To the Editor: We wish to express a number of concerns aboutthe methods used in the study of mild traumatic brain injuryby Hoge et al. (Jan. 31 issue).1 We learned through firsthandexperience in the combat zone that immediately after a concussion,the soldier's reported account is most accurate during the initial24 hours after the blast incident.2 We therefore would be concernedabout recall bias introduced 3 to 4 months after a return fromdeployment.
In addition, unlike perforation of the tympanic membrane, atransient neurologic event (e.g., a "split-second" loss of consciousness)after a blast incident is not a sentinel finding of direct-blastoverpressure.2 Rather, it is a combination of at least threebiodynamic variables: bodily displacement, direct-blast overpressure(involving intrinsic neural-tissue strains), and cardiopulmonaryinsufficiency.3,4,5
The adverse effects of cardiopulmonary-induced transient neurologicevents (e.g., vasodepressor presyncope) are neither necessarilypermanent nor cumulative, as a result of biologic restorativeprocesses.
Thus, we are concerned that the assessment methods used do notproperly reflect the dimensions of mild traumatic brain injury.Furthermore, we believe that the diagnosis of mild traumaticbrain injury can be made only over time.
Michael S. Xydakis, M.D., Lt. Col. Uniformed Services University of the Health Sciences Bethesda, MD 20814 michael.xydakis{at}usuhs.mil
Anthony S. Robbins, M.D., Ph.D. David Grant USAF Medical Center Travis Air Force Base, CA 94535
Gerald A. Grant, M.D. Duke University Medical Center Durham, NC 27710
The views expressed in this letter are those of the authorsand do not reflect an official position of the Department ofDefense.
References
Hoge CW, McGurk D, Thomas JL, Cox AL, Engle CC, Castro CA. Mild traumatic brain injury in U.S. soldiers returning from Iraq. N Engl J Med 2008;358:453-463. [Free Full Text]
Xydakis MS, Bebarta VS, Harrison CD, Conner JC, Grant GA, Robbins AS. Tympanic-membrane perforation as a marker of concussive brain injury in Iraq. N Engl J Med 2007;357:830-831. [Free Full Text]
Vander Vorst M, Ono K, Chan P, Stuhmiller J. Correlates to traumatic brain injury in nonhuman primates. J Trauma 2007;62:199-206. [ISI][Medline]
Dodd KT, Mundie TG, Lagutchik MS, Morris JR. Cardiopulmonary effects of high-impulse noise exposure. J Trauma 1997;43:656-666. [ISI][Medline]
Young AJ, Jaeger JJ, Phillips YY, Fletcher ER, Richmond DR. Intrathoracic pressure in humans exposed to short duration airblast. Mil Med 1985;150:483-486. [ISI][Medline]
To the Editor: Hoge and colleagues report that traumatic braininjury is strongly associated with psychiatric symptoms (e.g.,depression and post-traumatic stress disorder [PTSD]) that appearto mediate other physical health issues. The study, however,has at least two major limitations. First, subjects were recruitedand examined at a minimum of several months to 1 year aftertraumatic brain injury, making it somewhat difficult to establisha temporal relationship between traumatic brain injury and psychiatricsymptoms.1 Second and more important, the authors do not provideinformation on the soldiers' psychiatric history predating thetraumatic brain injury. Previous studies have shown that significantlylarge numbers of subjects with depression after traumatic braininjury had preexisting depression.2 Alcohol and substance abuseare also risk factors for psychiatric issues after traumaticbrain injury1,3; data regarding these issues are also not includedin the article by Hoge et al.
