“How many of you will commit malpractice?”files.academyofosteopathy.org/files/DecemberJournal2004.pdf · the top of the photo. Use a photocopy to in-dicate the placement of arrows

Official Publication of the American Academy of Osteopathy®

FORUM FOR OSTEOPATHIC THOUGHT

TRADITION SHAPES THE FUTURE • VOLUME 14 NUMBER 4 DECEMBER 2004

“How many of youwill commit

malpractice?”

2/The AAO Journal December 2004

Instructions to Authors

The American Academy of Osteopathy®

(AAO) Journal is a peer-reviewed publica-tion for disseminating information on thescience and art of osteopathic manipulativemedicine. It is directed toward osteopathicphysicians, students, interns and residentsand particularly toward those physicians witha special interest in osteopathic manipulativetreatment.

The AAO Journal welcomes contributions inthe following categories:

Original ContributionsClinical or applied research, or basic scienceresearch related to clinical practice.

Case ReportsUnusual clinical presentations, newly recog-nized situations or rarely reported features.

Clinical PracticeArticles about practical applications for gen-eral practitioners or specialists.

Special CommunicationsItems related to the art of practice, such aspoems, essays and stories.

Letters to the EditorComments on articles published in The AAOJournal or new information on clinical top-ics. Letters must be signed by the author(s).No letters will be published anonymously,or under pseudonyms or pen names.

Book ReviewsReviews of publications related to osteo-pathic manipulative medicine and to manipu-lative medicine in general.

NoteContributions are accepted from members ofthe AOA, faculty members in osteopathicmedical colleges, osteopathic residents andinterns and students of osteopathic colleges.Contributions by others are accepted on anindividual basis.

SubmissionSubmit all papers to Anthony G. Chila, DO,FAAO, Editor-in-Chief, Ohio University,College of Osteopathic Medicine (OUCOM),Grosvenor Hall, Athens, OH 45701.

Editorial ReviewPapers submitted to The AAO Journal maybe submitted for review by the EditorialBoard. Notification of acceptance or rejectionusually is given within three months after re-

ceipt of the paper; publication follows as soonas possible thereafter, depending upon thebacklog of papers. Some papers may be re-jected because of duplication of subject mat-ter or the need to establish priorities on theuse of limited space.

Requirementsfor manuscript submission:

Manuscript1. Type all text, references and tabular ma-terial using upper and lower case, double-spaced with one-inch margins. Number allpages consecutively.

2. Submit original plus three copies. Retainone copy for your files.

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6. For human or animal experimental inves-tigations, include proof that the project wasapproved by an appropriate institutional re-view board, or when no such board is inplace, that the manner in which informedconsent was obtained from human subjects.

7. Describe the basic study design; defineall statistical methods used; list measurementinstruments, methods, and tools used for in-dependent and dependent variables.

8. In the “Materials and Methods” section,identify all interventions that are used whichdo not comply with approved or standardusage.

Computer DisksWe encourage and welcome computer diskscontaining the material submitted in hardcopy form. Though we prefer Macintosh 3-1/2" disks, MS-DOS formats using either 3-1/2" or 5-1/4" discs are equally acceptable.

AbstractProvide a 150-word abstract that summarizesthe main points of the paper and it’sconclusions.

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2. Photos should be submitted as 5" x 7"glossy black and white prints with high con-trast. On the back of each, clearly indicatethe top of the photo. Use a photocopy to in-dicate the placement of arrows and othermarkers on the photos. If color is necessary,submit clearly labeled 35 mm slides with thetops marked on the frames. All illustrationswill be returned to the authors of publishedmanuscripts.

3. Include a caption for each figure.

PermissionsObtain written permission from the publisherand author to use previously published illus-trations and submit these letters with themanuscript. You also must obtain writtenpermission from patients to use their photosif there is a possibility that they might beidentified. In the case of children, permis-sion must be obtained from a parent or guard-ian.

References1. References are required for all materialderived from the work of others. Cite all ref-erences in numerical order in the text. If thereare references used as general source mate-rial, but from which no specific informationwas taken, list them in alphabetical orderfollowing the numbered journals.

2. For journals, include the names of all au-thors, complete title of the article, name ofthe journal, volume number, date and inclu-sive page numbers. For books, include thename(s) of the editor(s), name and locationof publisher and year of publication. Givepage numbers for exact quotations.

Editorial ProcessingAll accepted articles are subject to copy ed-iting. Authors are responsible for all state-ments, including changes made by the manu-script editor. No material may be reprintedfrom The AAO Journal without the writtenpermission of the editor and the author(s).

December 2004 The AAO Journal/3

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IN THIS ISSUE:AAO Calendar of Courses ................................................................................. 4Contributors ....................................................................................................... 6Component Societies’ CME Calendar ............................................................... 7

EDITORIAL

View from the Pyramids: Remembering Doctor Still .................................. 5Anthony G. Chila, DO, FAAO

REGULAR FEATURES

Dig On: A Program of Research ................................................................... 8From the Archives: Chapter VII, Table IV, Four Great Classesof Osteopathic Spinal Lesions ...................................................................... 9George Malcolm McCole, DO:An Analysis of the Osteopathic Lesion, 1935, pp. 35-39Book Review .............................................................................................. 32Elsewhere in Print ....................................................................................... 33

2004 SCOTT MEMORIAL LECTURE

Don’t Raise Your Hand – Put it on the Patient ........................................... 10Dennis J. Dowling, DO, FAAO

CLINICAL PRACTICE

A Case Study of Left Adhesive Capsulitis Presumably Resultingfrom Previous Treatment with Protease Inhibitors ..................................... 17James A. Lipton, DO, FAAO, CDR, MC, USN and Michele Neil, OMS-III

Case Study: An Osteopathic Resolution of a Neurocardiogenic Syncope .. 20Yvette Somoano, DO and Stefan Hagopian, DO

INTERNATIONAL COMMUNICATION

Could Joint Hypomobility Alter Optimal Proprioceptive Information? ..... 25Rafae; Zegarra-Parodi, DO, MROF

FORUM FOR OSTEOPATHIC THOUGHT

TRADITION SHAPES THE FUTURE • VOLUME 14 NUMBER 4 DECEMBER 2004

A PEER-REVIEWED JOURNAL

The Mission of the American Academy of Osteopathy® is to teach, advocate,and research the science, art and philosophy of osteopathic medicine, emphasiz-ing the integration of osteopathic principles, practices and manipulative treat-ment in patient care.

AMERICAN ACADEMY OF OSTEOPATHY®

Stephen D. Blood, DO, FAAO ............. PresidentKaren M. Steele, DO, FAAO ....... President ElectStephen J. Noone, CAE ......... Executive Director

AAO PUBLICATIONS COMMITTEE

Raymond J. Hruby, DO, FAAO ........ ChairpersonDenise K. Burns, DOStephen M. Davidson, DOEileen L. DiGiovanna, DO, FAAOEric J. Dolgin, DOStefan L.J. Hagopian, DOHollis H. King, DO, PhD, FAAOJohn McPartland, DOPaul R. Rennie, DOMark E. Rosen, DO

Ex-officio Members:Myron C. Beal, DO, FAAO ....... Yearbook EditorAnthony G. Chila, DO, FAAO ...... Journal Editor

THE AAO JOURNAL

Anthony G. Chila, DO, FAAO .... Editor-in-ChiefStephen J. Noone, CAE ......... Supervising EditorDiana L. Finley, CMP ............... Managing Editor

The AAO Journal is the official publication of theAmerican Academy of Osteopathy®. Issues are pub-lished in March, June, September, and Decembereach year.

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Opinions expressed in The AAO Journal are thoseof authors or speakers and do not necessarily re-flect viewpoints of the editors or official policy ofthe American Academy of Osteopathy® or the in-stitutions with which the authors are affiliated, un-less specified.

Official Publication of the American Academy of Osteopathy®


AAO Calendar of Courses

2005JANUARY

28-30 Winter OMT Update: Application ofOsteopathic Concepts in Clinical Medicineplus Preparation for Certifying BoardsTUCOM-NV; Henderson, NV

FEBRUARY

18-20 Clinical Applications of Muscle Energyin Primary CareMidwestern University/AZCOM; Glendale,AZ

MARCH

13-16 Advanced Visceral Manipulation:Visceral Approach to Cranial andPeripheral Nerve DysfunctionFeaturing: Jean-Pierre Barral, DO, MROFReno /Lake Tahoe, NV

16-20 2005 Annual Convocation:The Hand: The Instrument of Our DistinctionCharles J. Smutny, DO, FAAO, Program ChairReno /Lake Tahoe, NV

APRIL

9-10 Dr. Fulford’s Basic Percussion: A SystematicApproach to the Whole BodyMidwestern University/CCOM; Chicago, IL

MAY

13-15 Prolotherapy: Above the DiaphragmUNECOM; Biddeford, ME

JUNE

17-19 Visceral Approachto Cardiopulmonary DysfunctionUNECOM; Biddeford, ME

JULY

29-31 Muscle Energy: Three VisionsMidwestern University/CCOM; Chicago, IL

AUGUST

19-22 15th Annual OMT Update: Application ofOsteopathic Concepts in Clinical Medicineplus Preparation for Certifying BoardsThe Contemporary at Walt Disney World®

Buena Vista, FL

SEPTEMBER

16-18 Clinical Application of Principles ofLigamentous Articular Strain in Primary CareUMDNJ-SOM; Stratford, NJ

OCTOBER

22 Rapid OMT: Increase Your Reimbursementin an Ambulatory SettingOrlando, FL

23-27 AOA Unified Convention:AAO Program: Osteopathy in the Specialties:A Hands-on ApproachKenneth L. Lossing, DO, Program ChairOrlando, FL

NOVEMBER

11-13 Prolotherapy: Below the DiaphragmUNECOM; Biddeford, ME

DECEMBER

2-4 Lymphatic Approach to the VisceraAZCOM; Glendale, AZ

June 9-13, 2005Osteopathy in the Cranial Field

Course Director: Hugh M. Ettlinger, DO, FAAONYCOM

Old Westbury, NY

40 Category 1-A CME Hours

Contact: Judy Staser @ Phone: 817/926-7705or Fax: 817/924-9990

These programs anticipate being approved for AOA Category1-A CME credit pending approval by the AOA CCME

Visit our website at: www.sctf.com


View from the Pyramids

Anthony G. Chila

Andrew Taylor Still suffered a strokein 1914 from which he never fully re-gained his speech. Declining health even-tually resulted in his passing on Decem-ber 12, 1917. He was buried at Kirksville,MO on December 14, 1917. It is appro-priate that acknowledgment be given asa reminder of the osteopathic profession’sdebt to the contribution and vision of itsfounder.

George W. Riley, DO was a graduateof the American School of Osteopathy,Class of 1904. He also served as Presi-dent of the American Osteopathic Asso-ciation, 1917. Excerpted below are someof Doctor Riley’s recollections of his stu-dent days and the Old Doctor1:

“Although I had completely severedmy business relations in New York andhad come to Kirksville with every inten-tion of studying osteopathy, nevertheless,I spent my first two weeks in visitingclasses, talking with members of the fac-ulty, with students, with patients goingto and from the infirmary, with citizensof the town, trying to rid my mind of thatelement of doubt, aye ‘doubting Thomas’– like trying to find the pierced sidewherein I might place my hand and clinchmy faith in this momentously new ven-ture I was about to undertake.

Finally my mind was satisfied and Ientered into the work with a zest and faithseemingly impossible for one who hadbeen beset with such hesitancy.

The members of our class (June, 1904)came from all sections of the country –from village, farm, and city. I presumeevery member of the class was overtwenty-three years of age, maybe twenty-

four, many far beyond that age, and prob-ably everyone had learned the value of adollar by the sweat of his brow. Every-one gave the impression of knowing whathe was there for, of knowing, ‘what theshootin’ was all about.’ This possibly ismost pronounced in more mature classeswho probably look with greater zeal onthe practical goal sought than the morecommon cultural aim of classes com-posed of younger students.

I was very much impressed with thespirit of osteopathy that pervaded notonly the whole life of the student body,but that of the citizenry of the town aswell. This is easily accounted for whenwe take into consideration the fact thatthere came into the little city of Kirks-ville, each term, a combined outsidepopulation of between 600 and 1000 stu-dents and patients, whose aim and inter-est in life, for the time being, was oste-opathy and what it could do for afflictedhumanity. This number had to be takeninto the homes of the citizens. Their in-terests therefore pervaded the whole lifeof the town. As a result we all ate, drank,and slept with osteopathy.

We, as a class, were particularly for-tunate in having the subject, principlesand practice of osteopathy, under Dr. GuyHulett. Our diplomas were the last signedby that great teacher, cut off in the earlydawn of what gave promise of being aremarkable career. He was a conscien-tious believer in the science and a manthoroughly grounded in the fundamentalsof osteopathy. His was perhaps the keen-est, most logical, and scientific mind ofthe younger members of the professionof that day. A superior student himself,he possessed to an unusual degree the

faculties of a real teacher. It was alwaysa joy to watch the look of approval onthe face of the Old Doctor when listen-ing to a lecture by Dr. Hulett. His deathremoved from the profession one of itskeenest, most brilliant intellects.

We again were fortunate, indeed morefortunate than we perhaps realized, inhaving frequent visits to our class of ourrevered Old Doctor. In a spirit of sympa-thetic humility I feel sincerely sorry for allthose of the profession who never enjoyedthe privilege of knowing him personally,or of hearing his rare epigrammaticthought-provoking remarks, and thoseseemingly inspired diagnoses of his.

Frequently he would come into theclassroom, always unannounced, listenattentively to the lecture or discussion andmaybe after a few minutes pass out asquietly as he had entered. More often,however, he would make some quaintobservation that would forever fix in ourminds the fundamental osteopathic prin-ciple underlying the subject under discus-sion. …Perhaps the outstanding impres-sion I have of him was his eager, pas-sionate desire for every student to becomethoroughly imbued and grounded in thefundamentals of osteopathy. That was hisgreat goal, his supreme ambition. The onedisturbing thought that he seemingly hadsometimes, was that insufficient empha-sis was being given these fundamentalsin our class work. He wanted each stu-dent to know these principles and to knowthat he knew them.”

1. Hildreth, AG: The Lengthening Shadowof Andrew Taylor Still. Macon, MO.1938. 415-417.

Remembering Doctor Still


Contributors

Regular Features

Dennis J. Dowling. Don’t Raise Your Hand – Put it OnThe Patient. The 2004 Scott Memorial Lecture addresses es-sential osteopathic practice in the context of a significant con-temporary social occurrence: Malpractice. In recognizing thechanges in educational environment for osteopathic educationduring the past twenty years, the author makes the case that thebest defense for practice continues to be the application of thehand to the patient. (p. 10)

James A. Lipton and Michele L. Neil. A Case Study ofLeft Adhesive Capsulitis Presumably Resulting from Previ-ous Treatment with Protease Inhibitors. The authors presentan unusual case study in which circumstantial evidence sug-gested association of the chief complaint with prior administra-tion of agents for protection from an HIV infected source. Inthis instance, reconciliation of diagnostic findings and clinicalpresentation rested on the eventual casual reporting of an over-looked incident in the medical history. (p. 17)

Yvette Somoano and Stefan Hagopian. An OsteopathicResolution of Neurocardiogenic Syncope. The authors’ pre-sentation of this complaint (Neurocardiogenic Syncope) dem-onstrates the value of application of osteopathic thought. Theclinical history suggested that a complex series of imbalanceshad occurred over many years, probably associated with thecranial base and upper thorax. The rationale provided for thesuccessful use of osteopathic manipulative intervention is strik-ing given the variety of less than successful conventional medi-cal interventions. (p. 20)

Rafael Zegarra-Parodi. Could Joint Hypomobility AlterOptimal Proprioceptive Information? The author providesan opportunity for expanding thought in this review of contem-porary attitudes about Joint Complex Dysfunctions (JCD). Anosteopathic perspective begins with an expression by JohnMartin Littlejohn. The continuing search for understanding ofcomplexities associated with JCD has its current expression asSomatic Dysfunction. In today’s research environment, otherdisciplines are offering observations and interpretations, whichmay be helpful. (p. 25)

teopathic theory and practice. Seventy years ago this Montanapractitioner offered a classification of osteopathic spinal lesionswhich remains useful today. Of particular note from that era isthe descriptor The Osteopathic Greater Lesion Complex. (p. 9)

BOOK REVIEW. Principles of Manual Medicine. It isunusual to have the opportunity to follow the contribution ofthought of a single author through three consecutive editions ofa textbook. In the case of Philip E. Greenman, DO, FAAO, thisfact encompasses fifty years of practice and contribution to majordevelopments in osteopathic education, here and abroad. (p. 32)

ELSEWHERE IN PRINT. Do CAM therapies work forpain management? Authors Robert Bonakdar, MD and DavidE. Bresler, PhD address the fact that existing approaches to dis-ease and pain do not work for all patients. Four Complemen-tary Alternative Medicine approaches are discussed. In an ad-ditional citation, the pioneering work of Earl H. Gedney, DO(Hypermobile Joint) is recognized. (p. 33)

CME CREDIT. In response to reader requests, AAOJ willoffer CME Credit to readers completing the enclosed quiz. Atthis time, 1 Hour 2-B Credit will be offered, with request forupgrade as AAOJ qualifications are reviewed by the AmericanOsteopathic Association. (p. 24)

DIG ON. A Program Of Research. Albert E. Guy, DO prac-ticed in Paris, France and Mount Vernon, New York. A smallsampling of his extensive writing during the years 1930-1933 in-dicates that he was very proactive in suggesting an organizationalplan for research for the osteopathic profession. (p. 8)

FROM THE ARCHIVES. The name of George MalcolmMcCole is not frequently recognized in today’s teaching of os-

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Component Societies’CME Calendarand other Osteopathic Affiliated Organizations

January 8, 2005Osteopathic Dissection Projectof the Head & NeckCentral California Osteopathic Study GroupSoquel, CACME: 7 Category 1A (anticipated)Contact: Bonnie Gintis, DO

831/477-1200

January 20-23, 200516th Annual Osteopathic WinterSeminar and National Clinical UpdatePinellas CountyOsteopathic Medical SocietySt. Pete Beach, FLCME: 27 Category 1A (anticipated)Contact: Kenneth E. Webster, EdD

727/581-9069 or866/254-8798

January 21-24, 2005Biodynamics Phase II: The Fluid BodyPortland, ORCME: 23 Category 1A (anticipated)Contact: James Jealous, DO

207/778-9847

January 28-31, 2005Biodynamics Phase VI:The Embroyological HealthPortland, ORCME: 24.75 Category 1A (anticipated)Contact: James Jealous, DO

207/778-9847

February 11-13, 2005Energetically Integrated OsteopathicMedicine: The Life, Thought and Workof Robert Fulford, DO as Interpretedby Zachary Comeaux, DO, FAAOWVSOM; Lewisburg, WVCME: 12 Category 1A (anticipated)Contact: Zach Comeaux, DO, FAAO

304/647-6356

February 16-20, 2005Midwinter Basic CourseOsteopathic in the Cranial FieldCourse Director: Richard A. Feely, DO, FAAOThe Cranial AcademyTampa, FLCME: 40 Category 1A (anticipated)Contact: The Cranial Academy

317/594-0411

February 26, 2005OMM for the Family PractitionerArizona Academy of OsteopathyGlendale, AZCME: 7 hours Category 1A(anticipated)Contact: William Devine, DO

623/572-3350

March 5-8, 2005Biodynamics Phase I: BiodynamicsKona, HawaiiCME: 21.5 Category 1A (anticipated)Contact: Thomas Shaver, DO

207/778-9847

April 1-4, 2005Biodynamics Phase IV:The MidlineTopanga, CACME: 23 Category 1A (anticipated)Contact: Stefan Hagopian, DO

207/778-9847

April 2-5, 2005Biodynamics Phase II: The Fluid BodyFranconia, NHCME: 23 Category 1A (anticipated)Contact: Donald Hankinson, DO

207/778-9847

April 17-20, 2005Biodynamics Phase III: The Long Tideand the DuraFranconia, NHFaculty: James Jealous, DO andDonald Hankinson, DOCME: 22.5 Category 1A (anticipated)Contact: James Jealous, DO

207/778-9847

May 8-11, 2005Biodynamics Phase VI:The Embroyological HealthFranconia, NHCME: 24.75 Category 1A (anticipated)Contact: James Jealous, DO

207/778-9847

May 15-18, 2005Biodynamics Phase VII:The Health AloneCME: 22 Category 1A (anticipated)Franconia, NHContact: James Jealous, DO

207/778-9847

May 20-22, 2005Crash Recovery The Long Road Home:Treataing Victims of Motor VehicleAccidents and Brain InjuriesUMDNJ/SOM, Stratford, NJCME: 17 Category 1A (anticipatedContact: The Cranial Academy

317/594-0411

May 22-25, 2005Biodynamics Phase I: BiodynamicsFranconia, NHCME: 21.5 Category 1A (anticipated)Contact: Thomas Shaver, DO

207/778-9847


Dig OnAnthony G. Chila

The decade of the 1930s was a period of significant contri-bution to medical practice expressed through extensive writingby osteopathic physicians. From that period of time one caneasily construct a pantheon of distinguished practitioners andteachers who offered much direction and guidance for the con-tinuing development of the osteopathic profession. Among thosenames: Burns, Conley, Downing, Hildreth, and a host of othersnot all remembered or whose written contributions are now outof print. In pursuing the development of Andrew Taylor Still’sphilosophy, the American Osteopathic Association establishedthe Committee on Research in 1939.

