The AAO Journal - American Academy of Osteopathy

The AAOForum for Osteopathic ThoughtJOURNALOfficial Publication of the American Academy of OsteopathyTradition Shapes the Future Volume 22 Number 2 Summer 2012Special July 4 th Issue onMilitary Matters

The American Academy of Osteopathy is your voice . . ....in teaching, advocating, and researching the science, art and philosophy of osteopathic medicine, emphasizing theintegration of osteopathic principles, practices and manipulative treatment in patient care.The AAO Membership Committee invites you to join theAmerican Academy of Osteopathy as a 2012-2013 member.The AAO is your professional organization. It fosters thecore principles that led you to choose to become a Doctor ofOsteopathy.For just $5.01 a week (less than a large specialty coffee at yourfavorite coffee shop) or just 71 cents a day (less than a bottle ofwater), you can become a member of the professional specialtyorganization dedicated to the core principles of your profession!Your membership dues provide you with:• A national advocate for osteopathic manipulative medicine(including appropriate reimbursement for OMM services)with osteopathic and allopathic professionals, public policymakers, the media and the public.• Referrals of patients through the Search for a Physician toolon the AAO website, as well as calls to the AAO office.• Discounts on quality educational programs provided by AAOat its annual convocation and weekend workshops.• New online courses.• Networking opportunities with your peers.• Discounts on publications in the AAO Bookstore.• Free subscription to the AAO Journal publishedelectronically four times annually.• Free subscription to the online AAO Member Newsletter.• Access to the members only section of the AAO website,which will be enhanced in the coming months to include newfeatures such as resource links, a job bank, and much more.• Discounts in advertising in AAO publications, on the Website and at the AAO’s Convocation.• Access to the American Osteopathic Board ofNeuromusculoskeletal Medicine—the only certifying boardin manual medicine that exists in the medical world today.• Maintenance of an earned Fellowship program to recognizeexcellence in the practice of osteopathic manipulativemedicine.• Promotion of research on the efficacy of osteopathicmedicine.• Support for the future of the profession through the StudentAmerican Academy of Osteopathy on osteopathic medicalschool campuses.• Your professional dues are deductible as a business expense.If you have any questions regarding membership or renewalmembership, please contact Susan Lightle at (317) 879-1881 orslightle@academyofosteopathy.org. Thank you for supporting theAmerican Academy of Osteopathy.Founding Chair of Osteopathic Manipulative MedicineThe proposed Campbell University School of Osteopathic Medicine (CUSOM) is currently in the accreditation review process, with anticipatedmatriculation in August 2013.The Chair of Osteopathic Manipulative Medicine (OMM) is responsible for OMM program development, including participation in designing theOMM curriculum, as well as assisting the Associate Dean for Biomedical Affairs and Associate Dean for Clinical Affairs with development of the preclinicaland clinical curriculum. This role includes faculty recruitment and faculty development to ensure curriculum is successfully delivered to theCUSOM students. Other responsibilities include the supervision of the school’s OMM faculty and students to advance the student’s professionalism,knowledge, skills, and competencies to the level required for a graduate Osteopathic physician.This is a wonderful opportunity to help develop a creative, vibrant, student-centered learning community in a faith-based environment. Applicantsmust be AOA board-certified through the American Osteopathic Board of Neuromusculoskeletal Medicine or have received a Certifi cate of SpecialProfi ciency in Osteopathic Manipulative Medicine (C-SPOMM). Candidates with previous academic experience will be given preference. All offersare subject to background checks and reference reviews.Send CV, letter of application, and three references electronically to:Brian Kessler, DOAssociate Dean for Clinical Affairscusomemployment@campbell.eduCUSOM is committed to affirmative action, equal opportunity and the diversity of its workforce.www.campbell.edu/cusomPage 2The AAO Journal Volume 22, Issue 2, Summer 2012

THE AAO FORUM FOR OSTEOPATHIC THOUGHTOURNALOfficial Publication of the American Academy of OsteopathyJ3500 DePauw Boulevard, Suite 1080Indianapolis, IN 46268Phone: (317) 879-1881Fax: (317) 879-0563www.academyofosteopathy.orgAmerican Academy of OsteopathyJane E. Carreiro, DO..................................................................PresidentDavid Coffey, DO, FAAO................................................ President-ElectDiana L. Finley, CMP................................................ Executive DirectorEditorial Advisory BoardMurray R. Berkowitz, DO, MA, MS, MPHDenise K. Burns, DO, FAAOEric J. Dolgin, DOClaire M. Galin, DOWilliam J. Garrity, DOStephen I. Goldman, DO, FAAOStefan L. J. Hagopian, DO, FAAORaymond J. Hruby, DO, MS, FAAOBrian E. Kaufman, DOHollis H. King, DO, PhD, FAAOPaul R. Rennie, DO, FAAOHallie J. Robbins, DOMark E. Rosen, DOThe AAO JournalMurray R. Berkowitz, DO, MA, MS, MPH.....................Scientific EditorDiana Finley, CMP.......................................................Supervising EditorTessa Boeing....................................................................Managing EditorThe AAO Journal is the official publication of the American Academyof Osteopathy. Issues are published in March, June, September, andDecember each year.The AAO Journal is not responsible for statements made by anycontributor. Although all advertising is expected to conform to ethicalmedical standards, acceptance does not imply endorsement by thisjournal.Opinions expressed in The AAO Journal are those of authors or speakersand do not necessarily reflect viewpoints of the editors or official policyof the American Academy of Osteopathy or the institutions with whichthe authors are affiliated, unless specified.Please send address/e-mail address changes to:slightle@academyofosteopathy.orgDisclaimer: Dr. Berkowitz was not involved in the editorial decisionto publish the articles he co-authored, which was left up to the editorialcommittee of the journal.Correction: In the article “Manipulative Methods of Dr. Still” byJamie Archer, DO (UK), from the December issue of The AAO Journal,the quote from Dr. Edwards in the fifth paragraph of page 20 wasmisattributed to Dr. Still. On page 23, the following sentence wasomitted in reference to Figures 4 and 5: According to the dictionarythe very word “swinging” refers to an oscillating, rotary or repetitivemovement. Finally, “Figure 8: Hip Treatment” should have been labeled“Figure 9: Hip treatment.” The AAO Journal apologizes for these errors.Advertising rates for The AAO Journal are listed to the right. Please callTessa Boeing at (317) 879-1881 for more information.Subscriptions: $60.00 per yearTRADITION SHAPES THE FUTURE • VOLUME 22 NUMBER 2 • SUMMER 2012The mission of the American Academy of Osteopathy is to teach, advocateand research the science, art and philosophy of osteopathic medicine,emphasizing the integration of osteopathic principles, practices andmanipulative treatment in patient care.In this Issue:AAO Calendar of Events.......................................................................................7CME Certification of Home Study Form............................................................48Component Society Calendar of Events..............................................................64Regular Features:View from the Pyramids: A resource journal on traumatic brain injury and posttraumaticstress disorder in veterans......................................................................4Murray R. Berkowitz, DO, MA, MS MPHFrom the Archives...............................................................................................60Editorial:“The difference a DO makes” in welcoming home our troops.............................8William Bograkas, DO, MA, FACOEP, COL, MC, FS USA (retired)Original Contributions:Understanding blast-induced traumatic brain injury (bTBI) through mechanismsand patterns of injury...........................................................................................10Patrick M. Malie, MS, OMS III; Marc Quentin Sonnier, Jr., MS;Murray R. Berkowitz, DO, MA, MS, MPHClinical management and multipotential treatment strategies for blast-inducedtraumatic brain injury (bTBI)..............................................................................18Patrick M. Malie, MS, OMS III; Murray R. Berkowitz, DO, MA, MS, MPHBlast-induced mTBI as etiology of post-traumatic stress disorder in militaryveterans ...............................................................................................................25Marc Quentin Sonnier, Jr., MS; Murray R. Berkowitz, DO, MA, MS, MPHSociodemographic analysis of psychiatric emergency services in a state withgreater than average veteran density....................................................................36Livia Cara, MS; Murray R. Berkowitz, DO, MA, MS, MPHHolistic osteopathic approach to the care of veterans with post-traumatic stressdisorder: Case report...........................................................................................43Andrew Lovy, DO, FACN, DMOR; Murray R. Berkowitz, DO, MA, MS, MPHBiomarkers and neoroimaging techniques to detect blast-induced traumatic braininjury (bTBI).......................................................................................................49Patrick M. Malie, MS, OMS III; Murray R. Berkowitz, DO, MA, MS, MPHThe safety and efficacy of osteopathic manipulation in the treatment of mildtraumatic brain injury (mTBI) in U.S. service members as validated by SPECTscan: A report of planned research.......................................................................54Natalie A. Nevins, DO, MSHPE; Marcel Fraix, DO, FAAPMRAdvertising RatesPlaced 1 time Placed 2 times Placed 4 timesFull Page 7.5” x 10” $600 $575 $550Half Page 7.5” x 5” $400 $375 $350Third Page 7.5” x 3.3” $300 $275 $200Fourth Page 3.75” x 5” $200 $175 $150Professional Card 3.5” x 2” $60Classified$1.00 per wordVolume 22, Issue 2, Summer 2012 The AAO Journal Page 3

View From the PyramidsA resource journal on traumatic brain injury andpost-traumatic stress disorder in veteransMurray R. Berkowitz, DO, MA, MS, MPHAs part of the 2011 White House Joining ForcesInitiative aimed at taking action to better serve America’smilitary families, the American Association of Collegesof Osteopathic Medicine (AACOM) looked at the mannerin which the curricula taught at the nation’s osteopathicmedical colleges provide instruction in military-relatedmedical issues. An analysis of the complete curriculataught at these schools was performed. When the AACOMeffort was first announced in December 2011, this Editorsought to provide a special, themed issue of the AAOJournal that would emphasize the problems of traumaticbrain injury (TBI) and post-traumatic stress disorder(PTSD) in our veterans to coincide with the January 11public announcement of the Joining Forces Initiative. Fora number of reasons, this could not be accomplished inthe very short time that was available. Our colleagues atthe American College of Osteopathic Family Physicians(ACOFP), however, were able to publish a special, themedissue of the Osteopathic Family Physician in March 2012.My congratulations to Jay Shubrook, DO, Editor, andMeredith Norris, DO, Associate Editor.This month’s special, themed issue is the first for theAmerican Academy of Osteopathy and its Journal. Specificcontent includes, but is not limited to, post-traumatic stressdisorder (PTSD), traumatic brain injury (TBI), depressionand psychosocial issues related to military culture andfamilies. It was envisioned that this issue may serve as aresource for physicians, especially non-veteran civilianphysicians, who must be aware of how veterans can slipthrough the cracks of the Veterans Affairs system and haveissues tied to their military service.Our Guest Editor, Dr. William Bograkos, received hisDisaster and Chemical, Biological, Radiologic, Nuclearand Explosive (CBRNE) training during his 28 years ofmilitary service. He is a retired Colonel in the U.S. ArmyMedical Corps, and has served both the Army and the U.S.Air Force as a military Flight Surgeon and Family Practiceand Emergency Medicine Physician. Dr. Bograkos servedwith a Special Operations Weapons of Mass DestructionDetachment prior to, and during, the millennium. Heserved in the Balkans as a Division Surgeon and NATOMulti-National Peacekeeper from September 2001 to April2002. Dr. Bograkos chaired the U.S. Special OperationsCommand’s Curriculum Examination Board for theAdvanced Tactical Practitioner (SOF EMT-P) from 2004 to2006. He served the Pentagon’s Civil Military EmergencyPreparedness office as a Bioterrorism/Medical Consultantfor the Black Sea Initiative, and briefed at the First InterpolGlobal Conference on Preventing Bioterrorism in Lyon,France, in 2005.Of the contributing authors, several are veterans.Andrew Lovy, DO, FACN, DMOR, was the second DO tobe commissioned into the U.S. Army Medical Corps. Dr.Lovy served in Vietnam with the 506 th Infantry Regimentas part of the famed 101 st Airborne Division (“ScreamingEagles”). During World War II, the 506 th jumped intoFrance in the opening hours of D-Day, and fought their wayout of Bastogne during the Battle of the Bulge. Dr. Lovytook part in the 1968 Tet Offensive. For those not familiarwith the DMOR (Distinguished Member of the Regiment)designation, it is a special award conferred by theDepartment of the Army and sanctioned by the unit. Sincethe inception of the 506 th , approximately 40,000 troopshave been in the unit, and 112 have been so awarded. Untilthis year, Dr. Lovy was the only physician so awarded, andof the four medics who have since received the award, threeserved with him in Vietnam. This award is special becauseit is given by one’s peers to acknowledge service of thehighest magnitude.Murray R. Berkowitz, DO MA, MS, MPH, servedon active military duty as a Medical Corps Officer in theUnited States Army. Before attending medical school, Dr.Berkowitz served in numerous assignments in the U.S.Army and U.S .Air Force (USAF). He ultimately received aDirect Commission in the U.S. Army as an Armor/CavalryOfficer and served assignments as an Officer CandidatePage 4The AAO Journal Volume 22, Issue 2, Summer 2012

School (OCS) Instructor/Tactical Officer, TransportationOfficer, Chemical Officer and Infantry CompanyCommander with the Army, the Reserve, and the NationalGuard. He transferred to the USAF in January 1981. HisAir Force assignments included service with the StrategicAir Command, Military Airlift Command, DefenseCommunications Agency, USAF Headquarters (Pentagon)and the Office of the Secretary of Defense (OSD). Heserved for more than seven years in the space program,including assignments as Staff Development EngineeringManager for the space shuttle, Space Launch and ControlDivision; Directorate of Space Systems and Command,Control, Communications; Deputy Chief of Staff/Researchin the Department of Development and Acquisition at theUSAF Headquarters; Airborne Space Command, Control,Communications Flight Test Engineering Manager at theOSD; with attachment to the 89 th Military Airlift Wing(Special Air Missions/Presidential Support) at AndrewsAFB in Maryland; and as the Special Assistant for Spaceand Command, Control, Communications to the ChiefScientist of the Air Force. During the first Gulf War, Dr.Berkowitz served as a Special Assistant to the Directorof Plans; Directorate of Plans; and following cessation ofhostilities, Chief of Research Services for the Secretary’sGulf War Study. Dr. Berkowitz is a disabled veteran,medically separated from the military due to service-relateddisabilities. A former “Line of the Air Force” LieutenantColonel, he was a military aviator and parachutist, andalso holds the Master Space Badge and the Office of theSecretary of Defense Identification Badge. He has received26 military awards and decorations.Natalie A. Nevins, DO, MSHPE, is a former Majorin the United States Air Force Medical Corps. Dr. Nevinswas assigned to the 61 st Medical Squadron at Los AngelesAir Force Base as a Family Practice Physician, where sheheld positions as Chief of Medical Field Response; ClinicalDirector for Laboratory Services; Chairman of the InfectionControl Department; and Director of Radiology Services.She lectures for the California Preparedness and EducationNetwork on issues related to Disaster Preparedness,Bioterrorism, Chemical and Radiological Warfare andEmerging Infectious Diseases.Finally, I would like to gratefully acknowledge themany editing and other contributions of Ms. Tessa Boeing.Without her continuing efforts, this special issue of theJournal would have been delayed.Imagine expandingwhat you know every year.Chair, Department of Osteopathic Manipulative Medicine (OMM)Reporting directly to the Dean of the School and working closely with the Dean’s Cabinet, this extraordinary leader will guide the Department of OsteopathicManipulative Medicine toward excellence in teaching, research, patient care, administrative services and community activities. Yours will be a highly versatile role,encompassing everything from transforming our mission and vision into reality through coaching and mentoring, and creating an environment of cooperationand trust, to serving as spokesperson for the School, and directing the recruitment and retention of the highest quality faculty and staff. In addition, you will beresponsible for developing and managing the budget, creating effective work plans and conducting performance appraisals. You will also serve as the ProgramDirector for the Neuromuscular Medicine/Osteopathic Manipulative Medicine Plus One Residency Program. Crucial to your success will be your ability to identifythe needs of the University and School and take decisive action to meet them.The inspired candidate we seek must be a Doctor of Osteopathy (DO) with board certification in NMM/OMM, including five years of professional experiencethat include academic experience. Proven accomplishment in clinical and educational programs and a commitment to stimulating research activities required.Must have the academic and professional experience necessary to qualify at the rank of Professor (preferred) or Associate Professor and must be able to provideexamples of leadership (i.e. previous departmental leadership positions, involvement in regional/national organizations, etc.), teambuilding (i.e. previoussuccesses, experience, interpersonal skills), academic strength (i.e. teaching experience, research experience, publications), clinical strength (peer recognition,reputation, patient satisfaction) and management strength (coaching, type and quality of management experience, advanced degree with experience). Requires ademonstrated commitment to the values of osteopathy and continuous quality improvement, sound business acumen and a strong working knowledge of clinicalpractice in order to manage the OMM Department in a fiscally sound manner. NJ State medical license, DEA and CDS are required.Applicants should submit a letter of interest and curriculum vitae to: Vincent DeRisio, DO, AssociateDean for Clinical Affairs, c/o Ms. Tammy Merchant, UMDNJ-School of Osteopathic Medicine, OneMedical Center Drive, Academic Center, Suite 305, Stratford, NJ 08084, E-mail: merchata@umdnj.edu.Electronic submissions are encouraged, although paper applications will also be accepted. UMDNJ is anAA/EOE, M/F/D/V.Volume 22, Issue 2, Summer 2012 The AAO Journal Page 5AAO Journal6/1/2012

Osteopathic Considerations in Systemic Dysfunction:Common Clinical ProblemsJuly 20-22, 2012, at New York College of Osteopathic Medicine (NYCOM)Course DescriptionThis course presents a practical, hands-on osteopathicmanipulative treatment (OMT) approach to everyday patientsystemic complaints—ranging from sinusitis to pneumonia,gastritis to irritable bowel syndrome and headache to angina.The program centers on designing rational osteopathic care thatintegrates the five osteopathic care models and can be deliveredin a clinically-effective, time-efficient manner.It will teach clinicians to seek regional and segmental diagnosticsomatic clues to enhance and speed differential diagnosis.Participants will learn to integrate Chapman’s reflexes, collateralabdominal ganglia, and segmental diagnosis of the entire spineand sacroiliac joint. In treatment, the course will center on skillsused to enhance homeostasis. Participants will master skillsincluding sphenopalatine ganglia technique; collateral gangliainhibition; spleen pump; myofascial spray and stretch; ischialrectal fossa technique; mesenteric lifts; rib raising; lymph pumps;liver pump; diaphragm redoming; and direct and indirect OMTtechniques to remove somatic dysfunction in the cranial, cervical,thoracic, costal, lumbar and sacral regions.While a number of techniques will be taught, emphasis will beplaced on developing skills and strategies to speed diagnosisand recovery. Residents, residency trainers and directors ofmedical education will be accorded special tips for maximizingintegration of these skills and strategies into their specificprograms.FacultyHugh Ettlinger, DO, FAAO, is a 1987 graduate of NYCOM, wherehe serves as an Associate Professor of Osteopathic ManipulativeMedicine (OMM) and director of the NYCOM/St. Barnabas NMM/OMT Residency Program.Michael Kuchera, DO, FAAO, is a 1980 graduate of KirksvilleCollege of Osteopathic Medicine. He currently directs the OMMResearch and Human Performance and Biomechanics Laboratoryat Philadelphia College of Osteopathic Medicine. He is alsoclinical director of the Center for Chronic Disorders of Aging andsecretary-general of the International Federation of Manual/Musculoskeletal Medicine.CME20 hours of Category 1-A AOA CME credit is anticipated.Course LocationNYCOM at New York Institute of TechnologyNorthern BoulevardOld Westbury, NY 11568(516) 686-3747Course TimesFriday and Saturday: 8:00 am - 5:00 pm (lunch provided)Sunday: 8:00 am - 12:00 pm (lunch on your own)Travel ArrangementsCall Tina Callahan of Globally Yours Travel at (800) 274-5975.American Academy of Osteopathy Registration FormOsteopathic Considerations in Systemic Dysfunction...July 20-22, 2012 at NYCOMName: ___________________________________________ AOA#: _____________Nickname for Badge: __________________________________________________Street Address: __________________________________________________________________________________________________________________________________City: __________________________________ State: ________ Zip: ___________Phone: _______________________________ Fax: ____________________________E-mail: __________________________________________________________________By releasing your fax/e-mail, you have given the AAO permission tosend marketing information to your fax or e-mail.Billing Address (if different than above): ___________________________________________________________________________________________________Registration RatesOn or before 6/22/2012; After 6/22/2012AAO Member $ 680.00 $ 780.00AAO Non-Member $ 780.00 $ 880.00Student/Intern/Resident $ 580.00 $ 680.00The AAO accepts check, Visa, Mastercard or Discover payments inU.S. dollarsCredit Card #: ________________________________________________________Cardholder’s Name: ___________________________________________________Expiration Date: _____________________ 3-digit CVV#________________I hereby authorize the AAO to charge the above credit card for thefull course registration amount.Signature: ___________________________________________________________Click here to view the AAO’s Cancellation and Refund PolicyPlease submit registration form and payment via mail to the American Academy of Osteopathy,3500 DePauw Blvd., Suite 1080, Indianapolis, IN 46268 or by fax to (317) 879-0563.Or register online at www.academyofosteopathy.orgPage 6The AAO Journal Volume 22, Issue 2, Summer 2012

AAO Calendar of Events 2012-2013Mark your calendar for these upcoming Academy meetings and educational courses.July 17July 17-19July 20-22July 20-22August 10-11August 10-11August 16September 7-8October 6October 7October 8-10October 25-27November 9November 10November 11Nov. 30-Dec. 2Jan. 18-20, 2013Feb. 1-2, 2013Mar. 17-19, 2013Mar. 18-19, 2013Mar. 18-19, 2013Mar. 20, 2013Mar. 20-24, 2013AAO Board of Trustees Meeting—AOA Headquarters, Chicago, ILAOA Board of Trustees Meeting—The Farimont Hotel, Chicago, ILAOA House of Delegates Meeting—The Farimont Hotel, Chicago, ILOsteopathic Considerations in Systemic Dysfunction: Common Clinical ProblemsHugh Ettlinger, DO, FAAO; Michael Kuchera, DO, FAAO—NYCOM, Old Westbury, NYEducation Committee Meeting—University Place Conference Center & Hotel, Indianapolis, INSAAO Council Meeting—University Place Conference Center & Hotel, Indianapolis, INMembership Committee Teleconference, 8:30 pm ESTUltrasound Guided Injections—Millicent K. Channell, DO; Sajid Surve, DOUMDNJSOM, Stratford, NJFine-Tuning Your HVLA (Pre-AOA Convention)John G. Hohner, DO, FAAO—San Diego, CAAAO Board of Trustees Meeting—San Diego, CAAAO Program at the AOA Convention: Osteopathic Considerations for Head and Neck DisordersMillicent K. Channell, DO, Program Chair—San Diego, CAProlotherapy Weekend—Mark S. Cantieri, DO, FAAO; George J. Pasquarello, DO, FAAOUNECOM, Biddeford, MEAOBNMM Meeting—Wyndham Hotel West, Indianapolis, INAOBNMM Oral & Practical Exams—Wyndham Hotel West, Indianapolis, INAOBNMM Written Exam—Wyndham Hotel West, Indianapolis, INOscillatory & Energetically Integrated Osteopathic Medicine in a Contemporary SettingZachary J. Comeaux, DO, FAAO—NSUCOM, Fort Lauderdale, FLOsteopathic Approach to Clinically Relevant Myofascial Trigger PointsMichael Kuchera, DO, FAAO—AZCOM, Glendale, AZEducation Committee Meeting—Indianapolis, INPeripheral Nerve course (Pre-Convocation)—Kenneth J. Lossing, DO—Rosen Shingle Creek Resort,Orlando, FLPediatric ENT course (Pre-Convocation)—Program Chair TBD—Rosen Shingle Creek Resort,Orlando, FLOsteopathic Considerations in Systemic Dysfunction of the Geriatric Patient (Pre-Convocation)Drs. Kuchera and Ettlinger—Rosen Shingle Creek Resort, Orlando, FLCellular Biology and the Cellular Matrix (Pre-Convocation)–Frank H. Willard, PhDRosen Shingle Creek Resort, Orlando, FLAAO Convocation—Mechanotransduction and the Interstitium: The World In BetweenGregg C. Lund, DO—Rosen Shingle Creek Resort, Orlando, FLVolume 22, Issue 2, Summer 2012 The AAO Journal Page 7

“The difference a DO makes” in welcominghome our troopsWilliam Bograkas, DO, MA, FACOEP, COL, MC, FS USA (retired)The human spirit has not changed since Sun Tzuaddressed moral influence with the five fundamentals inThe Art of War 1 and Homer wrote of Odysseus’s journey toand from Troy in The Illiad 2 and The Odyssey. 3 What haschanged, however, is technology and the art of medicine.After World War II, our troops returned home by ship.They returned home from Vietnam by plane. During thelong “War on Terror,” our casualties have been treatedand stabilized through the modular Emergency MedicalServices (EMS) system of Joint Medical Force 2010.Through excellence in military EMS, survivors, notvictims, have received care and returned stateside within72 to 96 hours. Today, a surge of military patients requirethe unity of efforts between the Department of Defense, theDepartment of Veterans Affairs and our civilian medicalcommunities. We shall be judged by the homecomings ofthose we deploy.Recommended reading for those who care forveterans can be found at: www.ncptsd.va.gov,www.DCoE.health.mil and www.biausa.org.References1. Sun T. The Art of War. Griffith SB, trans. Oxford: OxfordUniversity Press;1963.2. Homer. The Iliad. Lattimore R, trans. Chicago: University ofChicago Press; 1951.3. Homer. The Odyssey. Butcher SH and Lang A, trans. New York:P.F. Collier & Son, 1909–14.4. Truhlar RE, ed. Doctor A. T. Still in the Living: His Conceptsand Principles of Health and Disease. Cleveland, OH: privatelypublished; 1950.Our own Civil War influenced the teaching andpractice of Major Andrew Taylor Still. Let us not forget histeachings when we welcome our Veterans home. The layingof hands on these patients will restore tissue perfusion andrelieve tissue congestion (tissue memory). We all need tofeel the safety of home.We all need to remember “an Osteopath asks no favorof drugs” 4 and be respectful of opiates. Fifty percent ofpatients with post-traumatic stress disorder (PTSD) selfmedicate—a great challenge in soldiers’ homecomings.Our teachers have taught us the importance of treatingboth body and mind. Let us do no harm as we receive ourreturning Veterans.As we treat and unwind the soma, memories release.Trauma to the autonomic nervous system (ANS) is seenin all disasters, not just man-made (war) disasters. Majordepression, anxiety disorders, PTSD and substance abuseare all reported in the disaster psychiatry literature. Asosteopathic physicians, we can make a difference throughthe restoration of the ANS, and through our support ofthose in recovery.I hope the reader will find these journal readings ofvalue. I am confident that our profession will continue towelcome our troops home and practice “the difference aDO makes.”Page 8The AAO Journal Volume 22, Issue 2, Summer 2012

Ultrasound-Guided InjectionsSeptember 7-8, 2012, at UMDNJSOM in Stratford, NJCourse DescriptionThis course is designed for physicians who are novices atsonographic guidance for injections. Under the directionof physiatrist Sajid Surve, DO, course participants will beintroduced to the basic principles of ultrasound, learn properinjection techniques with ultrasound guidance and learnproper billing and coding for this procedure. Cadavers willbe available for practice, and table trainers will facilitate alow faculty-to-participant ratio. The course will focus on theinjection of the major joints: glenohumeral, sacroiliac, hip, andknee.Course ObjectivesUpon completion of this course, participants will be able to:• Apply the basic principles of musculoskeletal ultrasound• Comfortably navigate the necessary equipment requiredfor sonographic guidance of injections• Utilize proper injection techniques under sonographicguidance for the glenohumeral, sacroiliac, hip and kneejoints.• Bill, code and document correctly for ultrasound-guidedinjections• Avoid common pitfalls associated with the aboveproceduresCME16 hours of AOA Category 1-A credit is anticipatedCourse DirectorsMillicent K. Channell, DO, FAAO, is a 2001 graduate of thePhiladelphia College of Osteopathic Medicine. After completingher Family Medicine residency and NeuromusculoskeletalMedicine/Osteopathic Manipulative Medicine (NMM/OMM) residency, she joined the faculty of UMDNJSOM in thedepartments of OMM and Family Medicine. She has madenumerous scholarly contributions to osteopathic medicine,most notably as co-author of the book The 5-Minute OsteopathicManipulative Medicine Consult.Sajid A. Surve, DO, is a 2005 graduate of the UMDNJSOM.After completing a traditional rotating internship at DelawareCounty Memorial Hospital in Drexel Hill, PA, he became aninaugural resident, and the irst Chief Resident, of the PhysicalMedicine and Rehabilitation residency at Long Beach MedicalCenter in Long Beach, NY. He joined the faculty of UMDNJSOMin 2009, and completed an NMM/OMM residency in 2010.Course LocationUMDNJSOMOne Medical Center DriveStratford, NJ 08084Course TimesFriday and Saturday: 8:00 am - 5:30 pm (lunch provided)Travel ArrangementsCall Tina Callahan of Globally Yours Travel at (800) 274-5975.Registration FormUltrasound-Guided InjectionsSeptember 7-9, 2012Name: ________________________________________ AOA#: _____________Nickname for Badge: _______________________________________________Street Address: ____________________________________________________________________________________________________________________________City: __________________________________State: ________ Zip: ___________Phone: _______________________________ Fax: ___________________________E-mail: ______________________________________________________________By releasing your fax/e-mail, you have given the AAO permission to sendmarketing information regarding courses to your fax or e-mail.Billing Address (if different than above): _________________________________________________________________________________________________Registration RatesOn or before July 9 After July 9AAO Member $ 1500.00 $ 1600.00AAO Non-Member $ 1600.00 $ 1700.00The AAO accepts check, Visa, Mastercard or Discover paymentsin U.S. dollarsCredit Card #: ________________________________________________________Cardholder’s Name: __________________________________________________Expiration Date: _____________________ 3-digit CVV#________________I hereby authorize the American Academy of Osteopathy tocharge the above credit card for the full course registrationamount.Signature: __________________________________________________________Click here to view the AAO’s Cancellation and Refund PolicyPlease submit registration form and payment via mail to the American Academy of Osteopathy,3500 DePauw Blvd., Suite 1080, Indianapolis, IN 46268 or by fax to (317) 879-0563.Or register online at www.academyofosteopathy.orgVolume 22, Issue 2, Summer 2012 The AAO Journal Page 9

