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Data publikacji: 2 listopada 2024

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1

Stujenske, Joseph Matthew. Prefrontal-Amygdala Circuits Regulating Fear and Safety. [New York, N.Y.?]: [publisher not identified], 2016.

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2

ill, Wiley Nancy 1964, red. The blammo--surprise! book: A story to help children overcome fears. New York: Magination Press, 1988.

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Bourguignon, Laurence. A friend for Tiger. Mahwah, NJ: BridgeWater Books, 1994.

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4

Gavin, Andrews, red. Stress-induced and fear circuitry disorders: Advancing the research agenda for DSM-V. Washington, DC: American Psychiatric Pub., 2009.

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Pedrozo, Sebastián. Abejas y flores marchitas. Montevideo, Uruguay: Alfaguara, 2007.

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McCully, Emily Arnold. Juliette et Bellini. [France]: Kaléidoscope, 1994.

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Michael, Zulli, i Cooper Alice, red. The compleat Alice Cooper: Incorporating the three acts of Alice Cooper - the last temptation. New York: Marvel Comics, 1994.

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8

When Panic Happens: Short-Circuit Anxiety and Fear in the Moment Using Neuroscience and Polyvagal Theory. New Harbinger Publications, 2024.

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Sargin, Derya, Chen Yan i Sheena Josselyn. Genetic Tools in the Erasure of Emotional Memory. Redaktor Turhan Canli. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.004.

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Fear is an important emotion; remembering fearful events/places/stimuli is key for survival. However, dysregulation of fear may underlie the etiology of several psychiatric diseases. Inappropriate storage and/or recall of fearful events can lead to maladaptive fear behaviors and physiological responses that contribute to emotional disorders. Much research has provided insights into the neural processes mediating the formation of fear memories. In addition, some new research has begun to provide insights into how fear memories may be weakened. A more thorough understanding of the molecular, cellular, and circuit basis of the formation and storage of fear memories may one day provide insights into how we can rid ourselves of aberrant fear memories associated with psychopathological responses.
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10

Cuthbert, Bruce N. The Nimh Research Domain Criteria Project. Redaktorzy Dennis S. Charney, Eric J. Nestler, Pamela Sklar i Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0071.

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The Research Domain Criteria (RDoC) project grew from recognized deficiencies in currently used diagnostic schemes for mental illness, such as the Diagnostic and Statistical Manual of Mental Disorders (DSM). While the latter is based on a series of signs and symptoms of illnesses that can co-occur in groups of individuals, without consideration of underlying biological factors, RDoC is based on the increasing ability to relate normal as well as abnormal behavior to particular molecules and circuits in the brain across animal species and humans. Behavioral domains include negative valence systems (e.g., fear and anxiety), positive valence systems (e.g., reward and motivation), cognitive systems, social processes, and arousal and regulatory systems, several of which might be affected in a given DSM disease classification. RDoC is seen as a step toward a “precision psychiatry,” where increasing knowledge of the genetic, molecular, cellular, and circuit basis of mental illness will yield biologically based diagnoses that offer important pathophysiological, treatment, and prognostic implications.
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11

Liberzon, Israel, i Kerry Ressler, red. Neurobiology of PTSD: From Brain to Mind. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.001.0001.

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Post-traumatic stress disorder (PTSD) is a maladaptive and debilitating psychiatric disorder characterized by an extreme sense of fear at the time of trauma occurrence, with characteristic re-experiencing, avoidance, and hyperarousal symptoms in the months and years following the trauma. PTSD can occur in up to 25% of subjects who have experienced severe psychological trauma, such as combat veterans, refugees, and assault victims. Why are some people resilient, whereas others develop debilitating PTSD? Notably, PTSD is among the most likely of psychiatric disorders to be understood from the perspective of environmental influences interacting with genetic vulnerability, since diagnosis requires a specific, highly traumatizing, fear-evoking experience. In addition, a large amount of evidence now supports a model in which PTSD can be viewed, in part, as a disorder of fear dysregulation. This is particularly exciting because the neural circuitry underlying fear behavior in mammals is among the most well-understood behavioral circuits in neuroscience. Further, the study of fear behavior and its underlying circuitry has led to rapid progress in understanding learning and memory processes. By combining molecular-genetic approaches with a mechanistic understanding of fear circuitry, great progress is possible in the understanding, diagnosis, and treatment of PTSD. This book examines the basic neural mechanisms that mediate complex responses and adaptations to psychological trauma; it describes what is currently known about how these biological processes are impaired in individuals with PTSD, and how environmental exposure to trauma interacts with the brain to create the syndrome of PTSD.
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12

Epstein, Joshua M. Mathematical Model. Princeton University Press, 2017. http://dx.doi.org/10.23943/princeton/9780691158884.003.0002.

