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Review Stress and brain atrophy. 2006
Bremner JD. · Departments of Psychiatry and Radiology, Emory University School of Medicine, Atlanta VAMC, Decatur GA 30306, USA. · CNS Neurol Disord Drug Targets. · Pubmed #17073653 No free full text.
Abstract: Studies in animals showed that stress is associated with changes in hippocampal function and structure, an effect mediated through decreased neurogenesis, increased glucocorticoids, and/or decreased brain derived neurotrophic factor. Antidepressants and some anticonvulsants block the effects of stress and/or promote neurogenesis in animal studies. Patients with posttraumatic stress disorder (PTSD) have been shown to have smaller hippocampal volume on magnetic resonance imaging and deficits in hippocampal-based memory. Symptom activation is associated with decreased anterior cingulate and medial prefrontal function, which is proposed as the neural correlate of a failure of extinction seen in these patients. Treatment with antidepressants and phenytoin reverse hippocampal volume reduction and memory deficits in PTSD patients, suggesting that these agents may promote neurogenesis in humans.
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Review PTSD: help patients break free. 2006
Neason K. · Harry S. Truman VA Medical Center, Columbia, MO, USA. · RN. · Pubmed #17069146 No free full text.
This publication has no abstract.
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Review Corticotropin releasing factor (CRF) receptor signaling in the central nervous system: new molecular targets. free! 2006
Hauger RL, Risbrough V, Brauns O, Dautzenberg FM. · San Diego VA Healthcare System, University of California San Diego, La Jolla, 929093-0603, USA. · CNS Neurol Disord Drug Targets. · Pubmed #16918397 links to free full text
Abstract: Corticotropin-releasing factor (CRF) and the related urocortin peptides mediate behavioral, cognitive, autonomic, neuroendocrine and immunologic responses to aversive stimuli by activating CRF(1) or CRF(2) receptors in the central nervous system and anterior pituitary. Markers of hyperactive central CRF systems, including CRF hypersecretion and abnormal hypothalamic-pituitary-adrenal axis functioning, have been identified in subpopulations of patients with anxiety, stress and depressive disorders. Because CRF receptors are rapidly desensitized in the presence of high agonist concentrations, CRF hypersecretion alone may be insufficient to account for the enhanced CRF neurotransmission observed in these patients. Concomitant dysregulation of mechanisms stringently controlling magnitude and duration of CRF receptor signaling also may contribute to this phenomenon. While it is well established that the CRF(1) receptor mediates many anxiety- and depression-like behaviors as well as HPA axis stress responses, CRF(2) receptor functions are not well understood at present. One hypothesis holds that CRF(1) receptor activation initiates fear and anxiety-like responses, while CRF(2) receptor activation re-establishes homeostasis by counteracting the aversive effects of CRF(1) receptor signaling. An alternative hypothesis posits that CRF(1) and CRF(2) receptors contribute to opposite defensive modes, with CRF(1) receptors mediating active defensive responses triggered by escapable stressors, and CRF(2) receptors mediating anxiety- and depression-like responses induced by inescapable, uncontrollable stressors. CRF(1) receptor antagonists are being developed as novel treatments for affective and stress disorders. If it is confirmed that the CRF(2) receptor contributes importantly to anxiety and depression, the development of small molecule CRF(2) receptor antagonists would be therapeutically useful.
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Review Developing an agenda for translational studies of resilience and vulnerability following trauma exposure. 2006
Yehuda R, Flory JD, Southwick S, Charney DS. · Bronx VA OOMH, 130 West Kingsbridge Road, Bronx, NY 10468, USA. · Ann N Y Acad Sci. · Pubmed #16891584 No free full text.