Albert E. Guy, DO wrote extensively about Vertebral Le-sions and Vertebral Mechanics. Some of his most importantobservations were published in The Journal of the AmericanOsteopathic Association during the years 1930-33. As a practi-tioner, he observed that “The practice of osteopathy has fullydemonstrated its worth, but the development of its theory, sourgently needed in view of the advance of others, has not pro-gressed very far beyond the dicta of A.T. Still. Guy proposedthe following considerations for osteopathic research1:

1. The vertebral column viewed as an entity2. The vertebral unit, composed of two adjacent articulated

vertebrae3. The intervertebral disk; the annulus lamellosus; the

nucleus pulposus; the exonuclear lesions4. The intervertebral ligaments; their innervation; their

control functions5. The apophyseal articulations; the mechanics of their

displacements6. The deep vertebral musculature; its innervation7. The contents of the intervertebral foramen8. The nerve sinu vertebral; its function as vaso-regulator of

the blood supply and drainage of the meningeal tissuesand of others located in the vertebral canal and in theintervertebral foramina

9. The supporting or connective tissue; its hygrometricproperties; its role in edematous and inflammatoryprocesses in relation with the lymphatic circulation

10. The purpose and physiological effects of the abrupt andintentional separation of the apophyseal articulations,with incidental “popping”; the physics of the latter

11. The analysis of the maintenance of the relative displace-ment of two adjacent vertebrae, or so-called “lesion”, in aposition within the normal range of motion, neverthelesspermitting a certain amount of mobility

12. The pathological effects of the maintenance in a fixedposition, either normal or abnormal, of the articulationsof two adjacent vertebrae; the remedial procedurethrough osteopathic manipulation for such a condition

A Program of Research

13. The analysis of the effects of osteopathic manipulation ofsoft tissues; drainage of the latter; abatement of conges-tive conditions; activation of arterial circulation; reduc-tion of acidosis, hence of irritation both to the nerveterminals and to the trunks, and consequent appeasementof superficial and deep-seated tenderness

14. The costovertebral articulations; the influence of theirdisordered conditions upon the nutrition of the costaltissues, ligaments, musculature, bones, marrow and itshematopoietic functions; study of the development oferuptive disturbances such as herpes zoster, of costogenicanemias and toxemias, of the influence of the latter uponthe genital functions

Guy’s challenge in offering this program was expressed as“In the field of research concerning the intimate parts of thespine it was our heritage to lead; shall we be contented withmerely joining?” Given the growth of the osteopathic profes-sion since that time, how far have we progressed?

1. Academy of Applied Osteopathy Yearbook. 1949. pp. 72-73.❒

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From the Archives

Osteopathic spinal lesions are classi-fied according (1) to their cause and (2)with respect to their age.

According to cause there are two greatclasses of spinal lesions, (1) Traumaticand (2) Reflex. With respect to state ofdevelopment or age of the lesion at thetime of observation there are two othergreat classes, (3) Acute and (4) Chronic.

In practice, however, classification isnot so simple as the following discussionshows.

The (1) Traumatic Spinal Lesion, in-stantly upon its formation, has reflexsymptoms caused by impulses from spi-nal cord centers in relation. The traumaticlesion may be either acute or chronic.

The (2) Reflex Lesion is caused byimpulses abnormal in intensity or con-tinuousness, which impulses arrive froma distant part. These stimuli first reachthe cord centers of the segment and fromthere are distributed to the surroundingjoint muscles and blood vessels. After itsformation the reflex lesion of itself sendsabnormal impulses into the cord centersof the segment thus increasing the volumeof stimuli distributed from these centers.

The (3) Acute Lesion, soon after for-mation, begins to develop chronic at-tributes from fibrous infiltration. Theacute lesion may be either traumatic orreflex.

The (4) Chronic Lesion always re-tains some acute symptoms, which withslight provocation definitely increase.The chronic lesion may be either trau-matic or reflex. There is no actual divid-ing line between the acute and thechronic.

The speed with which an acute lesiontakes on chronic attributes is governedby the reactions of the individual, the lifehe leads, and the burdens he requires hisspine to bear.

Chapter VII, Table IV, Four Great Classes ofOsteopathic Spinal LesionsGeorge Malcolm McCole, DO: An Analysis of the Osteopathic Lesion, 1935, pp. 35-39

Acute Lesion at Siteof Chronic Lesion

The acute lesion is often found at thesite of a chronic lesion, which has im-paired the muscular, and ligamentouscontrol of the joint and caused it to besusceptible to fresh insult. A chronic le-sion, hitherto unnoticed, may flare upwith acute symptoms and thus come un-der observation.

Chronic Lesion is theResult of Acute Lesion

The chronic lesion is often the resultof several acute lesions having at vari-ous intervals succeeded one another in acertain segment. Nature unaided, appar-ently removes many acute lesions, but theeffect of inflammation repeatedly occur-ring in the tissues of a certain joint is cu-mulative, and the formation of fibroustissue in muscle fasciculi and in ligament-fibers is stimulated. This formation iscalled the ‘fibrous contracture” of thechronic lesion.

The Causative LesionThe traumatic lesion is sometimes

called the causative lesion, and it is. How-ever, it must be remembered that the re-flex lesion becomes causative as soon asit is formed. If it were not, it would notbe an osteopathic lesion.

Reflex SymptomsComplicate TraumaticLesions

When a lesion of a certain spinal seg-ment (acting through efferent reflex nervepathways) causes disease in a part remotefrom the spine, that diseased part sends

abnormal nerve impulses streaming back(over afferent nerve pathways) to the le-sioned segment, to set up reflex tensionsin the muscles of that segment. There-fore, reflex lesion symptoms developwherever there is a traumatically lesionedsegment – the vicious circle.

Again: When abnormal nerve im-pulses are being sent out from a spinalcord segment, we think of them as goingto parts remote from the spinal joint.These abnormal impulses are distributedto the short, deep, segmental musclessurrounding the joint, just as they are sentto tissues remote from the spine. In fact,the distribution of abnormal nerve im-pulses seems to be more promptly con-centrated in the close-by short segmen-tal joint muscles than is the distributionto more distant tissues, which are occu-pied with other kinds of duties and wherethere is better opportunity to integrate.

Bone MalpositionIn the traumatic lesion the bone is usu-

ally held seated in position of abnormalside-bent rotation. Thus, bonemalpositions are more frequent in trau-matic than in reflex lesions. For the samereason the traumatic lesion is apt to beunilateral rather than bilateral.

Compound LesionsTherefore, although lesions are di-

vided into four great classes, they are allin some degree compound. All osteo-pathic spinal lesions tend toward the samepathology, irrespective of cause or timeelapsed since formation.

continued on page 19


➻

How many of you wish to commitmalpractice in the future? I see that nohands were raised.

As defined in the Merriam-Websterdictionary, Malpractice is:

1: a dereliction of professional dutyor a failure to exercise an accepted de-gree of professional skill or learning byone (as a physician) rendering profes-sional services which results in injury,loss, or damage

2: an injurious, negligent, or improperpractice1

Legally, there are several elements tomalpractice. In most states, in order toprove medical malpractice, a physician’sduty to act is judged according to certainstandards of care. Next, there is a breachof that standard of care. Usually, this re-sults in an injury and a causal connec-tion between the breach of care and theinjury can be established. A doctor mustact in a reasonable and prudent fashionas would anyone possessing the same orsimilar skills or knowledge. The expec-tation is that the same treatment interven-tion would be given by another physicianunder similar circumstances. The consid-eration of the caregiver’s location and thestandard of care to a similar communityhas shrunk due to the explosion in infor-mation availability.

There is also another element utilizedin malpractice situations known as “lossof chance”. The loss of chance doctrinein medical malpractice actions refers to“the injury sustained by a patient whosemedical providers negligently deprivedthe patient of a chance to survive or re-cover from a health problem, or wherethe malpractice lessened the effectivenessof treatment or increased the risk of anunfavorable outcome to the patient.”2

Legally and clinically, the patient is

Don’t Raise Your Hand –Put it on the PatientDennis J. Dowling

deprived of a chance for successful treat-ment. That decreased chance for success-ful treatment more likely than not resultedfrom the doctor’s negligence. In otherwords, the doctor could have done some-thing and did not. Please remember thaterrors can be ones of commission, wheresomething adversely is performed, andof omission, where something could or

should have been done but was not. Adoctor who fails to do therapeutic inter-ventions for which he or she has beentrained is depriving the patient of thegreatest chance to recover. Worse yetwould be if it was not only neglected, butknowingly withheld.

Now that these definitions of legalityhave been explained, I will ask the ques-tion again: “How many of you will com-mit malpractice”? There is a subtletythere. I asked the first time “How manyof you wish to commit malpractice in thefuture”? Now, I am asking the questionto determine how many of you think thatyou will commit malpractice. You maynot even realize that your future behav-ior may be considered malpractice. Donot worry, I am still asking a rhetoricalquestion. I do not expect any of you toraise your hands. We do know that intoday’s litigious American society that itis likely that for every three of you, onewill be sued. Being sued does not meanthat malpractice has been committed.That is not my question. My question ismore in regards to determining the fact

that by your actions, or, more to the point,inactions, patients will suffer becausethey have not been given optimal treat-ment. Some will suffer because they losta chance to get better or survive. It willbe your responsibility as an osteopathicphysician to assist them and failure to doso may place them at a critical disadvan-tage. I am interested in determining yourdesire to provide the best for your pa-tients. No matter which stage of training,we have all made the commitment to be-come practitioners of the osteopathicmedical profession. That means morethan getting a degree; it is a responsibil-ity that must be undertaken with eyeswide open. When I took the OsteopathicOath I swore to “be mindful always ofmy great responsibility to preserve thehealth and life of patients; to retain theirconfidence and respect, both as a physi-cian and a friend, who will guard theirsecrets with scrupulous honor and fidel-ity; to perform faithfully my professionalduties; and to employ only those recog-nized methods of treatment consistentwith good judgment and with my skilland ability, keeping in mind alwaysnature’s laws and the body’s inherent ca-pacity for recovery.” This is the oathtaken by all graduates of osteopathicmedical schools.

There are those who say that osteo-pathic manipulative medicine is un-proven. They will include, the health in-surance industry, hospital organizations,the community and unfortunately, evenyour colleagues and teachers, DOs aswell as MDs. If you are one of them, thenthe course in osteopathic manipulativemedicine will only be an obstacle tohurdle. That is sad. If you believe inOMM, then you will be put into the un-

2004 Scott Memorial Lecture

“How manyof you will commit

malpractice?”


enviable position of nearly constantly de-fending its effectiveness. We no longerappear to need to defend ourselves asphysicians in the arena of medicine, butmust do so in regards to our unique as-pects. What is it that others feel needs tobe proven? It is as if the standard of whatelse is being done in the name of medi-cine has been thoroughly proven. At onetime, the then U.S. Office of TechnologyAssessment (OTA) reported that, “Only10 to 20 percent of all procedures cur-rently used in medical practice have beenshown to be efficacious by controlledtrial.”3 However, osteopathic manipula-tion has been studied. Much of it was instep with the principles of statisticalanalysis of the time. We must rememberthat the practice of osteopathy beyond asingle practitioner is only 112 years oldand the use of single- and double-blindstudies is only a half-century old. Theterm “evidence-based medicine” is beingused frequently nowadays, and that is agood thing. We should control the careof patients in a way that has been dem-onstrated to cause no harm and, hope-fully, help. However, evidence-basedmedicine is best suited for pharmaceuti-cal studies and less so to other types ofcare and intervention. Evidenced-basedapproaches are actually a study of stud-ies. We hope that everything that we dofor the benefit of the patients actuallybenefits them.4 Any medication, surgery,and any other intervention, includingmanipulation, can help or injure. A col-league, Kenneth Johnson, DO uses aquote that “all treatments cause harm;some cause good.” Our goal is to maxi-mize and apply the good as much as pos-sible. Despite being used by students andothers with little experience, there arevery few instances where the applicationof OMT has caused any irreversible side-effects.

When compared to 20 years ago, thereare nearly twice as many osteopathicschools, three times as many graduates,and very few osteopathic hospitals. Ourgraduates are spending the large major-ity of time in their undergraduate andpost-graduate training in hospitals wherethere is little or no supervision for theapplication of osteopathy. However, theuse of OMT and the application of os-teopathic principles and practice are re-lated to ongoing learning of OMT after

graduation, continued interest during in-ternship and residency, and emphasisplaced upon these by the training institu-tions.5 Yet the evidence is mounting thatthe osteopathic approach is not only safe,but effective. If you as a physician coulddo something simple and decrease theneed for intravenous antibiotics, decreasehospital stays by days and makes it pos-sible for patients to go home days earlierthan they would have otherwise, wouldyou not do it? Hospitals are no places forsick people. That sounds like a contra-diction, but it is a sad ironic recognitionthat even in modern days, hospitals aredangerous places for the very people theyare designed to serve. It is a fact withwhich you will too soon be confronted.Medication and other errors as well asnosocomial (hospital-acquired) infec-tions are just a few of the dangers thatclaim the lives or injure tens of thousands

per year. A chance to be home, to get restat night or even during the day, to eat thefood that one chooses, to be more easilywith family and friends, and other ben-efits can be accrued by leaving the hos-pital. Anyone who has been in a hospitalknows that a hospital is one of the worstplaces to get rest. What could be done?There is good enough indication that os-teopathic approaches assists in earlierdischarge from the hospital setting witha concomitant decrease in medications.We have Dr. Noll, who is on faculty hereat KCOM to thank for this and severalother studies substantiating osteopathicmanipulative medicine.6,7 Another smallstudy of patients with pancreatitis showeda mean reduction of 3.5 days of hospitalstay with the treatment group receivingonly 10-20 minutes of an OMT standard-ized protocol.8 Think of the savings inmoney alone by multiplying this by each

day by approximately $1300-2500.9,10

Think of the lives saved.Would you spend a few minutes with

a patient and enhance his respiratory sta-tus? OMT has been compared favorablyto the use of incentive spirometry follow-ing surgery.11 Incentive spirometry is aplastic device given to patients, especiallypost-operatively, to use to increase theirability to breathe more deeply. They of-ten do not use them because it hurts. Thebiggest advantage is that patients can bepassive and receive OMT that facilitatesthe healing processes where they mayhave had difficulty in performing the in-centive spirometry. It all takes a few min-utes on the part of the osteopathic physi-cian. Patients with chronic asthma dem-onstrated measurements of both upperthoracic and lower thoracic forced respi-ratory excursion statistically increasedafter osteopathic manipulative proce-dures compared with sham procedures.12

A study done in the 1930s, the pre-anti-biotic era, demonstrated that hospitalizedchildren with bronchial pneumonia hadone third of the mortality rate of childrenin a non-osteopathic hospital with thesame condition. The hospitals werecounty facilities in similar types of com-munities in Los Angeles and New YorkCity respectively. It is also interesting tonote that the deaths from lobar pneumo-nia were equivalent. Think of the conse-quences: the children in Los Angeles whosurvived are quite possibly grandparentsnow all because they received osteopathicmanipulation.13 In a similar applicationof lymphatic pumping techniques, therewas at least 1/20th and as low as 1/40thof the reported mortality in those whowere treated by osteopathic physiciansduring the Spanish Flu pandemic of1917-18, depending on which article onereads.14,15 An estimated half a millionAmericans died directly or indirectlyfrom the flu those years. How many ofthose could have been saved had osteo-pathic approaches been the standard ofcare? A few hundred thousand, at least,may have lived. I know from an analysisof my own family that my grandfatherwas one of thirteen children, includinghis twin brother. Only three survived theflu, not the twin. Think of the toll on afamily to need to bury more than threequarters of their children within a year’stime. Had there been 20 times as many

…osteopathicapproaches assistsin earlier discharge

from the hospitalsetting with aconcomitantdecrease in

medications.


➻

osteopathic physicians as there actuallywere, perhaps the outcome would havebeen very much different.

If you needed to receive a vaccinationand were offered the opportunity to feelmore confident that you had greater im-munity earlier, wouldn’t you choose tobe in that group? It has been demonstratedthat there was greater immunity to themajority of the pneumococcal sub-sero-types in the OMT treated group versusthe untreated one16. Dr. Measel at theTexas College of Osteopathic Medicineperformed this study in the early ’80s.The researchers at the West VirginiaSchool of Osteopathic Medicine showedthat 50% of the OMT treated participantsin their study had what were consideredto be immune antibody levels after twoinoculations for hepatitis B as opposedto 16% of the control subjects. The meanantibody level, the innate immuno-pro-tecting armies of these individuals, re-mained higher for all 34 weeks of thefollowup but was statistically so for 25of the weeks of the study.17 Statistics is astrange tool. Years ago, my father-in-lawwas faced with the prospect of getting anangiogram. He did not have any realsymptoms and he was not sure that hewanted to take the risk. When he askedthem what were the chances of somethinggoing wrong, they answered 1/3000. Hisnext question was, “What number are youup to”? He understood their thinking, butI wonder if they understood his. Hewanted to be in the successful group orat least the group without complications.Would you not want to be in the groupwith the best chances.The current proto-col for exposure to Hepatitis B in a non-immunized person is to give an immedi-ate injection followed by another, onemonth later. Shouldn’t we be treating allof our patients with OMT following vac-cination for Hepatitis? Why isn’t it a stan-dard protocol to treat all patients present-ing for routine inoculation? These conceptschanged the way in which I practiced manyyears ago. Prior to this, I would have hadthe medical assistant give the injectionand I barely needed to do anything withthe patient. I subsequently offered treat-ment with OMT to all such patients. Yearsago, I had to coordinate immunization tohepatitis, measles, mumps, and rubellafor a whole class of osteopathic medicalstudents. There was a station where we

checked their records, another where wegave injections, and a third where theyperformed lymphatic pumping tech-niques to each other. I hope that in somesmall way, their chances of immunitywere assisted.