Understanding blast-induced traumatic brain injury(bTBI) through mechanisms and patterns of injuryPatrick M. Malie, MS, OMS III; Marc Quentin Sonnier, Jr., MS;Murray R. Berkowitz, DO, MA, MS, MPHAbstractObjective of review: To provide clinicians and researcherswith a comprehensive, evidence-based overview ofblast-induced traumatic brain injury (bTBI) and theimplications for a multi-disciplinary approach to treatingmilitary personnel. Understanding the effects of that injuryon the human brain is difficult due to the complexityof explosive forces. This review introduces new toolsand innovations being applied within the context ofbTBI research. Understanding blast injury—a commonoccurrence in military combat— by evaluating benchmarksfor concussive or mild traumatic brain injury (mTBI)with computational tools, neuroimaging, epidemiologyand neurophysiology in a multi-disciplinary approachto treatment, will help delineate subsequent effects thatmay complicate recovery and produce the majority ofmanifestations associated with this type of injury.Recent findings: Body and vehicular armor reducescombatants’ risk of higher severity blast exposure,which tends to increase the rate of bTBI incidence. Anincrease of mTBI literature has been found in a diverserange of science and medical journals from the fields ofimmunology, epidemiology, neuroscience and psychiatry,to computer science and blast forensics. This has improvedunderstanding of what differentiates bTBI, post-concussivesyndrome and post-traumatic stress disorder (PTSD) withthe goal of improving diagnosis.Conclusions: In the current state of the U.S. medicalcrisis, cost-effective solutions are needed to managethe new condition of chronic bTBI in our veterans.Understanding neurodegeneration with biomarkers,axonal damage, personality aberrations and inflammatoryresponses aimed at building treatment protocols improvesboth patient outcomes and scientific research progress.Through a multidisciplinary approach to understandingthe mechanisms and patterns of injury of blast-inducedtraumatic brain injury, research scientists and physicianshope to achieve optimal patient outcomes.IntroductionAs many as 320,000 American military combatveterans who have served in the current wars in Iraq andAfghanistan are estimated to have sustained a traumaticbrain injury (TBI) as of January 2008. 1 TBI has beendescribed as the “signature injury” of Operation Iraqi Freedom(OIF) and Operation Enduring Freedom (OEF). 2-5 Thegrowing number of conflicts in recent years has led to anunprecedented increase in the use of weaponry resultingin blast-induced TBI (bTBI). Such weaponry includesimprovised explosive devices (IEDs), rocket-propelledgrenades (RPG-7 to RPG-29), thermobaric “enhancedblastexplosives,” and explosive-formed projectiles. 6The negative effects of these devices are felt not only bymilitary personnel, but also civilians. In 2007, roughly14,000 terrorist attacks occurred worldwide, resultingin more than 44,000 injuries and 22,000 deaths, a 20 to30 percent increase from 2006. 7 Moreover, as a resultof modern warfare, it is estimated that 10 civilians arekilled for every one combatant casualty. 8 The studyand management of blast-related injuries is not a recentphenomena, despite its increased prevalence in recenttimes. The first known documented study of blast-relatedhead trauma occurred more than 90 years ago. 9During World War I, British Army physicians Drs.Gordon Holmes and Fred Mott studied soldiers subjectedto blasts who developed neuropsychiatric symptoms. 10Holmes and Mott had trouble differentiating betweenemotional trauma and physical brain injury. 9,11 Suchdifficulties persisted into World War II—some physiciansbelieved there was no brain injury, while others notedelectroencephalography changes similar to those previouslyseen in closed head injuries. 12 Although it was evident thatsecondary and tertiary blast injuries could result in braindamage, it remained unresolved whether primary blastinjuries could directly damage the brain.TBI OverviewTBI is defined as damage to the brain from anexternal mechanical force, including impact, accelerationor deceleration, penetration by a projectile and blastwaves. 13-14 It is an acquired form of brain injury. TBI isa complex injury with a broad spectrum of disabilitiesand symptoms that can be classified as mild, moderate orsevere, depending on the extent of the damage inflicted onthe brain. 15 Brain injury is also known as intracranial injuryPage 10The AAO Journal Volume 22, Issue 2, Summer 2012

Unfortunately, military-associated blast TBI is muchmore complex. Diffuse axonal injury occurs as a resultof rotational acceleration accompanying indirect loading.Of these rotational injuries, we are most susceptibleto sheer strain. This is due to the large cross-sectionalarea of the CNS providing many mediatory paths forcontradicting force vectors and causing both accelerationand deceleration forces. Animal models associate rotationalacceleration with concussion and linear accelerationwith contusions and subdural hematomas without loss ofconsciousness. As the lowest of TBI severity, mild bTBIhas a reported prevalence of 80 percent spanning threedecades of civilian traumatic brain injury. 33,39-41It is evident that many of the features observed inanimal models mimicking focal and diffuse TBIs arealso seen in bTBI. 42 According to Cernak and Noble-Haeusslein, 42 common features include vasospasmand barrier disruption, electroencephalogram (EEG)abnormalities, oxidative stress, elevated ICP, metabolicdisturbances and energy failure. Although some reportspropose varying temporal and spatial profiles, as well as adifferent frequency of pathological changes in bTBI versusnon-explosive TBI, other studies suggest a lack of strongevidence that blast is categorically different than othermechanisms of TBI. 43-45 For instance, Ling, et al., 44 proposethat the occurrence of vasospasm, which is often the causeof delayed neurological deterioration, appears to be moretypical following bTBI than other types of TBI, suchas penetrating TBI (pTBI) and closed head TBI (cTBI).As a result, military neurosurgeons have had to performdecompressive craniectomies more often than is typical forpTBI or cTBI. Moreover, there was an increased incidenceof PTSD symptoms reported among bTBI participants ina study designed to compare patterns of performance onneuropsychological measures. 45 However, with respect tocognitive sequelae, it was argued that there is no strongevidence that blast is categorically different than othermechanisms of TBI. 45Despite the aforementioned cases noting differingfeatures between bTBI and TBI from other mechanisms, itis still a challenge to confirm or refute a unique signatureclinical description for bTBI. Epidemiologic data aloneis not sufficient in differentiating the less-studied blastinjury features from the more well-known componentsof pTBI and cTBI. 44 Further complicating the issue isthat individuals who experience bTBI are also likely toexperience other severe injuries, including hemorrhagicshock and limb amputation. 42 Addressing other suchinjuries can mask features attributable to bTBI.Predicting Arousal Defects as a Long-TermConsequence of Blast-Induced mTBImTBI diagnosis is difficult due to its heavy relianceon patient recall of the history of the trauma. In the bestcasescenario, eyewitness accounts can substitute forthe memory of the injured. As a diagnostic componentof mTBI, loss of consciousness (LOC) is a result offunctional degradation of both cerebral hemispheres ofthe reticular activating system (RAS). Blyth proposes thatmTBI-associated alteration of consciousness is caused byinjury to consciousness as a state-dependent structure thatincludes the RAS. This structure is excited by input fromsurrounding sensory tracts, and transmits this excitationto the cortex to induce generalized cortical and behavioralarousal. Within the brainstem reticular formation, it extendsfrom the top of the spinal column to the rostral midbrainwith extensions into the thalamus and hypothalamus. 33,46Significant Forces of Blast EffectsBlast-induced TBI acts through multiple simultaneousevents occurring in succession, and as a result, canbe categorized according to three distinct actions ofinjury. 47 Blast waves traverse the explosives’ surroundingenvironment with an initial high-pressure shock waveleading to over-pressurization. An explosion createsballistic projectiles within a viscous medium, giving riseto blast-pressure waves. These projectiles, such as blastdebris, lose energy as they propagate toward the greaterforces generating the pressure waves. The magnitude ofthese waves is the sum of interfering wave points createdas it propagates, signature waves from conserved areas ofspatial expansion with a consequentially causal collapse,and reflected waves from stiffer boundaries. This propertyof energy dissipation is the inherit magnitude of explosiveblast waves. 48The over-pressurization mentioned earlier is followedby a subsequent blast wind that causally follows thesubsequent negative pressure created by the shock wavesimilar to an elastic-like pressure recoil. The ultimatevector of this reverse wind is directed toward the explosivesource, leading to rapid under-pressurization. 49 Thenegative transient pressures associated with reverse windcan create cavitation bubbles that are toxic to neurons.In vitro studies of mild TBI discovered induced circuitcrosstalk as a consequence of single, mild blast exposures.Multiple blasts increase neuronal tissue susceptibility todamage associated with excitotoxic insult. The action ofprimary blast injury relates to the wave action that theblast produces through the mediums it traverses. Tympanicmembrane rupture is generally considered a reliable patientpresentation for primary blast exposure, but interestingly,Page 12The AAO Journal Volume 22, Issue 2, Summer 2012

less than two percent of cases in the Madrid, Spain, trainstation explosion experienced pulmonary injury lacking thisindicator.Factors that complicate blast outcomes includeexplosive type, peak over-pressure and its duration, impulseas complex wave forms, location of the explosion and itsrelative proximity, environmental hazards, body orientationto the blast and barriers. All these factors impact, as wellas facilitate, bodily insult due to blast exposure. Secondaryacts by blast waves propulsion on fragmented objects thatbecome projectiles. This bTBI is more associated withpenetrating injury where, in the case of neurotrauma,the integrity of the skull becomes compromised by theblast’s projectiles. These projectiles create superficialpathology that is more apparent than the latter. Mild blastseldom causes injury of higher blast severity, but multipleexposures, like those seen in many military personneloverseas, creates acceleration/pressure forces that result inneuron associated soma swelling, nuclear prominence andsometimes neuronal death. 50 In vitro studies focusing onthe effects of direct laceration by cell scratching producedfindings that proposed the effects of micro-lacerationinduced a greater amount of neuronal cellular death thancompared to glial cells.Tertiary is relevant to the surroundings in which theblast’s action mediates a collision. Likely damage can beexpected between the hemispheres separating the cerebrumfrom the cerebellum due to sheer strains. Cytoskeletalalterations, organelle disruption and derangement haveoccurred in studies by Chen 51 when tertiary effects werequantified in vitro as an affect of mechanical deformationand quaternary involved burns to surface tissues proximalto those in contact with air, such as the respiratory tractsand skin. These are commonly seen with explosiveweapons capable of radiation delivery over largeareas. Injury findings of this type of blast would likelydemonstrate the neuronal damage similarly seen with heavycellular phone use. 42,51-58Computational Modeling of Blast InjuryChen describes researchers contrasting the virtualrepresentation of geometric deformations of blast wavesto that of experimentally similar effects of induced blasttrauma as an injury predictor. 51 With the aid of embeddedmonitoring systems consisting of cost-effective, helmetbasednanosensors capable of relaying digitalized forceinjury characteristics to a field hospital, medical teamsare able to explore new possibilities of guided, long-termtreatment into structurally precise areas of perceiveddamage. 59 Some are concerned that helmets, especiallywith the added weight of electronic sensors, may contributeto increased cerebral damage. But recent computational,three-dimensional analysis discredited this hypothesiswith findings that are suggestive of danger only whenforces are so high that the damage would be similarlydestructive either with or without protective headgear. Thecombined advantage of both recorded collateral damagecharacteristics as input for computational cell-deformationand cell-stretching modeling allows for estimates ofboundary zones between damaged and undamaged areas inthe brain. These data would be used to provide additionalinformation to the more obvious clinical findings. Theprecision of finite element models representing blastdynamics upon brain tissue will inevitably increase withmore research to meet the level of confidence needed to beuseful for diagnosticians to develop a structured approachto differential diagnosis for blast-related mTBI. 51,52,54,60-64Experimental Study of Blast EffectsThe more commonly studied methods forinvestigating blast effects are either by open-air blast,which is often done on large specimens, or closed-pressuresystems well suited to investigate blast wave kinetics withsmaller specimens in a more controlled fashion. Openairblast studies, while lacking the scalar precision andobjectivity of closed-air studies, presents the more realistic,multi-dimensional variability of forces experienced by U.S.military forces. One such study has attempted to combinethe more precise, closed-air blast tube investigationwith the varied, multi-mode shock of open blast studiesin a cost-effective and highly subjective TBI screeningexperiment as an alternative to the expensive Heliumbasedexperiment. The hypothesis is that multi-mode shockdraws correlate the severity of brain insult with a pressuretimesignature of varied blast signatures in an attempt toassociate a higher relevance to the variety and occasionallyoverlapping nature of injuries experienced by deployedcombat troops.Using several characteristically different gas typesin the experiment, expensive helium used to improve thevelocity performance of closed shock tube research wasreplaced with relatively inexpensive oxyhydrogen. Italso reduces conditional ischemia as an inherent propertyof the closed experiment’s atmospherically isolatedenvironment. This pressure-time signature compensatesfor the traditional lower resolution peak pressure as ameasure of the many different components of blast effects.The six parameters studied were shock wave velocity,positive phase magnitude, positive phase duration, positivephase impulse, negative phase magnitude, and the impulsedifference between reflected and free-field pressures. Thisallows the degrees of damage to be predicted as potentialcontributions of individual blast components. Greatercerebral vascular damage was seen using compressed airVolume 22, Issue 2, Summer 2012 The AAO Journal Page 13

ather than oxyhydrogen of similar peak pressure. Thissuggests that this method may be a more realistic and costeffectiveapproach to blast study. 65,66Long-Term Effects Associated with Blast mTBILong-term effects of mTBI on the CNS are elusivebecause conflicting findings in scientific and medicalliterature are unclear regarding mechanisms relative tothe nervous system. The combination of IEDs, along withdramatically improved soldier survivability since theinfancy of defining PTSD at the end of the Vietnam Warera, has bolstered a significant interest in blast-inducedneural injury. Although animal studies have indeed proventhat, of the many varied mechanisms of injury, blastoverpressure waves seem to cause the diffuse axonal-typeof neuropathological injury. 67 TBI injury findings of thesemechanisms illustrate primary blast wave as a uniquemechanism and injury variable. 49Blast-induced mild traumatic brain injury (bmTBI),whether occurring in a combat theater or berthing areas,is typically associated with instant, combustion-inducedcephalic blunt trauma, resulting in temporary debilitation ofneurological functionality. 23Helmet Protection from Blast mTBIThere has been much debate to whether helmetprotection adds to or lessens bTBI. Service memberswearing helmets were more likely to withstand both lowerTBI severity and Injury Severity Scores when comparedto those who weren’t, even though the helmet participatedin blast mechanisms. Less than 40 percent of IED attackswere accounted for by helmetless TBI as compared to thelarger 82 percent of operatives wearing helmets. This smallpercentage of victims unprotected from IED blast waslikely attributable to a combination of convoy-requiredhelmet use established by military protocol, and theincreased vulnerability that predisposes mobilized groundvehicles to this type of attack. Consequently, higher TBIseverity associated with projectile-type weapons, includingtheir associated injury specifics, was significantly higherwhen helmet protection wasn’t available. This is likelythe result of ambush or unexpected attacks on militaryservicemen in berthing areas where it is more difficult formilitant extremists to exercise timely IED staging, thuswarranting the use of focused weaponry. Unfortunately,these servicemen are most vulnerable because of laxedprecaution in these areas, leading to helmet disrobe andsubsequent maximum morbidity. Therefore, these results,along with current findings, seem fairly agreed that helmetsdo reduce TBI severity. But new helmet designs are neededfor improved facial protection to optimize TBI reductionduring explosive exposure. 62,68ConclusionsSymptoms are not only dependent on the type andseverity of TBI, but also by the particular region of thebrain that is affected. 15 Mild TBI may result in loss ofconsciousness, while other symptoms include nausea,vomiting, headache, dizziness, difficulty balancing, lack ofmotor coordination, blurred vision, lightheadedness, fatigueor lethargy, tinnitus and changes in sleep patterns. 13,19Emotional and cognitive symptoms associated with mildTBI include behavioral or mood changes, confusion,as well as impairment of concentration, attention, andthinking. 15 An individual with moderate or severe TBI maypresent the same symptoms associated with mild TBI, aswell as persistent headache, vomiting and nausea, agitation,restlessness, confusion, loss of coordination, slurredspeech, dysarthria, aphasia, weakness or numbness oflimbs, convulsions and dilation of one or both pupils. 13,15,19Long-term symptoms of moderate or severe TBIinclude cognitive changes, such as issues with attentionsustainment, processing speed and executive function, aswell as changes in typical social behavior and judgement. 20Cerebral concussive syndromes are common amongthose subjected to explosions, with cognitive deficits andsubstantial memory dysfunction typically resulting. 69 Theseresults indicate that bTBIs are capable of causing cognitivedeficits, particularly problems with memory.Hoge, et al., 70 found mild TBI occurring amongsoldiers deployed in Iraq was strongly correlated withPTSD and other physical health issues months afterreturning home. Furthermore, it was suggested thatboth PTSD and depression were critical mediators ofthe relationship between mild TBI and physical healthproblems. 70-74 Significant correlation was found betweentympanic perforation and unconsciousness in blast-injuryvictims, suggesting a relationship between concussive braininjury and tympanic perforation. 5 It has also been noted thatboth tympanic perforation and primary blast injury werescarce in service members subjected to explosions in therecent US-Iraq conflict. 69,75 This may suggest that tympanicperforation may correlate with concussive brain injury,but not with other primary blast-induced injuries. Furtherstudies need to be conducted to provide insight into therelationship between tympanic perforation and concussivebrain injury.Currently, many features of bTBI remain unknown.The relatively recent increase in the occurrence of bTBIhas warranted a research push to allow for a bettercharacterization of the injury. In so doing, the clinicalpersonnel will be better able to provide proper assessmentand treatment techniques. Furthermore, family membersand friends of bTBI victims will be better prepared forcoping with effects that may last a lifetime.Page 14The AAO Journal Volume 22, Issue 2, Summer 2012

References1. Tanielian T, Jaycox LH, editors. Invisible Wounds of War:Psychological and Cognitive Injuries, Their Consequences, andServices to Assist Recovery. Arlington, VA: Center for MilitaryHealth Policy Research, the Rand Corporation; 2008.2. Martin EM, Lu WC, Helmick K, French L, Warden DL. (2008).Traumatic brain injuries sustained in the Afghanistan and Iraqwars. Journal of Trauma Nursing. 2008;15(3):94-99,100-101.3. Okie S. Reconstructing lives—a tale of two soldiers. The NewEngland Journal of Medicine. 2006; 355(25):2609-2615.4. Warden D. Military TBI during the Iraq and Afghanistan wars. TheJournal of Head Trauma Rehabilitation. 2006;21(5): 398-402.5. Xydakis MS, Fravell MD, Nasser KE, Casler JD. Analysisof battlefield head and neck injuries in Iraq and Afghanistan.Otolaryngology-Head and Neck Surgery. 2005;133(4):497-504.6. Lew TA, Walker JA, Wenke JC, Blackbourne LH, Hale RG.Characterization of craniomaxillofacial battle injuries sustainedby United States service members in the current conflicts of Iraqand Afghanistan. Journal of Oral and Maxillofacial Surgery.2010;68(1):3-7.7. NCTC Report on Incidents of Terrorism 2007. NationalCounterterrorism Center Worldwide Incidents Tracking SystemWebsite. http://wits.nctc.gov/Reports.do. Updated April 30, 2008.Accessed January 23, 2010.8. Shuker ST. Maxillofacial air-containing cavities, blast implosioninjuries, and management. Journal of Oral and MaxillofacialSurgery. 2010;68(1):93-100.9. Mott FW. The effects of high explosives upon the central nervoussystem. Lancet. 1916;1: 441-49.10. Kocsis JD, Tessler A. Pathology of blast-related brain injury.Journal of Rehabilitation Research and Development. 2009;46(6):667-672.11. Macleod AD. Shell shock, Gordon Holmes and the Great War.Journal of the Royal Society of Medicine. 2004; 97(2):86-89.12. 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Neuropsychological test performance insoldiers with blast-related mild TBI. Neuropsychology. 2010;24(2):160-167.29. Hoge CW, McGurk D, Thomas JL, Cox AL, Engel CC, Castro CA.Mild traumatic brain injury in U.S. Soldiers returning from Iraq.New England Journal of Medicine. 2008;358(5):453-463.30. Martin EM, Lu WC, Helmick K, French L,Warden DL. TraumaticBrain Injuries Sustained in the Afghanistan and Iraq Wars. Journalof Trauma Nursing. 2008;15(3):94.31. Ling G, Bandak F, Armonda R, Grant G, Ecklund J. Explosiveblast neurotrauma. Journal of Neurotrauma. 2009;26(6):815-25.32. Jones E, Fear NT, Wessely S. Shell shock and mild traumatic braininjury: A historical review. Am J Psychiatry. 2007;164(11):1641-1645.33. Blyth BJ, Bazarian JJ. Traumatic Alterations in Consciousness:Traumatic Brain Injury. Emergency Medicine Clinics of NorthAmerica. 2010;28(3):571-594.34. Baskin TW, Holcomb JB. Bombs, mines, blast, fragmentationand thermobaric mechanisms of injury. In: Mahoney PF, Ryan J,Brookes A, Schwab CW, eds. Ballistic Trauma: A Practical Guide.London: Springer-Verlag;2005:45-66.35. Vanderploeg RD, Belanger HG, Curtiss G. Mild traumatic braininjury and post-traumatic stress disorder and their associationswith health symptoms. Arch Phys Med Rehabil. 2009;90(7):1084-1093.36. Warden D. Military TBI during the Iraq and Afghanistan wars. JHead Trauma Rehabil. 2006;21(5):398-402.37. Sbordone RJ and Liter JC. Mild traumatic brain injury does notproduce post-traumatic stress disorder. Brain Inj. 1995;9(4):405-412.38. DeKosky ST, Ikonomovic MD, Gandy S. Traumatic braininjury—Football, warfare and long-term effects. N Engl J Med.2010;363(14):1293-1296.39. Thompson JM, Scott KC, Dubinsky L. Battlefield brain:Unexplained symptoms and blast-related mild traumatic brainVolume 22, Issue 2, Summer 2012 The AAO Journal Page 15

Page 16injury. Can Fam Physician. 2008;54(11):1549-1551.40. Auerbach JM, Segal M. Muscarinic receptors mediatingdepression and long-term potentiation in rat hippocampus. TheJournal of Physiology. 1996;492(2):479.41. Beck AT, Alford BA. Depression: Causes and treatments.Philadelphia: University of Pennsylvania Press; 2009.42. Cernak I, Noble-Haeusslein NJ. Traumatic brain injury: Anoverview of pathobiology with emphasis on military populations. JCereb Blood Flow Metab. 2010;30(2):255-266.43. Armonda RA, Bell RS, Vo AH, Ling G, DeGraba TJ, Crandall B,et al. Wartime traumatic cerebral vasospasm: Recent review ofcombat casualties. Neurosurgery. 2006;59(6):1215-1225.44. Ling G, Bandak F, Armonda R, Grant G, Ecklund J. Explosiveblast neurotrauma. Journal of Neurotrauma. 2009; 26(6):815-825.45. Belanger HG, Kretzmer T, Yoash-Gantz R, Pickett T, Tupler LA.Cognitive sequelae of blast-related versus other mechanisms ofbrain trauma. Journal of the International NeuropsychologicalSociety. 2009; 15(1):1-8.46. Vanderploeg RD, Curtiss G, Belanger HG. Long-termneuropsychological outcomes following mild traumatic braininjury. J Int Neuropsychol Soc. 2005;11(3): 228-236.47. Elsayed NM. Toxicology of blast overpressure. Toxicology.1997;121(1): 1-15.48. Courtney A, Courtney M. A thoracic mechanism of mild traumaticbrain injury due to blast pressure waves. Med Hypotheses.2008;72(1): 76-83.49. Howe LL. Giving context to post-deployment post-concussive-likesymptoms: blast-related potential mild traumatic brain injury andcomorbidities. Clin Neuropsychol. 2009; 23(8): 1315-1337.50. Wolf SJ, Bebarta VS, Bonnett CJ, Pons PT, Cantrill SV. Blastinjuries. The Lancet. 2009;374(9687): 405-415.51. Chen YC, Smith DH, Meaney DF. In-vitro approaches for studyingblast-induced traumatic brain injury. Journal of Neurotrauma.2009;26(6):861-876.52. Cullis I. Blast waves and how they interact with structures. J RArmy Med Corps. 2001;147(1): 16-26.53. Ritenour AE, Baskin TW. Primary blast injury: update ondiagnosis and treatment. Critical Care Medicine. 2008;36(7):S311.54. Sogbesan EA. Design and Analysis of Blast Induced TraumaticBrain Injury Mechanism Using a Surrogate Headform:Instrumentation and Outcomes. Nebraska Univ.-Lincoln, Dept. ofMechanical Engineering. Master’s Thesis. May 2011.55. Margulies S, Hicks R. Combination therapies for traumatic braininjury: prospective considerations. Journal of Neurotrauma.2009;26(6): 925-939.56. Cernak I, Savic J, Ignjatovic D, Jevtic M. Blast injury fromexplosive munitions. J Trauma. 1999; 47(1):96-104.57. Moore DF, Radovitzky R, Shupenko L, Klinoff A, Jaffee MS,Rosen JM. Blast physics and central nervous system injury. FutureNeurol. 2008; 3(3): 243-250.58. Moore DF, Jaffee MS. Military traumatic brain injury and blast.Neuro Rehabilitation. 2010;26(3): 179-181.59. Watkin KL, Iyer R, Karbalczyk Z, Sanders W, Patel J. HelmetIntegrated Nanosensors, Signal Processing and Wireless RealTime Data Communication for Monitoring Blast Exposure toBattlefield Personnel. Report for U.S. Army Medical Research andMateriel Command, Ft. Detrick, Maryland. Dec 2009.60. Grujicic M, Bell WC, Pandurangan B, Glomski PS. Fluid/structureinteraction computational investigation of blast-wave mitigationefficacy of the advanced combat helmet. Journal of MaterialsEngineering and Performance. 2011; 20(6):877-893.61. Harrisson S, Kirkman E, Mahoney P. Lessons learnt fromexplosive attacks. J R Army Med Corps. 2007;153(4):278-282.62. Nyein MK, Jason AM, Yu L, Pita CM, Joannopoulos JD, MooreDF, et. al. In silico investigation of intracranial blast mitigationwith relevance to military traumatic brain injury. Proceedings ofthe National Academy of Sciences. 2010;107(48): 20703-20708.63. Nyein MK. Computational modeling of blast-induced traumaticbrain injury. Mass. Inst.of Technology, Dept. of Aeronautics andAstronautics. Thesis. 2010.64. Moore DF, Jerusalem K, Nyein MK, Noels L, Jaffee MS,Radovitzky RA. Computational biology—modeling of primaryblast effects on the central nervous system. Neuroimage.2009;47:T10-T20.65. Reneer DV, Hisel RD, Hoffman JM, Kryscio RJ, Lusk BT, GeddesJW. A multi-mode shock tube for investigation of blast-inducedtraumatic brain injury. Journal of Neurotrauma. 2011;28(1):95-104.66. Cernak I, Merkle AC, Koliatsos VE, Bilik JM, Luong QT, MahotaTM, et. al.The pathobiology of blast injuries and blast-inducedneurotrauma as identified using a new experimental model ofinjury in mice. Neurobiology of Disease. 2011;41(2):538-551.67. Elder GA, Cristian A. Blast-related mild traumatic brain injury:mechanisms of injury and impact on clinical care. Mt Sinai J Med.2009;76(2):111-118.68. Macgregor AJ, Dougherty AL, Galarneau MR. Injury-specificcorrelates of combat-related traumatic brain injury in operationIraqi freedom. J Head Trauma Rehabil. 2011;26(4):312-318.69. Wolf SJ, Bebarta VS, Bonnett CJ, Pons PT, Cantrill SV. Blastinjuries. Lancet. 2009;374(9687): 405-415.70. Hoge CW, McGurk D, Thomas JL, Cox AL, Engel CC, Castro CA.Mild traumatic brain injury in U.S. soldiers returning from Iraq.The New England Journal of Medicine. 2008; 358(5):453-463.71. Bryant RA, O’Donnell ML, Creamer M, McFarlane AC, ClarkR, Silove D. The psychiatric sequelae of traumatic injury. Am JPsychiatry. 2010;167(3): 312-320.72. Lannoo E, Colardyn F, Jannes C, de Soete G. Course ofneuropsychological recovery from moderate-to-severe head injury:a 2-year follow-up. Brain Injury. 2001;15(1):1-13.73. Snell FI, Halter MJ. A signature wound of war: mild traumaticbrain injury. J Psychosoc Nurs Ment Health Serv. 2010;48(2): 22-28.74. Bryant RA. Disentangling mild traumatic brain injury and stressreactions. N Engl J Med. 2008; 358(5):525-527.75. Harrison CD, Bebarta VS, Grant GA. Tympanic membraneperforation after combat blast exposure in Iraq: A poor biomarkerof primary blast injury. The Journal of Trauma. 2009: 67(1): 210-211.Accepted for publication: June 2012Address correspondence to:Patrick M. Malie, MS, OMS III; Marc Quentin Sonnier, Jr., MS;Murray R. Berkowitz, DO, MA, MS, MPHDepartment of Osteopathic Manipulative MedicinePhiladelphia College of Osteopathic Medicine—Georgia Campus625 Old Peachtree Road NWSuwanee, Georgia 30024murraybe@pcom.eduThe AAO Journal Volume 22, Issue 2, Summer 2012

Lighting theFlame ofKnowledge.Philadelphia College of Osteopathic Medicine (PCOM) brings to light a rich tradition of excellence in education and leadership.Currently, the Georgia Campus—Philadelphia College of Osteopathic Medicine, in the greater Atlanta area, has the following exciting positions available:Faculty Position: Department of Osteopathic Manipulative MedicineFull time faculty position in the Department of Osteopathic Manipulative Medicine. This individual will be expected to teach osteopathic medicalstudents in both lecture and laboratory sessions in all four years of the curriculum, see patients and develop an outpatient clinic for M-3 month longrotation, plan and supervise OMM Inpatient Student Service, assist in preparation of OMM video clips and tutorials, participate in existing researchand initiate new OMM research, assist in planning and production of new publications, and assist in planning and supervision of the OMM Residency.The successful applicant will have a D.O. degree and proficiency in osteopathic manipulative medicine. The candidate needs to have or be eligiblefor a license to practice Osteopathic Medicine in the State of Georgia. Board Certification or eligibility by the AOBNMM or AOBSPOMM is required.Additional Board Certification or eligibility by the AOBFM is desirable. The review of applications will begin immediately and continue until theposition is filled. Salary for this position will be commensurate with experience and qualifications.Clinical Education CoordinatorSeeking qualified Osteopathic Physician for a full-time Clinical Education Coordinator. This full time position reports to the Chair ofUndergraduate Clinical Education. This individual will be responsible as the Director of the Advanced Clinical Skills Program. He/Shewill supervise the Clinical Adjunct Facultyís participation in the didactic educational programs and assist the Chair in management ofthe Clinical Clerkship program. Minimum of five years in a clinical practice. Experience in clinical education as a Clerkship Director,Program Director, Didactic Educator, or similar activities. Must be Board Certified in a Primary Care specialty.To apply for these positions, send via E-mail a personal statement describing interest in and qualifications for this position, acurriculum vitae, and names and addresses of three references, preferably from current or former supervisors.All inquiries must include salary requirements and should be directed to: Department of Human Resources, GA-Campus, 625 OldPeachtree Road, Suwanee, GA 30024. Call (678) 225-7515; Fax (678) 225-7519; Email: hr@pcom.edu EOEWWW.PCOM.EDUBasic Musculoskeletal Manipulation Skills:The Job 15 Number: Minute 161960.1 Ofice MT EcounterClient:Publication: AAO Newsletterby Michael P. Rowane, DO, Size: MS, FAAFP, 7.5 x 4.5 FAAO & Paul Evans, DO, FAAFP, FACOFPArtist:Ad Delivery:Insertion Date(s):Color:Email Address:Confirmation:Phila. College of Osteopathic Medms--4-1-121----This material is developed by, and is the property of Alstin Communications, Inc. and is to beused only in conjunction with services rendered by Alstin Communications, Inc. and its agents. Itis not to be copied, reproduced, published, exhibited or otherwise used without the express writtenconsent of Alstin Communications, Inc. ©2008 Alstin Communications, Inc.Color depicted is for presentation purposes only and may not be an exact representation of thefinal product. Every effort and care has been made to simulate the colors of the finished product.See first page of Insertion Order for actual size and insertion date.NEW IN THE AAO BOOKSTORE!Purchase your copy on our Web site:www.academyofosteopathy.org(Select “AAO Store” from the left-hand menu)AAO member price: $89.95AAO non-member price: $99.95(plus shipping and handling)Volume 22, Issue 2, Summer 2012 The AAO Journal Page 17

