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BR A IN INJURY professional vol. 8 issue 1

The official publication of the North American Brain Injury Society

Post-Traumatic Headache Post-Traumatic Headache: A Pain in Search of a Brain? Pain and the Injured Brain: A Biopsychosocial Conceptualization Osteopathic Issues in Post-traumatic Headaches: A Neurological Perspective Physical Therapy Interventions For Musculoskeletal Dysfunction Related to Post-Traumatic Headache Application of the Bradford-Hill Criteria for Assessing Specific Causation in Post-Traumatic Headache BRAIN INJURY PROFESSIONAL


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BRAIN INJURY professional vol. 8 issue 1

The official publication of the North American Brain Injury Society

north american brain injury society

departments 4 Editor in Chief’s Message 6 Guest Editor’s Message

chairman Ronald C. Savage, EdD Immediate Past Chair Robert D. Voogt, PhD treasurer Bruce H. Stern, Esq. family Liaison Skye MacQueen executive director/administration Margaret J. Roberts executive director/operations J. Charles Haynes, JD marketing manager Megan Bell graphic designer Nikolai Alexeev administrative assistant Benjamin Morgan administrative assistant Bonnie Haynes

30 bip Expert Interview brain injury professional

publisher J. Charles Haynes, JD Editor in Chief Ronald C. Savage, EdD Editor, Legislative Issues Susan L. Vaughn founding editor Donald G. Stein, PhD design and layout Nikolai Alexeev advertising sales Megan Bell

32 Non-profit News 34 Legislative Roundup BRAIN INJURY professional vol. 8 issue 1

The official publication of the North American Brain Injury Society

Post-Traumatic Headache Post-Traumatic Headache: A Pain in Search of a Brain? Pain and the Injured Brain: A Biopsychosocial Conceptualization Osteopathic Issues in Post-traumatic Headaches: A Neurological Perspective Physical Therapy Interventions For Musculoskeletal Dysfunction Related to Post-Traumatic Headache Application of the Bradford-Hill Criteria for Assessing Specific Causation in Post-Traumatic Headache BRAIN INJURY PROFESSIONAL


features 8 Post-Traumatic Headache: A Pain in Search of a Brain? by Nathan D. Zasler, MD 14 Pain and the Injured Brain: A Biopsychosocial Conceptualization by Michael F. Martelli, PhD, and Keith Nicholson, PhD 18 Osteopathic Issues in Post-traumatic Headaches:

A Neurological Perspective bY Edward R. Isaacs, MD, FAAN 22 Physical Therapy Interventions For Musculoskeletal Dysfunction

Related to Post-Traumatic Headache by Tracey Adler, DPT, OCS, CMTPT 26 Application of the Bradford-Hill Criteria forAssessing Specific

Causation in Post-Traumatic Headache by Michael D. Freeman, PhD, MPH, and Sean S. Kohles, PhD

EDITORIAL ADVISORY BOARD Michael Collins, PhD Walter Harrell, PhD Chas Haynes, JD Cindy Ivanhoe, MD Ronald Savage, EdD Elisabeth Sherwin, PhD Donald Stein, PhD Sherrod Taylor, Esq. Tina Trudel, PhD Robert Voogt, PhD Mariusz Ziejewski, PhD

editorial inquiries Managing Editor Brain Injury Professional PO Box 131401 Houston, TX 77219-1401 Tel 713.526.6900 Fax 713.526.7787 Website: Email:

advertising inquiries Megan Bell Brain Injury Professional HDI Publishers PO Box 131401 Houston, TX 77219-1401 Tel 713.526.6900 Fax 713.526.7787

national office

North American Brain Injury Society PO Box 1804 Alexandria, VA 22313 Tel 703.960.6500 Fax 703.960.6603 Website: Brain Injury Professional is a quarterly publication published jointly by the North American Brain Injury Society and HDI Publishers. © 2011 NABIS/HDI Publishers. All rights reserved. No part of this publication may be reproduced in whole or in part in any way without the written permission from the publisher. For reprint requests, please contact, Managing Editor, Brain Injury Professional, PO Box 131401, Houston, TX 77219-1400, Tel 713.526.6900, Fax 713.526.7787, e-mail



editor in chief’s message

Ronald Savage, EdD We all have known the debilitating impact a headache can have on our functioning and daily activities, including problems with thinking and remembering, behavior changes and struggles with even working. Furthermore, as we are all well aware, headaches are common after TBI, but, as Dr. Nathan Zasler and his colleagues point out in this issue of BIP, while posttraumatic headaches are often misunderstood, multidisciplinary assessment most often leads to better treatment of headache symptoms.

Dr. Zasler, who is also Chairman of the International Brain Injury Association IBIA), points out in his lead article, “Headache and neck pain are the most common physical complaints following concussion (mild brain injury) and are experienced early after injury by up to 70% of persons with these types of injuries. Headache also occurs after more severe brain injury; however, for some reason, as yet unidentified, it tends to be a much less common phenomena in this group of patients when compared with the incidence following mild traumatic brain injury.” For example, in a study conducted at Fort Lewis, WA, involving 978 U.S. Army soldiers returning from Iraq or Afghanistan in 2008, all had experienced a concussion, head injury or blast exposure while deployed. Nearly 98 percent of the soldiers reported having headaches during the last three months of their deployment. The headaches started within one week of the traumatic brain injury for 37 percent of the soldiers, and within one to four weeks for 20 percent. Among the soldiers whose headaches started within a week of the injury, 60 percent had migrainelike headaches and 40 percent had headaches that interfered with their ability to do their daily activities. Thirty percent had headaches for 15 or more days each month.

NABIS and Brain Injury Professional very much appreciates Dr. Zasler and his colleagues for developing this issue on posttraumatic headaches. Dr. Zasler will also be one of the Plenary Speakers at this year’s annual NABIS conference in New Orleans on September 14-17, 2011. Additional information can be found in this issue, as well as at www. I am pleased to announce that Louis V. Sirausano has joined the NABIS Board of Directors. Lou brings a tremendous amount of experience to the table and has long been an advocate for persons with brain injury and their families. More information on Lou can be found below. Lastly, it was great sadness that we inform you that we have lost one of our beloved colleagues this past month. Dr. Jane Gillett, MD was a pediatric neurologist from Ontario, Canada who developed one of the truly exemplary pediatric and adolescent ABI model systems of care in the world. NABIS thanks Dr. Roberta DePompei for creating the Memorial page on Dr. Gillett in this issue. For all those who knew and loved Jane, this is a tragic loss of a gifted physician and wonderful friend. Ronald Savage, EdD

new board member The North American Brain Injury Society is pleased to welcome Louis V. Siracusano as a new member of our Board of Directors. Mr. Siracusano joined the Siracusano, Sleezer Group, an independent branch of Wells Fargo Financial Network, in 2005, after a thirty year career in the practice of law in the State of New York. A graduate of St. John’s University, Queens, NY, Mr. Siracusano obtained a B.A. in Business Administration in 1967, and J.D. from its School of Law in 1975. Admitted to the New York Bar in 1976, Mr. Siracusano became a founding partner of “Mckenna, Siracusano & Chianese” later that year, and was subsequently admitted to the Florida (1986) and Connecticut (1996) Bars. In addition to his duties as managing partner, Mr. Siracusano 4


concentrated his practice in the area of Family Law. Though no longer actively practicing law, Mr Siracusano has maintained an “Of Counsel” relationship with the successor firm, Albert W. Chianese & Associates, with offices in Rockville Centre, NY. Over the last six years Mr. Siracusano has sought to assist plaintiffs who have received settlements or verdicts in personal injury cases to manage these often life changing sums. From his experience in the legal world Mr. Siracusano recognized that the party who suffered a serious injury could find it even more traumatizing when confronted by a dramatic change in their economic status. This was even more problematic in the area of TBI, which prompted Mr. Siracusano’s membership in NABIS and

the American Association for Justice (formerly the American Trial Lawyers Association). A resident of Nassau County, New York, Mr. Siracusano is a member of the WE CARE Advisory Board, the Nassau County Bar Association’s charity arm, whose mission is to raise & distribute funds for those in need throughout Nassau County. For the past three years Mr. Siracusano has chaired the WE CARE Golf Outing, the charity’s largest fund raising event, and has helped, in these challenging times, to achieve record levels of sums in successive years. Mr. Siracusano continues to bring together the legal and financial communities, in order to maximize the benefits to those victims and their families who have suffered serious injuries or are otherwise in need.

Textbook of Traumatic Brain Injury, Second Edition Edited by Jonathan M. Silver, M.D., Thomas W. McAllister, M.D., and Stuart C. Yudofsky, M.D.


As soldiers and combat veterans have returned from the wars in Iraq and Afghanistan traumatic brain injury (TBI) has been identified as the “signature injury” of those wars. This new edition of Textbook of Traumatic Brain Injury has been thoroughly revised and updated from the 2005 first edition to reflect the exponential expansion of research and clinical data amassed in the intervening years. Each chapter was written and reviewed by the foremost authorities in neuropsychiatry, neurology, rehabilitation medicine, and the other specialties who assess, diagnose, and treat these patients. Key features include: ■ New chapters on epidemiology, neuropathology, and genetics of TBI ■ A new chapter on TBI in the military ■ A new chapter on posttraumatic stress disorder (PTSD), which emphasizes the common co-occurrence of TBI and PTSD ■ Enhanced coverage of psychopharmacology and psychotherapy for the psychiatric symptoms associated with TBI ■ Information on the social ramifications of TBI so that clinicians will better understand and help their patients cope with the complex legal, financial, and insurance-based struggles their patients who have sustained TBI encounter ■ Chapters that are complete, readable, and relevant in themselves, reflecting the editors’ understanding that few readers digest a work of this magnitude in a single sitting ■ A Foreword written by Bob Woodruff (the ABC World News correspondent who sustained a TBI while covering the war in Iraq) and his wife, Lee Woodruff, who underscore that although this volume is intended to be read primarily by professionals, patients and families may also find the information in the textbook to be of keen interest and practical application. The book has been closely edited to achieve a level of writing that is consistent and engaging and that addresses the needs of all medical professionals—including the full range of mental health professionals—who care for people who suffer from TBI. This new edition of Textbook of Traumatic Brain Injury represents a huge step forward for the diagnosis and treatment of TBI. 2011 • 704 pages • ISBN 978-1-58562-357-0 • Hardcover • $159.00 • Item #62357

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guest editor’s message

Nathan D. Zasler, MD

It was with great pleasure that I accepted the invitation of Dr. Ronald Savage to edit this issue of “The Brain Injury Professional” on the topic of post-traumatic headache. Over my 25 plus years of clinical practice, one of the most intriguing consequences of traumatic injury including TBI, cranial trauma, and whiplash injuries that I have treated has been that of post-traumatic headache disorders, also known as post-traumatic cephalalgia. As you will read, this is a complex, multidimensional condition that requires not only an adequate knowledge base to appropriately determine the factors contributing to the pain condition but also, an array of treatment skills ranging from a variety of treatment options including physical, psychological and pharmacological. As editor of this issue, I have tried to incorporate perspectives of a multidisciplinary authorship in the context of the discussion on PTHA assessment and treatment. The lead article on medical assessment and management authored by this clinician will hopefully provide readers with an overview of the topic and an introductory understanding of the com-



plexities involved in both identifying pain generators responsible for posttraumatic headache as well as treating said pain generators. The second article in this issue is authored by Drs. Michael Martelli and Keith Nicholson. I have worked with both these neuropsychologists before and both have excellent “pain pedigrees” in addition to being sophisticated clinicians. I have also had the pleasure of working with Dr. Martelli for close to 20 years and his assistance with patients with TBI including pain management has been truly invaluable. Their article deals with a biopsychosocial model for conceptualizing both PTHA assessment and treatment and should provide readers with an invaluable perspective on PTHA not typically discussed. Dr. Edward Isaacs provides us with both a neurological, and most importantly, an osteopathic perspective of PTHA as he examines skeletal somatic dysfunction issues as PTHA pain generators and discuss osteopathic treatment strategies to normalize such pathology. In my clinical experience, the use of manual therapy including osteopathic treatment can be an essential element in the treatment of a variety of posttraumatic headache disorders but all too often, these contributors are not recognized or acknowledged by clinicians evaluating these types of patients. The next article by Dr. Tracy Adler deals with physical therapy approaches to PTHA focusing particularly on treatment of referred myofascial pain. Again, this area of PTHA management often does not get the appropriate recognition that it deserves and the overall contribution of both myofascial, and more broadly, cervicogenic contributors to PTHA in this clinician’s opinion is often underestimated and/or misapportioned to other causes. Additionally, cervicogenic pain generators often serve as perpetuating fac-

tors for other types of headache disorders including migraine and tension headaches and when appropriately treated, often substantially modulate migraine-tension spectrum disorder type headaches. The last formal article in this issue is authored by Dr. Michael Freeman, an epidemiologist and chiropractor with a rather stellar publication record in the context of epidemiology of whiplash, as well as whiplash related disorders. Dr. Freeman will focus on epidemiological perspectives on PTHA causation and apportionment. I am sure readers will find this article quite fascinating, particularly those involved in the medicolegal arena; however, the approach is just as relevant to good differential diagnostic skills in a clinical context. The clinical interview in this issue is with Dr. Russell Packard, who has a longstanding history of providing clinical care to patients with post-traumatic headache as well as being a major contributor to the historical PTHA literature. His experiences treating headache disorders post-trauma over many years should be enlightening for BIP readers. I want to personally take this opportunity to thank all the contributors to this issue for their time, as well as their patience with my editorial scrutiny. I also want to, once again, thank Dr. Ronald Savage for the opportunity to edit this issue and disseminate what I hope will be well-valued information to fellow professionals about the very important, albeit often times confusing topic of PTHA. Nathan D. Zasler, MD, FAAPM&R, FACRM, FAADEP, DAAPM, CBIST CEO & Medical Director, Concussion Care Centre of Virginia, Ltd. CEO & Medical Director, Tree of Life Services, Inc. Chairperson, IBIA