Eight years ago, my family bought adog, a Shetland sheepherder that wenamed Amy. As part of the purchase, wewere given two free visits to a veterinar-ian. It turned out that Amy had otitismedia, an inner ear infection. After show-ing me how to clean her ears, administerher pills, and put in eardrops, Dr. Z., theveterinarian, then proceeded to show mea procedure of mandible and cervicalstroking that was very familiar to me. Hewas performing the Galbreath techniquefor Eustachian tube and cervical lym-phatic drainage. He informed me that hewas taught to do so in veterinarian schoolmany years before. Perhaps, they evolved

the technique independently or someoneyears ago learned it from an osteopathicphysician. Is it not strange that our petsreceive a standard treatment but our typi-cal patients do not? Miriam Mills, MDstudied osteopathic manipulative treat-ment in children with otitis media. Sheand her colleagues demonstrated that thetreated group had significantly lower in-cidence in almost all components: fewerepisodes of acute otitis media, fewer sur-gical procedures, great number of meansurgery-free months, and the relative ab-sence of hearing changes. The resultswere published in the Archives of Pedi-atrics and Adolescent Medicine18. Otherosteopathic sources have discussed theseadvantages for decades. You also shouldconsider that the American Pediatric As-sociation, the New York Health Depart-ment, and many other entities are highly

recommending that antibiotics not beused in children who have otitis media.The indications for use of antibiotics havenarrowed tremendously. The concern isthat frequent antibiotic exposure resultsin resistance and super-infections. Fordecades, doctors would try to mollifyparents and children by giving antibiot-ics. The most dangerous and destructivebacteria have been quite effectively pre-vented by the HIB vaccine. The prescrip-tion pad will more likely do harm andnot good by indiscriminate prescribing.What are the other alternatives? Childrenare uncomfortable and parents are dis-tressed by having to watch helplessly asthey suffer. The placement of myringo-tomy tubes to drain fluids has been un-successful in so many cases. What elsedo you have to offer the patient, or ratherthe anxious patient’s mother and father?Quite simply, you could use those instru-ments at the end of your arms to facili-tate the patient in finding health. You willwant studies to back up your use and theywill be coming. The Osteopathic Re-search Center is in the process of secur-ing funding for larger studies in this andother areas. However, you do not need toand should not wait for studies whenclinical practice has been demonstratedto help. Because of this, the use of osteo-pathic manipulative medicine should bethe standard of care.

We can go on and on with “evidence”.The literature is available. Standard medi-cal care combined with OMT was foundto be more efficacious in patients withfibromyalgia.19 It has enhanced the abil-ity of patients with Parkinson’s diseaseto move more easily as demonstrated byour study and work at the New York Col-lege of Osteopathic Medicine years ago.20

There are some clear and simple studiesindicating the effectiveness with low backpain.21,22 For any more proof, you haveonly to walk through the halls outside thisroom and read the poster presentationsof osteopathic research conducted hereat KCOM.

There will be people who say thatthere is no evidence that OMT is benefi-cial yet they will not have evidence thatit is not. By listening to them and with-holding treatment, you will be robbingthe patients who trust you of a chance tobenefit. As a graduate of an osteopathic

“What else do you have tooffer the patient, or rather

the anxious patient’s motherand father? Quite simply,

you could use thoseinstruments at the end ofyour arms to facilitate thepatient in finding health.”


medical school your training is equiva-lent to that of the other nearly three thou-sand new osteopathic physicians gradu-ating every year. To not incorporate os-teopathic principles and OMT into thecommon practice is to leave the dooropen for the “loss of chance” doctrine tobe employedwhen a patientcould have beenhelped. In yourfuture careers,you, and all DOsshould be held toa standard of carein which OMT isthe norm, the ex-pected, and thenecessary. Willfailure to useOMT be grounds for malpractice as somehave suggested? 23 I do not know that,but I do feel that we need to meet theneeds of our patients. The excuse thatthere is not enough time, desire, or recallof how to do treatment with osteopathicmanipulation is downright lame. It is notonly that, it is negligent. I find it incred-ible that students would admit to an at-tending physician that they forgot howto do OMT, when there is practically noother diagnostic or therapeutic skill thatthey had performed even once where theywould admit to a lack of ability. If theyhave seen and helped with doing a pro-cedure, you can be certain that they wouldwant the opportunity to do it themselves.The fact that osteopathic students andphysicians claim to forget gives an indi-cation that they had not put enough em-phasis on these aspects in the first place.It indicates that the individuals main-tained the practices that they used as col-lege students of earlier times; binge andpurge. One would learn what was re-quired for an exam and forget it soon af-terwards. Despite the overwhelming sub-stance of what you must learn to be agraduate of an osteopathic medicalschool, you must continue learning tolearn, retain any skills and knowledge thatwill help your patients survive and thrive,and be the best osteopathic physician thatyou can be. In order to diagnose the pa-tient correctly give the correct and thor-ough treatment then the most logical andappropriate approach would be the osteo-pathic one, including osteopathic ma-

nipulation. That should be the standardof care. There may come a time whenthose who do oversight might enforce it.Manipulation is already considered a firstline intervention for low back pain. Theremay come a time when the literature thatwe as a profession have been producing

to document and substantiate our unique-ness will be used to also demonstrate thatwe have not been holding to our ownstandard of care.

From personal experience, I havenever been disappointed in the advan-tages of my training. On my first rota-tion in a hospital as a third-year osteo-pathic medical student, I rounded thefloors with five MDs: an attending phy-sician, a third-year resident, a second-year resident, and two first-year internalmedicine residents. Even though they hadnever had experience with an osteopathof any type, they accepted me. I workedhard to make their jobs easier by doingeverything that was asked of me andmore. One day, we came to one of the in-patient service patients who had beenadmitted the day before for intensiveworkup and treatment of an intractableheadache. He had had this headache foreight weeks and they had done all pos-sible lab work, angiograms, EEGs, andCT scans. They had even shipped him byambulance to the one hospital in NewYork City that had a new MRI machine.Yes, those were days of archaic practice;there was only one MRI machine in allof New York City. Now, they are almostas common as pizza parlors. The physi-cians at our hospital were even going todo a temporal artery biopsy despite thefact that there was no other evidence toindicate doing this procedure. After ex-amining the patient, the others had ex-pressed their frustration in dealing withthe patient’s condition. I asked if I could

examine the patient and treat him. Theresidents were shocked but the attendingphysician stated that he did not knowwhat it was that I would do differently. Iexplained it to Dr. R., the attending, andhe agreed that I could do so after rounds.An hour later, I pulled the curtain around

Charlie’s bedand examinedhim. With nomore trainingthan one wouldhave after twoyears of educa-tion here atKCOM or anyother osteopathicmedical school, Itreated him withosteopathic ma-

nipulative medicine. He gave a gasp andthen a sigh 30 minutes into the treatment.I asked him to describe what it was thathe had felt. He stated that his headachewas gone for the first time in two months.It was all that I could do to keep him fromjumping out of bed. He got out anywayand went to the nurses’ station where hetold the residents and the nurses that Ihad “cured” his headache. When the at-tending heard, he called me to his office.The residents accused me of having somebrass body parts and advised that I shouldbe afraid since Dr. R. was the most fearedattending in the hospital. When I subse-quently met with him, Dr. R. asked whatI had actually done. We talked for awhileand he asked if I could treat the patientsin the Respiratory Intensive Care Unit.He was so pleased with the results that Iwas to go to the RICU every day and hewould include an order on all patients.Two years later, I rotated through thehospital again, this time on a Pulmonaryrotation, Dr. R.’s specialty. I met up withDr. R. the first day while he was doingRICU rounds. He did not immediately ac-knowledge my presence. As we finished,he told the crew that he was taking hisgeriatric boards the next day. This was aphysician who was already board certi-fied in internal medicine, pulmonarymedicine, critical care medicine, andemergency medicine. I asked him severalquestions about geriatrics and everyonelooked at me strangely. Remember, hewas still the “most feared Attending inthe hospital.” He said that I was to meet

“Despite the overwhelming substance of what you must learnto be a graduate of an osteopathic medical school,

you must continue learning to learn, retain any skills andknowledge that will help your patients survive and thrive,and be the best osteopathic physician that you can be.”


with him personally when he came backtwo days later. When we met, he told methat 8 out of 10 questions that I askedhim were on the geriatric boards. I wasto continue to treat all of the RICU pa-tients and anyone else whom he referred.Not only that, I met Charlie again in theoutpatient clinic when he brought his sonin for treatment of asthma. He was sothrilled and told everyone about our ex-perience and insisted that I alone treat hisson. This story does not end there. Yearslater when I was on the faculty at the NewYork College of Osteopathic Medicine,one of the students was in the clinic andasked if I remembered Dr. R. because myname came up one time when they wereon rounds. I asked the student how thathappened. He said that Dr. R. had askedthe osteopathic students to treat his pa-tients. When they informed him that theydid not know how, he proceeded to yellat them at length and stated that they werestupid and that he knew that at least I hadbeen able to treat his patients with OMT.I do not know if you will necessarily havea Dr. R. to berate you into doing OMT, butmaybe you should. Perhaps, like JiminyCricket, there should be some voice in yourhead urging you to do the right thing foryour patients.

Osteopathy is based on the principlesfirst presented by Andrew Taylor Still,MD and refined by others: The person isa whole; structure and function are inter-related as are abnormal structure and ab-normal function; disease occurs when theindividual is overwhelmed or under-pre-pared; the person has a unique ability torepair, defend, compensate and adapt; andthe physician is a facilitator who utilizesthese principles to assist the patients infinding health. Any physician should bepracticing in this manner. However, youhave and will be given an advantage; theability to use your hands and mind to di-agnose and treat. Many medical text-books decry the fact that palpation as atool is a lost art. Secondly, the directeduse of one’s hands to effect a change in apatient’s condition is a method that goesback thousands of years and throughoutmany cultures. In today’s medical prac-tice, it too has fallen by the wayside, withthe apparent exception of the osteopathicprofession. The tradition has been passeddown for 11 decades to us and is in dan-ger of dying despite the fact that medical

science is catching up. Too many ofour graduates take what they feel iseither the quick or “approved way” topatient care. With the acceptance intothe non-osteopathic theater has comemimicry. Many graduates of osteo-pathic medical schools claim more andmore that there is no difference in themedicine that they practice and thatpracticed by MDs. I do not doubt thatone can be a good osteopath and notdo manipulation if one applies theprinciples. I also know that many MDsare excellent physicians giving the bestcare possible for their patients. How-ever, I feel that one can not be a wholeosteopathic physician without inte-grating the knowledge and working tomaximize the patient’s abilities. Os-teopathic manipulative medicine al-lows us to do this. Yet, in a survey,somewhere in the neighborhood of50% of the responders stated that theytreated less than 5% of there patientswith OMT.24 Between 64% and 73%of osteopathic medical students haveresponded to surveys and reported theyhad few opportunities to use theseskills during clinical rotations. Mostheld some belief that they would usepalpatory diagnosis and OMT forfewer than 25% of their future patientsand then primarily for patients withmusculoskeletal complaints.25 Whyare the numbers not higher? Again,there is little opportunity and unlessyou and they make the commitmentto use it regularly or even look for in-stances that you would not otherwisethink of doing so, you will be givingyour patients less than optimal treat-ment. You and the people you willswear to protect will both have lostchances. For them it could be a matterof life and death. There may conse-quences for you as well.

When an Olympic skater is able tocompete after a severe laceration to histhigh without the use of medication,when patients can leave the hospitalsooner than their age-matched peers,when students are 30% more likely tobe immune following vaccination forhepatitis sooner than their peers, whenchildren with otitis media suffer fewerinstances of hearing loss and need lessantibiotics, and when patients withParkinson’s disease can move their

arms, legs, and head significantly better fol-lowing even just a single treatment withOMT, then there is more than proof enoughthat osteopathy works. In fact, many of theinterventions used are those taught withinthe first two years of the curriculum you asstudents are about to receive. Also, the re-search studies used protocols that were stan-dardized. The actual clinical application ofosteopathic manipulation is individualizedto the patient, as should all medical inter-ventions. That is part of the “Art of Medi-cine.”

When people tell me that the use of OMTis unnecessary and unproven, I frequentlywill reverse the situation and ask them toprove some aspect of their practice that iscommonplace. Over the years, I have heardso many directives that did or did not makesense. There are a million factoids and medi-cal practice has evolved. In my relativelyshort time of practice, I have seen the ACLSprotocols go through several changes and ithas not been all due to the development ofnewer medications. I have seen rapid cool-ing of patients with fever by alcohol and icebaths be replaced with tepid sponge baths.One of my professors, an MD specializingin pediatrics has often said that 75% of whathe had learned in medical school was wrong.My mentor, Dr. Schiowitz, replied that hemight not know which of the 75% was in-correct. Sometimes other physicians haverealized that in many instances the body’sown temperature variances were a goodthing and impaired the invaders’ own repli-cation system. I have seen physicians write“what if” orders to keep them, the physi-cian, from being disturbed. One of the mosttypical is the acetaminophen or ibuprofenorder for temperatures of a certain level.Rather than calling the physician, the nursegives the medication when the criterion isreached. Doctors as well as moms fed coldsand starved fevers. This may have mixedmeaning, but there is a physician in NewEngland who has “I fed fevers” on his cem-etery headstone. He was supporting his pa-tients by doing so in the face of overwhelm-ing “typical” medical practice for the nine-teenth century. He rebelled and did what hefelt was right. He showed a little piece ofartful practice in the face the incorrect ma-jority. Yet, a country physician from thebackwoods described that the physicianshould not get in the way of the patient’sown healing processes. We have not gottentoo far from the personal practices of Dr.


Still by coming around full circle to real-ize how correct he was in his thinking.

This lecture is named and is inmemory of John Herbert Bryce Scott, DOand Katherine Fraser MacLeod Scott,DO, graduates of this school in 1906 and1905 respectively. They practiced for 50years in Columbus, Ohio and taught inthe tradition of Andrew Taylor Still.26

When these doctors had practiced, therewere no specialists to speak of. Psychia-try was a branch of Neurology, the x-raymachine was barely a decade old, and theelectrocardiogram was a theory. Nowa-days, the numbers of specialties and sub-specialties have proliferated. We do needspecialists; those practitioners who aresmarter and better in some areas ofknowledge and who focus more intentlyand intensively upon the details. How-ever, I think that when we have a cardi-ologist treating chest wall pain withcounterstrain; when a pulmonologist re-quires that diaphragmatic and rib motionbe addressed in her patients with respi-ratory difficulties, when the internist re-duces edema in patients with lymphatictechniques, and the neurologist sees to itthat patients with parkinsonism or mul-tiple sclerosis are treated to maximizetheir musculoskeletal activities, then wewill be approaching the ideal of the prac-tice of osteopathic medicine. All gradu-ates of osteopathic medical schools mustdirect their attention to the full practiceof osteopathy. There is a mistaken beliefthat this requires a great deal of time.Actually, each treatment could last a fewminutes. According to Dr. Still, “Oste-opathy means a studious application ofthe best mental talents at the commandof the man or woman that would hold aplace in the profession.”27 We can allhonor him and the Drs. Scott by continu-ing their work. The osteopathic approachshould be the standard of care wherebyall patients are given the optimal chanceto heal, live, and return to their optimalconditions. We have to discard the choicethat we can not afford to spend the timeand energy to perform osteopathic ma-nipulative medicine. Those who state thatthey do not have time are not practicing avocation but are practicing business. Truth-fully, how can we afford not to use it? Thatis patient centered and necessary. A fewminutes spent assisting the patient can haveexponential benefits.

What can you do? You are being givenan exceptional opportunity to learnunique skills. Pay attention. Practice.Require that your educational experi-ences be expanded in opportunities, time,efforts, and assistance. The more that youhave, the more that you will be able tocontribute. Ask for opportunities. Learnas many skills as you possibly can andpractice so that you will be prepared.There has to be a paradigm switch; thedetermination that osteopathic graduateswill only become interested if they are atan institution that encourages them is notworking. Almost all of the colleges of os-teopathic medicine do a fine job in teach-ing osteopathic manipulative medicine inthe first few years. However, they haveless control over what occurs in the clini-cal rotations and the post-graduate train-ing. Many of the schools have tried andthere has been disappointing failure indoing so. Osteopathic students, interns,and residents must look for the opportu-nity and demonstrate osteopathic ma-nipulative medicine. You must take theresponsibility. By being determined andmaking your own attempts, you will beable to give your patients a better chancerather than depriving them of such. Putyour hands on the patient and try. Youmay be surprised. You most certainly willbe reinforced by the results. That is anexperiment worth trying.

I would like to thank PresidentMcGovern, Dean Slocum, the board oftrustees of Andrew Taylor Still Univer-sity of Health Science, the faculty of theKirksville College of Osteopathic Medi-cine, the members of the American Acad-emy of Osteopathy for their selection ofme for the honor and privilege of this lec-ture opportunity. Thank you for your at-tention and consideration as well. It hasbeen an honor to have this opportunityto address you.

References:1. Merriam-Webster on-line - http://

www.merriam-webster.com/cgi-bin/dictionary?va=malpractice

2. Legal database.com - http://www.legal-database.com/medical-malpractice.htm

3. Tunis SR and Gelband H. Health CareTechnology and Its Assessment in EightCountries. Health Care Technology inthe United States. Office of TechnologyAssessment (OTA). 1995.

4. Hampton, JR. Evidence-based medicine,opinion-based medicine, and real-worldmedicine. Perspectives in Biology andMedicine. Autumn 2002. 45:4:549-68.

5. Fry LJ. Preliminary findings on the useof osteopathic manipulative treatment byosteopathic physicians. JAOA. Feb 1996.96:91.

6. Noll DR, Shores JH, Gamber RG,Herron KM, and Swift, J Jr. Benefits ofosteopathic manipulative treatment forhospitalized elderly patients with pneu-monia. JAOA. Dec 2000. 100:776-782.

7. Noll DR, Shores J, Bryman PN, andMasterson EV. Adjunctive osteopathicmanipulative treatment in the elderlyhospitalized with pneumonia: a pilotstudy. JAOA. Mar 1999. 99:143.

8. Radjieski JM, Lumley MA, and CantieriMS. Effect of osteopathic manipulativetreatment of length of stay for pancre-atitis: a randomized pilot study. JAOA.May 1998. 98:264.