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This part of the book describes explicit mathematical models for the affective, cognitive, and social components of Agent_Zero. It first considers some underlying neuroscience of fear and the role of the amygdala before turning to Rescorla–Wagner equations of conditioning. In particular, it explains how the fear circuit can be activated and how fear conditioning can occur unconsciously. It then reviews some standard nomenclature adopted by Ivan Pavlov in his study, Conditioned Reflexes: An Investigation of the Physiological Activity of the Cerebral Cortex, with emphasis on David Hume's “association of ideas,” the theory of conditioning, and the Rescorla–Wagner model. After examining “the passions,” the discussion focuses on reason, Agent_Zero's cognitive component, and the model's social component. The central case is that the agent initiates the group's behavior despite starting with the lowest disposition, with no initial emotional inclination, no evidence, the same threshold as all others, and no orders from above.
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13

Bauer, Elizabeth P., i Denis Paré. Behavioral Neuroscience of Circuits Involved in Fear Processing. Redaktorzy Israel Liberzon i Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0002.

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Normal fear regulation includes the ability to learn by experience that some circumstances predict danger. This process, which can be modeled in the laboratory using Pavlovian fear conditioning, appears to be disrupted in individuals with post-traumatic stress disorder (PTSD). Understanding of the mechanisms underlying fear learning has progressed tremendously in the last 25 years, and constitutes a promising paradigm to study the neural bases of PTSD. This chapter first reviews current knowledge of the brain structures involved in fear learning, expression and extinction, including the contributions of the amygdala and prefrontal cortex. It then addresses how these circuits are affected by PTSD and how fear processing is altered in PTSD. Understanding PTSD within a fear-conditioning and extinction framework provides insight into why certain individuals are susceptible to developing PTSD and suggests potential therapies.
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14

Pace-Schott, Edward F., i Samuel Gazecki. The Role of Stress in the Etiology of PTSD. Redaktorzy Frederick J. Stoddard, David M. Benedek, Mohammed R. Milad i Robert J. Ursano. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457136.003.0012.

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This chapter reviews the biological features of stress and their correlation to symptoms of posttraumatic stress disorder (PTSD). Over the past 15 years, advances in understanding the neurobiology of stress and anxiety have revealed underlying neural abnormalities that might help explain why posttraumatic symptoms—intrusive memories or nightmares, avoidance of situations or stimuli associated with the event, persistent negativity of mood and cognition, and hyperarousal—persist in patients with PTSD. This chapter focuses on research that has discovered how abnormal hypothalamic-pituitary-adrenal axis activity, abnormalities of the catecholamingergic/autonomic system, and atypical physiologic and neural circuit responses during fear extinction recall may be important biological factors in the etiology and maintenance of PTSD symptoms.
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15

Milad, Mohammed R., i Kylie N. Moore. Neurobiology and Neuroimaging of PTSD. Redaktorzy Frederick J. Stoddard, David M. Benedek, Mohammed R. Milad i Robert J. Ursano. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457136.003.0015.

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This chapter provides a broad overview of the fear circuitry implicated in the development and maintenance of posttraumatic stress disorder. It begins by reviewing evidence from animal models of fear conditioning and extinction that unveiled the neural structures incorporated in the fear circuitry. Then it explores the translation of these findings to healthy human models of fear conditioning and finally examines the neural dysfunctions highlighted by neuroimaging studies of posttraumatic stress disorder (PTSD) in order to conceptualize mechanisms of fear extinction and the role of impaired fear extinction in contributing to the pathology of PTSD. The chapter ends with the potential therapeutic interventions for the treatment of PTSD in the scope of this model but with a note of caution regarding some of its limitations.
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16

High, Mette M. Fear and Fortune. Cornell University Press, 2017. http://dx.doi.org/10.7591/cornell/9781501707544.001.0001.