Post-Traumatic Headache: A Pain in Search of a Brain? Introduction

Headache and neck pain are the most common physical complaints following concussion (mild brain injury) and are experienced early after injury by up to 70% of persons with these types of injuries. Headache also occurs after more severe brain injury; however, for some reason, as yet unidentified, it tends to be a much less common phenomena in this group of patients when compared with the incidence following mild traumatic brain injury. This suggests that the TBI itself is probably not the primary cause because it would logically follow that if it was one would expect more headache problems with more severe TBI. Headache is also a common problem after cranial trauma, as well as spinal whiplash injuries. Often, injured persons will seek medical care following traumatic injuries only to be diagnosed with “post-traumatic headache� (PTHA). Such a non-specific diagnosis without elaboration as to pain generator etiologies leaves treaters and others (including patients and their families) with no real information regarding the true etiology of the headache disorder, its prognosis, or the appropriate treatment regimen that should be administered to modulate or ideally cure the headache. Although the majority of headache following mild brain injury is most likely benign relative to the fact that these conditions do not require surgical treatment, there are, on occasion, complications that occur, as is more commonly seen with more severe brain injury and associated headache, that may require surgical intervention. Subdural and epidural hematomas (blood collecting between the brain and the skull), carotid cavernous fistulas (abnormal communication between the venous blood flow and arterial blood flow), traumatic carotid artery dissection, cavernous sinus thrombosis, as well as post-traumatic intracranial pres8


by Nathan D. Zasler, MD

sure (ICP) abnormalities (high versus low ICP), among other conditions can all be responsible for PTHA and bring with them a potential need for surgical intervention. The experienced clinician should be able to determine the underlying cause for the PTHA with appropriate time taken to acquire an adequate pre-injury, injury and post-injury history, as well as conduct a careful physical evaluation and appropriate diagnostic testing. Treatment should be instituted in a holistic fashion with a goal of maximizing the benefit/risk ratio of any particular intervention, prescribing treatment that can be optimally complied with and educating the patient and family regarding the condition, its treatment and prognosis. Late onset headaches (i.e. greater than 6 months post-trauma) should cue the treating clinician to think of less common injury related conditions such as seizures or tension pneumocephalus as a cause for the headache disorder or just as likely a non-injury related cause such as a space occupying lesion (i.e. brain tumor), among other conditions. Categorization

The major types of headaches seen following trauma include: musculoskeletal headache (including direct cranial trauma, cervicogenic headache and TMJ disorders), neuromatous and neuralgic (nerve) headache, tension type headache, migraine, as well as more uncommon causes of headache including dysautonomic headaches, seizures, pneumocephalus (air in the head), cluster and paroxysmal hemicrania, post-traumatic sinus infections, drug induced headache, medication overuse headache (previously called rebound headache) and the surgical conditions previously mentioned. The most common cause of PTHA in this clinician’s extensive experience is cervicogenic headache which

may have several different possible causes. Referred cervical myofascial pain as a consequence of cervical acceleration-deceleration insult (i.e. whiplash) is a particularly common explanation for this condition, particularly when there is involvement of proximal aspects of cervical or associated musculature….such as trigger points in the sub-occipital musculature or proximal portions of the sternocleidomastoid and/or upper trapezius muscles. Etiology

There are multiple sources of head and neck pain, both inside and outside of the head. The brain itself, interestingly, is not a source of pain. Headache typically results from six major physiologic phenomena: • Displacement of intracranial (within the skull) structures. • Inflammation. • Ischemia (decreased blood flow) and/or metabolic changes. • Myodystonia (increased muscle tone). • Meningeal irritation (inflammation/irritation of the thin layers of tissue “coating” the brain). • Increased or decreased intracranial pressure. Natural History, Prognostic Factors and Outcome

There are inadequate evidence based studies to stipulate dogmatically the natural history, prognostic factors and outcomes of PTHA, in part, because PTHA is not one single pathophysiological disorder but rather a symptom descriptor that may involve multiple pain generators. Additionally, there are major methodological flaws in the existing literature relative to lack of prospective, controlled and blinded studies in this patient population. There are also multiple methodological challenges in studying an impairment that is predominantly based on subjective patient report including issues of misattribution bias, recall bias, and potential response bias regarding pain reporting, among other issues. Any study of chronic PTHA must also address the inherent co-morbidities of the psychological and medical effects of chronic pain (and stress) on not only the patient’s reporting of their pain but also on a myriad of other aspects of function including cognition, behavior and sleep. The majority of the studies to date have not based conclusions on comprehensive physical assessments that integrate neurological and musculoskeletal assessment and/or additionally link specific exam findings with current headache classification systems (the latter which have been criticized relative to their lack of applicability and relevance to this particular population). Studies to date have also, almost exclusively, not used pain validity or response bias measures of any kind to assess the accuracy of pain reporting which would significantly leave in doubt the accuracy of pain related disability reports (particularly with persons who had some potential secondary gain factor(s) in place such as a personal injury, worker’s compensation or disability claim) due to PTHA. Conversely, secondary gain may also apply to patients with PTHA underreporting their symptoms (e.g. the football player who wants to go back in the game or the soldier who wants to return to his unit). Studies have demonstrated that ongoing litigation has little to no effect on the persistence of headache complaints. Specifically, studies have shown that patients still continue to report significant symptoms even after litigation has ended (Note: the work in this area is limited and further research to confirm the

findings of prior studies is recommended). A small number of patients will develop intractable severe post-traumatic headache; however, this group of patients has been poorly studied and the influence of non-organic and/or psychogenic factors in such patients remains unclear. When properly diagnosed and treated, most PTHA is able to be modulated or cured and will not likely be disabling over the long term. PTHA prognosis must be based on an exact understanding of headache etiology (based on history and focused examination, overlay as relevant of psychogenic (including patient characterological issues) and secondary gain factors, response to appropriate historical treatment and consideration of whether the correct treatment for the pain generator was ever instituted at all. Evaluation

All too often, patients are simply given a diagnosis of post-traumatic headache (PTHA) and no further elaboration is made relative to the problem causing the pain. Often PTHA is incorrectly labeled and treated as migraine headache because no one bothers to adequately obtain a history of headache symptoms and/ or conduct an appropriately focused examination that considers injury mechanisms and/or headache symptoms. The examining clinician must keep in mind the different mechanisms of PTHA. Additionally, the mechanism of injury responsible for the initial insult should also be investigated (i.e. high speed MVA, fall, or assault as the most common mechanisms). Risk factors for three main phenomena that are typically associated with PTHA should be inquired about including brain injury, cranial or cranial/adnexal trauma (damage to the head or structures in the head but outside the brain) and/or cervical acceleration/deceleration (CAD) insult (also called whiplash injury). There is also a growing literature on blast related headache in returning military personnel that accounts for a significant level of post-conflict morbidity; however, the literature to date has been limited and without concurrent comprehensive assessments including physical examinations and/or pain response bias testing. Blast related injury may be primary (direct injury from pressure wave), secondary (due to injury from projectile elements), tertiary (due to effect of trauma from being thrown into other objects) or quaternary (from precipitation of explosion-related illnesses or diseases). One of the major clues as to the cause of PTHA should be the symptom profile for that particular headache condition. Clinicians must therefore have a very good grasp on the manner in which different post-traumatic headache disorders present from a symptomatic standpoint. Not infrequently, there is more than one type of PTHA pain generator present. For example, most patients with PTHA who have tension or migraine headaches typically have cervicogenic contributors and most patients with TMJD typically also have cervical involvement. A patient’s pre-injury headache history as well as their family headache history (e.g. relative to genetic loading risk for PTHA) is also very relevant in the context of understanding any PTHA disorder. Just because an individual had headache pre-injury does not mean that he or she could not develop a different type of headache or a worsening of the pre-injury condition following trauma. The major questions relative to the headache profile that need to be asked are expressed in the mnemonic “COLDER”: Character, Onset, Location, Duration, BRAIN INJURY PROFESSIONAL


Exacerbation, and Relief. Other important areas to inquire about include the frequency, severity, associated symptoms (including the presence/absence of aura), degree of functional disability associated with headache episodes, the time of day that headaches start and/or are worse, headache relationship with stress and/or menses, as well as seasonal variations are all important parameters to inquire about. Adequate physical examination is paramount to an appropriate diagnosis and should include inspection, palpation, auscultation and percussion as appropriate. The neurological exam should be a centerpiece of this assessment, however, adequate examination of cranial and cervical (i.e. neck) structures including inspection, percussion and palpation of the head, neck and shoulders, as appropriate, is a crucial yet often overlooked aspect of a complete exam for PTHA. Anecdotally, I would note that about 90% of the tertiary referrals this clinician has seen over the last 25 years report that no one had ever palpated their neck or head. Treatment

PTHA does not occur in a vacuum. Rather, it occurs in a biological system within specific psychological and social contexts. PTHA reflects an interaction of organic and emotional factors. Treatment decisions need to be made with an understanding of the differences between managing acute new onset PTHA versus chronic PTHA. In the acute setting, pharmacological and physical modalities generally are the prime interventions considered and appropriate. In the chronic setting, mental health assessment is paramount and when not included will often lead to sub-optimal clinical outcomes regardless of how “appropriately” the patient is otherwise managed. Unsophisticated medication management may lead to unwanted side effects (e.g., adverse effects on sleep, cognition, behavior, sexual functioning and/or work performance) and inadequate pain control; however, appropriate medication management can go a long way in modulating PTHA symptoms. There are now multiple different pharmacological approaches to the various types of PTHA that the treating physician must consider including enteral, intravenous, sublingual, transdermal, compounded and rectal formulations of medications. Physical interventions that are misdirected including physical therapy may augment costs for the payor but do nothing for ameliorating PTHA related pain and disability. Physical treatments may include various manual therapies including osteopathic, chiropractic, physical therapy and craniosacral therapies. Additional physical treatments may encompass interventional pain procedures such as nerve blocks, trigger point injections, acupuncture, facet blocks, and on rare occasion surgery, among a myriad of available techniques. Treatment in the “right hands” is crucial with these types of patients ….a fact often not appreciated by clinicians and payers not experienced and well acquainted with this post-traumatic disorder. PTHA patients have been reported to exhibit minimal response to psychological or physical treatments when utilized in a non-holistic fashion. Treatments that target not only the pain generator(s), but also the patient’s reaction to pain within their daily life (and their adaptation to it) typically fare better than treatments with a more narrow focus. Understanding vulnerability issues as predictors of poor chronic pain adaptation is also critical in this context. Currently, multicomponent treatment packages are the preferred treatment choice for PTH. For those 10 BRAIN INJURY PROFESSIONAL

interested in more detailed discussions of PTHA treatment options please refer to the attached recommended readings. Neuropsychology of Post-Traumatic Headache

Persons with chronic pain commonly develop emotional difficulties such as depression and/or anxiety which may further increase their perception of their pain and their subjective level of distress, as well as stress. Many times referral to a psychologist or pain specialist may be indicated to help the person with the headache condition learn to deal better with their pain. Biofeedback, stress management, cognitive-behavioral therapies, pain adaptation and/or disability counseling and pain cope groups, among a variety of possible interventions, do help many patients with headache including those without evidence of gross psychological problems. Such interventions should be provided by persons adept at chronic pain management, as well as, familiar with issues germane to working with persons with TBI and their families. Education of the patient with PTHA is crucial to optimizing treatment success, as well as decreasing distress and poor adaptation to pain, particularly when chronic. One of the most important pieces of education is making sure the patient understands their disease process and the expectations of treatment which may not necessarily be curing the headache but modulating it and optimizing general function. Another very important area of intervention is to make sure that the patient and their support system understands how to administer any prescribed treatments including medication and the potential detrimental effects of non-compliance such as delay of recovery, non-optimization of pain control, and medication overuse headache, as a few examples. Pain associated with PTHA can interfere with thinking in terms of decreased attention and concentration with perceived memory problems. Such interference can often produce false positive diagnoses of mild TBI in persons following cranial or cervical trauma with significant PTHA related pain and/or aggravate cognitive issues due to real post-TBI neurocognitive dysfunction. Pain can also disrupt sleep, behavior (i.e. predominantly manifesting as irritability, depression and/or anxiety), as well as promulgate symptoms of post-traumatic stress disorder (PTSD). Conclusions

PTHA is ultimately a symptom and not a diagnosis. This complex disorder has multiple potential causes and as a result has multiple potential ways to address the pain that is associated with the underlying pain generators. Assessing and treating PTHA is a process that requires adequate time commitment and knowledge by the treating clinician...some will consider this “a pain” and if that is the case, then those clinicians should defer treatment to others who make it their business to assess and treat these types of patients. Pejorative and potentially self-prophesising labels such as “chronic PTHA” are often a misnomer due to the fact that the actual pain generators were never diagnosed correctly in the first place. Ideally, such labels should be avoided. There is in fact hope for those with PTHA regardless of how long they have suffered from pain. The challenge is finding clinicians who understand the disorder and have experience in holistic assessment and treatment of post-trauma patients including those with TBI, cranial trauma and whiplash injuries.


Afari N, Harder LH, Madra NJ, Heppner PS, Moeller-Bertram T, King C, Baker DG.PTSD, combat injury, and headache in Veterans Returning from Iraq/Afghanistan. Headache. 49(9):126776, 2009. DeFelice M, Ossipov MH, Porreca F: Upddate on medication-overuse Headache. Curr Pain Headache Rep. Epub. 2010. Dobscha SK, Clark ME, Morasco BJ, Freeman M, Campbell R, Helfand M.: Systematic review of the literature on pain in patients with polytrauma including traumatic brain injury. Pain Med. 10(7):1200-17, 2009. Evans RW: Post-traumatic headaches. In Evans RW (Ed. ) Neurologic Clinics, 22(1), 237-249. Philadelphia: Saunders, 2004. Hecht JS: Occipital nerve blocks in post-concussive headaches: a retrospective review and report of ten patients. J Head Trauma Rehab. 19(1):58-71, 2004. Kozminski M.: Combat-related post-traumatic headache: diagnosis, mechanisms of injury, and challenges to treatment. J Am Osteopath Assoc. 110(9):514-9, 2010. Martelli, M.F., Zasler, N.D.: Post-traumatic pain disorders: Psychological Assessment and Management. In: Brain Injury Medicine: Principles and Practice. N. Zasler, D. Katz, R. Zafonte (Eds.). New York. Demos Publishers. 2007. Nampiaparampil, DE: Prevalence of chronic pain after traumatic brain injury. JAMA. 300(6):711719, 2008. Otis, J.D., Keane, T.M., Kerns, R.D., et al: The development of an integrated treatment for veterans with comorbid chronic pain and Post-traumatic Stress Disorder. Pain Med. 10:1300–1311, 2009. Packard RC: Epidemiology and pathogenesis of post-traumatic headache. J Head Trauma Rehabil. 14(1):9-21, 1999. Packard RC: The relationship of neck injury and post-traumatic headache. Current Pain and Headache Reports. 6:301-307, 2002. Peroutka SJ: 2010: Year in Review. Clinical Trials Update. Headache. 51:181-187, 2011. Sayer, N.A., Cifu, D.X., McNamee, S., et al. Rehabilitation needs of combat-injured service members admitted to the VA Polytrauma Rehabilitation Centers: The role of PM&R in the care of wounded warriors. PMR. 1:23–28, 2009. Walker RL, Clark ME, Nampiaparampil DE, McIlvried L, Gold MS, Okonkwo R, Kerns RD.: The hazards of war: blast injury headache. J Pain. 11(4):297-302, 2010. Walker WC, Seel RT, Curtiss G, Warden DL: Headache after moderate and severe traumatic brain injury: a longitudinal analysis. Arch Phys Med Rehabil. 86(9):1793-1800, 2005. Zafonte R, Horn L: Clinical assessment of post-traumatic headache. J Head Trauma Rehabil. 14:22-33, 1999. Zasler ND (Ed.): Post-traumatic headache. J Head Trauma Rehabil. 14(1), 1999. Zasler, N.D.: Post-traumatic Headache. Tip card. Lash & Associates Publishing. 2006. Zasler, ND: Post-traumatic pain. In: F. Zollman (Ed.). Manual of Traumatic Brain Injury. Demos


Medical Publishers. 2011 (In press). Zasler, ND: Pharmacotherapy and Post-traumatic Cephalalgia. Update on Pharmacology. JHTR. 2011 (In press). Zasler, N.D., Horn, L., Martelli, M.F. Nicholson K: Post-traumatic pain disorders: Medical Assessment and Management. In: Brain Injury Medicine: Principles and Practice. N. Zasler, D. Katz, R. Zafonte (Eds.). New York. Demos Publishers. 2007. Zasler, ND & Martelli, MF. Post-traumatic headache: Practical approaches to diagnosis and treatment. In: R.B. Weiner (Ed.): Pain Management: A Practical Guide for Clinicians, 6th edition. Boca Ratan, FL: St. Lucie Press, 313-344, 125-138, 2002. Zasler, N.D. Martelli, M.F.: Chronic pain. In: J.M. Silver, T.W. McAllister, S.C. Yudofsky (Eds.): “Textbook of Traumatic Brain Injury”, 2nd Edition. American Psychiatric Publishing, Inc. 2011: 375-396.

