Anxiety Disorders: Bracha HS

Bracha HS, Vega EM, Vega CB. · National Center for Posttraumatic Stress Disorder, Department of Veterans Affairs, Pacific Islands Health Care System, Spark M. Matsunaga Medical Center, Honolulu, Hawaii, USA. · Hawaii Dent J. · Pubmed #17152624 No free full text.

Abstract: In this brief review article, we suggest that the term "dental phobia" may be a misnomer. The problem with using the term "phobia" in a dental-care context is as follows: by definition, phobias involve a fear that is "excessive or unreasonable," which the individual recognizes as such, and in which the anxiety, panic attacks and phobic avoidance are not better accounted for by another disorder, including posttraumatic stress disorder (PTSD). In our experience, most individuals with dental "phobia" do not recognize their symptoms as "excessive or unreasonable" and in that sense, resemble individuals with PTSD. Our review of the dental-care literature suggests that true (innate) dental phobias (akin to unreasonable fear at the sight of blood or a syringe) probably account for a smaller percentage of cases, and that the vast majority of dental-care anxiety (DA) cases stem from aversive dental experiences. Research has documented that individuals who reported having experienced painful dental treatments and perceived a lack of control in the dental situation were approximately 14 times more likely to also report higher dental fear, and approximately 16 times more likely to report being less willing to return to the dental treatment. Therefore, we propose that this psychological condition should be conceptualized as Posttraumatic Dental-Care Anxiety (PTDA), and should be classified as part of the Posttraumatic Stress Disorder (PTSD) spectrum in the forthcoming Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-V).

Bracha HS. · Department of Veterans Affairs, Pacific Islands Health Care System, and Department of Tropical Medicine, Medical Microbiology and Pharmacology, John A. Burns School of Medicine, University of Hawaii, Honolulu 96813-2830, USA. · Prog Neuropsychopharmacol Biol Psychiatry. · Pubmed #16563589 No free full text.

