Thursday, December 3, 2015

Myofascial Release Technique in Chronic Lateral Epicondylitis: A Randomized Controlled Study

International Journal of Health Sciences & Research Vol. 3; Issue: 7; July 2013 (www.ijhsr.org) 

 Original Article

 Myofascial Release Technique in Chronic Lateral Epicondylitis: A Randomized Controlled Study 

P. Ratan Khuman*, Parth Trivedi, Surbala Devi, D. Sathyavani, Gopal Nambi, Kimi Shah 
Department of Musculoskeletal and Sports Physiotherapy C.U. Shah Physiotherapy College, Surendranagar, Gujarat, India 
*Correspondence Email: physiompt@gmail.com 
Received: 31/05//2013 Revised: 12/07/2013 Accepted: 13/07/2013

 Abstract 
Background & Objective: Lateral epicondylitis (LE) is a chronic overuse injury commonly affecting the common tendinous origin of the wrist extensors. The objective of the study was to find the effectiveness of   Myofascial Release Technique (MFR) on pain, functional performance and grip strength in Chronic Lateral Epicondylitis (CLE) subjects.

Study design: A randomized controlled study

Setting: Institutional based musculoskeletal Physiotherapy outpatient department.

Outcome measures: Numerical pain rated scale (NPRS), Patient rated tennis elbow evaluation (PRTEE), and Hand dynamometer (HD)

Material & Methods: 30 subjects with the CLE were included in the study. They were divided into two different groups; Group A: MFR & Conventional physiotherapy (n=15) and Group B: Conventional physiotherapy (n=15). The predefined treatment protocol was provided for four weeks. The pain, functional performance and grip strength were assessed at baseline and post treatment (4th week) using NPRS, PRTEE and HD.   

Result:  There was a significant decrease in pain, improvement in functional performance and grip strength (p<0.05) in both the groups. However, MFR group was found to have a greater effect on all outcome measures in CLE subjects

Conclusion: The result of this study indicates that 4 weeks of MFR was effective in improving pain, functional performance and grip strength in Chronic Lateral Epicondylitis (CLE) subjects compared to the control group.

Key words: Lateral epicondylitis, MFR, PRTEE, NPRS, Hand Dynamometer   

INTRODUCTION
Lateral Epicondylitis (LE) or tennis elbow affects about 1-3% of general population [1] and frequently encountered by physical therapist. It is one of the most common lesion of elbow characterized by pain at lateral epicondyle of humerus while dorsiflexing the wrist against resistance. [2] Subjects with LE complains of pain, functional difficulty affecting activities of daily living related to wrist and forearm movements.[3] The grip strength is affected due to voluntary decline of effort to avoid pain and due to wasting of affecting muscles seen in long standing conditions. The symptoms exacerbate with stressful activities in overuse syndromes but pain may persist even at rest as the condition progress. [4]
The LE is termed as chronic if symptoms last for more than three months. The causative factors of pain in chronic stage are uncertain. However, sensitization of peripheral nociceptors by an increase of neural transmitter in affected tissue may be responsible for the pain. The uncertainty about the causative factor of pain may explain the lack of a clearly effective intervention in CLE. [2]
Various other intrinsic causative factors of LE are enumerated in numerous studies. [5-11] The proposed patho-biology involves a tear of tendon at junction between muscle and bone leading to slow healing due to lack of overlying periosteal tissue. Repetitive micro trauma from overuse or abnormal joint biomechanics may overload the repairing tissue, mechanically distort scar tissue and thus stimulate free nerve endings to evoke mechanical nociceptive pain. The limited blood supply to muscle origin would be further reduced after injury. Patient’s age is also a significant factor in reduced vascularity. [12]
Traditionally, treatments for LE have focused primarily on pain control by rehabilitation of muscles. Numerous treatments have been tried for LE including anti-inflammatory medication, corticosteroid injection, electrical stimulation, laser, acupuncture, counterforce bracing or splint, ergonomics, ultrasound, iontophoresis, phonophoresis, exercises (flexibility, strengthening and endurance training), manual therapy techniques, (e.g, transverse frictions, joint mobilization and manipulation, myofascial release, strain and counter strain techniques) etc. [13]  
MFR is the application of a low load, long duration stretch (120 – 300s) to myofascial complex, intended to restore optimal length, decrease pain, and improves function. [14] Stanborough, myofascial practitioners believe that by restoring the length and health of restricted connective tissue, pressure can be relieved on pain sensitive structures such as nerves and blood vessels. MFR generally used are either by direct technique MFR or indirect technique MFR. [15]  The rationale for these techniques can be traced to various studies that investigated plastic, viscoelastic, and piezoelectric properties of connective tissue.[16-,17]  In this study direct technique MFR detailed by Stanborough was used through fingertips and knuckles in CLE subjects. [18]
Currently, no general consensus exists as the most appropriate management for CLE, even after several systematic reviews have been published. [19,20] A variety of physiotherapy treatments have been recommended which have different theoretical mechanism of action, but having same aim, to reduce pain and improve function. The available evidences comparing the effects MFR Technique in CLE are very few. Therefore our purpose was to find the effectiveness of   MFR Technique on pain, functional performance and grip strength in CLE subjects. So the result of this study could be implicated in clinical practice. We hypothesized that MFR would be effective in CLE subject.