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Mongolia over the last decade has seen a substantial and ongoing gold rush. The wide-spread mining of gold looks at first glance to be a blessing for a desperately poor and largely pastoralist country. Volatility and uncertainty as well as political and economic turmoil led many people to join the hopeful search for gold. This activity poses an intense moral problem; in the “land of dust,” disturbing the ground and extracting the precious metal is widely believed to have calamitous consequences. With gold retaining strong ties to the landscape and its many spirit beings, the fortune of the precious metal is inseparable from the fears that surround mining. This book considers the results of several years of fieldwork in Mongolia, time spent with the “ninjas,” as the miners are known locally, as well as the people who disapprove of their illegal activities and warn of the retribution that the land and its inhabitants may suffer as a result. As such, the book is a well-structured read on the Mongolian gold rush and the spirit forces that underpin it. It provides a uniquely up-close and personal view onto gold mining and its international circuitry, based on a sensitive study of Mongolian sociality, miners, religious knowledge and practice, and ways of envisioning and experiencing what counts as “value” in the Mongolian gold rush today.
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17

Maren, Stephen. Neural Circuits for Context Processing in Aversive Learning and Memory. Redaktorzy Israel Liberzon i Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0005.

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The nature and properties of emotional expression depend importantly on not only the stimuli that elicit emotional responses, but also the context in which those stimuli are experienced. Deficits in context processing have been associated with a variety of cognitive-emotional disorders, including post-traumatic stress disorder (PTSD). These deficits can be localized to specific neural circuits underlying context processing in the mammalian brain. In particular, the hippocampus has been implicated through numerous animal and human studies to be involved both in normal contextual memory formation, but also in discrimination of trauma-related cues. Decreased hippocampal functioning, as is observed in PTSD, is associated with increased generalization of fear and threat responses as well as deficits in extinction of fear. Understanding context processing offers the opportunity to further understand the biology of PTSD and to target new approaches to therapeutics.
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18

Hearn, Chester G. Circuits in the Sea. Greenwood Publishing Group, Inc., 2004. http://dx.doi.org/10.5040/9798400626531.

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This book tells the story of the scientific talent and technological prowess of two nations that joined forces to connect themselves with a communications cable that would change the world. In 1855 an American visionary named Cyrus West Field, who knew nothing about telegraphy, sought to establish a monopoly on telegraphic revenues between North America and Europe. Field and the wealthy New Yorkers who formed the first Atlantic cable-laying company never suspected that spanning the vast and stormy Atlantic would require 11 years of frustration and horrific financial sacrifice. The enterprise would eventually engage some of the most brilliant minds in England, Scotland, and the United States, attracting men of science, men of wealth, and men of curiosity. Message time would be cut from more than four weeks to about two minutes. Such a feat would not have been possible without the massive ship the Great Eastern, designed by Isambard Kingdom Brunel, Britain’s foremost engineer, or the financial backing of Thomas Brassey, the era’s greatest builder of railroads. Despite four failed attempts and the enmity that developed between the Union and Great Britain during America’s Civil War, Field never stopped urging his British friends to perfect a cable that could function in water as deep as two and a half miles. Without the unified effort of this small cadre of determined engineers, decades may have passed before submarine cables became reliable. This is the story of these men, their ships, and the technology that made it all possible. Behind the scenes were tough and worthy competitors who tried to beat them to the punch, adding a sense of urgency to their monumental task. Some called the Atlantic cable the greatest feat of the 19th century—with good reason. It perfected transoceanic communications and connected the world with circuits in the sea.
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19

Lankton, Stephen R. The Blammo-Surprise! Book: A Story to Help Children Overcome Fears. Magination Pr, 1989.

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Wiley, Nancy, i Stephen R. Lankton. The Blammo - Surprise! Book: A Story to Help Children Overcome Fears. Magination Pr, 1989.

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21

Goodkind, Madeleine S., i Amit Etkin. Functional Neurocircuitry and Neuroimaging Studies of Anxiety Disorders. Redaktorzy Dennis S. Charney, Eric J. Nestler, Pamela Sklar i Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0034.

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Anxiety and fear serve adaptive functions and include wide-ranging subjective, physiological, behavioral, and cognitive responses. When these reactions are present chronically, and to a heightened degree that generalizes to signals beyond those that are objectively dangerous, one sees emergence of clinical anxiety disorders. Historically, anxiety disorders have been conceptualized as disruptions in fear processing, though more recent accounts also highlight changes in emotional reactivity beyond fear and deficits in emotion regulation. In this chapter, we review the neural circuitry relevant for fear processing and for emotional reactivity and regulation more broadly. We then review neuroimaging studies of social anxiety disorder, specific phobia, generalized anxiety disorder, panic disorder, and posttraumatic stress disorder. We highlight areas of overlap between disorders as well as disorder-specific perturbations.
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22

Karpova, Nina N. Pharmacological Adjuncts and Evidence-Supported Treatments for Trauma. Redaktor Sara Maltzman. Oxford University Press, 2016. http://dx.doi.org/10.1093/oxfordhb/9780199739134.013.32.