9. http://www.fguide.org/Update/7_6u.htm10. http://64.233.161.104/search?q=cache:

M_xhjC6Vn6YJ:www.whitehouse.gov/omb/fedreg/tortfinal.pdf+hospital+stay+cost+per+day&hl=en&ie=UTF-8

11. Sleszynski SL and Kelso A. Comparisonof thoracic manipulation with incentivespirometry in preventing postoperativeatelectasis. JAOA. 1993. 93:834-845.

12. Bockenhauer SE, Julliard KN, Lo KS,Huang E, and Sheth AM. Quantifiableeffects of osteopathic manipulative tech-niques on patients with chronic asthma.JAOA. Jul 2002. 102:371-375.

13. Watson JO and Percival EN. Pneumo-nia research in children at Los AngelesCounty Hospital. JAOA. 39:3:153-159.

14. Smith RK. One hundred thousand casesof influenza with a death rate of one-for-tieth of that officially reported underconventional medical treatment. JAOA.1920. 20:172-175. Reprinted in: JAOA.2000. 100:320-323.

15. D’Alonzo GE, Jr. Influenza Epidemicor Pandemic? Time to Roll Up Sleeves,Vaccinate Patients, and Hone Osteo-pathic Manipulative Skills. JAOA. Sep2004. 104:370-371.

16. Measel JW, Jr. The effect of the lym-phatic pump on the immune response: I.Preliminary studies on the antibody re-sponse to pneumococcal polysaccharideassayed by bacterial agglutination andpassive hemagglutination. JAOA. Sep1982. 82:28.

17. Jackson KM, Steele TF, Dugan EP,Kukulka G, Blue W, and Roberts A. Ef-fect of lymphatic and splenic pump tech-niques on the antibody response to hepa-


titis B vaccine: a pilot study. JAOA. Mar1998. 98:155.

18. Mills MV, et al. The use of osteopathicmanipulative treatment as adjuvanttherapy in children with recurrent acuteotitis media, Archives of Pediatric andAdolescent Medicine. Sep 2003. 157:861-866.

19. Gamber RG, Shores JH, Russo DP,Jimenez C, and Rubin BR. Osteopathicmanipulative treatment in conjunctionwith medication relieves pain associatedwith fibromyalgia syndrome: results ofa randomized clinical pilot project.JAOA. Jun 2002. 102:321-325.

20. Wells MR, Giantinoto S, Dagate D,Areman RD, Fazzini EA, Dowling DJ,and Bosak A. Standard osteopathic ma-nipulative treatment acutely improvesgait performance in patients withParkinson’s disease, JAOA. 99:2:92-98.

21. Andersson GBJ, Lucente T, Davis AM,Kappler RE, Lipton JA, and LeurgansS. A Comparison of Osteopathic SpinalManipulation with Standard Care for Pa-tients with Low Back Pain. N Engl JMed. November 4, 1999. 341:19:1426-1431.

22. Licciardone JC, Stoll ST, Fulda KG,Russo DP, Siu J, Winn W, and Swift J,Jr. Osteopathic manipulative treatmentfor chronic low back pain: arqandomized controlled trial, Spine. Jul1, 2003. 28:13:1355-62.

23. Allen TW. Will failure to use OMT begrounds for malpractice? JAOA. May1997. 97:268.

24. Johnson SM and Kurtz ME. Osteopathicmanipulative treatment techniques pre-ferred by contemporary osteopathic phy-sicians. JAOA. May 2003. 103:219-224.

25. Chamberlain NR and Yates HA. A pro-spective study of osteopathic medical stu-dents’ attitudes toward use of osteopathicmanipulative treatment in caring for pa-tients. JAOA. Oct 2003. 103:470-478.

26. Walter GW. The First School of Osteo-pathic Medicine. The Thomas JeffersonUniversity Press. Kirksville, MO. 1992.p. 350.

27. Still AT. Early Osteopathy: in the Wordsof A.T. Still. Edited by Schnucker RV.The Thomas Jefferson University press.1991. Kirksville, MO. p. 342.

Address correspondence to:Dennis J. Dowling, DO, FAAOOMM Associates, PC575 Underhill Blvd., Suite 126Syosset, NY 11791Email: [email protected]

Errata: The references for the article, “Lymphatic Manipulative PumpResearch: A Brief Review of Literature” on pages 32-33 of the September2004 issue of the AAOJ by Sean McMillan, William T. Crow, Charlotte H.Greene was published without its references. Our apologies to the authors.Please find them listed below:

1. Smith RK. One hundred thousand casesof influenza with a death rate of one-for-tieth of that officially reported underconventional medical treatment. JAOA.Jan 1920. 19:172-175.

2. Still AT. Philosophy of Osteopathy.Kirksville, MO. A.T. Still. 1809. p. 108.

3. Amalfitano DM. The osteopathic tho-racic-lymphatic pump: A review of thehistorical literature. Journal of Osteo-pathic Medicine. Apr-May 1987. pp. 20-24.

4. Morey LW, Sr. The Morey lymphaticpump. JAOA. Mar 1971. 70:7:718-719.

5. Fagan CL. Lymph acceleration. The Os-teopathic Profession. Mar 1951. 18:6:46-47.

6. Young MD. Lymphatic pump speedsflow. The Osteopathic Profession. Nov1946. 14:2:8,10.

7. Good GW. Manipulative lymphatictherapy. The Osteopathic Profession. Oct1942. 10:1:10,59-60.

8. Dugan EP, Lemley WW, Roberts CA,Wager M, and Jackson KM. Effect oflymphatic pump techniques of the im-mune response to influenza vaccine.JAOA. Aug 2001. 101:8:472.

9. Jackson KN, Steele TF, Dugan EP,Kukulka G, Blue W, and Roberts A. Ef-fects of lymphatic and splenic pumptechniques of the antibody response tohepatitis B vaccine: a pilot study. JAOA.Mar 1998. 98:3:155-160.

10. Hampton D, Hultgren K, Goldstein J,Brutico A, Blackman C, Evans R, andMesina J. Basophilia occurs followinglymphatic pump techniques. JAOA. Jul1998. 98:7:391.

11. Mesina J, Hampton D, Evans R, ZieglerT, Mikeska C, Thomas K, and Ferretti J.Transient basophilia following the appli-cation of lymphatic pump techniques: apilot study. JAOA. Feb 1998. 98:2:91-94.

12. Cavanaugh SP. Application of osteo-pathic principles to a viral upper respi-ratory infection. AAOJ. Spring 1998.8:1:19-20.

13. Wright HL. Cystic Febrosis and a vic-tory for osteopathic methods: a case his-tory. AAOJ. Fall 1991. 1:3:11-12.

14. Allen TW and Pence TK. The use of thethoracic pump in treatment of lower res-piratory tract disease. JAOA. Dec 1967.67:4:408-411.

15. Jarski RW, Loniewski EG, Williams J,Bahu A, Shafinia S, Gibbs K, and MullerM. The effectiveness of osteopathic ma-nipulative treatment as complementarytherapy following surgery: A prospec-tive, match controlled outcome study.Alternative therapies in Health andMedicine. Sep 2000. 6:5:77-81.

16. Sleszynski SL and Kelso AF. Compari-son of thoracic manipulation with incen-tive spirometry in preventing postopera-tive atelectasis. JAOA. Aug 1993.93:8:834-838, 843-845.

17. Butler S, Carlton A, Carnell L, Kusel L,Timbury J, and Orrock P. Pregnancy –an osteopathic approach. AustralianJournal of Osteopathy. 1996. 7:2:17-24.

18. Anonymous: Intracranial hemorrhagefollowing obstetrical delivery. AAOYearbook. 1943. p. 87.

19. Sutton JB, Knouse CA, Heyman OG,and Chila AG. Thoracic lymphatic pump.JAOA. Jul 1998. 98:7:389.

20. Johnson MG. The intrinsic lymph pump:Progress and problems. Lymphology.1989. 22:116-122.

21. Oszewski WL, Engeset A. Intrinsic con-tractility of lymphatics in man. Prelimi-nary communication. Lymphology. 1979.12:81-84.

22. Dabney JM, Buehn MJ, and DobbinsDE. Constriction of lymphatics by cat-echolamines, carotid occlusion, or hem-orrhage. J Physiol. 1988. 255:(pt2):H514-H524.

23. Dery MA, Winterson BJ, and YonuschotG. The effect of lymphatic pump ma-nipulation in the healthy and the injuredrat. JAOA. 1998. 98:7:388.

24. Dery MA, Yonuschot G, and WintersonBJ. The effects of manually applied in-termittent pulsation pressure to rat ven-tral thorax on lymph transport.Lymphology. Jun 2000. 33:2:58-61.

25. Olszewski WL. Contractility patterns ofnormal and pathologically changed hu-man lymphatics. Annals of the New YorkAcademy of Science. 2002. 979:52-63.

26. Knott M, Tune JD, Stoll S, and DowneyHF. Lymphatic pump treatments increasethoracic duct flow. Osteopathic ResearchCenter News. Jun 2003. 1:2:4.

27. Degenhardt BF and Kuchera ML. Up-date on osteopathic medical concepts andthe lymphatic system. JAOA. Feb 1996.96:2:97-100.❒


AbstractAdhesive capsulitis may be linked to

the administration of protease inhibitorsused to treat the human immunodefi-ciency virus. One such case is presentedwhere left adhesive capsulitis was diag-nosed following an exhaustive workup.The etiology was presumed to stem fromadministration of protease inhibitors overone year prior to protect the patient fol-lowing a needle stick from an HIV-infectedsource. The adhesive capsulitis, which pre-sumably followed, was successfully treatedthrough the use of osteopathic manipula-tive medicine.

Presented is a case illustrating thetreatment of left adhesive capsulitis pre-sumably from unknown causes until a lit-erature search revealed a correlation be-tween the use of protease inhibitors andadhesive capsulitis.1-6 The case is remark-able for the lack of anatomic evidenceon imaging combined with the absolutereliability of the patient.

On 10 October 2000, the patient pre-sented in this case was seen by a physi-atrist. She was a 42-year-old active dutyfemale orthodontist complaining of leftshoulder adhesive capsulitis since May2000. She had been given medications

A Case Study of Left AdhesiveCapsulitis Presumably Resultingfrom Previous Treatment withProtease Inhibitors*James A. Lipton** and Michele Neil***

including celecoxib, ibubrofen, in-domethacin, and piroxicam without re-lief. Her worst pain was described as be-ing an 85 on a scale of 0-100. After pre-scribed treatment with medications herpain remained at a 15 out of 100 and atthe time of presentation 15 out of 100.The patient was searching for some mo-dality that would assist her in moving hershoulder. Patient was assessed and givendirections to continue indomethacin, toobtain an MRI of the left shoulder to ruleout a rotator cuff tear and was sent to thelab to obtain a CBC, ESR, and chemistrypanel.

An MRI (taken 9 November 2000),showed that the muscles and tendons ofthe rotator cuff demonstrated no evidenceof focal signal intensity abnormalities orevidence of rotator cuff rupture or tear.The subacromial subdeltoid bursa re-vealed no evidence of increased fluid ac-cumulation. The glenoid labrum and os-seous glenoid were normal in appearancewithout evidence of tear or fracture re-spectfully. There was no evidence ofintraarticular loose bodies or fracturefragments. The humeral head maintainednormal signal intensities and articularuniformity. The deltoid muscle in its ana-tomical acromial insertion appeared nor-mal. Acromioclavicular joint demon-

strated no evidence of abnormalities. Thelong head biceps tendon and its tendonsheath appeared normal. The impressionreported by the interpreting radiologistwas magnetic resonance imaging re-vealed an intact rotator cuff without tear.Normal appearance of the joint capsuleand synovial structures were also dem-onstrated.

The patient was followed up on 28November 2000 by the same physiatristand assessed as having an adhesivecapsulitis. She was prescribed rofecoxib25 mg taken by mouth once daily. Thenatural history of the disorder was dis-cussed and the patient was told to followup in two to three months.

On 1 February 2001, the patient hadher first visit with the author (also a phy-siatrist). The 42-year-old active duty fe-male was complaining of left shoulderpain with decreased range of motion sinceJune 2000, without injury. She had beenworked up and treated by a previous phy-siatrist as well as a general medical of-ficer and physician assistant. The work-ing diagnosis was adhesive capsulitis.The MRI of the left shoulder was nega-tive and ESR, Chem 17, and CBC werenormal. The past surgical history of thepatient was a C-section, tonsillectomy,and adenoidectomy. Past medical history

* “The opinions expressed in this article are those of the authors and do not reflect the official policy or position of the Department of theNavy, Department of Defense, or the United States Government.” “I am a military service member. This work was prepared as part of myofficial duties. Title 17 U.S.C. 105 provides that Copyright protection under this title is not available for any work of the United StatesGovernment. Title 17 U.S.C. 101 defines a United States Government work as a work prepared by a military service member or em-ployee of the United States Government as part of that person’s official duties”.

** Department of Orthopedics, Division of Physical Medicine and Rehabilitation, Naval Medical Center, Portsmouth, VA, 23708*** Oklahoma College of Osteopathic Medicine, Tulsa, OK, 74127

➻


was allegedly unremarkable according tothe patient. She was a gravida 4, para 3,ab 1. Her last menstrual period was aweek prior to her visit and normal. Herbreasts were normal and pap smears werenormal. Patient reported a history of mi-graine headaches. She was negative forhypertension, cancer, diabetes, and TB.She never smoked nor chewed tobacco.She was in bed by 2100, asleep by 2110and awake at 0500 for the day after hav-ing slept throughout the night. Her worstpain was assessed at 80 out of 100, aftermedication 50 out of 100, and at the timeof the interview 20 out of 100. Reviewof her family history revealed some ques-tion of arthritis in her mother and therewas also some question about whether ornot this was rheumatoid arthritis. She hadbeen to a chiropractor twice without re-lief. She had also undergone a left shoul-der arthrogram, which similarly wasnegative.

Physical exam revealed an extendedocciput, an atlantoaxial joint rotated leftand sidebent right, an elevated first ribon the right, a restricted left sternoclav-icular joint with decreased sternal motionand rib restrictions bilaterally (T-3through T-6). Pre-treatment (with 0MM)she was only able to achieve 90 degreesof abduction and post-treatment using avariety of soft tissue muscle energy, myo-fascial release, high velocity, low ampli-tude, cranial sacral, facilitated positionalrelease, and lymphatic pump techniques.Her post-treatment ability to abduct theleft shoulder was 120 degrees. Adhesivecapsulitis of the left shoulder with mul-tiple somatic dysfunctions were assessed.Obtained was an anti-nuclear antibody,rheumatoid factor, Denver panel, CK, abone scan, and an EMG (performed bythe author), as well as a followup re-evaluation. She was prescribed 0MMtreatments approximately two to threetimes per week until the end goal of fullrange of motion was achieved.

On 6 February 2001, the patient re-turned for her second OMM treatment.She had increased range of motion sincethe last visit, though she still felt tight.She had not received the results of herlabs or her bone scan as of yet. Thepre-treatment abduction was 90 degrees,versus post-treatment of 150 degrees withactive range of motion. Pre-treatmentwith passive range of motion, in abduc-

tion was 115 degrees. External rotationwas 0 degrees and post-treatment was 30degrees. It was noted that her left deltoidand supraspinatus were somewhat con-tracted and the assessment was that shehad improved, but it was necessary to ruleout a C5-6 involvement, perhaps with apossible herniated nucleus pulposus ormass. In addition, the rest of the differ-ential diagnosis was considered. The planwas to obtain her labs, bone scan, andEMG as directed. Also, an MRI of theneck and a chest x-ray (PA and lateral)were ordered.

On 8 February 2001, the patient fol-lowed up for Treatment #3. She said thatshe felt looser, less stiff. Thepre-treatment exam revealed she ab-ducted to 130 degrees, posttreatment 150degrees. She had improved and was di-rected to followup with her MRI, bonescan, and EMG.

On 13 February 2001, the patient un-derwent Treatment #4. She had abductedup to 160 degrees. She felt tight in herneck muscles and thought that she neededmore treatment. It agreed that treatmentfrequency should increase.

On 15 February 2001, after Treatment#5, she was able to abduct to 180 degrees.Her left biceps touched her left ear withher head in neutral position.

On 22 February 2001, treatment #6was administered. Patient was able toabduct her arm beyond 180 degrees.

On 27 February 2001, the patient re-turned for Treatment #7. Her bone scanshowed mild degenerative joint diseasein the left shoulder and mild degenera-tive joint disease in the thoracic spine.She was able to abduct to 180 degreesand the only remaining problem was flex-ion, which was only to 150 degrees whenlying on her back. Some tightness wasfelt in the pectoralis minor, and the cora-coclavicular ligament. Physical therapywas enlisted to assist with these areas.

On 1 March 2001, the patient returnedfor Treatment #8. She was able to abductto 180 degrees, and was 160 degrees inflexion. The teres minor insertion wastender on palpation as well as the deltoidinsertion. She was directed to keep work-ing and to obtain her c-spine MRI andEMG results.

On 5 March 2001, the patient returnedfor Treatment #9. She was able to abductto 180 degrees and flex to 170 degrees

with good release.On 8 March 2001, the patient returned

for Treatment #10. She was able to ab-duct 180 degrees and flex to 170 degrees.We again discussed with physical therapythe targeting of the areas of the pectora-lis minor tendon and coracoclavicularligament to maintain increased range ofmotion.

On 12 March 2001, the patient presentedfor an EMG. The EMG of the upper extrem-ity was performed by the author. The resultswere a normal study including examinationof the biceps, deltoid, triceps, trapezius,infraspinatus, supraspinatus, teres major,serratus anterior, paraspinal musculature,abductor pollicis brevis as well as addi-tional muscles. Nerve conduction studiesand EMG were normal.

On 14 March 2001, the patient re-turned and informed the author (jal) thatshe had been stuck by an HIV-infectedneedle and treated with protease inhibi-tors (stavudine, lamivudine, as nucleo-side analogs, and nelfinavir as a proteaseinhibitor) over one year prior. She hadforgotten to mention this and wonderedif it might be significant. The literaturewas searched and a cause and effect re-lationship was postulated.l-6 On 3 April2001, the patient returns for Treatment#11. Pre-treatment abduction was 160 de-grees, post-treatment was 180 degrees.Pre-treatment flexion was 110 and post-treatment was 170 degrees.

On 17 April 2001, Patient underwentTreatment #12. The use of facilitatedposition release resulted in progress. At thetime, there was a deficit of less than 15degrees of flexion in the supine positionwith arms over the head. The patient wasinstructed to return for her final treatment.

On 26 April 2001, the patient under-went Treatment #13. She was able to flexto 190 degrees and abduct to 190 degrees.At this point she was discharged fromPhysical Medicine and Rehabilitationwith directions to maintain range of mo-tion by using a pool for range of motionand flexibility.

DiscussionThe paucity of anatomic findings and

clues in the diagnostic workup were strik-ing compared to the patient’s frank mo-bility deficits. The clinical course of thistype of adhesive capsulitis is generallyself-limiting with appropriate treatment.


In this case, the etiology may have beensecondary to the use of protease inhibi-tor. Protease inhibitors had previouslybeen administered to the patient as treat-ment for an accidental needlestick. Thepatient was stuck with a needle from anHIV-infected host. She had been treatingover one year prior to the developmentof her adhesive capsulitis. The relation-ship, though circumstantial, is of someinterest in the literature, and as a result,was reported.

