Integrative Manual Therapy-Autonamic Nervous System and Related Disorders

Medicine/Rehabilitation This book Integrative Mamlal Therapy for the Autonomic Ner­ vous System and Related Disorders with Advanced Strain and Counterstrain Technique is the first of its kind: a text for system­ atic treatment of tissues and structures innervated by the auto­ nomic nervous system. Muscle spasm induced by stress, visceral and circulatory problems and central nervous system dysfunc­ tion can be alleviated. Arterial and venous blood flow will increase. Lymphatic drainage will improve. Muscles of organs and eyes and speech and swallowing will function more efficiently. Tendon Release Therapy for treatment of tendon lesions and scars is presented. Disc Therapy for effective elimina­ tion of discogenic problems is covered. Over one hundred tech­ niques are presented in this book. This approach is founded upon Dr. L awrence Jones' Strain and Counterstrain Technique; the authors acknowledge his con­ tribution to the field of manual therapy. All of the techniques in this text are original, developed by Weiselfish-Giammatteo, P h.D., P.T. and Giammatteo, D.G., P.T. Their unique experiences with clients of all populations has contributed to Advanced Strain and Counterstrain protocols and methodology for ortho­ pedics and sports medicine, chronic pain, pediatrics, cardiopul­ monary rehabilitation, neurology, and geriatrics. This approach has been used successfully for treatment of severe pain, spasticity and movement disorders, health and well­ ness. P hysicians, chiropractors, physical therapists, occupational therapists, massage therapists and other manual practitioners are excited regarding these new methods for health care. Key features include: • over 100 techniques for treatment of pain and disability for all client populations • clear, concise text • illustrations of related anatomy • photographs of positions of techniques • elaboration of application and integration • what symptomatology will be affected • procedures and protocols for multiple diagnosis � North Atlanric Books Jlllt If \\;J Berkeley, California ISBN: 1-55643-272-0 $65.00 Distnbutt\"d to Ute book rude b)\" Publishers Group West

INTEGRATIVE MAN UAl TH ERAPY FOR THE AUTONOMIC NERVOUS SYSTEM AND RElATED DISORDERS Utilizing Advanced Strain and Counterstrain Technique Thomas Giammatteo, D.C., P.T. Sharon Weiselfish-Giammatteo, Ph.D. P.T. North Atlantic Books Berkeley, California

Integrative Manual Therapy for the Autonomous Nervous System and Related Disorders Copyrighr © 1997 by Thomas Giammarreo and Sharon Weiselfish-Giammarteo. All righrs reserved. No portion of this book, except for brief review, may be reproduced, srored in a retrieval system, or transmitted in any form or by any means--electronic, mechanical, photo­ copying, recording, or otherwise-without written permission of the publisher. Published by North Atlantic Books P.O. Box 12327 Berkeley, California 94712 Cover and book design by Andrea DuFlon Printed in the United States of America Integrative Manual Therapy for the Autonomous Nervous System and Related Disorders is sponsored by the Society for the Study of Native Arts and Sciences, a nonprofit educational corporation whose goals are to develop an educational and crossculturai perspective linking various scientific, social, and artistic fields; ro nurture a holistic view of arts, sciences, human­ ities, and healing; and to publish and distribute literature on the relationship of mind, body, and nature. 2 3 4 5 6 7 8 9 I 00 99 98 97

ACKNOWLEDGMENTS The authors wish to acknowledge Lawrence jones, D.O., the developer of Strain and Counterstrain Technique, whose research and documentation during half a century contributed an outstanding procedure to health care and the field of manual therapy. Lawrence jones, Larry to his friends, was a humble and modest man, with integrity and truth as a model for all health care practitioners. We wish to extend our appreciation to Loren Rex, D.O., who intro­ duced us to Strain and Counterstrain Technique. We want to extend our gratitude to Carol Gordon, P.T., jay Kain, Ph.D., P.T., A.T.e., and our colleagues at Regional Physical Therapy in Connecticut, who supported the clinical research in this new area of man­ ual practice to address autonomic nervous system dysfunction. We extend our respect and appreciation to those original thinkers and developers who influenced us and thereby contributed to the unfolding of this approach: Frank Lowen, ICST, who refined the art of Listening for us, and contributed the results of his research for Synchronizerso; and jean Pierre Barral, D.O., whose research and instruction in visceral manipula­ tion and Listening is a foundation for all our work; Paul Chauffour, D.O., who developed Inhibitory Balance Testing, for more efficient rehabilitation; and Hildegaard Witrlinger, who brought Manual Lymph Drainage to North America. Many, many thanks to our clients who continue to return for more and improved manual therapy. We will always be here for you. Thanks and appreciation to john Giammatteo, for your artistry and skill in photography. Thank you Ayelet Weiselfish and Genevive Pennell, for the gift of your illustrarions. Love and appreciation to Nim, Ayelet and Amir, OUf children, whose blessings and encouragement have been such a gift. And, once again, thank you Margaret Loomer, whose creativity and skill makes books. With Love, Sharon and Tom iii

TABLE OF CONTENTS Foreword xi Chapter 1 Present Models of Strain and Counrerstrain Technique Jones' Model Uones) 2 MechanicaVCorrective Kinesiology Model (Weiselfish-Giammarreo) 2 Synergic Parrern Releasec Model (Weiselfish-Giammarreo) 2 Inhibitory Balance TestingC and Mechanical Link Model (Chauffour) 3 Behavioral Modification for Chronic Pain Model (Weiselfish-Giammatteo) 3 Chapter 2 Alternative Methods: Strain and Counrerstrain Technique Combined with Other Approaches 5 Inhibitory Balance Testing,C developed by Paul Chauffour, D.O. 5 Neurofascial Process,c developed by Sharon Weiselfish-Giammarreo, 5 Ph.D., P.T. Synchronizers,c developed by Lowen, LC.s.T. and Weiselfish- 6 Giammarreo, Ph.D., P.T. Chapter 3 A Hypothetical Model: Decreasing the Hypertonicity of Protective Muscle Spasm and Spasticity with Strain and Counrerstrain Technique and Advanced Strain and Counterstrain Technique 9 Chapter 4 Application: How to Perform Advanced Strain and Counrerstrain Technique 23 Chapter 5 Advanced Strain and Counrerstrain for the Viscera 24 OrglUG2: Bladder 24 OrglUGF3: Cervix 25 OrgIHTl: Heart I 26 OrglLll: Large Intestine 1 27 OrglLV1: Liver 1 28 OrglLUl: Lung 1 29 OrglLU2: Hilum of Lung 30 OrglPNl: Pancreas 1 31 OrglUGM 1: Prostate 1 32 OrglSl1: Small lntestine 1 33 OrglSTl: Stomach 1 34 OrglUGFl: Uterus 1 35 orglUG1: Ureter 36 OrglUG3: Urethra 37 v

vi ADVANCED STRAIN AND CDUNTERITRAIN OrglUGF2: Vagina 38 OrglUGM2: Vas Deferens 39 Chapter 6 40 40 Advanced Strain and Counterstrain for Vision 40 Visll: Eye ]-Superior 40 Vis/2: Eye 2-lnferior 40 Vis/3: Eye 3-Lateral Vis/4: Eye 4-lnferomedial 43 43 Chapter 7 44 Advanced Sttain and Counterstrain for Auditory Function 44 Aud/l: Tympanic Membrane 45 46 Chapter 8 47 Advanced Strain and Counterstrain for Speech and Swallowing 48 Speechll: Arytenoid Tendency to Adduct 48 Speech/2: Myelohyoid 50 Speechl3: Thyroid cartilage elevation 51 Speechl4: Vocal Cords 53 54 Chapter 9 56 Advanced Strain and Counterstrain for the Diaphragm System 56 Diaphll: Pelvic Diaphragm 57 Diaphl2: Respiratory Abdominal Diaphragm 58 Diaph/3: Thoracic Inlet 59 Diaph/4: Subclavius 60 Diaph/5: Cranial Diaphragm 61 62 Chapter 10 63 Advanced Strain and Counterstrain for Elemental Circulatory Vessels 63 Circ/l: Circulatory Vessels of the Lower Extremities 64 Circl2: Circulatory Vessels of the Upper Extremities 66 Circ/3: Circulatory Vessels of the Abdomen 67 Circl4: Circulatory Vessels of the Chest Cavity 68 Circl5: Circulatory Vessels of the Neck 69 Circl6: Circulatory Vessels of the Cranial Vault 70 Circl?: Circulatory Vessels of the Facial Vault Chapter 11 Advanced Strain and Counterstrain for the Muscles of Lymphatic Vessels Lymph/]: Lower Extremities Lymphatic Vessels Lymphl2: Upper Extremities Lymphatic Vessels Lymphl3: Abdomen Lymphatic Vessels Lymphl4: Chest Cavity Lymphatic Vessels Lymph/5: Neck Lymphatic Vessels Lymphl6: Facial Lymphatic Vessels Lymph/?: Cranium and IntraCranial Lymphatic Vessels

AU TONOMIC NERVOUIIYITEM vii Chopter 12 71 71 Advanced Strain and Counterstrain for Arteries: 72 Lower Extremities 73 ArtILEl: Iliac Arteries 73 ArtlLE2: Proximal Femoral Arteries 74 75 Chopter 13 76 Advanced Strain and Counterstrain for Arteries: 76 Upper Extremities 77 78 ArtlUEl: Arteries of the Arm 79 ArtfUE2: Axillary Artety 80 ArtfUE3: Brachial Artery 81 82 Chopter 14 83 84 Advanced Strain and Counterstrain for Arteries: 85 Cranial and Cervical Region 87 89 ArtlCranial1: Arteries of the Brain ArtlCranial2: Arteries of the Circle of Willis 90 ArtlCranial3: Arteries of the Eyes 90 ArtlCranial4: Arteries of the Hypothalamus 92 ArtlCranialS: Basilar Artery 93 ArtlCranial6: Carotid-Common Carotid Artery 94 ArtlCranial7: Carotid-External Carotid Artery 95 ArtlCranialS: Carotid-Internal Carotid Artery 96 ArtlCranial9: Cerebral-Anterior Cerebral Artery 97 ArtlCranial 10: Cerebral-Middle Cerebral Artery 98 ArtlCranial 11: Cerebral-Posterior Cerebral Artery 99 Art/Cranial 1 2 : Middle Meningeal Artery 1 00 Chopter 15 101 101 Advanced Strain and Counterstrain for Arteries: Cardiopulmonary System ArtlCardiol: Aorta Art/Cardio2: Arteries of the Lung Art/Cardio3: Intraventricular Coronary Arteries ArtlCardio4: Left Anterior Descending Coronary Artery ArtlCardioS: Left Coronary Arteries ArtlCardio6: Marginal Coronary Arteries ArtlCardio7: Posteriot Descending Coronary Arteries ArtlCardioS: Right Coronary Artery ArtlCardio9: Right Marginal Coronary Artery ArtlCardiol0: Subclavian Artery Chopter 16 Advanced Strain and Counterstrain for Arteries: The Urogenital Tissues ArtfUG1: Arteries of Capsule of Kidney