Clinical management and multipotential treatmentstrategies for blast-induced traumatic brain injury (bTBI)Patrick M. Malie, MS, OMS III; Murray R. Berkowitz, DO, MA, MS, MPHAbstractObjective of review: To gain an understanding of currentclinical management, treatment strategies and sequelae ofblast-induced traumatic brain injury (bTBI). Due to thenature of bTBI, the focus is placed on military populations.Recent findings: With the increased use of body armor inthe military, injuries that were once considered to resultfrom secondary and tertiary blast effects are increasinglybeing attributed to primary blast effects. The occurrenceof vasospasm and post-traumatic stress disorder (PTSD)symptoms appear to be more frequent in bTBI than withother mechanisms of brain injury. Diketopiperazine therapyand hyperbaric oxygen therapy are multipotential treatmentdesigns for bTBI.Conclusions: Due to the increased occurrence of bTBIas a result of modern warfare, a collaborative effort isrequired by all medical personnel involved in the clinicalmanagement, assessment and treatment processes in orderto increase the probability of favorable outcomes.Introduction and TBI OverviewIt is estimated that by January 2008, as many as320,000 American armed forces serving in the current Iraqand Afghanistan wars experienced a traumatic brain injury(TBI). 1 The growing number of conflicts in recent years hasled to an unprecedented increase in the use of weaponryresulting in blast-induced TBI (bTBI), so much so that TBIhas been designated as the “signature injury” of OperationIraqi Freedom (OIF) and Operation Enduring Freedom(OEF). 2-5TBI is defined as damage to the brain from anexternal mechanical force, including impact, accelerationor deceleration, penetration by a projectile and blastwaves. 6,7 TBI is a complex injury with a broad spectrumof disabilities and symptoms that can be classified asmild, moderate or severe, depending on the extent of thedamage inflicted on the brain. 8 Brain injury is also knownas intracranial injury or head injury, although the latterdoes not necessarily connote neurological defects. TBIis divided into two subcategories: (1) primary injuryoccurring at the moment of trauma and (2) secondary injuryoccurring after the trauma per se, which may persist for anextended period. 9 Secondary injury is promoted throughbiochemical cascades and further cellular damage from theeffects of the primary injury, and can take hours to daysto present following the initial injury. 10 Almost half of allTBI patients deteriorate after the initial injury, and manysuccumb days to weeks later. 11Symptoms are not only dependent on the typeand severity of TBI, but also by the particular regionof the brain affected. 8 Mild TBI may result in loss ofconsciousness, while other symptoms include nausea,vomiting, headache, dizziness, difficulty balancing, lackof motor coordination, blurred vision, lightheadedness,fatigue or lethargy, tinnitus and changes in sleep patterns. 6,12Emotional and cognitive symptoms associated with mildTBI include behavioral or mood changes, confusion,as well as impairment of concentration, attention andthinking. 8 An individual with moderate or severe TBImay present the same symptoms associated with mildTBI, as well as persistent headache, nausea and vomiting,agitation, restlessness, confusion, loss of coordination,slurred speech, dysarthria, aphasia, weakness or numbnessof limbs, convulsions and dilation of one or bothpupils. 6,8,12 Long-term symptoms of moderate or severe TBIinclude cognitive changes, such as issues with attentionsustainment, processing speed and executive function, aswell as changes in typical social behavior and judgement. 13Cerebral concussive syndromes are common amongthose subjected to explosions, with cognitive deficits andsubstantial memory dysfunction typically resulting. 14 Theseresults indicate that bTBIs are capable of causing cognitivedeficits, particularly problems with memory.According to Hoge, et al., 15 mild TBI occurringamong soldiers deployed in Iraq was strongly correlatedwith PTSD and other physical health issues monthsafter returning home. Recent studies have suggested thattympanic perforation, or rupture of the eardrum, mayforeshadow concussive brain injury, but not necessarily forother primary blast-induced injuries. 5,14,16It is evident that many of the features observedin animal models mimicking focal and diffuse TBIs arealso seen in bTBI. 17 According to Cernak and Noble-Haeusslein, 17 common features include vasospasmand barrier disruption, electroencephalogram (EEG)Page 18The AAO Journal Volume 22, Issue 2, Summer 2012

abnormalities, oxidative stress, elevated intracranialpressure (ICP), metabolic disturbances and energy failure.Though some reports propose varying temporal and spatialprofiles, as well as a different frequency of pathologicalchanges in bTBI versus non-explosive TBI, other studiessuggest a lack of strong evidence that blast is categoricallydifferent than other mechanisms of TBI. 18-20 For instance,Ling ,et al. 19 proposes that the occurrence of vasospasm,which is often the cause of delayed neurologicaldeterioration, appears to be more typical following bTBIthan other types of TBI, such as penetrating TBI (pTBI) andclosed head TBI (cTBI). As a result, military neurosurgeonshave had to perform decompressive craniectomies moreoften than is typical for pTBI or cTBI.Clinical ManagementClinical care for bTBI begins on the battlefield andis carried out in accordance with the ‘‘Guidelines forField Management of Combat-Related Head Trauma.” 19A primary objective of the guidelines is to serve as aresourceful tool for all the individuals involved in themanagement process, including the physician, commandingofficer, logistician and combat medic. 21 They provideevidence-based support for military medical personnel inthe assessment, treatment and transport of TBI combatcasualties. One of the assessment techniques included inthe guidelines involves the combatant’s Glasgow ComaScale (GCS) score.A more detailed clinical assessment should be madeupon arrival at a combat support hospital, beginningwith an immediate CT to identify lesions such as skullfractures, intracranial hemorrhage and cerebral edema. 22Critical issues to attend to include maintaining properoxygen levels, controlling ICP and ensuring propercerebral perfusion pressure. 21 A frequent observationamong clinicians is the presence of both hyperemia andsevere edema in the acute period, which tends to occurmore readily when a traumatic subarachnoid hemorrhageis observed. 19 A delayed increase in ICP has been observedin some individuals occurring two to three weeks aftersevere bTBI, although it may be attributable to othercomplications such as vasospasm. 18 In the first study toanalyze the effects of blast injury on cerebral vasculature,Armonda, et al. 18 found that clinical outcomes in bTBIvictims with traumatic vasospasm were worse whencompared to those who presented without it. Becauseinvestigations into the effects of blast injury on cerebralvasculature have only recently begun, further studieswill need to be conducted to determine if a significantrelationship exists between the two.General management of increased ICP includescontrolling the airway, elevating the patient’s head to 30degrees and administering Mannitol (0.5 to 1 g/kg over 10min). 23 Mannitol (Osmitrol) is a weak renal vasodilator thatis used as an osmotic diuretic. Hypertonic saline solutionsare an option that has shown efficacy in patients sufferingfrom an increase in ICP. 19 In particular, intravenousinjection of 23 percent NaCl can be used to alleviate acuteelevations of ICP, followed by repeated infusions of twopercent and three percent NaCl to stabilize ICP. 23 A criticalaspect of hypertonic saline therapy is that serum osmolalitycan be increased without compromising intravascularvolume, as many victims of severe blast injury presentwith hemorrhagic shock. 22 Unfortunately, many patientssuffering from intracranial hypertension do not respondupon implementation of the aforementioned strategies, andfurther intervention is required.Decompressive craniectomy is one such interventionthat played a critical role in alleviating adverse effectsof severe brain swelling following bTBI in OIF. 24 In adecompressive craniectomy, part of the skull is removedto permit space for the swelling brain to expand. Asidefrom easing the effects of increased ICP, it also improvesbrain oxygenation, cerebral blood flow and increasescompliance. 25 Some studies have suggested improvedoutcomes after decompressive craniectomy followingbTBI. 24,26 For instance, Aarabi, et al., 24 indicated anassociation between improved functional outcome anddecompressive craniectomy in patients with unmanageableICP and/or brain herniation. More than 61 percent ofpatients in an observational study with increased ICPdemonstrated favorable outcomes (defined as goodrecovery or moderate disability), following decompressivecraniectomy. 26 Moreover, decompressive craniectomyresulted in more favorable outcomes in patients with higherGCS scores. 22 Current randomized trials in Australia andthe United Kingdom could provide further insight intodecompressive craniectomy’s role in improving outcomeafter severe head injury. 27,28Positron emission tomography (PET) is an effectiveand resourceful technique for quantifying ischemic burdenafter TBI. 29 TBI studies implementing PET have shown thatearly reductions in cerebral perfusion can result in cerebralischemia, which is correlated with adverse outcomes. 29,30PET has demonstrated that in TBI, the threshold of cerebralblood flow (CBF) below which irreversible tissue damageoccurs varies from the classical CBF threshold for stroke. 30TreatmentStoica, et al., 31 discussed a multipotential treatmentdesign that has shown effectiveness for TBI and spinalcord injury. The approach was based on thyrotropinreleasinghormone (TRH)—a tripeptide hormone thatis metabolized to a cyclic dipeptide (CHP). CHP can beVolume 22, Issue 2, Summer 2012 The AAO Journal Page 19

classified as a diketopiperazine—a class of cyclic, organicsecondary metabolites with a wide variety of biologicalfunctions. 32 Similar to other diketopiperazines, CHP isable maintain substantial physiological function. 32 Ofall the diketopiperazines structurally similar to CHP thatwere developed by Faden, et al., 33 1-ARA-35b (35b) hasbeen evaluated both in vitro and in vivo experiments, andshowed neuroprotection in both necrotic and apoptoticcell death models. 31,34 When introduced intravenously, 35blowered lesion volume by almost 70 percent and improvedboth cognitive and motor skills in mice after either fluidpercussion-induced (FPI) TBI or controlled cortical impact(CCI). 31 35b is presently being investigated for humanclinical trials in head injury.Another multipotential treatment strategy that maybe beneficial in treating bTBI is hyperbaric oxygen therapy(HBOT). HBOT utilizes oxygen at pressures greater thanatmospheric pressure in an enclosed chamber to treatcertain disease processes, such as anemia, carbon monoxidepoisoning and air embolism. 35 The physiologic effects ofHBOT are dependent on the underlying pathology of thedisease. For instance, HBOT has been shown to causeproliferation in both normal and diabetic human fibroblastsin vitro. 36 Furthermore, HBOT has demonstrated the abilityto lower apoptosis and improve mitochondrial recovery inhypoxic neurons. 37 It is suggested that the enhancement inmitochondrial function facilitates cognitive recovery andlowers hippocampal neuron loss after TBI. 37In a case report conducted by Wright, et al., 38two U.S. servicemen who had suffered mild TBI froma roadside IED showed improvements in AutomatedNeuropsychological Assessment Metrics (ANAM) testingfollowing HBOT. ANAM is a library of more than thirtyelectronic-based test modules designed for a broad rangeof clinical and research applications across all servicebranches within the Department of Defense. 39 Specifically,ANAM4 TM serves as a neurocognitive assessment tool thathas been customized in the aforementioned case report tobe sensitive to cognitive changes that typically coincidewith mild TBI. 39 Following seven months of persistentmild TBI symptoms, the injured servicemen drasticallyimproved within ten days of HBOT. In particular, theirheadaches and sleep disturbances decreased, while theirirritability, cognitive and memory defects improved moreslowly. 38 Due to the reliability of the ANAM testing,and that HBOT was the only treatment received by theservicemen, the efficacy of HBOT in bTBI is noted.bTBI-related sequelaeThe sequelae of bTBI are diverse and can persist fora patient’s lifetime. Due to the scarcity of literature on thesubject, as well as an overlap of symptoms associated withcertain manifestations, understanding post-TBI disordershas proved troublesome for clinicians. 40 The chronicsequelae of TBI can be grouped into different categoriesbased on the various neuropsychiatric symptoms associatedwith each grouping. Specifically, they can be discussedas cognitive impairments, neurobehavioral disorders,somatosensory dysfunctions and somatic symptoms. 13Other post-injury manifestations that do not delineate intoseparate entities include post-concussion syndrome (PCS)and substance dependence. 41Any impairment of a sensory organ system canbe considered a somatosensory dysfunction. Auditorydisruption has become the most prevalent individual,service-connected disability, with compensation totalingmore than one billion dollars per year. 42 In particular,peripheral hearing loss, tinnitus, central auditory processingdeficits and vestibular impairment (leading to dizziness)can occur in bTBI. 42 Visual impairments, such as anomaliesof light sensitivity, accommodation and vergence(convergence or divergence) may also be present. 43Although disruption of olfactory and taste senses has notbeen thoroughly investigated in bTBI, alterations in senseof smell may alter social interactions, immune functionsand emotions. 44Chronic pain is a common complication of TBI,both in civilian and military populations. Nonetheless,somatic symptoms (i.e., chronic pain syndromes such asheadache) represent an underdiagnosed result of TBI. 13It is suggested that PTSD might arbitrate some TBIinducedsomatic symptoms; however, brain injury seems toassociate independently with chronic pain. 15 According toNampiaparampil, 45 chronic pain syndromes are independentof neurobehavioral disorders, and are typical amongindividuals with relatively minor brain injuries. Althoughit is thought that chronic pain is more likely to occurin patients with mild TBI, more studies will need to beconducted to establish a significant correlation between thetwo. 45 Although cognitive dysfunctions are commonlyreported following bTBI, their precise prevalence is poorlyunderstood, partly because of the difficulties associatedwith the classification of such conditions. 46 Cognitivedysfunctions can include impairments in attention,memory, language and communication, executive functionand visuospatial cognition. 13 Problems with memory areamong the most common dysfunctions following bTBI,and can be acute or chronic. Attention deficits are alsocommon following bTBI and are observed throughoutall TBI severities. 47 In particular, it is suggested thata pathophysiological association between TBI andattention deficit hyperactivity disorder (ADHD) mayPage 20The AAO Journal Volume 22, Issue 2, Summer 2012

exist. 47 Impairment of executive function, which canbe characterized as an integration of specific cognitivefunctions that allow an individual to perform dailytasks, has been associated with poor social integrationpost-injury. 48 Injury to the temporal and parietal lobesis associated with apraxia and agnosia; however, theprevalence and incidence of both conditions in mild ormoderate TBI is unknown. 13 Finally, there are an arrayof communication deficits associated with TBI, withthe precise location and severity of TBI determining theparticular type and degree of language dysfunction. 49As with cognitive dysfunctions, evidence of specificassociations between TBI and neurobehavioral disordersis scarce. The neurobehavioral sequelae of bTBI includedepression (mood down), mania (mood up), PTSD andother anxiety disorders, psychosis and other psychoticdisorders, and libido. 46 The incidence of TBI-induceddepression ranges from about 15 percent to 30 percentwhile the prevalence ranges from about 19 percent to61 percent 41,50 The broad ranges are due in part to theoverlap of depression symptoms with post-concussivetype symptoms, including fatigue, sleep disruptions, andconcentration impairments. 13 The incidence of TBI-inducedmania is nine percent, while the prevalence ranges fromabout one percent to 22 percent 51 While the majority ofmanic cases develop after one year following TBI, somestudies report a delay of four to five years after TBI. 52,53 Astrong relationship exists between OIF/OEF veterans andPTSD. In particular, about 11 percent of returning veteransscreen positive for PTSD, while about 62 percent of thosewith mild TBI screen positive. 54 The incidence of post-TBIpsychosis is about 20 percent, while the prevalence has notbeen determined. 55 Because the average onset of psychosisoccurs twelve years after TBI and manifests in manyvariations, diagnosing psychosis has proved troublesome. 41Finally, although sexual dysfunction is common afterTBI, data relating sexual health and veterans with bTBI isscarce. 56 Nonetheless, typical issues include impulsivenessand a decrease in both libido and sexual frequency. 56The criteria for PCS are intricate in that bothsomatic and cognitive impairments are included and itspathophysiological nature is contentious. 57 According to theInternational Classification of Diseases-10 (ICD-10), threeor more symptoms from a total of eight must be presentto classify as PCS. 41 The symptoms include headache,dizziness, fatigue, irritability, insomnia, concentrationimpairment, memory impairment, and intolerance ofstress, emotion or alcohol. 41 It is suggested that the term“PCS” may be deceptive in that it could falsely imply thatthe condition is solely the result of an observable braininjury. 57 Supportive of that argument are the high ratesof PCS found in individuals without brain injury. 58 Acutepain seemed to arbitrate acute outcome in mild TBI, whilesymptoms were more evident in patients with mild TBIcomorbid with PTSD than those without comorbid PTSD. 59Thus, even though bTBI may play a part in causing PCS,the relationship between PCS and other causative factorsdevalues its role as a marker for TBI severity and outcome.ConclusionsAs a result of the nature of modern warfare, bTBI hasbecome an increasingly occurring injury with devastatingeffects, both acute and chronic. Since many of the acuteeffects may not be observable by the naked eye, bTBIcan be referred to as “the invisible wound of war.”Because several of the chronic effects can persist for apatient’s lifetime, the costs associated with bTBI can bedeemed incalculable. Thus, not only is a patient foreveraffected, but so are the friends and family members of theinjured individual. Clinical management and treatmentof patients with bTBI require a multidisciplinary teamapproach. Primary care, neurology, physical medicineand rehabilitation, and neuromusculoskeletal medicinephysician specialists must team up with physical andoccupational therapists and nurses to provide the breadthand depth of care necessary to manage patients with thecomplex of symptoms inherent in those afflicted with bTBI.The present review highlights the need for aninvestigative surge so that bTBI can be better characterized.Studies encompassing both pharmacologic and nonpharmacologicmultipotential treatment strategies, such asHBOT, demonstrate the potential of combination therapiesfor bTBI. Since there are currently no clinically provenbiomarkers for brain injury, further research should beconducted on ways to improve and expedite the detectionof bTBI. Furthermore, a collaborative effort is needed byall medical personnel involved in the clinical managementprocess to become more aware of the tendencies andpatterns of bTBI. Finally, mandatory education programsshould be incorporated into the training regimens ofmilitary personnel stressing the importance of brain injuryrecognition and communication so fewer brain injuries willgo unnoticed and misdiagnosed.References1. Tanielian T, Jaycox LH, editors. Invisible Wounds of War:Psychological and Cognitive Injuries, Their Consequences, andServices to Assist Recovery. Arlington, VA: Center for MilitaryHealth Policy Research, the Rand Corporation; 2008.2. Martin EM, Lu WC, Helmick K, French L, Warden DL. (2008).Traumatic brain injuries sustained in the Afghanistan and Iraqwars. Journal of Trauma Nursing. 2008;15(3):94-99,100-101.3. Okie S. Reconstructing lives—a tale of two soldiers. The NewEngland Journal of Medicine. 2006; 355(25):2609-2615.Volume 22, Issue 2, Summer 2012 The AAO Journal Page 21

4. Warden D. Military TBI during the Iraq and Afghanistan wars. TheJournal of Head Trauma Rehabilitation. 2006;21(5): 398-402.5. Xydakis MS, Fravell MD, Nasser KE, Casler JD. Analysisof battlefield head and neck injuries in Iraq and Afghanistan.Otolaryngology-Head and Neck Surgery. 2005;133(4):497-504.6. Maas AI, Stocchetti N, Bullock R. Moderate and severe traumaticbrain injury in adults. Lancet Neurology. 2008; 7(8):728-741.7. Parikh S, Koch M, Narayan RK. Traumatic brain injury.International Anesthesiology Clinics. 2007;45(3):119-135.8. National Institute of Neurological Disorders and Stroke (NINDS).National Institutes of Health. http://www.ninds.nih.gov/disorders/tbi/tbi.htm. Updated May 6, 2010. Accessed February 17, 2010.9. Steyerberg EW, Mushkudiani N, Perel, P, Butcher I, Lu J, McHughGS, et al. Predicting outcome after traumatic brain injury:Development and international validation of prognostic scoresbased on admission characteristics. PLoS Medicine. 2008;5(8):165.10. Zink BJ. Traumatic brain injury. Emergency Medicine Clinics ofNorth America. 1996;14(1):115-150.11. Narayan RK, Michel ME, Ansell B, Baethmann A, Biegon A,Bracken MB, et al. Clinical trials in head injury. Journal ofNeurotrauma. 2002;19(5):503.12. Bagiella E, Novack TA, Ansel B, Diaz-Arrastia R, Dikmen S, HartT, et al. Measuring outcome in traumatic brain injury treatmenttrials: Recommendations from the traumatic brain injury clinicaltrials network. The Journal of Head Trauma Rehabilitation. 2010;25(5):375-382.13. Halbauer JD, Ashford JW, Zeitzer JM, Adamson MM, Lew HL,Yesavage JA. Neuropsychiatric diagnosis and management ofchronic sequelae of war-related mild to moderate traumatic braininjury. Journal of Rehabilitation Research and Development.2009;46(6), 757-796.14. Wolf SJ, Bebarta VS, Bonnett CJ, Pons PT, Cantrill SV. Blastinjuries. Lancet. 2009;374(9687):405-415.15. Hoge CW, McGurk D, Thomas JL, Cox AL, Engel CC, Castro CA.Mild traumatic brain injury in U.S. Soldiers returning from Iraq.New England Journal of Medicine. 2008;358(5):453-463.16. Harrison CD, Bebarta VS, Grant GA. Tympanic membraneperforation after combat blast exposure in Iraq: A poor biomarkerof primary blast injury. The Journal of Trauma. 2009: 67(1): 210-211.17. Cernak I, Noble-Haeusslein NJ. Traumatic brain injury: Anoverview of pathobiology with emphasis on military populations.J Cereb Blood Flow Metab. 2010;30(2):255-266.18. Armonda RA, Bell RS, Vo AH, Ling G, DeGraba TJ, Crandall B,et al. Wartime traumatic cerebral vasospasm: Recent review ofcombat casualties. Neurosurgery. 2006;59(6):1215-1225.19. Ling G, Bandak F, Armonda R, Grant G, Ecklund J. Explosiveblast neurotrauma. Journal of Neurotrauma. 2009; 26(6):815-825.20. Belanger HG, Kretzmer T, Yoash-Gantz R, Pickett T, Tupler LA.Cognitive sequelae of blast-related versus other mechanisms ofbrain trauma. Journal of the International NeuropsychologicalSociety. 2009; 15(1):1-8.21. Knuth T, Letarte PB, Ling G, Moores LE, Rhee P, Tauber D, etal. Guidelines for the field management of combat-related headtrauma. New York (NY): Brain Trauma Foundation; 2005.22. Aarabi B, Simard JM. Traumatic brain injury. Current Opinion inCritical Care. 2009;15(6):548-553.23. Ling GS, Marshall SA. Management of traumatic brain injury inthe intensive care unit. Neurologic Clinics. 2006;26(2):409-426.24. Aarabi B, Hesdorffer DC, Ahn ES, Aresco C, Scalea TM,Eisenberg HM. Outcome following decompressive craniectomyfor malignant swelling due to severe head injury. Journal ofNeurosurgery. 2006;104(4):469-479.25. Bell RS, Vo AH, Neal CJ, Tigno J, Roberts R, Mossop C, etal. Military traumatic brain and spinal column injury: A 5-yearstudy of the impact blast and other military grade weaponry onthe central nervous system. The Journal of Trauma. 2009;66(4Suppl):S104-111.26. Timofeev I, Kirkpatrick PJ, Corteen E, Hiler M, Czosnyka M,Menon DK, et al. Decompressive craniectomy in traumaticbrain injury: Outcome following protocol-driven therapy. ActaNeurochirurgica Supplement. 2006;96:11-16.27. Cooper DJ, Rosenfeld JV, Murray L, Wolfe R, Ponsford J, DaviesA, et al. Early decompressive craniectomy for patients with severetraumatic brain injury and refractory intracranial hypertension—Apilot randomized trial. Journal of Critical Care. 2008;23(3):387-393.28. Hutchinson PJ, Corteen E, Czosnyka M, Mendelow AD, MenonDK, Mitchell P, et al. Decompressive craniectomy in traumaticbrain injury: The randomized multicenter RESCUEicp study. ActaNeurochirurgica Supplement. 2006;96:17-20.29. Coles JP, Fryer TD, Smielewski P, Rice K, Clark JC, Pickard JD,et al. Defining ischemic burden after traumatic brain injury using15O PET imaging of cerebral physiology. Journal of CerebralBlood Flow and Metabolism. 2004;24(2):191-201.30. Cunningham AS, Salvador R, Coles JP, Chatfield DA, Bradley PG,Johnston AJ, et al. Physiological thresholds for irreversible tissuedamage in contusional regions following traumatic brain injury.Brain. 2005;128(8):1931–1942.31. Stoica B, Byrnes K, Faden AI. Multifunctional drug treatment inneurotrauma. Neurotherapeutics. 2009;6(1):14-27.32. Prasad C. Limited proteolysis and physiological regulation: Anexample from thyrotropin-releasing hormone metabolism. Thyroid.1998;8(10):969-975.33. Faden AI, Movsesyan VA, Knoblach SM, Ahmed F, Cernak I.Neuroprotective effects of novel small peptides in vitro and afterbrain injury. Neuropharmacology. 2005;49(3):410-424.34. Faden AI, Knoblach SM, Cernak I, Fan L, Vink R, Araldi GL, etal. Novel diketopiperazine enhances motor and cognitive recoveryafter traumatic brain injury in rats and shows neuroprotectionin vitro and in vivo. Journal of Cerebral Blood Flow andMetabolism. 2003;23(3):342-354.35. Harch PG, Kriedt C, Van Meter KW, Sutherland RJ. Hyperbaricoxygen therapy improves spatial learning and memory in arat model of chronic traumatic brain injury. Brain Research.2007;1174:120-129.36. Brismar K, Lind F, Kratz G. Dose-dependent hyperbaric oxygenstimulation of human fibroblast proliferation. Wound Repair andRegeneration. 1997;5(2):147-150.37. Palzur E, Zaaroor M, Vlodavsky E, Milman F, Soustiel JF.Neuroprotective effect of hyperbaric oxygen therapy in braininjury is mediated by preservation of mitochondrial membraneproperties. Brain Research. 2008;1221:126-133.38. Wright JK, Zant E, Groom K, Schlegel RE, Gilliland K. Casereport: Treatment of mild traumatic brain injury with hyperbaricoxygen. Undersea & Hyperbaric Medicine. 2009;36(6):391-399.Page 22The AAO Journal Volume 22, Issue 2, Summer 2012

39. Vincent AS, Bleiberg J, Yan S, Ivins B, Reeves DL, Schwab K,et al. Reference data from the Automated NeuropsychologicalAssessment Metrics for use in traumatic brain injury in an activedutymilitary sample. Military Medicine. 2008;173:836-852.40. Teasdale TW, Engberg AW. Subjective well-being and qualityof life following traumatic brain injury in adults: A long-termpopulation-based follow-up. Brain Injury. 2005;19(12):1041-1048.41. Kim E, Lauterbach EC, Reeve A, Arciniegas DB, Coburn KL,Mendez MF, et al. Neuropsychiatric complications of traumaticbrain injury: A critical review of the literature (a report by theANPA committee on research). The Journal of Neuropsychiatryand Clinical Neurosciences. 2007;19(2):106-127.42. Fausti SA, Wilmington DJ, Gallun FJ, Myers PJ, Henry JA.Auditory and vestibular dysfunction associated with blast-relatedtraumatic brain injury. Journal of Rehabilitation Research andDevelopment. 2009;46(6):797-810.43. Kapoor N, Ciuffreda KJ. Vision disturbances followingtraumatic brain injury. Current Treatment Options in Neurology.2002;4(4):271-280.44. Strous RD, Shoenfeld, Y. To smell the immune system: Olfaction,autoimmunity and brain involvement. Autoimmunity Reviews.2006;6(1):54-60.45. Nampiaparampil DE. Prevalence of chronic pain after traumaticbrain injury: A systematic review. The Journal of the AmericanMedical Association. 2008;300(6):711-719.46. Neurobehavioral Guidelines Working Group, Warden DL,Gordon B, McAllister TW, Silver JM, Barth JT, Bruns J, et al.Guidelines for the pharmacologic treatment of neurobehavioralsequelae of traumatic brain injury. Journal of Neurotrauma.2006;23(10):1468-1501.47. Whyte J, Hart T, Vaccaro M, Grieb-Neff P, Risser A, PolanskyM, et al. Effects of methylphenidate on attention deficits aftertraumatic brain injury: A multidimensional, randomized, controlledtrial. American Journal of Physical Medicine & Rehabilitation/Association of Academic Physiatrists. 2004;83(6):401-420.48. Reid-Arndt SA, Nehl C, Hinkebein J. The frontal systemsbehaviour scale (FrSBe) as a predictor of community integrationfollowing a traumatic brain injury. Brain Injury. 2007;21(13-14):1361-1369.49. Angeleri R, Bosco FM, Zettin M, Sacco K, Colle L, Bara BG.Communicative impairment in traumatic brain injury: A completepragmatic assessment. Brain Language. 2008;107(3):229-245.50. Rapoport MJ, McCullagh S, Shammi P, Feinstein A. Cognitiveimpairment associated with major depression following mild andmoderate traumatic brain injury. The Journal of Neuropsychiatryand Clinical Neurosciences. 2005;17(1):61-65.51. Van Reekum R, Bolago I, Finlayson MA, Garner S, Links PS.Psychiatric disorders after traumatic brain injury. Brain Injury.1996;10(5):319-327.52. Shukla S, Cook BL, Mukherjee S, Godwin C, Miller MG. Maniafollowing head trauma. The American Journal of Psychiatry.1987;144(1):93-96.53. Dalen P. Family history, the electroencephalogram and perinatalfactors in manic conditions. Acta Psychiatrica Scandinavica.1965;41(4):527-563.54. Schneiderman AI, Braver ER, Kang HK. Understandingsequelae of injury mechanisms and mild traumatic brain injuryincurred during the conflicts in Iraq and Afghanistan: Persistentpostconcussive symptoms and posttraumatic stress disorder.American Journal of Epidemiology. 2008;167(12):1446-1452.55. Thomsen IV. Late outcome of very severe blunt head trauma: A10-15 year second follow-up. Journal of Neurology, Neurosurgeryand Psychiatry.1984;47(3):260-268.56. Elliott ML, Biever LS. Head injury and sexual dysfunction. BrainInjury. 1996;10(10):703-717.57. Meares S, Shores EA, Taylor AJ, Batchelor J, Bryant RA, BaguleyIJ, et al. Mild traumatic brain injury does not predict acutepostconcussion syndrome. Journal of Neurology, Neurosurgeryand Psychiatry. 2008;79(3):300-306.58. Landre N, Poppe CJ, Davis N, Schmaus B, Hobbs SE. Cognitivefunctioning and postconcussive symptoms in trauma patients withand without mild TBI. Archives of Clinical Neuropsychology.2006;21(4):255-273.59. Bryant RA, Harvey AG. Relationship between acute stress disorderand post-traumatic stress disorder following mild traumatic braininjury. The American Journal of Psychiatry. 1998;155(5):625-629.Accepted for publication: June 2012Address correspondence to:Patrick M. Malie, MS, OMS III;Murray R. Berkowitz, DO, MA, MS, MPHDepartment of Osteopathic Manipulative MedicinePhiladelphia College of Osteopathic Medicine—Georgia Campus625 Old Peachtree Road NWSuwanee, Georgia 30024murraybe@pcom.eduVolume 22, Issue 2, Summer 2012 The AAO Journal Page 23

