. Normal muscle length requires normal joint function.⁴

Patients with labral tears usually complain of groin pain, a clicking hip, sharp, catching pain and popping. Sometimes the pain may be localized to the anterior groin, just proximal to the trochanter, or deep within the buttock.⁷ The hip symptoms may be subtle, such as a dull activity-related or positional pain that just does not seem to improve. I have treated patients with these types of symptoms and some of them definitely had shortened iliopsoas muscles. One was diagnosed with iliopsoas tendinosis and labral tearing that responded to manual therapy over the insertional tendinosis area.

References

1. Alpert JM, Kozanek M, Guoan Li, Kelly BT. Cross-sectional analysis of the iliopsoas tendon and its relationship to the acetabular  labrum: an anatomic study. Am J Sports Med, 2009;37(8):1594-1598.
2. Dobbs MB, Gordon JE, Luhmann SJ, Szymanski DA, et al. Surgical correction of the snapping iliopsoas tendon in adolescents. J Bone Joint Surg (U.S.), 2002;84:420-424.
3. Heyworht BE, Shindle MK, Voos JE, et al. Radiologic and intraoperative findings in revision hip arthroscopy. Arthroscopy, 2007;23:1295-1302.
4. Hammer W. “The Iliopsoas and the Hip Vascular-Compression Theory.” Dynamic Chiropractic, March 26, 2007.
5. Goodard JN, Gosling PT. Intra-articular fluid pressure and pain in osteoarthritis of the hip. J Bone Joint Surg (U.K.), 1988:52-55.
6. Hammer W. “The Psoas Major May Not Function As You Think.” Dynamic Chiropractic, Jan. 29, 2008.
7. Mason JB. Acetabular labral tears in the athlete. Clin Sports Med, 2001;20:779-790.

Management of Meralgia Paresthetica (lateral femoral cutaneous neuropathy) -- A Conservative Approach

By R. Vincent Davis, DC, PT, DNBPM

Any syndrome presenting clinically with numbness, paresthesias, and pain in the region over the anterolateral and lateral aspect of the thigh is suspicious of an inflammatory, degenerative lesion of the lateral femoral cutaneous nerve and is referred to as meralgia paresthetica.

Although it is commonly idiopathic, it may be due to kinking and constriction of the nerve where it exits the pelvis. The nerve arises from the posterior divisions of the second and third lumbar nerves and appears at the lateral border of the psoas muscle passing obliquely across the iliacus to the anterior superior iliac spine where it passes beneath the inquinal ligament where it proceeds down the anterolateral aspect of the thigh. If the nerve happens to penetrate between the two fasciculi of the inquinal ligament, when the hip is fully extended, it may be compressed by the posterior fibers of the ligament.This syndrome may present clinically as sensations which are described as burning, or tingling, or hyperesthetic, or as numbness, or severe pain. Pain may occur after physical activity, or direct pressure against the thigh which is relieved by rest. A reduction in tactile sensibility may be demonstrated over the lateral aspect of the thigh.

Although symptoms may persist for many months, they commonly subside over time. If the pain persists and is intolerable, conservative care involves application of interferential current with the electrodes placed with the point of intersection located at the position where the nerve emerges from the pelvis. The Davis procedure is recommended for actual clinical application of the current. Also, pulsed 2.5 percent lidocaine phonophoresis at 0.75 W/cm2 for 8-10 minutes p.r.n. for pain may also be applied, directing the cone of the ultrasonic beam at the point of emergence of the nerve from the pelvis. When at home, the patient may apply moist cryotherapy for 8-10 minutes at each treatment, allowing for 10 minute intervals prior to reapplying the moist cryotherapy p.r.n. over the area characteristic of the anatomic site where the nerve emerges from the pelvis.

In the unusual event that the pain should persist, referral for surgical division of the inquinal ligament, or neurectomy may become necessary.

References

1. Davis RV. Therapeutic Modalities for the Clinical Health Sciences, 2nd Edition, Library of Congress Card #TXU, 389-661, 1989.
2. Goss. Gray's Anatomy, 26th Edition, Lea & Febiger.
3. Griffin JE and Karselis TC. Physical Agents for Physical Therapists, 2nd Edition, Thomas Publishers, 1982.
4. Krusen, Kottke, Ellwood. Handbook of Physical Medicine & Rehabilitation, 2nd Edition, Saunders Publishers, 1971.
5. Schriber WA. A Manual of Electrotherapy, 4th Edition, Lea & Febiger Publishers, 1975.
6. Turek. Orthopedics, Principles & Practice, 3rd Edition, Lippincott.

Chiropractic Muscle Testers Rise to the Challenge of Validating Their Work

By Scott Cuthbert, DC

This article reviews a landmark study presenting the basic science and clinical research evidence for the reliability and validity of the manual muscle test (MMT). The study was published in March in the Journal of Chiropractic and Osteopathy.¹

"On the Reliability and Validity of Manual Muscle Testing: A Literature Review" presents the results of more than 100 peer-reviewed studies related to the MMT and the applied kinesiology chiropractic technique (AKCT).

Since the first peer-reviewed publication on the topic in 1915, the growth of knowledge about the MMT and the muscle system in general, has been exponential.

Founded by Dr. Goodheart (now in his 69^th year of chiropractic practice), the International College of Applied Kinesiology (ICAK) has functioned within the chiropractic profession as a self-appointed Greek chorus commenting upon and participating in the action, as knowledge about MMT has developed. Since 1964, Dr. Goodheart and the ICAK have won over (in a census taken by the National Board of Chiropractic Examiners in 2000) 43.2 percent of the chiropractic profession who now use AK in their practices.^2-4Similar numbers are reported in Australia.⁵

The role of the muscle system in spinal function has become increasingly well-acknowledged and MMT is the most commonly used method for documenting impairments in muscle strength. MMT is used by AK chiropractors to determine whether manipulable impairments to neurological function (controlling muscle function) exist. For example, chiropractic management using MMT for a patient with carpal tunnel syndrome may involve assessment of the opponens pollicis and flexor digiti minimi muscles (innervated by the median and radial nerves) and then adjustment as indicated to the carpal bones, radius and ulna; attention to an inhibited (on MMT) pronator teres muscle; adjustment of the cervical or thoracic spines; and evaluation of cranial nerve XI through MMT of the sternocleidomastoid and upper trapezius muscles. Any or all of these factors may require treatment in order to strengthen the inhibited opponens pollicis and flexor digiti minimi muscles, which are evidence of the carpal tunnel syndrome. This "continuous nervous system" thinking and testing in AK allows the identification of contributing sites to a pain state.