Abstract: Here we outline a translational research agenda for studies of resilience, defined as the process of adapting well in the face of adversity or trauma. We argue that an individual differences approach to the study of resilience, in which the full range of behavioral and biological responses to stress exposure is examined can be applied across human samples (e.g., people who have developed psychopathology versus those who have not; people who have been exposed to trauma versus those who have not) and even, in some cases, across species. We delineate important psychological resilience-related factors including positive affectivity and optimism, cognitive flexibility, coping, social support, emotion regulation, and mastery. Key brain regions associated with stress-related psychopathology have been identified with animal models of fear (e.g., extinction and fear conditioning; memory reconsolidation) and we describe how these regions can be studied in humans using neuroimaging technology. Finally, we cite recent research identifying neuroendocrine markers of resilience and recovery in humans (e.g., neuropeptide Y [NPY], dehydroepiandrosterone [DHEA]) that can also be measured, in some cases, in other species. That exposure to adversity or trauma does not necessarily lead to impairment and the development of psychopathology in all people is an important observation. Understanding why this is so will provide clues for the development of therapeutic interventions for those people who do develop stress-related psychopathology, or even for the prevention of adverse outcomes.
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Review Advances in understanding neuroendocrine alterations in PTSD and their therapeutic implications. 2006
Yehuda R. · Bronx VA OOMH, 130 West Kingsbridge Road, Bronx, NY 10468, USA. · Ann N Y Acad Sci. · Pubmed #16891568 No free full text.
Abstract: The findings from investigations of the neuroendocrinology of posttraumatic stress disorder (PTSD) have highlighted alterations that have not historically been associated with pathologic processes, and have, accordingly, raised several questions about the nature of the findings and their relationship to PTSD. The most infamous of these observations--low cortisol levels--has been the subject of much discussion and scrutiny because the finding has been both counterintuitive, and not uniformly reproducible. This fact notwithstanding, novel therapeutic approaches to the treatment of PTSD are in large part predicated on the assumption that glucocorticoid levels may be lower in PTSD. This article summarizes important neuroendocrine observations in cortisol and provides strategies for understanding what has emerged over the past two decades, to be a complex and sometimes contradictory literature.
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Review Neuroimaging studies of emotional responses in PTSD. 2006
Liberzon I, Martis B. · Trauma Stress and Anxiety Research Group, Department of Psychiatry, Ann Arbor VA Healthcare System, University of Michigan, 1500 E. Medical Center Drive UH9D 0118, Ann Arbor, MI 48109-0118, USA. · Ann N Y Acad Sci. · Pubmed #16891565 No free full text.
Abstract: Neuroimaging research offers a powerful and noninvasive means to understand healthy as well as dysregulated emotional processing in healthy subjects and PTSD patients. Functional neuroimaging findings suggest specific roles for subregions of the medial prefrontal (mPFC), orbito frontal (OFC), anterior cingulate (ACC), and insular cortices as well as the sublenticular extended amygdala (SLEA) and hippocampus in various components of emotional processing. Some of the same regions appear to be associated with emotional response to trauma, and with symptom formation in PTSD. Neuroimaging findings of emotional processing in healthy subjects and PTSD patients are discussed, addressing the specific roles of cortical regions like mPFC, ACC, and insula, and their potential contribution to PTSD pathophysiology. Processes of cognitive-emotional interactions and social emotions are discussed in an attempt to synthesize the prefrontal findings in healthy subjects and PTSD patients. Further links between functional neuroanatomy of emotional responses and neuroendocrine stress regulation are proposed.
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Review Memory performance in older trauma survivors: implications for the longitudinal course of PTSD. 2006
Golier JA, Harvey PD, Legge J, Yehuda R. · James J. Peters VA Medical Center, OOMH, 130 West Kingsbridge Road, Bronx, NY 10468, USA. · Ann N Y Acad Sci. · Pubmed #16891562 No free full text.
Abstract: Impaired declarative memory performance and smaller hippocampal volume have been observed in young and middle-aged adults with chronic posttraumatic stress disorder (PTSD). These alterations may put trauma survivors with PTSD at greater risk for cognitive decline in later life. This article focuses on the emerging literature on neuropsychological impairment in aging trauma survivors, in particular, elderly combat veterans and survivors of the Holocaust. In veterans and in Holocaust survivors, PTSD was associated with substantial impairments in learning, free and cued recall, and recognition memory compared to the respective nonexposed subjects; however, in neither group was PTSD associated with impaired retention or "rapid forgetting." Additionally, PTSD was not associated with smaller right or left hippocampal volume in either cohort. PTSD is associated with considerable cognitive burden with age. Longitudinal studies of older subjects are warranted to examine whether PTSD is associated with accelerated aging or progressive memory loss.