MATERIALS AND METHODOLOGY:
The subjects from an institutional based Musculoskeletal Physiotherapy outpatient department referred with lateral elbow pain were screened. The subjects were included if age 30-45 years, both gender, CLE > 3 months, unilateral involvement, NPRS score 4 to 8. They were excluded if any history of trauma, surgery, acute infections, any systemic disorders, cervical spine and upper limb dysfunction, neurological impairments, cardiovascular diseases, osteoporosis, recent steroid infiltration, ossification and calcification of soft tissue, malignancies, athletes, recently underwent physiotherapy interventions in least 3 months, unwillingness to attend all treatment sessions & assessments. Informed consent was obtained from all subjects. Demographic data were collected from the subjects (Table-1). The study obtained ethical clearance from institutional review board.

SAMPLING TECHNIQUE:
30 subjects diagnosed as CLE were included in study that fulfils the inclusion criteria after detailed physical therapy evaluation. They were randomly assigned with concealed allocation into one of the two treatment groups: Group-A (n=15) MFR & Conventional physiotherapy and Control Group-B Conventional physiotherapy (n=15). A block randomization method was implemented, where   subjects randomly chose one of the two enclosed envelopes to determine their group allocation. The next subject was then assigned to remaining group before the process was repeated.

INTERVENTION:
            Both groups were treated for four weeks by the same therapist. All subjects attended full treatment protocol without drop out. No blinding was done for intervention as well as subjects.         

MYOFACIAL RELEASE TECHNIQUE:
The subjects were in supine with affected side shoulder rotate internally, elbow flexion to around 15° and pronation, palm resting flat on table. Therapist stands at the side of table near shoulder and facing ipsilateral hand. Procedure 1: Treating from common extensor tendon (CET) to extensor retinaculum (ER) of wrist began on humerus, just proximal to lateral epicondyle. Using fingertips to engage periosteum and carries this contact inferior to common extensor tendon and then down to extensor retinaculum of the wrist (5min, 2 repetitions). Then, the patient slowly flexes and extends the elbow within range of 5° to 10° during this procedure. Procedure 2: Treating through periosteum of ulna, use knuckles of hand to work over periosteum of ulna (5min, 2 repetitions). Then the patients performed alternating ulnar and radial deviation of wrist. Procedure 3: Spreading radius from ulna, contacts head of ulna with finger pads of one hand and dorsal tubercle of radius with the pads of other. The therapist engaged through to the periosteum and put a line of tension in a lateral and distal direction. It is carried for just a few centimeters with a firm intent to spread the bones (5min, 2 repetitions). Dosage: 30 minutes/session, 3 times a week for 4 weeks. [15,18]