The expectation in a chiropractic setting is that the proper therapy immediately will improve muscle strength upon MMT taking the patient from "weak" to "strong." Chiropractic therapy can produce rapid responses for the innervation of muscles because the basic therapy required for chiropractic patients is decompression of the nervous system. This literature review, which evaluated randomized clinical trials (n=12), prospective cohort studies (n=26), retrospective studies (n=17), cross-sectional studies (n=26), case-control studies (n=10), and single-subject case series and case reports (n=19) from the PubMed and CINAHL (Cumulative Index to Nursing and Allied Health Literature) databases, suggests this can be done readily with chiropractic manipulative therapy (CMT).^6,37

The Reliability of the MMT

One way researchers determine if a clinical test is consistent and repeatable over several trials is to analyze its reliability. The reliability of a diagnostic method is the consistency of that measurement when repeated. Depending on the type of measurement performed, different types of reliability coefficients can be calculated.

The inter-examiner reliability of the MMT was reviewed from 19 studies.^7-18 Levels of agreement attained were excellent, ranging from 82 percent to 97 percent agreement for inter-examiner reliability, and from 96 percent to 98 percent for test-retest reliability. Despite this evidence, critics who remain unaware of the research literature underlying the MMT still assert that the method is unreliable. However this review of the scientific literature on MMT shows that this contention should be dismissed.

The Validity of the MMT

Validity is defined as the degree to which a meaningful interpretation can be inferred from a measurement or test. Validity refers to the appropriateness, truthfulness, authenticity or effectiveness of an observation or measurement.

The validity of Lovett's original MMT methods was based on the theoretical construct that properly innervated muscles could generate greater tension than the partially innervated muscles present in patients with anterior horn cell damage. Lovett (1915)^19,20 developed MMT as a method to determine muscle weakness in polio patients with damage to anterior horn cells in the spinal cord. The next development of the MMT was the measurement of physical weakness from faulty and painful postural conditions, injuries and congenital deformities.^21-23,25 The neurologists also adopted MMT as part of their physical diagnostic skills.²⁷ Then the chiropractic use of MMT began with AK in order to diagnose structural, chemical and mental dysfunctions.²⁴ The concept of manually examining the nervous system's status through MMT continues to evolve and gain adherents to this method.^2-4,28

AK extends Lovett's construct and suggests that physical, chemical and mental/emotional disturbances are associated with secondary muscle dysfunction affecting the anterior horn of the spinal cord - specifically producing a muscle inhibition often followed by overfacilitation of an opposing muscle and producing postural distortions in patients.

Contrary to the physiotherapeutic understanding of the time, Goodheart suggested that muscle spasm was not the major initiator of structural imbalance.^24,29-30 The primary cause of structural imbalance is muscle weakness. Muscle weakness (as observed by MMT) is understood as an inhibition of motor neurons located in the spinal cord's anterior horn motor neuron pool.³¹

Chiropractic AK research also has suggested that there are five factors or systems to consider in the evaluation and effective treatment of muscle dysfunction: the nervous system, the lymphatic system, the blood vascular system, cerebrospinal fluid flow and the meridian system.^29,30 A complication to the original construct of MMT from Lovett and others has emerged with the increasing awareness that the responses to the MMT are not solely due to the denervation effects on neural tissues in conditions like polio, but also co-existing inputs to the spinal cord's anterior horn and the processing state of the CNS.³¹

Lamb stated (1985) that MMT has content validity because the test construction is based on known physiologic, anatomic and kinesiologic principles.³² A number of research papers have dealt with this specific aspect of MMT in the diagnosis of patients.^33,34

In a paper by Panjabi, the world's most published biomechanical researcher, it is proposed that the function of muscles, as both a cause and a consequence of mechanoreceptor dysfunction in chronic back pain patients, should be placed at the center of a sequence of events that ultimately results in back pain.³⁵ This paper argues that as a result of spinal subluxations, muscle coordination and individual muscle-force characteristics are disrupted, i.e., inhibited muscles on MMT. The injured mechanoreceptors generate corrupted transducer signals which lead to corrupted muscle-response patterns (that research suggests may be detected by MMT, EMG and dynamometers).

This article is important for those in the manipulative professions who are evaluating the consequences of spinal dysfunction. The key technical factor in this hypothesis would be the MMT that makes the detection of the muscular imbalances producing the spinal dysfunction cited by Panjabi identifiable. Another paper by Hodges, et al. (2003) also suggests this hypothesis.³⁶ Pickar also has shown there is a substantial experimental body of evidence indicating that spinal manipulation impacts primary afferent neurons from paraspinal tissues, immediately affecting the motor-control system.³⁷

In a previous literature review, Lund, et al. (1991)³⁸ describes muscle function in five chronic musculoskeletal pain conditions (temporomandibular disorders, muscle tension headache, fibromyalgia, chronic lower back pain and post-exercise muscle soreness). That review concludes that the data did not support the commonly held view that some form of tonic muscular hyperactivity maintains the pain of these conditions. Instead, they maintain that in these conditions, the activity of agonist muscles often is reduced by pain even if this does not arise from the muscle itself.