Fine-Tuning Your HVLAOctober 6, 2012, at the San Diego Convention Center (Pre-OMED)Course DescriptionThis course will demonstrate variations from the usual“tried and true” HVLA techniques that are commonly usedthroughout the osteopathic profession. The primary goalis to present treatment options in dificult-to-manage bodyareas (transition zones), or those involving less typicalpresentations. Treatment of regional junctions will beaddressed as the outline for the session. It will focus on theHVLA treatment within each of these regions, and also includethe use of other modalities as appropriate. Participants areencouraged to bring relevant case histories to be addressed insmall group sessions.Course Objectives1. To understand the functional anatomy of each area.2. To diagnose somatic dysfunction in junctional areas.3. To formulate the manipulative prescription for each area.4. To appreciate the relationships between different regionaldysfunctions.5. To perform the techniques as taught, and to be able to varythem when appropriate.6. To know when to toss out the OMT rule bookCourse LocationSan Diego Convention Center111 West Harbor DriveSan Diego, CA 92101(619) 525-5000Program DirectorJohn G. Hohner, DO, FAAO, is a 1987graduate of Midwestern University ChicagoCollege of Osteopathic Medicine (CCOM).He is certiied by the American OsteopathicBoard of Special Proiciency in OsteopathicManipulative Medicine and the AmericanOsteopathic Board of Family Physicians, andis in private practice in Oak Forest, IL. He is aprofessor of Osteopathic Manipulative Medicine (OMM) andFamily Practice at CCOM, where he is also Division Directorfor the OMM’s Department’s MS-I curriculum. He currentlyserves on the AAO Board of Trustees, and is the former chairof the Education Committee.Pre-requisitesA basic understanding of the relevant functional anatomy andof HVLA.CME8 hours of Category 1-A AOA CME credit is anticipated.Course Times8:00 am - 5:00 pm (lunch on your own)Travel ArrangementsCall Tina Callahan of Globally YoursTravel at (800) 274-5975.See AOA OMED Web site for lodginginformation.Registration FormFine-Tuning Your HVLAOctober 6, 2012, in San Diego, CAName: __________________________________________ AOA#: ____________Nickname for Badge: ______________________________________________Street Address: ____________________________________________________________________________________________________________________________City: _________________________________ State: _______ Zip: ___________Phone:____________________________ Fax: ____________________________E-mail: ______________________________________________________________Registration RatesRegistration fee...............................................................................$225.00The AAO accepts check, Visa, Mastercard or Discover paymentsin U.S. dollarsCredit Card #: ________________________________________________________Cardholder’s Name: __________________________________________________Expiration Date: _____________________ 3-digit CVV#________________I hereby authorize the AAO to charge the above credit card forthe full course registration amount.Signature: ___________________________________________________________By releasing your fax/e-mail, you have given the AAO permissionto send marketing information to your fax or e-mail.Billing Address (if different than above): _________________________________________________________________________________________________Click here to view the AAO’s Cancellation and Refund PolicyPage 24Please submit registration form and payment to:American Academy of Osteopathy,3500 DePauw Blvd., Suite 1080Indianapolis, IN 46268Fax to: (317) 879-0563Or register online at www.academyofosteopathy.orgThe AAO Journal Volume 22, Issue 2, Summer 2012

Blast-induced mild traumatic brain injury as etiology ofpost-traumatic stress disorder in military veteransMarc Quentin Sonnier, Jr., MS; Murray R. Berkowitz, DO, MA, MS, MPHAbstractObjective of Review: To provide clinicians and researcherswith a comprehensive, evidence-based overview of mildtraumatic brain injury (mTBI) and the implications for amulti-disciplinary approach to the treatment of militarypersonnel. Blast injuries occur in a variety of ways, butgrasping a comprehensive understanding of their effectson the human brain is difficult due to the chaotic natureof explosive forces. Less obvious are the effects of mTBI.Confusion over adequate testing methods to examinethese effects continues to occur. Advanced methods withinthis field of research are just beginning to reveal a newunderstanding of the debilitating effects of blast-relatedmTBI. These new discoveries are producing a significantunderstanding of the causes of reduction in both life qualityand life expectancy. Along with this come new insights intotreating mTBI.Recent Findings: Body and vehicular armor reducesmilitary combatants’ risk of higher severity blast exposure,which tends to increase the rate of mTBI incidence.This, along with a proliferation of sabotage explosiveattacks, has resulted in an awareness of injury patternsseen in a large proportion of U.S. military ground combatunits exposed to mTBI. An unraveling of the overlap ofmTBI with post-traumatic stress disorder (PTSD) andpost concussive syndrome (PCS) has progressed, as wellas neurophysiological associations with excite-toxicdamage occurring with further blast exposure. This hasimproved our understanding of what separates biologicalmanifestations, such as mTBI, PTSD and PCS, from otherindicators that might complicate the differential diagnosis.Conclusions: In the current state of the U.S. medicalcrisis, it is imperative that cost-effective solutions arecreated to manage the new chronic disease of mTBIin our demobilized military forces. Understandingneurodegeneration indicated with biomarkers, axonaldamage, personality aberrations and inflammatoryresponses aimed at building treatment regimes haveimproved both patient outcomes and the progressionscientific research. Through patterns of injurycharacteristics and standardizing baselines of physicaland psychological fitness risk, patient assessments andfollow-ups will help to establish relative foundationsfrom which mTBI disease manifestation can be measuredon an individual level. A multidisciplinary approach byphysicians and research scientists is necessary to achieveoptimal patient outcomes.Psychological manifestations and co-morbidity relatedto blast mTBIPatterns of mTBI should be distinguished fromblast trauma to build a greater understanding of theirpsychological effects. The incidence of hospitalizationassociated with non-blast mTBI in adults encompasses300/100,000 per year. With transient symptoms typicallytranspiring within a time frame of days to weeks, thistrauma can be easily overlooked. Evidence of developinga psychiatric disorder was 2.8 times greater for mTBIpatients. 1 Studies performed in Level I trauma centersreveal the influence mTBI has on the risk of manifestingpsychiatric illness. Comparing mTBI to the lack thereof,injured patients had a greater likelihood of developingPTSD, panic disorder, agoraphobia and social phobiaat 12 months in a study outlined by Bryant. 2 More thana third of mTBI patients had a coexisting diagnosis ofPTSD in a Veterans Affairs study for screening accuracy.Inconsistent mTBI screening systems between civilian andmilitary healthcare are believed to be a major confounderto PTSD research related to TBI. 3,4 Damage associated withthe frontal brain compromises emotional control, whichis believed to mediate the stress of traumatic injury. Butevidence that disproves the linkage between mTBI andgreater post-injury functional impairment make it difficultto predict subsequent health problems in afflicted militarypersonnel following control of both PTSD and depressiveeffects. It is noteworthy that psychological disorders amongmilitary personnel could be sustained, if not increased,during combat theaters. 5-8Health problems occurring with mTBI and associatedwith PTSD begin to appear three to four monthsafter soldiers return home. 9 The term post-traumaticstress disorder (PTSD) refers to the development ofa set of specifics symptoms following exposure to apsychologically distressing event that is outside the rangeof usual human experience. 10 These symptoms sharea stronger association than any other pair of injuries inrecent military theaters. 11 But Meares has shown thatVolume 22, Issue 2, Summer 2012 The AAO Journal Page 25

mTBI diagnosis wasn’t a reliable predictor of acute PCS,whereas pain was associated with the two. 12 Evidenceamong non-blast studies suggest traumatic events atthe onset of mTBI play a protective role against causalmemory retention for PTSD. 10,13 This contradicts PTSDas a more probable sequela of mTBI (compared to moresevere trauma) because of its likelihood to occur in lesssevere brain injury. 14 This may in part be due to the lowerincidence of memory defect hindering the experientialrecall of traumatic events. The co-morbidity of duallydiagnosed PTSD and mTBI may make it difficult to reducethe differential diagnosis because of the association withtraumatic memory retention or loss in both. 10,15 Someof the persistent symptoms are of a somatic, cognitiveand psychological nature. 16 While PCS shares manyoverlapping symptoms with mTBI, patients may presentless than the full spectrum of symptoms. Because civilianPTSD carries a clinician’s warning not to diagnosemTBI or PCS, military doctors are confronted with thecomplications of warfare trauma within the context ofpatient assessment. 3,17-20Associated symptomsSymptoms of military personnel exposed to blastmTBI when other bodily injuries were present did notdiffer. The Department of Veteran Affairs demonstratedcontrasting patterns of injury between blast and nonblastpolytrauma. Excluding brain injury from similarcases of polytrauma didn’t improve negative neurologicalproblems. High rates of neurobehavioral symptoms frompolytrauma are similar to those leading to PCS. Thesignificance of predicting and treating PCS continues toincrease in the fragile healthcare crisis in the U.S. 14,21-23The mTBI group had more reported injuries overall. Theyalso had higher reporting of PTSD with increasing injuryseverity. Overexposure to combat-related stressors actedto compound psychological dissolution and fatigue, whichultimately lead to chronically high states of alertnessand thus predisposing blast victims to experience moresymptoms. 24Soldiers’ environments and internal states throughoutcombat operations worked to exacerbate these effects (inparticular, the response to environmental stressors and thereciprocal reaction to their environment due to internalstressors) through deviations in normal functional responseand regression (consequences of poor interdependencebetween cognition and response). Poor outcomes, as aresult of additive chronic symptoms, were best protectedagainst when emotional disorders were taken into accountduring clinical investigation, the functional outcomes ofwhich were mediated by PTSD as it relates to symptomsof mTBI. 11,25 PTSD findings and depression can makerecovery from such injuries exceedingly difficult. Evidencehas suggested that a large portion of mTBI damageinducing PTSD causes neural network disruption. Damageto the amygdale, contained in the pre-frontal cortex, couldperpetuate anxieties through emotionally charged traumaassociated with an injury event. Almost half of the servicemembers with burn injuries were exposed to mTBI and 32percent had PTSD. 21Retrospective reviews of Operation Iraqi Freedom(OIF) clinical cases involving mTBI have shown certainblast dynamics that are often apparent upon examination forspecific injury patterns. In one of the largest sample sizesof Iraq combat operatives to date, 95 percent of participantswere injured by blast mechanics and 90 percent sustainedmTBI. The demographics revealed that injuries were 89.3percent likely to involve mTBI when case findings werestratified against TBI severity. This is significantly greaterthan moderate and severe TBI, with 4.3 percent and 6.4percent, respectively. Head injuries sustained without skullfracture were 99.6 percent likely to have mTBI symptompresentations.Injuries from improvised explosive device (IED)explosions dominated all TBI instances. Afflictionsfrom the detonation of these ordinances showed up in alarge percentage of mTBI clinical cases. In recent years,military activity has delivered a payload of mild braintrauma in significantly greater numbers than any previousengagements because of the stockpiles of these ordinances.Without guidance equipment or tactical platforms to launchfrom, these otherwise useless “dumb bombs” of old warfarefill the effectiveness gap between the heavily armoredmodernized forces and resourceful militant guerilla fighterswho are less likely to directly engage the enemy withtraditional gunfire. This leads to a greater contrast betweenthat of mild and the historically more frequent TBI ofgreater severity associated with gunshot wounds.Other bodily injuries that predominate higher severityTBI are sub-clavicular and sub-cervical. In particular,simulation injuries to upper and lower extremities were notheavily present in mTBI, except when the spine or backwas involved. Blast mechanisms appeared in a greaterpercentage of these type of injuries, which raises thepossibility that the effective blast radius associated withmTBI may exert a greater force of injury than initiallythought. Macgregor, Dougherty and Galarneau theorize thatif the spine is involved in some cumulative force that servesto magnify the injurious effects on the CNS (includingthe brain and spinal cord), the blast wave spread over alarger, cross-sectional area may mediate an increase in thequalitative effects that blast vectors force on the nervoussystem. But these observations are purely speculative. 26Page 26The AAO Journal Volume 22, Issue 2, Summer 2012

Demographic findings of blast mTBImTBI in recent, war-related demographics has beentaken ever more seriously because of the high risk forphysical and mental degradation due to the corrosiveeffect imposed on biological processes associated withexposure to extreme stress. When a blast creates sensoryimpairments, repercussions might worsen depending onhow much of a sense remains or what can be restoredfrom its baseline. Multiple sensory losses can have drasticimplications to quality of life and create increased risksfor depression. Dual sensory disabled patients struggledto recover functional independence and required moreassistance that dampened motor-function conditioning.This was made worse by the dizzying sequela followinga blast’s effect on vestibular balance. Soldiers serving inAfghanistan and Iraq frequently complain of vestibularsymptoms that are not typical of blunt head trauma andsignificantly worsen if the gap between time of injury andpresentation of symptoms increases. 21 The civilian clinicalscreening and treatment guidelines for mTBI lack sufficientspecificity for environmental effects of combat, and makethe discernment of the overlapping alteration of mentalstatus with dissociative symptoms of acute stress disorder,post-concussive symptoms and PTSD that much moredifficult.In an effort to assess the prevalence and significanceof combatants’ self-reported history of mTBI three to fourmonths after an incident, epidemiologic data was used toadvance the prevention and treatment strategies of healthprofessionals. Due to the effects of combat-related TBI,the debilitation that persistent post-concussive symptomsleave behind might pose a serious threat to the livelihoodof many recent veterans for years to come. These longterm effects concern mTBI, which is characterized bybrief loss of consciousness or altered mental status as aresult of deployment-related head injuries, particularlythose resulting from proximity to blast explosions.From a population of 2,525 soldiers with injury, 124(4.9 percent) reported loss of consciousness and 260(10.3 percent) reported altered mental status withoutloss of consciousness. The significance of injury reports,including those related to mTBI, lies in the likelihoodthat the incident coincided with high intensity combat, ablast mechanism of injury, more than one exposure to anexplosion and hospitalization during deployment. WhilePTSD was strongly associated with mTBI, in cases withloss of consciousness, 43.9 percent met criteria for thediagnosis of PTSD; logistical regression demonstratedthat this was significant only when associated with combatintensity. 11,21Neurophysiology and anxiety-related sequelaePTSD and its association with anxiogenic effects onthe amygdala have been established as the fundamentalmechanisms underpinning the conditioned fear reactionsplaguing many mTBI-exposed veterans. Mild blast TBI hasbeen the suspected culprit for the large majority of casesof prefrontal cortex blast shearing, which exerts forcesthat cause the frontal region to collide against the skull.But just as it is possible for mTBI to impair one’s capacityto regulate the exaggerated fear response, recent findingssuggest that the amygdala possesses a built-in anxietyreversal circuit.The prevalence of anxiety is approximately 28percent for lifetime disorders and, within the scope of thispaper, there exists equal implications for understandingwhat neuronal circuitry plays a role in neurologicaland psychological dysfunctions associated with mTBI.Exploring the underpinnings of anxiety with cellularprecision, the amygdala micro-circuitry was optogeneticallydissected using viruses that induced the synthesis of photoresponsiveproteins similar to those expressed within retinalcells. This allows individual cells to be stimulated byselectively induced depolarization using light. The majorityglutamatergic basolateral amygdala and the centrolateralnuclei of the amygdala together compose a neural substratefor real-time bidirectional modulation of unconditionedanxiogenic activity. 27Mild TBI, upon initial examination, is differentiatedinto complicated and uncomplicated types based onstructural injury that is visualized on imaging and/or acuteneurological signs. 28 Complicated mTBI better parallels thesymptom pathology of moderate TBI in severity. This islikely to include Alzheimer’s disease because TBI is its bestknown environmentally related exposure. In a retrospectivecohort study of World War II veterans with documentedclosed head injury, Blyth is clear to point out an increasedrisk of Alzheimer’s type dementia when compared to nonhead-injured controls (hazard ratio 2.00, 95 percent CL1.03-3.90). 29Vasterling explored the effects of deployment onneuropsychological health. Some important differencesare now being noted between severe and penetratingCNS trauma and increasing emphasis on battle-relatedmTBI. Behavioral discharges among military personnelfollowing mTBI increased 1.8 fold, and when confoundedwith alcohol or drugs, ultimately increased 2.6 fold.Hypovolemic shock from hemorrhage is the mostdetrimental to cerebral blood flow, making the brain highlysusceptible to post-traumatic hypoxemia, the long-termeffects of which need further investigation. 21,30Volume 22, Issue 2, Summer 2012 The AAO Journal Page 27

Blast mTBI has the potential to cause neuronaldamage that subjects otherwise long, healthy lives tomultiple brain-related disturbances. When characterizedas a chronic, mild discomfort, neglected treatment canoften promote irrational mood swings that can disturbsocial structures and seclude patients from healthyneurobehavioral habits. Because pharmacological andpsychiatric therapies for mTBI remain largely unknown, itis critical to isolate adverse effects from the baseline beforefurther therapies are pursued. The neuropsychologicaleffects of blast mTBI present challenges that warrant aninterdisciplinary approach at both the microscopic neuronallevel, as well as the macroscopic neuroanatomical andneurophysiological levels.Much of the newly relevant medical and scientificliterature commonly expresses a need for furtherinvestigation into these stratified layers of depth. This isnecessitated by the difficulty of blast trauma differentialdiagnosis. Animal research with primary blast wavesadversely affected the white matter of the brain andconsequently affected areas by neuronal death-inducedastrocyte proliferation. The hippocampus, at a cellularlevel, had abnormal myelin with cytoplasmic vacuoles.Although the likelihood of these effects being seen in blastmTBI cases is small, it has occurred. 31 This may involvealtered neurobehavioral patterns with implications ofhippocampal defects associated with memory and specialawareness. 32-35Reporting errors involving blast mTBI can manifestanomalies, such as false symptoms, remediation andrecovery, when environmental variables of post-deploymentaren’t taken into consideration. 31 When examined for theneurophysiological outcomes of deployment, a prospectivecohort-controlled study of OIF revealed an associated riskof increased compromise in learning and memory withalterations in response times. The study was based ondifferences recorded among two separate deployments,each with subdivisions of deployed and non-deployedpersonnel, and measured the outcomes for each. The firstdeployment group had a sample size of 600 personneldrawn from a unit of 1,368 personnel and a sample of300 non-deployed personnel. There was a 94 percentcompliance rate in the deployed volunteer group and a 75percent compliance rate in the non-deployed volunteergroup. Comparisons between the two found that the seconddeployment group performed significantly poorly in visualreproductions of immediate recall (P < .001). 30 Primaryoutcomes as a function of deployment revealed significantlosses with greater distress when tested for Profile ofMood States confusion and tension (P < .001). TheNeurobehavioral Evaluation System (third edition) revealedsignificantly less proficiency toward omission errors (P< .001), and the Wechsler Memory Scale (third edition)similarly revealed proficiency compromise (P = .003) inverbally paired associated learning trials.Although visual-spatial impairments weresignificantly less proficient when it came to percentretention of visual reproduction in the Wechsler MemoryScale (P < .001), there was a significant increase in simplereaction time throughout proficiency in the AutomatedNeuropsychological Assessment Metric test (P = .003).This improvement is suggested to be a conditionedsurvival response advantageous in reacting swiftly towardan aggressor. This is likely attributed to an autonomicassociated neuroendocrine effect of the hypothalamicpituitary-adrenalaxis in response to life-threatening stimuliwithin combat settings. While initial benefits pertain todeployed infantrymen, this may yield a false sense ofsecurity likened to that of a Western quick draw. In theseoperations, a soldiers’ safety heavily relies on their wits andtact to counter the cunning tactics aimed at outsmarting amodern military.Once more, these findings point out negativeoutcomes that cannot be attributed to pre-existingneuropsychological outcomes that are ruled out frombaseline measurements. Significantly poor effects onsustained attention, learning and memory have little ifany likelihood of inaccuracy due to variability betweensubjects because of relatively short, intermittentdeployment times and score compensation for worseningPTSD and/or depression symptoms. Neurobehavioraloutcomes demonstrated skewed associations withemotional symptoms that were found to be independentfrom emotional responses to deployment-relatedneuropsychological alterations. These may, in fact, be dueto varying degrees of coping mechanisms developed todiminish the emotional burden of warfare. Even withoutevidence to associate mTBI as a mechanism of injury, thefindings clarify that war deployment has shown negativehealth outcomes that compromise neuropsychologicalfunctions. 30Compromised brain stress systems have beenhypothesized to promote a compulsory dependence onreward-seeking behavior. This behavior can lead to avicious cycle with a perceived resolution of anxiolyticeffects. The paradox has to do with the way this stressrelatedbehavior depresses the gamma-aminobutyricacid (GABA) activity associated with stress relief.Corticotrophin-releasing factor (CRF) localized incomponents of the amygdala, whereby it, along withnorepinephrine binding to the α1 receptors, participatesin allostatically related addictive tendencies. Within thePage 28The AAO Journal Volume 22, Issue 2, Summer 2012

context of the emotional state, CRF engages hypothalamicand midbrain systems that reciprocate norepinephrineinducedrelease of more CRF from the amygdala.Alcohol-augmented GABA release in thecentral nucleus of the amygdala can be linked to CRFdepreciation, as its effects also depreciate the ability tomotivationally overcome drug/alcohol-seeking behavior.Similarly, anxiolytic drugs used to treat PTSD mightsabotage an mTBI-exposed patient’s successful treatmentneurophysiological alterations due to the fact that itdepresses GABA transmission in the brain. The resultantmodifications in regions downstream to the amygdalamight compromise the healthy, synergistic rationale ofemotionally driven behavioral response. 36,37The amygdala comprises a role in the CNS that isas emotionally prevalent as it is complex. The amygdalaneurocircuits contain associated GABA pathways thatperform mixed inhibitory and stimulatory roles that areimportant to the mechanics of anxiety disorders likePTSD. Neurocircuits comprised of basolateral amygdala,centrolateral and centromedial nuclei within the nuclei areconsidered causally anxiogenic. As basolateral pyramidalneurons have mixed roles, centrolateral nuclei inhibitcentromedial nuclei output associated with stimulatoryeffects toward autonomic and behavioral responsesassociated with fear and anxiety by feed-forward inhibition.The centromedial, containing the majority of GABAneurons, is the primary output region of the amygdale,and is therefore associated with fear- and anxiety-relatedprojections within the brain. But stimulation to theamygdaloid basolateral terminals in the central nucleusof the amygdala reflected a measured reduction inanxiety. These circuits, therefore, illustrate a bidirectionalequilibrium effect between the anxiogenically associated,centrolaterally induced diminishment of inhibition to thecentromedial output and the anxiolytically associated,basolateral amygdaloid terminals within the central nucleusof the amygdala. For mTBI patients with compromisedmemory, learning and emotional compromise associatedwith blast sequel, these illuminate strong implicationsof brain arousal/stress systems affecting the amygdala.As components relating to mood and general well being,induced negative emotional states are the driving force ofthe substance dependencies of war veterans that magnifythe damages of conflict. Interestingly, Trudeau mentionsthat persons with attention-deficit/hyperactivity disorder(ADHD) are more prone to mTBI. 38Some of the psychological outcomes followingmTBI are of great preventative importance in targetingsecondary and tertiary disabling sequelae. The prevalenceof psychiatric illness following mTBI within the first yearwas 34 percent. For those who did not succumb withinthis time frame, the adjusted relative risk of psychiatricillness post-mTBI following an additional six months was2.8, with a 95 percent confidence interval and P value lessthan .001. With prior psychiatric illness post-mTBI, theadjusted relative risk was 1.6, with a 95 percent confidenceinterval and P value of .005. Within the age range of 15to 44 years, greater TBI effects were often seen in mTBIcases without prior psychiatric illness. For those adjustedfor exposure, mTBI disorders were not significant untilfollowing the second year. When the incidence of theexposed was expressed as a proportion of the unexposed,substance abuse became significant in groups without priorpsychiatric illness and individual significance continued for30 months. This may illustrate a risk of prior conditioningof substance mediation of emotional stress propitiated bythe emotional cost of war-related trauma.Nearly all substance abusers with TBI had mTBI.Substances being used to minimize prior, sub-levelpsychiatric illness may explain this finding. A relativelylonger subsequence of relative psychiatric illness risk wasnominally statistically significant for mTBI. This prolongedpattern of elevated risk exhibited by pre-nonpsychiatricmTBI eventually surpassed that of TBI of higher severity,suggesting mTBI may contribute to a significantlylarge proportion of the population whose persistentsymptoms continue to perplex healthcare professionals.Etiologically related, post-TBI psychiatric symptoms withneurophysiological effects may have been a contributingfactor in subjects with prior pre-psychiatric mTBI. 1,39PCS presents injurious outcomes in addition tomTBI, and represents more than 500,000 new casesafter mTBI annually. The disabling nature of this diseasemarks causes great concern considering today’s economicfragility. 1 Blast mTBI treatment planning and managementcould be more effectively planned if an identifying ruleoutlined patients for high or low risk of PCS. One studyexamined how effective testing for PCS in non-blast mTBIcomparatively, using both logistical regression (LR) andrecursive partitioning (RP), might help shed light on thisrisk determinant. LR helped determine relative risk andRP used an intuitive tree design more easily understood byclinicians. The combination of LR and RP found notablyhigh, similarly low and distinctly divergent high-risk PCSpatients following mTBI injury, reducing the difficult-toclassifymiddle zone. Males with mTBI were less proneto succumb to PCS symptoms over time than women withmTBI. 40Neuroimaging may eventually prove the existenceof a cerebellar cognitive affective syndrome wherecerebellar and subcortical brain structures exhibit relativeVolume 22, Issue 2, Summer 2012 The AAO Journal Page 29

hypometabolism and neuroanatomy of cortico-cerebellarcorticalcircuits. As these afferent cortical projectionsconverge in the pons and pass through the cerebellarpeduncles to the cerebellar hemispheres and vermis, leadingto efferent convergence in the deep cerebellar nuclei, theytraverse the peduncles returning to the thalamus wherethey associate with motor cortices. Functional imaginganalysis of mTBI veterans demonstrated further posteriorcerebellar cortex lesion impairments to executive, visualspatialand linguistic impairments, along with vermallesion impairments of affective dysregualtion. Animal testsexplain the vulnerability cerebellar Purkinje neurons havetoward mechanical trauma.These chronic, post-concussive symptoms betweenOIF and Operation Enduring Freedom (OEF) maytherefore be due to repetitive, blast-related acute mTBIdamage to the infratentorial and medial temporal brainregions. 41-43 Neuroimaging was also used to study majordepression’s effects on veterans from the two recent combattheaters to analyze what other effects mTBI may haveon neuroanatomically related damage. Major depressivedisorder, when compared to its absence, demonstratedsignificantly greater activity within the bilateral amygdaladuring fear processing. Since there were not any relativelynoticeable behavioral changes, either group’s brain activitywas unlikely to be driven by behavioral differences.Whole-brain analysis revealed significantly greateractivation in the cerebellum, thalamus and middletemporal gyrus, with only a lowered level of corticalactivity. Diffusion tensor imaging showed significantlylower fractional anisotropy by a count of white-matterassociated tracts. These included the corona radiata, corpuscallosum and superior longitudinal fasciculus. The superiorlongitudinal fasciculus connects the dorsolateral prefrontalcortex with a wide distribution of nodes in the parietal,occipital and temporal lobes. This comprised heteromodalneural network is of paramount importance to coreprocessing executive to attention, memory, language andemotional processing with modulation. This lowered levelof fractional anisotropy was significantly related in the leftsuperior longitudinal fasciculus, as was demonstrated inpost-mTBI major depressive disorder. These hypothesizedmicrostructural changes caused by the mechanistic forcesof concussive, blast-induced trauma dampen normal,healthy emotional processing and regulation, leading torisky cognitive states for major depressive disorder. 44-46The major depressive disorder group also exhibited asignificantly negative correlation of fractional anisotropyin the left superior longitudinal fasciculus and the BeckDepression Inventory-II, 44,45 which tests depression severitybased on psychodynamic prospective instead of thoughts.As a salience detector, the amygdala orchestrates the samesomato-motor, visceral and cognitive responses utilizedby rigorous, repetitive conditioning used in military basictraining self-defensive exercises. This neurostructure, asits role in threat response implicates, is deeply rooted andhas been shown to preferentially participate in negativeemotional states. Neuroanatomical structures additionallyinvolved with emotional processing of stimuli, such asthe cerebellum and middle frontal gyrus, also exhibited aheightened fear response. This was shown to be associatedwith major depressive disorder and hyperactivity ofemotional processing circuitry and hypoactivity instructures of emotional regulation. The hyperactivitywas caused by blast-induced disruptions of white mattertracts, but whether or not these changes were structuralor functional remains to be discovered. Major depressivedisorder due to mTBI, as it relates to microstructural andfunctional changes, is hypothesized to be the emotionallyand cognitively responsive driving force that comprises amajor depressive disorder symptom complex. 41,47Blast mTBI symptoms as they related to the adverseeffects on normal homeostasisPain following mTBI can be associated withlesional damage at any point along the ascendingpathways. This referred or central pain can be attributedto trauma delivered at the first synapse in the dorsalhorn of the spinal cord or trigeminal nuclei, thalamicpathways, subcortical white fibers and cerebral cortex.The ventroposterior thalamus, and to be more specific,damage to the ventroposterior thalamic nucleus causescentral pain if lesions occur. Interestingly, the reticularthalamic nucleus as a GABA projection plays an inhibitoryrole in pain perception, and a lesion in this area will leadto hypersensitivity to pain. If patients suffering frommTBI-related central pain are not treated in a fashionthat’s conducive to a healthy lifestyle, this may causallycontribute to worsening neuropsychological outcomes.Chronically administered pain medication will lead toincreased dosages, which have a high risk of addiction andmay create or worsen a patient’s substance abuse. Theserisks present patients returning from deployment withsignificant concern over their general stress and discomfortlevels. The attributed euphoric effects may temporarilyresolve these stressors psychologically, and establish afunctional dependency to cope with civilian life in a postrecessioneconomy. 48Chronic pain, like that of post-mTBI headaches,is often associated with troubled sleep. This, alongwith sleep cycle disruption due to nightmares, candesynchronize hormones and lead to excessive daytimedrowsiness. Consequentially, more time is needed toPage 30The AAO Journal Volume 22, Issue 2, Summer 2012