Websites of Interest:

American Council for Headache Education: National Headache Foundation: The American Council for Headache Education provides a listing of on-line and local support groups. Visit An on-line headache diary is available at

About the Author

Dr. Zasler is CEO & Medical Director, Concussion Care Centre of Virginia, Ltd., as well as, CEO & Medical Director, Tree of Life Services, Inc. He is an adjunct Professor, VCU Department of Physical Medicine and Rehabilitation, Richmond, Virginia and an adjunct Associate Professor, Department of Physical Medicine and Rehabilitation, University of Virginia, Charlottesville, Virginia where he also serves on the UVA Brain Injury and Sports Concussion Institute Professional Advisory Board. Dr. Zasler is also an adjunct Professor in the Graduate School of Psychology, Institute for Neurobehavioral Studies, Touro College, New York, NY. Dr. Zasler has published and lectured extensively on TBI related neuromedical issues including PTHA and is internationally recognized for his work in brain injury medicine. He currently serves as the Chairperson of the International Brain Injury Association and is co-editor of two peer reviewed international scientific journals: Brain Injury and NeuroRehabilitation. E-mail:



Restore Neurobehavioral Center is a residential, post acute healthcare organization dedicated exclusively to serving adults with acquired brain injury who also present with moderate to severe behavioral problems. Services range from intensive inpatient neuro-rehabilitation and transitional community re-entry services to long term supported living services. Restore Neurobehavioral Center, located in a suburb north of Atlanta, is the site of our inpatient post acute neuro-rehabilitation program as well as one of our supported living sites. We operate two other community living sites, Restore-Lilburn (GA) and Restore-Ragland (AL). 800-437-7972 ext 8251 BRAIN INJURY PROFESSIONAL


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Pain and the Injured Brain: A Biopsychosocial Conceptualization by Michael F. Martelli, PhD, and Keith Nicholson PhD Pain is described as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (Merskey and Bogduk, 1994). Acute pain usually occurs in response to identifiable tissue damage or noxious event, has a time-limited course and any needed treatment targets underlying pathology. Chronic pain persisting beyond 6 months is often not associated with obvious tissue damage or pathology and may be characterized by anxiety, maladaptive protective responses or pain behaviors, protracted medication use, minimally effective medical services, marked behavioral or emotional changes and restrictions in daily activities. Pain-related avoidance behaviors can result in a self-perpetuating disability pattern; as pain persists, it becomes increasingly recalcitrant and treatment goals refocus on improved coping with pain and concomitants (Martelli et al., 2004, 2007). Increasing evidence associates persistent pain with peripheral and/ or central sensitization effects involving hyper-responsiveness in components of the pain system (Zasler et al, 2007; Nicholson & Martelli, 2004, 2006). An association between post-traumatic stress reactions and development of chronic pain suggests that uncontrollable pain after physical injury and anticipated pain (Wager et al, 2004; Porro et al, 2002) can represent a core trauma producing post-traumatic stress symptomatology and/or perpetuating it (Hart et al, 2003). Pain is a multidimensional subjective experience mediated by emotion, attitudes and other perceptual influences. Variability in pain responses is expected and appears to reflect complex biopsychosocial interactions between genetic, developmental, cultural, environmental and psychological factors (Gatchel & Turk, 1999). Important distinctions between pain and suffering, impairment 14 BRAIN INJURY PROFESSIONAL

and disability and presentations ranging from possibly exaggerated suffering or disability to a “belle indifference” and absence of distress or interference despite high apparent pain intensity reflect the variability in response to pain problems and the importance of always considering both psychological and organic factors in the presentation of any chronic pain patient (Nicholson & Martelli, 2004, 2006; Zasler & Martelli, 2002). Complex pain presentations, especially when intractable or functionally disabling, acute or chronic, warrant referral to pain management specialists or specialty interdisciplinary pain programs. Competent, specialized, early intervention offers the greatest hope of facilitating adaptation to pain. Notably, the requirement for specialized assessment and management of pain has been incorporated into the prevailing standards of healthcare practice in the United States, while psychological assessment is a required element of pain treatment programs accredited by the Commission on Accreditation of Rehabilitation Facilities (Martelli, Nicholson, et al, 2007). Pain can be triggered by sensory inputs (e.g., acute) or independently (e.g., chronic) from sensitization effects or hyper-responsiveness in peripheral or central components of the medial pain system and related limbic structures (Zasler et al, 2007). Central pain control processes seem to encompass the cognitiveevaluative, motivational-affective, and sensory-discriminative systems that characterize the pain response. The pain system is intimately related to other systems in the brain (e.g., motor, mnemonic, and social). TBI, cranial trauma and cervical whiplash injuries are all associated with a high comorbidity of chronic pain problems. Head-

ache is the primary complaint in surveys of postconcussion syndrome (e.g., Nicholson & Martelli, 2004, 2006). Posttraumatic headache (PTHA) frequency in the immediate post accident period has been reported to be as high as 90%, with problems continuing beyond 6 months in as many as 44% of patients (Martelli, Nicholson, Zasler, 2007). In addition to headache, many other pain problems may follow trauma, including back pain, complex regional pain syndrome (CRPS), and fibromyalgia, among others. Although PTHA problems are common, most studies report greater head and other pain problems in mild versus more severe TBI (Nicholson & Martelli, 2004, 2006; Zasler and Martelli 2002). Mahmood et al, (2004) reported that while severe TBI is more likely to produce subcortical damage and reduce pain experience, mild TBI is associated with increased pain and sleep disturbance and that sleep disturbance is associated with frontal hypoactivation that especially when associated with depression heightens vulnerability to cognitive dysfunction.

TBI, Chronic Pain and Neuropsychological Dysfunction There is increasing recognition of the disruptive effect pain may play in symptom presentation after TBI, including cognitive complaints (Nicholson & Martelli, 2004, 2006; Hart et al., 2000, 2003; Martelli et al, 2004, 2007). Available evidence from acute, as well as chronic animal and human pain studies involving experimental, clinical and neurophysiological studies strongly supports the conclusion that pain and pain-related symptomatology, independent of TBI or neurological disorder, can and often do produce impairment of cognitive functioning as assessed on neuropsychological and functional tests, especially on measures of attentional capacity, processing speed, memory, and executive functions (Martelli, Nicholson, Zasler, 2007). Recent reviews have also indicated that the associated symptoms of chronic pain, singly and in combination, may be more important than pain severity in producing cognitive and other impairment, including hyperalgesic changes and disruption of serotonergic and opioidergic processes (Pilcher & Huffcutt, 1996). Cognitive impairment in chronic pain patients has been associated with sleep disturbance / partial sleep deprivation, major depression, mood change/emotional distress, medication use, somatic preoccupation and pain catastrophization and perceived interference with daily activities that are potential sources of chronic stress (Hart et al, 2000, 2003; Nicholson & Martelli, 2004, 2006; Mooney et al, 2005; Kunderman et al, 2004). Chronic pain and its concomitants can complicate the symptom picture in TBI. PTHA and associated problems can present a differential diagnostic challenge especially in cases of persistent sequelae following milder TBI, as well as complicate neuropsychological assessment when untreated and/or contribute to, exacerbate or maintain symptoms associated with TBI. This evidence provides strong support for the argument that resolution of the post-concussive syndrome and successful adaptation to residual sequelae frequently relies on successful coping with post-traumatic craniocervical pain and associated symptomatology.

Assessment of Post-traumatic Headache Anticipation of pain activates cortical networks similar to pain itself (Wager et al, 2004; Porro et al, 2002). This highlights a

complex, multidimensional, subjective perceptual pain process comprised of behavioral, affective, cognitive and sensory components. Hence, a comprehensive, biopsychosocial assessment is considered the standard of care when pain is chronic (Gatchel, Turk, 1999). In addition to medical findings, pain assessment should address self-report, via interview of patient, relevant others and use of appropriate assessment instruments, in the following areas: (1) Pain onset, location, intensity level, duration, course, quality /characteristics; (2) Affective and autonomic stress related effects (including psychophysiological assessment as indicated); (3) Pain behaviors, environmental effects / responses, specific effect on mood, activity, cognition, affect, sleep, appetite, irritating / relieving factors, etc.; (4) Medications and effects; (5) Beliefs about the pain condition; (6) Coping strategies and effectiveness; (7) Psychosocial context and social responses to pain; (8) Personality and psychoemotional status and adjustment, including general coping, specific pain coping and how these affect or are affected by pain; (8) Activity, level of function / disability, quality of life, including current activities, pain related changes. See Martelli, Nicholson, Zasler (2007) for a survey of useful pain assessment instruments (link: at PainAssessTable.pdf ), including ones for special populations. These are intended to be integrated with a thorough history taking, interview (patient, relevant others) and examination of relevant medical and health records. Included are measures of response bias or tendency to report or present pain / related disability inaccurately. This is important given the nature of pain (avoidance is a reflexive response), frequent forensic contexts, frequent pain related anxieties (fear of re-injury, avoidance of unpleasant situations) and possible dependency or avoidance personality traits, among other factors. See Martelli, Nicholson, Zasler et al (2007) for a thorough analysis and strategy for this challenging task.

Behavioral and Psychological Management of Pain Pain management parallels pain assessment with treatment evolving over time from (1) analgesia; promoting healing and/ or correcting pathophysiology; minimizing physical, cognitive or emotional distress reactions and preventing “chronification�, i.e., peripheral or CNS sensitization effects, to (2) improving adaptation and reducing functional disability. Comprehensive biopsychosocial assessment provides the framework for individually tailored treatment interventions and recommendations. Behavioral and psychological treatment interventions in persons with chronic post traumatic headache include individualized interventions that follow from the biopsychosocial assessment that provides a treatment framework, defines goals, expectations and sequences and provides psychoeducational information about the particular type of chronic pain and rationale for treatment (Martelli, et al, 2004, 2007). Specific outcome studies that examine PTHA treatments are recently emerging. These are demonstrating the clear phenomenological similarities in clinical presentation and treatment response of PTHA compared to non-traumatic headache disorders. Martelli et al (2004, 2007) reviewed evidence supporting the utility of behavioral interventions for PTHA that include patient education, biofeedback, relaxation training, operant beBRAIN INJURY PROFESSIONAL


havioral therapies, cognitive behavioral treatments, social, assertiveness, stress management and coping skills training. They noted that in cases of post-traumatic pain: (a) the severity and frequency of pain attacks and chronic pain-related sequelae such as coping abilities, depression, and anxiety may be significantly improved by combined behavioral treatment protocols; (b) supportive counseling that begins early after trauma and is continuous results in better patient response; and (c) combination medical and behavioral treatments increase likelihood of benefit. Several authors have systematically reviewed evidence supporting the efficacy of behavioral interventions for chronic pain that includes chronic headache and posttraumatic headache. Kröner-Herwig’s (2009) review confirmed efficacy of behavioral treatment outcomes for chronic back pain, headache, fibromyalgia, and temporomandibular pain. Lake (2001), found that controlled studies of cognitive behavioral therapies (CBTs) for migraine, such as biofeedback and relaxation therapy, had a prophylactic efficacy of about 50%, roughly equivalent to propranolol, while the combination of behavioral therapies greatly increased efficacy. Rains et al, (2005) note that meta-analytic reviews have consistently shown behavioral interventions (relaxation training, biofeedback, cognitive-behavioral therapy, and stress-management training) to yield 35% to 55% improvements in migraine and tension-type headache. Finally, supportive evidence now includes randomized clinical trials (e.g., Thorn et al, 2007) and the interesting finding of Ruff et al, (2009) that a combined behavioral (sleep hygiene counseling) and pharmacologic (prazosin) treatment effectively improved sleep and decreased average frequency and intensity of PTH by 66% and improved cognitive assessment scores with results maintained at 6 months.

References 1.

2. 3. 4. 5. 6. 7. 8.




12. 13. 14.

15. 16. 17. 18.

Conclusions and Future Directions The assessment and treatment of chronic pain associated with TBI is a challenging process. Pain and its concomitants can have a more disabling effect across a wider range of functions than brain injury itself, particularly when mild. Available evidence strongly supports the conclusion that resolution of the post concussive syndrome and successful adaptation to residual sequelae frequently relies on successful coping with PTHA and associated symptomatology. Early, competent, specialized intervention offers the greatest hope of facilitating adaptation to pain. Complex or persistent pain presentations warrant referral to pain management specialists or specialty interdisciplinary pain programs. Biopsychosocial assessment and treatment strategies have emerged as the standard of care in chronic pain. The most promising current treatment interventions are combination treatments that are holistic in nature and target the patient’s reaction to pain within his/her daily life and ability to exercise self-control. Multicomponent treatment packages are currently the preferred treatment choice for chronic pain generally and especially when it accompanies TBI (Martelli, et al, 2004, 2007). Early, competent, specialized intervention that includes education and combination medical and behavioral interventions directed at simultaneously improving adaption to PTH and improving its associated symptoms of sleep disturbance, emotional distress and depression, is indicated. 16 BRAIN INJURY PROFESSIONAL

19. 20.