Lund's paper describes with fascinating similarity one of the major hypotheses in MMT and chiropractic, namely that physical imbalances produce secondary muscle dysfunction, specifically a muscle inhibition (usually followed by overfacilitation of an opposing muscle). A paper by Falla, et al. (2004) describes a similar model but involving patients with chronic neck pain.³⁹ A paper by Mellor, et al. (2005) presents this model in relationship to anterior knee pain⁴⁰ and Cowan, et al. (2004) in relationship to chronic groin pain with another paper demonstrating this mechanism in patellofemoral pain syndrome.^41,42 A review of 13 papers showed that patients with low back pain have lower mean trunk strength than asymptomatic subjects.^43-55

Convergent validity exists when a test, as predicted, demonstrates a strong correlation between two variables. Discriminant validity exists when the test, as predicted, demonstrates a low correlation between two variables. These tests, when found to have the proper correlations, lend support to the construct validity of the method of testing. The convergent and discriminant validity of MMT was good to excellent in 35 studies that were reviewed. These studies examined the relationship between MMT findings in patients with and without neurological, musculoskeletal or viscerosomatic symptoms.

The concurrent validity of MMT was reviewed from 12 studies comparing strength scores obtained with MMT with strength readings obtained with quantitative instruments. The 12 studies showed the concurrent reliability of MMT to be excellent. Nineteen published peer-reviewed case reports (with patient cohorts ranging from 1 to 88 patients in the trials) using AKCT have been published and were reviewed.^56-74

To provide the strongest evidence for the use of chiropractic MMT techniques, more randomized controlled clinical trials (RCTs) and systematic reviews like this one in the Journal of Chiropractic and Osteopathywill be essential. However, because the etiology of a muscle weakness can be multifactorial, and because these multiple factors may be required in successful therapy, RCTs that employ only one mode of therapy to only one area of the body may produce outcomes that are poor due to these limitations. This is frustrating because it is the clinician who depends on scientific proof that these techniques work.

Although RCTs will be required to document a cause-effect relationship between treatment and outcome, they frequently are impractical projects for the practicing clinician. One alternative is for groups such as ICAK and others who use MMT methods to organize and fund these RCTs. The ICAK USA currently is funding RCTs on MMT.

In conclusion, this paper demonstrates that good to excellent reliability and validity exist for the use of MMT for patients with neuromusculoskeletal dysfunction. The studies demonstrated good external and internal validity and the 12 randomized controlled trials (RCTs) on MMT showed that MMT findings are not dependent upon examiner bias.

In order to evaluate the effectiveness of MMT in the diagnosis of patients with musculoskeletal and nervous system disorders, it is necessary to survey the full range of research studies that have addressed the topic, giving due consideration to the strengths and weaknesses of the studies in the literature. After such a review critics of chiropractic MMT and of AK in particular, should consider many of their critiques answered. Muscle testing, which is the backbone of AK, has good evidence to support its use in the field of chiropractic to diagnose and treat neuromusculoskeletal dysfunction.

Hopefully this presentation has stimulated a desire for others to review the current MMT literature and become effective users of and contributors to chiropractic MMT research.^1,75-76