CONVENTIONAL PHYSIOTHERAPY:
It includes pulse ultrasound therapy and graduated exercise therapy regimen of stretching and strengthening exercises. Stretching: Self-stretching of wrist extensors (wrist being palmar-flexed using other hand) 15 sec hold, 10 stretches/session/day. Strengthening: Wrist extensor isometric exercise in sitting position with elbow 90° flexion, while unaffected hand applying manual resistance over dorsum of hand and held for 5 to 10 seconds, 15 contractions/ session/day. It was progressed by increasing resistance.[21]  Pulse ultrasonic therapy (PUS): Using ultrasound device, (Chattanooga Intellect Advanced, Model no-2762cc, Series no-4003) in seated position, over tenoperiosteal junction of ECRB with 1MHz, 1.5 W/cm2, 1:4 ratios, for 5 minutes 3 session/week total 12 sessions were given.[22]  The stretching exercise, strengthening exercise and pulse ultrasound therapy were given to both groups.

OUTCOME MEASURES:
Pain was assessed by 11 Point NPRS, where the end points are extremes of no pain and worst pain. The NPRS is a reliable and valid pain assessment scale in CLE.[23]  Functional Disability was measured by PRTEE, a 15-item questionnaire designed to measure forearm pain and disability in patients with LE. The PRTEE was found to be a reliable, reproducible and sensitive instrument for the assessment of pain and disability in CLE subjects. [24] The hand grip strength was evaluated using baseline hand dynamometer (HD) which has been used extensively in studies for assessing hand function. The devices have test-retest reliability in various age groups and have been used to validate other instruments. [25] All outcome measures were used to assess baseline value and progressions at 4th week.

STATISTICAL ANALYSIS:
All statistical analysis for the subjects in both the groups was done using SPSS 16 for windows software. The level of significant was set at 95% (p=0.05). Descriptive analysis was used to calculate Mean and Standard deviation. The inter group comparison of demographic details were performed using independent “t” test. Non parametric Mann Whitney “U” Test was used for inter group and Wilcoxon Sign Rank Test for intra group comparisons.

RESULT:
The demographic details (age; p=0.739, duration of condition; p=0.631) of groups were homogenous with p>0.05(Table-I). Pre-treatment NPRS (p=0.713), PRTEE (p=0.161) and HD (p=0.202) shows no significant difference (p>0.05) (Table-II) (Figure-5, 6, 7). All the subjects in both groups show positive effect in pain, functional performance and grip strength. Pre and post treatment comparison for NPRS (Group-A: p=0.001, Group-B: p=0.002), PRTEE (Group-A: p=0.001, Group-B: p=0.001) and HD (Group-A: p=0.00) shows significant difference (p<0.05) whereas the HD (Group-B: p=0.063) did not shows significant difference. (Table-III) (Figure: 5, 6, 7). Post treatment inter group comparison of NPRS (p=0.000), PRTEE (p=0.000) and HD (p=0.001) shows highly significant difference (p<0.05) among groups (Table-IV) (Figure: 5, 6, 7) proving MFR, an effective treatment in improving pain, functional performance and grip strength.


DISCUSSION:
The treatment of CLE has been attempted using varieties of intervention in previous studies. [13] None of the studies were strongly suggesting to any specific treatment strategy. This study of 4 weeks MFR technique was found to have significant improvement in pain (NPRS), functional performance (PRTEE) and hand grip strength (HD) compared to control group. The superior effect of MFR group compared to control group is similar to finding of previous authors. [18] This may be the fact that pain relief due to MFR is secondary to returning the fascial tissue to its normative length by collagen reorganization. [18] As with any massage therapy techniques, the analgesics effect of MFR can also be attributable to the stimulation of afferent pathways and the excitation of afferent Ad fibres, which can cause segmental pain modulation [26] as well as modulation through the activation of descending pain inhibiting systems. [27]   
All the outcome measures were recorded at baseline and at 4th week.  The domain of pain in NPRS score and functional performance in PRTEE score was found to have more changes than the grip strength domain in HD score. The relative poor outcome in grip strength may be due to the large variation in the duration of condition (5-12 months), as in long standing case there may be wasting of affected muscles and grip become weak.  This may lead to the hypothesis that graded griping muscles strengthening exercise may be required to further improve grip strength in CLE subjects. The results of this study may be applied to a population with a clinical diagnosis of CLE subjects. The predominance of male (GroupA-60%; GroupB-53.3%), dominant side (GroupA-80%; GroupB-86.63%) with age range 30-45 years (mean age GroupA-37.20±3.35, GroupB-37.70±2.79) and right dominant (GroupA-66.6%; GroupB-73.3%) are likely to experience CLE in general population.
The study has certain limitations like no blinding procedure performed, the sample size were small and long-term improvements in the pain; functional performance and grip strength with MFR technique were not recorded. The intervention was of only 4 weeks’ duration in a small sample size; it is possible that longer treatment protocol may achieve greater effects especially on grip strength. Further controlled studies, confirming these findings with blinding process, larger sample size for longer observation period in acute and sub-acute LE may be considered to establish whether these interventions result in long term improvement. Future research comparing the effectiveness of MFR techniques with any other treatment which have been proven effective in CLE subjects should be conducted. In summary, our results suggest that MFR technique may improve pain, functional performance and grip strength in CLE subjects.