Bibiliography1. Grasland A, Ziza JM, Raguin G, Pouchot

J, and Vinceneux P. Adhesive capsulitisof shoulder and treatment with proteaseinhibitors in patients with human immu-nodeficiency virus infection: report of 8cases. J Rheumatol. 2000 Nov. 27:11:2642-6.

2. Peyriere H, Mauboussin JM, Rouanet I,Rouveroux P, Hillaire-Buys D, andBalmes P. Frozen shoulder in HIV pa-tients treated with indinavir: report ofthree cases. AIDS. 1999 Nov 12. 13:16:2305-6.

3. Kolb C, Mauch S, Krawinkel U, andSedlacek R. Related Articles Matrixmetalloproteinase-19 in capillary endot-helial cells: expression in acutely, but notin chronically, inflamed synovium. ExpCell Res. 1999 Jul 10. 250:1:122-30.

4. Leone J, Beguinot I, Dehlinger V,Jaussaud R, Rouger C, Strady C,Pennaforte JL, and Etienne JC. Adhesivecapsulitis of the shoulder induced by pro-tease inhibitor therapy. Three new cases.Rev Rhurn Engi Ed. 1998 Dec.65:12:800-1.

5. Pappalardo A, Pulizzi C, and Sossio M.Value and significance of the immuno-logic determination of various serumsialoglycoproteins in rheumatic diseasesof inflammatory nature. Minerva Med.1979 Sep 19. 70:39:2667-72.

6. Paque GR. Trials using a protein inhibi-tor in scapulo-humoral periarthritis. JBelge Rhumatol Med Phys. 1971Jul-Aug. 26:4:179-90. French.

Accepted for publication, July 2002.

Address Correspondence to:Cdr. James A. Lipton, MC, USNDept. of Orthopedics,Division of Physical Medicine andRehabiliationNaval Medical CenterPortsmouth, VA 23708

From the Archives – continued from page 9

ReflexSensitive points: Present if lesion is acute. May

spread into superficial muscles. Always presentin deep spinal muscles if the lesion is chronic.

Fatigue in back: Not present when there is pain.Functional capacity impaired: Probably is if lesion

is acute. Probably note if lesion is chronic.History: No injury to back.

TraumaticSensitive points: Present in deep muscles and

spreading to superficial muscles if lesion isacute. Present in deep tissues only if lesion ischronic.

Fatigue in back: Not present when there is pain.Functional capacity impaired: Seriously if lesion

is acute. Insidiously if lesion is chronic.History: Injury to back.

Objective Symptoms of the Spinal LesionRigidity in joint tissues: Very pronounced if lesion

is acute. Pronounced if lesion is chronic.

Malposition: Usually present.Lesion: Usually unilateral.Oedema: Pronounced if acute. Slight if chronicPerversion of movement: Cause by malposition and

tonic muscle shortening.Postural changes: Caused by bony maladjustment.Gait changes: Apparent

Rigidity in joint tissues: Noticeable in all musclesif lesion is acute. Noticeable in deep muscleonly if lesion is chronic.

Malposition: Usually none.Lesion: Usually bilateral.Oedema: Present if acute. Slight if chronic.Perversion of movement: Caused by tonic muscle

shortening.Postural changes: Caused by muscular tension.Gait Changes: Slight.

Subjective Symptoms of the Spinal LesionAcute

Tender points on palpation: Acute and easilyelicited.

Pain in joint: Acute.Fatigue in back: Present (not present when there

is pain).Functional capacity: Openly impaired.History of injury: Usually easily discovered.

ChronicTender points on palpation: Present but not easily

elicited.Pain in joint: Present but not acute.Fatigue in back: Present (not present if pain is

acute).Functional capacity: Insidiously impaired.History of injury: Often not easily discovered.

Objective Symptoms of the Spinal LesionOedema over facets: ConsiderablePerversion of joint movement: Present by test of

all tissues.Malposition of bony parts: Difficult to test for on

account of inflammation.Thickening of deep short muscles: Present and

oedematous-like.Postural stress: Apparent.Gait changes: Apparent.

Oedema over facets: Slight or absent.Perversion of joint movement: Present by test of

deep tissues.Malposition of bony parts: Present and easy to test

for, (not present in reflex lesion).Thickening of deep short muscles: Present and rope-

like.Postural stress: InsidiousGait changes: Insidious

Subjective Symptoms of the Spinal Lesion

Lesion Causes Disease Symptoms in Two PlacesThe Spinal lesion may cause disease either

(1) in the spine itself or (2) in tissue distant from the spine.

(1) In the spine itself. Patients present them-selves with the complaint in the spine. The spinallesion itself is the disability.

These patients have a disturbance in tissues re-mote from the spine, but a disease has not as yetmade itself apparent there.

The spinal lesion may be chronic, but usually itis acute – very often it is a chronic lesion with pro-nounced acute symptoms.

The lesion usually has been produced bytrauma, but reflex irritations may complicate it. Itmay be a purely reflex lesion.

(2) In tissue remote from the spine. Patientspresent themselves with the complaint in tissue re-mote from the spine.

These patients have spinal lesions, but they maynot be aware of them.

In chronic organic diseases the spinal lesionfound is chronic, but it may also show acute, reflexsymptoms in addition.

In fevers, acute, reflexly formed spinal lesionsare present. They may be at the site of chronic le-sions.

A reflexly formed spinal lesion is alwayspresent. A traumatic causative lesion is also fre-quently present.❒


AbstractUnexplained intermittent neurocar-

diogenic syncope in a 24-year-old patient,managed, but unresolved by chemicaltreatment, is treated osteopathically and re-solved. Description of this case and a briefdiscussion of questions raised addresses adeficit in the osteopathic literature.

Neurocardiogenic syncope is a con-dition in which cerebral metabolism istemporarily impaired by a reflex reduc-tion in blood pressure causing a decreasein cerebral blood flow and loss of con-sciousness.1 Recent investigations showthis to be a broad spectrum of autonomicdisorders variously triggered, all mani-festing with syncope, hypotension, andorthostatic intolerance.2 In cases of un-explained syncope, this diagnosis is madewith a positive tilt-table test.3 It is knownthat neurogenic syncope involves inter-play between an imbalanced autonomicnervous system and cardiovascular regu-lation.4 What is still unclear, is the exactmechanism causing this disorder.

Case ReportThe patient first presented in Febru-

ary 2001, age 24, with a seven-year his-tory of neurocardiogenic syncope, forwhich she was taking Disopyramide, asshe had since shortly after diagnosis.

A healthy-looking woman, she relatedthe beginnings of her problem in 1994,at age 18. At a roller-coaster ride at anamusement park, she would repeatedlyhit her head on the back of the seat andhad briefly blacked out, with residual lossof memory for parts of the ride. A weeklater while rollerblading, she would be-

Case Study:An Osteopathic Resolutionof a Neurocardiogenic SyncopeYvette Somoano and Stefan Hagopian

come lightheaded and dizzy; the first timethis had happened in years of active dailyexercise. Diagnosis resulted from a franksyncopal episode during the subsequentexam by her primary physician. Whiletaking deep inspirations during lung aus-cultation, she blacked out. On waking,confused, after a few seconds, she wasrushed to the hospital for observation.

Findings were not significant, with anormal CT, EKG, and EEG. While beingmonitored on telemetry, awaiting a lum-bar puncture, the patient experienced yetanother syncopal episode during which shewent into asystole for a few seconds. A tilt-table test was done; results were positive,with decreases in blood pressure and pulseleading to asystole (HR 86 to 113, BP 101-118/62-70, until syncope, when neither HRnor BP could be monitored).

Started on Lopressor, a beta-blocker,which after two weeks eventuated a simi-lar positive result on the tilt table (HR75-86; BP 85-111/57-70), the patient wasswitched to Disopyramide, a sodiumchannel blocker. After two more weeks,a tilt-table test proved negative for 15minutes (HR 61-120; BP 62-136/32-81);an Isoproterenol challenge producednegative results (HR 120-152, BP 73-146/40-89). Within a few months, thepatient’s Disopyramide dosage was re-duced from 300mg BID to 300mg QAMand 150mg QHS, and the patient re-mained stable on this dose for seven yearsduring which only three events sugges-tive of syncope occurred. Twice she ex-perienced tachycardia secondary to de-hydration – quickly resolved with intra-venous fluids – and once, prodrome tosyncope during a neck massage. In one

episode the patient had been supine, notupright as is commonly described in theliterature.

On this day, in addition to her historyof syncope, the patient complained ofchronic upper back pain on the left side.

Birth/Childhood HistoryThe patient had been born at 42 weeks

of gestation after being “engaged” forover a month. As an infant, she wouldhad emesis with every meal.

Past Medical/Surgical/Trauma History

Nine months prior to first noted syn-copal episode, the patient had sustainedthoracic strain injuries in an MVA; nosurgeries. Medical history insignificant,except as above noted.

Initial Physical Exam/Osteopathic Findings

The physical exam was grossly nor-mal except for the following: an imbal-ance in the autonomic nervous system asindicated by diaphragm and thorax re-stricted in inhalation position; emotionaldistress regarding even the memory of anaborted lumbar puncture; and a slight butpalpable muscular hypertonicity. The pa-tient was also found to have compressionthrough the cranio-vertebral junction andmarkedly decreased thoracic kyphosis. Shehad restrictions in movement in segmentsC7-T3 and T11-L2 and at the sacroiliacjoint, and a decrease in the excursion ofher thoracic and pelvic diaphragms.


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Treatment and ResultsOsteopathic treatment was begun on

the initial visit by performing an EV4(phasic inverse of a cranial CV4); per-forming condylar decompression; andbalancing ligamentous tension through-out the lower cervical and upper thoracicregions, as well as the thoraco-lumbarjunction and sacroiliac joints. Post-treat-ment, over the next month the patient

experienced no syncopal episodes andfelt fine.

On a second visit, the strain pattern inthe patient’s upper thoracic region wasstill present, but this time resolved withthe use of respiratory cooperation duringosteopathic treatment. A compression ofthe right occipital-mastoid suture wasfound and treated by balancing the duralmembranous tension in the region.

During a third visit, the patient wastreated similarly, and was newly foundto be expressing a marked restriction inthe region of the right middle face. Bynow, the strain patterns in the upper tho-racic region had improved, but side ef-fects of medication were increasing. Thepatient’s cardiologist suggested she stoptaking Disopyramide and return for test-ing in a week.

Figure 1. Heart Rate during tilt-table test without Isoproterenol Challenge.

Figure 2. Heart rate during tilt-table with Isoproterenol Challenge on 10/11/94 and 1/13/98,and without Isoproterenol Challenge on 8/28/01

Heart Rate During Tilt Table Test

Heart Rate During Tilt Table Test

➻


Eight days later, tilted for 30 minutesat 65 degrees [HR 103-146, BP 112-155/46-103], the patient experienced no syn-cope nor near syncopal episodes. The testwas negative, even though she was anx-ious, even tachycardic (figure 1). Herheart rate reached levels comparable tothose previously experienced only whenstimulated by Isoproterenol (figure 2).The patient was symptom-free. The car-diologist discontinued the medication. Tothis day, 26 months later, the patient hasexperienced no further episodes. She tol-erates a full range of activities and con-tinues to be monitored and supported withosteopathic treatment approximatelyquarterly.

DiscussionWhat caused this patient’s

neurocardiogenic syncope, what trig-gered the episodes and how was the con-dition resolved?

A complex series of imbalances oc-curring over a period of many years,probably resulted from or compensatedfor injuries to the cranial base and upperthorax. Such injuries can have occurredin the process of birth and in early child-hood through falls and maladaptive pos-tural patterns. These imbalances can cre-ate a chronic neurocardiologic instability.Several texts note that syncope can be aresponse to strong emotions, stress, pain,fear, fatigue, hunger or thirst, over-crowded or humid environments, CO

2/0

2

imbalance, medications, exercise or evenprolonged standing.5,6 This patient hadindicated deep breathing during lung aus-cultation, exercise, stress, and dehydra-tion as triggers at various points in herhistory.

In this case, autonomic imbalance re-solved with the decompression of the cra-nial base and a release with restorationof the originally flattened kyphotic curvein the upper thoracic region. Treatmentresults suggest as cause, some physicalinterference with the nerves in these ar-eas, which may have developed second-ary to birth trauma. Support for thistheory is found in the patient’s history ofinfantile emesis. Such emesis is docu-mented in infants with strain patterns atthe cranial base,7 where the vagus nerveexits the cranium through the jugular fo-ramen, which lies between the occiput

and the temporal bone.As for the thoracic restrictions, al-

though they may have originated frompostural adaptations to emotional stress(decreased kyphosis), they may havebeen exacerbated by the patient’s inju-ries, such as the unresolved upper tho-racic injury from an MVA. And, thoughrelatively minor, the multiple blows to thehead during the amusement park ride can-not be discounted.

An exact mechanism for neuro-cardio-genic syncope is still unknown. The cur-rent literature suggests that central hypo-volemia sparked by venous pooling whilein an upright posture, causes a decreasein atrial pressure.8 A reflex tachycardiastimulates C-fibers (atrial and ventricu-lar afferent stretch receptors) within themyocardium. A consequent afferenttransmission is sent to the vagal nucleiof the brainstem, mimicking hyperten-sion, causing a decrease in sympatheticactivity, bradycardia and hypotension,classically known as Bezold-Jarisch re-flex.9 This theory is controversial: stud-ies show that syncope can occur evenwith sudden volume depletion in animalswho have surgically denervated hearts.9

Osteopathic and other research showsthat the autonomic imbalance in syncopecan be caused by a mechanical impinge-ment or irritation of the nervous system,either peripherally or centrally. Such dis-ruption may occur with inflammation,nerve or vaso-neural compression fromsurrounding anatomical structures, or asa response to chemical stimulation.10

Animal studies have shown that long-term impingement of nerves at the thirdor fourth thoracic level destabilizes thenervous system, leaving the subject un-able to compensate under the stress of,for example, central hypovolemia.11 Anda lesion of the atlas in rabbits producesvasodilation of the extremities and varia-tion of heart rate and rhythm—responsesseen with autonomic imbalance.12 Va-sodilation has long been thought to in-fluence the Bezold-Jarisch reflex.9 Thestructural impingement on these nervesis thought to cause a magnification of ef-ferent impulses that pass through thesesegments to the viscera, strongly affect-ing the tissue.13 The facilitation of the ner-vous system due to this structural im-pingement could be a cause of

neurocardiogenic syncope secondary tostress placed anywhere along the auto-nomic nervous system.

Other than osteopathic treatment,therapeutic approaches for neuro-cardio-genic syncope include general measuressuch as volume expansion; pharmaco-logic approaches; and even invasivemethods such as placement of a dual-chamber cardiac pacemaker.14 Experi-mentally, the simple measures of orthos-tatic training (standing against a wall)15

and tilt-table training,16 and maintainingproper hydration17 and CO

2/O

2 balance,18

show promise in improving orthostatictolerance and diminishing probability ofsome syncopal episodes. By far the mostcommon treatment choice, though, ispharmacologic.

Further research is essential to deter-mine a more precise mechanism, andrange of treatments, for neurocardiogenicsyncope. The theories noted in this casereport piece together a complex mecha-nism with both a cause and an effect, incases where autonomic imbalance is sec-ondary to somatic dysfunction.

A large portion of the population –28% in one study of 400 healthy youngadults19 – suffers from syncopal episodesof unknown causes. Surely many of thesepeople can be helped without the needfor chemical treatment, if the biophysicalcomponents are properly identified andaddressed, as they can with complete os-teopathic diagnosis and treatment.

AcknowledgementsThe authors gratefully acknowledge

assistance from Jacqueline Austin.

References1. Grubb BP. Pathophysiology and Differ-

ential Diagnosis of NeurocardiogenicSyncope. The American Journal of Car-diology. 1999. 84:3Q-9Q.

2. Grubb BP and Karas B. Clinical Disor-ders of the Autoimmune Nervous Sys-tem Associated with Orthostatic Intol-erance: An Overview of Classification.Clinical Evaluation and Management.Pacing Clinical Electrophysiology. May1999. 22:5:798-810.

3. Sutton R and Bloomfield DM. Indications,Methodology, and Classification of Re-sults of Tilt-Table Testing. American Jour-nal of Cardiology. 1999. 84:10Q-19Q.

4. Calkins H. Pharmacologic Approaches


The purpose of the quiz found on thenext page is to provide a convenientmeans of self-assessment for your read-ing of the scientific content in the ar-ticle, An Osteopathic Resolution ofNeurocardiogenic Syncope by YvetteSomoano, DO and Stefan Hagopian,DO.

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CME QUIZ

to Therapy for Vasovagal Syncope.American Journal of Cardiology. 1999.84:20Q-25Q.

5. Schnipper JL and Kapoor WN. Diagnos-tic Evaluation and Management of Pa-tients with Syncope. Medical Clinics ofNorth America. 2001. 85:423-456.

6. Bhandari AK. Electrophysiologic Test-ing: General Principles and Clinical Ap-plications. In Kloner RA (ed): The Guideto Cardiology, Third Edition. Greenwich,CT, Le Jacq Communications, Inc. 1995.165-182.

7. Frymann VM. Relation of Disturbancesof Craniosacral Mechanism to Symp-tomatology of the Newborn: Study of1,250 Infants. JAOA. 1966. 65:1059-175.

8. Grubb BP and Kosinski D. Syncope re-sulting from Autonomic InsufficiencySyndromes Associated with OrthostaticIntolerance. Medical Clinics of NorthAmerica. 2001; 85:457-472.

9. Grubb BP. Neurocardiogenic syncope. InGrubb BP, Olshansky B (eds): Syncope:Mechanisms and Management. Armonk,NY, Futura Publishing. 1998. 73-106.

10. Goehler LE, et al. Interleukin-1ß in Im-mune Cells of the Abdominal VagusNerve: a Link between the Immune andNervous System? The Journal of Neu-roscience. April 1, 1999. 19:7:2799-2806.

11. Burns L. Early Pathogenesis FollowingVertebral Strain. JAOA. Oct 1946.49:2:103.

12. Cole WV. The Osteopathic Lesion Com-plex, The Effects of the Atlas LesionAfter Six Months. JAOA. Apr 1948.47:399-406.

13. Korr IM. Somatic Dysfunction, Osteo-pathic Manipulative Treatment, and theNervous System: A Few Facts, SomeTheories, and Many Questions. JAOA.1986. 86:109-114.

14. Nair N, Padder FA, and Kantharia BK.Pathophysiology and Management ofNeurocardiogenic Syncope. AmericanJournal of Managed Care. April 9, 2003.4:327-34.

15. Abe H, Kondo S, Kohsi K, andNakashima Y. Usefulness of OrthostaticSelf-Training for the Prevention ofNeurocardiogenic Syncope. PacingClinical Electrophysiology. Oct 2002.25:10:1454-8.

16. Ector H, Reybrouck T, Heidbuchel H,Gewillig M, and Ven de Werf F. TiltTraining: A New Treatment for Recur-rent Neurocardiogenic Syncope and Se-vere Orthostatic Intolerance. PacingClinical Electrophysiology. Jan 1998.21:1 Pt 2:193-6.