each a sleeping state due to over-resting throughoutdaytime hours. This desynchronization may largely beattributed to the impaired attention and reduced learningand memory capacity of OIF/OEF veterans. Many studiesdemonstrate that these cognitive processes suffer becausethe consolidation and intergradation they require are partof sleep-dependent processes. 49,50 With a prevalence of 30percent to 70 percent, post-TBI sleep disturbance is animportant differential diagnosis sequela for the purpose ofnormalization of blast victims. This is especially true formTBI-associated sleep disturbances, which are significantlymore frequent than those of any greater severity.Insomnia is also a common occurrence with TBIinjury. 51 A survey of 452 TBI patients found that up tohalf met the criteria for insomnia and more than halfwent untreated. Not only was there a greater incidenceof sleep dysfunction, there were also reportings ofhigher frequencies of sleep disturbance. These circadianaberrations all surmount to more somnolence arousalevents during sleep and longer sleep-onset latency.Strangely, these dysfunctions and their related symptomsare more prevalent in mTBI. In an overall sleep study of175mTBI patients there was a two- to three-fold increase insleep disturbance from a time frame of 11 days to 6 weeksfollowing injury. This coincides with the physiologicaloutcome of animal exposure to mTBI and a post-day sevennormalization of increased of heart rate, followed by a day14 return to increased heart rate. Therefore, these, alongwith discharge complaints of greater neurobehavioralimpairments that impair occupational outcomes, aggravatemTBI-associated risk factors that include higher levels offatigue, depression and pain.Some studies suggest that mTBI, to a greater degreethan any other severity of TBI, contributes to daytimesleepiness scores in excess of 10 on the Epworth SleepinessScale. When driving, a score greater than nine can be lifethreatening. Sleepiness becomes a disease when it placesindividuals at higher risks of adverse consequences. 52 Somemight argue that sleep deprivation may contribute to aprotective mechanism through resultant insomnia-relatedmemory loss. As memory consolidation and encoding areheavily sleep-dependent, sleep deprivation may extinguishimplicit fear recognition and physiological response tofear lingering from a spontaneously forgotten traumaticevent memory. 53 If this is the case for civilians, then mTBIexposed deployed and veteran military service memberscould be less likely to experience PTSD symptoms. mTBI’sincreased prevalence with insomnia over other blastTBI severities could better explain the controversy overwhether or not it shares any causality with PTSD. A civilianstudy of mTBI found it was associated with lower sleepefficiency, more nocturnal wake time and more awakeningslasting longer than three minutes. These same patientspresented altered sleep architecture with significantlyhigher proportions of Stage 2 sleep over Rapid EyeMovement slumber. This can lead to deficits in the healthyreplenishment of neurotransmitters and subsequently poorneurophysiological outcomes.Electroencephalogram analysis in an awakened staterevealed significantly greater delta activity and less alphaactivity—a pattern indicative of sleep deprivation and/ora sleep disorder. Low hypocretin-1 levels within cerebralspinal fluid, an indicator of hypothalamic damage, havealso been observed six months after TBI. In excess, lowlevels of hypocretin-1 are associated with post-traumaticexcessive daytime sleepiness, and are therefore a potentialbiomarker for service members ailing from sleep-relatedsymptoms post-mTBI. 54 If the evidence of endocrinedamage substantiates civilian sleep disturbance, a greaterrisk ism, in fact, likely to affect military blast victims dueto blast’s effects on the brain’s inflammatory responseson neurophysiology. Other animal studies have found thatdirect brain injury produces diffuse degeneration of whitematter or diffuse axonal injury. These injuries, producedby angular accelerations, inflict blunt trauma onto areasclosely associated with sleep-wake mechanisms in theseptum pellucidum, corpus callosum, deep gray matter anddorso-lateral pons and midbrain. Subsequent biochemicalprocesses associated with mTBI injury and response,including excitotoxicity, inflammation, free radicals,hyperglycolysis, hyperglycemia and apolipoproteinE e4 synthesis, likely increase the severity of sleepdysfunction.For post-rest period somnolence in particular,sleepwalking can be associated with damage to the perilocuscoeruleus area. This type of sleep disturbance canbe triggered by excitatory impulses, which are typicallysuppressed during Rapid Eye Movement sleep, and reachthe nucleus reticularis magnocellularis within the medulla.This can lead to the unintended activation of motorpathways as the spinal motorneurons of the ventrolateralreticularspinal tract have become hyperpolarized. 49,55-60Predicting the psychological and physical outcomes ofblast mTBIFor military injury related to blast exposure, stressis rarely excluded from TBI, PTSD or PCS symptoms.To what degree does stress add to mTBI injury insult?In a newly published study by Kwon, mice exposed tostress, with and without mild blast exposure, were studiedto examine what complications stress-induced anxietyhas on blast exposure. An open field test used to measureVolume 22, Issue 2, Summer 2012 The AAO Journal Page 31

anxiety found significantly higher levels in stressed blastrats. This normalized after one to two months. In contrast,anxiety levels measured by the count of rat entrance ontoan exposed, elevated ledge that projected from an enclosurewere significantly greater for stressed non-blast rats in thefirst 48 hours.These results draw on differences between the twomethods, and therefore imply that fear perception may bea factor. Three to eight days post-blast, spatial learningand memory testing found that stressed non-blast ratsneeded significantly more time to locate the escape boxentrance. Similar effects for the stressed blast rats werenot seen until 33 to 36 days after. The stressed blast ratsalso performed very poorly in Barnes maze, a less stressfulalternative to water a maze, after day 64. Histologicaltissue from the prefrontal cortex and hippocampus wereexamined two months post-injury as a proteomics andimmunohistochemical analysis of mental defects.Tissue samples showed elevated levels of S100β,VEGF, GFAP, Tau-protein and IFNγ in both the neuralstructures of stressed blast rats, with IL-6 only having asignificantly higher level in the hippocampus of stressednon-blast rats. Stress alone had no effect on IFNγ levels inthe hippocampus. Cellular examinations to subjugate theseobservations found that stressed blast rats experiencedan increase in glial fibrillary acidic protein (GFAP)immunoreactivity of the prefrontal cortex and ventralhippocampus. Such findings were significant for long-termmemory impairments associated with conditions similarto those our military forces confront. Unlike that relatedblast exposure, stress alone was found to cause a transientincrease in anxiety, but no lasting memory impairments.A recent surge in astrocyte research involvingneurodegenerative disease has proliferated TBI findings,which is not to be excluded from this study. Increasedstellar morphology characteristic of reactive astrocytes wasin the previously mentioned structures of stressed blastrats. TUNEL-measured neuronal apoptotic activity in theventral and dorsal hippocampus was significantly increasedin stressed blast rats. Overall, stress alone contributed nomajor cellularly or molecularly induced defects, unlikestress combined with blast. Neuroinflammatory, vascular,neuronal and glial causally destructive outcomes arebelieved to contribute primarily to increased anxiety andchronic memory faults. The tress aspect of war-relatedblast exposure might selectively impair regenerationof inflammatory damage as chronic levels of anxietysignificantly reduce somal volume of astroglia of thehippocampus. 62The long-term effects of mTBI aren’t limited tocognitive deficits. mTBI can also have longstandingconsequences related to increased mortality. Compared togreater severity trauma, veteran mTBI is marginally greaterin the significance of premature death. All injury preventionaccounted for on the battlefield only delays fatality toa later time if long-term medical care isn’t properlymaintained. Given that today’s military combatantsare frequently exposed to mTBI, prototypical medicaldischarge should always follow a plan for scheduledcheckups throughout the lifespan of these patients. TBI isa chronic disease, which could lead to untimely death if itsprogression goes unchecked. 63,64ConclusionsBlast mTBI has been, and continues to be, a majorhurdle in the recovery of many military personnel andveterans faced with debilitating occurrences, includingsignificant changes made on both the patients’ lives andthose with whom they share them. Injuries related toblast mTBI are more prevalent, and even more so formultiple insults. This review covered a broad spectrum offindings and correlations about mTBI. In this review, italso becomes apparent that research tools, combined witha diversity of novel investigatory approaches, may lead towhat wasn’t available to veterans of Vietnam and DesertStorm– a new chance at living better lives.This review describes the complexity of findingsin which clinical methods may be more fruitful whenoverlapping with cutting-edge research tools. Unlikelethal diseases such a cancer, mTBI clinical trials are moreconcerned with more quality of life than certain mortality,which argues the necessity of risky endeavors, such asthose taken in chemotherapy treatments. The exceptionfor mTBI is that the quality of life lost is progressive andunpredictable in nature. This provocation is not to makea difficult situation more hopeless—in fact, quite thecontrary. mTBI patients stand at the forefront of wherenew medicine can make great strides to develop innovativepractices among a community of interconnected physiciansand researchers in this digital age.New branches in astrocyte research are opening doorsfor a new understanding of human neurophysiology inthe hope that brain-injured veterans can aid in the studyof other related neurological diseases. Research scientistsand physicians are working to turn state-of-the-art medicalresearch into state-of-the-practice medical care. Moreover,there was an increased incidence of PTSD symptomsamong blast TBI participants in a study designed tocompare patterns of performance on neuropsychologicalmeasures. 65 However, with respect to cognitive sequelae,it was argued that there is no strong evidence that blast iscategorically different than other mechanisms of TBI. 65Page 32The AAO Journal Volume 22, Issue 2, Summer 2012

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Advances in neuroimaging of traumatic braininjury and post-traumatic stress disorder. J Rehabil Res Dev.2009;46(6):717-757.47. Pare D, Quirk GJ, Ledoux JE. New vistas on amygdala networksin conditioned fear. Journal of Neurophysiology. 2004;92(1):1.48. Usunoff KG, Popratiloff A, Schmitt O, Wree A. FunctionalNeuroanatomy of Pain. New York: Springer Verlag; 2006.49. Ruff RL, Ruff SS, Wang XF. Improving sleep: Initial headachetreatment in OIF/OEF veterans with blast-induced mTBI. Journalof Rehabilitation Research and Development. 2009;46(9):1071.50. Schreiber S, Barkai G, Gur-Hartman T, Peeles E, Tov N, DolbergOT, et al. Long-lasting sleep patterns of adult patients with minortraumatic brain injury (mTBI) and non-mTBI subjects. Sleep Med.2008;9(5):481-487.51. Zeitzer JM, Friedman L, O’Hara R. Insomnia in the context oftraumatic brain injury. J Rehabil Res Dev. 2009;46(6):827-836.52. Sangal RB. When is sleepiness a disease? How do we measure it?Sleep Medicine. 2006;7(4):310-311.53. Kuriyama K, Soshi T, Kim Y. Sleep deprivation facilitatesextinction of implicit fear generalization and physiologicalresponse to fear. Biological Psychiatry. 2010;68(11): 991-998.54. Orff HJ, Ayalon L, Drummond SP. Traumatic brain injury andsleep disturbance: a review of current research. J Head TraumaRehabil. 2009;24(3):155-165.55. Wallace BE, Wagner AK, Wagner EP, McDeavitt JT. A history andreview of quantitative electroencephalography in traumatic braininjury. J Head Trauma Rehabil. 2001;16(2):165.56. Jones C. Glasgow coma scale. The American Journal of Nursing.1979;79(9):1551.57. Duff, J., The Usefulenss of Quantitative EEG (QEEG) andNeurotherapy in the Assessment and Treatment of Post-Concussion Syndrome. Clinical EEG and Neuroscience, 2004.35(4): p. 198-209.58. Chaput G, Giguere JF, Chauny JM, Denis R, Lavigne G.Relationship among subjective sleep complaints, headachesand mood alterations following a mTBI. Sleep Medicine.2009;10(7):713-716.59. Verma A, Anand V, Verma NP. Sleep disorders in chronic traumaticbrain injury. J Clin Sleep Med. 2007;3(4):357-362.60. Stulemeijer M, Van Der Werf SP, Jacobs B, Biert J, Van Vugt AB,Brauer JMP. Impact of additional extracranial injuries on outcomeafter mTBI. J Neurotrauma. 2006;23(10):1561-1569.61. Bulut M, Koksal O, Dogan S, Bolca N, Ozguc H, Korfali E,et al. Tau protein as a serum marker of brain damage in mTBI:preliminary results. Advances in Therapy. 2006;23(1):12-22.62. Kwon SKC, Kovesdi E, Gyorgy AB, Wingo D, Kamnaksh A,Walker J, et al. Stress and traumatic brain injury: A behavioral,proteomics and histological study. Frontiers in Neurology.2011;2:112.63. Masel BE, DeWitt DS. Traumatic brain injury: A disease process,not an event. J Neurotrauma. 2010;27(8):1529-1540.64. Weightman MM, Bolgla R, McCulloch KL, Peterson MD.Physical therapy recommendations for service members withmTBI. J Head Trauma Rehabil. 2010;25(3):206-218.65. Belanger HG, Kretzmer T, Yoash-Gantz R, Pickett T, Tupler LA.Cognitive sequelae of blast-related versus other mechanisms ofbrain trauma. Journal of the International NeuropsychologicalSociety. 2009;15(1):1-8.Accepted for publication: June 2012Address correspondence to:Marc Quentin Sonnier, Jr., MS;Murray R. Berkowitz, DO, MA, MS, MPHDepartment of Osteopathic Manipulative MedicinePhiladelphia College of Osteopathic Medicine—Georgia Campus625 Old Peachtree Road NWSuwanee, Georgia 30024murraybe@pcom.eduPage 34The AAO Journal Volume 22, Issue 2, Summer 2012

Prolotherapy WeekendOctober 25-27, 2012, at UNECOM in Biddeford, MECourse OutlineThursday, October 25, 5:00 pm - 10:00 pm: Physicians whohave not taken a prior course in prolotherapy are requiredto attend this session. It will include an introduction toprolotherapy, wound healing, degenerative postural cascade,coding and billing.Friday and Saturday, October 26-27, 8:00 am - 5:30 pm:Participants will be divided into two groups—beginners andadvanced. These two groups will alternate between lecturesin anatomy and injection technique, and time in the anatomylab performing injections under supervision and reviewingprosections.Principles of Prolotherapy by Cantieri MS, Pasquarello GJand Ravin TH, will serve as the course syllabus. Please seehttp://principlesofprolotherapy.com/index.html for details.PrerequisitesFunctional anatomy: (1) Level I course or equivalent.Participants must indicate upon registration whetherthey are a beginner or advanced prolotherapy student. Ifyou are unsure, please contact Lisa Susemichel at the AAO.CME20 hours of AOA Category 1-A credit is anticipatedTravel ArrangementsCall Tina Callahan of Globally Yours Travel at (800) 274-5975.A rental car is recommended since the campus is locatedabout 15-20 minutes from most hotels and restaurants.Course DirectorsMark S. Cantieri, DO, FAAO, is a 1981graduate of Des Moines University Collegeof Osteopathic Medicine, and is boardcertiied in NMM/OMM. He has served onvarious hospital staffs as a consultant inOMM—treating newborns, post-operativepatients and patients in intensive care units.He currently operates a private practice,Corrective Care, PC, in Mishawaka, IN, whichspecializes in the treatment of chronic musculoskeletal pain.Dr. Cantieri is a Past President and Secretary-Tresurer of theAAO.George J. Pasquarello, DO, FAAO, graduatedfrom UNECOM in 1993. Board-certiied inNMM/OMM, he has served as a ResidencyProgram Director and Associate Professorof OMM at UNECOM. He has also workedas a clinical specialist at Maine Spine &Rehabilitation and University Healthcare.He is currently in private practice at EastGreenwich Spine & Sport in East Greenwich,RI. Dr. Pasquarello is a Past President of the AAO.Course LocationUniversity of New England College of Osteopathic Medicine11 Hills Beach RoadBiddeford, ME 04005(207) 283-0171Registration FormProlotherapy WeekendOctober 25-27, 2012Name: ________________________________________ AOA#: _____________Nickname for Badge: _______________________________________________Street Address: ____________________________________________________________________________________________________________________________City: __________________________________State: ________ Zip: ___________Phone: _______________________________ Fax: ___________________________E-mail: ______________________________________________________________By releasing your fax/e-mail, you have given the AAO permission to sendmarketing information regarding courses to your fax or e-mail.Billing Address (if different than above): _________________________________________________________________________________________________Registration Rates $1,500 - I already own a copy of Principles of Prolotherapy $1,810 - Please order me a copy of Principles of ProlotherapyI am a Beginner Advanced prolotherapy student.Please notify us of any special dietary restrictions.The AAO accepts check, Visa, Mastercard or Discover paymentsin U.S. dollarsCredit Card #: ________________________________________________________Cardholder’s Name: __________________________________________________Expiration Date: _____________________ 3-digit CVV#________________I hereby authorize the American Academy of Osteopathy to chargethe above credit card for the full course registration amount.Signature: __________________________________________________________Click here to view the AAO’s Cancellation and Refund PolicyPlease submit registration form and payment via mail to the American Academy of Osteopathy,3500 DePauw Blvd., Suite 1080, Indianapolis, IN 46268 or by fax to (317) 879-0563.Or register online at www.academyofosteopathy.orgVolume 22, Issue 2, Summer 2012 The AAO Journal Page 35

Sociodemographic analysis of psychiatric emergencyservices in a state with greater than average veteran densityLivia Cara, MS; Murray R. Berkowitz, DO, MA, MS, MPHAbstractObjective: The purpose of this study is to examinethe socio-demographic and clinical characteristics ofpsychiatric patients who utilize the emergency department(ED) of a hospital in the Northeast part of the state ofAlabama as a resource for treatment. The results of thisstudy have the potential to help healthcare providers inearly detection and intervention strategies. One objectiveof this research is to expose the prevalence of mentalhealth emergencies and the importance of management ofpsychiatric crises in the state of Alabama and the nation atlarge.Methods: This study analyzed regression model datacollected from an emergency department in the Northeastregion of Alabama from May 2010 to July 2010 of allpatients presenting with mental health-related issues.Statistical Package for the Social Sciences (SPSS) softwarewas used to analyze descriptive statistics.Results: During this three-month period, 502 psychiatricpatients were seen in the emergency department. A randomsample of 218 patients was used for statistical analysis. Theaverage age was 36.7 years, and 54.6 percent of the patientswere female. Mood disorders were the most frequentdiagnosis with 41.3 percent, followed by anxiety disorderswith 37.6 percent, suicidal ideation in 10.2 percent andpsychosis in 10.2 percent. Suicidal ideation was present in49.1 percent of patients, and more were discharged fromthe hospital than were admitted (47.2 percent).Conclusions: This research demonstrates the importanceof understanding the population served, as well as thecharacteristics of the care delivered to psychiatric patientsseeking emergency services. This research also revealed theneed for further attention to developing strategies that couldprovide greater support to the ever-increasing demand formental healthcare.IntroductionThe use of emergency departments as a sourcefor treatment for psychiatric and social problems hasincreased dramatically in the last decade. 1 Overcrowdingin emergency departments has led to a state of crisis allover the nation, with an even greater concern in the stateof Alabama, where local laws and a decreased numberof psychiatrists and psychiatric inpatient beds havecontributed to this chaotic situation. 2,3The National Institute of Mental Health estimated that26.2 percent of Americans ages 18 and older (about onein four adults) suffer from a diagnosable mental disorderin a given year. 4 In the 2004 census, this figure translatedto 57.7 million people. The Centers for Disease Controland Prevention’s (CDC) National Vital Statistics Systemreported that suicide was the fourth-leading cause of deathin the U.S. for adult ages 18 to 64 years. 5The lack of available and appropriate psychiatricservices, especially for short-term care and stabilization,has turned emergency departments into holding areasfor patients in crisis. 6 This consumes limited emergencydepartment resources (e.g., staff, beds and ancillarypersonnel), thus prolonging the amount of time that allpatients spend waiting for services. 7One objective of this research is to exposethe prevalence and characteristics of mental healthemergencies, and examine whether there is a need toimprove the management of psychiatric services in the stateof Alabama and the nation at large to prevent exacerbationof an already existing crisis.Psychiatric Services in AlabamaStatistics provided by the Substance Abuse andMental Health Services Administration (SAMHSA)and other federal agencies reveal that Alabama has 7.1practicing psychiatrists per 100,000 persons, comparedwith the entire Southeast region of the U.S. having a ratioof 8.2 per 100,000, and with the New England regionhaving a ratio of 26.9 per 100,000. 8,9 An important factorthat needs to be taken into consideration in the state ofAlabama is its number of veterans. Alabama’s civilianpopulation consists of 12.8 percent veterans. Male veteransin the general U.S. population are twice as likely as theircivilian peers to die by suicide. Compared with civilianmen who died by suicide, veterans were 58 percent morelikely to use a firearm to end their lives. 10 By taking thisimportant concept into consideration, more appropriatepsychiatric emergency services can be made available in agiven location.Page 36The AAO Journal Volume 22, Issue 2, Summer 2012

Northeast Alabama Regional Medical CenterNortheast Alabama Regional Medical Center (RMC)is located in the city of Anniston. RMC is a 330-bedhospital. The emergency department (ED) is a Level IITrauma Center with 35 beds, and sees approximately55,000 patients annually. The hospital has an inpatient adultpsychiatric program and a geriatric inpatient psychiatricprogram, as well as outpatient and partial-day treatmentprograms. RMC does not treat adolescent psychiatricpatients, who must be transferred to another facility.Methods and MaterialsThis study analyzed regression-model data collectedfrom an emergency department in the Northeast regionof Alabama from May 1, 2010, to July 31, 2010, of allpatients presenting with mental health-related issues. Arandom sample of 218 was drawn from the population of502 psychiatric emergency patients seen during this threemonthperiod.Table 1. Descriptive statistics for patient demographicsStatistical Package for the Social Sciences (SPSS)software was used to perform the analyses. All theanalyses were descriptive statistics. The mean and standarddeviation was calculated on the continuous variablesand frequencies, and percentages were calculated for thecategorical/ordinal data. Logistic-regression analysis wasperformed.Results and DiscussionAnalysis of the socio-demographic characteristics ofthe patients in this study revealed that 54.6 percent werefemale. Their ethnicity was overwhelmingly Caucasian(78.6 percent). The majority of the patients seen wereeither unemployed (49.9 percent) or disabled (22.9 percent)(Table 1). Mental health-related visits to the emergencydepartment between sexes were consistent with nationalreports, showing a prevalence of females over males. 11Ethnicity was not consistent with national trends, however,which showed a prevalence of African Americans overCaucasians. 12 The national prevalence of any disabilityamong those with a mental disorder is 69.8 percent. 13People with mental disorders were twice as likely to beunemployed than those with no disorder (49.6 percentcompared with 24.5 percent). Our research results wereremarkably similar to the national results. 14Among this research of mental health-related visits,the most common diagnoses were acute depression (22.9percent), followed by anxiety (12.8 percent) and suicidalideation (10.1 percent) (Table 2). The overall consolidateddiagnosis data (Table 3) shows the most common diagnosiswas that of a mood disorder (41.3 percent), followed bythat of an anxiety disorder (37.6 percent); the results wereTable 2. Descriptive statistics for patient diagnosisVolume 22, Issue 2, Summer 2012 The AAO Journal Page 37

the same for suicidal ideation (10.2 percent) and psychosis(10.2 percent).Comprehensive research done by Larkin andAssociates using data from the National HospitalAmbulatory Medical Care Survey (NHAMCS) wasused for comparison. The NHAMCS surveys emergencyhealthcare services nationwide annually. Larkin andhis colleagues reported that the most prevalent nationalmental health-related diagnoses were substance-relateddisorders (30 percent), mood disorders (23 percent) andanxiety disorders (21 percent). 12 Our research revealedthat 66.1 percent of the patients had positive results in adrug or alcohol screening (Table 3). Table 3 also showsthat suicidal ideation was reported in 49.1 percent ofthe patients, and a well thought-out plan for suicide waspresent in 40.4 percent. Plans ascertained for furtheranceand lethality varied, with the most common being selfmutilationwith 35 percent, closely followed by overdosewith 31.6 percent and shooting oneself with 12.7 percent.Forty-two percent of all the patients reported being suicidalin the past, 17.9 percent reported suffering from domesticviolence, and a positive family history of psychiatric illnesswas seen in 26.5 percent.More than 300,000 people attempt suicide eachyear in the United States. 15 This research, as well as otherreports, reveal that suicidal behavior is a frequent problemin psychiatric ED patients. In two similar studies, suicidalideation was present in 38 percent 16 and 39 percent 17 of thepatients. It is our interpretation that a ten percent increasein the suicide rate in the state of Alabama may be due tothe lack of involuntary commitment laws, which make thepatient more comfortable to state suicidal ideation withoutbeing forced to be hospitalized for a 72-hour period formental evaluation.It is possible that our study may have been subjectedto under-reporting of suicidal behavior. 18 Suicidal ideationdata was also obtained from the patients’ family members,emergency medical personnel and police reports, but if thepatient denied being suicidal while answering the face-tofacesuicide risk assessment tool, he/she was not consideredto be at risk for suicide. Past studies have concluded thatface-to-face assessments of suicidal behavior reveal lowerrates of suicide risk when compared with anonymous19, 20surveys.Psychiatric treatment was received by 46.8 percent ofthe patients in the ED. This percentage is lower comparedwith the percentage obtained from NHAMCS in a nine-yearresearch study, which showed that 61 percent of patientsreceive psychiatric medication while in the ED. 12 Amongsuicidal patients, 40.4 percent reported having a wellthoughtout plan for suicide.Table 3. Descriptive statistics for patient informationThe incidence and pattern of drug abuse is reportedin Table 4. Fifty-five percent of the patients tested positivefor drug use. Marijuana (THC) was the most commondrug used by the patients that were seen in the emergencyroom for mental health evaluation. THC was followedby benzoates and cocaine as the drugs of choice for thesepatients. For the patients who tested positive for two ormore drugs, the combination varied, but the most commoncombinations were amphetamines and THC, benzoates andecstasy, and benzoates and THC (Table 4). In agreementwith the SAMHSA (Substance Abuse and Mental HealthPage 38The AAO Journal Volume 22, Issue 2, Summer 2012

Service Administration), THC is the most commonsubstance abused by psychiatric patients, followed bycocaine and opiates. 2Surprisingly, only 11.1 percent of the patients hadpositive alcohol screenings, and their mean blood-alcohollevel was found to be 150.77 milligrams per deciliter (mg/dL). The SAMHSA reported alcohol abuse in 35.7 percentof the patients—a far higher percentage than the 11 percentreported by our patients. 22 Blood-alcohol level is reportedin milligrams per deciliter. At present, 32 states have lawsmaking it illegal to drive with a blood-alcohol level of 80mg/dL or above. 23ConclusionIn summary, 502 psychiatric patients were seen inthe ED during the specified three-month period. A randomsample of 218 patients was used for statistical analysis. Theaverage age was 36.7 years, and 54.6 percent of the patientswere female. Mood disorders were the most frequentdiagnosis with 41.3 percent, followed by anxiety disorderswith 37.6 percent, suicidal ideation with 10.2 percent andpsychosis in 10.2 percent. Suicidal ideation was present in49.1 percent of cases, and more patients were dischargedfrom the hospital than were admitted (47.2 percent).Table 4. Descriptive statistics for postive drug screeningsVolume 22, Issue 2, Summer 2012 The AAO Journal Page 39

The socio-demographic analysis was very similarto that of other studies, with the exception that patients’ethnicity was overwhelmingly more Caucasian in ourresearch compared with African American in the nationaldata. The most common diagnoses in other studies weresubstance-related disorders, whereas, in our study, mooddisorders were more predominate. Furthermore, alcoholabuse had very low incidence in our research with only 11percent compared to nation results of 32.4 percent. 21Suicidal ideation was 10 percent higher in ourresearch compared to the national data. Our patients weremore likely not to receive treatment while in the ED whencompared with patients seen in other EDs across the nation.Admission rates for all patients were also higher in ourresearch.According to the SAMHSA, in 2002, out of the $1.6trillion of all healthcare expenditures, $100 billion wasspent on mental healthcare. 24 Mental healthcare representedaround six percent of all medical expenditures in the UnitedStates. Mental healthcare expenditures are tied with canceras the nation’s third costliest medical conditions. 25These statistics show the need for mental healthservices to continually be researched and evaluated inorder to improve the gaps that exist in the healthcaresystem related to psychiatric services and costs.Significant changes in treatment methods and servicedelivery have occurred during the past 50 years, withdeinstitutionalization being the most striking transition. 3,26These changes mandate that psychiatric emergency servicesbe available to provide psychiatric patients with crisisevaluation, management and treatment outside of inpatientsettings. However, due to political and economic forces,mental healthcare services have declined. 27,28 A lack ofresources and community support, underpaid providersand a decline in psychiatric inpatient beds all increase thechances of relapse in patients with mental illnesses. Withnowhere appropriate to go, these patients have been seekingcare in emergency departments. 29,30Analysis of the characteristics of psychiatric patientsis important because it has the potential to reveal diversityin the clinical decisions made by different providers inthe emergency department. Since general physicians andpractitioners are the ones making the decision betweenhospitalizing a patient and referring him/her to anoutpatient mental health service, it is of great importancethat an analysis of these characteristics is done. 31 Inaccuraterecognition of symptoms has been associated with theoveruse of expensive services such as hospitalization. 32Pain, cognitive disorders, post-traumatic stressdisorder 33 and depression 34.35 are often found amongveterans, especially those of the recent conflicts in Iraqand Afghanistan. Many of these veterans have beenfound to self-medicate with various drugs or alcohol. Thesociodemographics of this study is consistent with pastresults. 33-35 This research demonstrates the importanceof understanding the population served, as well as thecharacteristics of the care delivered to psychiatric patientsseeking emergency services. This research also reveals theneed for further attention to developing strategies that couldprovide greater support for the ever-increasing demand formental healthcare.Lastly, this data provides insight on the differenttype of issues psychiatric emergency systems face in thestate of Alabama. It allows public officials to recognizegaps and consider the implantation of more hospital bedsfor psychiatric patients and the improvement of resourcesavailable for outpatient treatment, using other statesand national data as models for a more plausible mentalhealthcare system. This analysis is limited with respectto its generalizability beyond the local rural area of thissingle state. Questions comparing veteran vs. non-veteransociodemographics could not be analyzed due to the lackof patient data regarding veteran status in this civilianmedical center. Questions regarding whether the sample isrepresentative of both the general U.S. population and theveteran population remain. More research is warranted.References1. Larkin GL, Claassen CA, Emond JA, Pelletier AJ. Trends in U.S.emergency department visits for mental health conditions, 1992 to2001. Psychiatry Serv. 2005;56:671–677.2. Powers MD, Richard E. Understanding the shortage ofpsychiatrists in Alabama. Scribd. http://www.scribd.com/doc/2175651/. April 25, 2007. Accessed February 3, 2011.3. Tuttle G. Access to Psychiatric Beds and Impact on Emergency.Report of the Council on Medical Service. American MedicalAssociation. http://www.ama-assn.org/resources/doc/cms/a-08cms2.pdf. March 22, 2009. Accessed May 5, 2011.4. Kessler RC, Chiu WT, Demler O, Walters EE. Prevalence, severityand comorbidity of twelve-month DSM-IV disorders in theNational Comorbidity Survey Replication (NCS-R). Archives ofGeneral Psychiatry. 2005;62(6):617-627.5. U.S. Census Bureau Population Estimates by DemographicCharacteristics. Table 2: Annual Estimates of the Population bySelected Age Groups and Sex for the United States: April 1, 2000to July 1, 2004 (NC-EST2004-02). Source: Population Division,U.S. Census Bureau Release. June 9, 2005. http://www.census.gov/popest/national/asrh/6. Baraff LJ. A mental health crisis in emergency care. BehavioralHealthcare. 2006.26(11):39-40.7. Carolla B. Emergency departments see dramatic increase in peoplewith mental illness seeking care. National Alliance on MentalIllness- Mental Health Support, Education and Advocacy. http://www.nami.org/Content/ContentGroups/Press_Room1/20041/April3/Emergency_Departments_See_Dramatic_Increase_in_People_with_Mental_Illness_Seeking_Care.htm. April 27, 2004.Accessed May 12, 2011.Page 40The AAO Journal Volume 22, Issue 2, Summer 2012