CONCLUSION:
This investigation of MFR technique provided evidence of its use in the treatment of CLE subjects. It can be concluded that 4 weeks MFR technique improves pain, functional performance & hand gip in CLE subjects probably by normalizing the fascial tissue length and excitation of afferent A-d fibres, which can cause segmental pain modulation. The MFR technique was more effective than that of control group in pain, functional performance and grip strength.   

ACKNOWLEDGEMENT:
Our best wishes to those valuable subjects & supporter of this study.

CONFLICT OF INTEREST:
We declare that there were no conflicts of interest in the entire journey of the study.

REFERENCE:
  1. Choudhary KA, Rathore FA, Hanif S, Rashid MH. Lateral epicondylitis; Steroid injections for the management. Professional Med J Mar 2011; 18 (1):133-138.
  2. Peterson M, Butler S, Eriksson M, Svärdsudd K. A randomized controlled trial of exercise versus wait-list in chronic tennis elbow (lateral epicondylosis). Ups J Med Sci.2011;116(4):269-279
  3. Briggs CA, Elliot BG. Lateral epicondylitis: A review of structures associated with tennis elbow. Anat clin. 1985; 7(3):149-53.
  4. Kivi P. The etiology and conservative treatment of humeral epicondylitis. Scand J Rehabil Med. 1983; 15(1):37-41.
  5. Bosworth DM. The role of orbicular ligament in tennis elbow. J Bone Joint Surg Am, 1955 Jun 01;37(3):527-533
  6.  Roles NC, Maudsley RH. Radial tunnel syndrome: resistant tennis elbow as a nerve entrapment. J Bone Joint Surg Br. 1972 Aug; 54(3):499-508.
  7. Chard MD, Hazleman BL. Tennis elbow-a reappraisal. Br J Rheumatol. 1989 Jun; 28(3):186-90.
  8. Nirschl RP, Pettrone FA. Tennis elbow. The surgical treatment of lateral epicondylitis. J Bone Joint Surg Am. 1979 Sep; 61(6A):832-9.
  9.  Plancher KD. Medial and lateral epicondylitis in the athletes. Clin Sports Med 1996; 290-305.
  10. Abrahamsson. Lateral elbow pain caused by anconeus compartment syndrome. Acta Orthop Scand 1987; 58:589-591.
  11. Roetert EP, Brody H, Dillman CJ, Groppel JL, Schultheis JM. The biomechanics of tennis elbow. An integrated approach. Clin Sports Med. 1995 Jan; 14(1):47-57.
  12. Mark A. Jones, Darren A. Rivett. A chronic case of mechanic's elbow. Clinical reasoning for manual therapist. 1st ed. UK: Butterworth Heinemann; 2004. p78-102.
  13. Greg w. Johnson. Treatment of Lateral Epicondylitis. American Academy of Family Physicians. 2007; 76: 843-53.
  14. Barnes JF. Myofascial release: the search for excellence. 10th ed. Paoli, PA: Rehabilitation Services Inc; 1990.
  15. Michael Stanborough. The upper extremities. Direct release myofascial technique: an illustrated guide for practitioners. UK: Churchill Livingstone; sep 2004. p172-175.
  16. Greenman PE. Principles of manual medicine. Philadelphia: Lippincott, Williams & Wilkins; 2003. p 155–8.
  17. Pischinger A. Matrix and matrix regulation: basis for a holistic theory in medicine. Brussels: Haug International; 1991.
  18. Ajimsha MS, Chithra S, Thulasyammal RP. Effectiveness of myofascial release in the management of lateral epicondylitis in computer professionals. Arch Phys Med Rehabil. 2012 Apr; 93(4):604-9.
  19. L Bisset, A Paungmali, B Vicenzino, et al. A systematic review and meta-analysis of clinical trials on physical interventions for lateral epicondylalgia. Br J Sports Med 2005 39: 411-422
  20. Smidt N, Assendelft WJ, Arola H, Malmivaara A, Greens S, Buchbinder R, van der Windt DA, Bouter LM. Effectiveness of physiotherapy for lateral epicondylitis: a systematic review. Ann Med. 2003; 35 (1):51-62.
  21. Shimose R, Matsunaga A, Muro M. Effect of submaximal isometric wrist extension training on grip strength. Eur J Appl Physiol. 2011 Mar; 111(3):557-65.
  22. A. P. D’Vaz, A. J. K. Ostor et al Pulsed low-intensity ultrasound therapy for chronic lateral epicondylitis: a randomized controlled trial. Rheumatology 2006;45:566–570.
  23. Amelia Williamson, Birmingham Hoggart, Pain: a review of three commonly used pain rating scales, 2005 Blackwell Publishing Ltd, Journal of Clinical Nursing, 14, 798–804.
  24. Rompe JD, Overend TJ, MacDermid JC. Validation of the Patient-rated Tennis Elbow Evaluation Questionnaire, J Hand Ther 2007 Jan-Mar; 20(1):3-10; quiz 11.
  25. C.B. Irwin and M.E. Sesto. Reliability and Validity of the MAP (Multi-Axis Profile) Dynamometer with Younger and Older Participants. J Hand Ther. 2010 Jul–Sep; 23(3): 281–289.
  26. Melzack R, Wall PD. Pain mechanisms: a new theory. Science 1965; 150: 971-9.
  27. Le-Bars D, Dickenson AH, Besson JM. Diffuse noxious inhibitory controls (DNIC). II. Lack of effect on non-convergent neurons, supraspinal involvement and theoretical implications. Pain 1979; 6: 305-27