References

1. www.chiroandosteo.com/content/15/1/4.
2. Christensen MG, Delle Morgan DR. Job Analysis of Chiropractic: A Project Report, Survey Analysis, and Summary of the Practice of Chiropractic Within the United States. Greeley, Colo.: National Board of Chiropractic Examiners, 1993:78.
3. Christensen MG, Delle Morgan DR. Job Analysis of Chiropractic in Australia and New Zealand: A Project Report, Survey Analysis, and Summary of the Practice of Chiropractic Within Australia and New Zealand. Greeley, Colo.: National Board of Chiropractic Examiners, 1994;92:152.
4. Christensen MG. American Chiropractic Association. Available from:www.amerchiro.org/techniques.
5. LeBoeuf C. A survey of registered chiropractors practicing in South Australia in 1986, J Aust Chiro Assoc, 1988:105-10.
6. Shambaugh P.Changes in electrical activity in muscles resulting from chiropractic adjustment: a pilot study. J Manipulative Physiol Ther, 1987;10(6):300-304.
7. Florence JM, Pandya S, King WM, et al.Clinical trials in Duchenne dystrophy. Standardization and reliability of evaluation procedures. Phys Ther, Jan. 1984;64(1):41-5.
8. Mendell JR, Florence J.Manual muscle testing, Muscle Nerve, 1990;13 Suppl:S16-20.
9. Caruso B, Leisman G. A force/displacement analysis of muscle testing. Percept Mot Skills2000;91:683-92.
10. Lilienfeld AM, Jacobs M, Willis M. A study of the reproducibility of muscle testing and certain other aspects of muscle scoring. Phys Ther Rev, 1954;34:279-89.
11. Blair L. The role of the physical therapist in the evaluation studies of the poliomyelitis vaccine field trials. Phys Ther Rev, 1955;37:437-47.
12. Iddings DM, Smith LK, Spencer WA. Muscle testing: Part 2. Reliability in clinical use, Phys Ther Rev, 1961,41:249-56.
13. Silver M, McElroy A, Morrow L, Heafner BK. Further standardization of manual muscle test for clinical study: applied in chronic renal disease. Phys Ther, 1970;50:1456-66.
14. Frese E, Brown M, Norton BJ. Clinical reliability of manual muscle testing. Phys Ther, 1987;67:1072-6.
15. Barr AE, Diamond BE, Wade CK, et al. Reliability of testing measures in Duchenne or Becker muscular dystrophy. Arch Phys Med Rehabil, 1991;72:315-19.
16. Perry J, Weiss WB, Burnfield JM, Gronley JK. The supine hip extensor manual muscle test: a reliability and validity study. Arch Phys Med Rehabil, Aug. 2004;85(8):1345-50.
17. Jacobs G. Applied kinesiology: an experimental evaluation by double blind methodology. J Manipulative Physiol Ther, 1981;4:141-5.
18. Wadsworth CT, Krishnan R, Sear M, et al. Intrarater reliability of manual muscle testing and hand-held dynametric muscle testing. Phys Ther, Sept. 1987;67(9):1342-7.
19. Martin EG, Lovett RW. A method of testing muscular strength in infantile paralysis. JAMA, Oct. 30, 1915;LXV(18):1512-3.
20. Lovett RW, Martin EG. Certain aspects of infantile paralysis with a description of a method of muscle testing. JAMA, Mar. 4, 1916;LXVI(10):729-33.
21. Harms-Ringdahl K. Muscle Strength. Edinburgh: Churchill Livingstone, 1993.
22. Kendall FP, McCreary EK, Provance PG. Muscles: Testing and Function. Baltimore: Williams & Wilkins; 1993.
23. Daniels L, Worthingham K. MuscleTesting - Techniques of Manual Examination, 7thEdition. Philadelphia: W.B. Saunders Co., 2002.
24. Walther DS. Applied Kinesiology, Synopsis, 2nd Edition. Pueblo, Colo.: Systems DC, 2000.
25. Kendall HO, Kendall FP, Boynton DA. Posture and Pain. Baltimore: Williams & Wilkins Company; 1952.
26. Janda V. Muscle Function Testing. London: Butterworths, 1983.
27. Barbano RL. Handbook of manual muscle testing. Neurology, 2000;54(5):1211.
28. A number of chiropractic "name techniques" have evolved from AK that also employ MMT as part of their diagnostic system, including: Neuro Emotional Technique (N.E.T.); Neural Organization Technique (N.O.T.); Clinical Kinesiology; Contact Reflex Analysis (C.R.A.); Total Body Modification (T.B.M.), and others.
29. Green BN, Gin RH. George Goodheart, Jr., D.C., and a history of applied kinesiology. J Manipulative Physiol Ther, 1997;20(5):331-7.
30. Goodheart GJ. Applied Kinesiology Research Manuals. Detroit: Privately published annually, 1964-1998.
31. Schmitt WH, Yannuck SF. Expanding the neurological examination using functional neurological assessment Part II: Neurologic basis of applied kinesiology. Intern J Neuroscience, 1999;97:77-108.
32. Lamb RI. Manual Muscle Testing. In: Measurement in Physical Therapy. Rothstein JM, Ed. New York: Churchill Livingstone, 1985:47-55.
33. Michener LA, Boardman ND, Pidcoe PE, Frith AM.Scapular muscle tests in subjects with shoulder pain and functional loss: reliability and construct validity. Phys Ther, Nov. 2005;85(11):1128-38.
34. Great Lakes ALS Study Group.A comparison of muscle strength testing techniques in amyotrophic lateral sclerosis. Neurology, Dec. 9, 2003;61(11):1503-7.
35. Panjabi M. A hypothesis of chronic back pain: ligament subfailure injuries lead to muscle control dysfunction. Eur Spine J, July 27, 2005.
36. Hodges PW, Moseley GL. Pain and motor control of the lumbopelvic region: effect and possible mechanisms. J Electromyogr Kinesiol, Aug. 2003;13(4):361-70.
37. Pickar JG. Neurophysiological effects of spinal manipulation. Spine J, Sep-Oct. 2002;2(5):357-71.
38. Lund JP, Donga R, Widmer CG, Stohler CS. The pain-adaptation model: a discussion of the relationship between chronic musculoskeletal pain and motor activity. Can J Physiol Pharmacol, 1991;69:683-94.
39. Falla DL, Jull GA, Hodges PW. Patients with neck pain demonstrate reduced electromyographic activity of the deep cervical flexor muscles during performance of the craniocervical flexion test. Spine Oct. 1, 2004;29(19):2108-14.
40. Mellor R, Hodges PW. Motor unit synchronization is reduced in anterior knee pain. J Pain, Aug. 2005;6(8):550-8.
41. Cowan SM, Schache AG, Brukner P, et al.Delayed onset of transversus abdominus in long-standing groin pain. Med Sci Sports Exerc, Dec. 2004;36(12):2040-5.
42. Cowan SM, Bennell KL, Hodges PW, et al. Delayed onset of electromyographic activity of vastus medialis obliquus relative to vastus lateralis in subjects with patellofemoral pain syndrome. Arch Phys Med Rehabil, Feb. 2001;82(2):183-9.
43. Nummi J, Jarvinen T, Stambej U, Wickstrom G:Diminished dynamic performance capacity of back and abdominal muscles in concrete reinforcement workers. Scand J Work Environ Health, 1978;4(Suppl 1):39-46.
44. Addison R, Schultz A. Trunk strengths in patients seeking hospitalization for chronic low-back disorders. Spine, Nov-Dec. 1980;5(6):539-44.
45. Karvonen MJ, Viitasalo JT, Komi PV, et al. Back and leg complaints in relation to muscle strength in young men. Scand J Rehabil Med, 1980;12(2):53-9.
46. MacNeill T, Warwick D, Andersson G, Schultz A. Trunk strength in attempted flexion, extension, and lateral bending in healthy subjects and patients with low-back disorders.Spine, Nov-Dec 1980;5(6):529-38.
47. Nordgren B. Schele R, Linroth K. Evaluation and prediction of back pain during military field service. Scand J Rehabil Med, 1980;12(1):1-8.
48. Mayer TG, Gatchel RJ, Kischino N, et al: Objective assessment of spine function following industrial injury. A prospective study with comparison group and one-year follow-up.Spine, Jul-Aug. 1985;10(6):482-93.
49. Rantanen J, Hurme M, Falck B, et al.The lumbar multifidus muscle five years after surgery for a lumbar intervertebral disc herniation. Spine, April 1993;18(5):568-74.
50. Hides JA, Richardson CA, Jull G. Multifidus muscle recovery is not automatic after resolution of acute first-episode low back pain. Spine, 1996;21:2763-9.
51. Hodges PW, Richardson CA. Inefficient muscular stabilization of the lumbar spine associated with low back pain. Spine 1996, 21:2640-2650.
52. Chaffin DB, Park KS. A longitudinal study of low-back pain as associated with occupational weight lifting factors. Am Ind Hyg AssocJ, Dec. 1973;34(12):513-25.
53. Biering-Sorensen F: Physical measurements as risk indicators for low-back trouble over a one-year period. Spine, Mar. 1984;9(2):106-19.
54. Mayer TG, Barnes D, Nichols G, et al.Progressive isoinertial lifting evaluation. II. A comparison with isokinetic lifting in a disabled chronic low-back pain industrial population.Spine, Sept. 1988;13(9):998-1002.
55. Nachemson A, Lindh M. Measurement of abdominal and back muscle strength with and without low back pain. Scand J Rehabil Med, 1969;1(2):60-3.
56. Cuthbert S. Proposed mechanisms and treatment strategies for motion sickness disorder: a case series. J Chiro Med, Spring 2006;5(1):22-31.
57. Cuthbert S, Blum C.Symptomatic Arnold-Chiari malformation and cranial nerve dysfunction: a case study of applied kinesiology cranial evaluation and treatment. J Manipulative Physiol Ther, May 2005;28(4):e1-6.
58. Meldener R: Post-surgical hip dislocation. Int J AK and Kinesio Med, 2005;19:27.
59. Chung AL, Shin EJ, Yoo IJ, Kim, KS.Reliability of the kinesiologic occlusal position. Int J AK and Kinesio Med, 2005;20:6-10.
60. Caso ML.Evaluation of Chapman's neurolymphatic reflexes via applied kinesiology: a case report of low back pain and congenital intestinal abnormality. J Manipulative Physiol Ther,Jan. 2004;27(1):66.
61. Cuthbert S.Applied kinesiology and Down syndrome: a study of 15 cases. Int J AK and Kinesio Med, 2003;16:16-21.
62. Maykel W.Pediatric case history: cost effective treatment of block naso-lacrimal canal utilizing applied kinesiology tenets. Int J AK and Kinesio Med, 2003;16:34.
63. Weiss G.A 39-year-old female cyclist suffering from total exhaustion caused by over-training and false nutrition. Int J AK and Kinesio Med, 2003;15:39.
64. Sprieser PT. Episodic paroxysmal vertigo. Int J AK and Kinesio Med, 2002;14:35.
65. Leaf D. Severe equilibrium problems non-responsive to pharmacological care treated with chiropractic and applied kinesiology: a case history. Int J AK and Kinesio Med, 2002;13:27.
66. Gregory WM, Mills SP, Hamed HH, Fentiman IS.Applied kinesiology for treatment of women with mastalgia. Breast, Feb 2001;10(1):15-9.
67. Cuthbert S.An applied kinesiology evaluation of facial neuralgia: a case history of Bell's Palsy. Int J AK and Kinesio Med, 2001;10:42-45.
68. Calhoon J. Applied kinesiology management of multiple sclerosis: a case history. Int J AK and Kinesio Med, 2001;12:28-29.
69. Mathews MO, Thomas E, Court L. Applied kinesiology helping children with learning disabilities. Int J AK and Kinesio Med, 1999:4.
70. Masarsky CS, Weber M. Somatic dyspnea and the orthopedics of respiration. Chiro Tech, 1991;3(1):26-9.
71. Masarsky CS, Weber M. Chiropractic management of chronic obstructive pulmonary disease. J Manipulative Physiol Ther, 1988;11(6):505-10.
72. Moncayo R, Moncayo H, Ulmer H, Kainz H. New diagnostic and therapeutic approach to thyroid-associated orbitopathy based on applied kinesiology and homeopathic therapy. J Altern Complement Med, Aug. 2004;10(4):643-50.
73. Goodheart G: Failure of the musculo-skeletal system may produce major weight shifts in forward and backward bending. In: Proc Inter Conf Spinal Manip, May 1990:399-402.
74. Jacobs G. Applied kinesiology: an experimental evaluation by double blind methodology. J Manipulative Physiol Ther, 1981;4:141-5.
75. ICAK-International and ICAK USA Web sites: "Applied Kinesiology Research and Literature Compendium." Available at:www.icak.com/college/research/publishedarticles.shtml andwww.icakusa.com/. (Accessed Feb. 15, 2007)
76. Sacro Occipital Technique Organization Web site; SOT literature. Available at:www.sotousa.org/SOTLiterature/. (Accessed Feb. 15, 2007)