21. 22.


Campbell JK. Penzien DB. Wall EM, Evidence-based guidelines for migraine headache: behavioral and physical treatments. April 25, 2000. http: // www.aan .com /professionals/ practice/pdfs/g 10089.pdf. Accessed January 2011. Gatchel RJ Turk DC (Eds.): Psychosocial Factors in Pain. New York: The Guilford Press, 1999. Hart RP. Martelli MF. Zasler ND., Chronic pain and neuropsychological functioning. Neuropsychol Rev, 10(3):131-149, 2000. Hart RP. Wade JB. Martelli MF: Cognitive Impairment in Patients with Chronic Pain: The Significance of Stress. Current Pain and Headache Reports. 7:116-226. 2003. Kröner-Herwig B., Chronic Pain Syndromes and Their Treatment by Psychological Interventions. Curr Opin Psychiatry, 22(2):200-204, 2009. Kundermann B. Krieg JC. Schreiber W. Lautenbacher S., The effect of sleep deprivation on pain. Pain Res Manag, 9(1):25-32, 2004. Lake AE, Behavioral and nonpharmacologic treatments of headache. Med Clin North Am, 85(4):1055-75, 2001. Mahmood O. Rapport LJ. Hanks RA. Fichtenberg NL., Neuropsychological performance and sleep disturbance following traumatic brain injury. J Head Trauma Rehabil, 19(5):37890, 2004. Martelli MF Nicholson K Zasler ND: Psychological Approaches to Comprehensive Pain Assessment and Management Following TBI. In: Brain Injury Medicine: Principles & Practice. ND Zasler DI Katz RD Zafonte (Eds.) Demos, New York. Pages 723-742, 2007. Martelli MF Nicholson K Zasler ND Bender MC: Assessment of Response Bias in Clinical and Forensic Evaluations of Impairment Following Brain Injury. In: Brain Injury Medicine: Principles & Practice. ND Zasler DI Katz RD Zafonte (Eds.) Demos, New York. Pages 1183-1204, 2007. Martelli MF. Zasler ND. Nicholson K. Bender MC., Psychological, neuropsychological and medical considerations in the assessment and management of pain. J Head Trauma Rehabil, 19(1):10-28, 2004. Merskey H Bogduk N (Eds.): Classification of Chronic Pain. 2nd Ed. Seattle: IASP Press, 1994. Mooney G. Speed J. Sheppard S., Factors related to recovery after mild traumatic brain injury. Brain Injury, 19(12):975-87, 2005. Nicholson K Martelli M. The confounding effects of pain, psychoemotional problems or psychiatric disorder, premorbid ability structure, and motivational or other factors on neuropsychological test performance. In Psychological Knowledge For Court: PTSD, Chronic Pain and TBI. G Young A Kane K Nicholson (Eds.) Springer, New York, NY. Pages 335-351, 2006. Nicholson Kl Martelli MF., The problem of Pain. J Head Trauma Rehabil, 19(1):2-9, 2004. Pilcher JJ. Huffcutt AL., Effects of sleep deprivation on performance: A meta analysis. Sleep, 19:318–326, 1996. Porro CA. Baraldi P. Pagnoni G, et al., Does anticipation of pain affect cortical nociceptive systems? J Neurosci15;22(8):3206-14, 2002. Rains JC. Penzien DB. McCrory DC. Gray RN., Behavioral headache treatment: history, review of the empirical literature, and methodological critique. Headache, May;45 Suppl 2:S92-109, 2005. Ruff RL. Ruff SS. Wang XF., Improving sleep: initial headache treatment in OIF/OEF veterans with blast-induced mild traumatic brain injury. J Rehabil Res Dev.; 46(9):1071-84, 2009. Thorn BE. Pence LB. Ward LC. et al: A randomized clinical trial of cognitive behavioral treatment targeted at the reduction of catastrophizing in chronic headache sufferers. Journal of Pain, 68(12), 938-949, 2007. Wager TD. RillingJK. Smith EE., et al., Placebo-induced changes in FMRI in the anticipation and experience of pain. Science, 303:1162-1167, 2004. Zasler N.D Horn LJ Martelli MF Nicholson K: Post-Traumatic Pain Disorders: Medical Assessment and Management. In: Brain Injury Medicine: Principles & Practice. ND Zasler DI Katz RD Zafonte (Eds.) Demos, New York. Pages 697-722, 2007. Zasler ND Martelli MF: Post-traumatic headache: Practical approaches to diagnosis and treatment. In Pain Management: A Practical Guide for Clinicians, 6th edition. : RB Weiner (Ed.). St. Lucie Press, Boca Ratan, FL. Pages 125-138, 2002.

About the Authors

Michael F. Martelli, PhD, directs Rehabilitation Neuropsychology at Tree of Life, a residential & transitional neurorehabilitation facility. He has 25 years of experience providing specialized, holistic assessment & treatment services, academic appointments, a diplomate in pain management, serves on editorial review and brain injury related boards, is a past President of the Brain Injury Assoc. of VA & has written & lectured widely in areas of rehabilitation, psychology, neuropsychology, pain and disability. E-mail: Keith Nicholson, PhD, is a psychologist with extensive clinical experience working with many different patient populations. He obtained his Ph.D. in Clinical Neuropsychology from the University of Victoria and, since then, has worked at the University Health Network in Toronto, Ontario in addition to working at several community clinics and maintaining a private practice. He has particular interest in the psychology of chronic pain and clinical neuropsychology. E-mail:



Osteopathic Issues in Post-traumatic Headaches: A Neurological Perspective

bY Edward R. Isaacs, MD, FAAN

Headaches following cranial/head trauma can originate from within the central nervous system but more often the source of the pain will be from the musculoskeletal structures of the thoracic and cervical spine (Gorbis, 2006), the cranium and even occasionally from the lumbosacral spine. There remains ongoing debate regarding the use of osteopathic manipulative techniques, primarily because of the inability to satisfactorily demonstrate long lasting effectiveness either by double blind, or outcome studies. Without citing all of these numerous studies, they remain limited by using pain reduction as the criteria for a successful outcome (Mlor, 2001) and (Gross et al, 2010), while failing to further define what specific musculoskeletal dysfunctions are being treated and by what techniques other than labeling them as “OMT” (Osteopathic Manipulative Therapy) or “spinal manipulation” (Bronfort, et. al, 2001). It would be best if a complaint was further described with a specific structural diagnosis that defines the actual motion restrictions between vertebrae, followed by specific treatments to correct these restrictions, and then review any changes in the initial complaints. 18 BRAIN INJURY PROFESSIONAL

At the least, these techniques can be considered as part of a theoretical construct from which more specific musculoskeletal diagnoses can be made and to then provide clinically useful and appropriate treatment options (DeStephano 2011).

Headaches of Cervicothoracic Origin

Any injury to the head that is capable of causing headache is usually coupled with flexion-extension or side bending injuries to the cervical and thoracic spine. After the acute phase of the “soft tissue” injuries, persistent injury patterns remain and can be identified by observing localized motion loss between individual spinal segments in the cervical and thoracic spine. These restrictions are the consequence of persistent muscle imbalances of the smaller muscles responsible for motion between individual vertebrae and a shortening of associated supportive connective tissue structures that influence individual zygapophyseal joint function. The ability for these joints to glide apart or open for flexion and to approximate or close for extension is the basis for a structural diagnosis that de-

fines these motion restrictions. Side bending occurs when the ipsilateral zygapophyseal joint closes and the contralateral one opens. Furthermore, if side bending is introduced while the vertebra is in the flexed or extended position, there is a coupled rotational motion of the superior vertebra rotating it in the same direction as the side bending, around the zygapophyseal joint that has closed. If a zygapophyseal joint is restricted from closing, then extension will be restricted at that level, and when attempted the vertebral body will rotate in the same direction toward the other zygapophyseal joint that can still close. Flexion restrictions will cause the vertebra to rotate to the side of the zygapophyseal joint that will not open completely when the spine is flexed. If both zygapophyseal joints are symmetrically restricted there will not be a rotational component. If the restrictions are asymmetrical there will be still be a rotational component with rotation around the joint that is capable of further closure. If one zygapophyseal joint is restricted from opening and the other from closing, the rotation will not change between the flexed or extended positions as it would if the joint open/closed positions become symmetrical. For example, if the left joint will not open then the vertebra will rotate left when the spine is flexed, but it will de-rotate when the spine is extended and both left and right zygapophyseal joints have closed. Similarly if the left zygapophyseal joint cannot close, the vertebra will rotate right when the spine is extended and de-rotate when the spine flexes and both left and right joints are open. In addition to the changes noted by motion testing, segments that are restricted are also identified by a sense of hardness in the overlying tissues that can be palpated that is different from the tissue texture overlying unrestricted segments. Persistent abnormal motion between vertebrae is a functional representation of the spinal injury and will be unilateral if the injury is more one sided or bilateral if a more midline impact is experienced. Through muscular and ligamentous attachments the mechanics of the upper five thoracic vertebrae have a profound effect upon cervical spinal mechanics and in fact one can consider normal neck motion to occur between the occipital-cervical junction and the 5th thoracic vertebra. Thoracic spine motion is limited by rib attachments, which can be viewed as extensions of the transverse processes of the vertebral bodies allowing the interaction between the ribs and the thoracic spine to be observable both anteriorly and posteriorly. Thoracic spine restrictions for flexion or extension not only influence the mechanics of the cervical spine but also the motion of the rib cage for either inhalation, exhalation or both, and as a cause for chest wall pain. Rotation of the cervical spine between C3 and C7 is always coupled with side bending in the same direction as the rotation (Ishii et al, 2004). The motion at C1-C2 is almost purely rotational. Because of the ligamentous attachments and unique anatomical shape of the articulation at the occipital-cervical junction, rotation of the occiput is always coupled by its side bending in the opposite direction in relation to C1. This reversed coupling serves to keep the eyes level when the head rotates. Pain from musculoskeletal structures originates from mechanical stimulation of nocicpetive nerve fibers (Cusick et al, 2001). Ligamentous structures overlying restricted, dysfunctional joints are tender but, because motion is restricted, mechanical distortion of these nociceptors does not occur during normal movement. Therefore, even though these joint regions are tender they are probably not the pain generators. The spinal adaptation for a restricted segment is hypermobility of the still normal joints, permitting a continued more normal overall range of motion elsewhere. These hypermobile zygapophyseal joints can locate at the same segment,

at adjacent segments or at more distant locations and are probably the true pain generators since the nociceptors at these sites are susceptible to mechanical distortion from the increased mobility. Treating the pain by identifying locations that are concordant with the pain complaint makes less sense if these concepts are valid, and the lasting improvement achieved by the successful practitioner using osteopathic techniques, suggests that they are. Headaches originating from cervical and thoracic structures often begin at the occiput and then migrate, with increasing pain, into frontal and temporal regions. Associated neck pain is often an added component to this headache. The spinal restriction causing these headaches is primarily for extension and localized at least to T3 and T1. When the upper cervical complex is involved, especially at the occipital- cervical junction, the head pain is often described as being behind the eyes. The pain is often steady but increases in intensity as an aching or pressure-like sensation which when intense may be associated with nausea, vomiting and photophobia. The pain may also “throb� and be asymmetrically more intense on one side. With appropriate osteopathic manipulative treatment, these restrictions can be removed and normal motion and posture becomes possible again, often with a consequent reduction in pain both in the head and neck.

Headaches of Lumbosacral Origin

There is a connection between the cranium and the sacrum defined by synchronized motion between the occipital bone and sacrum by the dural coverings of the brain and spinal canal with attachments to the cranium, thoracic spine and sacrum. If there is a strain to the lumbosacral junction, and a subsequent loss of motion between L5 and the sacrum, and at one of the sacroiliac joints, there can be an associated, asymmetrical tension within the Cranio-sacral system. The resultant head pain is derived from distorted nociceptors within in these supporting structures and is often described as a constant, generalized aching which may be more intense frontally. Normally L5 can rotate and flex and extend in a direction opposite to the sacral base or S1. When there is a bend and twist type injury straining this junction, abnormal non-adaptive mechanics can persist and the ability to extend at this level is lost. This injury can also occur in motor vehicle accidents when the seated position (bent) is reversed and rotated (twist) by an impact from the behind and accompanies injury patterns to the cervical and thoracic spine and head. Once these dysfunctions are identified by physical examination of the spine and cranium, appropriate osteopathic treatment can be very effective in reducing both the back pain and the associated headache.

Headaches of Cranial Origin

There has been an extensive body of work developed by our osteopathic colleagues that concern the motion characteristics of the cranium that is also reflected throughout the musculoskeletal system (Magoun 1966; Gehin 1985). Basic to the concept of the craniosacral system is the observation of a very subtle palpable movement of the cranium that can be described as an internal and external rotation of lateral structures and a craniad-caudad motion of the midline structures. The cranial sutures are actually articulating joints, that allow for the expansion (external rotation) and contraction (internal rotation) of the cranial vault. Key to this motion is the flexibility of the junction between the occipital and sphenoid bones which permits the craniad-caudad motion. One of the generators for this motion is thought to be the consequence of the production of spinal fluid which increases intracranial pressure expanding the cranial vault followed by the opening of the arachnoid villae and the decompression of the vault as spinal fluid siphons back into the veBRAIN INJURY PROFESSIONAL


nous system. These oscillations occur at frequencies between eight and fourteen cycles/ minute and can be palpated throughout the musculoskeletal system between breaths. An identical pattern of motion occurs with inhalation and exhalation. Inhalation while expanding the chest causes an external rotation of the limbs and extension through the spinal axis while exhalation promotes spinal flexion and internal rotation of the extremities. These basic coupled motion patterns are responsible for a particular involuntary motion of the sacrum between the ilia which in a normal state would move synchronously with the occipital bone. Cranial motion is also influenced by the tension within the intracranial dural membranes. Cranial compressions can be the source of chronic tenderness and pain in a fashion similar to other joint restrictions in the axial skeleton. Specialized treatment techniques have been successful in restoring normal cranial motion by freeing restricted sutures and when appropriately applied provide another means of reducing or eliminating the pain following skull trauma. Localized pain can result when trauma directly compresses the skull at individual sutures thereby distorting the normally symmetrical cranial rhythmic movements. Compression can also be an indirect result of increased muscle tension from overlying muscles origination from the cranium or from cervical attachments. Both cervical spine dysfunction and compression of the temporal-occipital sutures are components of temporomandibular joint pain. Loss of motion at the sphenobasilar junction can severely affect cranial motion and cause rather profound generalized headaches. Loss of normal nasal bone motion at the frontal/nasal suture line from a direct frontal impact can be the source of frontal pain associated with a loss of normal frontal bone motion that can be relieved using a cranial technique of gently distracting the nasal bones with thumb and index finger of one hand and the orbital ridge with the finger tips of the other hand.

uses a follow-up examination to determine if that motion has been restored. If the restoration of normal motion within the spinal axis and cranium results in a reduction and elimination of the head pain from a traumatic event, then there was an added benefit to the intervention. If there was no change in the complaint then it is unlikely that the abnormalities that were identified and successfully treated by restoring normal motion were also the source of the problem causing the pain. Rather than typifying the success or failure of a treatment in the general sense, manipulative techniques need to be considered as an appropriate treatment option for an individual situation. An accurate diagnosis is most often the result of an analysis of data derived from a complete history and physical examination. Without additional post doctoral training most physicians are not able to perform the kind of musculoskeletal examination that is capable of defining the localized specific dysfunctions that have been described here. This is a significant handicap for anyone who hopes to fully understand and treat individuals with these problems.