8. Manderscheid RW, Berry JT, eds. Center for Mental HealthServices, Substance Abuse and Mental Services Administration.www.samhsa.gov. 2004.9. An action plan for Behavioral Health Workforce Development:A framework for discussion. http://www.samhsa.gov/workforce/annapolis/workforceactionplan.pdf10. Kaplan M, Huguet N, McFarland B, Newsom J. Suicide amongmale veterans: A prospective population-based study. Journal ofEpidemiology and Community Health. 2011;61(7):619-624.11. NIMH Statistics—Prevalence of serious mental illness amongU.S. adults by age, sex and race. National Survey on Drug Use andHealth (NSDUH). http://www.nimh.nih.gov/statistics/SMI_AASR.shtml. July 29, 2010. Accessed May 6, 2011.12. Larkin GL. Trends in U.S. emergency department visits for mentalhealth conditions, 1992 to 2001. Psychiatric Serv. 2005;56(6):671-677.13. Jans L, Stoddard S, Kraus, L. Chartbook on mental health anddisability in the United States. National Institute on Disability andRehabilitation Research. http://www.infouse.com/disabilitydata/mentalhealth/14. Burke-Miller JK, Cook JA, Grey DD, Razzano LA, Blyler CR,Leff HS, et al. Demographic characteristics and employmentamong people with severe mental illness in a multi-site study.Community Mental Health Journal. 2006;42(2):143-15915. Weissman MM. The epidemiology of suicide attempt, 1960 to1971. Arch Gen Psychiatry. 1974:30:737-746.16. Dhossche DM. Suicidal behavior in psychiatric emergency roompatients. Southern Medical Journal. 2000;93(3):310.17. Szuster R, Schanbacher B, McCann S. Characteristics ofpsychiatric emergency room patients with alcohol or drug-induceddisorders. Hop Community Psychiatry. 1990;41:1342-1345.18. Malone KM, Szanto K, Corbitt EM, Mann JJ. Clinical assessmentversus research methods in the assessment of suicidal behavior.Am J Psychiatry. 1995;152:1601-1607.19. Meehan PJ, Lamb JA, Saltzman LE, O’Carroll PW. Attemptedsuicide among young adults: Progress toward a meaningfulestimate of prevalence. Am J Psychiatry. 1992;149:4144.20. Safer DJ. Self-reported suicide attempts by adolescents. Ann ClinPsychiatry. 1997;9:263-269.21. The TEDS Report—Characteristics of Clients Who Left OutpatientTreatment During the First 30 Days. Alcohol, Tobacco & DrugAbuse and Mental Health Data from SAMHSA, Office of AppliedStudies. http://oas.samhsa.gov/2k11/203/203TxDropouts2k11.htm.April 5, 2011. Accessed May 5, 2011.22. The TEDS Report—Characteristics of Clients Who Left OutpatientTreatment During the First 30 Days. Alcohol, Tobacco & DrugAbuse and Mental Health Data from SAMHSA, Office of AppliedStudies. http://oas.samhsa.gov/2k11/203/203TxDropouts2k11.htm.April 5, 2011. Accessed May 5, 2011.23. Howard P. Psychiatric care in the emergency department—Chaosor crisis? Psychiatric Emergencies. 2006;41-43.24. Mark TL, Levit KR, Coffey RM, McKusick DR, Harwood HJ,King EC, et al. National Expenditures for Mental Health Servicesand Substance Abuse Treatment, 1993–2003. 2005. http://www.samhsa.gov/spendingestimates/samhsafinal9303.pdf. AccessedMay 6, 2011.25. Mark TL, Levit KR, Coffey RM, McKusick DR, Harwood HJ,King EC, et al. National Expenditures for Mental Health Servicesand Substance Abuse Treatment, 1991–2001. 2005. http://www.samhsa.gov/spendingestimates/SEPGenRpt013105v2BLX.pdf.Accessed May 6, 2011.26. Brown JF. Psychiatric Emergency Services: A Review ofthe Literature and a Proposed Research Agenda. PsychiatricQuarterly. 2005;76(2):139-165.27. Kates N, Eaman S, Santone J, Didemus C, Steiner M, Craven M.An integrated regional emergency psychiatry service. Gen HospPsychiatry. 1996;18(4):251–256.28. Manderscheid RW, Atay JE, Hernández-Cartagena MR, EdmondPY, Male A, Zhang H. Chapter 14: Highlights of OrganizedMental Health Services in 1998 and Major National and StateTrends. Mental Health, United States, 2000. Rockville, MD: U.S.Department of Health and Human Services, 1999. Available at:http://www.mentalhealth.org/publications/allpubs/SMA01-3537/default.asp.29. Fitzgerald M. Structuring psychiatric emergency services forsmaller communities in response to managed care. PsychiatricServices. 1996; 47:233–234.30. Claassen C, Hughes C, Gilfillan S, McIntire D, Roose A, BascoM. The nature of help seeking during psychiatric emergencyservice visits by a patient and an accompanying adult. PsychiatricServices. 2000;51:924–927.31. ACEP Psychiatric and Substance Abuse Survey 2008.American College of Emergency Physicians. http://www.acep.org/uploadedFiles/ACEP/Advocacy/federal_issues/PsychiatricBoardingSummary.pdf. March 22, 2009. AccessedApril 5, 2011.32. Novacek J, Raskin R. Recognition of warning signs: Aconsideration for cost-effective treatment of mental illness.Psychiatric Services. 1998;49:376–378.33. Halbauer JD, Ashford JW, Zeitzer JM, Adamson MM, Lew HL,Yesavage JA. Neuropsychiatric diagnosis and management ofchronic sequelae of war-related mild to moderate traumatic braininjury. Journal of Rehabilitation Research and Development.2009;46(6):757-796.34. Neurobehavioral Guidelines Working Group, Warden DL,Gordon B, McAllister TW, Silver JM, Barth JT, Bruns J, et al.Guidelines for the pharmacologic treatment of neurobehavioralsequelae of traumatic brain injury. Journal of Neurotrauma.2006;23(10):1468-1501.35. Rapoport MJ, McCullagh S, Shammi P, Feinstein A. Cognitiveimpairment associated with major depression following mild andmoderate traumatic brain injury. The Journal of Neuropsychiatryand Clinical Neurosciences. 2005;17(1): 61-65.Accepted for publication: June 2012Address correspondence to:Livia Cara, MS; Murray R. Berkowitz, DO, MA, MS, MPHDepartment of Osteopathic Manipulative MedicinePhiladelphia College of Osteopathic Medicine—Georgia Campus625 Old Peachtree Road NWSuwanee, Georgia 30024murraybe@pcom.eduVolume 22, Issue 2, Summer 2012 The AAO Journal Page 41

Oscillatory and Energetically IntegratedOsteopathic Medicine in a Contemporary SettingNovember 30-December 2, 2012, at NSUCOM in Fort Lauderdale, FLCourse DescriptionThe course will give practitioners an introduction to, oran organized context in which to use, rhythmic force inthe application of osteopathic manipulation—either tocomplement their current methods or as a new alternativestrategy. Three major trains of thought emerge, namelythe use of the mechanical percussion vibrator updatedfrom Dr. Fulford’s introductory view; a purely manualapplication (Facilitated OscillatoryRelease); and a phenomenologicalapproach to mindfulness in manipulation.Contemporary neuroscience and cognitivescience pertinent to these skills will bereviewed. Each of the three areas willbe dealt with conceptually, but also with practical exercisesintended to integrate them rapidly into practice.Dr. Comeaux’s attitude toward each is that vibratory methodsshould be most appropriately viewed not as separate models,but as part of an eclectic, integrated approach to the intendedend, facilitating normal function. This includes engagementon multiple levels of dynamic physiology. Integration relieson having strategies and skills, but also a perceptive, mindfulapproach. The use of oscillation and managed perception,furthermore, develop insight into the common features ofmany approaches to subtle Osteopathy and advanced practice.CME20 hours of AOA Category 1-A credit is anticipatedCourse DirectorsZachary J. Comeaux, DO, FAAO, a student/protegé ofRobert C. Fulford, DO, has researched neuroscience/cognitive science relevant to Dr. Fulford’s “energetic”patient/practitioner interraction. The result is an integrativesynthesis taught to avid osteopathic communities overseasfor years. As president of the World Osteopathic HealthOrganization and active in the Osteopathic InternationalAlliance, he has a broad view ofosteopathic history, concept and practice.A 1988 graduate of OUCOM, he iscertiied in FM and NMM, and carries thisintegrative perspective into workshops.PrerequisitesLevel I course and basic understanding of functional anatomy.Course TimesFriday and Saturday: 8:00 am - 5:30 pm (lunch provided)Sunday: 8:00 am - 12:30 pm (lunch on your own)Course LocationNSUCOM3301 College Ave.Fort Lauderdale, FL 33314(800) 541-6682Travel ArrangementsCall Tina Callahan of Globally Yours Travel at (800) 274-5975.Registration FormOscillatory & Energetically Integrated Osteopathic MedicineNovember 30-December 2, 2012Name: ________________________________________ AOA#: _____________Nickname for Badge: _______________________________________________Street Address: ____________________________________________________________________________________________________________________________City: __________________________________State: ________ Zip: ___________Phone: _______________________________ Fax: ___________________________E-mail: ______________________________________________________________By releasing your fax/e-mail, you have given the AAO permission to sendmarketing information regarding courses to your fax or e-mail.Billing Address (if different than above): _________________________________________________________________________________________________Registration RatesOn or before Oct. 2 After Oct. 2AAO Member $ 680.00 $ 780.00AAO Non-Member $ 780.00 $ 880.00Student/Intern/Resident $ 580.00 $ 680.00Please notify us of any special dietary restrictions.The AAO accepts check, Visa, Mastercard or Discover paymentsin U.S. dollarsCredit Card #: ________________________________________________________Cardholder’s Name: __________________________________________________Expiration Date: _____________________ 3-digit CVV#________________I hereby authorize the American Academy of Osteopathy to chargethe above credit card for the full course registration amount.Signature: __________________________________________________________Click here to view the AAO’s Cancellation and Refund PolicyPlease submit registration form and payment via mail to the American Academy of Osteopathy,3500 DePauw Blvd., Suite 1080, Indianapolis, IN 46268 or by fax to (317) 879-0563.Or register online at www.academyofosteopathy.orgPage 42The AAO Journal Volume 22, Issue 2, Summer 2012

Holistic osteopathic approach to the care of veterans withpost-traumatic stress disorder: Case reportAndrew Lovy, DO, FACN, DMOR; Murray R. Berkowitz, DO, MA, MS, MPHAbstractPost-traumatic stress disorder (PTSD) is an anxietydisorder, the differential diagnosis of which includesgeneralized anxiety, somatoform disorder, major depressionwith or without psychosis, secondary chemical dependencyand schizophreniform disorder. The epidemiology andetiology of PTSD are briefly discussed. Pharmacotherapyis presented. The purposeof this paper is to alertphysicians of what tolook for, since the cluesare sometimes in themusculoskeletal system,but do not respond toOsteopathic ManipulativeMedicine (OMM) treatmentuntil the origin of the traumais also discovered.IntroductionPTSD is a valid diagnosis, with many differentvalid treatment options that work for some. There isan overabundance of contradictory medical literature.In general, we are doing a poor job with the diagnosis,treatment, and even validation of, PTSD. The purpose ofthis paper is to alert physicians of what to look for, sincethe clues are sometimes in the musculoskeletal system,but do not respond to OMM treatment until the origin ofthe trauma is also discovered. Since September 11, 2001,even World War II veterans have been having symptomsthey cannot explain until they receive therapy and PTSDis uncovered. We now have many Iraq and Afghanistanveterans facing the terrors of their tour(s).Post-traumatic stress disorder (PTSD) is an anxietydisorder, the differential diagnosis of which includesgeneralized anxiety, somatoform disorder, major depressionwith or without psychosis, secondary chemical dependency,and even schizophreniform disorder when in the middle ofan “attack.” 1• Approximately 20 percent of women andeight percent of men who have been exposedto significant traumatic events will eventuallydevelop symptoms of PTSD. The lifetimeprevalence of this disorder is approximately 10 to14 percent for women and five to six percent formen. 2• PTSD is a debilitating anxiety disorder seen in25 to 30 percent of individuals who experience atraumatic event. 2• PTSD has been described throughout Americanmilitary history, originating in veterans ofthe American Civil War. Then called “DaCosta syndrome” or “soldier’s heart,” it wascharacterized by cardiac symptoms associatedwith irritability and increased arousal. DuringWorld War I, “shell shock” was thought to resultfrom brain trauma caused by exploding shells.• In World War II, the terms “combat neurosis”and “operational fatigue” were used to describecombat-related symptoms. The Vietnam Warsignificantly influenced the current concept ofPTSD, with the lifetime prevalence of the disorderin these veterans estimated to be approximately30 percent. 2Etiology of PTSDAlthough the etiology of PTSD is unknown,patients with a personal or family history of majordepression or anxiety disorder may be at risk for symptomdevelopment. 2-4• Overall, there is “an increased likelihood ofsuffering from physical health conditions withincreased exposure to traumatic events, in a linearpattern.” 2Volume 22, Issue 2, Summer 2012 The AAO Journal Page 43

• Some people are more likely to develop PTSDafter a traumatic event. Risk factors includesevere or prolonged trauma, trauma/abuse duringchildhood, pre-existing history of psychiatricillness, comorbid substance abuse, 5 poor socialsupport and female gender.• Common forms of trauma that cause PTSDinclude involvement in military conflict(particularly combat or medical roles), violentcrime, rape and other sexual assault, torture,natural disasters and severe injury or medicalillness. 2• Current evidence suggests that the underlyingphysiology of PTSD probably involvesdysregulation of multiple neurochemical systems,including those regulated by noradrenalin, thehypothalamic-pituitary-adrenocortical (HPA) axis,the thyroid and endogenous opioid systems.• Major medical illnesses are common amongpeople with severe PTSD.• In a large cohort ofVietnam veterans examinedapproximately 20 years aftertheir combat experiences,there was a higher lifetimeprevalence of circulatory,digestive, musculoskeletal,endocrine, nervoussystem, respiratory andnon-sexually-transmittedinfectious diseases amongveterans with PTSD. 2• There is considerable evidence to suggest thatnoradrenergic mechanisms play a fundamentalrole in the underlying neurophysiology of PTSD,in particular with respect to disturbances ofarousal response and memory function.Troops serving in Iraq and Afghanistan may be morevulnerable to mental disorders for several reasons:• Due to the lack of a formal battlefront, soldiersdeal with constant threat and combat uncertainty.• Many of the troops are from National Guardunits. These soldiers frequently receive much lesstraining than active-duty units.• Tours of duty are long and frequently includedirect-combat exposure.• Many military service members face redeployment.According to the DSM-IV, for a diagnosis of PTSD,a person has to have been exposed to a traumatic event inwhich both of the following were present: 1• The person experienced, witnessed, or wasconfronted with, an event or events that involvedactual or threatened death or serious injury, ora threat to the physical integrity of oneself orothers.• The person’s response involved intense fear,helplessness or horror. Note: In children, it maybe expressed instead by disorganized or agitatedbehavior.True trauma, in the clinical sense, refers to situationsin which one is rendered powerless and great danger isinvolved. The fundamental dynamic underlying PTSDis a cycle of re-experiencing the trauma, followed byattempts to bury the memories of the trauma and thefeelings associated with it. This cycle of intrusive recall,followed by avoidance and numbing, has a strongbiological component. The patientexperiences persistent avoidance ofstimuli associated with trauma and anumbing of general responsiveness.The patient experiences hyperarousalsymptoms (“fight or flight” and“freeze” reactions). This results inimpaired functioning. It is possiblefor individuals to develop PTSDwithout meeting this stressorcriterion. There also appears to be agenetic predisposition to developingPTSD. 6PTSD is more likely to develop if one dissociates(defense mechanism); has the perception that they wereresponsible or acted inappropriately; perceives that theyare alone or isolated; has post-trauma factors; the recoveryenvironment is negative; there is emotional unavailability;the victim is disbelieved, stigmatized, shamed or shunned;the victim does not receive treatment; or the victim hasineffective coping skills. There are various triggers: sensory(visual–seeing blood, etc.–sound, smell, taste); physical/bodily; tactile; pain; significant dates or seasons of the year;stressful events/arousal; and strong emotions, thoughts,memories or behaviors. Symptoms may come “out ofthe blue” when the patient is tired, relaxing or his/herdefenses are down. These symptoms may appear in variouscombinations.Pharmacotherapy for PTSDPharmacotherapy should be directed at thecore symptoms of PTSD and attempt to reduce thePage 44The AAO Journal Volume 22, Issue 2, Summer 2012

therapeutic modality addresses the issue. The medicationmakes the brain more amenable to therapy; the therapycannot proceed as well without the medication; the groups;the returning in the mind, if not actually physically, to theoriginal site of the trauma—all are part of the situation. Formany, it is a lifelong struggle, since the damage to the brainis irreversible, but can be attenuated. For others, once thetherapy proceeds and is successful, the symptoms relent,possibly forever.frequency and intensity of symptoms and their disability.The primary target symptoms for pharmacotherapy includedifficulties with sleep, hypervigilance, exaggerated startleresponse, irritability or outbursts of anger, and difficultyconcentrating or completing tasks.Antidepressants are currently the preferred medicationfor PTSD, with the most substantial evidence availableto support the use of the selective serotonin reuptakeinhibitors (SSRIs). The SSRIs should be regarded asthe first-line pharmacotherapy for PTSD. Antipsychoticmedications may be helpful, particularly in cases wherethere are severe hyperarousal symptoms or psychoticphenomena; these include Olanzapine, Quetiapine andAripiprazole. Adrenergic modulators appear to be effectivein treating symptoms of PTSD. There is considerableevidence to suggest that noradrenergic mechanisms playa fundamental role in the underlying neurophysiology ofPTSD, in particular with respect to disturbances of arousalresponse and memory function.An estimated 70 to 87 percent of patients sufferingfrom PTSD experience sleep disruption. Prazosin, a highlylipophilic α 1-adrenergic receptor blocker that is traditionallyused to treat hypertension and benign prostatic hyperplasia,has been shown to decrease the occurrence of traumanightmares in both combat veterans and patients withnon-combat-related PTSD. Drawbacks to the medicationinclude the side effects of weight gain, Diabetes Mellitusand Tardive Dyskinesia.For years, the treatment for the depression componentof those with PTSD was Buproprion (Wellbutrin). This isa very good dopaminergic medication and an especiallygood one for depression. However, the depression ofPTSD is predominantly serotonergic. It is the decreasein serotonin, possibly due to the shock of the incidentor incidents, that depletes the serotonin, and it is thatreplacement that is crucial during the effective treatment ofPTSD. Patients who were switched to Zoloft (sertraline),or any other SSRI, did better. Now we understand thatthe replacement of serotonin is not the single answer; itis part of the chemicals the brain needs in order to thenprocess the therapy. So, as is frequently the case, no singleCasesAt a medical conference, one doctor (a psychiatrist)came up to me and told me that he had never been incombat or ever assigned to a combat unit; his job was tocounsel newly returning veterans from combat zones andhelp them re-adjust and get their new assignments. Thehorrors they talked about to him, over and over again,caused him to develop a full-blown case of PTSD, meetingall the criteria. This emphasizes the criterion of beingpersonally involved in the horrors—hearing about it enoughtimes, and personalizing it, can lead to developing PTSD.Another case, one that is still in my active files, is thatof an airborne paratrooper suffering from PTSD. He was onpatrol, had a Vietcong person in his sights, and shot first,killing the person. When they went to the site, they foundthat the person was a woman, and brought him back herbloodied bra. He sees this in his dreams continually, hasnightmares about it and cannot get it out of his mind, evenwhen he is not thinking about it. When we chatted yearsago, I mentioned that, at the time, this was not a woman,but a dedicated enemy and, had he not fired, she surelywould have killed him. He looked at me and said that mostof his life, he wished she would have, so he would not haveto go through this for the rest of his life.Another case is that of a 60-year-old veteran whohas had PTSD symptoms since a few years after he leftthe military. One of his symptoms was that he could notstand changing the diaper of his children, or even beingin the same room as his grandchildren when their diaperswere being changed. We worked on this for six months. Idid relaxation therapy and OMM to his very tight musclesVolume 22, Issue 2, Summer 2012 The AAO Journal Page 45

when he described his symptoms and discomfort (hebabysat his grandchildren frequently). Then, one daywhile working with him in therapy and doing myofascialrelease, he had a flashback in my presence. He was inthe South Pacific and watching a Canberra (twin-engineBritish aircraft) that was landing, when an engine brokeloose and went ahead of the plane. It then turned aroundand went through the cabin, burning and dismemberingthe occupants. One of his tasks was cleanup—pickingup burnt body parts and bagging them. It finally hit himthat the smell of burning flesh and diesel fuel smelled (tohim) very much like a soiled baby’s diaper! Once that wasrevealed, he went through a catharsis, and in a few months,his symptoms completely disappeared and he could changediapers. For some reason, locked in the way the brainworks, once the original issue is discovered and workedthrough, and the emotional and physical are recombinedin the present, the symptoms either disappear or aresufficiently attenuated to no longer be so pervasive as toprevent function.PTSD is not limited to military situations, but acommon result of any type of trauma, such as rape, murder,sudden death, etc. I work with two nurse practitioners, andit surprises me just how many ladies in this rural area meetthe criteria for PTSD, having been in terrible relationships,beaten, accosted, etc.It has been reported that children in California,thousands of miles away from ground zero on September11, 2001, have the same incidence of PTSD as those atGround Zero, so distance is not a factor.Women face the same situations and dangers as theirmale counterparts, plus the additional trauma inherentin being women. Accurate data was presented to me bya female Colonel in the Army, who had statistics that, inaddition to dealing with combat-related issues, almost 75percent of women in the military, sometime during hercareer, will be sexually harassed, raped or accosted by theirmale counterparts. If the theories are correct regardingorigins and etiological mechanisms, any severe traumacan lead to repressed or unrepressed memories resulting inPTSD.I have seen many cases over the years of patients whohave had muscle aches and pains, and musculoskeletalor somatic issues, where the origin is not in the tissuesthemselves, but in the tissues reacting to the emotionalcomponent. Unless physicians are sensitive to thispossibility, they can fail to identify the root cause(s) andmiss coming to the correct, overarching diagnosis.ConclusionThe parameters for making a diagnosis of PTSD areconstantly changing. We still have many more questionsthan definitive answers. Much has been made of geneticvulnerability that is valid. Current state-of-the-practiceplaces more emphasis on early diagnosis, and even moreon effective ways to attenuate it when there is suspicionof it occurring now or in the future. Treatments can bevery effective, perhaps in spite of the theories rather thanbecause of them.Physicians need to recognize that the brain cancompartmentalize and move psychic trauma to unconsciouslevels so the individual can function. They must alsounderstand that if anything pushed into the unconsciousor subconscious is not resolved, it may make a full-blownreturn under certain circumstances. There are somaticfunctional complaints that do not resolve with appropriateand effective somatic therapy until and unless the originalinsult to the body and/or brain is also exposed, understoodand worked through.There are five fundamental “victim” questions:• What happened?• Why did it happen?• Why did I act as I did then?• Why do I act as I have since then?• How will I act if it happens again?Patients with PTSD often experience guilt over actsthey performed or observed—“survivor guilt,” gaps inawareness, depersonalization and de-realization. In additionto the management of core PTSD symptoms, it is alsoPage 46The AAO Journal Volume 22, Issue 2, Summer 2012

necessary for clinicians to address important associatedcomorbidities, most notably, substance-use disorders andmood disturbances.It is a myth that PTSD will go away and be forgottenif you do not talk about it. Treatment can be very helpful,and is recommended if the patient’s symptoms are causingconsiderable suffering; the symptoms are interfering withhis/her capacity to work, enjoy life and connect to others;his/her symptoms are causing physical illness; 7 symptomsdo not lessen within one to three months; the patientexperiences suicidal thoughts; or if the patient is taking anymedications for his/her symptoms. 5Physicians, especially non-veteran civilian physicians,need to be aware of how veterans can slip through thecracks of the military and VA systems, and have issues tiedto their military service. Somatic dysfunctions may not onlyreflect viscerosomatic reflexes, but may also announce thatthe patient is suffering from psychic trauma. This psychictrauma may be the reflection of wartime experiencespresenting as PTSD.6. Cornelis MC, Nugent NR, Amstadter AB, Koenen KC. Geneticsof post-traumatic stress disorder: Review and recommendationsfor genome-wide association studies. Curr Psychiatry Rep.2010;12(4):313-326.7. Cohen BE, Gima KS, Bertenthal D, Kim S, Marmar CR, Seal KH.Mental health diagnoses and utilization of VA non-mental healthmedical services among returning Iraq and Afghanistan veterans. JGen Intern Med. 2010;25(1):18-24.Accepted for publication: June 2012Address correspondence to:Andrew Lovy, DO, FACN, DMOR;Murray R. Berkowitz, DO, MA, MS, MPHDepartment of Osteopathic Manipulative MedicinePhiladelphia College of Osteopathic Medicine—Georgia Campus625 Old Peachtree Road NWSuwanee, Georgia 30024murraybe@pcom.eduReferences1. Diagnostic and Statistical Manual of Mental Disorders,4 th Ed. DSM-IV. Washington, DC: American PsychiatricAssociation;1994.2. Tanielian T, Jaycox LH, eds. Invisible wounds of war:Psychological and cognitive injuries, their consequencesand services to assist recovery. Santa Monica, CA: RANDCorporation; 2008.3. Seal KH, Metzler TJ, Gima KS, Bertenthal D, Maguen S, MarmarCR. Trends and risk factors for mental health diagnoses amongIraq and Afghanistan veterans using Department of VeteransAffairs health care, 2002-2008. American Journal of PublicHealth. 2009; 99(9):1651-1658.4. Sundin J, Forbes H, Fear NT, Dandeker C, Wessely S. The impactof conflicts of Iraq and Afghanistan: A UK perspective. Int RevPsychiatry. 2011;23(2):153-159.5. Seal KH, Shi Y, Cohen G, Cohen BE, Maguen S, Krebs EE, et al.Association of mental health disorders with prescription opioidsand high-risk opioid use in U.S. veterans of Iraq and Afghanistan.JAMA. 2012;307(9):940-947.CME QUIZThe purpose of the quiz found on page 48 is to providea convenient means of self-assessment for your reading ofthe scientific content in “Holistic osteopathic approach tothe care of veterans with post-traumatic stress disorder: Casereport” by Andrew Lovy, DO, FACN, DOMR and Murray R.Berkowitz, DO, MA, MS, MPH.Please answer each question listed. The correct answerswill be published in the September 2012 issue of the The AAOJournal.To apply for Category 2-B CME credit, record youranswers to the AAOJ CME quiz application form answersheet on page 48. The AAO will note that you submittedthe form, and will forward your results to the AOA Divisionof CME for documentation. You must score a 70 percent orhigher on the quiz in order to receive CME credit.Volume 22, Issue 2, Summer 2012 The AAO Journal Page 47

American Osteopathic Association Continuing Medical EducationThis CME Certification of Home Study Form is intended to document individual review of articles in the American Academyof Osteopathy Journal under the criteria described for Category 2-B CME credit.CME Certification of Home Study FormThis is to certify that I, ____________________________Please print nameREAD the following article for AOA CME credits.Name of Article: Holistic osteopathic approach to the careof veterans with post-traumatic stress disorder: Case reportAuthor(s): Andrew Lovy, DO, FACN, DMOR; Murray R.Berkowitz, DO, MA, MS, MPHPublication: The AAO Journal, Volume 22, No. 2, Summer2012, pp. 43-47.Category 2-B credit may be granted for these articles.00____________AOA NumberFull name: ______________________________________(Please print)Street address: ___________________________________City, state, zip: ___________________________________Signature: _______________________________________FOR OFFICE USE ONLYCategory: 2-B Credits:_________ Date: ____________December 2011 AAO Journal CME quiz answers:1. D2. B3. D4. AAnswers to June 2012 AAOJ CME quiz willappear in the September 2012 issue.Complete the quiz below by circling the correct answer.Mail your completed answer sheet to the AAO. The AAOwill forward your results to the AOA. You must have 70percent accuracy in order to receive CME credits.Mail this page to:American Academy of Osteopathy3500 DePauw Blvd,Suite 1080Indianapolis, IN 462681.Which of the following mechanisms are believed to playa fundamental role in the neurophysiology of PTSD, inparticular with respect to disturbances of arousal responseand memory function?A) AdrenergicB) Exogenous opioid systemsC) NoradrenergicD) Serotonergic2.Which of the following should be regarded as first-linepharmacotherapy for PTSD?A) AntipsychoticsB) MAOIsC) SNRIsD) SSRIsE) TCAs3.Musculoskeletal somatic dysfunctions due to thedepression of PTSD may not be resolved with OMT untilthe emotional component is successfully addressed.A) TrueB) False4.Which of the following is NOT one of the DSM-IVcriteria for PTSD?A) AvoidanceB) ExposureC) HypoarousalD) Impaired functioningE) Re-experiencing the traumaPage 48The AAO Journal Volume 22, Issue 2, Summer 2012