Lateral Femoral Cutaneous Nerve Entrapments

By Scott Cuthbert, DC

The lateral femoral cutaneous nerve arises from the 2nd and 3rd lumbar nerves. It is formed in the psoas muscle¹ and emerges from its lateral border to cross the iliacus muscle and exit the pelvis.

The most common point for possible entrapment is as the nerve passes between the two slips of the inguinal ligament's lateral attachment to the anterior-superior iliac spine, where it exits the pelvis. The nerve is tightly bordered by the tendinous fibers of the inguinal ligament at this point and makes a right-handed bend to change direction from a horizontal course in the pelvis to a more vertical course in the lateral and anterolateral thigh. The lower slip of the inguinal ligament also gives origin to some sartorius fibers.² The nerve may pass in front of or through the sartorius into the thigh.³

Shortly after it leaves the abdomen, the nerve divides into an anterior and a posterior branch. The anterior branch supplies the skin of the anterior and lateral parts of the thigh to the knee. The posterior branch supplies the skin on the lateral surface of the thigh, from the greater trochanter down the lateral thigh. The lateral femoral cutaneous nerve is strictly sensory, giving no motor supply.

As the nerve reaches a point just medial to the anterior-superior iliac spine where it enters the thigh, it changes its course from nearly horizontal to vertical. This angulation is increased by extension and lessened by flexion of the thigh. In addition to this major point of possible entrapment, other locations may be where the nerve emerges from the psoas muscle,⁴ the passage underneath the fascia lata, and the area where the nerve leaves the fascia.²

After the lateral femoral cutaneous nerve exits the pelvis at the opening of the inguinal ligament, it is held down as it pierces the fascia lata; thus, movement between the thigh and pelvis can stretch the nerve and increase entrapment at the opening of the inguinal ligament.⁵

Entrapment is prone to occur in obesity, with a lax abdominal wall, and in pregnancy.^{2, 6}Diabetics have an increased susceptibility to compression neuropathy, which is especially apparent in this nerve.⁷

Symptoms of Nerve Entrapment

Nerve entrapment causes pain calledmeralgia paresthetica (Barnhardt-Roth syndrome) in the anterolateral thigh.^6,8 ( Interestingly, Sigmund Freud reported in 1895 that he and one of his sons suffered from the condition.)⁹ The condition affects men more than women due to possible occupational considerations, and can also be bilateral in some 25 percent of cases.¹⁰ It most commonly develops from the nerve's fascial attachment in the thigh pulling the nerve tightly against the opening at the lateral end of the inguinal ligament,² which usually relates to thigh obesity and/or a lateral shift in trunk posture.⁴ Generally, meralgia paresthetica develops without prior trauma.