Abstract: The DSM-III, DSM-IV, DSM-IV-TR and ICD-10 have judiciously minimized discussion of etiologies to distance clinical psychiatry from Freudian psychoanalysis. With this goal mostly achieved, discussion of etiological factors should be reintroduced into the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V). A research agenda for the DSM-V advocated the "development of a pathophysiologically based classification system". The author critically reviews the neuroevolutionary literature on stress-induced and fear circuitry disorders and related amygdala-driven, species-atypical fear behaviors of clinical severity in adult humans. Over 30 empirically testable/falsifiable predictions are presented. It is noted that in DSM-IV-TR and ICD-10, the classification of stress and fear circuitry disorders is neither mode-of-acquisition-based nor brain-evolution-based. For example, snake phobia (innate) and dog phobia (overconsolidational) are clustered together. Similarly, research on blood-injection-injury-type-specific phobia clusters two fears different in their innateness: 1) an arguably ontogenetic memory-trace-overconsolidation-based fear (hospital phobia) and 2) a hardwired (innate) fear of the sight of one's blood or a sharp object penetrating one's skin. Genetic architecture-charting of fear-circuitry-related traits has been challenging. Various, non-phenotype-based architectures can serve as targets for research. In this article, the author will propose one such alternative genetic architecture. This article was inspired by the following: A) Nesse's "Smoke-Detector Principle", B) the increasing suspicion that the "smooth" rather than "lumpy" distribution of complex psychiatric phenotypes (including fear-circuitry disorders) may in some cases be accounted for by oligogenic (and not necessarily polygenic) transmission, and C) insights from the initial sequence of the chimpanzee genome and comparison with the human genome by the Chimpanzee Sequencing and Analysis Consortium published in late 2005. Neuroevolutionary insights relevant to fear circuitry symptoms that primarily emerge overconsolidationally (especially Combat related Posttraumatic Stress Disorder) are presented. Also introduced is a human-evolution-based principle for clustering innate fear traits. The "Neuroevolutionary Time-depth Principle" of innate fears proposed in this article may be useful in the development of a neuroevolution-based taxonomic re-clustering of stress-triggered and fear-circuitry disorders in DSM-V. Four broad clusters of evolved fear circuits are proposed based on their time-depths: 1) Mesozoic (mammalian-wide) circuits hardwired by wild-type alleles driven to fixation by Mesozoic selective sweeps; 2) Cenozoic (simian-wide) circuits relevant to many specific phobias; 3) mid Paleolithic and upper Paleolithic (Homo sapiens-specific) circuits (arguably resulting mostly from mate-choice-driven stabilizing selection); 4) Neolithic circuits (arguably mostly related to stabilizing selection driven by gene-culture co-evolution). More importantly, the author presents evolutionary perspectives on warzone-related PTSD, Combat-Stress Reaction, Combat-related Stress, Operational-Stress, and other deployment-stress-induced symptoms. The Neuroevolutionary Time-depth Principle presented in this article may help explain the dissimilar stress-resilience levels following different types of acute threat to survival of oneself or one's progency (aka DSM-III and DSM-V PTSD Criterion-A events). PTSD rates following exposure to lethal inter-group violence (combat, warzone exposure or intentionally caused disasters such as terrorism) are usually 5-10 times higher than rates following large-scale natural disasters such as forest fires, floods, hurricanes, volcanic eruptions, and earthquakes. The author predicts that both intentionally-caused large-scale bioevent-disasters, as well as natural bioevents such as SARS and avian flu pandemics will be an exception and are likely to be followed by PTSD rates approaching those that follow warzone exposure. During bioevents, Amygdala-driven and locus-coeruleus-driven epidemic pseudosomatic symptoms may be an order of magnitude more common than infection-caused cytokine-driven symptoms. Implications for the red cross and FEMA are discussed. It is also argued that hospital phobia as well as dog phobia, bird phobia and bat phobia require re-taxonomization in DSM-V in a new "overconsolidational disorders" category anchored around PTSD. The overconsolidational spectrum category may be conceptualized as straddling the fear circuitry spectrum disorders and the affective spectrum disorders categories, and may be a category for which Pitman's secondary prevention propranolol regimen may be specifically indicated as a "morning after pill" intervention. Predictions are presented regarding obsessive-compulsive disorder (OCD) (e.g., female-pattern hoarding vs. male-pattern hoarding) and "culture-bound" acute anxiety symptoms (taijin-kyofusho, koro, shuk yang, shook yong, suo yang, rok-joo, jinjinia-bemar, karoshi, gwarosa, Voodoo death). Also discussed are insights relevant to pseudoneurological symptoms and to the forthcoming Dissociative-Conversive disorders category in DSM-V, including what the author terms fright-triggered acute pseudo-localized symptoms (i.e., pseudoparalysis, pseudocerebellar imbalance, psychogenic blindness, pseudoseizures, and epidemic sociogenic illness). Speculations based on studies of the human abnormal-spindle-like, microcephaly-associated (ASPM) gene, the microcephaly primary autosomal recessive (MCPH) gene, and the forkhead box p2 (FOXP2) gene are made and incorporated into what is termed "The pre-FOXP2 Hypothesis of Blood-Injection-Injury Phobia." Finally, the author argues for a non-reductionistic fusion of "distal (evolutionary) neurobiology" with clinical "proximal neurobiology," utilizing neurological heuristics. It is noted that the value of re-clustering fear traits based on behavioral ethology, human-phylogenomics-derived endophenotypes and on ontogenomics (gene-environment interactions) can be confirmed or disconfirmed using epidemiological or twin studies and psychiatric genomics.

Bracha HS, Ralston TC, Williams AE, Yamashita JM, Bracha AS. · National Center for Posttraumatic Stress Disorder, Dept. of Veterans Affairs, Pacific Islands Health Care System, Spark M. Matsunaga Medical Center, 1132 Bishop Street, Ste, 307, Honolulu, HI 96813, USA. · CNS Spectr. · Pubmed #15788958 links to  free full text