Rohit R. Das, M.B., B.S., M.P.H. Brigham and Women's Hospital Boston, MA 02115 rohitdas{at}yahoo.com
References
Deb S, Lyons I, Koutzoukis C, Ali I, McCarthy G. Rate of psychiatric illness 1 year after traumatic brain injury. Am J Psychiatry 1999;156:374-378. [Free Full Text]
Jorge RE, Robinson RG, Arndt SV, Forrester AW, Geisler F, Starkstein SE. Comparison between acute- and delayed-onset depression following traumatic brain injury. J Neuropsychiatry Clin Neurosci 1993;5:43-49. [Free Full Text]
Federoff JP, Jorge RE, Robinson RG. Depression in traumatic brain injury. In: Starkstein SE, Robinson RG, eds. Depression in neurologic disease. Baltimore: Johns Hopkins University Press, 1993:139-49.
To the Editor: As an endocrinologist with a special interestin pituitary dysfunction secondary to traumatic brain injury,I question the conclusions drawn in the article by Hoge et al.These authors report that soldiers with traumatic brain injurieshave significantly higher rates of self-reported physical andmental health problems than soldiers with other injuries, andthey imply that many of these symptoms could be related to PTSD.What the authors have overlooked, however, is the idea thatthese symptoms could also be related to hypopituitarism andgrowth hormone deficiency related to head trauma.
Pituitary deficiency occurs in 20 to 50% of patients with traumaticbrain injury1,2,3,4; growth hormone deficiency is common andoften occurs without other deficiencies.1,2,3,4 The psychologicaland neurobehavioral complications after head injury, usuallyattributed to brain damage itself or currently to PTSD, mayin some cases be related to growth hormone deficiency or otherpituitary dysfunction, and treatment could improve the rehabilitationof these patients.2,4 Good clinical practice therefore suggeststhat these patients should at least be screened for pituitarydisease.
Larry D. Stonesifer, M.D. St. Francis Medical Center Federal Way, WA 98003 ldstonesi{at}aol.com
References
Aimaretti G, Ambrosio MR, Di Somma C, et al. Residual pituitary function after brain injury-induced hypopituitarism: a prospective 12-month study. J Clin Endocrinol Metab 2005;90:6085-6092. [Free Full Text]
Agha A, Rogers B, Sherlock M, et al. Anterior pituitary dysfunction in survivors of traumatic brain injury. J Clin Endocrinol Metab 2004;89:4929-4936. [Free Full Text]
Agha A, Phillips J, O'Kelly P, Tormey W, Thompson CJ. The natural history of post-traumatic hypopituitarism: implications for assessment and treatment. Am J Med 2005;118:1416-1416. [Medline]
Kelly DF, Gonzalo IT, Cohan P, Berman N, Swerdloff R, Wang C. Hypopituitarism following traumatic brain injury and subarachnoid hemorrhage: a preliminary report. J Neurosurg 2000;93:743-752. [ISI][Medline]
To the Editor: Hoge and colleagues and Bryant,1 in an accompanyingeditorial, argue for caution in assigning a diagnosis of mildtraumatic brain injury solely on the basis of reported history.The Department of Veterans Affairs (VA) appreciates the importanceof appropriately diagnosing and treating traumatic brain injuryand the mental health consequences of military service, includingPTSD. Military personnel entering the VA system undergo a detailed,multistep screening for traumatic brain injury. The initialstep is a questionnaire. Veterans identified by the initialscreening undergo a second-level evaluation for traumatic braininjury. The evaluation team includes physicians and psychologistswho are trained to detect traumatic brain injury and mentalhealth issues, including PTSD and depression. We evaluate findingsto determine whether they are best attributed to traumatic braininjury, mental health issues, or preexisting conditions. Consequently,although the initial part of the screening process for traumaticbrain injury depends on self-report, the second-level assessmentrelies on physical examination, psychiatric assessment, neuroimaging,and neuropsychological test results. The care of veterans isdirected at treating both physical and mental problems. TheVA aims to return veterans as closely as possible to their precombatstate.