The Goal of Osteopathic Manipulative Techniques


Although the reduction of head pain is the outcome most sought after response to any intervention directed at this complaint, successful manipulative treatment should first be determined by the ability to demonstrate a restoration of normal motion and not the reduction of pain. Osteopathic manipulative techniques are based upon a physical examination that defines a specific motion loss and then after a physical intervention, 20 BRAIN INJURY PROFESSIONAL


Gorbis, S. Cervical Mobilization in Post Traumatic Headache/ Cervicalgia. January 01, 2006 Mlor, S. Manipulation and mobilization in the treatment of chronic pain. Clin J Pain 17 (4 Suppl): S70-6, 2001 Gross, A., Miller J., D’Sylva, J. et al. Manipulation or mobilisation for neck pain: A Cochrane Review. Man Ther 15 (4):315-33, 2010 Bronfort, G., Assendelft. W. J. J., Evans, R. et al.: Efficacy of Spinal Manipulation for Chronic Headache: A Systematic Review. J Manipulative Physiol Ther 24; 457-466. September 2001. DeStephano, L: Greenman’s Principles of Manual Medicine, 4th Ed. Philadelphia: Wolters Kluwer/ Lippincott Williams & Wilkins, 2011. Cusick, J.F., Pintar, F.A., and Yoganandan, N. Whiplash Syndrome: Kinematic Factors Influencing Pain Patterns. Spine; 26:1252-8. June 2001 Gehin A. Atlas of Manipulative Techniques for the Cranium and Face. Seattle: Eastland Press, 1985. Isaacs, E. M.D. or D.O.: Is that a Question? Triad Quarterly Publication of the Michigan Osteopathic Association 2009. Ishii, T., Mukai, Y., Honsono, N., et al. Kinematics of the Subaxial Cervical Spine in Rotation In Vivo Three-Dimensional Analysis. Spine. 29 (24)2826-2831, December 15, 2004 Magoun HI. Osteopathy in the Cranial Field. 2nd Ed. Kirksville, MO: Journal Printing Co., 1966.

Edward R. Isaacs, MD, FAAN, is a board certified neurologist with additional training and expertise in osteopathic manipulative techniques. Dr. Isaacs practices musculoskeletal medicine in Richmond, Virginia and is regarded as an expert in manual medicine treatments for post-traumatic pain disorders including headache. The author has had the privilege of participating in a series of continuing medical education courses offered by Michigan State University, College of Osteopathic Medicine and participating as an active faculty member in these same courses since 1988 while continuing a very active clinical practice incorporating and advancing these skills. E-mail:

conferences 2011 APRIL 7-10 – 20th Annual Multi-Disciplinary Conference, Atlanta, GA. For more information, visit www. MAY 5 - 6 – Rehabilitation of the Adult and Child with Traumatic Brain Injury: Practical Solutions to Real-World Problems, May 5 - 6, Williamsburg, VA, USA. For more information, visit 21 – Johns Hopkins Traumatic Brain Injury A National Conference: From Impact to Recovery, May 21, Baltimore, MD. For more information, visit aspx/80026209. 24-25 – The 5th Annual National Brain Injury Employment Conference, Denver, CO. For more information, please visit JUNE 13-15 – Federal Interagency Conference on Traumatic Brain Injury, Washington, D.C. For more information, visit July 10-13 – The 29th Annual National Neurotrauma Symposium, including the AANS/CNS Section on Neurotrauma & Critical Care, Fort Lauderdale, FL. For more information, visit 12 - 14 – Brain Injury in Children, July 12-14, Four Seasons Hotel in Toronto, Ontario, Canada. For more information, visit AUGUST 24 -26 – Brain Injury Association of Canada Annual Conference, August 24-26, Charlottetown, PEI, Canada. For more information, visit www. SEPTEMBER 14-17 – 23rd Annual Conference on Legal Issues in Brain Injury, New Orleans, LA. For more information, visit 14-17 – 8th Annual Conference on Brain Injury, New Orleans, LA. For more information, visit www.


JANUARY 9 -11 – 2012 Brain Injury Summit - A Meeting of the Minds, January 9 -11, Beaver Creek, CO. For more information, visit www.braininjurysummit2012. org. MARCH 21-25 – Ninth World Congress on Brain Injury, Edinburgh, Scotland. For more information, visit This is the official World Congress of IBIA.



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Physical Therapy Interventions For Musculoskeletal Dysfunction Related to Post-Traumatic Headache

by Tracey Adler, DPT, OCS, CMTPT


Post-traumatic headaches, or PTHA, occur following traumatic brain injuries (TBI), closed head injuries (CHI) and cervical whiplash injuries. Due to various definitions and methods of study the incidence of post-traumatic headaches following these types of insults has been described as occurring in 15 to 80 percent of those individuals (Packard, 1999; Faux, 2008, Nampiaparampil, 2008). In addition to headaches, patients experience dizziness, fatigue, disruption of sleep, and anxiety among other symptoms. There remains debate as to the true incidence of the various types of post-traumatic headache. According to Lew et al (2006), the most common types of headaches following traumatic brain injury include tension-type headaches and migraines; however, if the injury includes a whiplash, it is more likely that the cervical spine will also be involved (Packard, 2002). Whiplash injuries may cause a cervicogenic headache, musculoskeletal headaches, temporomandibular disorder (TMD), and tensiontype headaches (Freund, 2002; Rachlin, 2002). In a study by Freidman M.H. et al (2002), three hundred patients that had suffered a whiplash injury and subsequent temporomandibular joint internal derangements, presented with trigger points in the masseter muscles. Physical therapists evaluate and treat musculoskeletal injuries and can play an integral part in the management of many patients with post-traumatic headaches. Over the years, specialty areas of physical therapy have evolved. Those therapists, who have had additional training in musculoskeletal evaluations, trigger point identification, and manual therapy techniques, will most likely 22 BRAIN INJURY PROFESSIONAL

have a higher treatment success. There are several advanced certifications available, for physical therapists that become proficient in orthopedics, manual therapy, and trigger point dry needling. The American Physical Therapy Association offers a Orthopedic Certified Specialist (OCS) exam. Additionally, physical therapists may be certified through the North American Institute of Orthopaedic Manual Therapy (NAIOMT) and/or The American Academy of Orthopaedic Manual Physical Therapists (AAOMPT). The National Association of Myofascial Trigger Point Therapist (NAMTPT) certifies physical therapists in trigger point dry needling that have completed rigorous course work including a written and practical exam.

Physical Therapy Evaluation

As with many other kinds of soft tissue injuries, no outward signs of dysfunction may be noticed or observed in persons with PTHA. Additionally, imaging of the cervical and/or thoracic spine and/or shoulder may not yield information that explains the symptoms of the patient with PTHA. An adequate history exploring what might intensify the headache, what positions relieve or aggravate the headache, and what other associated symptoms occur is essential. Questions regarding the mechanism of injury, description of pain character (ie. sharp, dull, achy, burning, tingling, numbness), associated symptoms, pain constancy, and/or pain intensity levels on the VAS (visual analogue scale) are all highly relevant areas of inquiry. Past medical history information regarding previous injuries and surgeries, completes the puzzle.

A thorough physical therapy evaluation includes range of motion measurements (ROM), strength testing of the upper and lower extremities and neurological testing for deep tendon reflexes in the elbows, wrists, knees and ankles. Assessment of posture includes, forward head, protracted shoulders, scoliosis and excessive lordosis or kyphosis. Questions related to activities of daily living and work duties shed light on possible repetitive activities that may be perpetuating some of the symptoms. The range of motion evaluation should include spinal, glenohumeral, and jaw mobility. Palpation of the muscles in the surrounding area that are responsible for referring pain into the head and neck region include the upper trapezius, sternocleidomastoid, suboccipitals, temporalis, frontalis, masseter, and the splenius capitis and cervicis muscles. Additional muscles that may not specifically refer headache pain, but are typically irritable in these individuals, include the scalenes and levator scapulae muscles (Fernandez, 2010; Baldry,2005). Distribution of pain referred from these muscles includes the suboccipital region from the upper trapezius and pain in the forehead region, around the eye, the top of the head, and the posterior skull, from the sternocleidomastoid muscle. Supra-orbital pain and pain imitating temporomandibular joint dysfunction is referred from the masseter muscle. Temporal headaches may be triggered from the temporalis muscle. Posterior orbital (also called retro-orbital) pain is referred from the splenius cervicis. Pain in the vertex of the head, as well as vice-like pain, emanate, from trigger points in the splenius capitis and can easily be confused with tension type headache pain. The short suboccipital muscles, including rectus capitis posterior major and minor and the oblique inferior and superior, produce a less defined and vague headache (Travell, 1983). Associated complaints may include dizziness, blurred vision, and pain when hair brushing. Even after what appears to be a minor injury, musculoskeletal symptoms may cause severe limitations in activity and mobility, along with paralyzing pain. The primary goals of physical therapy treatment should be determining the musculoskeletal source of pain, reproducing the symptoms, and treating the structures responsible for referring the pain.

Referred Myofascial Pain

Referred pain from trigger points is a commonly overlooked source of PTHA. Travell and Simons (1983) have demonstrated referral patterns from upper quarter and cervical muscles that radiate into the occipital region, superior skull region, orbital region, and facial region. In addition to referring pain, trigger points in the sternocleidomastoid muscle can cause dizziness, vertigo, and ptosis of the eye which can mislead the less sophisticated clinician into thinking that there was a brain injury related cause for these symptoms/findings. Trigger points, the source of referred pain from the muscle, differ from tender points. Trigger points are defined as nodules in the muscle within a taut band. The criterion for indentifying a trigger point includes referred pain, tenderness, and a twitch when palpated. Tender points do not exhibit these characteristics. Tender points may exist along with trigger points, however, to properly treat the areas of referred pain the active trigger points must be deactivated. Evaluation should include a progressive (i.e., from superficial to deeper layers) palpatory exam of not only the posterior cervical musculature, but also the anterior cervical and shoulder girdle muscles to determine the exact sources of referred pain. Often times, inadequate palpatory skills and/or inadequate attention to a

detailed exam result in spurious conclusions of the absence of soft tissue pathology. Since temporomandibular disorders (TMD) are a source of headaches following a traumatic event, the jaw and muscles of mastication require evaluation (Rachlin, 2002). During the evaluation questions regarding pain related to eating, chewing or talking are essential to determine any sort of related TMD symptoms. According to Freund and Schwartz (2002), more than 75% of patients that presented to their center with TMD had associated head and neck complaints. Although TMD may begin with micro-trauma, such as bruxing and clenching, macro-trauma such as a TBI, CHI or cervical whiplash must be considered when evaluating these individuals. Even without a previous history of TMD, the individual may develop symptoms indirectly related to poor posturing, due to pain following these types of injuries. Cervico-cepahlic pain patients may begin clenching and bruxing as a result of stress related to chronic pain and headaches. Additionally, headaches that are bitemporal in location and reported upon awakening typically suggest nocturnal bruxing. Lastly, trigger points in the masseter and pterygoid muscles are known to refer pain into the jaw and facial region.

Treatment Techniques

Following a thorough evaluation and adequate reproduction of symptoms to correlate the source of pain, numerous techniques are used by physical therapists to reduce painful symptoms, increase range of motion, and improve posture. Analyzing a patient’s workstation and posture that is perpetuated by either pain or specific activities is essential. Keeping the neck in a neutral position, so as to not overwork the anterior cervical muscles and over stretch the posterior cervical muscles, is the goal of posture exercises and improved ergonomic workstations. Modalities to decrease pain, muscle spasm, and inflammation, include electrical treatments, such as a TENS unit, interferential, and muscle stimulation. Additionally, ultrasound, cold laser, and spray and stretch directed at specific trigger points may be effective. Ice, heat, and specific exercises are also part of the rehabilitation to decrease inflammation, increase mobility, increase flexibility, and strength. Cold laser is a relatively new modality and is believed to decrease inflammation on a cellular level (Rachlin,2002). Spray and stretch techniques consist of using a vapocoolant spray, placing the muscles in an elongated position, and directing the spray at a 30 to 60 degrees angle over the area to be treated (Travell,1983; Rachlin,2002). All treatments are aimed at deactivating the trigger points that are causing referred pain and limiting ROM. On occasion, excessive stretching of an area with trigger points can increase the intensity of the individual’s symptoms. Hands-on treatments for decreasing trigger points and referred pain, include manual therapy techniques such as myofascial release, muscle energy, strain/counterstrain, and soft tissue mobilization. These techniques require skilled palpation, assessment, and treatment of the mechanical position of the spine, as well as the integrity of the soft tissue. Myofascial release techniques, muscle energy, and soft tissue mobilization are all direct techniques that address limitations in the skin, fascia, and muscle. Normal play between the muscles and fascia is essential for freedom of movement without pain. Fascia is connective tissues that cover organs and muscle. Similar to joints allowing bones to articulate, fascia allows muscle to glide on muscle. Following an injury or prolonged immobility, restrictions develop in the fascia. Several theories regarding the exact mechanism have been proposed. (FernanBRAIN INJURY PROFESSIONAL


dez, 2010) The physical therapist uses a gentle pressure, through the layers of muscle and fascia, to restore mobility of the soft tissues. Muscle energy techniques address the mechanical aspects of pain and limitation of motion, and use gentle muscle contractions to normalize the positioning of the affected joint. Strain/ counterstrain technique, which is an indirect technique, works by shortening the affected muscles to decrease the pain/spasm cycle. This soft tissue technique focuses on releasing tender points by approximating origin and insertion of a muscle and holding the position for 90 seconds. Dr. Lawrence H. Jones, DO, developed this latter treatment technique in 1955.