viii ADVANCED STRAIN AND (OUNTERSTRAIN 102 104 ArtIUG2: Renal Artery 105 ArtfUG3: Suprarenal Artery ArtlUGF/M 1: Testicular/Ovarian Artery 106 106 Chapter 17 108 109 Advanced Strain and Counterstrain for Arteries: Arteries to the Spine 110 110 Art/Spinel: Anterior and Posterior Spinal Arteries Art/Spine2: Middle Sacral Artery 111 Art/Spine3: Pial Arterial Plexus 111 112 Chapter 18 113 Advanced Strain and Counterstrain for Veins: 113 Lower Extremities 114 1 15 VeinlLEl: Superficial Veins of rhe Lower Limbs 116 Chapter 19 116 117 Advanced Strain and Counterstrain for Veins: 118 Upper Extremities 119 120 VeinlUEl: Superficial Veins of the Arms VeinlUE2: Superficial Veins of the Shoulder 122 122 Chapter 20 123 Advanced Strain and Counterstrain for Veins: 124 Cranial and Cervical Veins 124 Vein/Craniall: Superficial Cerebral Veins Vein/CraniaI2: Superficial Veins of the Head Vein/CraniaI3: Superficial Veins of the Neck Chapter 2 1 Advanced Strain and Counterstrain for Veins: Cardiopulmonary Veins Vein/Cardiol: Alveolar-Inferior Pulmonary Veins Vein/Cardio2: Alveolar-Superior Pulmonary Vein Vein/Cardio3: Superficial Veins of the Trunk Vein/Cardio4: Inferior Vena Cava Vein/CardioS: Superior Vena Cava Chapter 22 Advanced Strain and COllnterstrain for Veins: Visceral Veins 1. Vein/Orgl: Hepatic Vein 2. Vein/Org2: Portal Vein Chapter 23 Advanced Strain and Counterstrain for Veins: Spinal Veins Vein/Spinel: Anterior and Posterior Spinal Veins

AUTONOMIC NERVOUS SYSTEM ix Chapler 24 126 Advanced Strain and Counterstrain: 127 Skin Therapy Level One 131 Chapler 25 135 Advanced Strain and Counterstrain: Disk Therapy 137 139 Chapler 26 140 1 41 Advanced Strain and Counterstrain: 1 42 Tendon Release Therapy 144 146 Chapler 27 147 149 Muscle Rhythm Therapy 149 151 Chapler 28 153 Procedures and Protocols Anterior Compartment Syndrome Cardiac Syndromes Carpal Tunnel Syndrome Headaches Reflex Sympathetic Dystrophy Respiratory Syndromes Spinal Syndromes Speech and Swallowing Disorders Thoracic Outlet Syndrome Vision Disorders Index

FOREWORD Considering the frequency of asthma, hypertension, hypotension, glau­ coma, ulcer disease, and abnormalities of sweating, temperature, cardiac rhythm, respiration, sexual, bowel and bladder function, it is amazing that the autonomic system gets essentially no direct treatment. Rather, those symptoms produced by lack of homeostasis of this system have been attacked with a vengence but with no correction of the problematic system. Diabetes mellitus, brainstem multiple sclerosis, Guillain-Barre's syn­ drome and infarction are often associated with disorders of autonomic function. And our medical response has been reduced to a barrage of phar­ macological antidotes: antihypertensives, psychotropic drugs, atropinics, alpha- and beta-adrenergic stimulating and inhibiting agents but in no sin­ gle case is this treatment directed at the problem, only the symptom. None of this central or peripheral clinical pharmacology addresses the system directly. The autonomic nervous system is the normally involuntary or uncon­ scious division of the peripheral nervous system. Irs efferent stimulation of all smooth muscles from blood vessels, lymphatic vessels, organs and glands as well as the resting muscle tone that allows us to sit up is a func­ tion of this autonomic nervous system. The autonomic nervous system has two divisions, the sympathetic and the parasympathetic. The parasympa­ thetic system regulates the funcrions necessary for long term survival. Everything from salivation and digestion to heart rate, respiratory rate, pancreatic function, liver and gallbladder function, and urine excretion through the kidneys, ureters and bladder, are only a few of the things that fall under autonomic control. The sympathetic system meets all crises; it spares no expense. The parasympathetics pick up after the sympathetics, replenishing, restoring and replacing, preparing for a rainy day. And when the parasympathetics can no longer \"keep up\" all life becomes a crisis and the overload escalates more and more with less and less provocation. All cells have sympathetic innervation, including blood vessels which, when hypertonic, decrease distribution of oxygen even to the brain in crisis. The impact of this is reduced healing, increased hypertension, facilitated segments, changes in endocrine function impacting metabolism, brain func­ tion and ultimately all homeostatic mechanisms. But when this system is balanced, cells have their optimal potential to repair and replace themselves for an estimated 120-140 years. We die from lack of homeostasis in this system and are disabled when its harmaony is simply out of sync. It affects every fiber of our being-so where is the treatment? xi

xii ADVANCED ITRAIN AND COUNHRITRAIN Well, you're holding it in your hands! Dr. Sharon Weiselfish-Giammateo has, using the basic principles of Lawrence Jones' Strainlcounterstrain, developed a mechanical/corrective kinesiology model. This technique brought marked changes in her neurologic patients. Dr. Weiselfish-Giam­ mateo further observed a synergic pattern of spastic muscles whether the client was a pediatric cerebral palsy, geriatric hemiplegic, chronic pain or other patient. When the mechanical model was applied from proximal to distal, to the muscles which contribute directly to the synergic pattern, spasticity and severe protective muscle spasm are remarkably reduced. When synchronizers, developed by Frank Lowen and Weiselfish-Giam­ mateo, (energetic relexogenic points which control and/or inhibit different body funcrions) were added to the mechanical and synergistic model and held past the ninery seconds of Jones, a \"De-Facilitated Fascial Release\" occurred. The resultant tissue \"unwinding\" occurs secondary to the elimi­ nation andlor decrease of hyporoniciry and appears to occur at a cellualar level, specifically in the ground substance or matrix of the connective tissue. I have found in my clinic after literally thousands of hours of application rhar a homeostasis is returned to the autonomic system as a direct and immediate response to this treatment. The body's ability to heal depends on creating a balanced environment in the tissues. This environment is directly controlled by the autonomic system and its balance. Advanced Strainlcounterstrain of the Autonomic Nervous System provides a direct and ongoing impact on the homestasis of this system thereby creating the environment in which our bodies do what they do best- HEAL. Without autonomic balance, there can be no health, only various levels of dis-ease. I have never worked with any treatment whether it be surgical, pharmacologic or manual therapy which has such an incredible impact on the individual's body. It doesn't just relieve symptoms, it allows for true recovery of the autonomic system. Its simplicity allows it to be managed by all levels from physicians to manual therapists, to patients themselves in certain instance. The work is profound, the results are profound and, when integrated with other directed manual therapies, can establish a state of ongoing health improvement and potential that is limited only by your patience and belief systems. This text is a jewel, that when incorporated into an informed treatment setting, will change your life as a manual therapy practitioner. Your patients will be the recipients of this simple straightforward work that is elegant in its simplicity and lasting in its effects and reproducibility. I have found no contraindication to rhe work, and done in rhe proper context ir can do no harm. In twenty years in medicine I have never found such a versatile tool and I'm truly excited that it can now be shared with the rest of the world. Mary A. Lynch, MS, M.D., P.A. The Center for Spores Medicine and Rehabilitation Wichita, Kansas

CHAPTER 1 PRESENT MODElS OF STRAIN AND COUNTERSTRAIN TECHNIQUE The History of the Phenomenon the phenomenon of Strain and Counterstrain of Strain and Counterstroin Technique generated a comprehensive approach for the treatment of somatic dysfunction and pain. Since Lawrence Jones, D.O. started his studies Approximately one hundred and seventy five and documentation of Strain and Counterstrain (175) Tender Points and their correlating precise Technique in the early 1990's, the art and sci­ positions were documented by Jones. Elimina­ ence of this approach has progressed to the re­ tion of muscle spasm with Jones' Strain and markable techniques presented in this text. Counterstrain Technique is a phenomenon. The When he discovered that precise positions art of this approach is described in several texts would eliminate pain and disability in persons by different authors. The science of this proce­ with similar painful postures, he searched for dure is still under investigation. other typical correlations. He detected Tender Points, which were exquisitely painful on palpa­ The following descriptions of the various tion, at the exact same locations in all persons models of Strain and Counterstrain Technique with identical postural deviations. He deter­ are presented in order to facilitate extrapo­ mined that the e postural deviations were be­ lation of this approach for various patient cause of protective muscle spasm. He discerned populations. that the shortened muscles in spasm were pulling on bony articular surfaces, contributing Jones' Model (Jones) to joint dysfunction. He appreciated that the precise positions which resulted in improved Lawrence Jones, D.O. was the original devel­ movement and decreased discomfort also dissi­ oper of Strain and Counterstrain Technique. pated the pain of the Tender Point. He spent over half a century perfecting this approach for the treatment of somatic dysfunc­ Thus Jones began his search for painful Ten­ tion. Dr. Jones discovered that there are ex­ der Points in the bodies of all of his patients. tremely tender points on the body, which people When he discovered a new painful point which present in a similar manner. The Tender Points was present in the same exact location in the are exhibited in the same exact locations. Each typical person, his investigation towards finding Tender Point is a reflection of a muscle in spasm, the precise position to dissipate the pain of this or of a joint and/or suture in a state of compres­ Tender Point ensued. Later he defined the prob­ sion. His discovery that positional therapy lem: which muscle in spasm was reflected by would eliminate the pain of the Tender Point led which Tender Point. During his quest for infor­ to his further understanding that holding this mation he learned that these precise positions position for 90 seconds would result in elonga­ would need to be maintained for exactly ninety tion of the muscle and decompression of the (90) seconds. Although Lawrence Jones did not joint and/or suture. Dr. Jones created an ap­ understand the neuroscience underlying this proach which changes arthrokinematics and os­ clinical phenomenon, his faith and his vision teokinematics in a remarkable manner. Joint conquered questions of relevance. mobility and joint play is usually restored with Strain and Counterstrain Technique. Articular Over fifty years of his investigation of