Other symptoms consist of increased ² or decreased sensitivity. ⁶ Rubbing of clothing and other cutaneous stimuli causes a characteristic burning pain on the outer side of the thigh. Pelvic and hip motion, such as walking and running, aggravates the pain. In general, those with meralgia paresthetica have poor posture; consequently, the postural muscles are overactive and fatigued with prolonged standing, which also aggravates pain.

The postural deficiency most common with meralgia paresthetica is lumbar hyperlordosis and a protuberant abdomen.^4,11 Manual muscle testing examination usually finds weak abdominal and gluteus maximus muscles failing to provide support to prevent anterior rotation of the pelvis, with subsequent hyperlumbar lordosis.¹¹ Aggravating the condition will probably be hypertonic lumbar extensor muscles and shortening of the iliopsoas. Sitting and recumbent positions relieve the pain; however, sitting with one leg crossed over the other – especially the ankle on the knee – can exacerbate the pain.

Postural shifts by a short leg, whether physiological or anatomical, may be a factor in the condition. Other factors include the muscle fibers from the internal oblique and transverses abdominus muscles originating from the inguinal ligament, or the external oblique muscle inserting into it.³ Additional causes have been reported, including body-building,¹² falling asleep in Siddha yoga position,¹³ seat-belt¹⁴ and pocket-watch trauma,¹⁵ and misplaced injections.¹⁶

Presentation and Diagnosis

Meralgia paresthetica presents more often to chiropractors than is generally recognized.¹⁷ In 215 consecutive examinations of patients in a chiropractic office, 12 cases of meralgia paresthetica were diagnosed. The method of diagnosis was "standard orthopedic and neurologic testing procedures that evaluate the lateral femoral cutaneous nerve territory for superficial tactile sensation, superficial pain, sensitivity to vibration, sensitivity to temperature, and temperature gradient studies."¹⁸

Patients had been aware of their condition from two days to 12 years. Five of the 12 had received treatment by the medical profession, with an unsatisfactory diagnosis or results.

The condition should be differentially diagnosed from conditions such as 2nd and 3rd lumbar nerve root compression, appendicitis, spinal cord tumor, colon cancer, and trochanteric or iliopsoas bursitis.² Disturbance at the lumbar level is usually associated with diminished or absent patellar reflex and weakness of the quadriceps muscles. Because the lateral femoral cutaneous nerve is purely sensory, there is never weakness or reflex change when disturbance is limited to its entrapment.^{2, 6}

In femoral neuropathy or L2-3 root lesions, sensory changes usually spread out to extend more anteromedially than in entrapments of the lateral femoral cutaneous nerve, where the sensory change is limited to its dermatome.⁶ Staal¹⁹ considers meralgia paresthetica rare and suggests that "one should look carefully for vertebral or disc lesions, intrapelvic anomalies, old operation scars, compression from outside due to clothing or chronic microtrauma: in short for all kinds of local pathology along the course of the nerve, from its beginning until distal to the anterior superior iliac spine. In the majority of the cases no obvious cause will however be found even after thorough investigation."

Failure to find a cause for meralgia paresthetica is not consistent with chiropractic findings. This may be due to a more functional evaluation of spinal, pelvic and muscular function with chiropractic methods.

There will usually be pain below and slightly medial to the anterior superior iliac spine, close to the inguinal ligament attachment. To determine the attachment of the inguinal ligament, palpate along the ligament to the bone. A positive indication that meralgia paresthetica is present occurs when deep pressure in this area causes radiation of pain in the skin supplied by the lateral femoral cutaneous nerve.

Another source of pain at the anterior superior iliac spine is the origin of the sartorius, especially when there is a category II pelvic involvement. Since skeletal muscular imbalance is often present in meralgia paresthetica, sartorius pain and a category II may be present in combination with lateral femoral cutaneous nerve entrapment. To differentiate sartorius pain, palpate its origin at the anterior superior iliac spine and the upper half of the notch below it. From the sartorius origin, palpate down the sartorius tendon into the muscle, observing for pain; this indicates muscle involvement rather than, or in addition to, nerve entrapment. Usually the muscle will also test weak.

Low back derangement may cause pain in the greater trochanteric region or in the tensor fascia lata. It is distinguished from meralgia paresthetica by the absence of sensory alteration in the skin, and lack of pain on digital pressure to the nerve.⁴

Entrapment of the superior gluteal nerve that supplies the gluteus medius and minimus and tensor fascia lata, as well as the greater trochanteric region and a portion of the hip joint, can cause what has been termed false meralgia paresthetica.² In this condition there is pain over the gluteus medius and minimus that radiates down the lateral aspect of the thigh to the knee. Lack of cutaneous sensory findings and no tenderness of the lateral femoral cutaneous nerve differentiate this from true meralgia paresthetica. Structural correction of the spine and pelvis typically corrects the condition.

Body language that first indicates that entrapment of the lateral femoral cutaneous nerve and meralgia paresthetica may be present is the location of the pain, and whether it is relieved in seated or recumbent positions and exacerbated by standing, walking and hip extension. Hip extension applied as a provocative test for meralgia paresthetica will aggravate the paresthesia and discomfort.²⁰

A therapeutic test that is sometimes done is a local anesthetic injection at the point of probable entrapment.²¹ Williams and Trzil²¹ reported on an impressive series of 277 patients for whom only 24 cases required surgery. In a surgical study for the relief of meralgia paresthetica, there were findings of constrictive fascial bands around the lateral femoral cutaneous nerve in 19 of 21 cases, indicating that soft-tissue disturbances of the mechanical interface with the nerve the most common etiology.²²

Corrective Strategies

Correction of entrapment of the lateral femoral cutaneous nerve is usually readily accomplished using chiropractic techniques. Even without the effective procedures of applied kinesiology, exercises directed toward improvement of muscles that support the pelvis – especially the abdominals – have been shown to be effective in treating this condition.⁴ Surgical procedures are usually not done as a method of treatment.²³ Correction of spinal subluxations has been indicated as a method of treatment.⁴ Obviously, the optimal approach is to evaluate all aspects of the condition and correct any dysfunction that is present.