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Monday, July 9, 2012

"Neuromuscular Spindle Cell Dysfunction & Its Correction"



Fig: Neuromuscular Spindle Cell
           Neuromuscular spindle cells are throughout the muscle, but concentrated in its "belly,". A neuromuscular spindle is 2-20 mm in length and is enclosed in a fluid-filled sheath of connective tissue. Within are 3-10 thin intrafusal muscle fibers. These lie parallel to the much larger extrafusal muscle fibers located outside the sheath. The extrafusal fibers makeup the bulk of a muscle and they are responsible for the strength of contraction. Spiralling around the central portion of the intrafusal fibers are the neuromuscular spindle cell receptors. These stretch-sensing nerve receptors send their messages along the "primary" type 1a afferent nerves to the central nervous system. The efferent nerves that send the response of the CNS back to the muscle are the alpha motor neurons and gamma motor neurons.

A neuron is one complete nerve cell. It consists of:
  1. The cell body with its nucleus
  2. Along extension called the axon or nerve fiber
  3. Many short branching extensions (dendrites) that connect the nerve via synapses with nerve receptors or other nerves
  4. The synapse.
         The signal that a nerve conducts cannot be stronger or weaker. The nerve impulse always has the same strength. The intensity of a nerve signal is determined by how often the nerve "fires" per second.

           Alpha motor neurons have their origin in the ventral horn of the gray matter of the spinal cord. When a nerve signal from type Ia afferent nerves reaches the spinal cord, the response returns to the muscle along the alpha motor neurons. There are two types of alpha motor neurons. "Tonic" alpha motor neurons innervate postural muscles that are active for extended periods of time. "Phasic" alpha motor neurons innervate phasic muscles that only contract for short periods of time. About 70% of the motor neurons going to the muscles are alpha motor neurons. These innervate the thick extrafusal muscle fibers that are responsible for the force of muscular contraction. The remaining 30% are the gamma motor neurons, which innervate the intrafusal muscle fibers. The intrafusal muscle fibers do not contribute to the strength of muscular contraction. Instead, gamma stimulation causes contraction of the intrafusal muscle fibers, which stretch the neuromuscular spindle. This process produces fine motor control, not raw force. The nerve impulses traveling through gamma motor neurons to the intrafusal muscle fibers originate in the cerebellum.