2 ADVANCED STRAIN AND CDUHTERSTRAIN balance, which is the relative normal positions technique for the pectoralis muscle (called the of the articular surfaces of a joint during physio­ second depressed rib, because Lawrence Jones logic motion, is improved. Ranges of motion are observed that contraction of the pectoralis always increased dramatically. Utilization of this minor depresses the second rib) will eliminate approach educates the practitioner about the the postural dysfunction. The protraction of the normal elongation capacity of a muscle. While shoulder girdle will disappear, even if it is severe documenting his findings during the initial and chronic. Weiselfish-Giammatteo developed stages of creation, he did not know that his ap­ a postural evaluation of sagittal, coronal and proach worked on decreasing the hyperactivity transverse plane posture. When postural devia­ of the myotatic reflex arc. He believed; he was tion and limitations of ranges of motion are guided; he followed with humility and with ad­ assessed, a knowledge of kinesiology will deter­ miration of the results of his creation. Dr. Jones mine which muscles are in spasm. When these will be remembered for his contribution of enor­ muscles are treated with Strain and Counter­ mous proportion to manual therapy. strain Technique, there is an elongation of the muscle fiber, increased ranges of motion, and a Mechanical/Corrective Kinesiology Model remarkable improvement in postural symmetry. (Weiselfish-Giammatteo) This mechanical/kinesiologic model works Sharon Weiselfish-Giammatteo, Ph.D., P.T., co­ exceptionally well for the neurologic patient. author of this text, began to work with For example, a typical dysfunction in a CVA Lawrence Jones' Strain and Counterstrain Tech­ client is a painful subluxation of the gleno­ nique in 1981. Sharon observed how a 90 sec­ humeral joint, described in the literature as a onds technique eliminated a 'locked jaw' \"subluxed hemiplegic shoulder.\" Berta Bobath secondary to a masseter spasm after surgery for defined this disorder as a latissimus dorsi in a parotid gland tumor excision. She began to state of hypertonicity within a flaccid shoulder teach herself this approach from Jones' book, girdle after stroke. The latissimus dorsi is the and learned that many clients with moderate only depressor of the humeral head. When the and severe hypertonicity would not experience Strain and Counterstrain technique is used for pain on palpation of the Tender Point. They pre­ the latissimus dorsi there will usually be a total sented an atypical response to pressure on that reduction of the subluxation of the humeral point. She began to develop a 'mechanical' head, because the latissimus dorsi muscle fibers model for treatment of patients with atypical will elongate, and they will no longer pull on the pain perception, such as the neurologic, pedi­ humeral head in a caudal direction. This ap­ atric, geriatric and chronic pain patient. Her proach will be successful in acute and chronic development of this model was based on shoulder subluxation, no matter how severe the knowledge of kinesiology and muscle function. presentation. The neurologic patient requires For example, the pectoralis minor which origi­ nates on the second, third and fourth rib, and that the position be held for three (3) to five (5) inserts on the coracoid process, protracts the shoulder girdle. When the shoulder girdle is pro­ minutes, rather than for 90 seconds. tracted, the pectoralis muscle is in protective muscle spasm. There will be a limitation of hor­ Synergic Pattern Release@ Model izontal abduction. Whenever there is a shoulder (Weiselfish-Gia mmatteo) girdle protraction, the Strain and Counterstrain Sharon Weiselfish-Giammatteo, Ph.D., P.T., uti­ lized Jones' Strain and Counterstrain to treat spasticity in the neurologic patient, nOt only to

AUTONOMIC NERVOUS SYSTEM 3 treat protective muscle spasm in the orthopedic­ which discovers the primary dominant lesion like client. She realized that the hypertonicity of which is contributing to all of the other lesions spasticity was similar in nature and characteris­ in the body. With this approach, the practitioner tics to the hypertonicity of protective muscle can find the one major problem in the spinal col­ spasm. There is primary dysfunction: hyperac­ umn, in the rib cage and sternum, in the cra­ tivity of the myotatic reflex arc. This hyperactiv­ nium, in the extremiry joints, and in the visceral ity is reduced with Strain and Counterstrain system which affects the whole person. Technique, whether the manifestation is protec­ tive muscle spasm or spasticity. The positions re­ Weiselfish-Giammatteo, Ph.D., P.T. and 0'Ambrogio, P.T., adapted Chauffour's Inhib­ quire holding patterns of three (3) to five (5) irory Balance Testing\" to Jones' Strain and Counterstrain Technique. The Jones' Tender minutes, rather than 90 seconds, for optimal Points are 'balanced' against each other with In­ results. hibitory Balance Testing\". The whole body can be assessed in this manner, or the Tender Points Sharon further observed that the synergic of a region can be 'balance tested'. The primary, pattern of spastic muscles was similar in presen­ dominant Tender Point will be evident, which tation for all severely impaired clients, whether indicates which muscle in spasm is contributing pediatric cerebral palsy, geriatric hemiplegic, to the protective muscle spasm of most of the chronic pain or other. When the Strain and other muscles. This muscle can be treated with Counterstrain techniques are applied proximal the specific Strain and Counterstrain technique, ro distal, to the muscles which contribute di­ which will cause a general decrease in the hyper­ rectly ro the synergic pattern, spasticity and tonicity of all of the other muscles. severe protective muscle spasm is remarkably reduced. For example, the synergic pattern of Also, Weiselfish-Giammatteo discovered the upper extremity is as follows: an elevated 'Muscle Rhythm.' Muscle Rhythm of the major shoulder girdle; a protracted shoulder girdle; an muscles can be assessed and 'balanced' against adducted shoulder in internal rotation; a flexed each other. In this manner, Inhibitory Balance elbow; a pronated forearm; a flexed wrist in Testing\" can be utilized for Strain and Counter­ ulnar deviation; flexed fingers; a flexed and ad­ strain Technique. The muscle with the dysfunc­ ducted thumb. The Strain and Counterstrain tional 'Muscle Rhythm' which is contributing to techniques can be applied to eliminate the the dysfunctional 'Muscle Rhythm' of the other synergic pattern of presentation in the follow­ muscles can be treated with Strain and Counter­ ing sequence: the supraspinatus; the elevated strain Technique. first rib; the pectoralis minor; the biceps; the wrist flexors; the finger flexors; the first meta­ Behavioral Modification for Chronic Pain Model carpal technique. The spastic synergic pattern (WeiseIfish-Giammalleo) can be reduced, and even eliminated, with this approach. Treatment of clients with chronic pain syn­ drome is difficult. These persons believe that life Inhibitory Balonce Testing© and without pain does not exist. In order to affect Mechanical link Model (Chauffour) these belief systems, they require proof that pain can be eliminated, and will not rerurn. Behav­ Paul Chauffour, D.O. developed a remarkably ioral modification can be utilized with Strain efficient approach for treatment of somatic, cra­ and Counterstrain Technique. The practitioner nial and visceral dysfunction called Mechanical can isolate the Jones' Tender Point. The client Link\". He created Inhibitory Balance 'Testing\

,"4 ADVANCED STRAIN AND (DUNlERSTRAIN can press on the Tender Point and experience presses on the Tender Point, and finds that there the exquisite pain on palpation of the point. The is no longer any pain present. After several repe­ Strain and Counterstrain technique is then per­ titions, the client begins to question whether or formed by the therapist. The patient once again not pain is a requirement for living!

CHAPTER 2 ALTERNATIVE METHODS Strain and Counterstrain Technique Combined with Other Approaches This chapter presents alternate methods for uti­ hypertonicity which is affecting many muscles. lization of Strain and Counterstrain Technique. Many unique approaches were developed which When Inhibitory Balance TestingO is used can be adapted to use with Jones' procedures. with the total body format, the dominant Ten­ Inhibitory Bolonce Testing© Adaptoted der Point is determined for each of the following for Strain ond (ounterstroin Technique body parts: 1. right lower extremity; 2. left Strain and Counterstrain Technique is an ap­ lower extremity; 3. right upper extremity; 4. left proach to treat hypertonicity, developed by upper extremity; 5. abdomen; 6. pelvis and low Lawrence Jones, D.O.. Inhibitory Balance Test­ back; 7. sternum and anterolateral rib cage; B. ingO is a evaluation process to discover domi­ nant restrictions in the body, developed by Paul upper back; 9. neck; 10. cranium; 11. face. Chauffour, D.O.. Inhibitory Balance TestingO is A nullification process with Inhibitory Bal­ an integral component of Mechanical Linko, a manual therapy approach which addresses total ance TestingO determines, by comparison, which body somatic dysfunction. When Inhibitory Bal­ is the primary dominant Jones' Tender Point Ollt ance TestingO is incorporated into Strain and of the 11 dominant Tender Points remaining, as Counterstrain Technique, the practitioner can determine which muscle, in a state of hyper­ outlined in the above paragraph. tonicity, is contributing to hypertonicity of other muscles. Neurofosciol Process© Utilized with Stroin ond (aunterstroin Technique It is possible to perform Inhibitory Balance Neurofascial Processo, developed by Sharon TestingO in a regional format and in a total body . format. In a regional format the Jones' Tender Points of a body part (for example the right Weiselfish-Giammatteo, Ph.D., P T., is a differ­ ential diagnosis and treatment approach which lower extremity) can be compared, one to the addresses body and mind dysfunction. This ap­ proach allows the practitioner two premises. other. A nullification process can determine One premise gives the ability to recognize areas when the pressure on one Tender Point nullifies The Process Center for hypertonicity is the mental the pain of another Tender Point. All Jones' Ten­ body (lowen and Weiselfish-Giammatteol. The der Points can be compared. The Tender Points mental body access is approximately 1 cm anterior which remain painful to pressure, resist nullifi­ to/above the left frontal eminence. cation, but nullify other Tender Points, are the dominant Tender Points. When the muscles of dysfunction which contribute to the dysfunc­ which have dominant Tender Points are treated tions of other parts of the body. Another premise of this work gives the ability to deter­ with Strain and Counterstrain Technique, the re­ mine the non-physical process which is part of the physical dysfunction. Certain typical body sult can be a total elimination of primary self­ areas surface as part of the client's problem perpetuating protective muscle spasm and when emotions, cognitive thoughts, and/or spir- 5