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Review Predictors of posttraumatic stress in police and other first responders. 2006
Marmar CR, McCaslin SE, Metzler TJ, Best S, Weiss DS, Fagan J, Liberman A, Pole N, Otte C, Yehuda R, Mohr D, Neylan T. · San Francisco Veterans Affairs Medical Center, 4150 Clement St. (116 P), San Francisco, CA 94121, USA. · Ann N Y Acad Sci. · Pubmed #16891557 No free full text.
Abstract: We provide an overview of previous research conducted by our group on risk and resilience factors for PTSD symptoms in police and other first responders. Based on our work, the findings of other investigators on individual differences in risk for PTSD, and drawing on preclinical studies fear conditioning and extinction, we propose a conceptual model for the development of PTSD symptoms emphasizing the role of vulnerability and resilience to peritraumatic panic reactions. We tested this conceptual model in a cross-sectional sample of police officers (n = 715). Utilizing an hierarchical linear regression model we were able to explain 39.7% of the variance in PTSD symptoms. Five variables remained significant in the final model; greater peritraumatic distress (beta = 0.240, P < .001), greater peritraumatic dissociation (beta = 0.174, P < .001), greater problem-solving coping (beta = 0.103, P < .01), greater routine work environment stress (beta = 0.182, P < .001), and lower levels of social support (beta = -0.246, P < .001). These results were largely consistent with the proposed conceptual model. Next steps in this line of research will be to test this model prospectively in a sample of 400 police academy recruits assessed during training and currently being followed for the first 2 years of police service.
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Review N-acetylaspartate as a marker of neuronal injury in neurodegenerative disease. free! 2006
Schuff N, Meyerhoff DJ, Mueller S, Chao L, Sacrey DT, Laxer K, Weiner MW. · Magnetic Resonance Unit VA Medical Center, Department of Radiology, University of California, San Francisco, CA 94121, USA. · Adv Exp Med Biol. · Pubmed #16802717 links to free full text
This publication has no abstract.
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Review Functional weakness and sensory loss. 2006
Lanska DJ. · VA Medical Center, Tomah, Wisconsin 54660, and Department of Neurology, University of Wisconsin, Madison, Wisconsin, USA. · Semin Neurol. · Pubmed #16791776 No free full text.
Abstract: Functional weakness and sensory loss are common clinical problems with variable presentations. Functional weakness commonly presents as weakness of an entire limb, paraparesis, or hemiparesis, with observable or demonstrable inconsistencies and nonanatomic accompaniments. Documentation of limb movements during sleep, the arm drop test, the Babinski thigh-trunk test, Hoover tests, the Sonoo abductor test, and various dynamometer tests can provide useful bedside diagnostic information on functional weakness. Functional sensory loss typically affects all sensory modalities, either in a hemisensory distribution or affecting an entire limb. Although often inconsistent over serial examinations with nonanatomic features, many clinical findings reported to be helpful in diagnosing functional sensory loss are neither sensitive nor specific for functional sensory loss. The yes-no test, Bowlus-Currier test, and forced-choice tests can provide useful bedside diagnostic information on functional sensory loss. Clinicians must be prepared to make more than one diagnosis in some cases, including an organic neurological diagnosis and a diagnosis of functional overlay. Recent studies have reported relatively low rates (<5%) of misdiagnosis of functional weakness or sensory loss as indicated by subsequent diagnosis of neurological or psychiatric conditions that explained the presenting symptoms. Most neurologists find such patients more difficult to help than patients with organic disease. Management focuses on supportive psychotherapy and behavioral management, exploration of social and psychological issues, treatment of comorbid depression or anxiety, and facilitation of development of more appropriate and constructive coping methods. Many patients with functional weakness, and to a somewhat lesser extent functional sensory loss, have persisting or relapsing-remitting somatic symptoms and persistently impaired social/interpersonal, occupational, and psychological functioning.
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Review Exploring the links between posttraumatic stress disorder and social support: processes and potential research avenues. 2006
Guay S, Billette V, Marchand A. · Centre de Recherche Fernand-Seguin de l'Hôpital Louis-H. Lafontaine and Veterans Affairs Canada. · J Trauma Stress. · Pubmed #16788995 No free full text.