Biomarkers and neuroimaging techniques to detectblast-induced traumatic brain injury (bTBI)Patrick M. Malie, MS, OMS III; Murray R. Berkowitz, DO, MA, MS, MPHAbstractDetection of blast-induced traumatic brain injury(bTBI) is discussed by looking at potential biomarkers ofinjury and current neuroimaging techniques. Due to thenature of bTBI, the focus is placed on military populations.Biomarkers of injury that have demonstrated pre-clinicalpotential include glial fibrillary acid protein (GFAP),myelin basic protein (MBP), S-100b and neuron specificenolase (NSE). The application of neuroimaging techniquesto the evaluation and management of patients who havesuffered bTBI is presented. Additional translationalresearch is needed to study the effectiveness and efficiencyof using biomarkers of injury and neuroimaging techniquesin the evaluation and management of patients withsuspected exposure to bTBI.IntroductionIt is estimated that, by January 2008, as many as320,000 American armed forces serving in the current Iraqand Afghanistan wars have experienced a traumatic braininjury (TBI). 1 TBI has been designated as the “signatureinjury” of Operation Iraqi Freedom (OIF) and OperationEnduring Freedom (OEF). 2-5 The nature and effects ofblast-induced traumatic brain injury (bTBI) are more fullyreviewed and described elsewhere. 6Biomarkers for bTBIA thorough understanding of the biomarkers of bTBIis yet to be achieved. One reason is because the symptomsof bTBI often do not manifest until sometime after theinjury has occurred. 7 Another is that brain injuries, mild andmoderate in particular, often go undiagnosed and untreatedsince medical attention is issued toward more visibleinjuries. 8 Although there are currently no biomarkers withproven clinical utility for bTBI, or any mechanism of braininjury for that matter, there are several proteins that havedemonstrated pre-clinical potential. 9 The candidates includeglial fibrillary acid protein (GFAP), myelin basic protein(MBP), S-100b and neuron specific enolase (NSE).GFAP is a filamentous protein found in the astroglialcytoskeleton, and is not located outside the central nervoussystem (CNS). 10 In a study conducted by Nylen, et al., 11 onsevere TBI patients, those with unfavorable outcomes hadsignificantly higher maximal serum GFAP (s-GFAP) levelsin the acute phase than patients with favorable outcomes.Another study indicated that GFAP had the capability todistinguish injury severity based on the Marshall scaleclassification of computed tomography (CT) scans. 12The Marshall scale is a classification scale of intracranialpathology as observed by CT, and has been shown tobe predictive of clinical outcome. 13 Although GFAPhas not been studied in mild or moderate brain injury, itdemonstrates potential as a diagnostic tool in predictingoutcome after severe TBI. Furthermore, it shows potentialin discriminating brain injury magnitude, and may prove tobe a better diagnostic tool than S-100b, since it is specificfor brain tissue and not affected by hemorrhagic shock orextracranial trauma. 9MBP, an abundant protein in white matter, is thoughtto be important in the myelination of nerves in the CNS. 14It has been examined as a biomarker of axonal damagein many insults relevant to neurointensive care. 9 In TBI,serum and cerebrospinal fluid (CSF) levels of MBP haveshown excellent specificity, but limited sensitivity. 15More recently, it was shown that MBP serum levels, aswell as NSE and S-100b serum levels, may function inpredicting outcomes after pediatric TBI. 16 Specifically,Berger, et al. 16 demonstrated that initial MBP and NSEserum concentrations were more strongly correlated withoutcomes in children younger than or equal to four years ofage, as compared to children older than four. Because MBPis yet to be studied in bTBI, further research is needed toverify its utility as a biomarker of brain injury.Among the most well researched biomarkers for TBIis S-100b, a small dimeric calcium binding protein mostabundant in glial cells of the CNS (astrocytes) and PNS(Schwann cells). 9 A downside to S-100b as a biomarkerfor brain injury is that it is not exclusively located in thebrain, as it has been found to be expressed in melanocytes,adipocytes and chondrocytes. 17 Many studies have shownan association between S-100b and injury outcome andmagnitude in TBI. 15,16,18 In a study using patients withsevere TBI, Korfias, et al., 18 concluded that S-100bserum levels reflected TBI severity, improved predictionof outcomes, and may also have a role in assessing theVolume 22, Issue 2, Summer 2012 The AAO Journal Page 49

efficacy of treatment after severe TBI. Conversely, otherstudies have suggested that S-100b is a poor predictorof outcomes following brain injury, particularly mildand pediatric TBI. 19,20 Specifically, while attempting todetermine the relationship between S-100b serum levelsand long-term outcomes after mild TBI, Bazarian, etal., 19 found no statistically significant correlation betweenmarker levels and PCS three months after injury. Despitethe contradictions, S-100b has potential as a biomarker forbrain injury, and should be further studied in bTBI.NSE is a protein located in the neuronal cytoplasmand is involved in regulating intracellular chloride levels. 21Although NSE was originally believed to be exclusivelyneuronal, it was later located in both erythrocytes andplatelets, decreasing its value as a biomarker for braininjury. 22 Elevated NSE levels have been observed aftermultiple trauma, however, systemic levels have increasedby similar amounts with and without TBI, limiting itscapability of distinguishing brain injury magnitude. 23 Inaddition, NSE has a half-life of more than twenty hours inserum, which may further limit its use as a biomarker forTBI. 22 Although associations of NSE serum levels withbrain injury magnitude and outcomes are controversial,NSE measured in conjunction with S-100b hasdemonstrated utility in predicting TBI outcomes. 9,16 Furtherresearch will need to verify whether NSE concentrationsalone are valuable in predicting and distinguishing bTBIoutcome and severity, respectively.Neuroimaging techniquesIdeally, a detailed clinical assessment should be madeupon arrival at a combat support hospital, beginning withimmediate CT to identify lesions such as skull fractures,intracranial hemorrhage and cerebral edema. 24 Althoughcomputed tomography (CT) and standard magneticresonance imaging (MRI) structural images are efficient indemonstrating bleeds and large focal contusions (i.e., TBIscharacterized by bruises in specific locations), they are lesseffective in detecting diffuse axonal injury. 25 Diffuse axonalinjury is one of the more common and destructive types ofTBI, and is characterized by extensive lesions in the whitematter. Diffuse axonal injury can be detected by diffusiontensor imaging (DTI), or indirectly by volumetric analysis(brain volume loss). 25DTI is an MRI technique that enables themeasurement of the restricted diffusion of water in certaintissues in order to produce neural tract images. 26 Datais used to produce images rather than for the purpose ofassigning contrast or colors to pixels in a cross-sectionalimage. 27 DTI is resourceful when a tissue, such as theneural axons of white matter in the brain, has an internalfibrous structure that is similar to the anisotropy of somecrystals. 28 The value that describes the degree of anisotropyof a diffusion process is known as the fractional anisotropy(FA), and when applied to diffusion imaging, it provides ameasure of fiber density, axonal diameter and myelinationin white matter. 29 Some DTI studies have shown reductionsin FA at sites of traumatic axonal shearing injury,corresponding to a loss of microstructural fiber integrity. 29,30An increasing number of DTI studies in TBI have beenemerging recently, a couple of which indicate correlationsbetween DTI findings and neurocognition. 31,32 For instance,Salmond, et al., 31 demonstrated a significant correlationbetween learning and memory indices and diffusivity inareas known to subserve the cognitive functions. Moreover,DTI was found to be sensitive to white matter injury threemonths after the occurrence of a moderate or severe TBI. 32Positron emission tomography (PET) is an effectiveand resourceful technique for quantifying ischemic burdenafter TBI. 33 TBI studies implementing PET have shown thatearly reductions in cerebral perfusion can result in cerebralischemia, which is correlated with adverse outcome. 33,34In addition, PET has been employed to demonstrate that,in TBI, the threshold of cerebral blood flow (CBF) belowwhich irreversible tissue damage occurs varies from theclassical CBF threshold for stroke. 34 Aside from PET, manystudies have confirmed the potential of single-voxel protonMR spectroscopy ( 1 H-MRS or MRS) for the detection ofneuronal injury following TBI. 35-40 MRS is a metabolicscreening technique that has been shown to be moresensitive than PET in depicting metabolic abnormalities ofthe temporal lobe in individuals with epilepsy. 41MRS is resourceful in that it allows for the acquisitionof biochemical (metabolic) information from tissues ina non-invasive manner. While MRI can determine thelocation of a particular injury, MRS has the capacity, intheory, to determine the severity of the injury. 41 A commonfinding among the MRS studies is the presence of alteredmetabolite concentrations that appear normal on structuralMR images, suggesting diffuse neuronal tissue damage.Specifically, a significant correlation has been foundbetween N-acetylaspartate (NAA), a biomarker of neuronalintegrity, and adverse clinical outcome in studies usingsingle-voxel methods. 42,43A method similar to MRS, known as proton MRspectroscopic imaging (MRSI), collects spectroscopicinformation from multiple voxels during the same imagingacquisition. 25 Thus, MRSI differs from MRS in that thedata acquired is not restricted to a single region or voxel.However, both have been found resourceful in findingPage 50The AAO Journal Volume 22, Issue 2, Summer 2012

metabolic abnormalities that present as markers for longtermsequelae, which includes neuronal loss and glialproliferation. 36 Moreover, some studies have implementedMRS and MRSI in the effort of finding a correlationbetween metabolic abnormalities and neurocognitiveeffects. 44,45 In short, Friedman, et al., 45 found that theassociation between neurometabolic levels and behavioralfunction supports the hypothesis that diffuse axonal injuryis an important contributor to brain dysfunction after TBI.Furthermore, it was determined that acute MR spectroscopyof the pediatric brain injury patient improves prognosticability and may provide valuable information for earlytreatment and intervention planning. 44Studies using functional MRI (fMRI) in individualswith TBI demonstrate unusual patterns of brain activationwhen compared with healthy control subjects. 46-48Functional MRI is a type of specialized MRI scan thatmeasures the hemodynamic response, or change in bloodflow, related to neural activity in the brain or spinal cordof humans and other animals. 49 It uses blood-oxygen-leveldependent (BOLD) contrast that enables detection ofchanges in the concentration of oxygenated hemoglobin,which becomes altered by the hemodynamic response. 49Prigatano et al. 46 demonstrated that the different patternsof brain activation in individuals with TBI compared tohealthy controls can be observed even when the level ofbehavioral performance between groups is generally withinnormal parameters.Furthermore, it was concluded that the impairmentof working memory in TBI seems to be correlated withalterations in functional cerebral activity. 48 Anothervariation of MRI, known as dynamic contrast-enhancedperfusion-weighted MRI (PW-MRI), is a method that canprovide information about the functional status of cerebraltissue with a high spatial resolution of morphology. 50Although PW-MRI has demonstrated that regions of bothnormal-appearing and contused brain can have an unusualregional cerebral blood volume (rCBV), and that changesin rCBV can play a role in determining the clinical resultsof patients, there have not been any publications using PW-MRI in TBI patients. 51ConclusionsSince many of the effects of bTBI may not beobservable by the naked eye, bTBI has been referred to as“the invisible wound of war.” Since there are no clinicallyproven biomarkers for brain injury to date, further researchshould be conducted on the potential candidates to improveand expedite the detection process. Furthermore, theapplication of neuroimaging techniques to the evaluationand management of patients who have suffered bTBIwas briefly presented. Additional translational research isneeded to study the effectiveness and efficiency of usingbiomarkers of injury and neuroimaging techniques in theevaluation and management of patients with suspectedexposure to bTBI so that fewer brain injuries will gounnoticed or misdiagnosed.References1. Tanielian T, Jaycox LH, editors. Invisible Wounds of War:Psychological and Cognitive Injuries, Their Consequences, andServices to Assist Recovery. Arlington, VA: Center for MilitaryHealth Policy Research, the Rand Corporation; 2008.2. Martin EM, Lu WC, Helmick K, French L, Warden DL. (2008).Traumatic brain injuries sustained in the Afghanistan and Iraqwars. Journal of Trauma Nursing. 2008;15(3):94-99,100-101.3. Okie S. Reconstructing lives—a tale of two soldiers. The NewEngland Journal of Medicine. 2006; 355(25):2609-2615.4. Warden D. Military TBI during the Iraq and Afghanistan wars. TheJournal of Head Trauma Rehabilitation. 2006;21(5): 398-402.5. Xydakis MS, Fravell MD, Nasser KE, Casler JD. Analysisof battlefield head and neck injuries in Iraq and Afghanistan.Otolaryngology-Head and Neck Surgery. 2005;133(4):497-504.6. Malie PM, Berkowitz MR. Understanding blast-induced traumaticbrain injury (bTBI) through mechanisms and patterns of injury.American Academy of Osteopathy Journal, June 2012;22(2):.7. Yilmaz S, Pekdemir M. An unusual primary blast injury traumaticbrain injury due to primary blast injury. The American Journal ofEmergency Medicine. 2007;25(1):97-98.8. Belanger HG, Scott SG, Scholten J, Curtiss G, Vanderploeg RD.Utility of mechanism-of-injury-based assessment and treatment:Blast injury program case illustration. Journal of RehabilitationResearch and Development. 2005;42(4):403-412.9. Svetlov SI, Larner SF, Kirk DR, Atkinson J, Hayes RL, Wang KK.Biomarkers of blast-induced neurotrauma: Profiling molecular andcellular mechanisms of blast brain injury. Journal of Neurotrauma.2009;26(6):913-921.10. Galea E, Dupouey P, Feinstein DL. Glial fibrillary acidic proteinmRNA isotypes: Expression in vitro and in vivo. Journal ofNeuroscience Research. 2005;41(4):452-461.11. Nylen K, Ost M, Csajbok LZ, Nilsson I, Blennow K, NellgardB, et al. Increased serum-GFAP in patients with severe traumaticbrain injury is related to outcome. Journal of the NeurologicalSciences. 2006;240(1-2):85-91.12. Pelinka LE, Kroepfl A, Leixnering M, Buchinger W, RaabeA, Redl H. GFAP versus S100B in serum after traumatic braininjury: Relationship to brain damage and outcome. Journal ofNeurotrauma. 2004;21(11):1553-1561.13. Cunningham RM, Maio RF, Hill EM, Zink BJ. The effects ofalcohol on head injury in the motor vehicle crash victim. Alcoholand Alcoholism. 2002;37(3):236-240.14. Harauz G, Ladizhansky V, Boggs JM. Structural polymorphismand multifunctionality of myelin basic protein. Biochemistry.2009;48(34):8094-8104.15. Berger RP, Adelson PD, Pierce MC, Dulani T, Cassidy LD,Kochanek PM. Serum neuron-specific enolase, S100B, andmyelin basic protein concentrations after inflicted and noninflictedtraumatic brain injury in children. Journal of Neurosurgery.2005;103(1 Suppl):61-68.Volume 22, Issue 2, Summer 2012 The AAO Journal Page 51

16. Berger RP, Beers SR, Richichi R, Wiesman D, Adelson PD. Serumbiomarker concentrations and outcome after pediatric traumaticbrain injury. Journal of Neurotrauma. 2007;24(12):1793-1801.17. Michetti F, Gazzolo D. S100B protein in biological fluids: A toolfor perinatal medicine. Clinical Chemistry. 2002;48(12):2097-2104.18. Korfias S, Stranjalis G, Boviatsis E, Psachoulia C, Jullien G,Gregson B, et al. Serum S-100B protein monitoring in patientswith severe traumatic brain injury. Intensive Care Medicine.2007;33(2):255-260.19. Bazarian JJ, Zemlan FP, Mookerjee S, Stigbrand T. Serum S-100Band cleaved-tau are poor predictors of long-term outcome aftermild traumatic brain injury. Brain Injury: [BI]. 2006;20(7):759-765.20. Piazza O, Storti MP, Cotena S, Stoppa F, Perrotta D, Esposito G.,et al. S100B is not a reliable prognostic index in pediatric TBI.Pediatric Neurosurgery. 2007;43(4):258-264.21. Vinores SA, Herman MM, Rubinstein LJ, Marangos PJ. Electronmicroscopic localization of neuron-specific enolase in rat andmouse brain. The Journal of Histochemistry and Cytochemistry.1984;32(12):1295-1302.22. Johnsson P, Blomquist S, Luhrs C, Malmkvist G, Alling C, SolemJO, et al. Neuron-specific enolase increases in plasma duringand immediately after extracorporeal circulation. The Annals ofThoracic Surgery. 2000;69(3):750-754.23. Pelinka, L. E., Hertz, H., Mauritz, W., Harada, N., Jafarmadar,M., Albrecht, M., et al. (2005). Nonspecific increase of systemicneuron-specific enolase after trauma: Clinical and experimentalfindings. Shock (Augusta, Ga.), 24(2), 119-123.24. Aarabi B, Simard JM. Traumatic brain injury. Current Opinion inCritical Care. 2009;15(6):548-553.25. Van Boven RW. Harrington GS, Hackney DB, Ebel A, Gauger G,Bremner JD, et al. Advances in neuroimaging of traumatic braininjury and post-traumatic stress disorder. Journal of RehabilitationResearch and Development. 2009;46(6):717-757.26. Manenti G, Carlani M, Mancino G, Colangelo V, Di Roma M,Squillaci E, et al. Diffusion tensor magnetic resonance imaging ofprostate cancer. Investigative Radiology. 2007;42(6):412-419.27. Basser PJ, Pajevic S, Pierpaoli C, Duda J, Aldroubi A. In vivofiber tractography using DT-MRI data. Magnetic Resonance inMedicine. 2000;44(4):625-632.28. Filler A. Magnetic resonance neurography and diffusiontensor imaging: Origins, history and clinical impact of the first50,000 cases with an assessment of efficacy and utility in aprospective 5000-patient study group. Neurosurgery. 2009;65(4Suppl):A29-43.29. Arfanakis K, Haughton VM, Carew JD, Rogers BP, Dempsey RJ,Meyerand ME. Diffusion tensor MR imaging in diffuse axonalinjury. American Journal of Neuroradiology. 2002;23(5):794-802.30. Huisman TA, Schwamm LH, Schaefer PW, Koroshetz WJ,Shetty-Alva N, Ozsunar Y, et al. Diffusion tensor imaging aspotential biomarker of white matter injury in diffuse axonal injury.American Journal of Neuroradiology. 2004;25(3):370-376.31. Salmond CH, Menon DK, Chatfield DA, Williams GB, PenaA, Sahakian BJ, et al. Diffusion tensor imaging in chronic headinjury survivors: Correlations with learning and memory indices.NeuroImage. 2006;29(1):117-124.32. Levin HS, Wilde EA, Chu Z, Yallampalli R, Hanten GR, Li X, etal. Diffusion tensor imaging in relation to cognitive and functionaloutcome of traumatic brain injury in children. The Journal of HeadTrauma Rehabilitation. 2008;23(4):197-208.33. Coles JP, Fryer TD, Smielewski P, Rice K, Clark JC, Pickard JD,et al. Defining ischemic burden after traumatic brain injury using15O PET imaging of cerebral physiology. Journal of CerebralBlood Flow and Metabolism. 2004;24(2), 191-201.34. Cunningham AS, Salvador R, Coles JP, Chatfield DA, Bradley PG,Johnston AJ, et al. Physiological thresholds for irreversible tissuedamage in contusional regions following traumatic brain injury.Brain. 2005;128(8):1931–1942.35. Holshouser BA, Tong KA, Ashwal S. Proton MR spectroscopicimaging depicts diffuse axonal injury in children withtraumatic brain injury. American Journal of Neuroradiology.2005;26(5):1276-1285.36. Holshouser BA, Tong KA, Ashwal S, Oyoyo U, Ghamsary M,Saunders D, et al. Prospective longitudinal proton magneticresonance spectroscopic imaging in adult traumatic brain injury.Journal of Magnetic Resonance Imaging. 2006;24(1):33-40.37. Hunter JV, Thornton RJ, Wang ZJ, Levin HS, Roberson G,Brooks WM, et al. Late proton MR spectroscopy in children aftertraumatic brain injury: Correlation with cognitive outcomes.American Journal of Neuroradiology. 2005;26(3):482-488.38. Yoon SJ, Lee JH, Kim ST, Chun MH. Evaluation of traumaticbrain injured patients in correlation with functional statusby localized 1H-MR spectroscopy. Clinical Rehabilitation.2005;19(2):209-215.39. Govindaraju V, Gauger GE, Manley GT, Ebel A, Meeker M,Maudsley AA. Volumetric proton spectroscopic imaging of mildtraumatic brain injury. American Journal of Neuroradiology.2004;25(5):730-737.40. Garnett MR, Blamire AM, Corkill RG, Cadoux-Hudson TA,Rajagopalan B, Styles P. Early proton magnetic resonancespectroscopy in normal-appearing brain correlates with outcomein patients following traumatic brain injury. Brain: A Journal ofNeurology. 2000;123(10):2046-2054.41. Achten E, Santens P, Boon P, De Coo D, Van De Kerckhove T, DeReuck J, et al. Single-voxel proton MR spectroscopy and positronemission tomography for lateralization of refractory temporal lobeepilepsy. American Journal of Neuroradiology. 1998;19(1):1-8.42. Brooks WM, Friedman SD, Gasparovic C. Magnetic resonancespectroscopy in traumatic brain injury. The Journal of HeadTrauma Rehabilitation. 2001;16(2):149-164.43. Shutter L, Tong KA, Lee A, Holshouser BA. Prognostic roleof proton magnetic resonance spectroscopy in acute traumaticbrain injury. The Journal of Head Trauma Rehabilitation.2006;21(4):334-349.44. Babikian T, Freier MC, Ashwal S, Riggs ML, Burley T,Holshouser BA. MR spectroscopy: Predicting long-termneuropsychological outcome following pediatric TBI. Journal ofMagnetic Resonance Imaging. 2006;24(4):801-811.45. Friedman SD, Brooks WM, Jung RE, Hart BL, Yeo RA. ProtonMR spectroscopic findings correspond to neuropsychologicalfunction in traumatic brain injury. American Journal ofNeuroradiology. 1998;19(10):1879-1885.46. Prigatano GP, Johnson SC, Gale SD. Neuroimaging correlates ofthe Halstead finger tapping test several years post-traumatic braininjury. Brain Injury. 2004;18(7):661-669.Page 52The AAO Journal Volume 22, Issue 2, Summer 2012

47. Wiese H, Tonnes C, de Greiff A, Nebel K, Diener HC, Stude P.Self-initiated movements in chronic prefrontal traumatic braininjury: An event-related functional MRI study. NeuroImage.2006;30(4):1292-1301.48. Christodoulou C, DeLuca J, Ricker JH, Madigan NK, Bly BM,Lange G, et al. Functional magnetic resonance imaging of workingmemory impairment after traumatic brain injury. Journal ofNeurology, Neurosurgery and Psychiatry. 2001;71(2):161-168.49. Gusnard DA, Raichle ME, Raichle ME. Searching for a baseline:Functional imaging and the resting human brain. Neuroscience.2001;2(10):685-694.50. Arioz U, Oguz KK, Senturk S, Cila A. Multislice mapping andquantification of brain perfusion MR imaging data: A comparativestudy of homemade and commercial software. Diagnostic andInterventional Radiology. 2005;11(4):182-188.51. Garnett MR, Blamire AM, Corkill RG, Rajagopalan B, YoungJD, Cadoux-Hudson TA, et al. Abnormal cerebral blood volumein regions of contused and normal appearing brain followingtraumatic brain injury using perfusion magnetic resonanceimaging. Journal of Neurotrauma. 2001;18(6):585-593.Accepted for publication: June 2012Address correspondence to:Patrick M. Malie, MS, OMS III;Murray R. Berkowitz, DO, MA, MS, MPHDepartment of Osteopathic Manipulative MedicinePhiladelphia College of Osteopathic Medicine—Georgia Campus625 Old Peachtree Road NWSuwanee, Georgia 30024murraybe@pcom.eduCLASSIFIED ADVERTISEMENTSSEATTLE PHYSICIAN OPPORTUNITYContact Stephen Cavanaugh, DO, at seattledo@gmail.com or (206) 834-5438. Web site for the practice isSeattleDO.com.NEW NMM PLUS 1 RESIDENCY PROGRAM IN NEW YORKThere is a new NMM Plus 1 Residency at Southampton Hospital in beautiful Southampton, Long Island.Applications are currently being accepted. If interested, please contact Program Director Denise K. Burns, DO,FAAO, at drdenise@optonline.net or Education Department Secretary Karen Roberts at (631) 726-0409.DO/MD/NP WANTED IN NEBRASKAFor Omaha, NE, wellness center offering Christian-based prayer and emotional conflict resolution, cranialosteopathy, nutritional/homeopathic/herbal support, ondamed, lymphstar, sauna, intravenous therapies and naturalskin aesthetics, etc., for all types of conditions. Four-day work week, no hospital call. “Fee for service,” no thirdpartycontracts. Send resume to kay@cph.omhcoxmail.com or call (402) 343-7963.PRACTICE OSTEOPATHY IN BEAUTIFUL COLORADOSuccessful integrative practice seeks a board-certified/eligible NMM/OMM physician for its busy Denver office.Preferably someone comfortable with a broad variety of techniques. Very competitive compensation. Friendly andprofessional atmosphere. Please call (303) 781-7862 or e-mail CV to mgentile@cointegrative.com. Our Web site iswww.cointegrative.com.DO SOUGHT IN BOSTONInnovative primary care practice seeks primary care physician also interested in OMM. Balanced lifestyle, workingwith academically trained MDs, started by original designer of Epocrates. If interested, please send a brief intro andCV to: jobs@onemedical.com.Volume 22, Issue 2, Summer 2012 The AAO Journal Page 53

The safety and efficacy of osteopathic manipulation in thetreatment of mTBI (mild traumatic brain injury) in U.S.service members as validated by SPECT scan: A report ofplanned researchNatalie A. Nevins, DO, MSHPE; Marcel Fraix, DO, FAAPMRIntroductionTraumatic brain injury (TBI) is one of the signaturewounds of the Global War on Terrorism (GWOT). TBIis a common injury in Unites States service men andwomen who have served in Operation Enduring Freedom(OEF) and Operation Iraqi Freedom (OIF). The ArmedForces Health Surveillance Center (AFHSC) report to theDepartment of Defense (DoD) from February 2012 statesthat there have been 233,425 TBIs, including all levels ofseverity in all branches of the Armed Forces from 2000-2011. Additionally, of these, 178,961 were classified asmild in nature. 1The Centers for Disease Control (CDC) approximatesthat 1.7 million individuals sustain a TBI in the UnitedStates each year. 2 In 2007, The Report to the SurgeonGeneral from the Traumatic Brain Injury Task Forcecommented that, if mild TBI (mTBI) is also accountedfor, then at least 5.3 million Americans currently havelong-term or life-long disabilities resulting from TBI. 3TBI is clearly a factor affecting the overall function andproductivity of both U.S. military personnel and those inthe general population.The leading causes for non-military TBI includefalls, motor vehicle accidents and assault involving headtrauma. According to the Defense Manpower Data Center,explosive devices, including Improvised ExplosiveDevices (IED), are responsible for two-thirds of thewounded-in-action casualties from the conflicts in Iraq andAfghanistan. 4 IEDs are the leading cause of blast-inducedmTBI. The financial burden of direct medical costs andindirect costs (i.e., loss of productivity) resulting from TBItotaled an estimated $60 billion to $76.5 billion in the U.S.in 2000. 5,6,7 Additionally, the one-year costs for militaryservice members with TBI accessing the health care systemin 2007 ranged from $27,259 to $32,759 for mild cases,and $268,902 to $408,519 in moderate to severe cases. 8TBI is often referred to as one of the invisible woundsof warfare. Our service men and women are returningwith mental health and cognitive dysfunctions, many ofwhich are directly related to TBI. Research related to thelong-term treatment of TBI is lacking and underfunded.At the Concussion Restoration Care Center at CampLeatherneck in Helmand province, Afghanistan, patientswith a history of acute concussion and possible mTBIreceive a neurological evaluation, balance assessment andevaluation via Automated Neuropsychological AssessmentMetric (ANAM), which is an advanced neurocognitivetest. Current test results from ANAM are comparedwith a baseline study that was established back in theStates prior to deployment. Additionally, the patient mayreceive a CT or MRI scan. 9 Treatments are designed to becomprehensive and may include acupuncture, osteopathicmanipulative therapy, occupational or physical therapy,counseling and chaplain visits. Rest, both physical andmental, is emphasized for all patients. This treatmentprotocol has 98 percent of Marines treated at the centerreturning to their units in theater. Before it opened inAugust 2010, the Marine Expeditionary Force in RegionalCommand-Southwest was losing about 20 Marines a monthto concussions. 10Definition of TBIThe definition of TBI has been continually evolvingover the last 10 years, with no consensus definition agreedupon by those treating these patients. The Defense andVeterans Brain Injury Center defines TBI simply as ablow or jolt to the head that disrupts the normal functionof the brain. The severity of the TBI is determined atthe time of the injury, and may be classified as mild,moderate or severe. 11 The DoD definition is far moreexplanatory—a traumatically induced structural injury and/or physiological disruption of brain function as a result ofexternal force that is indicated by new onset or worseningof at least one of the following clinical signs, immediatelyfollowing the event:• Any period of loss of or a decreased level of consciousness;Page 54The AAO Journal Volume 22, Issue 2, Summer 2012

• Any loss of memory for events immediately before orafter the injury;• Any alteration in mental state at the time of the injury(confusion, disorientation, slowed thinking, etc.);• Neurological deficits (weakness, loss of balance,change in vision, praxis, paresis/plegia, sensory loss,aphasia, etc.) that may or may not be transient;• Intracranial lesion.External forces may include any of the followingevents: the head being struck by an object, the head strikingan object, the brain undergoing an acceleration/decelerationmovement without direct external trauma to the head,a foreign body penetrating the brain, forces generated fromevents, such as blast or explosion, or other force yet to bedefined. 12The severity of TBI is based on the status of thepatient at the time of injury, based on observable signs.Severity of injury does not predict the functional orrehabilitative outcome of the patient. 13 (Table 1).Signs and Symptoms of TBICommon signs and symptoms are generally brokendown into physical, emotional and cognitive changes. TheNational Academy of Sciences published an executivesummary, which provides a general description of thesymptoms of TBI. 14 It states that the majority of people whosustain a TBI are mobile and able to care for themselves,but physical health problems are common. Such problemsinclude balance and motor coordination, fatigue, headache,sleep disturbance, seizures, sensory impairments, slurredspeech, spasticity and tremors, problems with urinarycontrol, dizziness and vestibular dysfunction, andweakness. Psychiatric sequelae can also occur after TBI,with major depressive disorder being the most commonin civilian and military populations. Other psychiatricdiagnoses associated with TBI include generalized anxietydisorder, PTSD, bipolar disorder and personality changes. 15,16,17Other symptoms can include memory impairment anddisordered thinking. 18 (Table 2).AOC – Alteration of consciousness/mental stateLOC – Loss of consciousnessPTA – Post-traumatic amnesiaTable 1. Severity of TBITable 2. Common signs and symptoms of mTBIVolume 22, Issue 2, Summer 2012 The AAO Journal Page 55