17. Schroeder C, Bush VE, Norcliffe LJ,

Luft FC, Tank J, Jordan J, andHainsworth R. Water Drinking AcutelyImproves Orthostatic Tolerance inHealthy Subjects. Circulation. Nov 26,2002. 106:22:2806-11.

18. Blaber AP, Bondar RL, Moradshahi P,Serrador JM, and Hughson RL. Inspira-tory CO

2 Increases Orthostatic Tolerance

During Repeated Tilt. Aviation, Space,and Environmental Medicine. Nov 2001.72:11:985-991.

19. Silberstein TA and Cox MM. The Preva-lence of Syncope in a Population ofHealthy Young Adults. JAOA. 1996.96:8:485.

Accepted for publication, Sept. 2004

Adddress correspondence to:Yvette Somoano, DO7533 Cecilia St.Downey, CA 90241E-mail: [email protected]

or

Stefan Hagopian, DO1448 15th St., Suite 207Santa Monica, CA 90404Fax: 310/576-2501

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1. In this case study, neurocardiogenic insta-bility was thought to be caused by:

___A. Compression of the lower cervical regionfrom multiple whiplash injuries.

___B. Multiple falls during childhood causing com-pensation of L5 and the Sacrum.

___C. Birth trauma and maladaptive postural pat-terns causing compensation of the cranialbase and upper thorax.

___D. Birth trauma and multiple falls causing com-pression of the sacrum.

2. Autonomic imbalance triggering syncopymay be initiated by:

___A. Inflammation___B. Nerve or vaso-neural compression from sur-

rounding anatomical structures.___C. A response to chemical stimulation.___D. All of the Above

3. A lesion of the atlas in animal models hasbeen shown to cause:

___A. Vasoconstriction of the extremities.___B. Variation of heart rate with vasodilation

of the extremities.___C. Hypertension with vasoconstriction

of the extremities.___D. Autonomic balance with vasodilation

of the extremities.

4. Infantile emesis, noted in this patient, hasbeen previously documented in the literatureto be caused by strain patterns at the:

___A. Upper thorax.___B. Lower thorax involving the diaphragm___C. Lower cervical region.___D. Cranial Base.

5. It is thought that in a patient with struc-tural impingement of the nerves at the thirdor fourth thoracic levels and/or the vagusnerve, neurocardiogenic syncopy could befacilitated.

___A. Only if stress is placed directly on the pointof impingement.

___B. If stress is placed anywhere affecting theautonomic nervous system.

___C. Only if multiple stressors occur at once.___D. None of the above.

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Key Words:joint complex dysfunctionproprioceptiondysafferentationhypomobilityadjustment

AbstractIt has long been thought that “joint

complex dysfunctions” (JCD) such asthose treated by osteopaths only had det-rimental effects on local joints and sur-rounding soft tissues due to the focus onthe kinesiopathological component ofJCD. More recent theories emphasize onthe neurophysiological component, in-volving afferent inputs to the spinal cordBy reviewing recent papers, it has beenshown that joint hypomobility is associ-ated with altered reflex responses involv-ing mechanoreceptive and nociceptivepathways. As these pathways are crucialfor an optimal proprioceptive function,alteration of these inputs to the spinalcord created by a JCD could decreaseappropriate proprioceptive informations.In this light, osteopathic treatment shouldbe seen as more than treatment for mus-culoskeletal conditions. While improvingmobility to restricted joints, it could havea favourable influence on several neuro-logical reflex responses: by reducing ab-normal inputs to the spinal cord, it couldimprove the body’s ability to recover anoptimal proprioceptive function.

IntroductionLittlejohn stated in 1901. “Osteopa-

thy may be defined as a system, or sci-ence, of healing that uses the natural re-sources of the body for the adjustment ofits structure, to stimulate the preparation,

and distribution of the fluids and forcesof the body, and to promote cooperationand harmony in the body mechanism.”1

Osteopathy then is a system of clinicalpractice that looks at a person from a me-chanical point of view and recognizes themusculoskeletal system as crucially im-portant to the overall function and healthof a person.2 The musculoskeletal systemis intimately connected with all other sys-tems of the body through both the somaticand the autonomic nervous system andis, therefore, considered as a mirror ofboth health and disease, responding as itdoes to inflammation and pain from dis-order in other body systems.3

A host of interacting factors have theability to produce dysfunction of the mus-culoskeletal system, including stress re-sponse, postural anomalies and overload,repetitive physical actions (sport, occu-pation, hobbies, and so on), emotionaldistress, trauma, structural factors (con-genital short leg, cranial distortion atbirth), visceral, and other reflex activity.These can be summarised as overuse,misuse, and abuse of the musculoskel-etal system.4

The purpose of adjustment is to restorejoint mobility by manually applying acontrolled force into joints, which havebecome hypomobile. When a joint is ad-justed, compression of corpuscular end-ings of somatic receptors will create de-polarization of afferent neurons. Theseafferent inputs have a variety of effectsin the central nervous system (CNS) thataffect the amount of pain, different pri-mary perceptual experiences, the integ-rity of the motor system, as well as thefunction of autonomic nervous system forthe integrity of life itself. Since biome-chanical integrity will give us the high-

Could Joint Hypomobility AlterOptimal ProprioceptiveInformation?Rafael Zegarra-Parodi

est population of receptor afferents, it isvery simple to understand that a decreasein biomechanical integrity or aberrantbiomechanical relationships will have avery high probability of decreasing thepopulation of receptor afferents. This, inturn, will modify our primary perceptualexperiences.5

Proprioception refers to kinaestheticawareness. Proprioception occurs as aconsequence of the integration of vesti-bular input, visual input, and tissuemechanoreceptor input to the cerebralcortex and cerebellum. It is thought thatmechanoreceptor input is of the utmostimportance for proprioception. Neuronsof the motor cortex respond to activationof peripheral somatosensory and proprio-ceptive afferents. These input pathwaysmay be involved in the control of theoutput of the motor cortex. Thus, mecha-noreceptors give rise to local segmentalreflexes and suprasegmental propriocep-tive reflex effects.6 Various areas of themusculoskeletal system are extensivelyand richly innervated with mechanorecep-tors, especially around the spinal column,which seems to operate as one vast prop-rioceptive organ.7

We will use in this paper thezygapophyseal joint (ZJ) as a model fordescription. Our purpose is to review re-cent scientific literature about physiologi-cal relations between a biomechanicaldysfunction such as hypomobility (struc-ture) and proprioception (function). Sincesuch biomechanical dysfunction is re-versible in nature, we will discuss theopportunity and the aim of osteopathiccare for patient-specific conditions.

➻


DiscussionThe adjustable spinal disorder

Several terms have been coined todescribe the adjustable spinal disorderfrom a mechanical point of view: “sub-luxation” in chiropractic; “somatic dys-function” in osteopathy; and “fixation”or “functional blockage” in manual medi-cine. For a better comprehension of thefollowing paper, a single term will beused: “joint complex dysfunction (JCD)”.

This is characterized as a ZJ strain/sprain with associated local and referredpain and muscle spasm. The function ofthe ZJ is deranged by virtue of static mis-alignment and/or reduction of motion(i.e., “fixation,” “blockage,” or the moregeneric term “hypomobility”).8 The hall-marks of diagnostic criteria for segmen-tal JCD are asymmetry, range of motionabnormality, and segmental tissue texturechange. Some authors include tendernessamong these criteria.9

Mechanisms that have been proposedfor this dysfunction, particularly thehypomobility, include:1. Entrapment of a ZJ inclusion or

meniscoid, which have been shown tobe heavily innervated by nociceptors.

2. Entrapment of a fragment of posteriorannular material from the interverte-bral disc, again, innervated bynociceptors.

3. Stiffness induced by adhesions andscar tissue from previous injury and/or degenerative changes and adaptiveshortening of myofascial tissues.

4. Excessive activity (spasm, hypertonic-ity) of the deep intrinsic spinal mus-culature, particularly in unilateral,asymmetric patterns.8

Common to all concepts of JCD aresome form of kinesiologic dysfunctionand some form of neurologic involve-ment, let’s onto the anatomy of receptorsaffected by JCD.

Zygapophyseal joint receptorsZygapophyseal joint (ZJ) receptors are

innervated by a variety of neuroreceptorsall derived from the dorsal and ventralrami as well as the recurrent meningealnerve of each segmental spinal nerve. In-formation from these receptors crossesmany segmental levels because of multi-

level ascending and descending primaryafferents. There are two categories of so-matic receptors: nociceptors and mecha-noreceptors. McLain stated, “The pres-ence of mechanoreceptive andnocicepttve nerve endings in cervicalfacet capsules proves that these tissuesare monitored by the CNS and impliesthat neural input from the facets is im-portant to p roprioception and pain sen-sation in the spine.” McLain’s statementreinforces the concept that the very pres-ence of neural structures in spinal tissuesprovides the evidence of the integrationbetween the spinal joints and the nervoussystem.10 More than half of all nerve fi-bers ascending and descending in the spi-nal cord are propriospinal fibers, whichrun from one segment to another, provid-ing pathways for multisegmental re-flexes.

There are four types of somatic recep-tors: nociceptors and three types of mecha-noreceptors. D’Astolfo8 gives us an over-view of their location and function.

Type I mechanoreceptors are confinedto the outer layers of the joint capsule andare stimulated by active or passive jointmovements. Stimulation of type I recep-tors is involved with:1. Reflex modulation of posture and

movement.2. Perception of posture and movement.3. Tonic effects on neck, eye, limbs, jaw,

and eye muscles.4. Inhibition of pain from receptors via

an enkephalin interneuron transmitter.

Type II mechanoreceptors are foundwithin the deeper layers of the joint cap-sule. They are stimulated when minorchanges in tension within the inner jointoccur. Type II receptors are likely toachieve the following:1. Inhibition of pain from receptors via

an enkephalin transmitter.2. Monitoring for reflex actions.3. Phasic effects on neck, eye, limbs, jaw,

and eye.

Type III mechanoreceptors are locatedonly in ligaments of the peripheral jointsand like Golgi tendon organs, impose aninhibitory effect on motoneurons. Thesereceptors:1. Monitor direction of movement.2. Create reflex effects on segmental

muscle tone.3. Recognize potentially harmful joint

movements.

Mechanoreception refers to the pro-cess by which tissue mechanoreceptorsare stimulated by mechanical input suchas touch, muscle stretching, and joint mo-tion. A-alpha and A-beta fibers carrymechanoreceptive information into theCNS. Segmental reflex effects ofmechanoreceptor input can be both exci-tatory and inhibitory. An important in-hibitory effect is the presynaptic andpostsynaptic inhibition of the nociceptivepathways. There are also suprasegmentalreflex effects of mechanoreceptor stimu-lation, which are proprioceptive in na-ture.11 Human facets contain mechanore-ceptors to detect motion and distortion.Spinal proprioceptors may play a role inmodulating protective proprioceptivemechanoreceptors. The densities ofmechanoreceptors are greater in areasrelated to extreme movements, explain-ing why cervical facets have more recep-tors.12 Mechanoreceptors are the first lineof defense in sensing the safe limit ofrange of motion of a joint. This input ac-tivates reflex mechanisms that act to pre-vent joint injury.13

Type IV receptors or nociceptors arefree nerve endings located throughout thefibrous portion of the joint capsule andligaments. Type IV receptors are absentfrom articular cartilage and synovial lin-ings but have been found in synovialfolds and within the annulus fibrosus ofthe disc. These receptors are associatedwith the following:1. Evoke pain.2. Tonic effects on neck, limb, jaw, and

eyes muscles.3. Central reflex connections for pain in-

hibition and autonomic effects.8

Nociception is the process by whichnociceptive receptors receive tissue-damaging stimuli which are then carriedinto the CNS by nociceptive axons(A-delta and C fibers). The receptors in-volved in pain detection are referred toas nociceptors (receptors for noxiousstimuli). It is important to note that al-most all body tissue is equipped withnociceptors as pain has primary warningfunctions. If we did not feel pain and ifpain did not impinge on our well-being,


we would not seek help when our bodyaches. Nociceptors are free nerve endingsthat terminate just below the skin so as todetect cutaneous pain. Nociceptors arealso located in tendons and joints for de-tection of somatic pain and in body organsto detect visceral pain. Pain receptors arevery numerous in the skin, hence pain de-tection here is well defined and the sourceof pain can be easily localized. In tendons,joints, and body organs the pain receptorsare fewer.14

We must remember that nociceptionand pain are completely different: pain isa combination of sensory (discriminative)and affective (emotional) components.The sensory component of pain is definedas nociception.15 Potential outcomes of no-ciceptive input to the cord include pain,autonomic symptoms, vasoconstriction,and muscle spasm. A devastating conse-quence of both pain and nociceptive stimu-lation of the hypothalamus is the releaseof cortisol by the adrenal glands. Overtime, elevated levels of cortisol will pro-mote glucose intolerance, inhibit collagenformation, increase protein breakdown,inhibit secretory IgA output, and inhibitwhite blood cell function. Clearly, theclinical importance of pain andnociception should not be minimized.11

Joint receptors contribute both to thecoordination of muscle tone around jointsand provide neurologic feedback to en-hance joint stability. Spinal ligaments, likethose around knee joints, are richly inner-vated, responsive to mechanical stimula-tion, and provide proprioceptive feedbackthat mediates reflex muscular stabilizationabout the joint. This provides dynamicjoint stability which is part of a neurologicprotective mechanism.16 Joint and musclereceptors detect limits of movement of ajoint and play a role in synchronizingmechanisms involved with control ofmovement. While the kinesiologic com-ponent of the JCD is largely accepted bythe medical community, the neurologic in-volvement is poorly accepted, even re-jected. The description given below ofsomatic receptors involved during normalfunction could help provide a bettercomprehension of neurologic involve-ment associated with JCD when dys-function occurs.

Joint ComplexDysfunction

The osteopathic profession gives thefollowing definition: “Somatic dysfunc-tion is impaired or altered function of re-lated components of the somatic system(body framework): skeletal, arthrodial,and myofascial structures, and relatedvascular, lymphatic, and neural ele-ments”; while the chiropractic professiongives this one: “A subluxation is a com-plex of functional and/or structural and/or pathological articular changes thatcompromise neural integrity and may in-fluence organ system function and generalhealth”.

JCD is now described by Seaman as akinesiopathogical joint lesion (usuallyhypomobility) that develops as a conse-quence of:1. Micro and/or macrotraumatic tissue in-

jury and the associated inflammatoryresponse.

2. Inflammatory damage that may be per-petuated by a nutritional status that ispro-inflammatory in nature.

3. Degenerative changes in muscularand connective tissues due to seden-tary living.

4. Decreased descending inhibitory path-way activity due to aberrant psycho-logical states.

5. “Dysafferentation” (This term refers toan imbalance in afferent input such thatthere is an increase in nociceptor inputand a reduction in mechanoreceptorinput.17

Korr, et al. have provided experimen-tal evidence to lend support to a neuro-logical explanation for JCD.18,19 The fa-cilitated segment is a concept that is pro-posed to explain the behaviour of JCD: aninjured somatic or visceral structure pro-duces a barrage of discordant afferent im-pulses into the dorsal horn of the spinal cord,which “sensitises” that segment. It is pro-posed the spinal interneuron thresholds arelowered, allowing an exaggerated responseto pathways synapsing at that level, thuscontributing to increased pain perception,sympathetic outflow, and segmentally sup-plied muscle tone.9

Van Buskirk (1990) proposed a modelof JCD where nociceptive input to the cordappeared to be the driving force behind

the pathogenesis of JCD. He argued thatnociceptors were the only receptors ca-pable of producing reflex muscle contrac-tion and sympathetic discharge, and pro-posed a cascade of events that produceJCD. Noxious stimuli (from viscera orsoma) produce reflex axon effects promot-ing inflammation at all the terminal branchesof that axon, which further sensitises othernociceptors. Afferents reaching the dorsalhorn produce reflex muscle contraction andsympathetic discharge (producing visceraland immune effects). Over time the musclebecomes fibrotic and, if stretched or re-strained, activates nociceptors once again.20

Nociceptor activation produces furthersegmental tissue inflammation and sym-pathetic stimulation and the cycle becomesself-sustaining. Pain perception need notbe involved. However, nociceptive process-ing in the dorsal horn may become dis-turbed, producing what has been describedas “central sensitization” by Woolf leadingto hyperalgesia and chronic pain.9

Subsequently, Fryer refined this con-cept of JCD. Same neurological eventswere described but the origin of JCD wasmuch more a mechanical one, focusing onjoint strain as a primary source of aber-rant inputs to the CNS.

Strain to the ZJ capsule and ligamentscreates inflammation, synovitis, synovialeffusion, and activates nociceptors. Axonreflexes produce vasodilatation and in-flammation at the terminal ends of all theaxon branches, producing segmental tis-sue texture change and tenderness (possi-bly even segmental muscle inflammationand engorgement). Range of movementand end feel is altered due to tissue en-gorgement and joint effusion.

The research work of Lewit, Janda, andothers has shown that postural muscles,when chronically abused, misused, over-used, will tend to shorten and eventuallyto contract. Phasic muscles, however,when faced with the same insult, will tendto weaken but will not shorten.4 Theseconclusions were applied for this model.Deep segmental “stabilising” muscles, likemultifidus, are reflexly inhibited; excit-ability of longer polysegmental muscleslike the erector spinae increase, makingthe joint less stable and vulnerable to fur-ther strain. Over time connective tissuechanges in the strained capsule occur, pro-ducing long-term joint range of movement

➻


asymmetry. The multifidus atrophies,functional stability, and control are im-paired and the joint undergoes continu-ing strain.

JCD may produce a variety ofpatient-specific symptoms dependingupon specific end organ changes initiatedby nociceptive reflex activity and, whichcentral autonomic, endocrine, limbic,motor and/or sensory nuclei are most af-fected by “dysafferent” input.17

Common to these theories is the fo-cus on aberrant inputs to CNS comingfrom a joint. This phenomenon some-times becomes self-sustaining due to con-nective tissue changes and could alterother neurological pathways due to cen-tral sensitization. Nociception, mechan-oreception, and proprioception are all in-timately associated with the normal andabnormal function of the ZJ: nociceptioninduces JCD (whether the source is lo-cated in somatic or visceral structures),which subsequently reduces mechanore-ception and proprioception.11

DysafferentationSeaman, a chiropractor highly in-

volved in neurophysiologic theories forJCD, concluded that an emerging bodyof research indicates that abnormal jointcomplex function can alter the activityof nociceptors mechanoreceptors, suchthat nociceptive activity increases andmechanoreceptive activity decreases.

Many authors and researchers in-volved in joint adjusting and manipula-tion realize this and use the terms “al-tered afferent input”, “abnormal afferentinput”, or similar terms when discussingthe neuropathophysiological componentof JCD. Seaman cites several authors inhis paper:21

“1.Peterson stated that, “somatic dysfunc-tion and/or joint dysfunction inducepersistent nociceptive input and al-tered proprioceptive input”.

2. Peterson and Bergmann described ver-tebral joint dysfunctions (and their as-sociated mechanical alterations, pain,and potential local inflammation) as“lesions capable of inducing chroni-cally altered nociceptive and proprio-ceptive input”.

3. Hooshmand illustrated how restrictedjoint mobility results in decreased fir-

ing of large diameter mechanorecep-tor axons (A-beta fibers) and increasedfiring of nociceptive axons (A-deltaand C fibers).

