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REVIEWAcupuncture for Posttraumatic Stress Disorder: Conceptual,Clinical, and Biological Data Support Further ResearchMichael HollifieldThe Behavioral Health Research Center of the Southwest, Albuquerque, NM, USA; The Department of Psychiatry and Behavioral Sciences, University ofLouisville School of Medicine, Louisville, KY, USA; The Department of Family and Community Medicine, University of New Mexico School of Medicine,Albuquerque, NM, USA; The Institute for Stress Medicine at Sage Neurosciences, Albuquerque, NM, USAKeywordsAcupuncture; Anxiety disorders; Mechanisms;Posttraumatic stress.CorrespondenceMichael Hollifield, M.D., The Behavioral HealthResearch Center of the Southwest, 612 EncinoPlace N.E., Albuquerque, NM 87202, USA.Tel.: (505) 765-2322;Fax: (502) 244-3408;E-mail: mhollifield@bhrcs.orgdoi: 10.1111/j.1755-5949.2011.00241.xSUMMARYPosttraumatic stress disorder (PTSD) is common, debilitating, and has highly heterogeneousclinical and biological features. With the exception of one published preliminary clinicaltrial, rationale in support of the efficacy of acupuncture, a modality of Chinese medicine(CM), for PTSD has not been well described. This is a focused review of conceptual and clin-ical features of PTSD shared by modern western medicine (MWM) and CM, and of biolog-ical mechanisms of acupuncture that parallel known PTSD pathology. MWM and CM bothrecognize individual developmental variables and interactions between external conditionsand internal responses in the genesis of PTSD. There is one published and one unpublishedclinical trial that preliminarily support the efficacy of acupuncture for PTSD. Although therehave been no mechanistic studies of acupuncture in human PTSD, extant research showsthat acupuncture has biological effects that are relevant to PTSD pathology. Conceptual,clinical, and biological data support possible efficacy of acupuncture for PTSD. However,further definitive research about simultaneous clinical and biological effects is needed tosupport the use of acupuncture for PTSD in health care systems.IntroductionPosttraumatic Stress Disorder (PTSD) is a common and complexillness with high psychiatric and medical comorbidity and impair-ment in daily functioning. Interventions for PTSD are similarlyvaried and have complex mechanisms of action. There is prelim-inary evidence that acupuncture may be an efficacious, safe, andacceptable treatment for PTSD. Efficacy may be due to similari-ties between the known pathology of PTSD and mechanisms ofaction of acupuncture. The stage is set in this article by reviewingthe known epidemiology and pathology of PTSD from a modernwestern medicine (MWM) perspective, which is then comparedand contrasted with a Chinese medicine (CM) perspective. Giventhe wealth of knowledge about PTSD, this review only summa-rizes major findings. Effective treatments are then reviewed. Fi-nally, data are presented showing that acupuncture has effects inbiological systems that are relevant to PTSD. This is not a compre-hensive review of PTSD pathology or mechanisms of acupuncture,nor is the intent to contrast acupuncture with other interventionsor offer “relative worth” of established interventions. Rather, thisreview summarizes the potential value of and need for further re-search about acupuncture for PTSD.Two Perspectives on the Genesis of PTSDMWM’s Understanding of PTSDPTSD is characterized by reexperiencing aspects of the originaltrauma, avoidance and numbing of trauma reminders, and generalhyperarousal [1,2]. Cognitive, emotional, and somatic symptomsother than those defined in the DSM-IV also occur in PTSD suf-ferers [3]. Lifetime prevalence of PTSD in community samples isaround 6.8% [4] and as high as 30% among Vietnam veterans [5]and female victims of rape [6]. Recent Iraq and Afghanistan warveterans have 13–16% PTSD prevalence, dependent on the degreeof combat exposure [7]. The estimated cost for mental health-related expenses in these veterans is $4–6 billion over 2 years[8]. PTSD is heterogeneous by individual variables and develop-mental period during which it emerges, by supposed causal events(trauma exposure), and by the complexity of its comorbidity andknown pathology.Individual VariablesWhat an individual “has” or “brings to” a traumatic experienceare critical determinants of whether or not PTSD will develop.CNS Neuroscience & Therapeutics17(2011) 769–779c2011 Blackwell Publishing Ltd769