Robert L. Ruff, M.D., Ph.D. Louis Stokes Veterans Affairs Medical Center Cleveland, OH 44106
References
Bryant RA. Disentangling mild traumatic brain injury and stress reactions. N Engl J Med 2008;358:525-527. [Free Full Text]
The authors reply: We agree with Xydakis and colleagues that concussion (i.e., mild traumatic brain injury) can be accuratelydiagnosed only at the time of injury. We remain concerned thatpopulation screening for concussion and postconcussive symptomsmonths after injury will result in unintended iatrogenic effectsfrom misdiagnosis, inconclusive neuropsychological or neuroimagingstudies, costly referrals, or side effects of medication.1,2The letter by Xydakis and colleagues, however, is also an exampleof the circular arguments and speculation about injurious primary-blasteffects that permeate the recent literature about mild traumaticbrain injury.3 The conclusion that "the diagnosis of mild traumaticbrain injury can be made only over time" does not logicallyfollow from the guidance regarding assessment within 24 hoursafter injury. Experimental blast models, such as air shock tubes,do not take into account vehicle and body armor, the high proportionof explosions that occur in open spaces, or the devastatingeffects of fragment dispersion and fire on persons close enoughto be exposed to the primary overpressure wave.4
We agree with the comments by Das on the limitations of ourstudy. However, our study focused on causal inferences at animportant time when screening is becoming routine. If the suspectedpostconcussive symptoms 3 to 4 months after the return fromdeployment were caused by concussions, then we would expectthis association both in soldiers with PTSD and in the largergroup of soldiers without PTSD. This association was not observedin both groups; instead, the physical symptoms were clusteredin the group with PTSD. The likely mechanism pertains to thevery life-threatening context. PTSD is not known to be associatedwith sports-related concussions. Being knocked unconscious froma blast during combat is a life-threatening event that occursin the context of other traumatic events. These experiencescan precipitate stress responses and traumatic memory encodingthat underlie the development of acute stress disorder and PTSD,which, in turn, are strongly associated with generalized symptoms,including those in the "postconcussive" category, through autonomicnervous system and neuroendocrine dysregulation.5
We appreciate Stonesifer's suggestion regarding pituitary dysfunction,but the literature to which he refers pertains almost exclusivelyto moderate or severe traumatic brain injury. We thank Rufffor detailing the multistep screening intervention in VA facilities.We only ask that Ruff consider the assumptions underlying eachstep and use scientific rigor to ensure that the expected risksand costs do not outweigh the hypothesized benefits. The valueof screening would obviously be greater if effective treatmentswere available for concussions identified months after injury.
Charles W. Hoge, M.D. Walter Reed Army Institute of Research Silver Spring, MD 20910 charles.hoge{at}us.army.mil
Charles C. Engel, M.D., M.P.H. Uniformed Services Universityof the Health Sciences Washington, DC 20910
Carl A. Castro, Ph.D. U.S. Army Medical Research and Materiel Command Ft. Detrick, MD 21702
The views expressed in this reply are those of the authors anddo not reflect an official position of the Department of Defense.
References
Iverson GL, Zasler ND, Lange RT. Post-concussive disorder. In: Zasler ND, Katz DI, Zafonte RD, eds. Brain injury medicine: principles and practice. New York: Demos Medical Publishing, 2007.
Wood RL. Understanding the `miserable minority': a diathesis-stress paradigm for post-concussional syndrome. Brain Inj 2004;18:1135-1153. [CrossRef][Medline]
Bhattacharjee Y. Shell shock revisited: solving the puzzle of blast trauma. Science 2008;319:406-408. [Free Full Text]
Wade CE, Ritenour AE, Eastridge BJ, Young LA, Blackbourne LH, Holcomb JB. Explosion injuries treated in combat support hospitals in the global war on terrorism. In: Elsayed NM, Atkins JL, eds. Explosion and blast-related injuries. Amsterdam: Academic Press (in press).
Boscarino JA. Posttraumatic stress disorder and physical illness: results from clinical and epidemiological studies. Ann N Y Acad Sci 2004;1032:141-153. [Free Full Text]
Previous