4. Henderson used the term “altered so-matic afferent input theory” to clas-sify a neurophysiologic theory of chi-ropractic subluxation.”

Because researchers in different pro-fessions have acknowledged the fact thatcompromised joint function will alter af-ferent input such that nociception is en-hanced and mechanoreception is reduced,Seaman proposed that the chiropractic pro-fession adopt the word “dysafferentation”to describe the abnormal afferent input as-sociated with JCD.

Aim of theOsteopathic Treatment

Where possible, the aim is to under-stand the anatomical and physiologicalbreakdown and the resulting dysfunctionin the context of the whole person. Theosteopath should attempt to discoverwhere and what the cause of the symp-toms are, and also why the dysfunctionhas occurred, considering aetiological,predisposing, and maintaining factors.The purpose of osteopathic treatment andmanagement is then to enhance thebody’s response by encouraging the res-toration of normal function and also toremove or reduce the person’s predispo-sition to the problem.2

The hypothesized effects of adjust-ment commonly accepted today can cat-egorized as either mechanical or neuro-logical. Some authors describe adjust-ment as mechanical treatment with reflexeffects.

Mechanisms of action of adjustment,which have been proposed to affect me-chanical issues, include:1. Release of entrapped synovial or disc

tissues, thus reducing pain restoringmobility.

2. Stretching and breaking of adhesions.3. Dynamic stretching of musculature

and myofascial tissues.22

Spinal adjustments produce ashort-lasting (100-300 milliseconds),high velocity impulse into the body.Triano, et al. have quantified the appliedforces of an adjustment and correlated

them with physiologic responses(changes in leukocyte function) such thata threshold of approximately 500 N dis-tinguishes potentially effective from“noneffective” procedures.22 An audiblerelease (cavitation) was not necessary forthe burst of muscle activity to be stimu-lated, but the adjustment did have to befast to produce this response (it is impor-tant to remember that these findings re-late to immediate responses, not thosemeasured a period of time after the treat-ment).

Proposed mechanisms of action ofadjustment on neurological phenomenacan be divided into two categories: re-duction of compressive insult to neuraltissues, and creation of stimulus-inducedreflex changes.

The first mechanism is relativelystraightforward in that adjustment is hy-pothesized to relieve the compressiveinsult on nerve roots and autonomic fi-bers within the intervertebral foraminae,or affect disc/facet athropathy.22 As an ex-ample, intersegmental tractions producetheir attenuating effects on peripheralstructures via pumping action which in-creases the removal of inflammatorybyproducts and reduces swelling.23 Ad-justment might exert its effect by dy-namic stretching of the muscle spindlesand Goigi tendon organs, copiously lo-cated in the deep spinal muscles, therebyresetting the length/tension ratio in thesemuscles. This would help break the pain/spasm/pain cycle by alleviating signalsemanating from spastic muscle and irri-tated joint. Similarly, massage has theeffect of sedation of pain and relaxationof muscle spasms via the attenuation oftrigger points and other foci of irritationwithin the muscle.24 Spinal adjustmenthas been proposed to reduce motor neu-ron excitability and produce reflexmuscle relaxation, but results of studiestesting this proposal have been conflict-ing. A recent study has demonstrated re-flex electromyographic responses in spi-nal and limb muscles follow high veloc-ity technique, but the responses wereshort lived (100 - 400msec) and no studyhas examined the effects in symptomaticpatients.9

In the second mechanism it is pro-posed that the dynamic stretching pro-duced by adjustment induces a barrageof activity in joint and muscular mecha-


noreceptors that is transmitted along largediameter afferents and, which producesinhibitory effects within the nervous sys-tem. These effects are proposed to be bothlocal (at spinal level) and “central,” in thatthey may involve so-called descendinginhibitory pathways.22

Adjustment might inhibit incomingmessages of pain according to the “gatecontrol” theory of Melzac and Wall.9

Action potentials from joint mechanore-ceptors are conducted by fast large di-ameter axons, which reach the dorsalhorn of the spinal cord before the noci-ceptor potentials, and can “close the gate”on the incoming pain messages. The spi-nal tissues appear to be particularly ame-nable to this process, probably becauseof their unique patterns of afferent inputinto the CNS, with a high level of con-vergence existing with other somatic andvisceral inputs onto the same spinal tractprojection cells.21 Whether manual tech-niques produce a significant analgesiceffect that lasts longer than the manualevent is yet to be determined.9

There is a third target site for interac-tion between nervous system and adjust-ment, the enkephalin mediated pain con-trol. It involves activating brainstemstructures responsible for enkephalin pro-duction. Experimentally, analgesia hasbeen produced by electrical stimulationof the skin, peripheral nerve trunks, dor-sal and ventral columns of the spinal cord,thalamus, cortex, periaqueductal graymatter of the midbrain, and the nucleusraphe magnus of the medulla.24 There areother effects of physiological therapeu-tic modalities, such as psychosomatic re-sponses, which should also be consid-ered, but they are beyond the scope ofthis paper.23

Joint ComplexDysfunction andProprioception

Potential symptoms may develop as aconsequence of JCD and may produce avariety of patient-specific symptoms. Wewill just focus on possible altered prop-rioception. Alteration in mechanorecep-tor function may affect postural tone.Murphy summarized the neurologicalpathways associated with the mainte-nance of background postural tone:“Weight-bearing disc and mechanorecep-

tor functional integrity regulates anddrives background postural neurologicinformation and function (muscular)through the unconscious mechanorecep-tion anterior and posterior spinocerebel-lar tract, cerebellum, vestibular nuclei,descending medial longitudinalfusciculus (medial and lateral vestibu-lospinal tracts), regulatory anterior horncell pathway.” The anterior horn cellsprovide motor output, which travels viamotor nerves to muscle fibres.25

The evidence that the neck plays acritical role in posture is overwhelming.Muscle receptors may be of great impor-tance in sensing joint position. A charac-teristic of neck muscles is an abundanceof muscle spindles; spindle density inlarge muscle of the neck range from46-106 per gram, among the highest ofanywhere. High spindle density is char-acteristic of muscle executing fine musclecontrol. The abundance of afferent infor-mation may not only be due to fine mo-tor control. Polysynaptic pathways fromneck muscles afferents to neck motoneu-rons are powerful. Afferents leaving neckmuscles can exert profound effects onhind-limb motoneuron excitability. Theneck structures are unusually rich in re-ceptors. Small muscles close to the cer-vical vertebrae may have up to 500muscle spindles per gram, a density al-most 100 times as great as some muscles,of locomotion and 5 times greater thanthe large dorsal neck muscles, which areregarded as spindle rich. These deepstructures play an important role in re-flexes and maintenance of posture andprovide precise information with respectto position.26 Articular structure, like liga-ments, not only provides mechanical re-straint but also provide neurological feed-back that directly mediates reflex mus-cular stabilization about the joint, provid-ing dynamic joint stability.

According to these anatomical andphysiological particulars, some studieswere conducted to access relationshipsbetween JCD and proprioception. Sea-man reviewed some of these:

“In a study lead by Rogers in 1997,20 patients with chronic neck pain wereevaluated at the beginning of the studyfor pain levels and proprioceptive func-tioning. The patients were then dividedinto two groups: Group A, who received6 sessions of spinal adjustment; Group

B: who were instructed to performstretching exercises twice daily for 3-4weeks. After the study period, the spinaladjustment patients showed a 44% im-provement in pain symptoms on average,while the stretching patients showed justa 9% improvement. In regard to proprio-ceptive functioning, similar results werefound: a 41% improvement in the adjust-ment group, but only an 11% improve-ment in the stretching group. How spinaladjustment affects proprioception is notyet known, but the authors speculate thatchiropractic treatment somehow stimu-lates the deep articular mechanoreceptorsin the spine, in turn leading to improvedfunctioning.

In 1991, Revel, et al. demonstratedthat patients with neck pain have an al-teration in neck proprioception. The au-thors developed a proprioceptive test,which involved head and neck reposition-ing after an active head movement. Pa-tients with neck pain consistently per-formed this test significantly worse thanpain-free controls. The authors concluded:“The test may also permit a completion ofpost-trauma cervical pain investigation bystudying the responsibility of neck prop-rioceptors in dizziness and unclear‘pseudovestibular’ disorders.”

In 1994, Revel et al. performed astudy, which sought, in part, to determineif an exercise program based on eye-headcoordination can improve cervicocepha-lic kinesthesia. The results demonstratedthat such a rehabilitation program wassuccessful. The authors concluded: “Therehabilitation of cervico-cephalic kines-thesia could be particularly appropriatefor patients with neck pain and dizzinessafter neck trauma, because it has beenpostulated that this syndrome some-times called ‘cervical vertigo’, couldbe the result of damage to cervicalproprioceptors.”27

McPartland, et al, studied the relation-ship between chronic neck pain, stand-ing balance, and suboccipital muscle at-rophy. They hypothesize that patientswith chronic neck pain have more JCDin the cervical spine than control subjectswithout neck pain. They also hypothesizethat patients with chronic neck pain andJCD exhibit more atrophy of suboccipi-tal muscles than control subjects. Lastly,because suboccipital muscles have a highdensity of proprioceptors, they hypoth-


esize that chronic pain patients with at-rophied suboccipital muscles demon-strate a loss in standing balance. This pre-liminary study suggests that there is arelationship between chronic pain, JCD,muscle atrophy and standing balance.They hypothesize a cycle initiated bychronic JCD, which may result in muscleatrophy, which can be expected to reduceproprioceptive output from atrophiedmuscles. The lack of proprioceptive in-hibition of nociceptors at the dorsal hornof the spinal cord would result in chronicpain and a loss of standing balance.28

It appears that JCD (abnormal jointmotion and abnormal afferent inputs)could decrease optimal proprioceptiveinformation, and that alteration could beeither symptomatic or not. Several hy-potheses were formulated to explain thisclinical phenomenon: muscle atrophy de-creasing proprioceptive inputs,hypomobility decreasing afferent inputs,JCD resulting in dysafferentation. It is im-portant to remember that this phenomenoncould become chronic as soon as JCD hasbecome self-sustaining due to connectivetissue reorganization throughout surround-ing soft tissues. Once again, this could beasymptomatic and predispose the affectedcord segments to further dysfunctioningdue to central sensitization.

ConclusionJCD of the ZJ is truly based upon two

events with a cascade of effects: segmen-tal kinesiopathogical spinal lesion anddysafferentation. Since the nervous sys-tem controls and coordinates every func-tion in the body, all the other componentsare merely effects of the JCD. It appearsthat adjustment might normalize articu-lar afferent input to the CNS system,which reestablishes normal nociceptiveand kinaesthetic reflex thresholds.“Structure governs function”, one of thetraditional osteopathic principle, findshere a major clinical application throughphysiological relationship betweenhypomobility and proprioception. Thepathways explaining both physiopathol-ogy and improvement with adjustmentare not totally known.

This concept can be further extendedto other functions. The osteopath shouldkeep in mind the crucial relationshipsbetween biomechanical integrity andoptimal afferent inputs and consider these

inputs as a major component of an opti-mal health status. Afferent inputs are in-forming the CNS about self-awareness,which in turn will respond adaptivelythrough efferent inputs (self-regulation).Alteration of these neurological reflexpathways could decrease the optimal stateof health. It is fundamental to understandthat while JCD could implicate mechan-oreceptive and nociceptive pathways,JCD does not systematically induce painand these aberrant inputs to CNS couldexist without any symptomatology. Thisunique concept in health care explains themajor focus we place in osteopathic carefor the musculoskeletal system and whyit is so important for the health of eachindividual.

References1. Littlejohn JM. The Principles of Oste-

opathy. 1901. Maidstone College of Os-teopathy. IPR. 1998.

2. Sammut E. and Searle-Barnes P. Osteo-pathic Diagnosis. Stanley Thornes.1998.

3. DiGiovanna EL and Schiowitz S. An Os-teopathic Approach to Diagnosis andTreatment. Lippincott-Raven. 1997.

4. Chaitow L. Palpation Skills. ChurchillLivingstone. 1997.

5. Ferezy J. Sensory innervation of the spi-nal joint and effects of manipulation. Thechiropractic neurological examination.University Chiropractic Consultants.Minneapolis, MN. 1992.

6. Zarzecki, Assanuma. Progress in BrainResearch. 1979. 50:113-119.

7. Patterson. Somatic dysfunction in osteo-pathic medicine. The role of subluxationin chiropractic. FCER. 1997. pp. 26-31.

8. D’Astolfo C. The role of chiropractic inpain management.

9. Fryer G. Somatic dysfunction: updatingthe concept. Australian Journal of Oste-opathy. 1999. 10:2:14-19

10. Colloca C. Neurophysiological researchhold a key to understanding mechanismsof adjustments. American Journal ofClinical Chiropractic. April 2002.

11. Seaman D. Nociception, mechanorecep-tion, and proprioception... What’s the dif-ference and what do they have to do withsubluxation? Dynamic Chiropractic.2002.

12. McLain and Pickars. Spine. 1998. 21:2:168-173.

13. Zinny (Dept. of Anatomy). AmericanJournal of Anatomy. 1988. 182:16-32.

14. Perna L. Biology 202. 1998 Third WebReports on © Serendip. 1994-2002.

15. Kuner R. Universitat Heidelberg, Ger-many. [email protected]

16. Hongxing et al. Spine. 1997. 22:1:17-25.17. Seaman D. Subluxation: cause and ef-

fects. Dynamic Chiropractic. 2002.18. Korr I. The Collected Papers of Irvin

Korr. AAO Yearbook. 1979.19. Korr I. The Collected Papers of Irvin

Korr. Vol 2. AAO Yearbook. 1997.20. Van Buskirk RL. Nociceptive Reflexes

and the Somatic Dysfunction: A Model.JAOA. 1990. 90:9.

21. Seaman D. and Winterstein J.Dysafferentation: a novel term to de-scribe the neuropathophysiological ef-fects of joint complex dysfunction. Alook at likely mechanisms of symptomgeneration. www.chiro.org

22. Vernon H. Biological rationale for pos-sible benefits of spinal manipulation.

23. Lederman E. Fundamentals of manualtheapy. Churchill-Livingstone. 1997.

24. McKechnie B. A three-step neurologi-cal approach for the application of mo-dalities. Dynamic Chiropractic. 2002.

25. Kent C. Models of vertebral subluxation:a review. Journal of Vertebral Sublux-ation Research. August 1996. 1:1.

26. Abrahams (Dept. of Physiology). In:Garlick D (Ed). Proprioception, posture,and emotion. Committee in postgradu-ate medical education. Kensington, NewSouth Wales. 1982.

27. Seaman D. The dizzy patient. DynamicChiropractic. 2002.

28. McPartland M, Brodeur R, and HaligrenR. Chronic neck pain, standing balance,and suboccipital muscle atrophy – a pi-lot study. The Chiropractic News Source.Dec. 1996. 14:26.

Accepted for publication, July 2004

Address correspondence to:Rafael Zegarra-Parodi, DO MROFResearch Department of CEESOCEESO Osteopathic College175, Boulevard Anatole France93200 Saint-Denis, FranceFax: 00.33.1.48.09.33.66Email: [email protected]


Energetically Integrated Osteopathic MedicineThe life, thought, and work of Robert Fulford, DO as interpreted by Zachary Comeaux, DO, FAAO

February 11-13, 2005WVSOM Campus • Lewisburg, WV

Course Description: Level IIThis course serves as an introduction or enhancement to thepractitioner’s use of subtle energy to complement other aspects ofosteopathic diagnosis and treatment.

Learning Objectives:• Review of the philosophical background bioenergetic work• Reconciliation of energetic and biomechanical models• Introduction to energetic palpation• Discussion/demo and practice of Dr. Fulford’s methods of

diagnosis and treatment• Introduction of percussion vibrator, Vogel crystal, and magnets

in context• Practical integration of these methods into primary care

medicine/osteopathic practice

Contact: Zachary Comeaux, DO, FAAO, Program Chairpersonand author of Robert Fulford, DO and the PhilosopherPhysicianPhone: 304/647-6270 or E-mail: [email protected]

• This approach is especially helpful in cases resistant to tradi-tional methods. Often the symptoms are due to unrecognized orunresolved latent effects of trauma.

• This course is based on material presented and well receivedoverseas over the last five years. This material draws on Dr.Fulford’s sources including some not disclosed by himself in hiscourses. Although it includes work with the percussion vibrator, itcomplements and does not reduplicate the Basic and AdvancedPercussion Vibrator courses taught through the AmericanAcademy of Osteopathy.

• Dr. Comeaux has practiced Family Medicine since 1988 and hadprovided care to both Dr. and Mrs. Fulford. In this capacity hespent significant time over the last years of Dr. Fulford’s lifediscussing and co-treating patients with the Doctor as welldiscussing concepts and cooperating in the writing of Dr.Fulford’s Touch of Life. He currently is an Associate Professor atthe West Virginia School of Osteopathic Medicine.

• Early enrollees will receive a bibliography for pre-course studyif desired.

CME: 18 Category 1A

(anticipated)Course Fee:

$475.00

A Biodynamic View of Osteopathyin the Cranial Field

Course offerings by Tom Shaver, DO

Phase I – An introduction to a biodynamic model ofO.C.F. C. N. S. motion and development. Balanced fluidtension.

Date: March 5-8, 2005 Course Fee: $650 (US)Location: Kona, Hawaii CME: 21.5 Category 1A

Registration Deadline: January 30, 2005

Phase II – An in-depth perception of fluid dynamics.Therapeutic/diagnostic use of balanced fluid tensionaround the fulcrum incited by the tidal forces. Rates/CV-4/EV-4 techniques. Automatic shifting.

Date: September 3-6, 2005 Course Fee: $650 (US)Location: Kona, Hawaii CME: 23 Category 1A

Registration deadline: July 8, 2005

(“The AAO designates these programs for AAO co-sponsorship asmeeting the criteria for CME credits awarded through the AOA.”)

Questions/Registration information, contact:Tari Sargent

196 Weeks Mills Road, Farmington, ME 04938Phone: 207/778-9847; E-mail: [email protected]


Book ReviewReviewer: Anthony G. Chila

PRINCIPLES OF MANUAL MEDICINEPhilip E. Greenman, DO, FAAO, Emeritus ProfessorDepartments of Osteopathic Manipulative Medicine & Physical Medicine &Rehabilitation; College of Osteopathic Medicine; Michigan State University; EastLansing, Michigan

pp. 613, incl. Index. Third Edition, ©2003 by Lippincott Williams & Wilkins: 530Walnut Street; Philadelphia, PA 19106, USA. LWW.com; $99.00

The author, a nationally and internationally respected osteopathic physician, conveys 50 years’ experiencein the use of manual medicine in a single author attempt. Previous editions were released in 1989 and 1996by Williams & Wilkins.

Three sections of this text utilize 23 chapters to address Principles and Concepts, Technique Procedures,Clinical Integration, and Correlation. Adjunct disciplinary procedures including the use of exercise are pro-vided. Each chapter begins with a detailed review of appropriate anatomy. This serves to build understand-ing and focus therapy. Complete disciplinary coverage is assured through the provision of information onboth diagnostic testing and treatment techniques. Practical visual guidance is enhanced through the use ofmore than 1000 clinical photographs. Clear and thorough instructions provide the procedural detail neces-sary to assure proper performance and best results.