6 ADVANCED mAINAND (OUNTERITRAIN itual disturbances are contributing to the symp­ work is ongoing, and has culminated in a series of manual therapy courses called Biologic tomatology. These body areas are called Process AnalogsC, presented by Therapeuric Horizonsc, Centers, and present in rypical manifestations a continuing education institution for advanced learning for manual practitioners. Lowen and for similar situations in all persons. The body re­ Weiselfish-Giammatteo have discovered almost sponds in these Neurofascial Processc patterns, in a similar behavioral model, for all persons, no one hundred (100) Synchronizersc which facili­ matter the age, gender, personal traits. tate restoration of multiple body functions. Strain and Counterstrain Technique with Neurofascial A Synchronizerc is an energeric reflexogenic Processc for Treatment of Hypertonicity point which controls and/or inhibits different When performing Jones' Strain and Counter­ body functions. These points are found on the strain Technique, or Advanced Strain and Coun­ lungs, on the cranium, in the abdomen and low terstrain Technique, whatever the etiology back, and in the pelvic region. (protective muscle spasm, spasticity, other), con­ When protective muscle spasm and/or spas­ tact on the mental body will augment the out­ ticiry is diffuse throughout the body, further in­ hibition of the hyperactive myoratic reflex arc is come. Position the body in the Strain and attained wirh contact on two (2) specific Syn­ Counterstrain Technique position (Jones' posi­ chronizersc. tions, and also the Advanced Strain/Counter­ strain positions by Weiselfish-Giammatteo and During the StrainiCounterstrain technique, Giammatteo).There is an apparent association contact can be maintained on these Synchroniz­ ersc and must also be maintained on the muscle. between the mental body energy and the The Jones', or Advanced StrainiCounterstrain position is maintained while hand contact is actin/myosin interface of the sarcomere. maintained on these Synchronizersc. There are When performing Strain and Counterstrain two (2) Synchronizers for improved muscle function which are appropriate to use with Technique with Neurofascial Processc, hand Strain and Counterstrain Technique; since the contact must be maintained on the muscle. The practitioner has only two hands, it is not possi­ Jones, or Weiselfish-Giammatteo/Giammatteo ble to perform all of the following at once: Strain/Counterstrain position is maintained throughout the technique. Hand contact is 1. Attain and maintain the Strain and Counterstrain position. maintained at the access of the mental body. The 2. Maintain hand contact on the muscle client's hand can maintain this contact, or the belly. hand of another person can be used. After the 3. Maintain hand contact on the Process 90 seconds (1 minute for the Advanced Center. Strain/Counterstrain techniques) there will be 4. Maintain hand contact on the two (2) continued unwinding of the fascial tissue. Main­ Synchronizersc. tain the position and the hand contacts for the duration of the De-Facilitated Fascial Releasec. 5. Maintain hand contact on the access to the Mental Body. Synchronizersc Utilized with Note: #1 and #4 are the most important Strain and Counterstrain Technique steps of the above. Synchronizersc were discovered by Frank There are a few options for practical appli­ Lowen and Sharon Weiselfish-Giammatteo dur­ cation of all of the above. One option is as fol­ ing their clinical research with manual therapy lows: The practitioner can maintain the Strain to affect the tissues of the brain and heart. Their

AUTONOMI( NERVOUIIYITEM 7 and Counterstrain position with hand contact l on the muscle belly, while contacting the Process Center. When the fascial release is complete, the hand contact on the Process Center can be changed to hand contact on the first Synchro­ nizerCl• When this fascial release is complete, the hand contact can be changed to the second Syn­ chronizerCl• The second option is to have multi­ ple hands performing this technique with hands contacting the Process Center, the two Synchro­ nizersCl, and the muscle belly at the same rime. The Synchronizers© for Improved Muscle Function SYNCHRONIZERCl #1 Goal: Apparently To Release Tetanic Reflex to Motor End Plate. • Location of Right and Left SynchronizersCl: 3 em's lateral to both Ll Transverse Processes. • Procedure: To be used with Strain/Counter­ strain positions. Maintain hand contact on muscle. SYNCHRONIZERC #2 Goal: Apparently To Unlock Actin/Myosin Complex. Location of Left SynchronizerCl: at interface of mesosigmoid/sigmoid colon. Procedure: To be used with Strain/Counter­ strain positions. Maintain hand contact on muscle. (Biologic Analogs, Copyright 1995 LowenIWeiselfish­ Giammatteo) Neurologic Phenomenon for lreotment lntegrotion (Weiselfish-Giommolleo) 1. Tonic and Anti-tonic Neuronal Activity Increase Muscle Tone with Strain/Counter­ strain and 'Tonic FacilitationCl.' Left frontal and parietal lobes are tonic, which means their neuronal activity will predetermine the tone of muscles, ligaments and tendons. In­ creased muscle, ligament and tendon tone can

8 ADVANCED STRAINAND CDUNTERITRAIN be attained when the Strain and Counterstrain 3. Neurofascial Processc for Agonistic and position is maintained while hand contact is Antagonistic Neuronal Activity Treatment maintained on the left frontal and left parietal of the Neurologic Patient with Spasticity. regions. For the neurologic patient with hypertonicity Step One: Maintain the StrainiCounterstrain Position. (spasticity), 'alltagonistic' neurollal activity can Step Two: Maintain hand contact on the left be induced with right frontal and parietal hand frontal and left parietal region of contact. Antagonistic neuronal activity de­ the cranium. creases the tone of agonist muscle. 2. Tonic and Anti-tonic Neuronal Activity Step One: Maintain the Strain/Counrerstrain Decrease Muscle Tone with Strain/Counter­ position. strain and 'Anti-Tonic De-Facilitationc.' Step Two: Maintain hand contact on the Right frontal and parietal lobes are anti-tonic, right frontal and right parietal region of the cranium. which means their neuronal activity will \"tone­ down\" muscle, ligament, and tendon tension. 4. Neurofascial Processc for Agonistic and Decreased muscle, ligament and tendon tone Antagonistic Neuronal Activity Treatment can be attained when the Strain and Counter­ of the Neurologic Patient with Hypotonia. strain position is maintained while hand contact is maintained on the right frontal and parietal For the neurologic patient with hypotonia, 'ago­ regions. lIistic' neuronal activity can be induced with left Step One: Maintain the Strain/Counterstrain frontal and left parietal hand contact. Agonistic position. neuronal activity increases the tone of the ago­ nist muscle. Step Two: Maintain hand contact on the right frontal and right parietal Step One: Maintain the Strain/Counterstrain region of the cranium. position. Step Two: Maintain hand contact on the left frontal and left parietal region of the cranium.

CHAPTER 3 A HYPOTHETICAL MODEl Decreasing the Hypertonicity of Protective Muscle Spasm and Spasticity with Strain and Counterstrain Technique and Advanced Strain and Counterstrain Technique The musculofascialskeletal system receives most The site of this \"endogenous origin\" is the pro­ of the efferent outflow from the central nervous prioceptors, especially the muscle spindles. They system; the largest portion of this efferent dis­ charge exits the spinal cord via the ventral roots are sensitive to musculofascialskeletal stresses. to the muscles. The musculofascialskeletal sys­ They are non adapting receptors, sustaining tems are also the source of much of the wide­ streams of impulses for as long as they are me­ spread, continuous, and variable sensory input chanically stimulated. Their influence is specific to the eNS. This sensory feedback relayed from to the muscles acting on the affected joints, receptors in myofascial, visceral, articular com­ which are innervated by corresponding spinal ponents, and others, enters the spinal cord via segments. the dorsal roots. This sensory reporting is routed to many centers throughout the central The Myotatic Reflex Arc nervous system, including the cerebral cortex, the cerebellum, the brain stem, and the auto­ The Myotatic Reflex Arc (also known as the nomic nervous system. This sensory input from sttetch reflex arc, the monosynaptic reflex arc, the musculofascialskeletal body is extensive, in­ and the gamma motor neuron loop), has long tensive, and continuous, and is a dominant in­ been considered as the basis of muscle tone. The fluence on the central nervous system. components of this reflex arc include: the muscle fiber, which has the ability to contract, and to The Premise relax and elongate; the muscle spindle, the pro­ prioceptor, which is responsive to length and ve­ Disturbances in the sensory afferent input from locity stretch; the gamma neuron which the neuromusculoskeletal systems, whether dif­ innervates the muscle spindle; the a fferent neu­ fuse or local, affect motor functions and other ron, which transcribes the information regard­ functions. This premise is a core concept, clini­ ing stretch to the spinal cord; and the alpha cally significant for hypertonicity (protective motor neuron, which transcribes the impulse muscle spasm and spasticity), the facilitated seg­ from the spinal cord to the muscle fibet, eliciting ment, and Structural Rehabilitation. a muscle contraction. [n 1947, Denslow stated a hypothesis which The Muscle explained this concept: The muscle is the focus of dysfunctional move­ \"(An) osteopathic lesion represents a facili­ ment, when considering the hypertonicity of tated segment of the spinal cord maintained protective muscle spasm and spasticity. The muscle is active, self-energized, independent in in that state by impulses of endogenous ori­ motion and capable of developing great, widely gin entering the corresponding dorsal root. variable, and rapidly changing forces. Other tis­ sues are passively moved, immobilized, pushed, All StruCtures receiving efferent nerve fibers pulled, compressed, and altered in shape by from that segment are, therefore, potentially those forces of muscular origin. Muscles exposed to excessive excitation or inhibi­ tion.\" 9

1 0 ADVANCED ITRAIN AND CDU NTERITRAIN /Jroduce motion by their contraction, but those motor activity via the stretch reflex arc, al­ same contractile forces also oppose motion. though this premise is presently under investiga­ tion. Contracting muscle absorbs momentum, and regulates, resists, retards, and arrests movement. The Colgi tendon receptors are located in Irvin Korr stares that this energy-absorbing function of skeletal muscle is as important to the tendons close to the musculotendinous j unction. control of motion as its energy-imparting func­ A pull on the tendon causes discharge of im­ tion. But the same cellular mechanisms are in­ pulses into the spinal cord via afferent fibers. volved in these functions. This pull is usually exerted by active contraction of the muscle. The tendon endings are respon­ Joint mobility, range of motion, and ease of sive to changes in force, not in length. When the initiation of active motion are results of healthy muscle contracts against a load, or fixed object, muscle function. Limited capacity of muscles or against the contraction of antagonistic mus­ often appears to be the major impediment to cles as in spasticity and protective muscle spasm, mobility of a dysfunctional joint. Korr states the discharge of the tendon endings is in propor­ that muscular resistance is not based on inexten­ tion to the tension that is developed. The affer­ sibility, as with connective tissues, but on ent input from the Colgi tendon varies with the changes in the degree of activation and deactiva­ tension exerted by the muscle on the tendon, re­ tion of the contractile tissue. The hypothetical gardless of the muscle length. The discharges of cause for a muscle to increase or decrease its the tendon endings enter the spinal cord by dor­ contraction and braking power is variations in impulse flow along the motor axons, the alpha sal root fibers, where they excite illhibitory in­ neurons, which innervate the muscle. This neu­ ronal impulse traffic varies with changing levels terneurons that synapse with motor neurons of excitation within the anterior horn cells, controlling the same muscle. The effect of their which change according to varying afferent discharge is inhibitory; it tends to oppose the input. further development of tension by the muscle. Proprioceptors The Musde Spindle The muscle spindle, the proprioceptor within The muscle spil1dles are complex. Each spindle the muscle fibers which responds to stretch, is a basic component of the myotatic reflex arc, and has two kinds of sensory endings with different has been implicated as a basic component of reflex influences, each with its own motor inner­ protective muscle spasm, and of spasticity. The vation. Spindles are scattered throughout each proprioceptors are the sensory end organs that muscle, the quantity varying according to the signal physical changes in musculofascialskeletal function of the muscle and the delicacy of its tissues. The three main categories of propriocep­ control. The greater the spindle density, the finer tors are sensitive to joint position and motion, the control. The complex anatomy and physiol­ to tendon tension, and to muscle length. ogy of the muscle spindles is well documented in the literature. The joint receptors are located in joint cap­ Spindles are within the muscle itself, sur­ sules and ligaments; they report joint motion rounded by muscle fibers, arranged in parallel and position. The Ruffini endings in the capsules with them and attached to them at both ends. report direction, velocity of motion, and posi­ Stretching the muscle causes stretch of the spin­ tion very accurately. These joint receptors do dle; shortening of the muscle slackens the spin­ not appear to have significant influence on dle. Each spindle, enclosed in a connective tissue sheath, about 3 mm long, has several thin mus­ cle fibers. These are the intrafllsal fzbers. The