Acupuncture for PTSDM. HollifieldAs examples, there are genetic [9], morphologic [10], and so-cial determinants (such as gender, age, and socioeconomic sta-tus) of PTSD [11]. These determinants are interactive. For exam-ple, the social context in which a primate is reared is a determi-nant of long-term morphological changes in stress-sensitive brainareas [12].Unfortunately, young children and adolescents are exposed tovarious traumata. The risk of developing PTSD likely varies bytrauma type, age of exposure, and moderating environmental andgenetic variables. It has become clear that trauma exposure dur-ing early development is a significant risk factor for altered bi-ology, stress reactivity, and later medical and psychiatric illness[13–15]. It is unclear if there are developmental periods duringwhich trauma exposure is more likely to lead to PTSD than otherperiods.Supposed Causal EventsCommon events that comprise traumatic exposure include mo-tor vehicle accidents, natural and human-caused disasters, child-hood abuse and neglect, interpersonal violence, tragic death ofa loved one, witnessing of violence, and war-related events. Ap-proximately 60% of men and 51% of women in the United Statesreport exposure to one or more traumatic event [4]. Trauma ex-posure coupled with a host response involving intense fear, help-lessness, or horror comprises the first, or “A,” criterion of PTSD[1], and is by definition necessary but not sufficient for develop-ing PTSD [16]. Perceptions of threat and psychological prepared-ness also mediate the association of traumatic experience withPTSD [17,18]. Trauma exposure alone is a risk factor for develop-ing distressing symptoms, severe medical/psychiatric illness, poorhealth habits, and decreased life expectancy [19–25]. The risk ofdeveloping PTSD after trauma exposure varies by type of exposure[6,26].ComorbidityPTSD is highly comorbid (83–90%) with other psychiatric disor-ders, including mood, substance use, personality, and panic disor-der [27]. Approximately 50% to 60% of PTSD patients have ma-jor depressive disorder (MDD) [27]. Among veterans with PTSD inprimary care, 87% have one or more comorbid psychiatric disor-der, the most common being depression [28]. Both self-reportedcardiovascular symptoms [29–33] and objectively assessed cardio-vascular diseases [34–37] are more prevalent in PTSD patientsthan in community samples [38]. There is also a higher prevalenceof self-reported arthritis, hypertension and autoimmune diseases[39], diagnosed rheumatoid arthritis, psoriasis or other autoim-mune diseases [40,41], and diagnosed fibromyalgia and irritablebowel disease [31] in PTSD compared to control subjects. Diabetesmellitus is more prevalent in PTSD patients (15%) compared tothose with trauma but no PTSD (9%) and to those with no trauma(6%) [42].Known PathologyPhenomenologically, stress exposure coupled with a host responseof severe fear and/or helplessness defines psychological trauma,which is the manifestation of gene–environment interactionscritical for the genesis of PTSD. Clinicians often observe that itis as if the PTSD sufferer is “stuck” in the “freeze” response, un-able to successfully process the event by fighting or fleeing dan-ger. Thus, perceived threat continues even when the acute dan-ger is no longer present, and stimuli that are reminiscent of thosethat occurred during the trauma (triggers) continue to provokefear and alarm. This state of a frozen stress response, or the fail-ure of processing a traumatic experience, involves multiple bio-logical systems. The known pathology of PTSD thus parallels itscomplex clinical comorbidity. For example, neurological mech-anisms of PTSD, depression, and other anxiety disorders havemany similarities [43,44], and the known genetic variance for de-pression and other anxiety disorders accounts for the majority ofknown genetic variance for PTSD [45]. Major summative find-ings to date indicate a complex pathological state that includesalterations in central nervous system (CNS) processes that influ-ence cognition, emotion, and somatic functioning, hypothalamic-pituitary-adrenal (HPA) axis dysfunction, and autonomic nervoussystem (ANS) dysfunction. Recent work has identified a low-levelproinflammatory state in PTSD that may be a mediator of the in-creased risk for medical illness. There is also a burgeoning liter-ature about the genetics of PTSD that points to polygenetic andgene expression control.The CNSAn expert review identifies the complex and heterogeneous neu-rological response to symptom provocation in PTSD [46]. Sub-stantial corroborative data implicate the medial prefrontal cortex(mPFC) and amygdala as being critically involved in PTSD: manyneuroimaging studies show increased amygdala reactivity– mostlyright sided [47]—and a failure of mPFC and anterior cingulate cor-tex (ACC) activation during traumatic reexperiencing [48]. Theseinterconnected functions are thought to be the neural correlateof the failure of recovery of the stress response that is central toPTSD. The mPFC is also implicated in emotional and cognitiveinteractions involved in fear conditioning, habituation, and en-docrine responses relevant to PTSD [49,50]. However, these func-tions are complex. For example, a recent study concluded thatfocal damage to the amygdala or the ventromedial PFC appearsprotective against the development of PTSD [51], contrary to ex-pectations that such lesions would confer an increased risk due toloss of fear-controlling inhibitory actions on the amygdala. Otherbrain areas are involved in PTSD, such as the subcallosal cortex,rostral and caudal ACC, hippocampus, hypothalamus, insula, andother frontal nuclei, which are integral parts of the limbic systeminvolved in regulating the HPA axis and the ANS.The HPA AxisEssential HPA disturbances in PTSD are low cortisol signaling,increased responsiveness of glucocorticoid receptors, enhanced770CNS Neuroscience & Therapeutics17(2011) 769–779c2011 Blackwell Publishing Ltd