Abstract: This review discusses the clenching-grinding spectrum from the neuropsychiatric/neuroevolutionary perspective. In neuropsychiatry, signs of jaw clenching may be a useful objective marker for detecting or substantiating a self-report of current subjective emotional distress. Similarly, accelerated tooth wear may be an objective clinical sign for detecting, or substantiating, long-lasting anxiety. Clenching-grinding behaviors affect at least 8 percent of the population. We argue that during the early paleolithic environment of evolutionary adaptedness, jaw clenching was an adaptive trait because it rapidly strengthened the masseter and temporalis muscles, enabling a stronger, deeper and therefore more lethal bite in expectation of conflict (warfare) with conspecifics. Similarly, sharper incisors produced by teeth grinding may have served as weaponry during early human combat. We posit that alleles predisposing to fear-induced clenching-grinding were evolutionarily conserved in the human clade (lineage) since they remained adaptive for anatomically and mitochondrially modern humans (Homo sapiens) well into the mid-paleolithic. Clenching-grinding, sleep bruxism, myofacial pain, craniomaxillofacial musculoskeletal pain, temporomandibular disorders, oro-facial pain, and the fibromyalgia/chronic fatigue spectrum disorders are linked. A 2003 Cochrane meta-analysis concluded that dental procedures for the above spectrum disorders are not evidence based. There is a need for early detection of clenching-grinding in anxiety disorder clinics and for research into science-based interventions. Finally, research needs to examine the possible utility of incorporating physical signs into Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition posttraumatic stress disorder diagnostic criteria. One of the diagnostic criterion that may need to undergo a revision in Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition is Criterion D (persistent fear-circuitry activation not present before the trauma). Grinding-induced incisor wear, and clenching-induced palpable masseter tenderness may be examples of such objective physical signs of persistent fear-circuitry activation (posttraumatic stress disorder Criterion D).

Bracha HS. · United States Department of Veterans Affairs, Pacific Islands Health Care System, Spark M Matsunaga Medical Center, National Center for Posttraumatic Stress Disorder, Honolulu, HI, USA. · CNS Spectr. · Pubmed #15337864 links to  free full text

Abstract: This article reviews the existing evolutionary perspectives on the acute stress response habitual faintness and blood-injection-injury type-specific phobia (BIITS phobia). In this article, an alternative evolutionary perspective, based on recent advances in evolutionary psychology, is proposed. Specifically, that fear-induced faintness (eg, fainting following the sight of a syringe, blood, or following a trivial skin injury) is a distinct Homo sapiens-specific extreme-stress survival response to an inescapable threat. The article suggests that faintness evolved in response to middle paleolithic intra-group and inter-group violence (of con-specifics) rather than as a pan-mammalian defense response, as is presently assumed. Based on recent literature, freeze, flight, fight, fright, faint provides a more complete description of the human acute stress response sequence than current descriptions. Faintness, one of three primary physiological reactions involved in BIITS phobia, is extremely rare in other phobias. Since heritability estimates are higher for faintness than for fears or phobias, the author suggests that trait-faintness may be a useful complement to trait-anxiety as an endophenotype in research on the human fear circuitry. Some implications for the forthcoming Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition as well as for clinical, health services, and transcriptomic research are briefly discussed.

Bracha HS. · National Center for Posttraumatic Stress Disorder, Department of Veterans Affairs, Pacific Islands Health Care System, Spark M. Matsunaga Medical Center, 1132 Bishop Street, #307, Honolulu, HI 96813-2830, USA. · Int J Psychophysiol. · Pubmed #14693362 No free full text.

Abstract: While laboratory methods for estimating genetic susceptibility for adult psychopathology have received much recent attention, laboratory methods for objectively estimating a person's early autonomic nervous system perturbations have been under-researched. Research on heart rate variability suggests that early life episodes of diminished vagal tone may predict poor stress resilience in adults. This article will detail a research method for retrospectively estimating in adults the chronology of diminished vagal tone episodes experienced prior to age 10. This method makes use of the developing enamel matrix, one of very few tissues that cannot recover after being stressed.

Bracha HS, Bienvenu OJ, Eaton WW. · National Center for Posttraumatic Stress Disorder, Pacific Islands Division Department of Veterans Affairs, Pacific Islands Health Care System, Spark M. Matsunaga Medical Center, Honolulu, HI 96813-2830, United States. · J Affect Disord. · Pubmed #16860872 No free full text.