Abstract: Social support after a traumatic event is linked to posttraumatic stress disorder (PTSD). However, little is known about the ways in which social support influences the adaptation to trauma and development of PTSD. The aim of the present article is threefold: to outline the various processes by which social support is linked to PTSD, to review the most relevant research in the field, and to suggest potential future research.
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Review Long-term pharmacotherapy for post-traumatic stress disorder. 2006
Davis LL, Frazier EC, Williford RB, Newell JM. · VA Medical Center, Tuscaloosa, Alabama 35404, USA. · CNS Drugs. · Pubmed #16734498 No free full text.
Abstract: This article reviews the literature on the long-term pharmacological treatment of post-traumatic stress disorder (PTSD). A PUBMED search was conducted; only studies on the effects of long-term (>14-weeks) pharmacological treatment for PTSD in adults or children were considered. Our search identified three randomised, double-blind, placebo-controlled studies (one each for sertraline, fluoxetine and risperidone), four open-label studies (one each for sertraline, paroxetine, nefazodone and valproate), one retrospective case series (clozapine) and one pooled analysis (sertraline). All studies involved adult populations, with the exception of the study of clozapine. The studies demonstrate that long-term treatment of PTSD with SSRIs effectively maintains the previous treatment response and improvement in quality of life, converts more patients to responder status and accounts for one-third of overall treatment gains. Greater PTSD severity predicts a longer time to response to these drugs. Discontinuation of SSRI treatment after 12 weeks results in a greater risk of relapse and symptom exacerbation compared with extended treatment. In addition to improved PTSD symptoms, extended treatment with paroxetine improves verbal declarative memory and increases hippocampal volume. Long-term treatment of PTSD with atypical antipsychotics (risperidone and clozapine), non-SSRI antidepressants (nefazodone) and antiepileptic drugs (AEDs; valproate) also appears to result in significant improvements in PTSD symptoms. In conclusion, long-term treatment of PTSD with SSRIs improves the psychiatric and clinical outcome of patients with the disorder and prevents relapse and symptom exacerbation. The effect of other agents (atypical antipsychotics, AEDs and other psychotropic medications) requires further controlled study.
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Review Posttraumatic stress disorder: clinical features, pathophysiology, and treatment. 2006
Vieweg WV, Julius DA, Fernandez A, Beatty-Brooks M, Hettema JM, Pandurangi AK. · Psychiatry, Hunter Holmes McGuire Veterans Affairs Medical Center, Richmond, Va, USA. · Am J Med. · Pubmed #16651048 No free full text.
Abstract: Posttraumatic stress disorder (PSTD), classified as an anxiety disorder, has become increasingly important because of wars overseas, natural disasters, and domestic violence. After trauma exposes the victim to actual or threatened death or serious injury, 3 dimensions of PTSD unfold: (1) reexperiencing the event with distressing recollections, dreams, flashbacks, and/or psychologic and physical distress; (2) persistent avoidance of stimuli that might invite memories or experiences of the trauma; and (3) increased arousal. Traumatic events sufficient to produce PTSD in susceptible subjects may reach a lifetime prevalence of 50% to 90%. The actual lifetime prevalence of PTSD among US citizens is approximately 8%, with the clinical course driven by pathophysiologic changes in the amygdala and hippocampus. Comorbid depression and other anxiety disorders are common. General principles of treatment include the immediate management of PTSD symptoms and signs; management of any trauma-related comorbid conditions; nonpharmacologic interventions including cognitive behavioral treatment; and psychopharmacologic agents including antidepressants (selective serotonin reuptake inhibitors most commonly), antianxiety medications, mood stabilizing drugs, and antipsychotics. This review of PTSD will provide the reader with a clearer understanding of this condition, an increased capacity to recognize and treat this syndrome, and a greater appreciation for the role of the internist in PTSD.
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Review Human brain evolution and the "Neuroevolutionary Time-depth Principle:" Implications for the Reclassification of fear-circuitry-related traits in DSM-V and for studying resilience to warzone-related posttraumatic stress disorder. 2006
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.