AUTONOMIC NERVOUS SY STEM 11 larger and more powerful extrafl/sal fibers com­ arrachments, slows the discharge proportion­ ately, and may even silence it. prise the bulk of the muscle. The intrafusal fibers are attached ro the sheath at each end. The spindle, an essential feedback mecha­ nism by which the muscle is controlled, continu­ The intrafl/sal ml/scle fibers are innervated by ally reports back ro the central nervous system. The feedback from the primary endings of each gamma motor lIel/ron fibers originating in the spindle is conveyed by dorsal root fiber directly, that is, monosynaptically, to the alpha motoneu­ ventral horn, passing through the ventral roOt. rons of the same muscle. This afferent discharge of the spindle results in excitation of the alpha The alpha motor neurOlls supply innervation to motor neurons of the same muscle. How does the extrafusal muscle fibers. this occur? When a muscle is stretched, it is re­ flexly stimulated by its spindles to COlitract, and The sensory endings of the spindle are in close relation to the central, nucleated, noncon­ thereby resists stretching. This protective reflex tractile portion of the intrafusal fibers. This sen­ response is at the spinal cord level of the same sory ending, called the primary ending, is spinal segment. The protective shortening of the muscle decreases the afferent discharge, and wound around the intrafusal fi bers, described as thus reduces the excitation of the alpha moror the annulospiral ending. Secondary, flower­ spray elldillgs occur on either side of the pri­ neurons, cal/sing relaxation and lengthening of the ml/scle. mary ending and are connected ro thinner myelinated axons. Both are sensitive ro stretch The muscle spindle causes the ml/scle to re­ of the central portion of the spindle. sist chmtge ill length ill either direction. The There is a static and a dynamic response ro spindle is the sensory component of the stretch, stretch by the muscle: static is proportional ro reflex arc, or myotatic reflex arc. It is important muscle length; dynamic is proportional ro the in maintenance of posture. The intrafusal mus­ rate of change in muscle length. The intrafusal cle fibers influence spindle discharge. Their ends muscle fiber is relatively elastic: the IA afferent are anchored, and contraction of these intra­ endings, which innervate the primary nerve end­ fusal fibers stretches the middle portion in which ings, end here. Therefore, the IA fiber has a dy­ the sensory endings are situated, increasing their namic and a static response ro stretch. The group II afferent fibers, which innervate the sec­ d ischarge. The effect of intrafusal contractioll ondary endings, end on the small nuclear chain On the sensory endings is illdistinguishable from fibers. This is at the area of the hearr of the my­ the effect produced by stretch of the extrafl/sal ofibril striations of the intrafusal fibers: a less fibers. The two effects are cumulative. At any elastic, stiffer area. Therefore there is only a sta­ tic response ro stretch which is proportional ro lengthening of the muscle, intrafusal contraction muscle length. Since these fibers have no dy­ would increase the spindle discharge; stretch of namic response, they will nOt carry central ner­ the muscle while the intrafusal fibers are con­ tracted produces a more intense spindle dis­ vous system feedback regarding the velocity of charge than when the intrafusal fibers are at rest the stretch. or less contracted. The primary endings, or alllllllospiral end­ The Gamma Neuron ings, respolld to challge ill muscle length. When The gamma neuron, a component of the my­ the muscle is stretched beyond its resting length, otatic reflex arc, (or gamma motor neuron the spindle is stretched, causing the primary and loop), innervates the muscle spindle, is affected secondary endings ro fire at increased frequen­ cies in proportion ro the degree of stretch. Short­ ening of the muscle, whether by its own contraction or by passive approximation of its

1 2 ADVANCED ITRAIN AND [OUNTERITRAIN by dysfunction within the neuromusculoskeletal tion when the muscle is already shorrer than irs system, and is controlled by the brain and resting length. I f the increased gamma gain is supraspinal neurons. The function of the sustained, the muscle contraction is mainrained. gamma neurons is to control contraction of the This is muscle spasm. intrafusal fi bers, the frequency of the spindle d ischarge at a given muscle length, and the sen­ The sensory endings of the spindle are stim­ sitivity or change in that frequency per millime­ ulated by mechanical distorrion, whether caused ter change in length. The higher the gamma by conrraction of the inrrafusal fibers or by activity, the larger the spindle response; the stretch of the main muscle, or both. The spindle higher the spindle discharge at a given muscle length, the shorter the length of muscle at which in effect reporrs length relative to that of the in­ a given impulse frequency is generated. This ex­ trafusal fibers. The greater the disparity in plains the threshold to stretch of the spindle. length, the greater the discharge and the greater the contracrion of the muscle. Increase in inrra­ The gamma neurons, also known as fusal-exrrafusal disparity increases the afferent \"fusimotor\" neurons are small in size and their discharge, which results in a contractile re­ sponse of the extrafusal fibers, which in turn axons are rhino Fusimotor innervation by the tends to reduce the disparity and to silence the gamma fibers comprise one-third of the ventral root outflow from the spinal cord. Alpha-to­ spindle. The greater the gamma activity, the gamma and extrafusal-to-intrafusal relation­ more the muscle must shorten before the spindle ships regulate the activity of skeletal muscles. is turned back down to resting discharge and The higher the spindle discharge, the greater the reflex contraction of the muscle. What that mus­ normal gamma bias. The central nervous system can elicit and precisely control gamma bias. cle contraction accomplishes depends on the other forces acting on the joints crossed by that There is always some activity around this muscle. Generally, the greater the contraction, the more the muscle shortens and moves the myotatic reflex arc. There is a certain gamma joint, and the more it resists being stretched in bias: a certain level of activity along the gamma the opposite direction. neuron which results in a resting threshold to Gamma Bias stretch of the muscle spindle, controlled by the Normal resting conditions of gamma activity maintain a tonic afferent discharge from the central nervous system. Evidently the gamma spindle. This is the gamma bias. This maintains neuron is inhibited by supraspinal structures. When there is a cortical lesion, the suppressor the alpha motor neurons in a moderately facili­ areas of the brain which inhibit the gamma neu­ tated state, and the muscles in low-grade tonic ron are damaged. The inhibition process via the contraction at their resting lengths. Thus, people medial rericular formation is affected. An in­ are not flaccid and hypotonic, but maintain creased level of activity within the myotatic re­ some muscle tone. Gamma activity may be flex arc occurs because of the resultanr increase turned up or down. The higher the gamma ac­ in gamma bias. Gamma bias is no longer nor­ tivity, because of its influence on the excitatory mal, due to disinhibition of the central nervous spindle discharge, the more forceful the m uscle's system. The result is spasticity, which is hyper­ contraction and the greater its resistance to tonicity, plus other characteristics of the syn­ being lengthened. During high gamma activity, drome of spasticity. The gamma gain and the hyperactivity of the myotatic reflex arc resulr in or gamma gain, the spindle may elicit contrac- the hyperronicity of protective muscle spasm and spasticiry.

AUTONOMIC NERVOUS SY STEM 13 The Afferent Neuron Neuramusculoskeletal Dysfunction Causes Whenever the muscle spindle is stimulated, via Afferent Gain; Afferent Gain Causes Alpha Gain stretch stimulus, that information passes along the afferent neuron into the posterior horn of When a person has a supraspinatus tendinitis, the spinal cord of that spinal segment. Some of the brain is apprized of this status. The person this sensory input is distributed throughout the perceives pain at the shoulder. The pain is central nervous system. Much of the sensory generic: the person does not know that the pain input passes as discharge along the same affer­ ent neuron to the anterior horn of that same is the result of a supraspinarus dysfunction. The spinal segment. In the ventral horn, this dis­ afferent neuron, bringing the sensory informa­ charge passes across the synapse to the neuron of the alpha mOtor nerve, and passes along the tion about this dysfunction /0 the spinal cord, length of the alpha motor neuron axon, to the muscle fiber. When the muscle fiber receives the will pass this information as excessive alld high impulse, it contracts and shortens. frequellcy discharge. This is similar to the exces­ Neuromusculoskeletal Dysfunction sive and high frequency discha rge of gamma and the Hyperactive Myotatic Reflex Arc gain, but it is \"afferent gain\". The afferent neu­ ron from the supraspinatus muscle and tendon This hypothetical model expands on Denslow's will pass the sensory information along the af­ and Korr's hypothesis of the Osteopathic lesion, ferent neuron as increased afferent gain, which in order to provide a model which explains the enters the spinal cord via the dorsal roots and results of Manual Therapy for treatment of neu­ posterior horn of C5 spinal segment. romusculoskeletal dysfunction. These results in­ clude increased resting muscle length, increased This excessive and high frequency discharge joint mobility, and increased ranges of motion. is distributed throughout the central nervous system: cortex, brain stem, up one or more A Hypothetical Model spinal segmenrs, down one or more spinal seg­ menrs, across to the opposite side of the spinal Envision a cross section of the spinal cord at the cord, and more. Some of this excessive and high level of C5. The embryologic segmenr of C5 frequency discharge is also passed along the af­ spinal cord innervates certain tissues and struc­ ferent neuron to the anterior horn. At the ven­ tures. Among these tissues and structures are: tral horn, the excessive and high frequency the supraspinatus muscle, the deltoid muscle, discharge passes across the synapse and affects the infraspinatus muscle, the subscapularis mus­ the alpha motor neuron which innervates the cle, the biceps muscle (C5,6), and more. When supraspinatus muscle. This same excessive and there is dysfunction in one or more of the tissues high frequency discharge passes along the length and structures which are innervated by the C5 of the alpha motor neuron which innervates the embryologic segment, there is resultant increase supraspinatus muscle. in gamma gain, and protective muscle spasm of the muscularure innervated by rhat same C5 This excessive and high frequency discharge, segment. passing down the length of the alpha motor neu­ ron to the muscle fiber, is alpha gain, or the in­ crease in discharge and activity of the alpha motor neuron. When an impulse reaches the muscle fiber, the muscle fiber contracts and shortens. If excessive and toO frequent discharge passes along the alpha motor neuron, the muscle fiber will go into a state of contraction which is sustained by the continuous volley of impulses. The muscle fiber, the supraspinatus, can no