Purpose of StudyThe purpose of our study is to measureneurobehavioral and brain changes following theapplication of osteopathic manipulation in the treatment ofchronic mTBI. Current standards of evaluation in mTBIwill be recorded before and after treatment to validateoutcomes. Single-photon emission computer tomography(SPECT) imaging will be used to evaluate the brain beforeand after treatment.MethodsThe objectives of this study are:• To assess the safety of osteopathic manipulativetreatment (OMT) in participants experiencingchronic mTBI;• To measure the response to OMT by usingSPECT imaging and neurobehavioral testing inparticipants experiencing chronic mTBI.Design: Prospective randomized controlled cohortcomparative effectiveness study1. Evaluationa. Outcome Measuresi. Neuropsychological TestingANAM testing is conducted prior todeployment, and can be used to identify andmonitor changes in function before and afteran injury. ANAM is a proven, computerbasedcognitive assessment tool used by theU.S. military designed to detect the speed andaccuracy of attention, memory and thinkingability. It records every service member’sperformance through responses provided ona computer. 19 Additionally, we will use theNeurobehavioral Symptom Inventory (NSI) andthe Amen Brain System and Symptom Checklist.ii. SPECT Imaging“SPECT is a functional imagingtechnique used to determine blood flowin the brain based on the distribution ofradioactive pharmaceuticals in the brain. Theradiopharmaceuticals are injected into thebloodstream of patients and, as the radioisotopedecays, the photons emitted are detected andrecorded by gamma cameras. This producestomographic images of the activity of theradiopharmaceutical in the brain. These imagescan then be reconstructed in three dimensions.” 20The most common radiopharmaceuticalused for SPECT imaging in the brain istechnetium-99 m-hexamethylpropyleneamineoxime (99mTc-HMPAO). Technetium-99 m is ametastable radionuclide that releases the photonsdetected by the SPECT scan. 21 “99mTcHMPAOis injected, and accumulates in areas of bloodflow with detectable concentrations for up to24 hours, and is therefore utilized as a restingstate functional neuroimaging technique, similarto functional magnetic resonance imagingmethods.” 22 “Given the long half-life of theSPECT radionuclide, subjects can be injectedand time can be taken to establish a calm andquiet environment to eliminate background brainactivity.” 23Given the disturbances to metabolismthat are expected to occur after brain injury, itis expected that blood flow would be alteredin mTBI. SPECT is an ideal tool for makingblood flow assessments after mTBI due to itsavailability, and non-invasive nature. As a result,there is a rich body of medical and scientificliterature surrounding the use of SPECT in braininjury. 24It is agreed that imaging studies are notnecessary for all mTBI patients. The absenceof pathologic signs on computed tomography(CT) does not rule out the presence of mTBI.Structural magnetic resonance imaging (MRI)has a low incidence of positive findings inmTBI. 25 It is contraindicated in patients withshrapnel and is of limited use with acute mTBI.SPECT and functional MRI (fMRI) may bemore useful for patients who manifest symptomsof cognitive dysfunction after the acute phase ofTBI has passed. 26b. InterventionOMT will be used as an intervention in thisstudy. Patients will receive OMT with the objectiveof treating diagnosed somatic dysfunction,which will entail the use of specific indirect anddirect techniques. These can include soft tissue,inhibitory, myofascial release, Osteopathy in theCranial Field, articulatory and high-velocity/lowamplitude(HVLA) techniques, but not muscleenergy techniques, which are active, and passivemotion maneuvers that could confound thedata. Direct-action OMT procedures, includingHVLA, involve the application of a force in thePage 56The AAO Journal Volume 22, Issue 2, Summer 2012

Table 3. OMT techniquesdirection of restricted joint motion in order toresolve somatic dysfunction. Indirect techniques,including counterstrain, balanced ligamentoustension and myofascial release, entail applying aforce away from the restrictive barrier of a jointor soft-tissue structure. A descripton of thesetechniques is listed in Table 3. Each participant inthe intervention groups using OMT will receive atotal of three treatments spaced approximately oneweek apart. The same physician will perform allthe OMT to ensure it is applied as consistently aspossible. Additionally, OMT will not be restrictedto a specific region of the body, since there isnot evidence that demonstrates that somaticdysfunction of a specific region causes, or iscorrelated with, mTBI. This is also in keeping withthe theory of Osteopathy, which attempts to resolvestructural imbalances and improve the overallfunction of the body.The schedule for each group regardingevaluation and treatment is illustrated in Table 4.Volume 22, Issue 2, Summer 2012 The AAO Journal Page 57

ParticipantsSubjects: Men and women who have served in the U.S.armed forces above the age of 18. Participants will notbe excluded based on their race, color, national origin,religion, disability, gender or sexual orientation.Inclusion criteria:• Diagnosis of mTBI during deployment;• Baseline ANAM testing done before deployment.Exclusion criteria:• Pre-existing psychiatric disorder;• Refusal to participate in the study.Timeline: We will recruit participants and randomlyassign them to the varying treatment arms of the study. Thetreatment phase of the study will last one month. Data willbe collected pre-treatment and immediately post-treatment.Data Analysis: After the treatment phase of the study iscompleted and data from SPECT and the neurobehavioraltesting is collected, descriptive statistics will be used tocharacterize the study population at baseline and at theconclusion of treatment. Frequencies and percentages willbe computed for categorical variables; means, standarddeviations, medians and ranges will be computed forcontinuous variables. Pre- to post-treatment change scoreswill be computed and reported in terms of both absoluteand percentage changes. Ninety-five percent confidenceintervals for the differences between pre-treatment andpost-treatment measures will be computed, and generallinear modeling will be used to estimate and test theeffects of treatment on SPECT and neurobehavioral testingchanges. Data management and statistical analyses willbe conducted with Microsoft Excel and SAS (version 9.1,Cary, NC).References1. Department of Defense Surveillance System (DMSS) and TheaterMedical Data Store (TMDS) prepared by the Armed ForcesHealth Surveillance Center (AFHSC), numbers for 2000-2011Q4. Defense and Veterans Brain Injury Center Web site. February10, 2012. http:/www.dvbic.org/sites/default/files/uploads/dodtbi-2012.pdf.Accessed June 5, 2012.2. Faul M, Xu L, Wald MM, Coronado VG. Traumatic brain injury inthe United States: emergency department visits, hospitalizations,and deaths. Atlanta, GA: Centers for Disease Control andPrevention, National Center for Injury Prevention and Control;2010. http://www.cdc.gov/traumaticbraininjury/pdf/blue_book.pdf.Accessed June 11, 2012.3. Traumatic Brain Injury (TBI) Task Force Report RecommendationSummary. Report to The Surgeon General. Homeland SecurityDigital Library Web site. May 15, 2007. http://www.hsdl.org/?view&did=482727. Accessed June 1, 2012.Global War on Terrorism Casualty Statistics by Reason. DefenseManpower Data Center Web site. http://siadapp.dmdc.osd.mil/personnel/CASUALTY/gwot_reason.pdf. Accessed May 24, 2012.4. Thurman DJ. Epidemiology and economics of head trauma. In:Miler L, Hayes R, eds. Head Trauma: Basic, Preclinical andClinical Directions. New York: Wiley and Sons; 2001: 1193–1202.5. Finkelstein E, Corso P, Miller T. The Incidence and EconomicBurden of Injuries in the United States. New York (NY): OxfordUniversity Press; 2006. Accessed June 5, 2012.6. Coronado, McGuire, Faul, Sugerman, Pearson. The Epidemiologyand Prevention of TBI (in press). 2012.7. Adamson DM, Burnam MA, Burns RM, Caldarone LB, Cox RA,D’Amico E, et al. Invisible Wounds of War: Psychological andCognitive Injuries, Their Consequences, and Services to AssistRecovery. Santa Monica, CA: RAND Corporation; 2008. http://www.rand.org/pubs/monographs/MG720. Accessed June 11, 2012.8. News Transcript. DOD News Briefing with Cmdr. Bensonand Cmdr. Stuessi via Teleconference from Afghanistan. U.S.Department of Defense, Office of the Assistant Secretary ofDefense (Public Affairs) Web site. http://www.defense.gov/Transcripts/Transcript.aspx?TranscriptID=4760.January 27, 2011.Accessed June 11, 2012.9. Rauch L. Concussion center in Afghanistan offers full treatmentfor troops. Stars and Stripes Web site. June 24, 2012. http://www.stripes.com/news/concussion-center-in-afghanistan-offers-fulltreatment-for-troops-1.181226.Accessed June 27, 2012.10. Signs and Symptoms of Concussion (Mild Traumatic BrainInjury). Defense and Veterans Brain Injury Center Web site. http://www.dvbic.org/sites/default/files/DVBIC_S%26S_English_FINAL.pdf. Accessed June 11, 2012.Table 4. Group schedule for evaluation and treatmentPage 58The AAO Journal Volume 22, Issue 2, Summer 2012

11. Military Health System Coding Guidance: ProfessionalServices and Specialty Coding Guidelines, Version 1.0, UnifiedBiostatistical Utility, 2005. Appendix G: Special Guidance onTraumatic Brain Injury Coding. 2009. The Defense Centersof Excellence for Psychological Health and Traumatic BrainInjury Web site. http://www.dcoe.health.mil/Content/navigation/documents/Department%20of%20Defense%20Coding%20Guidance%20for%20Traumatic%20Brain%20Injury%20Fact%20Sheet.pdf. Accessed June 11, 2012.12. Military Health System Coding Guidance: ProfessionalServices and Specialty Coding Guidelines, Version 1.0, UnifiedBiostatistical Utility, 2005. Appendix G: Special Guidance onTraumatic Brain Injury Coding. 2009. The Defense Centersof Excellence for Psychological Health and Traumatic BrainInjury Web site. http://www.dcoe.health.mil/Content/navigation/documents/Department%20of%20Defense%20Coding%20Guidance%20for%20Traumatic%20Brain%20Injury%20Fact%20Sheet.pdf. Accessed June 11, 2012.13. National Research Council. Evaluating the HRSA Traumatic BrainInjury Program. Washington, DC: The National Academies Press;2006. http://books.nap.edu/catalog/11600.html. Accessed June 11,2012.14. Gordon WA, Zafonte R, Cicerone K, Cantor J, Brown M, LombardL, et al. Traumatic brain injury rehabilitation: State of the science.Am J Phys Med Rehabil. 2006;85(4): 343-82.15. Salazar AM, Warden DL, Schwab K, Spector J, Braverman S,Walter J,et al. Cognitive rehabilitation for traumatic brain injury: Arandomized trial. JAMA. 2000;283(23):3075-3081.16. Salazar AM, Warden DL, Schwab K, Spector J, Braverman S,Walter J,et al. Cognitive rehabilitation for traumatic brain injury: Arandomized trial. JAMA. 2000;283(23):3075-3081.17. Traumatic Brain Injury (TBI) Among U.S. Troops Fightingthe Global War on Terrorism: Finding the Gaps and PresentingSolutions for Care and Treatment. Institute for Combat WoundedPolicy Web site. August 3, 2008. http://woundedpolicy.org/I4CWP_TBIWhitePaper.pdf. Accessed June 11, 2012.18. Automated Neuropsychological Assessment Metrics. Defense andVeterans Brain Injury Center. Association of American MedicalColleges Web site. https://www.aamc.org/download/268440/data/204_resource.pdf. Accessed June 15, 2012.19. Lin AP, Liao HJ, Merugumala SK, Prabhu SP, Meehan 3 rd , WP,Ross BD. Metabolic imaging of mild traumatic brain injury. BrainImaging and Behavior. 2012;6(2):208-223.20. Leonard JP, Nowotnik DP, Neirinckx RD. Technetium-99 m-d,1-HM-PAO: A new radiopharmaceutical for imaging regionalbrain perfusion using SPECT—a comparison with iodine-123HIPDM. J Nucl Med. 2006;27(12):1819–1823.21. McDonald BC, Saykin AJ, McAllister TW. Functional MRI ofmild traumatic brain injury (MTBI): Progress and perspectivesfrom the first decade of studies. Brain Imaging and Behavior.2012;6(2):193-207.22. Lin AP, Liao HJ, Merugumala SK, Prabhu SP, Meehan 3 rd , WP,Ross BD. Metabolic imaging of mild traumatic brain injury. BrainImaging and Behavior. 2012;6(2):208-223.23. Lin AP, Liao HJ, Merugumala SK, Prabhu SP, Meehan 3 rd , WP,Ross BD. Metabolic imaging of mild traumatic brain injury. BrainImaging and Behavior. 2012;6(2):208-223.24. Lewine JD, Davis JT, Bigler ED, Thoma R, Hill D, Funke M, et al.Objective documentation of traumatic brain injury subsequent tomild head trauma: Multimodal brain imaging with MEG, SPECT,and MRI. J Head Trauma Rehabil. 2007;(3):141-55.25. Updated Mild Traumatic Brain Injury (mTBI) Clinical Guidance.Office of the Assistant Secretary of Defense Web site. May 8,2008. http://www.evans.amedd.army.mil/srp/pdf/final%20HA%20mTB. Accessed June 11, 2012.26. Glossary of Osteopathic Terminology. American Association ofColleges of Osteopathic Medicine Web site. 2011. www.aacom.org/resources/bookstore/Documents/GOT2011ed.pdf. AccessedJune 18, 2012Accepted for publication: June 2012Address correspondence to:Natalie A. Nevins, DO, MSHPEDowney Regional Medical CenterDirector/Medical Education/DRMC11500 Brookshire Ave. - PO Box 7010Downey, CA 90241docnnevins@aol.comVolume 22, Issue 2, Summer 2012 The AAO Journal Page 59

From the ArchivesEdited by Raymond J. Hruby, DO, MS, FAAO; From: Still AT. The Autobiography of A.T.Still. Kirksville, MO: Published by the author; 1908: 71-81.In September 1861, at Fort Leavenworth, I enlisted inthe Ninth Kansas Cavalry, in Company F, T. J. Mewhinne,captain. The regiment was composed mainly of Kansasmen who had been christened in the baptism of fire duringthe pro-slavery contest. Soon after enlisting, we drew ourclothing and equipment. We were men who meant businessand had started out to do some very severe and successfulfighting. From Leavenworth, we were ordered to KansasCity to complete our outfit, and were placed in the brigadeof James H. Lane, then commissioned to organize theWestern army. In a short time, we received marching ordersto report at Springfield, MO.We left Kansas City on the day that Mulligansurrendered to General Price at Lexington. Price, fromsome cause, chose to march his army south by way ofSpringfield. Each night we camped on the ground, whichPrice had camped on the night previous, until Springfieldwas reached. During this march, the rebel army seemedaware of the fact that pursuers were in their rear. Thoughwe did not come in sight of the Confederates during themarch, we took down many flags that Price had flung tothe breeze. At Pleasant Hill, Greenfield and other points,the stars and bars were lowered to give place to the starsand stripes. Many loyal hearts that had sought concealmentduring Price’s march came forth from the woods andbushes to fall in with us and swell our numbers, so by thetime we reached Springfield, our brigade was considerablylarger than when we left Kansas City. We arrived atSpringfield just before General Fremont was removed fromcommand of the Western Department.The whole army assembled at Springfield was thengiven in round numbers at 120,000 men. The east and westsides of a forty-acre field were protected by lines of artillerya quarter-of-a-mile long. We remained at Springfield untilabout the first of November, and were then ordered back toFort Scott, and then to different points along the Missouriborder, until we finally reached Harrisonville, where wewent into winter quarters. During the winter that followed,we were continually harassed by bushwhackers, who notonly ambushed and shot our soldiers, but loyal citizens aswell. This guerrilla warfare grew to be such an annoyancethat a Colorado brigade under Colonel Ford, to whom wehad reported, set out to take summary vengeance on theenemy. The Colorado troops were cavalry, and in squadsof 20 to a company, scoured the country from Kansas Cityto the Osage River. It was reported that they killed 1,700in that Territory in 11 days. I counted 62 fresh graves inone graveyard near Harrisonville. For some time after this,there was no trouble from guerrillas.About the first of April 1862, the Third Battalion ofthe Ninth Kansas was disbanded, which let me out of theservice. I went home and organized a company of Kansasmilitia, and about May 15, 1862, was commissionedCaptain of Company D, 18 th Kansas militia. I receivedorders to drill my men once a week, and patrol the roadknown as the Old Santa Fe Trail, running from KansasCity to Old Mexico. My beat extended east and west acrossDouglas County, KS. The drilling and training continueduntil an order was issued to organize the 18 th Regiment ofKansas militia, of which I was chosen major.A few months later, there came another order toconsolidate with some other battalions, by which I wastransferred and commissioned major of the 21 st Kansasmilitia. I did service in this capacity in Kansas until theautumn of 1864, when on the 10 th of October, GeneralCurtis ordered us to the borderline between Missouri andKansas to fight General Price, who was expected at KansasCity or Independence at an early day. Militia regimentsfrom Kansas were hurried to the border until our numbersequaled 127,000. By the addition of General Totten, wenumbered 35,000. We were stationed south of Westport,forming a line extending for ten miles. During Thursdayand Friday of October 22 and 23 there was heavy fightingat Lexington and Independence. On the morning of 24 th ,General Price moved west, formed his men and openedthe battle, from Westport running south to the Little Blue,a distance of six miles. He took the aggressive, and wemet and fought his forces, who were under the commandof Joe Shelby, Quantrell and numerous other Confederatecommanders.About four o’clock on Saturday the 24 th , the battleraged all along the line, from Westport to the Little Blue, onwhich ground the 21 st Kansas State Militia was stationed.Being east of the Kansas line, General Joe Shelby seemedto regard us as intruders, and expressed his conviction byshowers of bullets. We considered this an uncivil way toPage 60The AAO Journal Volume 22, Issue 2, Summer 2012

treat visiting neighbors, and resented by an equally hotfire. The 21 st Kansas nobly held its ground while we weresurrounded by fire, smoke and blood. I remembered thegood old Scriptural admonition, that “it is more blessed togive than to receive,” and told the boys to give them thebest they had—and we gave them 42 rounds—not withouta charge, but with a charge behind each one of them.During the hottest period of the fight, a musketballpassed through the lapels of my vest, carrying away a pairof gloves I had stuck in the bosom of it. Another minie ballpassed through the back of my coat, just above the buttons,making an entry and exit about six inches apart. Had therebels known how close they were to shooting Osteopathy,perhaps they would not have been quite so careless. Duringthis engagement, I was mounted on the same mule, whichhad walked the log with me back in Kansas. The antics ofthis creature when the leaden balls came whizzing thickestabout her were amusing. She seemed under the impressionthat they were nit flies, while I was thoroughly convincedthey were bullets.Many amusing incidents occurred during our conflict.Some of our boys fell to praying for the Lord to save them.Under the circumstances, I deemed it best to suspenddevotional services and get into line to fight the rebels,who were spattering us with lead, so I leaped from mymule, and planting my foot close behind some of them, Ibroke the spell. They closed up the front and made goodsoldiers throughout the remainder of the fight. We held thefield until Price’s forces withdrew, leaving 52 dead on theground and 127 horses, which fell into our hands.Shortly after the departure of the enemy, night spreadher friendly mantle over the scene, shutting out from oursight the horrors of war. Our regiment marched west twomiles, then north six, east one, and went into camp nearShawneetown. About six o’clock the next morning, theartillery under General Totten opened fire east of Westportand south for six or eight miles—28 pieces joining in thechorus with a spattering of small arms, which made asullen roar, rolling along the entire line. The fighting wassevere until about eight o’clock, when General Price beganhis retreat south. We followed him, skirmishing all theway, until we had pursued him a distance of 90 miles, hadcaptured 28 cannon and were only a mile or two east ofFort Scott.At this point, we decided not to escort General Priceany farther, but leave him to take care of himself. Findingthe Confederate General Marmaduke in bad company, weinvited him to go home with us; and as we were prepared toenforce the invitation, he consented with some reluctance,for the general had “a hankering after the stars and bars.”After Price’s forces began their retreat, the firing ceasedfor a while, and they had gone fully 20 miles before itwas again resumed. The privilege was given the enemy tobury their dead, and soon a company of 140 of our bravefoes came to my headquarters under a flag of truce, whichwe always respected. I ordered the captain and his mento dismount and stack their arms, which they did. I theninstructed the officer in command to form his men in linebefore me, and stationed a guard over their arms.Addressing the Captain, I asked, “How are you off forgrub?” “Almost out, major!” he answered. Then in a toneand manner as serious as I could assume, I said, “I wantyou to listen to what I have to say for about five minutes,and not move a muscle until I get through.” Then I wenton to picture the horrors of war and the extreme measuressometimes necessary. I wound up by saying the rebelshad been in the habit of shooting many of our men, andnotwithstanding they had come in under a flag of truce, Iintended to shoot the captain and every man with him.At this, every cheek blanched and their breath camequick. Some were about to interpose, when I broke in with,“I mean I will shoot you all in the mouth with food andcoffee, as I want to convert all your sorrows into joy. Breakranks, go to the commissary and get enough to fill up.” Thecaptain and officers gave me a friendly grasp, and regrettedthat war made us (who should be by all laws of natureVolume 22, Issue 2, Summer 2012 The AAO Journal Page 61

friends) enemies, and hoped that the Angel of Peace mightsoon spread her white wings over our beloved land. Thoserebels certainly enjoyed that meal, and it was no doubt thefirst good meal the poor fellows had had for many days.After chasing Price for 90 miles, as stated, we wentinto Kansas at De Soto, and on Tuesday morning, October27, 1864, I received orders to disband the 21 st Regimentand go home. I kept the order to myself, determined to trythe grit of the boys and have a little fun at their expense.Ordering the whole regiment to be drawn up in line, I madea speech in which I said we had a very long march beforeus and a desperate battle at the end of it. I stated that Idid not wish anyone to undertake this arduous march, orto engage in the terrible conflict, who was not fully equalto the emergency. If any felt too sick, faint or weak toaccompany us, or for any cause felt they could not endurethe hardship and danger, they would not be forced to go.All who would volunteer to go with me through any trial ordanger were requested to step six paces to the front.About one-third of the command stepped out sixpaces and thus declared their willingness to followanywhere. Then, in a tone loud enough to be heard byall, I read the order for the disbanding of the regiment,told those who did not feel well enough to accompany usto go to the hospital under the doctor’s care, and to theothers said, “Boys, we will go home!” Shouts and roars oflaughter drowned any further utterance, and in ten minutes,we had not a sick man in the regiment. The regiment wasdisbanded, we all went home and that ended my experienceas a soldier.BOOKS & BONEfrom Pacific DistributinggS951-677-0652Featured Releases• NEW EDITION in Hard Cover, with New Preface• Biokinetics and Biodynamics of Human Differentiation:Principles & Applications E. Blechschmidt & R.F. Gasser $34.95• Human Embryology from a Biodynamic Perspective6 DVD Set - 12 hours of Lecture Brian Freeman $119.95• Visceral Osteopathy: The Peritoneal Organs $85.00• The Polyvagal Theory: NeurophysiologicalFoundations of Emotions, Attachment, Communication,and Self-Regulation Stephen Porges PhD. $45.00• Strolling Under the Skin Micro-cinematographyDVD of the Fasciae Tissue Jean-Claude Guimberteau• Protoplasm of a Slime Mold - Now in DVD$53.95Newly Re-Mastered from original film William Seifriz $29.95• Pediatric Manual Medicine: An OsteopathicApproach Jane Carreiro, D.O. $74.95• In the Realm of Hungry Ghosts Gabor Mate‘ $17.95• In an Unspoken Voice: Healing Trauma P. Levine $21.95• Visceral and Obstetric Osteopathy Caroline Stone $83.95• Mystic Spiral: Journey of the Soul Jill Purce $19.95booksandbones@verizon.net951-677-0652 Fax 951-677-3911www.booksandbones.comNew! Magnetic Didactic Colored Skull - 22 parts $367Magnets at sutures hold skull together. Easy to assemble and hasall the important anatomical landmarks- A wonderful teaching toolFetal Skulls • 20-22-29-30-31-32-34-35-40-401/2 weeks $71Male or Female sacrum w/ sacral nerve canal open $65Sphenoid and Occiput Set From Germany made by Somso _$1303B Re-Articulating 22 Piece Skull - New Price ReductionPastel colors • Good sutural detail • Easy disassembly / assembly• Ideal for teaching and educating patients $357Swiss DisarticulatedSkullThis museum quality disarticulatedskull is handmolded in limited quantitiesto ensure the finest possiblefit and finish. All pieceshave the exact weight,texture, color and feel of realbone. The entire vault andbase will re-articulate onsutural contact without theuse of snaps or eyelets. Thefrontal has an open metopicsuture and the occiput hasbeautiful wormian bones.Comes with a hard shell,foam lined case. Call formore details. $1085.00Page 62The AAO Journal Volume 22, Issue 2, Summer 2012

AAOJ Submission ChecklistFor more information on the elements in this checklist, see “AAOJ Instructions for Contributors” at www.academyofosteopathy.orgManuscript SubmissionSubmission e-mailed to AAOJ’s Scientific Editor ateditoraaoj@gmail.com or mailed on CD-ROM to the AAOJ’sManaging Editor, American Academy of Osteopathy, 3500DePauw Boulevard, Suite 1080, Indianapolis, IN 46268Manuscript formatted in Microsoft Word for Windows (.doc),text document format (.txt) or rich text format (.rtf)Manuscript ComponentsCover letter addressed to the AAOJ’s Scientific Editor,Murray R. Berkowitz , DO, MA, MS, MPH, with any specialrequests (e.g., rapid review) noted and justifiedTitle page, including the authors’ full names and financial orother affiliations, as well as disclosure of the financial supportrelated to original research described in the manuscript“Abstract” (see “Abstract” section in “AAOJ Instructions forContributors” for additional information)“Methods” section• the name of the public registry in which the trial islisted, if applicable• ethical standards, therapeutic agents or devices, andstatistical methods definedFour multiple-choice questions for the continuing medicaleducation quiz and brief discussions of the correct answersEditorial conventions adhered to• units of measure given with all laboratory values• on first mention, all abbreviations other than measurementsplaced in parentheses after the full names of theterms, as in “American Academy of Osteopathy (AAO)”Numbered references, tables and figures cited sequentially inthe text• journal articles and other material cited in the “References”section follow the guidelines described in themost current edition of the AMA Manual of Style: AGuide for Authors and Editors.• references include direct, open-access URLs to posted,full-text versions of the documents“Acknowledgments” section with a concise, comprehensivelist of the contributions made by individuals who do notmerit authorship credit and permission from each individualto be named in printFor manuscripts based on survey data, a copy of the originalvalidated survey and cover letterGraphic ElementsGraphics should be formatted as specified in the “GraphicElements” section of “AAOJ Instructions for Contributors”Each graphic element cited in numerical order (e.g., Table 1,Table 2, and Figure 1, Figure 2) with corresponding numericalcaptions in the manuscriptFor reprinted or adapted tables, figures and illustrations, a fullbibliographic citation given, providing appropriate attributionRequired Legal DocumentationFor reprinted or adapted tables, figures and illustrations, permissionto reprint from the publisher in the AAOJ’s print andonline versions accompanied by photocopies of the originalworkFor photographs in which patients are featured, signed anddated “Patient-Model Release” forms submittedFor named sources of unpublished data and individuals listedin the “Acknowledgments” section, permission to publishtheir names in the AAOJ obtained.For authors serving in the U.S. military, the armed forces’approval of the manuscript and institutional or military disclaimerssubmittedFinancial Disclosure and Conflict of InterestAuthors are required to disclose all financial and non-financialrelationships related to the submission’s subject matter. All disclosuresshould be included in the manuscript’s title page. See the“Title page” section of “AAOJ Instructions to Contributors” forexamples of relationships and affiliations that must be disclosed.Those authors who have no financial or other relationships to disclosemust indicate that on the manuscript’s title page (e.g., “DrJones has no conflict of interest or financial disclosure relevant tothe topic of the submitted manuscript”).• photocopies provided for referenced documents notaccessible through URLsVolume 22, Issue 2, Summer 2012 The AAO Journal Page 63

Component Societies and Affiliated OrganizationsUpcoming Calendar of EventsJuly 15-18Alabama Osteopathic Medical Association22 nd Annual Emerald Coast ConferenceHilton Sandestin Beach, Destin, FLCME: 25 Category 1-A AOA credits anticipatedPhone: (256) 447-9045 Fax: (256) 447-9040E-mail: alosteoma@aol.com Web site: http://aloma.org/July 19-22Opthalmalogic Principles and their Relationship toOsteopathy in the Cranial FieldCourse Director: Paul Dart, MDPrivate office, Eugene, ORCME: 26 Category 1-A AOA credits anticipatedPhone: (317) 581-0411 Fax: (317) 580-9299E-mail: info@cranial academy.orgWeb site: http://www.cranialacademy.orgJuly 20-22Manual Medicine: An Osteopathic ApproachIntroduction to Osteopathic Medicine andEvaluation & Treatment: Lumbar SpineUNECOM, Biddeford, MECME: 20 Category 1-A AOA credits anticipatedPhone: (207) 602-2589 E-mail: cme@une.eduWeb site: www.une.edu/com/cme/manualmedicine.cfmAugust 9-12Colorado Society of Osteopathic Medicine2012 Annual Meeting and Summertime CME:Primary Care Medicine in the RockiesBeaver Run Resort & Conference Center, Breckenridge, COCME: 25 Category 1-A AOA credits anticipatedPhone: (303) 322-1752 Fax: (303) 322-1956E-mail: rachel@coloradodo.orgWeb site: http://www.coloradodo.orgAugust 17-19Indiana Academy of Osteopathy &Indiana Osteopathic Association: A Sutural Approach toOsteopathy in the Cranial FieldHoliday Inn Indianapolis North, Carmel, INProgram Chair: Charles A. Beck, DO, FAAOFaculty: Edward G. Stiles, DO, FAAOCME: 20 Category 1-A AOA credits anticipatedPhone: (317) 926-3009 Fax: (317) 926-3984E-mail: info@inosteo.orgWeb site: http://www.inosteo.orgSeptember 7-9Integrated Neuromuscular and Myofascial ReleaseCourse Chairperson: Lisa DeStefano, DOMSUCOM, East Lansing, MICME: 19 Category 1-A AOA credits anticipatedPhone: (517) 353-9714 Fax: (517) 432-9873E-mail: cme@com.msu.eduWeb site: http://www.com.msu.edu/cme/courses.htmlSeptember 14-16Osteopathic Physicians & Surgeons of California23 rd Annual Fall Conference - CME by the BayIntercontinental Clement Monterey Hotel, Monterey, CACME: 22 Category 1-A AOA credits anticipatedPhone: (916) 822-5246 Fax: (916) 822-5247E-mail: opsc@opsc.org Web site: http://www.opsc.org/September 21-23Orthopedics, Posture and thePrimary Respiratory MechanismCourse Director: Maurice Bensoussan, MDAssociate Course Director: R. Paul Lee, DO, FAAOHilton Hotel, Providence, RICME: 21.5 Category 1-A AOA credits anticipatedPhone: (317) 581-0411 Fax: (317) 580-9299E-mail: info@cranial academy.orgWeb site: http://www.cranialacademy.orgSeptember 21-23Manual Medicine: An Osteopathic ApproachIntroduction to Osteopathic Medicine andEvaluation & Treatment: Thorax & Rib CageUNECOM, Biddeford, MECME: 20 Category 1-A AOA credits anticipatedPhone: (207) 602-2589 E-mail: cme@une.eduWeb site: www.une.edu/com/cme/manualmedicine.cfmSeptember 21-23ACOFP Intensive Update & Board Review inOsteopathic Family MedicineIntercontinental Chicago O’Hare Hotel, Rosemont, ILCME: 21 Category 1-A AOA credits anticipatedPhone: (800) 323-0794 Fax: (847) 228-9755Web site: http://www.acofp.org/CME_Center/Conventions/Workshops/Page 64The AAO Journal Volume 22, Issue 2, Summer 2012