Trigger Point Dry Needling

A treatment technique that is relatively new to physical therapists in the United States is trigger point dry needling. This technique has been used in Europe and Canada for over twenty years by physical therapists. Presently, in the US, there are 18 states and the District of Columbia that have determined that trigger point dry needling is within the scope of physical therapy practice (Dommerholt, 2011). Trigger point dry needling is most effective when utilized by a physical therapist with excellent palpation skills in order to treat the appropriate areas. It is a skill that requires additional training and a certification test in some states. This technique uses small solid needles that are placed into the trigger point that has been identified following the criteria stated earlier. No medicine is injected and a twitch response is elicited to confirm the existence and location of the trigger point. In 2005, Shah et al, investigated trigger point biochemical milieu using a hollow acupuncture needle. He found that active trigger points possessed high levels of substance p, serotonin, and norepinephrine. Furthermore, he demonstrated that the pH level of the trigger point was always lower than areas without trigger points. According to Shah’s 2005 study, after a local twitch response occurred, the biochemical milieu returned to normal as did the pH level.


Post-traumatic headaches often have a musculoskeletal component but in order to diagnose these contributors an adequate history and exam are necessary. Patients with PTHA should be evaluated by a physical therapist for posture related issues, limitations of motion, and musculoskeletal dysfunction, including trigger points. Referred pain from trigger points in the face, jaw, neck, upper quarter, and anterior/posterior cervical region are frequently involved. Traditional physical therapy treatment, such as exercise, modalities, and manual therapy techniques may help to alleviate some or all of the headache symptoms. In addition to traditional physical therapy treatment, trigger point dry needling into the active trigger points that are referring pain may serve as a valuable adjunct to more traditional treatment (Dommerholt, 2011; Fernandez, 2010). A recent search of the literature, by this author for physical therapy treatment of PTHA, did not produce any results. Controlled prospective randomized studies to further determine the effectiveness of trigger point dry needling and physical therapy treatments in general in patients with PTHA are clearly needed. References

Baldry, PE: Pain in the Head and Face. In: Acupuncture, Trigger Points and Musculoskeletal Pain. Elsevier Churchill Livingstone UK. Pgs: 251-274, 2005. Dommerholt J; Huijbregts P: Myofascial Trigger Points – Pathophysiology and Evidence – Informed Diagnosis and Management. Boston: Jones and Bartlett Publishers, 2011. Faux S, Sheedy J. A Prospective Controlled Study in the Prevalence of Post-traumatic Headache Following Mild Traumatic Brain Injury Pain Medicine. Vol 9. No. 8 p. 1000-1011, 2008.


Fernandez DE Las Renas C; Aprdent-Nielsen A; Gerwin RD Tension-Type and Cervicogenic Headache – Pathophysiology, Diagnosis, and Management. Boston; Jones and Bartlett Publishers, 2010. Freund B. Schwartz M. Post-Traumatic Myofascial Pain of The Head and Neck Current Pain and Headache Reports 6:361-369, 2002. Friedman MH, Weisberg J: The Craniocervical Connection: A Retrospective analysis of 300 Whiplash Patients With Cervical and Temporomandibular Disorders. Cranio 18 (3):163-167, 2000. Lew HL, Lin P-H, Fuh J-L, et al. Characteristics and Treatment of Headache after Traumatic Brain Injury – A Focused Review Am.S. Physical Medical Rehabil. Vol. 85(7):619-627, 2006. Nampiaparampil DE: Prevalence of Chronic Pain after Traumatic Brain Injury. A Systematic Review JAMA. 300(6):711-719, 2008. Packard RC The Relationship of Neck Injury and Post-Traumatic Headache. Current Pain and Headache Reports. 301-307, 2002. Rachlin, ES; Rachlin, IS: Myofascial Pain and Fibromyalgia – Trigger point Management. St. Louis Mosby, 2002. Shah JP et al: An in Vivo Microanalytical Technique for Measuring the Local Biochemical Milreu of Human Skeletal Muscle. J. Appl Physical. 99 p. 1977-1984, 2005 Travell, JG; Simons, DG: Myofascial Pain and Dysfunction – The Trigger Point Manual, Baltimore: Williams and Wilkins, 1983.

Web Resources Referenced APTA NAIOMT AAOMPT NAMTPT

About the Author

Tracey Adler, DPT, OCS, CMTPT, is a physical therapist with over thirty years of experience evaluating and treating people with musculoskeletal dysfunctions and has extensive experience dealing with post-trauma pain disorders including PTHA. Throughout her career, she has treated individuals with chronic pain using manual therapy techniques and since 2002, trigger point dry needling. She started her private practice in Richmond, Virginia in 1984. She is on the faculty of Myopain Seminars. E-mail:

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Application of the Bradford-Hill Criteria for Assessing Specific Causation in Post-Traumatic Headache by Michael D. Freeman, PhD, MPH, and Sean S. Kohles, PhD

Introduction Post-traumatic headache (PTH) is a difficult condition to evaluate epidemiologically because of variations in presentation, evaluation, definition, and pathogenesis. While it is readily accepted that patients with direct head trauma may develop persisting headache (and approximately 15% of patients with mild head injury have PTH at 3 months), headache is also a prominent feature of neck injury resulting from whiplash trauma.1, 2 To confuse matters further, the classical and most common cause of whiplash trauma, a rear impact collision, results in potentially injurious loads to both the neck and the head. Because PTH is often allegedly due to the negligence of another individual (as with a rear impact collision) there is often polarization of expert opinions regarding the most probable cause of the headaches. A treating clinician will most typically take a history from the patient, and if they have new headache complaints that they did not have prior to the injury event then an attribution of causation is made. An expert who is retained by an insurer or other party defending a claim of injury may find in the pre-trauma history of the patient prior complaints of headaches, and thus conclude that the onset of the headaches only coincided with the trauma, and that the trauma did not alter the natural history of the headaches. Fact finders such as judges and juries are thus left at an evidentiary impasse, without a standard by which to compare the validity of the conflicting opinions. A large part of this difficulty is the lack of general familiarity amongst clinicians with the standards of epidemiologic (general) causation, and how they may be systematically applied in cases of specific (individual) causation. The purpose of this paper is to describe these criteria and how they may be used in a forensic setting to evaluate disputed causation in a case of alleged posttraumatic headache. Causation Generally, the cause of a disease or injury event is an event or condition that preceded the disease or injury and without 26 BRAIN INJURY PROFESSIONAL

which the disease or injury would not have occurred (at the time at which it occurred). In the current era, a practical approach to causation was described in a systematic fashion by Hill in 1965 with a list of nine criteria that could be evaluated for determinations of epidemiologic causation.3, 4 The Hill Criteria have served as the seminal basis from which virtually all subsequent systematic approaches to general (population) and specific (individual) causation have been derived, including those for a variety of injuries such as traumatic brain injury,5 carpal tunnel syndrome,6 needle stick injuries7 and spinal disk injuries,8 among others. Hill’s original nine criteria are briefly summarized as follows: 1. Strength of association – A strong association is more likely to indicate a causal relationship than is a modest or weak association. Strength of association is generally considered to be the most important determinant of causation. Most simply stated, a strong association is more likely to indicate a causal relationship than is a modest or weak association.4 In specific causation, strength of association is determined by the lack of more probable alternative or competing explanations. 2. Consistency – The repetitive observation of a causal relationship in different circumstances strengthens the causal inference. 3. Specificity – In general causation, specificity refers to the degree to which a factor is associated with a particular outcome or population. Specificity has value in specific causation when it’s present, but a lack of specificity does not imply lack of causation. 4. Temporality – the potential causal factor must precede the outcome it is assumed to affect, and the outcome cannot either occur before it is physiologically feasible or after too great of a latency period. Temporality is the one factor that must always be present in general and specific causation. 5. Biological gradient – The injury outcome increases proportionately with increasing dose of exposure (also known as

dose-response). 6. Plausibility – For both general and specific causation, plausibility refers to the degree to which the observed association can be explained by known scientific principles. Hill did not put much weight in plausibility, having commented that a hypothesized disease cause that is thought to be implausible today may be found to be plausible at some time in the future as a result of new scientific inquiry. The plausibility criterion is met when there is a lack of established implausibility (impossibility). For example, a brain tumor found on CT scan the day of a head trauma and loss of consciousness is implausibly related to the trauma. A common error in specific causation is to consider a rare outcome to be the same as an implausible outcome. 7. Coherence – A causal conclusion should not fundamentally contradict present substantive knowledge – it should “make sense” given current knowledge. Experiment – In some cases there may be evidence from randomized experiments on animals or humans, although in most cases of injury there will not. 8. Analogy – An analogous exposure and outcome may be translatable to the circumstances of a previously unexplored causal investigation.

Application of Hill Criteria to Post-traumatic Headache For practical determinations of specific causation of PTH in a forensic setting (cause and effect in individuals as evaluated for a legal matter) Hill’s criteria can be grouped into 2 major categories: criteria that answer the question “could the exposure have caused the disease or injury outcome in this case?” and those that answer the question “did the exposure cause the disease or injury outcome in this case?” To this end, Hill’s criteria can be grouped into three subcategories, as follows:9 Biologic Plausibility – This criterion is meant to demonstrate whether or not the exposure could have caused the disease or injury outcome, regardless of how often, and is an amalgam of Hill’s plausibility, coherence, consistency, specificity, biologic gradient, analogy, and experiment criteria. No single factor must be present to establish biologic plausibility, which simply means that the probability of a cause and effect cannot be said to be 0 (that it is implausible). In applying the criteria that comprise biological plausibility to the evaluation of the relationship between persisting headaches and trauma, the first question that often arises is whether there is an injury force threshold for PTH. The epidemiologic concept of the asymptote, that there is no way to know at what point the nth most fragile member of the population falls on an injury risk versus traumatic force plot, dictates that implausibility cannot be concluded for virtually any degree of forceful loading of the head as a possible cause of PTH. The conclusion begs the question (for some) as to whether a light tap on the head with a finger can cause PTH, and the answer is almost certainly not, but then again such a question would not arise in a forensic setting. For most clinicians, the recognition of the potential for injury of a described traumatic event in a patient’s history is something like the well known quote of US Supreme Court Justice Potter Stewart regarding the definition of obscenity, that one “knows it when one sees it.” With no reliably established injury thresholds for mild traumatic brain injury/PTH the prevailing standard for judging plausibility is clinician common sense (the coherence criterion referred to by Hill). Further, because of the lack of implausibility for PTH and vir-

tually any traumatic head loading scenario, there is no need for the clinician to be able to quantify head loading forces in order to make an evaluation of plausibility in evaluating causation of PTH. As a result a post hoc biomechanical analysis of an injury mechanism may be helpful to fully describe how an injury occurred, such an analysis cannot be useful in a determination as to whether an injury occurred. Temporality – This criterion is the first step in establishing whether a biologically plausible exposure resulted in a case of PTH. Each case must be evaluated individually, but as a general rule, the headaches must start after the trauma and within a reasonable amount of time. In the case of a head trauma with a loss of consciousness, for example, a delay of one year from the last symptoms of head injury and the development of headaches would not be in keeping with a reasonable period of latency for PTH. A careful history of the nature of the headache with regard to intensity, distribution, frequency, and duration both following and, if necessary, preceding a trauma is critical to determining if there has been a substantive change in a patient’s history that is temporally associated the trauma. Strength of Causal Association – This is the final step in determining whether an exposure caused an injury or disease outcome in which the risk of the condition relative to the suspected exposure is compared to the competing risk of the condition had the exposure not occurred, and given the timeframe of the exposure. If a competing traumatic exposure has taken place then a comparison of dose may be appropriate, and the temporal relationship of the competing exposure must be compared to that of the exposure that is under investigation. Often, the only other explanation for an injury or disease outcome aside from a suspected exposure is the coincidental onset of the condition (the probability the condition was going to occur at the same time regardless of the injury exposure). The temporal relationship between a traumatic exposure and the development of PTH becomes the most important factor in evaluating the strength of the causal association between the two. This is primarily because the closer the temporal relationship between trauma and development of symptoms the lower the probability that another unknown or unseen cause has coincidentally intervened. The simplest way to think of this relationship is to consider a light that is controlled by one of 5 switches in 5 different rooms. For the example we can say that we are in room #1, and when we switched the light switch to the on position the lights immediately turned on. The natural conclusion would be that this was the switch with the causal relationship to the light, and the reason for the conclusion would be that the close temporal relationship between the action and the outcome reduced the probability that someone in rooms 2 through 5 also switched their light switch at the exact same moment as us. If we switched the light switch and there was a 5 second delay before the lights came on we may still think that we have the causal light switch, but we would be less certain, and this certainty would rapidly evaporate as the latency between the action and the light turning on increased. The same relationship exists with causal determinations of PTH relative to the timing of a traumatic exposure. In the patient who develops PTH within a matter of hours to days of a head trauma, unless the patient is a frequent and chronic headache sufferer prior to the trauma, the temporal proximity is such that a coincidental onset of headache is far less probable than is a causal relationship between the injury and the PTH. In cases in which there is a greater period of latency between the trauma BRAIN INJURY PROFESSIONAL


and the onset of headache more scrutiny is required to assess the probability of coincidence, with particular attention paid to precrash history of headache. The question the practitioner must ask is “had the trauma not occurred, would I have predicted that these headaches would be present regardless?” Unless this question can be answered yes then the trauma is the most probable cause.

Conclusion Determinations of cause and effect in cases of headache following trauma need not be a matter of blind belief, but rather a systematic approach can be employed to justify a conclusion that a causal relationship is or is not present, given the facts in a case, and focusing on the temporal relationship between the trauma and the onset of the headaches. References 1. 2. 3. 4. 5.

6. 7.



Faux S, Sheedy J. A prospective controlled study in the prevalence of posttraumatic headache following mild traumatic brain injury. Pain Med. 2008 Nov;9(8):1001-11. Crutebo S, Nilsson C, Skillgate E, Holm LW. The course of symptoms for whiplash-associated disorders in Sweden: 6-month followup study. J Rheumatol. 2010 Jul;37(7):1527-33. Hill AB. The environment and disease: association or causation? Proc Roy Soc Med 1965;5:295-300. Morabia A. On the origin of Hill’s causal criteria. Epidemiology 1991; 2:367-369. van Reekum R, Streiner DL, Conn DK. Applying Bradford Hill’s criteria for causation to neuropsychiatry: challenges and opportunities. J Neuropsychiatry Clin Neurosci. 2001;13(3):318-25. Lozano-Calderón S, Anthony S, Ring D. The quality and strength of evidence for etiology: example of carpal tunnel syndrome. J Hand Surg Am. 2008;33(4):525-38. Batty L, Holland-Elliott K, Rosenfeld D. Investigation of eye splash and needlestick incidents from an HIV-positive donor on an intensive care unit using root cause analysis. Occup Med (Lond). 2003;53(2):147-50. Freeman MD, Centeno CJ, Kohles SS. A systematic approach to clinical determinations of causation in symptomatic spinal disk injury following motor vehicle crash trauma. PM R. 2009;1(10):951-6. Freeman MD, Rossignol AC, Hand M. Forensic Epidemiology: A systematic approach to probabilistic determinations in disputed matters. J Forensic Legal Med 2008;15(5):281-90.