1 4 ADVANCED ITRAIN AND CDUNTERITRAIN longer voluntarily relax and elongate. This is vate the subscapularis, infraspinatus, deltoid, and biceps (CS,6), can also pass the excessive the model of protective muscle spasm of the and high frequency discharge accumulating in the ventral horn, as the condition of the supra­ supraspinatus which results from a supraspina­ spinatus tendinitis becomes more severe and tuS tendinitis dysfunction. more chronic. This excessive and high frequency discharge in the anterior horn, when sufficient If there is a supraspinatus tendinitis, the to inAuence the other neurons, will pass along supraspinatus muscle will go into a state of pro­ those other alpha motor neurons innervated by tective muscle spasm, contracted and shortened, incapable of attaining full resting length due the same CS spinal segment. Thus there is a po­ to an inability to relax and elongate. The telltial al1d tel1del1cy for protective muscle supraspinatus crosses the glenohumeral joint. spasm of all the muscles il1nervated by that same The joint surfaces will become approximated, C5 embryologic segmel1t which innervates the resulting in joint hypomobility and limitations supraspil1atus. This situation becomes exacer­ in ranges of motion. bated as the tendinitis becomes more severe and more chronic. Gamma Gain: Increased Sensitivity of the Musde The gamma neurons, which innervate the in­ Spindle and Decreased Threshold to Stretch trafusal muscle fibers of the muscle spindles of all the muscles innervated by this same CS em­ The excessive and high frequency discharge bryologic segment, can also pass this excessive which is passed into the alpha motor neuron in and high frequency discharge, as the dysfunc­ the anterior horn is also passed into the gamma motor neuron. Alpha and gamma signals are tion becomes more severe and more chronic. As linked and coordinated in the spinal segment. a result, the sensitivity of these spindles to The gamma motor neuron passes this excessive stretch is increased, and the threshold of stretch and high frequency discharge down to the mus­ of all the muscle spindles inl1ervated by this cle spindle. The muscle spindle is now hyper­ spil1al segment is decreased. The potential for innervated. Therefore, the sensitivity of the spindle to stretch is increased; the threshold of protective muscle spasm and dysfunction is ex­ the muscle spindle to stretch will be decreased. acerbated. All these muscle cross the gleno­ The spindle will be \"hyperactivated\", and will humeral j oint, therefore the approximation of react to smaller stretch, and lower velocity of the humeral head in the glenoid fossa, the joint stretch, than before the supraspinatus tendinitis hypomobility, the disturbance of articular bal­ was present. There is a facilitation of the my­ ance, and the limitations in ranges of motion are exacerbated. otatic reAex arc: the stretch ref/ex arc is hyperac­ tive. This phenomenon is called a \"facilitated Somatovisceral Reflex Am segment. \" Neurons exiting the spinal cord innervate more The Facilitated Segment and than muscle spindles and muscle fibers. They also provide innervation of viscera via the auto­ Efferent Gain of Alpha and Gamma Neurons nomic nervous system. For example, L1 inner­ vates the cecum. If a patient with a history of an Increased efferel1t gail1 is characteristic of the fa­ appendectomy has scarring within the lower right abdominal cavity, this information will cilitated segment. The alpha motor neurons be passed as sensory feedback via the afferent which innervate the supraspinatus muscle fibers neurons to the central nervous system. Afferent are not the only neurons to exit from the ante­ rior horn of CS embryologic segment. The other alpha neurons, for example, those which inner-

AUTONOMIC NERVOUI IYITEM 15 neurons, passing this information a s excessive activity by the suppressor areas of the brain does and high frequency discharge, enter the spinal not appear to be effective in maintaining a nor­ cord via the posterior horn of Ll. From here the mal gamma bias. The hypertonicity of the mus­ sensory information is distributed throughout cle spindles and the fi bers is maintained. Is this the central nervous system. Some of the infor­ situation possible? It is this situation which oc­ mation is also relayed to the anterior horn of curs when there is a cortical lesion, for example, this same Ll embryologic segment. All the alpha with the hemiplegic: a self-perpetuating hyper­ motor neurons which are innervated by Ll em­ active reflex arc due to disinhibition of supra­ bryologic segments can potentially pass this ex­ spinal structures. cessive and high frequency discharge, which is accumulating in Ll anterior horn, and can pass In these cases, it is necessary to address this this hyperactivity along the alpha motor neu­ self-perpetuating hyperactive reflex arc as a pri­ rons, which would result in protective muscle mary problem. Initially, this myotatic reflex arc spasm of the muscle fibers innervated by that became hyperactive secondary to the supra­ same Ll segment. Also, all the muscle spindles spinatus tendinitis. Now, due to a chronic and innervated by the gamma neurons from this Ll severe supraspinatus dysfunction, it is a primary segment which could potentially pass the exces­ self-perpetuating problem. A Manual Therapy sive and high frequency discharge will be af­ technique developed by Lawrence Jones, D.O., fected, so that the threshold to stretch of all called Strain and Counterstrain Technique, ap­ these muscle spindles would be decreased. This pears to successfully \"shut down\" the hyper­ facilitated segment at Ll, the result of dysfunc­ activity within this reflex arc. In the case of a tional tissue surrounding the cecum, may cause self-perpetuating protective muscle spasm of somatic dysfunction of the pelvis and hip joint this supraspinatus muscle, the technique would region because of the sustained contraction of result in an apparent reduction and arrest of the the muscles crossing those joints. propriocepror activity of the muscle spindles of the supraspinatus muscle fibers. There is a de­ The Self-Perpetuating Hyperactive Reflex Arc crease in the gamma gain. This technique is performed by shortening the muscle fibers and Occasionally, the supraspinatus tendinitis may spindles of the muscle (for example, the supra­ be so severe and so chronic that healing of the spinatus m uscle), while putting a stretch on the tendinitis with effective Manual Therapy inter­ Golgi tendon of the antagonist of this muscle. vention is not sufficient to decrease the hyperac­ Korr and others have provided evidence that tivity of the stretch reflex arc. The hyperactivity shortening of the muscle spindle, together with of the myotatic reflex arc has become self-per­ the stretch on the Golgi tendon of the antagonist petuating. There remains some excessive and muscle, results in a decrease and even an arrest high frequency discharge passed along the neu­ in the gamma neuronal and proprioceptor activ­ rons within this gamma motor neuron loop, in ity. There is apparently a general decrease of this spite of the Manual Therapy which \"cured\" the excessive and high frequency discharge passed supraspinatus tendinitis. There is an apparent around this hyperactive reflex arc. This tech­ disinhibition of this hyperactive reflex arc: the nique results in an effective elimination of pro­ increased gamma gain is maintained in spite of tective muscle spasm of the muscle treated, with the decrease in afferent gain. The gamma gain is a relaxation and elongation of the resting increased, as it is in cases of spasticity, when the muscle fibers. There are increases in joint mo­ brain and supraspinal struCtures are affected in bility and ranges of motion as a result of the the neurologic patient. The inhibition of gamma elimination of the protective muscle spasm. The

1 6 ADVANCED STRAIN AND CDUNTERSTRAIN mechanism o f correction is not known. This au­ musculature deprived of voluntary control. In thor speculates that the shut-down of the hyper­ the neurologic patient, these associated reac­ activity of the muscle spindle will decrease the tions produce a widespread increase of spastic­ gamma gain to a normal gamma bias, which ity throughout the affected side. will facilitate a linking and a coordination be­ tween the inhibition process of the central ner­ Spasticity is considered a major affliction, vous system and the myotatic reflex arc. This and although the neurophysiology of spasticity linking process is a neurophysiologic phenome­ has been considered in detail by several re­ non which requires 90 seconds. searchers, there is no unanimous agreement of its definition. The most commonly discussed Spasticity and the Myotatic Reflex Arc: characteristics of spasticity include: 1. exagger­ ated stretch reflexes; 2. tendon (phasic) reflexes A Hypothetical Model with a increased threshold to tapping; 3. in­ creased response by tapped muscles; 4. in­ The Therapist with an understanding of spastic­ creased response of tonic stretch reflexes; 5. ity can util ize this hypothetical model to explain clonus which may be induced. the results of Manual Therapy on reducing hy­ pertonicity in the neurologic patient. The abnor­ Characteristics af Spasticity mal muscle tone and coordination in the neurologic patient are due to the release of ab­ • increased passive/resistance to stretch normal postural reflexes. The normal postural • clonus reflex mechanism consists mainly of three • flexor spasm groups of automatic reactions. These include the • alternating flexor and extensor spasm righting reactions, which attain and maintain • overflow the position of the head in space (face vertical • hyperreflexia and mouth horizontal) and its symmetrical rela­ • extensor synergy tionship with the trunk. The equilibrium reac­ • flexor synergy tions attain and maintain balance during • spastic equinovarus activities to prevent falling. Reactions which au­ • co-contraction tomatically adapt muscles to postural changes in • dyssynergy the trunk and extremities are the third group in­ • clasp-knife response cluded in this category. • flexor withdrawal • spastic gait The described postural reflex mechanisms • associated movements are necessary for voluntary functional activity. • irradiation They provide normal postural tone via central • spastic paraplegia nervous system activation of muscles in pat­ • spastic hemiplegia terns, involving large groups of muscles. Nor­ • \"alpha\" spasticity mal reciprocal interaction of muscles allows • \"gamma\" spasticity stabilization of proximal body parts; this allows • increased tone distal mobility. Automatic protective reactions, • abnormal tone such as righting and equilibrium reactions, in • excessive or increased motor unit gross movement patterns, are the background for voluntary functional activity. Associated re­ activity actions as described by Walshe are tonic re­ • alternating clonus flexes; they are released postural reactions in