There is usually a pelvic category I or II and weak abdominal and gluteus maximus muscles. Total postural balance should be evaluated and corrected, as well as modular interaction of PRYT, cloacal synchronization, and dural tension.11, 24 These techniques restore organization to the muscles and postural balance, and are often important in improving range of motion.

A painful myofascial trigger point (MTrP) may be found just medial to the anterior superior iliac spine.²⁵ Muscle stretch reaction of the hip flexors differentiates this from radiating pain due to pressure on the entrapped nerve. The trigger point is treated with the usual chiropractic methods of percussion, trigger-point pressure release, or stretch-and-spray methods.^11,24,26

A recently published systematic review of the literature on the chiropractic management of myofascial trigger points and myofascial pain syndromes²⁷ reviewed 112 publications and came to the recommendation that moderately strong evidence supports some manual therapies (manipulation and ischemic pressure) for immediate pain relief for myofascial trigger points.

After these chiropractic techniques have been applied, evaluate hip extension range of motion; if limited, evaluate the hip flexors for muscle stretch reaction and apply either trigger point pressure release, percussion, or stretch and spray technique to obtain improved range of motion. Frequently the percussion and/or trigger point pressure release technique is the appropriate one. This appears to release the fascial pull on the lateral femoral cutaneous nerve that is causing the entrapment at its pelvic outlet. Stretching exercises designed to stretch the iliopsoas and rectus femoris muscles are usually contraindicated since they will cause additional irritation to the entrapped nerve. Generalized body organization or local muscle treatment is usually satisfactory for obtaining effective correction.

Medical approaches have included ultrasound at L2 and where the nerve leaves the pelvis; and high-voltage electrogalvanic stimulation. "The medical approach, after attempting to relieve external stress to the nerve, would include mild analgesia or local injection of xylocaine or corticosteroids."²⁸ These procedures are usually not necessary in a comprehensive chiropractic practice.

Kopell and Thompson²⁹ found that stretching exercises to relax the tensor fascia lata and shoe lifts are ineffective. They do, however, state that most often the condition can be corrected without neurolysis.

References

1. Moore KL, Dalley AF, Agur AMR. Clinically Oriented Anatomy, 6th Edition. Lippincott Williams & Wilkins; 2009.
2. Staal A, van Gijn J, Spaans F. Mononeuropathies: Examination, Diagnosis and Treatment.WB Saunders: London; 1999.
3. Gray's Anatomy: The Anatomical Basis of Clinical Practice. Churchill Livingstone: Edinburgh; 2004.
4. Skaggs CD, Winchester BA, Vianin M, Prather H. A manual therapy and exercise approach to meralgia paresthetica in pregnancy: a case report. J Chiropr Med, 2006;5(3):92-6.
5. Kopell HP, Thompson WAL. Peripheral Entrapment Neuropathies, 2nd Edition. Robert E. Krieger Pub Co: Huntington, NY; 1976.
6. Harney D, Patijn J. Meralgia paresthetica: diagnosis and management strategies. Pain Med, 2007;8(8):669-77.
7. Veves A, Giurini JM, LoGerfo FW. The Diabetic Foot: Medical and Surgical Management.Humana Press: Totowa, NJ; 2002.
8. Pearce JM. Meralgia paraesthetica (Bernhardt-Roth syndrome). J Neurol Neurosurg Psychiatry, 2006;77(1):84.
9. Freud S. Ueber die Bernhardtsche Sensibilitaetsstoreung. Neurol Centralbl, 1895. 14491–14492.
10. Sunderland S. Nerves and Nerve Injuries, 2nd Edition. Churchill-Livingstone: New York; 1978.
11. Cuthbert S. Applied Kinesiology: Clinical Techniques for Lower Body Dysfunctions. The Gangasas Press: Pueblo, CO; 2013.
12. Szewczyk J, Hoffmann M, Kabelis J. Meralgia paraesthetica in a body-builder. Sportverletz Sportschaden, 1994;8(1):43-5.
13. Mattio TG, Nishida T, Minieka MM. Lotus neuropathy: report of a case. Neurology,1992;42(8):1636.
14. Beresford HR. Meralgia paresthetica after seat-belt trauma. J Trauma, 1971;11(7):629-30.
15. Mack GJ. Watchpocket meralgia paresthetica. IMS Ind Med Surg, 1968;37(10):778-9.
16. Ecker AD, Woltman HW. Meralgia paresthetica: a report of one hundred and fifty cases. 1938;110:1650-1652.
17. Arcadi VC. Lower back pain in pregnancy: chiropractic treatment and results of 50 cases.Collected Papers International College of Applied Kinesiology, Shawnee Mission, KS. 1996: 55-57.
18. Kadel RE, Godbey WD, Davis BP. Conservative and chiropractic treatment of meralgia paresthetica: Review and case report. J Manip Physiol Ther, 1982;5(2):73-8.
19. Staal A. The Entrapment Neuropathies. In: Handbook of Clinical Neurology, Volume 7. (Editors: Vinken PJ, Bruyn GW). American Elsevier Pub Co.: New York; 1970.
20. Russell SM. Examination of Peripheral Nerve Injuries: An Anatomical Approach. Thieme Medical Publishers, Inc.: New York; 2006.
21. Williams PH, Trzil KP. Management of meralgia paresthetica. J Neurosurg, 1991;74(1):76-80.
22. Edelson R, Stevens P. Meralgia paresthetica in children. J Bone Joint Surg (U.S.), 1994;76(7):993-9.
23. Aguayo AJ. Neuropathy Due to Compression and Entrapment. In: Peripheral Neuropathy, Vol I. (Editors: Dyck PJ,. Thomas PK, Lambert EH). W.B. Saunders Co: Philadelphia; 1975.
24. Walther DS. Applied Kinesiology Synopsis, 2nd Edition. ICAKUSA: Shawnee Mission, KS; 2000.
25. Biemond A. Femoral Neuropathy. In: Handbook of Clinical Neurology, Volume 8. (Editors: Vinken PJ, Bruyn GW). American Elsevier Pub Co: New York; 1970.
26. Cuthbert S. Applied Kinesiology and the Myofascia. Int J AK and Kinesio Med, 2002;13-14.
27. Vernon H, Schneider M. Chiropractic management of myofascial trigger points and myofascial pain syndrome: a systematic review of the literature. J Manipulative Physiol Ther, 2009;32(1):14-24.
28. Stites JS. Meralgia paresthetica: a case report. Research Forum, 1986;2(2).
29. Kopell HP, Thompson WAL. Peripheral entrapment neuropathies of the lower extremity. N Engl J Med, 1960;262:56-60.