About the Authors

Michael Freeman, PhD, MPH, is a Forensic and Medical Epidemiologist specializing in the application of probability and epidemiologic data to forensic venues. He serves as an Affiliate Professor of Epidemiology at Oregon Health and Science University School of Medicine, Department of Public Health and Preventive Medicine. Dr. Freeman is also an Adjunct Associate Professor of Forensic Medicine and Epidemiology at the Institute of Forensic Medicine, Faculty of Health Sciences, University of Aarhus, Denmark. Dr. Freeman has more than 100 published scientific papers, books, and book chapters on forensic applications of epidemiology, crash-related injuries and death, general and specific causation, and a variety of other areas of interest. Dr. Freeman is an associate editor of The Spine Journal, the journal of Physical Medicine & Rehabilitation (PM R), and the Journal of Forensic Biomechanics. He has served in US, Canadian, European and Australian courts, applying the principles of forensic epidemiology to a variety of disputed matters including injury and death litigation, product liability, toxic tort litigation, tobacco litigation, medical negligence, and has served as both prosecution and defense expert in a number of homicide cases. E-mail: Dr. Kohles, PhD, is a Research Associate Professor at Portland State University and an Adjunct Associate Professor at the Oregon Health & Science University. He completed a doctoral degree in Bioengineering and bachelors/masters degrees in Engineering Mechanics all at the University of Wisconsin-Madison. He has published over 170 journal and conference papers in the areas of cell, tissue, joint, biomaterial, implant, and forensic biomechanical engineering and serves on the Editorial Boards for the Journal of Biomechanics and the Annals of Biomedical Engineering. He has maintained funding for his research from the National Science Foundation, the National Institutes of Health, and private foundations. He has trained over 1,100 students in lecture-based settings and 122 students during individualized project-based design/research experiences. These students have won awards from the American Society of Mechanical Engineers, the American Society of Biomechanics, the Sigma Xi Scientific Honor Society, and great jobs. E-mail: 28 BRAIN INJURY PROFESSIONAL

In Memoriam ~ Dr. Jane Gillett Dr Jane Gillett passed away on Wednesday February 16, 2011. Jane was the Medical Director of the Acquired Brain Injury Program at Hamilton Health Sciences and an Associate Professor at McMaster University. Jane was the Founder and President of the International Paediatric Brian Injury Society (IPBIS) and developed the Paediatric Acquired Brain Injury Community Outreach Program (PABICOP) in London, Ont. Because of her tireless advocacy for youths with neurological disorders, PABICOP is known and duplicated in many other countries. Jane was also the founder and first president of the International Paediatric Brain Injury Society (IPBIS).Following are some of the comments from her friends around the world.

“Jane was a wonderful blend of strong and sensitive who could see the big picture yet always relate warmly to the individual. Her PABICOP “flower” model showed great respect for the child and family as the center point yet recognized the key importance of the community that surrounds them. She has always been willing to see brain injury rehabilitation as a collaborative team process, all coming together to help the child and family. Though we will miss her dearly, her legacy will live on and children will be better for it.” Gerard Gioia, USA “Jane’s flower model is, in fact, a living legacy of someone who was a wonderful colleague and an effective advocate. I am sure her family is surrounded by flowers, however none so lovely as the one she crafted for the children of the world.” Joe Tepas, USA “Jane was a rare flower, the kind that opens up in surprising ways. Being informal when others were strict, being generous in a way that passed it on to the rest of us. Clear in mind, turning complicated into easy.” Catherine Aaro Jonsson, Östersunds, Sweden “The first time I met Jane she was rushing; busily organising numerous activities at once. It was the same whenever I saw her subsequently in a work setting, which was just characteristic of her drive, determination and impatience to achieve so much. This is why she was so successful in her aims of improving the lives of young people with acquired brain injury and their families and she was an inspiration to us all. Then, there was the other Jane, who was such fun to be with and a generous and relaxed host with an infectious smile. She will be sadly missed but we will attempt to continue the work of IPBIS as she would have wanted.” Beth Wicks, United Kingdom “From our first meeting in NYC at the Sarah Jane Brain Foundation advisory board inception, through the extra work she put in to get the first draft of the PABI plan completed, to her participation in our Sports Concussion symposium at last fall’s Child Neurology Society meeting, it was always a pleasure to talk and work with her. We’ve lost a friend and colleague, but the effort that she championed for kids with brain injuries goes on!” Chris Giza, USA “Jane was worldwide known as a true expert in pediatric brain injury. In Holland her PABICOPproject has always been an inspiring example for Dutch workers in the field of pediatric brain injury. Jane has always been a true motivator of our efforts to replicate the PABICOP model in Holland. Only a few years ago she was the keynote speaker on a Dutch congress and a few hundreds of professionals were impressed by her vision, her passion and her eloquence. Holland will never forget Jane”. Eric Hermanns, Netherlands

“She loved chocolate, wine, cats, dogs, music and mostly people. She was passionate, whip-smart and forever cheering on the people she cared about. Jane was truly collaborative, both as a doctor and a leader in the brain injury community, and it is very telling that many of her colleagues have become her close friends. Jane nurtured each of her relationships carefully, and then introduced us all to each other.” We stand on the shoulders of giants and these larger than life individuals come into our lives for differing amounts of time and reasons. Jane came for too short of a time. While here, she was our philosopher, thinker, planner, innovator, writer, organizer, mentor and incredible friend. Who else would write a prescription for potato chips for a teen with low sodium! She is gone. However, her work will live on in all who were touched by her. Our future is bright because of her willingness to share her knowledge and skills freely. We can carry her hopes forward, but what we will never be able to duplicate is her amazing ability to always select a perfect bottle of wine! We miss you Jane.

“The idea for an international paediatric brain injury society (IPBIS) emerged over dinner in a restaurant in Lisbon with Jane, Eric Hermanns, myself and Dianne Henderson. With Jane’s drive and motivation it soon became a reality, with Jane as President. This is just one example of how Jane made things happen and her wonderful ability to bring people together. She was always so positive and quick to find solutions and new ways of doing things. She was a true inspiration and motivator of others, we shall miss her so much, and will endeavour to achieve her vision for IPBIS.” Carol Hawley, United Kingdom “Jane was the one who invited me into the international circle of colleagues and friends working with ABI. Her way of doing this was characterized with never ending kindness, friendship and a wish that everybody would share and spread their knowledge among each other. In IPBIS this took a more organized form and it has been such an interesting and rewarding experience to be part of it. With Jane’s role as the one that gathered people together combined with her experience and enthusiasm it felt so natural that Jane should be our first president. For us in Sweden her work with PABICOP has also been an important source of inspiration. Ingela Kristiansen, Sweden “Jane truly represented the best that medicine and humanity can offer as both a physician and friend. As a colleague, her loss pushes me to do more. As a friend, her loss leaves a void and she will be remembered with love and respect. “ Deborah M. Little, USA

To read more tributes to Jane Gillett, visit BRAIN INJURY PROFESSIONAL


bip expert interview Dr. Russell Packard Dr. Russell Packard graduated from the University of California, Irvine with an M.D. in 1971. He then did a year of Internal Medicine Internship, a Psychiatry Residency and then a Neurology Residency, all at US Navy Facilities. He subsequently became Board Certified in both Psychiatry and Neurology. He was the Director of a Headache and Head Injury Clinic in Pensacola, Florida until 2000, when he joined the faculty at Texas Tech University as a Professor of Psychiatry and Neurology until 2005. He was Professor of Neurology and Vice Chair of the Department of Psychiatry at the University of North Texas until 2007, when he decided to reenter private practice in Palestine, Texas. He is a Fellow of the American College of Physicians and the American Academy of Neurology. He has written over 100 professional papers and chapters in his career, mainly on headache and head injury. He was presented with Awards for Excellence in Neurologic Education from Texas Tech and the American Academy of Neurology in 2003, and was chosen as one of America’s Top Physicians in 2009. Good afternoon Dr. Packard this is Dr. Nathan Zasler. I’m looking forward to interviewing you regarding the topic of “Post-traumatic Headache” (PTHA) given your clinical background in this area of post-TBI care and your historical contribution to the scientific literature in this area. I have a number of questions I’d like to go over with you today, so if you’re ready to go, I’m sure the readers of “Brain Injury Professional” will be interested in your thoughts and insights. Where do you see our knowledge relative to post-traumatic headache, relative to what it was a decade ago? Well, I think now there is more acceptance that there really are mild traumatic brain injuries, concussions and headaches that result from those injuries. I know 10 years ago there were battles about whether mild traumatic brain injury and concussion were even real entities, but I think since concussion in sports and combat injuries have come to the front over the past 10 years or so it has brought more acceptance to this whole area. Okay… thank you for that thought. Certainly, you would agree that we see post-traumatic headache not just after mild injury, but also after moderate to severe. In terms of the general evaluation of persons with traumatic brain injury who present with complaints of post-traumatic headache, what do you see as the greatest area of deficit in the general medical community? Well, from what I’ve seen there is often an inadequate history from the patient and more of an emphasis on imaging. Consequently, when the imaging is normal, which it most often is, the patient is sometimes told there is nothing wrong with them, even though there clearly is.

physical exam, looking at the types of pain generators that are typically responsible for post-traumatic headache or do you see that as one of the deficits in the context of the typical community physician evaluation for PTHA? I think that has generally been inadequate and I say that because patients that I’ve seen will often say nobody even tested their neck range of motion, felt their neck muscles or head, or looked for trigger points to find the pain generators that are often very obvious when a careful exam is performed. Thank you for those thoughts. My next question, Dr. Packard, is what has been your experience with the way PTHA is treated in the general medical community? I’ve not seen a lot of successful treatments for patients prior to the time that they are referred to me. One of the first things that I usually go over with patients are goals of treatment… not only from my point of view but what are the patient’s goals of treatment? What are they after? If they want a total cure and you are working to make the headaches less frequent and less severe, you may never satisfy the patient. If you get on the same page, where you both are working to make the headaches less frequent and less severe, then I think you will be pretty successful most of the time. Good point. How often do you see migraine as the cause of headache after trauma versus other types of headache disorders that we see post-traumatically such as tension headache, cervicogenic headache, and as related to that, do you find that it makes a difference as far as peoples’ training background (i.e. neurologist vs. physiatrist vs. neurosurgeon) as far as how often they make a diagnosis of a particular type of headache disorder?

I literally see it all the time and I have for years. Or even that the patient is just seeking compensation or malingering.

It is really kind of like the diagnosis of migraine in general because when I see patients referred for headache evaluations, many times, they have already been diagnosed as “sinus,” dental problems or cluster headache, and after a careful history, they have typical migraine. So, the diagnoses really vary. I don’t see very many that I would call pure post-traumatic migraine. What I do see are people who have had migraines and their migraine is aggravated by trauma. I also see people who have a rather typical migraine headache that is mixed in with neck pain and/or a tension headache, and have a pattern of chronic daily headache.

As far as patients that get referred to you from other clinicians, do you typically feel that those patients have undergone an adequate

How about tension headache and cervicogenic headache… in practice, do you see these headache sub-types commonly after trauma?

All too often if people don’t find anything (or at least that is what they conclude), they will diagnose the problem as psychogenic. Do you often see that as a conclusion that is drawn incorrectly by people who don’t take the time to elicit an adequate history, do an appropriate physical exam, and find nothing on the imaging?


I think, very often, there is a tension or muscle contraction headache component to PTHA. From my point of view, most people with just tension type headaches don’t even come into the doctor. They actually take overthe-counter remedies and just go on with life but I do think they are mixed in with posttraumatic headaches a lot. I think there is often a cervicogenic neck component as well to PTHA. As a neurologist, what role do you feel invasive pain management techniques or interventional pain management more specifically, have in treatment of post-traumatic headache, based on your extensive clinical experience with that population? I, personally, have not seen it as being very helpful and, again the population I see often tends to be people who have had those procedures and they didn’t work… so it may be a little bit skewed, but the ones that do seem to get some brief relief usually have the pain return. On the other hand, if there is a fairly specific neck injury that you can pinpoint and somebody can treat that specific area, then I think that they may do better with that type of approach. If it is just an injection because they have a “headache,” they do not seem to be very helpful. Cleary, then, it is important to not just treat the symptom of pain but to try to identify what the pain generator or generators are and treat those more directly. In this context, how much do you think cervical pain generators potentially perpetuate or aggravate other kinds of PTHA such as migraine or tension headache? I think they are a big part actually, even in patients without trauma who come in with a migraine. Migraine patients will often say that their headaches start at the back of their neck or after they’ve had the migraine their neck still hurts. After an injury, I think the neck is often part of that injury and it tends to keep the whole process going in a vicious cycle: neck pain triggers the headache and the headache tightens up the neck muscles. Often times, patients are referred with headache diagnosis labels that are potentially self-prophysizing such as chronic posttraumatic headache or intractable posttraumatic headache because they haven’t responded to prior treatment. Would you agree that physicians who are looking at these kind of patients shouldn’t necessarily be locked into those kinds of labels and should relook at their diagnosis to make sure they were appropriately diagnosed in the first place. The unfortunate thing is that all too often, doctors whip out a prescription pad and write for an opiate…what are your thoughts on that trend? I do agree with that and I have seen many patients referred and the only treatment they have ever had have been opiates and they have never been tried on preventative medicine or trigger point injections or even a trial of physical therapy. It might be helpful for readers to understand the kinds of folks that you see. Do you see a combination of people more acute-