AUTONOMIC NERVOUS SYITEM 17 Studies performed by Sherrington on decere­ imposed by extrapyramidal impulses; the result brate cats were important in providing a useful animal model for the conception of pathogenic of this disinhibition is the hyperactivity of the factors in spasticity. The motor manifestations were found to be those of human spasticity. gamma neuron system, and the excessive and Sherrington concluded that decerebrate rigidity high frequency discharge of the gamma motor is reflexly maintained by the extrapyramidal tract, which is phylogenetically newer than the Ileurons. Therefore, there is an excessive and pyramidal system. He concluded that the muscle high frequency discharge from the primary end­ proprioceptors, which are the muscle spindles, are responsible for this decerebrate rigidity. ings of the muscle spindles. Thus, within the The gamma motor neuron loop, and the monosynaptic ref/ex arc, the alpha motor neu­ gamma motor system discussed in this Learner's Workbook, were first described by Leskell in rons will also have high frequency firing. The 1945. As described, it is assumed that the gamma system controls the length and velocity result is h)lperactivity, hypertonicity, and spas­ of the spindles' primary endings, and the length sensitivity of the secondary endings. Gamma ac­ ticity, of the skeletal muscle. tivity maintains appropriate spindle discharge at all muscle lengths during movement. This phe­ Apparently, the alpha motor neuron system nomenon is also true for the patient with spas­ is rarely released from higher inhibitory control. tici ty. Occasionally, brain lesions disrupt their supraspinal inhibition. In these cases, interrupt­ As described above, the muscle spindles lie ing the gamma-spindle loop will not reduce the parallel to, and are attached to, the extrafusal spasticity. Typically, brain lesions result in disin­ muscle fibers. Passive muscle stretch causes spin­ hibition of the gamma neuron system. dle discharge from the primary endings. This re­ sults in a depolarization of alpha motor neurons The lateral rericular formation appears to be until muscle contraction occurs. This is via a a major source of facilitation of rhe gamma negative feedback control circuit, called the motor neurons; their supraspinal inhibition ap­ monosynaptic reflex arc, or stretch reflex arc, or pears to synapse from the medial reticular for­ myotatic reflex are, or gamma mOtor neuron mation. Alrhough the lateral reticular formation loop, to counteract changes in muscle length, is inherently active, neurons from the medial due to passive stretch. rericular formarion need impulses from suppres­ sor areas in order to release the impulses which There is dual innervation of the muscle by exert an inhibitory effect upon the lower motor the alpha: motor neuron to the extrafusal muscle fibers, and by the gamma neurons to the intra­ neurons. Therefore, brain lesions which destroy fusal muscle fiber of the muscle spindle. Their these suppressor areas reduce the inhibitory motor neurons are coordinated. Influenced by brain impulses, they fire at appropriate rates to drive of the medial reticular formation. This attain smooth movements. The neurologic pa­ tient with a brain lesion no longer has these sig­ lack of inhibition results in all imbalance of the nals linked and coordinated. system: there is excessive facilitation to gamma Spasticity is considered the release of inhi­ motor neurOIIS. Signs of hyperactive muscle spindles and spasticity appear. Normal gamma bition of the gamma neuron system, normally bias cannot be maintailled. Increased gamma gain results. Although rhe gamma neurons are smaller than the alpha neurons, borh are locared in rhe ventral horns of the spinal cord. These smaller gamma neurons, which terminate on the intra­ fusal fibers as trail endings and plate endings, need less excitatory input to discharge than do the larger neurons. Without sufficient input to fire, the alpha neurons can remain quiet; gamma

1 8 ADVANCED ITRAIN AND (OUNTEiITRAIN neurons are tonically firing. This is the gamma those which excite flexor motor neurons. There­ bias. A muscle spindle with increased gamma fore the tonic stretch reflex is typica lly sup­ bias (gamma gain) will be more responsive to pressed in extensor muscles and enhanced in the stretch than a passive spindle. Therefore the in­ flexor muscles. trafusal fibers innervated by gamma neurons, with gamma gain, are in a active state of con­ Hyperactive phasic stretch reflexes is an­ traction. other characteristic of spasticity. The monosy­ naptic reflex arc is as follows: the tendon is If indeed the sensitivity of the primary and tapped; the muscle spindle is thus stretched; pri­ secondary sensory endings is a function of the mary endings then fire; action potentials travel level of the gamma bias, then with high gamma to the spinal cord via lA afferents; alpha moror bias, or gamma gain, there will be a high fre­ neurons are then excited; there is a muscle con­ quency discharge from these sensory endings of traction. With the phasic response, there is no the muscle spindle. dependency upon velocity sensitivity of the pri­ mary endings. There are static and dynamic gamma motor neurons; 3/4 of these are static. Different areas These hyperactive stretch reflex arcs impede of the brain control static and dynamic gamma voluntary control. Agonist function is impeded activity. Thus the brain lesion location will de­ by the hyperactivity of the antagonist and dys­ fine the dysfunction as static, dynamic, or both. function of the agonist. Sahrman and Norron gave evidence through electromyography that Patients with spasticity may have similar primary impairment of movement in the hemi­ motor signs, bur their underlying neural mecha­ plegic patient is not due to this antagonist spas­ nisms differ. The final common pathway is the ticity, but due to limited and prolonged recruitment of agonist contraction. They state alpha motor neuron. Hypertonicity as found in that these muscles are slower to attain maximal the spastic state is a reflection of the excessive EMG levels, and do not elicit the quantity or frequency of moror unit discharge produced by excitatory drive to these alpha neurons, trans­ normal individuals. mitted to them via the hyperactive monosynap­ There is an intimate relationship between spasticity and movement in the neurologic pa­ tic reflex arc, due to release of inhibition causing tient: lack of voluntary movement appears largely due to spasticity. The weakness of mus­ excessive gamma gain. This is evidenced by the cles, documented by Sahrman and Norron, may not be real, but relative ro the opposition of hyperactive tonic stretch reflexes: upon passive their spastic antagonists and the gamma gain of stretch to a limb, resistance is encountered. The strength of this resistance depends upon the ve­ the muscle itself. Reduce the spasticity and these locity of the movement: slower motion, de­ weak muscles often show increased power. creased resistance. This reflex appears to be an objective measure of dynamic gamma motor Therefore, the techniques used to test muscle nerve involvement. Since most spastic muscles strength in clinical orthopedic disotdets are not do not respond to static stretch, the static appropriate for the neurologic patient because gamma nervous system is possibly not the site of of the compromise of muscle control. Muscle excitatory excess. Tonic stretch reflexes elicit ex­ testing in non-central nervous system lesions de­ aggerated responses only after exceeding certain pends upon the ability to simultaneously con­ velocity threshold, after which the response is tract the agonist and relax the antagonist. The proportional to the velocity of the movement. muscle function must be independent of stretch The Group II afferents, which innervate the secondary endings that respond only to static srretch, synapse on two types of neurons: those which inhibit extensor mOtor neurons, and

AUTONOMIC NERVOUI IYITEM 19 and rate o f stretch. porting reaction is also released from supra­ These muscle tests also rely on the patient's spinal control; when combined with extensor spasticity of the leg it becomes a severe spastic ability to be indifferent to the posture of the response. This positive supporting reaction is limb and body. But the associated movements in the static modification of the spinal extensor the neurologic patient which also cause the im­ thrust described by Sherrington: a brief extensor pairment of selectivity of movement are primi­ reaction, evoked by a stimulus of sudden pres­ tive, stereotypic synergies: patterns of mass sure to the pads of the foot, and affecting all the flexion and extension, rhese synergies are nOt extensor muscles of the limb, with relaxation of pathological movements, but normal humans their antagonists. Adequate stimulus for this can perform relatively independently of these reaction includes: proprioceptive stimulus by patterns. These synergies are the same as those stretching foot intrinsic muscles, and exterocep­ found in the primitive withdrawal and thrust re­ tive stimulus by contacting pads of the foot with flexes. Bur a reflex is an involuntary reaction to the ground. The reaction is characterized by si­ a sensory srimulus; the primitive pattern re­ multaneous contraction of flexors and exten­ sponse is a voluntary action. It is initiated when sors, so that joints are fixated. the neurologic patient wants to perform an act. No sensory stimulus is needed to elicit these Brain lesions can affect nOt only the gamma patterns. and alpha systems, and the release of primitive patterns of movement, but also the interneurons The effects of these repetitive primitive in the intermediate grey matter of the spinal patterns are severe: they could almost become cord. In the animal model, flexor withdrawal permanent changes in movement patterns. cannot be elicited. To elicit flexor withdrawal Although the neural mechanism is not clearly during extensor spasticity, the flexor mOtor neu­ understood, it is known that the repetition of rons must be excited, while hyperactive exten­ movement patterns can cause long term alter­ sors are inhibited. There is a polysynaptic reflex ation of performance. The abnormal postures arc with one neuron to excite flexors and an­ and muscle activity will cause structural changes other to inhibit extensors. In brain stem tran­ in joints and muscles. Hyperactive m uscles will sections there is depression of this reciprocal hypertrophy; inactive muscles will atrophy. inhibition. Post-tetanic potentiation will occur: central ner­ vous system synapses exposed to repetitive ac­ Manual Therapy for Treatment of (tVlry present a long lasting pre-synaptic facilitation. The repetitive action caused by Neuromusculoskeletal Dysfunction and Spasticity these recurring patterns could induce an exag­ gerated response in the nerve to synthesize, The reduction of excessive gamma activity is the mobilize, and transmit neurotransmitters. basic rationale which explains why Manual Repetitive activity has shown increased ampli­ Therapy reduces spasticity in the neurologic pa­ tude in the excitatory post-synaptic potential, tient. Manual Therapy which is effective in when evoked by single nerve impulse repetition. This pOSt- tetanic potentiation may aggravate treatment of neuromusculoskeletal dysfunction the spasticity. The high frequency discharge of will rypically result in: reducing the hyperactiv­ the lA fibers may cause post-tetanic potentiation ity and gamma gain; decreasing the primitive at the monosynaptic connections of rhe alpha patterns of movement; strengthening voluntary neurons. controls. The same hyperactive Myotatic Reflex In the neurologic patient, the positive sup- Arc implicated in protective muscle spasm is as­ sociated with the hypertonicity component of

2 0 ADVANCED IIRAIN AND (OUNTERIIRAIN spasticity. Due ro brain lesions and lesions of hyperactivity within that reflex arc. This con­ tributes ro a decrease of the hypertonicity of supraspinal structures, there is an apparent hy­ spasticity as well as a decrease of the hyperronic­ peractivity of this reflex arc secondary to a disin­ ity of primary protective muscle spasm. hibition of the gamma neuron system. Effect of Manual Therapy on Central Nervous Pre-injury Neuromusculoskeletal Dysfunction System Activity of the Neurologic Patient in the Neurologic Patient Afferent information of sensory input is distrib­ Human beings typically present with varying de­ uted throughout the central nervous system, ro grees of neuromusculoskeletal dysfunction the brain and the spinal cord. Manual Therapy somewhere in the body. Statistics indicate that 8 which corrects neuromusculoskeleral dysfunc­ of 10 Americans suffer back pain during their tion achieves a decrease in general afferent gain. lifetimes. This pain probably is the result of neu­ Therefore, a decrease in the efferent gain which romusculoskeletal dysfunction: biomechanical is affecting the muscle fibers innervated by other dysfunction and joint hypomobility; protective spinal segments can be expected. Utilization of muscle spasm; connective tissue dysfunction; Manual Therapy ro correct and heal neuromus­ and more. It may be assumed that there is pre­ culoskeletal dysfunction results in more than the existing neuromusculoskeletal dysfunction and decrease of protective muscle spasm of the mus­ protective muscle spasm in the neurologic pa­ cles innervated by the segment that innervates tient, prior ro the central nervous system insult. The hyperactive Myotatic Reflex Arc is present the dysfunctional tissue or structure. There is a due ro neuromusculoskeletal dysfunction in all resultant decrease ill the severity of the protec­ patient populations: clinical orthopedic, sports tive muscle spasm in muscles innervated by medicine, chronic pain, pediatric, and neuro­ other segments of the spinal cord as well. There logic. will be a resultant decrease in the general level of spasticity also. The gamma neuron, with increased gamma gain, and the muscle spindle, is the seat of pro­ Utilization of Strain and Counterstrain tective muscle spasm and spasticity. According Technique ro decrease and arrest the inappropri­ ate propriocepror activity of the muscle spindle, ro this model, normalization and healing of neu­ and to eliminate the hyperactivity within the re­ romusculoskeletal dysfunction with effective flex arc of a muscle, will result in a decrease in Manual Therapy should result in decrease of ex­ general efferent gain as well. Therefore, the pro­ cessive and high frequency discharge within this tective muscle spasm of all the muscles inner­ hyperactive myotatic reflex arc in the neurologic vated by that same segment, as well as muscles patient population, as in other patient popula­ innervated by other segments, will diminish. For the neurologic patient, the general level of spas­ tions. Effective Manual Therapy techniques, ticity of the musculature surrounding the treated which correct neuromusculoskeletal dysfunc­ muscle will also decrease. Utilization of Manual tion, achieve decreased hypertonicity, whether Therapy Techniques will beneficially affect spas­ in the form of protective muscle spasm or spas­ ticity. ticity, for the orthopedic and the neurologic pa­ The facilitated segment as described above tient. In the case of a self perpetuating is a concept basic to the philosophy of Struc­ hyperactive reflex arc, associated with primary tural Rehabilitation for the neurologic patient. hypertonicity, utilization of Strain and Coun­ terstrain Techniques results in a decrease in The author has presented a model. If research proprioceptor activity and a decrease in the