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Review Response style and posttraumatic stress disorder (PTSD): a review. 2005
Franklin CL, Thompson KE. · VA Medical Center, Mental Health Service Line COS6, 1601 Perdido Street, New Orleans, LA 70112, USA. · J Trauma Dissociation. · Pubmed #16172084 No free full text.
Abstract: Response style is an important issue that is often not addressed when assessing or treating patients with posttraumatic stress disorder (PTSD). In this paper, various response styles are discussed along with their relevance to clinical work and research with PTSD patients. Two of the most prevalent measures of response style, the Minnesota Multiphasic Personality Inventory-2 (MMPI-2) and Structured Interview of Reported Symptoms (SIRS) scales are evaluated for use in assessing for PTSD. In addition, the Trauma Symptom Inventory's potential for use in evaluating response style is briefly discussed. Implications for future work and directions for future investigation are outlined.
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Review Physiological markers for anxiety: panic disorder and phobias. 2005
Roth WT. · Department of Veterans Affairs Health Care System, Palo Alto, CA 94304, USA. · Int J Psychophysiol. · Pubmed #16137780 No free full text.
Abstract: Physiological activation is a cardinal symptom of anxiety, although physiological measurement is still not used for psychiatric diagnosis. An ambulatory study of phobics who were afraid of highway driving showed a concordance between self-reported anxiety during driving, autonomic activation, hypocapnia, and sighing respiration. Patients with panic attacks do not exhibit autonomic activation when they are quietly sitting and not having panic attacks, but do have the same respiratory abnormalities as driving phobics, suggesting that these abnormalities could be a marker for panic disorder. Such abnormalities are compatible with both the false suffocation alarm (D. Klein) and hyperventilation (R. Ley) theories of panic. Hypocapnia, however, is often absent during full-blown panic attacks. Since activation functions as preparation for physical activity, it may not occur when a patient has learned that avoidance of fear by flight or fight is futile. We developed a capnometry feedback assisted breathing training therapy for panic disorder designed to reduce hyperventilation and making breathing regular. Without feedback, conventional therapeutic breathing instructions may actually increase hyperventilation by increasing dyspnea. Five weekly therapy sessions accompanied by daily home practice with a capnometer produced marked clinical improvement compared to changes in an untreated group. Improvement was sustained over a 12-month follow-up period. The therapist avoided any statements or procedures designed to alter cognitions. Improvement occurred regardless of whether patients initially reported mostly respiratory or non-respiratory symptoms during their attacks. There is evidence that modifying any of the three systems comprising a fear network can be therapeutic, as exemplified by cognitive therapy modifying thoughts, exposure therapy modifying avoidance, and breathing training procedures modifying pCO(2).
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Review War-related mental health problems of today's veterans: new clinical awareness. 2005
Reeves RR, Parker JD, Konkle-Parker DJ. · G.V. (Sonny) Montgomery VA Medical Center, Jackson, Mississippi 39216, USA. · J Psychosoc Nurs Ment Health Serv. · Pubmed #16116923 No free full text.
Abstract: 1. Veterans of the military conflicts in Iraq and Afghanistan may have been exposed to significant psychological stressors, resulting in mental and emotional disorders. 2. Posttraumatic stress disorder (PTSD) is characterized by symptoms in three domains: reexperiencing the trauma, avoiding stimuli associated with the trauma, and symptoms of increased autonomic arousal. 3. Treatment of PTSD often requires both psychological and pharmacological interventions. 4. In addition to PTSD, other mental disorders may be precipitated or worsened by exposure to combat, including depression, anxiety, psychosis, and substance abuse.
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Review The neurobiology of PTSD: implications for nurses. 2005
Olszewski TM, Varrasse JF. · PTSD Outpatient Clinic, Department of Veterans Affairs, Hampton, VA 23667, USA. · J Psychosoc Nurs Ment Health Serv. · Pubmed #16018133 No free full text.