ly and tertiary care referrals with more chronic post-traumatic headache or traditionally more of the latter. I tend to see people who have persistent headaches for weeks or months. I do also get some referrals now of people who have had accidents and go to the emergency room and are referred directly to me, so I think I see more newly injured patients now than I used to, but in general, I still see more that have had their headaches for weeks or months and haven’t improved. In your prior practice setting, you were seeing more chronic cases? Yes. I used to be the director of a headache and head injury clinic both in private practice and at Texas Tech and referrals would often be the most refractory and persistent cases. In general, based on your years of experience, how do you feel patient’s fare relative to prognostically if their diagnosed and treated appropriately? I think they do pretty well. I think I’ve had pretty good success working with this group and I’ve worked with them for a long time, and I think the key is going back to the beginning, like we talked about… getting a good history and exam and identifying the type or types of headache that you want to target your treatment to. I totally concur with that and just to throw my two cents in here. Often times, the current health care system structure doesn’t necessarily lend itself to taking that kind of time with patients and that’s why you end up with people grabbing their prescription pad and writing for an opiate… which is of course covering up the symptom and not addressing the cause. You mention something there that I think is really important and I have often discussed this in talks that I have given. I think the most important thing with these patients is just giving them time, and very often, the patients have stated, “you’re the very first doctor I’ve had that has actually listened to me”. I always appreciate that because I do spend time with them and I think that is very important. I think that is a very salient point to end on because I think that ultimately, we are not practicing the art of medicine if we are not taking the time to elicit an adequate history as you shared with us and get a good physical exam and, ultimately, that the art of touch, which you eluded to, and people not even touching their patients might seem surprising to some people reading this, that you have many clinicians that aren’t even examining patients but, unfortunately, that does happen and I think your point is very well made there as far as taking the time in doing so. I’d like to thank you on behalf of myself, as the editor of this issue, as well as our readers of “Brain Injury Professional” for taking the time to talk with me today. Thank you very much Dr. Packard. BRAIN INJURY PROFESSIONAL


non-profit news North American Brain Injury Society

The North American Brain Injury Society will hold its annual meeting on September 14-17, 2011, at the InterContinental Hotel in New Orleans, Louisiana. An educational planning committee comprised of nationally recognized multidisciplinary leaders from the brain injury field is currently developing an integrated educational program that promises to be of interest to researchers, clinicians, administrators and other professionals working with persons with brain injury and their families. Brain injury professionals are encouraged to submit their original research for possible presentation at the conference. All accepted abstracts will be published in the Journal of Head Trauma Rehabilitation. NABIS values presentations that highlight current and best practices, including information that compliments the conference’s topical themes including: basic research (animal and human), medical/clinical research (including acute care and rehabilitation), and post acute care (including education, life-long living and vocational issues). Also encouraged are innovative approaches to brain injury assessment, treatment, intervention, rehabilitation, advocacy and public policy initiatives. In addition to the invited speakers and the oral and poster presentations, the conference will feature a special pre-conference workshop on how to design, develop and implement a comprehensive cognitive rehabilitation program. This unique full-day session will focus on practical activities that can be used in the rehabilitation of attention, visual processing, information processing, memory and executive functions. Also, incorporated into the main conference program, will be focused sessions addressing the critical and growing issue of blast injury and TBI. The highlight of these sessions will be a one half day discussion panel for professionals working with blast induced brain injured military and non-military personnel. ACBIS training will also be available on-site. For more information, please visit www.

Brain Injury Association of America

BIAA and its affiliates celebrate Brain Injury Awareness Month in March, with the focus on concussions: “A concussion is a brain injury. Get the facts.” Brain Injury Awareness Day takes place on Capitol Hill on March 16, 2011. Go to for more information. 32 BRAIN INJURY PROFESSIONAL

Media coverage featuring BIAA as a resource increased substantially due to the TRICARE cognitive rehabilitation issue and the tragic shooting of Rep. Gabrielle Giffords. BIAA contributed to a front-page USA Today story on March 2, about access to a continuum of care following brain injury. The BIAA board approved its 2011 slate of officers: Chair Gregory J. O’Shanick, M.D.; Chair-elect James S. Misko, Psy.D.; Vice Chair for Finances & Records James F. Humphreys, Esq.; and Vice Chair for Program Outcomes Virginia (Ginny) Lazzara, RN, BSN, CRRN. More than 80 people attended this year’s Brain Injury Business Practice College, “Sharing Exemplary Strategies to Ensure Access to Quality Health Care,” which was held in February in San Antonio. This interactive program included a number of speakers, as well as smaller roundtable discussions and case study breakouts. In other news, BIAA adopted a new definition of TBI. Dr. Brent Masel, president and medical director at the Transitional Learning Center at Galveston, Texas, was named BIAA’s National Medical Director. Susan Connors was appointed by the National Association of Insurance Commissioners (NAIC) as a consumer liaison representative. Go to for details.

Defense Centers of Excellence

In January 2011, Navy Capt. Paul Hammer became the new director of the Defense Centers of Excellence for Psychological Health and Traumatic Brain Injury (DCoE). Capt. Hammer, a psychiatrist, previously served as director of the Naval Center for Combat and Operational Stress Control at the Naval Medical Center (NCCOSC), San Diego, Calif. DCoE’s mission is to assess, validate, oversee and facilitate prevention, resilience, identification, treatment, outreach, rehabilitation and reintegration programs for psychological health and traumatic brain injury (TBI) to ensure the Defense Department meets the needs of the nation’s military communities, warriors and families. To meet those needs, DCoE has launched many initiatives, including its monthly webinar series. DCoE will host an online webinar titled “Mild TBI and Co-Occurring Disorders” March 24 at 1 p.m. (EST). The webinar will provide an overview of the relationship between mild TBI and co-occurring disorders commonly seen with mild TBI. To register

for this online learning event, or for more information on the DCoE Monthly Webinar Series, contact DCoE.MonthlyWebinar@ DCoE also recently published the Winter 2011 edition of the “Military TBI Case Management Quarterly Newsletter.” This newsletter is aimed at sharing best practices, resources and ideas specifically for the Military TBI Case Management COI (Community of Interest). The newsletter is available for download at Case managers interested in joining the military TBI Case Management COI should contact Sue Kennedy at Susan.Kennedy.CTR@tma. For more information about DCoE, please visit and www.


To date over 30 international associations and professional societies have provided their official endorsement of the International Brain Injury Association’s Ninth World Congress on Brain Injury. This biennial event will be held March 21-25, 2012, in the historic city of Edinburgh, Scotland. Progress continues to be made in the planning of the Congress; international and local planning committees have been established, comprised of some of the leading experts in brain injury research and rehabilitation. The oral and poster abstract submission categories are being revised and expanded for the Congress to accommodate the significant increase in scientific submissions enjoyed at the previous two events in Lisbon, Portugal, and Washington, DC. The Congress will be relevant to professionals who work with people with acquired brain injury and will provide a forum for education, formal and informal discussion and debate. Up to date research will be presented on a variety of topics ranging from neurobiology to neurorehabilitation and from the theoretical to the applied. The IBIA awards will be presented, including the Jennett & Plum Award for Clinical Achievement in the Field of Brain Injury Medicine, the Henry Stonnington Award for best review article in Brain Injury, the IBIA Young Investigator Award and the Car of the Year Award. IBIA will have a host of exhibitors to complement more formal aspects of the conference and to encourage collegial networking. Edinburgh, the capital of Scotland, is a picturesque historic city, dominated by its famous castle with many fine hotels, restaurants, museums and traditional

“Imagine my joy when I was able to move back home again...” pubs! There is easy access to Glasgow, the Highlands and to tourist and sporting opportunities. A number of social events will be organized, including a post-congress excursion to Glasgow, that will give attendees the opportunity to explore the depth and breadth of Scottish culture and the beautiful scenery of Scotland. The abstract submission system will open in April, 2011. Please visit for more details.

National Association of State Head Injury Administrators

The National Association of State Head Injury Administrators (NASHIA) is pleased to announce that it has engaged the services of Rebeccah Wolfkiel as its Government Relations Consultant. She is replacing Jean E. Bérubé, Esq., who is assuming a new position as the Legislative Liaison for the National Center for Complementary and Alternative Medicine (NCCAM) at the National Institutes of Health (NIH). Rebeccah, who is a Sr. Government Relations Specialist with the Ridge Policy Group, worked on Capitol Hill for over six years where she served as Legislative Director to Congressman Todd R. Platts, co-chair of the Congressional Brain Injury Task Force. She has worked most extensively in the health care, education, energy, and national security fields. During her tenure on the Hill, Rebeccah became keenly aware of the importance of bipartisanship and developed strong Congressional relationships with Republicans and Democrats alike. She often bridged partisan gaps and facilitated communication between contrasting view points. The Ridge Policy Group brings over 28 years of policy and political experience to its clients. The firm also employs former senior aides to Tom Ridge, who also have vast experience at the state and federal levels, overseeing every aspect of government programs, policies, and budgets. Tom Ridge was first elected to the U.S. Congress in 1982, served as the Governor of Pennsylvania (19952001), and was the nation’s first Homeland Security Secretary, serving from 2003- 2005. Plans are finalized for the annual Congressional Brain Injury Task Force (CBITF) Awareness Day, scheduled for Wednesday, March 16, 2011, on Capitol Hill in Washington, DC. A schedule, as well as additional information about contacting your representative and senators for those who wish to make Hill visits is available at NASHIA’s website:

- Mike Tarry

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Services include: • Physical, occupational, speech, language and cognitive therapies and psychological counseling • Case management • Medical services including on-site nursing, neurological, physiatricand psychiatric treatment • Vocational services from sheltered employment through to community placement • Residential services on a main campus, in community group homes and supported community apartments • Outpatient services

A COMMUNITY-INTEGRATED BRAIN INJURY PROGRAM An affiliated service of Woods Services, Inc • Program Locations in PA 1-800-782-3299 • 215-750-4299 • Beechwood does not discriminate in services or employment on the basis of race, color, religion, sex, national origin, age, marital status, or presence of a non-job related medical condition or handicap.



legislative roundup “A billion here and a billion there, and soon you’re talking about real money.” Everett Dirksen US Senate Minority Leader (from 1959 - 1969)

The 112th Congress convened in January, with the US House of Representatives changing leadership as the result of the Republicans winning the majority of seats during the November election. Immediately, the new leadership announced its intentions to cut spending, starting with its own House. As the previous Congress failed to pass spending bills to fund federal governmental programs through September 30th, the end of the current fiscal year, legislators passed a Continuing Resolution (CR) to fund government through March 4th at level funding, meaning the same level as the previous year (FY 2010). On February 12th, the House proceeded to pass a CR extending funding through September 30th, with around $61 billion cuts to discretionary programs, including the full elimination of the Corporation for National and Community Services (-$1 billion); the supported employment State grants (-$28 million) and Projects with Industry; as well as a significant cut to the Maternal and Child Block Grant of $50 million. The House adopted amendments to defund the health care law, including an amendment to ban all payments to “any employee, officer, contractor, or grantee of any department or


agency” to implement the law. The Senate, however, balked at this drastic measure, so a compromise was made to cut $4 billion to this year’s budget and fund government through March 18th. Discussions are taking place as to how much can be cut from the current budget. Meanwhile, the President has released his budget proposals for FY 2012, which starts October 1st, and his proposed budget eliminates or trims more than 200 programs and reduces the deficit by $1.1 trillion over the next decade. Two-thirds of the savings would come from cuts to domestic spending. In keeping with the health reform law, the Affordable Care Act, the US Department of Health and Human Services recently announced $4.3 billion in new funds to help establish and expand community-based alternatives to institutional long-term care through the Money Follows the Person (MFP) demonstration and the Community First Choice option program. Thirteen states will together receive more than $45 million in MFP grants to start the program in their states. Under the Community First Choice Option, which will start in October, all states will have opportunity to access a potential $3.7 billion in increased federal funding to provide long-term services and supports through the program. States would receive a six percent increase in federal matching funds for serving Medicaid eligible individuals with disabilities in a community setting, in accordance with a erson-centered plan. Concussion prevention, education and management continues to be a priority for members of Congress. In January, Rep. Timothy H. Bishop (D-NY) introduced H.R. 469, the Protecting Student Athletes from Concussions Act of 2011, requiring each state educational agency to issue regulations establishing minimum requirements for the prevention and treatment of concussions in order to be eligible for federal education

funds. The bill also requires each local educational agencies to develop and implement a standard plan for concussion safety and management that includes: (1) the education of students, parents, and school personnel; (2) supports for students recovering from a concussion; and (3) best practices designed to ensure the uniformity of safety standards, treatment, and management. Public school personnel who suspect that a student has sustained a concussion during a schoolsponsored activity would be required to: (1) remove the student from the activity and prohibit such student from participating in school athletic activities until the student submits a written release from a health care professional; and (2) report to the student’s parent or guardian regarding such injury and the treatment provided. As March is Brain Injury Awareness month, the Congressional Brain Injury Task Force will sponsor Brain Injury Awareness Day on March 16th, which will feature a Fair, a briefing of national experts on rehabilitation and research, and a reception. The Fair provides an excellent opportunity for federal agencies and national organizations to provide information on brain injury research, prevention, treatment and reintegration programs and supports. The Fair is held in the Foyer of the Rayburn House Office Building. Equally important, is that state and local organizations also promote awareness activities during this time around the country. Anyone interested in helping is certainly welcome to join forces. About the Editor

Susan L. Vaughn of S.L. Vaughn & Associates, consults with states on service delivery and serves as the Director of Public Policy for the National Association of State Head Injury Administrators. Ms. Vaughn retired from the State of Missouri after nearly 30 years, where she served as the first director of the Missouri Head Injury Advisory Council. She founded NASHIA in 1990, and served as its first president.

Real Challenges, Real Outcomes, Real Life Learning Services’s programs are designed to provide specialized support for adults with brain injuries in a real life setting. All of our programs are equipped to maximize each resident’s quality of life as they take on the challenges of a brain injury. Our approach supports outcomes by offering individuals the tools necessary to live life on their terms. •

Neurobehavioral Rehabilitation

Residential Rehabilitation

Supported Living

Therapeutic Day Activities

To learn more about our programs nationwide, call 888.419.9955, or visit



from focus comes excellence •









Craig Hospital in Denver is dedicated exclusively to specialty rehabilitation and research for people with

spinal cord injury and traumatic brain injury. Craig is committed to helping rebuild lives after catastrophic injury — and to unsurpassed clinical outcomes,

patient and family satisfaction, and financial value for the insurance industry and society.

As an international leader in the field, Craig

consistently serves more than 1,700 inpatients and

outpatients from 47 to 50 states each year. Craig is

federally designated by NIDRR as a Model Systems Center for SCI and TBI, and is the NIDRR TBI National Data and Statistical Center. Craig has been ranked in the Top 10 Rehab Hospitals for 21 years — every year since the rankings began in 1990, and is one of only a few Magnet® Recognized rehabilitation hospitals

in the U.S.

The success of our patients is due to Craig’s focused expertise and resources, remarkable longevity of staff

and physicians, large patient milieu, family services and on-site housing, financial stability, and an upbeat culture of contagious caring and compassion.

As a non-profit, independent hospital governed by a volunteer board of directors, the Craig “family” is

dedicated to delivering the highest quality of rehabilitation treatment available anywhere. Ask anyone who has ever been associated with Craig Hospital and you’ll receive a consistent answer: Craig is a very special place.

3425 South Clarkson Street | Englewood, Colorado 80113 | 303-789-8000 |

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January 9-11, 2012 | Beaver Creek, CO | brought to you by Craig Hospital

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