AUTONOMIC NERVOUI IY ITEM 21 discovers new information, which negates this Hypersensitivity: The sensitivity to stretch of model, then a new hypothesis for a new model the muscle spindle is increased. The threshold will be needed. Structural Rehabilitation for the of tolerance of the muscle spindle to stimuli neurologic population does not require a hypo­ and stretch and dysfunction is lowered. A thetical model for the successful integration of smaller stimulus can activate the facilitated this work for improved rehabilitation results. segment. • The Facilitated Segment: efferent gain of the Summary: A Canceptual Model gamma and alpha neurons potentiates protec­ tive muscle spasm of all muscles innervated for the Neurologic Patient by that segment. • Hyperactivity: Not only is the segment hyper­ • The muscle spindle innervation by the gamma sensitive with a decreased threshold to become neuron. more activated, but the segment overreacts to Inhibitory control of the gamma neuron by stimuli. The excessive and high frequency dis­ the central nervous system. charge in that segment will influence every tis­ sue and structure innervated by that segment. • Afferent Gain: excessive and inappropriate Central netvous system inhi bitory effects on sensory input into the spinal cord due to neu­ the segment are less effective. romusculoskeletal dysfunction. • Protective Muscle Spasm of the musculature Distribution of excessive and high frequency innetvated by that segment. d ischarge throughout the central nervous • Protective Muscle Spasm of musculature in­ system: hyperactivity of the central nervous nervated by other segments. system. Dysautonomia: Sympathetic ganglia are af­ Alpha Gain: excessive and high frequency dis­ fected by the excessive and high frequency charge affecting the alpha motot neuron in­ discharge of the spinal segment. The thresh­ nervation of the muscle fiber. old to \"fight and flight\" and stress is lowered. Hyperinnervated sarcomere: a contracted and Healing is affected. Visceral function, lym­ shortened muscle due to alpha gain. phatic system function, connective tissue Hyperactive myotatic reflex arc: afferent gain; function, immune system function is affected. alpha gain; gamma gain. There is a correlating attempt for parasympa­ thetic nervous system balancing, which af­ • Protective muscle spasm: a hyperactive my­ fects digestive and cardiovascular function. otatic reflex arc causing sustained contracted • Dystrophic Effect: Irwin Korr discovered the and shortened sarcomeres. A basis of trophic effect of the neuron which manufac­ pathokinesiology: muscles crossing the joints will cause approximation of joint surfaces, tures and transports protein to vitalize the joint hypomobility and limitations of ranges end organs: e.g. the muscle fiber. This func­ of motion. tion is affected when the neuron is \" facili­ tated. \" The reduction of this trophic effect is • Articular Balance: imbalance in the resting dystrophy, which affects all end organs. position of articular surfaces due to protective Defacilitation: can be achieved with Manual muscle spasm in muscles crossing the joint Therapy: 1 ) by correcting and healing the and exerting pathologic forces on the bones neuromusculoskeletal dysfunction, 2) by re­ at muscle insertion and origin. ducing and artesting inappropriate proprio­ ceptor activity and the self-perpetuating • Gamma Gain: due to excessive and high frequency discharge in the ventral horn; re­ sulting in inapproptiate and excessive propri­ oceptor activity.

2 2 ADVANCED STRAIN AND CD U N TERST i l i N hyperactive reflex arc with Strain and Coun­ there is improved articular balance, with a terstrain Technique, 3) by Manual and Cra­ more normal resting position of articular sur­ nial Therapy ro defacilitate the facilitated faces. There is decreased muscle resistance ro segment and the spinal cord. movement, increased joint mobility, increased Corrective Kinesiology: As a result of the re­ ranges of motion, and improved posture for laxation and elongation of the muscle fiber the orthopedic and the neurologic patient. achieved with effective Manual Therapy,

CHAPTER 4 APPLICATION How to Perform Advanced Strain and Counterstrain Technique A Note of (aution to maintain the precise position of the tech­ nIque. Use the \"Mechanical Model.\" Do not use the 2. Maintain this position precisely, without any Tender Point. The autonomic nervous system is movement added, until there is no sensation especially susceptible to stimulation by pressure of movement, or any other sensation. on the tender points! 3. The De-Facilitated Fascial Release is the tis­ sue \"unwinding\" which occurs secondary to At Regional Physical T herapy we use the the elimination anrlol r decrease of hyper­ Mechanical Model/Corrective Kinesiologic tonicity. This unwinding appears to occur at Model with Jones' Strain and Counterstrain the level of the ground substance (matrix) of Technique. During more than a decade of re­ the connective tissue. search, we have discovered that many persons 4. Use the Synchronizersc! do not have\"normal\" sensory perception; the Tender Points may not reflect the true status of Application hypertonicity of the patient. We also discovered that stimulation of the Tender Points of Ad­ 1. Do not\"use\" the Tender Point. Pressure on vanced Strain and Counterstrain Technique can these Tender Points will further stimulate the set off a long-term treatment reaction which is autonomic reflex arcs and will contribute to difficult to contain. problems associated with existing hyper­ tonicity. De-Facilitated Fascial Release 2. Know where the Tender Point is situated if De-Facilitated Fascial Release (Weiselfish-Gi­ the treatment requires this knowledge. For ammatteo) is the phenomenon of \"tissue un­ example, position of the body part is occa­ winding\" which occurs when there is sionally relative to the location of the Tender \"de-facilitation.\" De-facilitation is the decrease Point. of afferent and efferent discharge. Strain and Counterstrain Technique, and Advanced Strain 3. Position the body, one-step-at-a-time, ac­ and Counterstrain Technique cause de-facilita­ cording to treatment directions. Maintain tion. precisely the positions for at least one minute. Maintenance of the position for one Maintain the precise position of the Strain and minute will eliminate anrlol r decrease the hy­ Counterstrain Technique or Advanced Strain and pertonicity of the contractile tissues. Counterstrain Technique throughout the duration of 4. Every technique should be continued beyond tissue tension transformation. the one-minute duration in order to attain a De-Facilitated Fascial Release. Maintain the How to perform a De-Facilitated Fascial Release position until the end of the release. The re­ lease is the tissue tension change and trans­ 1. After one-minute duration of the Advanced formation, which can be palpated. Strain and Counterstrain technique, continue 5. Use the Synchronizersc for more effective and efficient results! 23

CHAPTER S ADVANCED STRAIN AND COUNTERSTRAIN FOR THE VISCERA Org/UG2: Bladder (Netter's plate # 341 - 348, 355, 357, 362) (Bilateral) TENDER POINT On the inferior pubic ramus, at the medial bor­ der of the bone, 1 inch caudal from the inferior border of the pubic symphysis. TREATMENT • Supine. • Abduct both hips 20 degrees. • Internally rotate the ipsilateral hip 10 degrees. • Extend the knee (straight leg). • Internally rotate the tibia on the femur with one lb. of force. GOAL Alleviate the hypertonicity of the bladder muscle. INTEGRATIVE MANUAL THERAPY This technique will decrease the hypertonicity of the bladder and can be used with the other Advanced StrainiCounrersrrain techniques for the kidneys, ureter and urethra. Often incontinence is due to the muscle spasm of the bladder muscle. Edema of the legs can be associated with hypertonicity of the bladder. Muscle spasm of the bladder is commall, often the result of prolonged pubic symphysis dysfunction. This technique can be performed with the Advanced SrrainlCoumer­ strain Urogenital sequence. 24

AUTONOMIC NERVOUS SYSTEM 2S Org/UGF3: Cervix , (Netter's plate #341-352, 355) Cervix (Bilateral) of Uterus TENDER POINT There is no Tendet Point for this musculature. The technique must be petformed with the 'Mechanical Model.' TREATMENT • Supine. • Flex both hips to 60 degrees. Knees are flexed to 50 degrees. Cross the legs, with the ipsilateral leg on top. Move both knees toward the ipsilateral side 20 degrees. GOAL To decrease hypertonicity of the cervix muscu­ lature. INTEGRATIVE MANUAL THERAPY This technique will often affect pain, cramping, men­ strual cramps, and other PMS symptomatology. This technique occasionally causes large changes in sitting pain and sitting wlerance. This technique can be per­ formed with the Advanced StrainiCounrerstrain Uro­ genital Sequence. \"--\"'

26 ADVANCED \\TRAIN AND (OUNmmAIN Org/HTl: Hearl (Netter's plate #182, 184, 194, 200, 202, 214) (Unilateral) TENDER POINT 1 inch left of the left 4th sternocostal joint and slightly inferior. (At the junction of the ventri­ cles and atria which is approximately at the 4th rib.) TREATMENT • Supine. Neck flexion to the end of cervical range of mOtion. Neck sidebending to the right 10 degrees. Left shoulder in horizontal adduction to the end of range of motion. GOAL Release of the heart muscle. INTEGRATIVE MANUAL THERAPY This technique is useful for all patients with chest tight· ness, andlor any rib cage sympromarology. There are no comra-indications to [he use of this technique. There may be limitations of T3, T4, T5 mobility. There may be upper and/or mid-thoracic limitations of mo­ tion. There may be left shoulder girdle limitations of motion which are all indications for use of OrglHTl Advanced StrainlCounrerstrain technique.