Abstract: Posttraumatic stress disorder (PTSD) is a disabling and prevalent psychiatric disorder. Researchers and scientists have developed a neurobiological basis, which provides a framework for understanding the complexities of PTSD, for many symtoms of the disorder. The estimated lifetime prevalence of PTSD among adult Americans is 7.8%, with women twice as likely as men to have PTSD. Onset of symptoms can occur years after exposure to trauma, and the duration of the illness can last a lifetime. Patients with PTSD often encounter multiple psychosocial problems that result from the symptoms they experience, and their distorted perceptions can affect relationships within the family and the workplace. Nurses in various roles (e.g., educator, therapist, prescriber, case manager, staff nurse) may encounter individuals with PTSD. The nursing profession has traditionally sought to explain sophisticated language to patients in understandable terms, and nurses serve in encouraging, supporting, and evaluating roles, all of which will be increasingly important as science and technology discover more information about the neurobiological basis for mental illnesses.
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Review Pathological responses to terrorism. free! 2005
Yehuda R, Bryant R, Marmar C, Zohar J. · Psychiatry OOMH, Bronx Veterans Affairs Medical Center, 130 West Kingsbridge Road, Bronx, NY 10468, USA. · Neuropsychopharmacology. · Pubmed #16012535 links to free full text
Abstract: Many important gains have been made in understanding PTSD and other responses to trauma as a result of neuroscience-based observations. Yet there are many gaps in our knowledge that currently impede our ability to predict those who will develop pathologic responses. Such knowledge is essential for developing appropriate strategies for mounting a mental health response in the aftermath of terrorism and for facilitating the recovery of individuals and society. This paper reviews clinical and biological studies that have led to an identification of pathologic responses following psychological trauma, including terrorism, and highlights areas of future-research. It is important to not only determine risk factors for the development of short- and long-term mental health responses to terrorism, but also apply these risk factors to the prediction of such responses on an individual level. It is also critical to consider the full spectrum of responses to terrorism, as well as the interplay between biological and psychological variables that contribute to these responses. Finally, it is essential to remove the barriers to collecting data in the aftermath of trauma by creating a culture of education in which the academic community can communicate to the public what is and is not known so that survivors of trauma and terrorism will understand the value of their participation in research to the generation of useful knowledge, and by maintaining the acquisition of knowledge as a priority for the government and those involved in the immediate delivery of services in the aftermath of large-scale disaster or trauma.
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Review Interaction of sleep disturbances and anxiety in later life: perspectives and recommendations for future research. 2005
Spira AP, Friedman L, Flint A, Sheikh JI. · Veterans Affairs Palo Alto Health Care System, CA 94025, USA. · J Geriatr Psychiatry Neurol. · Pubmed #15911939 No free full text.
Abstract: Both sleep disturbances and anxiety are quite common in older adults. Although increasing research efforts have investigated sleep disturbances and anxiety in older adults, little has been written concerning the relation between sleep disturbances and anxiety in this population. This article reviews the epidemiological and clinical literature concerning the overall prevalence of sleep disturbances and relations between sleep and anxiety in later life. The article begins with a discussion of the prevalence of sleep and anxiety problems in older individuals, continues with a clinical review of the complex interrelationship between sleep and anxiety in older adults, and briefly considers possible neurobiological underpinnings of this interrelationship. This is followed by a brief discussion of the impact of medical illness on both anxiety and sleep disturbances. The article ends with a summary of findings from this review and provides recommendations for future research.
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Review Emerging roles for atypical antipsychotics in chronic post-traumatic stress disorder. 2005
Hamner MB, Robert S. · Department of Psychiatry, Ralph H Johnson Department of Veterans Affairs Medical Center and Medical University of South Carolina, Charleston, SC 29401, USA. · Expert Rev Neurother. · Pubmed #15853496 No free full text.