Idiopathic Scoliosis: How Chiropractic Can Help

By Mark Charrette, DC

Scoliosis is a lateral curvature of the spine that measures 10 degrees or more. An idiopathic scoliosis is accompanied by vertebral rotation and rib-cage deformity, and usually becomes progressively apparent as the spine grows during childhood.

There is currently no known cause for idiopathic scoliosis.¹ Recent scientific research has focused on hormonal and neurological causes, with some promising early results that suggest recommendations for conservative management.

Spinal Development

The pineal gland produces melatonin, a hormone that appears to influence the development of a balanced spine. Surgical removal of the pineal gland in young chickens² and in bipedal rats³ has produced spinal curvatures very similar to human idiopathic scoliosis, including vertebral rotation and rib humps. In the rat study, the investigators found that providing a source of melatonin prevented the development of scoliosis in pinealectomized rats. They theorized that "melatonin may facilitate the fine neuromuscular coordination needed to maintain the 24 stacked vertebrae in balance."

While some studies have found that human patients with progressive scoliosis may have lower levels of melatonin, other investigations have not been able to establish a direct correlation.⁴ A 2004 study of 41 patients with adolescent idiopathic scoliosis found defects in the melatonin signaling pathways in their osteoblasts.⁵

What Gait Observations Reveal

Numerous studies have shown that humans with scoliosis have various deficiencies in muscle coordination and standing balance, but the source of these difficulties with fine motor control is still unknown. The gait of children with scoliosis has been found to be somewhat abnormal, but there is controversy about whether this causes a curvature to develop or is simply a result ofwalking with a curved spine.

A study that used sophisticated measuring devices and advanced computer analysis has provided some initial answers.⁶ The investigators found several significant differences in gait between normal children and those with scoliosis, and they found that children with scoliosis had substantially higher inter- and intrasubject variability. There was also substantial bilateral asymmetry in their lower limbs when walking. This was most noticeable in the medial-lateral component of gait, indicating problems with pronation and supination control.

They observed: "These findings indicate a different functional role for the left and right limbs during gait," and that the "differences between the scoliosis and the control group, together with previously reported abnormalities of torsion in the tibia and femur and the hypothesis of pelvic rotation, suggests these are primary mechanisms of the cause of idiopathic scoliosis."

The researchers concluded that patients with scoliosis "exhibit balance problems during the stance phase of gait and have significant asymmetry in the frequency characteristics. These findings could be a primary effect that contributes to the medial-lateral deformity of the spine and its initiation and progression."6 Later research has concluded that "Somatosensory dysfunction in AIS patients shows to have an impact on dynamic balance control."⁷

Chiropractic's Role

These studies are exciting, as they open up the very real possibility of preventing or at least significantly slowing the progression of idiopathic scoliosis with conservative methods. While much more study needs to be done, it is quite possible that chiropractic care will be the accepted scoliosis treatment of the future. This care will likely include careful spinal adjustments, individually designed stabilizing orthotics for better foot function and gait symmetry, and nutritional supplementation of melatonin levels, along with exercise recommendations to improve body balance and neuromuscular coordination.

Each young patient with a scoliosis must be evaluated to determine the classification of the spinal curvature and its potential for progression. When conservative treatment is indicated, nutritional support for the pineal gland should be considered. Perhaps most importantly, the neurological and musculoskeletal systems need to be checked thoroughly – starting with the feet. Exercises to develop fine control of balance and posture, as well as gait training, may be helpful. Some type of stabilizing orthotics should be considered early in the treatment of all patients with scoliosis to help improve bilateral balance and gait symmetry.

References

1. de Baat P, van Biezen EC, de Baat C. Scoliosis: review of types, aetiology, diagnostics, and treatment 1. Ned Tijdschr Tandheelkd, 2012;119(10):474-478.
2. Dubousset J, Queneau P, Thillard MJ. Experimental scoliosis induced by pineal and diencephalic lesions in young chickens: its relation with clinical findings. Orthop Trans,1983;7:7.
3. Machida M, Murai I, Miyashita Y, et al. Pathogenesis of idiopathic scoliosis: experimental study in rats. Spine, 1999;24(19):1985-1989.
4. Brodner W, Krepler P, Nikolakis M, et al. Melatonin and adolescent idiopathic scoliosis. J Bone Joint Surg Br, 2000;82:399-403.
5. Moreau A, Wang DS, Forget S, et al. Melatonin signaling dysfunction in adolescent idiopathic scoliosis. Spine, 2004;29:1772-1781.
6. Giakas G, Baltzopoulos V, Dangerfield PH, et al. Comparison of gait patterns between healthy and scoliotic patients using time and frequency domain analysis of ground reaction forces. Spine, 1996;19:2235-2242.
7. Lao ML, Chow DH, Guo X, et al. Impaired dynamic balance control in adolescents with idiopathic scoliosis and abnormal somatosensory evoked potentials. J Pediatr Orthop,2008;28(8):846-849.