          At each end of the neuromuscular spindle, the intrafusal muscle fibers attach to the muscle sheath and are thereby automatically lengthened or shortened with the rest of the muscle. In the middle of each intrafusal fiber is an area with no actin and myosin, which therefore does not contract. So when the gamma motor neurons stimulate the intrafusal muscle fibers to contract, the intrafusal muscle fibers pull toward each end and thus lengthen the central portion upon which the Ia nerve receptor fibers are wound.

         Ia nerves are afferent nerves. They and their nerve receptors are called "primary" to distinguish them from the finer type II nerves. The primary Ia receptors of neuromuscular spindle cells are always sending signals into the spinal cord. When the central portion is stretched, the output from the "primary" receptors is increased. Type Ia nerves are thick and the nerve signals travel through them swiftly. When the receptor area between the contractile portions of the intrafusal fibers is suddenly lengthened, it sends an especially intense signal (high number of nerve firings per second) through its type Ia nerves to the dorsal horn of the spinal cord. Only one synapse in the spinal cord needs to be stimulated before the speedy "monosynaptic" response is sent back to the same muscle to contract. This is the basis of reflex reactions such as the knee-jerk reflex. This type of response is called "monophasic" because it occurs once and immediately stops.

       "Secondary" type II afferent nerves connect directly into the contractile portions of the intrafusal muscle fibers. Type II nerves are slender and slower than type Ia nerves. They are responsible for the second type of neuromuscular spindle response which, when stimulated, causes the muscle to raise its tension slowly and remain in a state of elevated tonus.

      During the muscle test or any weight-bearing activity, there is both alpha and gamma efferent stimulation to the muscle. Alpha stimulation of the extrafusal fibers produces the force of contraction. Gamma stimulation of the intrafusal fibers stretches the central receptor area of the neuromuscular spindle cell. The receptor, which is always sending impulses, then sends a greater than normal impulse into the spinal cord and cerebellum. This is, in effect, an order for greater contraction in the muscle to meet the current demand. This results in a greater nerve signal being sent back through the alpha motor nerves to the extrafusal fibers of the muscle, increasing the force of contraction.

      The neuromuscular spindle cells are responsible for signalling the nervous system to increase the tension in a muscle that is lacking adequate tone. As the examiner applies more force in the muscle test, the patient's neuromuscular spindle cells monitor the amount of force applied and signal the nervous system to produce the appropriate intensity of alpha nerve signal to contract the muscle enough to hold the limb or other body part in position. Thus if the neuromuscular spindle cells in a muscle are not sending an adequate signal, the muscle will test weak.

       The activity of the neuromuscular spindle cells excites its own muscle to contract. It further facilitates contraction of the muscle's synergists and its stabilizers. At the same time, the antagonists to the muscle are inhibited. As mentioned, the reflex excitation of the muscle itself occurs swiftly because only one single synapse in the spinal cord must be traversed between the neuromuscular spindle cell and the extrafusal muscles that provide the force of contraction. This allows the body to protect itself by very quickly jerking away from potentially damaging stimuli. The neural circuits that facilitate the synergists and stabilizers and those that inhibit the antagonists, each have two synapses in the spinal cord to traverse and thus are somewhat slower.

       It is the coupled activity of the alpha and gamma nerves in the neuromuscular spindle cells that makes muscular contraction smooth and coordinated. Postural or "tonic" muscles typically hold relatively high levels of tone for long periods of time. Such muscles have a high proportion of slow tonic fibers. The activity of such muscles does not require fine coordination. Therefore, tonic muscles have few neuromuscular spindle cells. "Phasic" muscles have a higher proportion of fast "phasic" fibers and far more neuromuscular spindle cells to provide for their faster, more intricate, finely coordinated movements.