Abstract: OBJECTIVE: The research agenda for the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V) has emphasized the need for a more etiologically-based classification system, especially for stress-induced and fear-circuitry disorders. Testable hypotheses based on threats to survival during particular segments of the human era of evolutionary adaptedness (EEA) may be useful in developing a brain-evolution-based classification for the wide spectrum of disorders ranging from disorders which are mostly overconsolidationally such as PTSD, to fear-circuitry disorders which are mostly innate such as specific phobias. The recently presented Paleolithic-human-warfare hypothesis posits that blood-injection phobia can be traced to a "survival (fitness) enhancing" trait, which evolved in some females of reproductive-age during the millennia of intergroup warfare in the Paleolithic EEA. The study presented here tests the key a priori prediction of this hypothesis-that current blood-injection phobia will have higher prevalence in reproductive-age women than in post-menopausal women. METHOD: The Diagnostic Interview Schedule (version III-R), which included a section on blood and injection phobia, was administered to 1920 subjects in the Baltimore ECA Follow-up Study. RESULTS: Data on BII phobia was available on 1724 subjects (1078 women and 646 males). The prevalence of current blood-injection phobia was 3.3% in women aged 27-49 and 1.1% in women over age 50 (OR 3.05, 95% CI 1.20-7.73). [The corresponding figures for males were 0.8% and 0.7% (OR 1.19, 95% CI 0.20-7.14)]. CONCLUSIONS: This epidemiological study provides one source of support for the Paleolithic-human-warfare (Paleolithic-threat) hypothesis regarding the evolutionary (distal) etiology of bloodletting-related phobia, and may contribute to a more brain-evolution-based re-conceptualization and classification of this fear circuitry-related trait for the DSM-V. In addition, the finding reported here may also stimulate new research directions on more proximal mechanisms which can lead to the development of evidence-based psychopharmacological preventive interventions for this common and sometimes disabling fear-circuitry disorder.

Bracha HS, Garcia-Rill E, Mrak RE, Skinner R. · National Center for Posttraumatic Stress Disorder, Department of Veterans Affairs, Pacific Islands Health Care System, Spark M. Matsunaga VA Medical Center, 1132 Bishop St. #307, Honolulu, HI, USA. · J Neuropsychiatry Clin Neurosci. · Pubmed #16387990 links to  free full text

Abstract: The authors investigated whether war-related posttraumatic stress disorder (WR-PTSD) is associated with a postmortem change in neuronal counts in the locus coeruleus (LC) since enhanced central nervous system (CNS) noradrenergic postsynaptic responsiveness has been previously shown to contribute to PTSD pathophysiology. Using postmortem neuromorphometry, the number of neurons in the right LC in seven deceased elderly male veterans was counted. Three veterans were classified as cases of probable or possible WR-PTSD. All three veterans with probable or possible WR-PTSD were found to have substantially lower LC neuronal counts compared to four comparison subjects (three nonpsychiatric veterans and one veteran with alcohol dependence and delirium tremens).To the authors' knowledge, this case series is the first report of LC neuronal counts in patients with PTSD or any other DSM-IV-TR anxiety disorder. Previous postmortem brain tissue studies of Alzheimer's Disease (AD) demonstrated an upregulation of NE biosynthetic capacity in surviving LC neurons. The finding reported is consistent with the similar upregulation of NE biosynthetic capacity of surviving LC neurons in veterans who developed WR-PTSD. Especially if replicated, this finding in WR-PTSD may provide further explanation of the dramatic effectiveness of propranolol and prazosin for the secondary prevention and treatment of PTSD, respectively. The LC neurons examined in this study are probably the origin of the first or second "leg" of what might be termed the PTSD candidate circuit. Larger neuromorphometric studies of the LC in veterans with WR-PTSD and in other development-stress-induced and fear-circuitry disorders are warranted, especially using VA registries.

López HH, Bracha AS, Bracha HS. · National Center for PTSD, Department of Veterans Affairs, Spark M. Matsunaga Medical and Regional Office Center, 1132 Bishop St., Suite 307, Honolulu, HI 96813, USA. · Hawaii Med J. · Pubmed #12422383 No free full text.

Abstract: Increasing scientific evidence point to a non-pharmacological complementary treatment for insomnia: white noise. Its presentation has been shown to induce sleep in human neonates and adults, probably by reducing the signal-to-noise ratio of ambient sound. White noise may be a simple, safe, cost-effective alternative to hypnotic medication in many psychiatric disorders, especially acute stress disorder and PTSD.

Bracha HS, Hayashi K. · No affiliation provided · Arch Gen Psychiatry. · Pubmed #18180435 No free full text.

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Bracha HS, Lenze SM, Tsang Mui Chung M. · No affiliation provided · Br J Dermatol. · Pubmed #17107409 No free full text.

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Bracha HS, Lenze SM, Shelton J. · No affiliation provided · Br J Psychiatry. · Pubmed #17077449 links to  free full text

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Bracha HS, Lenze SM. · No affiliation provided · Clin Auton Res. · Pubmed #16865325 No free full text.

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Bracha HS, Chronicle EP. · No affiliation provided · CNS Spectr. · Pubmed #16496463 links to  free full text

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