In this third edition, extensive new material in soft tissue considerations includes Chapman’s Reflexes,tender points of the Counterstrain System, and visceral techniques. Chapter 12, which addresses Osteopathyin the Cranial Field, has been completely revised. New information is provided regarding the use of cranialapproaches in the management of brain injury patients. Chapters 18 (Upper Extremity) and 19 (LowerExtremity) have been expanded to include new treatment options such as neural and dural mobilization of theextremities.

Doctor Greenman’s assessment of his single author evolution in writing is worth noting, given in his ownwords:

“The first edition of this book was originally designed to support the Continuing Medical Education’scourses offered through Michigan State University and its Colleges of Osteopathic Medicine and HumanMedicine. Since that time it has been used in a number of colleges of osteopathic medicine, chiropracticcolleges, schools of physical therapy, and schools of massage therapy. The second edition has been trans-lated into seven foreign languages.

This third edition attempts to bring current new information, as well as answers to many of the questionsI have received when teaching this material. This edition also adds newer techniques and visuals and clarifi-cation to some of the concepts presented. As an art form, manual medicine cannot be mastered by reading atext and requires considerable practice using the hands as a diagnostic and therapeutic instrument. For thebeginner, be diligent and not discouraged. For the experienced, continue to explore this fascinating field.Our patients are always grateful for the personalized nature of manual medicine. Happy voyage.”


Elsewhere in Print

Do CAM therapies work for pain management?Patient Care: September 2004, 52-58Robert Bonakdar, MD: Director of Pain Management; Scripps Center for Integrative Medicine, LaJolla, CA

David E. Bresler, PhD: Health psychologist and board-certified acupuncturist, founder and former director, UCLA Pain ControlUnit; President, Academy for Guided Imagery, Malibu, CA

The authors offer a guide to making informed choices of CAM treatments for pain. As a consensus article, evidence supporting theuse of CAM treatments and suggestions regarding incorporation into daily practice are provided.

Acupuncture“Efficacy is seen with treatment of headache, joint pain, cancer pain, and low back pain (LBP). Transcutaneous electrical nervestimulation (TENS) has shown efficacy for osteoarthritis pain in elderly patients. Percutaneous electrical nerve stimulation (PENS)and electroacupuncture have shown efficacy for fibromyalgia, headache, LBP, diabetic neuropathy, and cancer pain.”

Mind-Body Therapy“Mindfulness-based Stress Reduction (MBSR) incorporates meditation, yoga, and exercise to reduce pain. Studies show thattreatment of cancer pain, tension headache, fibromyalgia, and acute pain with guided imagery is particularly efficacious.”

Massage“A reduction in blood pressure (BP) and an improvement in heart rate variability have been associated with massage. Efficacy isseen in soft tissue pain and LBP.”

Manipulation“Ideally suited to patients with recent emergence of pain when first-line medications have failed. Efficacy is seen in LBP andheadaches.”

The authors acknowledge that distinctions are made between chiropractic treatments and osteopathy, but consider that both prac-tices can be reasonably discussed under the larger rubric of manipulation. Having said this, the remainder of their commentssimply compare chiropractic care and medical treatment. Such reporting unfortunately completely omits the significance of struc-tural diagnosis as evolved by osteopathic medicine in its contribution to the history of manipulative medicine. Had the differentia-tion been more thorough, the concepts of holism, neurologic control, circulatory function, energy expenditure and self-regulationwould have considerably broadened the assessment.

Special Technic: Hypermobile JointThe Pain Clinic: Volume 6, Number 6; September 2004, 14-16

This publication is the official journal of The Florida Academy of Pain Medicine and The Ohio Pain Initiative. Special Technic:Hypermobile Joint (A Preliminary Report) is the first in a series of historical articles of interest. Introduction and editorial com-ments are provided by Felix S. Linetsky, MD. The contributions of Earl H. Gedney, DO (1901-1976) are appropriately recognized:First described application of sclerotherapy for treatment of painful knee and sacroiliac instabilities; First described application ofsclerotherapy and developed the injection technique for painful lumbar discs; Emphasized the pathology of sacroiliac joint andligaments. Doctor Gedney’s article was published in Osteopathic Profession, 4:9:30-31, June 1937.


Back, Heather D. OMS-IIICystic Fibrosis: A Case HistoryVol. 14, No.1, March 2004,pp. 20-21

Booth, E. R. DOCollege and General Osteopathic HospitalsVol. 14, No. 2, June 2004, pp. 9-14

Buser, Boyd R. DOAcademy Contributions:What have you done for us lately?Vol. 14, No. 1, March 2004, pp. 16-19

Capobianco, John D. DO, FAAOThe Neuroendocrine-Immune ComplexIllustrated in the work of Dr. Frank ChapmanVol. 14, No. 1, March 2004, pp. 33-40

Crow, William T. DO, FAAOLymphatic Manipulative Pump Research: ABrief Review of LiteratureVol. 14, No. 3, September 2004, pp. 32-33 withreferences appearing in Vol. 14, No. 4,December 2004, p. 16

Dowling, Dennis J. DO, FAAODon’t Raise Your Hand –Put it on the PatientVol. 14, No. 4, December 2004, p. 10-16

Drew, Brendon OMS-IVA Case of Right First Rib Somatic DysfunctionDiagnosed and TreatedVol. 14, No. 1, March 2004, pp. 24-31

Gamber, Russell G. DOCystic Fibrosis: A Case HistoryVol. 14, No.1, March 2004, pp. 20-21

Geletta , Simon PhDHealth Promotion and Disease Prevention(HPDP) Programs of Osteopathic Hospitals: AComparative AnalysisVol. 14, No. 2, June 2004, pp. 20-27

Glonek, Thomas PhDCranial Manipulation Induces SequentialChanges in Blood Flow Velocity on DemandVol. 14, No. 3, September 2004, pp. 15-17

Greene, Charlotte H. PhDLymphatic Manipulative Pump Research: ABrief Review of LiteratureVol. 14, No. 3, September 2004, pp. 32-33 withreferences appearing in Vol. 14, No. 4,December 2004, p. 16

Gregg, Tammy OMS-IIIChronic Fatigue Syndrome: The Misunder-stood DiseaseVol. 14, No. 3, September 2004, pp. 20-25

Hagopian, Stefan DOCase Study: An Osteopathic Resolution of aNeurocardiogenic SyncopeVol. 14, No. 4, December 2004, pp.20-23

2004 Journal IndexBY AUTHOR Kravchenko, Tamara I MD, PhD, DO

Wave Phenomena in Movementsof Intracranial Liquid Media and the PrimaryRespiratory MechanismVol. 14, No. 2, June 2004, pp. 29-40

Lipton, James A. DO, FAAO,CDR, MC, USNA Case of Right First Rib SomaticDysfunction Diagnosed and TreatedVol. 14, No. 1, March 2004, pp. 24-31

A Case Study of Left Adhesive CapsulitisPresumably Resulting from PreviousTreatment with Protease InhibitorsVol. 14, No. 4, December 2004, pp.17-19

Mann, Josalyn M. OMS-IVThe Effect of Osteopathic ManipulativeTreatment on Gait Disturbance in MultipleSclerosis PatientsVol. 14, No. 3, September 2004, pp. 27-31

McCarty, Claudia DO, FAAOA Case of Right First Rib SomaticDysfunction Diagnosed and TreatedVol. 14, No. 1, March 2004, pp. 24-31

McCole, Malcolm DOAnalysis of the Osteopathic LesionVol. 14, No. 4, December 2004, p. 9

McMillan, Sean OMS-IVLymphatic Manipulative Pump Research:A Brief Review of LiteratureVol. 14, No. 3, September 2004, pp. 32-33 withreferences appearing in Vol. 14, No. 4,December 2004, p. 16

Moskalenko, Yuri E. D.Sci., DO(Hon)Wave Phenomena in Movementsof Intracranial Liquid Media and the PrimaryRespiratory MechanismVol. 14, No. 2, June 2004, pp. 29-40

Neil, Michele OMS-IIIA Case Study of Left Adhesive CapsulitisPresumably Resulting from PreviousTreatment with Protease InhibitorsVol. 14, No. 4, December 2004, pp.17-19

A Case of Right First Rib Somatic DysfunctionDiagnosed and TreatedVol. 14, No. 1, March 2004, pp. 24-31

Nelson, Kenneth E. DO, FAAOCranial Manipulation Induces SequentialChanges in Blood Flow Velocity on DemandVol. 14, No. 3, September 2004, pp. 15-17

Sergueef, Nicette DO (France)Cranial Manipulation Induces SequentialChanges in Blood Flow Velocity on DemandVol. 14, No. 3, September 2004, pp. 15-17

Sinay, Tony DOHealth Promotion and Disease Prevention(HPDP) Programs of Osteopathic Hospitals:A Comparative AnalysisVol. 14, No. 2, June 2004, pp. 20-27

Somoano, Yvette DOCase Study: An Osteopathic Resolution of aNeurocardiogenic SyncopeVol. 14, No. 4, December 2004, pp.20-23

Steele, Karen M. DO, FAAOThe Effect of Osteopathic ManipulativeTreatment on Gait Disturbance in MultipleSclerosis PatientsVol. 14, No. 3, September 2004, pp. 27-31

Williams, Stuart F. DOChronic Fatigue Syndrome:The Misunderstood DiseaseVol. 14, No. 3, September 2004, pp. 20-25

Wilson, Perrin T. DOOsteopathy with a Background of 5,000 YearsVol. 14, No. 3, September 2004, p. 10

Zegarra-Parodi, Rafael DO, MROFCould Joint Hypomobility Alter OptimalProprioceptive Information?Vol. 14, No. 4, December 2004, pp.25-30

BY SUBJECTBook Reviews Reprinted with Permission of:

Institute of Noetic SciencesGetting at the Root: Treating the DeepestSource of Disease by Andrew LangeVol. 14, No. 3, September 2004, pp. 34

Physicians of the Soul by Robert M. MayVol. 14, No. 3, September 2004, pp. 34

The Medium, the Mystic, and the Physicist byLawrence LeShanVol. 14, No. 3, September 2004, pp. 34

Book Reviews by Anthony G. Chila, DO, FAAOA Fulford Trilogy:Dr. Fulford’s Touch of Life;Philosopher Physician; andAre we on the Path?Vol. 14 No. 1 Fall 2004, p. 41;

Hands On: A Clinical Companionby Simon Browning, DO, Cert Ed.Vol. 14, No. 2, June 2004, pp. 42;

Healing Outside the Margins: the Survivor’sGuide to Integrative Cancer Careby Carole O’Toole(with Carolyn B. Hendricks, MD)Vol. 14, No. 2, June 2004, pp. 42

Principles of Manual Medicineby Philip E. Greenman, DO, FAAOVol. 14, No. 4, December 2004, pp.32


Silent Waves: Theory and Practice of LymphDrainage Therapyby Bruno Chikly, MDVol. 14, No. 2, June 2004, pp. 41

Case HistoryA Case of Right First Rib Somatic DysfunctionDiagnosed and TreatedLipton, James A. DO, FAAO, CDR, MC,USN; Michele Neil, OMS-IV; Brendon Drew,OMS-IV; Claudia McCarty, DO, FAAOVol. 14, No. 1, March 2004, pp. 24-31;

Cystic Fibrosis: A Case HistoryGamber, Russell G. DO;Heather D. Back, OMS-IIIVol. 14, No.1, March 2004, pp. 20-21

A Case Study of Left Adhesive CapsulitisPresumably Resulting from PreviousTreatment with Protease Inhibitors Lipton,James A. DO, FAAO, CDR, MC, USN,Michele Neil, OMS-IIIVol. 14, No. 4, December 2004, pp.17-19

Case Study: An Osteopathic Resolution of aNeurocardiogenic SyncopeSomoano, Yvette DO; Stefan Hagopian, DOVol. 14, No. 4, December 2004, pp.20-23

Chronic Fatigue Syndrome:The Misunderstood Disease;Williams, Stuart F. DO;Tammy Gregg, OMS-IIIVol. 14, No. 3, September 2004, pp. 20-25

Chapman ReflexesThe Neuroendocrine-Immune ComplexIllustrated in the work of Dr. Frank Chapman;Capobianco, John D. DO, FAAOVol. 14, No. 1, March 2004, pp. 33-40

Cranial ManipulationCranial Manipulation Induces SequentialChanges in Blood Flow Velocity on DemandNelson, Kenneth E. DO, FAAO; NicetteSergueef, DO (France), Thomas Glonek, PhDVol. 14, No. 3, September 2004, pp. 15-17

Cystic FibrosisCystic Fibrosis: A Case History;Back, Heather D. OMS-III; Russell G.Gamber, DOVol. 14, No. 1, March 2004, pp. 20-21

Dig OnA Program of ResearchChila, Anthony G. DO, FAAOVol. 14, No. 4, December 2004, p. 8

Parallel and DistinctChila, Anthony G. DO, FAAOVol. 14, No. 3, September 2004, p. 8

Russian School of Osteopathic Medicine Chila,Anthony G. DO, FAAOVol. 14, No. 2, June 2004, pp. 8, 14

They were ContemporariesChila, Anthony G. DO, FAAOVol. 14, No. 1, March 2004, p. 8

From The ArchivesCollege and General Osteopathic HospitalsBooth, E. R. DOVol. 14, No. 2, June 2004, pp. 9-14;

Chapter VII, Table IV, Four Great Classes ofOsteopathic Spinal Lesionsfrom McCole, Malcolm DO’s An Analysis ofthe Osteopathic Lesion, 1935Vol. 14, No. 4, December 2004, p. 9;

Osteopathy with a Background of 5,000 YearsWilson, Perrin T. DO;Vol. 14, No. 3, September 2004, p. 10

The Lymphatic System; Applied AnatomyMillard, F. P. DOVol. 14, No.1, March 2004, p. 9

Health Promotion and Disease PreventionHealth Promotion and Disease Prevention(HPDP) Programs of Osteopathic Hospitals: AComparative AnalysisGeletta , Simon PhD;Tony Sinay, DOVol. 14, No. 2, June 2004, pp. 20-27

Intracranial Liquid MediaWave Phenomena in Movementsof Intracranial Liquid Media and the PrimaryRespiratory MechanismMoskalenko, Yuri E. D.Sci., DO(Hon)Tamara I. Kravchenko, MD, PhD, DOVol. 14, No. 2, June 2004, pp. 29-40

Joint Complex DysfunctionCould Joint Hypomobility Alter OptimalProprioceptive Information?Zegarra-Parodi, Rafael DO, MROFVol. 14, No. 4, December 2004, pp.25-30

Left Adhesive CapsulitisA Case Study of Left Adhesive CapsulitisPresumably Resulting from PreviousTreatment with Protease InhibitorsNeil, Michele OMS-III;James A. Lipton, DO, FAAO, CDR, MC, USNVol. 14, No. 4, December 2004, pp.17-19

Lymphatic Manipulative PumpLymphatic Manipulative Pump Research: ABrief Reviewe of LiteratureMcMillan, Sean OMS-IV; William T. Crow,DO, FAAO; Charlotte H. Greene, PhDVol. 14, No. 3, September 2004, pp. 32-33 withreferences appearing in Vol. 14, No. 4,December 2004, p. 16

Multiple SclerosisThe Effect of Osteopathic ManipulativeTreatment on Gait Disturbance in MultipleSclerosis PatientsMann, Josalyn M. OMS-IV;Karen M. Steele, DO, FAAOVol. 14, No. 3, September 2004, pp. 27-31

Neurocardiogenic SyncopeCase Study: An Osteopathic Resolution of aNeurocardiogenic SyncopeHagopian, Stefan DO; Yvette Somoano, DOVol. 14, No. 4, December 2004, pp.20-23

Northup Memorial LectureAcademy Contributions: What have you donefor us lately?;Buser, Boyd R. DOVol. 14, No. 1, March 2004, pp. 16-19

Osteopathic HospitalsOsteopathic HospitalsHealth Promotion andDisease Prevention (HPDP) Programs ofOsteopathic Hospitals: A ComparativeAnalysisSinay, Tony DO; Simon Geletta, PhDVol. 14, No. 2, June 2004, pp. 20-27

Scott Memorial LectureDon’t Raise Your Hand – Put it on the Patient.Dowling, Dennis J. DO, FAAOVol. 14, No. 4, December 2004, p. 10-16;

Are you interested inbecoming

BOARD CERTIFIED

inNeuromusculoskeletalMedicine and OMM?

PRACTICE TRACK

CLOSES

December 31,2005

May 1, 2005Application Deadline

for theNovember 2005

Exam

Contact:Dee Kieffaber, certification coordinator

for more information!American Osteopathic Board ofNeuromusculoskeletal Medicine3500 DePauw Blvd., Suite 1080

Indianapolis, IN 46268Phone: (317) 879-1881Fax: (317) 879-0563

E-mail: [email protected]

3500 DePauw Boulevard, Suite 1080Indianapolis, IN 46268

ADDRESS SERVICE REQUESTED

NON-PROFIT ORG.U.S. POSTAGE

PAIDPERMIT #14

CARMEL, INDIANA

®

COURSE OBJECTIVES: LEVEL IIIThis Academy program was designed to meet the needs of thephysician desiring the following:

• OMT Review - hands-on experience and troubleshooting• Integration of OMT in treatment of clinical cases• Preparation for OMT practical portions of certifying boards• Preparation for AOBNMM (American Osteopathic Board of

Neuromusculoskeletal Medicine) certifying/licensing boards• Information on CODING for manipulative procedures• Good review with relaxation and family time

PREREQUISITES: The participant should have a basicunderstanding of functional anatomy and (1) Level II course.

PROGRAM TIME TABLE:Friday, January 28 ....................................... 8:00 am - 5:30 pmSaturday, January 29 .................................... 8:00 am – 5:30 pmSunday, January 30 ..................................... 8:00 am –12:30 pm(Friday & Saturday include (2) 15 minute breaks and a (1) hour lunch;

Sunday includes a 30 minute break.)

Winter OMT Update“APPLICATION OF OSTEOPATHIC CONCEPTS IN CLINICAL MEDICINE”

PLUS PREPARATION FOR CERTIFYING BOARDS

Henderson, Nevada • January 28-30, 2005

HOTEL ACCOMMODATIONS:Holiday Inn Express Hotel & Suites441 Astaire Drive, Henderson, NV 89014 • 702/990-23231.3 Miles northwest from course location

Hampton Inn & Suites Henderson421 Astaire Drive, Henerson, NV 89014 • 702/992-92921.3 Miles northwest from course location

For other hotels in area, check out the internet:www.hotels.com or www.expedia.com

“LAST OMT UPDATEbefore May 1, 2005

AOBNMM Application Deadline”

The program anticipates being approved for 20 hours of AOACategory 1-A CME credit pending approval by the AOA CCME.

For Registration Information, contact:Christine Harlan, Membership Services Coordinator

American Academy of Osteopathy®

3500 DePauw Blvd., Suite 1080Indianapolis, IN 46268Phone: 317/879-1881

E-mail: [email protected] on-line at: www.academyofosteopathy.org

COURSE LOCATION:

NEVADA’S NEW SCHOOL OF OSTEOPATHIC MEDICINE

Documents

“How many of you will commit malpractice?”files.academyofosteopathy.org/files/DecemberJournal2004.pdf · the top of the photo. Use a photocopy to in-dicate the placement of arrows