   Normally, the neuromuscular spindle cells continuously send signals to the nervous system concerning the length of the muscle. The length of a muscle may be manually adjusted by manipulation of the neuromuscular spindle cells. Pushing or pinching the neuromuscular spindle cells together (parallel to the length of the muscle) reduces the tension on the intrafusal muscle fibers. They then send signals of less intensity than normal through their Ia afferent nerves to the spinal cord. This temporarily reduces the level of alpha efferent nerve signalling, which results in less tension in the extrafusal fibers responsible for muscle strength. Thus, pinching the spindle cells together will cause a muscle to temporarily test weak. This may be used to determine whether a muscle is responding correctly.

      Stretching and activating the neuromuscular spindle cells by pushing the two hands or fingers into the belly of a muscle and pulling apart stretches the intrafusal fibers, increasing their output to the spinal cord. As a result, more nerve impulses per second are sent through the alpha efferent nerves to the extrafusal fibers of the muscles, which then contract more strongly. Thus, pulling the neuromuscular cells apart increases the tension in a muscle.

     When a muscle (the agonist) acts, the action of its neuromuscular spindle cells causes its antagonist to be inhibited. When the antagonist to a muscle acts, the agonist is inhibited. This principle is call "reciprocal inhibition." Were both the agonist and antagonist to act simultaneously, they would be fighting against each other, which would be a waste of energy. Also, the two bones in the joint over which the two muscles act would be jammed together. Reciprocal inhibition occurs automatically at the level of the spinal cord where the synapses meet between the afferent nerve from the neuromuscular spindle cell and the efferent nerve that returns to the antagonist. However, higher brain centers can override this effect. A conscious decision can be made in the cerebral cortex to flex whole groups of agonists and their antagonists simultaneously. This is conveyed to the cerebellum and from there to the appropriate spinal segments and then on to the muscles. This is what occurs when a bodybuilder flexes most of his or her muscles at once to make an impressive pose.

         It is normal that while a muscle is active, its antagonists are inhibited. An incorrectly functioning neuromuscular spindle cell may send impulses so overly strong that any activity of the muscle causes its antagonist(s) to subsequently test weak, even after the agonist has relaxed. This condition is called "reactive muscles." Dysfunctioning neuromuscular spindle cells will usually therapy-localize (TL). That is, if the muscle tests weak because of dysfunction of the neuromuscular spindle cell, touching the neuromuscular spindle cell will cause the muscle to test strong. Conversely, just about any normotonic indicator muscle will weaken when a dysfunctioning neuromuscular spindle cell is therapy-localized.

       A dysfunctioning neuromuscular spindle cell is usually palpable as a hard lump. Locating it through therapy localization and palpation makes treatment more direct and easy to perform.

        To strengthen a muscle that tests weak because of a dysfunctioning neuromuscular spindle cell, the examiner presses his fingers rather deeply into the muscle on each side of the neuromuscular spindle cell and then pulls his fingers apart from each other along the direction of the fibers of the muscle. This also can be used to "wake up" normally functioning muscles and thereby prepare them for strong contraction before or even during athletic competition.

         To weaken a muscle that tests hypertonic (one that tests strong but cannot be weakened by usual means) because of a dysfunctioning neuromuscular spindle cell, the examiner presses his fingers into the muscle on each side of the problematic neuromuscular spindle cell and then repeatedly presses his fingers together along the line of the direction of muscular contraction (the line of the muscle fibers themselves). This effectively "pinches" the neuromuscular spindle cell together. This type of manipulation of the neuromuscular spindle cells can swiftly return full extension to shortened, tight muscles. It is not the most pleasant type of massage, but it is one of the most effective in promoting the relaxation of overly contracted muscles. For example, the application of this technique to a tight upper trapezius muscle between the neck and shoulder can swiftly reduce tension and pain in the muscle. This is assuming that the tension in the upper trapezius is primary and not caused only by its antagonist, the latissimus dorsi, having inadequate tone. Such treatment to the upper trapezius muscle may lengthen it so much that the shoulder sinks a few centimetres.