Abstract: Post-traumatic stress disorder is an anxiety disorder that may occur after the individual is exposed to severe psychologic trauma such as combat, sexual assault, or childhood physical or sexual abuse. Chronic post-traumatic stress disorder may result in considerable psychologic pain and suffering for the individual in addition to significant functional impairment. In addition to the heterogeneity of symptoms that occur in post-traumatic stress disorder, there may also be extensive comorbidity with other anxiety disorders, mood disorders, psychotic disorders, and other psychiatric disorders. This complicates the treatment picture. Currently, accepted treatments for post-traumatic stress disorder include psychotherapy, in particular cognitive behavioral-based approaches and antidepressant medication. However, many patients are refractory to these initial treatments or have only a partial response. In light of this, may clinicians combine additional classes of psychotropic agents and different psychotherapeutic approaches to enhance treatment response. This article reviews the literature on the use of atypical antipsychotics in the treatment of post-traumatic stress disorder. Most of the research to date has involved combat veterans partially responsive or refractory to treatment, namely with antidepressants. Studies have shown improvement across post-traumatic stress disorder symptom clusters, as well as improvement in comorbid psychotic symptoms or disorders. More research is needed to confirm these recent findings and further delineate the role of atypical antipsychotics in the treatment of post-traumatic stress disorder. Currently, possible indications for their use include treatment-resistant post-traumatic stress disorder and post-traumatic stress disorder with comorbid psychotic features.
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Review The clenching-grinding spectrum and fear circuitry disorders: clinical insights from the neuroscience/paleoanthropology interface. free! 2005
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).
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Review Psychiatric barriers to readiness for treatment for hepatitis C Virus (HCV) infection among injection drug users: clinical experience of an addiction psychiatrist in the HIV-HCV coinfection clinic of a public health hospital. 2005
Scheft H, Fontenette DC. · Lemuel Shattuck Hospital, Massachusetts Department of Public Health, Jamaica Plain, MA, USA. · Clin Infect Dis. · Pubmed #15768337 No free full text.
Abstract: Among injection drug users, psychological and psychiatric barriers to readiness for treatment for hepatitis C virus (HCV) infection include mood and anxiety disorders, cognitive deficits, temperament disorders, and personality vulnerabilities, as well as ongoing drug use. Many aspects of these barriers can be overcome with direct treatment or social support. To establish effective treatment for HCV infection in this population of patients, it is essential that the patient and providers develop a rapport that allows for active communication. It is also important that the patient make an effort to adhere to the treatment requirements and that the patient receive the appropriate evaluation and management of treatable barriers.
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Review Understanding the interface of HIV, trauma, post-traumatic stress disorder, and substance use and its implications for health outcomes. 2004
Brief DJ, Bollinger AR, Vielhauer MJ, Berger-Greenstein JA, Morgan EE, Brady SM, Buondonno LM, Keane TM, Anonymous00258. · Boston University School of Medicine, Boston, MA, USA. · AIDS Care. · Pubmed #15736824 No free full text.
Abstract: Many individuals living with HIV have been exposed to some type of traumatic event during their lives and may be living with symptoms of post-traumatic stress disorder (PTSD). A substantial number of these individuals are also likely to show evidence of a co-morbid substance use disorder (SUD). There is reason to believe that the co-occurrence of HIV and PTSD or co-morbid PTSD and SUD (PTSD/SUD) may predict poorer health outcomes. There are several pathways through which PTSD or PTSD/SUD might adversely impact the health of individuals living with HIV, including participation in negative health behaviours, low levels of adherence to antiretroviral medications, and/or a direct, deleterious effect on immune function. Psychological interventions are needed to treat PTSD and PTSD/SUD in HIV-positive individuals, and reduce the negative impact of these conditions on health outcomes. This article will explore data on the prevalence of trauma exposure, PTSD, and PTSD/SUD among individuals living with HIV, the pathways through which these conditions might affect health, possible interventions for PTSD and PTSD/SUD for individuals living with HIV, and methods for integrating care for individuals with these disorders. Future directions for research related to HIV, PTSD, and PTSD/SUD will also be discussed.
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Review Chest pain in patients with cardiac and noncardiac disease. free! 2004
Sheps DS, Creed F, Clouse RE. · University of Florida and the Malcom Randall VA Medical Center, P.O. Box 100181, Gainesville, FL 100181-0181, USA. · Psychosom Med. · Pubmed #15564350 links to free full text
Abstract: OBJECTIVE: To describe factors influencing chest pain expression in patients with cardiac or noncardiac disease. METHODS: The authors conducted a case presentation and review of literature. RESULTS: Causes of chest pain are diverse. Psychologic factors influence chest pain expression commonly in patients with or without cardiac disease. CONCLUSIONS: Physicians and other therapists must be aware of psychologic influences on chest pain expression to provide optimal treatment to their patients.
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