        Treatment of neuromuscular spindle cells requires 1-7 kilograms of pressure. Sometimes even more pressure is required for the desired effect. Patients who have little tone in their muscles should be treated with less pressure. The pressure should be applied to a particular neuromuscular spindle cell several times. If the muscle is very wide and several neuromuscular spindle cells are involved, the treatment is repeated upon each active spindle cell, or simply across the whole width of the muscle. After adequate treatment, the neuromuscular spindle cells should no longer therapy-localize and the muscle should have the proper level of tension as measured by muscle testing.

      If the same dysfunction of the neuromuscular spindle cell returns, or if there are neuromuscular spindle a cell problem in many separate muscles, a nutritional correction is indicated. Goodheart recommends that the patient chew raw bone concentrate or raw bone nucleoprotein extract. He suspects that the helpful factor in the bone concentrate is phosphatase. As long as one has no allergy to the nightshade family of plants (potatoes, tomatoes, eggplant and peppers), the phosphatase in raw potato also seems to work well for this purpose.

 Correction of a Muscle that Tests Weak Due to Dysfunctioning Neuromuscular Spindle Cells

 Indications of possible dysfunction of the neuromuscular spindle cells:
  1. The muscle has too little tone (is hypotonic).
  2. The muscle is palpatory hypertonic but tests weak.
  3. There are firm lumps in the belly of a muscle that hurt when pressed upon.
  4. The muscle contains neuromuscular spindle cells that therapy-localize.
Test:
  1. Palpate the muscle for firm l umps. They will usually be in the belly of the muscle but may     be located anywhere in the contractile fibers.
  2. Touch (therapy-localize) the suspect area (on the lumps if any are palpated).
  3. Test the muscle again while the suspect area is therapy-localized.
  4. If the previously weak-testing muscle now tests strong, there are dysfunctioning neuromuscular spindle cells in the area therapy-localized.
Correction:
  1. To raise the tone of a muscle that tests weak because it contains a dysfunctioning neuromuscular spindle cell, push the fingers (or sides of the hands) into the muscle on each side of it and pull the tissues apart along the direction of the muscle fibers. Do this several times with 1-7 kilos of pressure.
  2. Retest the previously weak-testing muscle. It should now test strong. If not, return to test step 1, check for and correct other areas of dysfunction.
  3. Therapy-localize the previously dysfunctioning neuromuscular spindle cell and retest the muscle. The muscle should again test strong. If not, repeat correction step 1.
  4. Have the patient chew raw potato or raw bone concentrate at this time to lock in the correction.


Fig: Neuromuscular Cells  "Pulling Apart" to increase tension in a muscle

Correction of a Muscle that is Hypertonic Due to a Dysfunctioning Neuromuscular Spindle

 Indications of possible dysfunction of the neuromuscular spindle cells:
  1. The muscle has too much tone (palpatory hypertonic) and is hard and painful.
  2. There are firm l umps in the belly of a muscle that hurt when pressed upon.
  3. Neuromuscular spindle cells therapy-localize.
Test:
  1. Palpate the muscle for firm lumps.
  2. Therapy-localize the suspect area (on the l umps if any are palpated).
  3. Test another normotonic indicator muscle while therapy localizing the suspect area.
  4. If the previously normotonic indicator muscle now tests weak, there are dysfunctioning neuromuscular spindle cells in the area therapy-localized.
Correction:                                                                                                                   
  1. To correct a muscle that is too tight because of dysfunctioning neuromuscular spindle cells, push the fingers (or sides of the hands) into the muscle on each side of the area that therapy-localized and push the tissues together (pinch the neuromuscular spindle cell together) along the direction of the muscle fibers. Do this several times with 1-7 kilos of pressure.
  2. Therapy-localize the previously dysfunctioning neuromuscular spindle cell area and retest the indicator muscle. The indicator muscle should now remain strong. If not, repeat correction step l.
  3. Test if the muscle that could not be weakened previously (hypertonic), now can be weakened (is normotonic).
  4. Have the patient chew raw potato or raw bone concentrate to lock in the correction.
    Fig: Neuromuscular spindle cell "Pressing Together" to decrease in a muscle

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