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A large proportion of humans experienced a traumatic event in their lifetime, with more than 10% developing posttraumatic stress disorder (PTSD), panic disorder, phobias, and other fear/anxiety disorders. The neural circuitry of fear responses is highly conserved in humans as well as rodents, and this allows for translational research using animal models of fear. Fear/anxiety disorders in humans are most efficiently treated by exposure-based psychotherapy (i.e., cognitive behavioral therapy; CBT), the main aspects of which are closely modeled by extinction training in Pavlovian fear conditioning and extinction paradigms in rodents. To improve the efficacy of psychotherapy, pharmacological agents potent for enhancing learning and memory consolidation processing should be developed to combine with exposure-based therapy. The purpose of these adjunctive pharmacological agents is to promote fear memory erasure and the consolidation of extinction memories, thus providing a combined treatment of increased effectiveness. This review discusses established pharmacological adjuncts to behavioral therapeutic interventions for fear/anxiety disorders. The mechanisms of action of these adjuncts, as well as the evidence for and against the pharmacological treatment strategies and their limitations are discussed.
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23

Javanbakht, Arash, i Gina R. Poe. Behavioral Neuroscience of Circuits Involved in Arousal Regulation. Redaktorzy Israel Liberzon i Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0007.

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This chapter evaluates the evidence that hyper-reactive noradrenergic responses during trauma contribute to hyperarousal symptoms in PTSD, including disturbances in sleep. Some genetic vulnerability for PTSD involves the adrenergic system, and a hyperactive central noradrenergic system might serve to over-consolidate and sustain the affective component of fear memories. Reduced moderation of noradrenergic reactions during low hormone phases of the menstrual cycle could also lead to increased susceptibility to PTSD. This chapter considers a mechanism by which hyperactivity in the noradrenergic system during sleep would impair REM sleep theta and non-REM sleep spindles in the limbic system, both of which are implicated in the consolidation of new safety memories, thereby compromising extinction recall and setting into motion a positive feedback loop in PTSD pathophysiology, involving hyperarousal, failure to integrate contextual information, and biased attention to threat. If so, novel pharmacotherapeutic interventions inhibiting the noradrenergic system during sensitive periods in sleep should be considered.
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24

Catcher. New York: Farrar, Straus, Giroux, 1994.

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Mirette Highwire Post. Penguin Publishing Group, 1992.

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Fabulous Flying Fandinis. Penguin Publishing Group, 1999.

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The Fabulous Flying Fandinis. New York: Cobblehill Books/Dutton, 1996.

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Charney, Dennis S., Gavin Andrews, Paul J. Sirovatka i Darrel A. Regier. Stress-Induced and Fear Circuitry Disorders: Refining the Research Agenda for DSM-V. American Psychiatric Association Publishing, 2009.

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Fox, Nathan A., Bethany C. Reeb-Sutherland i Kathryn A. Degnan. Personality and Emotional Development. Redaktor Philip David Zelazo. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199958474.013.0002.

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Over the past 20 years, research on the development of emotions and interest in the emotion–cognition interface has blossomed. Coinciding with this growth has been research on the neural circuitry and development of two basic motivational/emotion states: one brought on by threat and danger (i.e., fear) and one resulting from actively pursuing or receiving reward (i.e., reward/joy). The current chapter reviews traditional approaches to thinking about emotional development and temperament in infants and children. It then reviews the neuroscience work associated with fear and reward with a focus on the development of these systems. A particular emphasis will be placed on how this research and the examination of gene X environment interactions can influence research in personality and emotion development.
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Felger, Jennifer C., Ebrahim Haroon i Andrew H. Miller. Inflammation and Immune Function in PTSD. Redaktorzy Israel Liberzon i Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0013.

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Numerous reports have described an association between PTSD and alterations in the immune response primarily characterized by increased biomarkers of inflammation, including inflammatory cytokines and acute phase reactants as well as increased inflammatory responses to immune stimuli. When considering systems that evolved to protect and prepare organisms during challenge, it is not surprising that the immune system is affected by exposure to trauma, or to the chronic stress associated with PTSD symptoms. Conversely, inflammatory cytokines have been shown to affect the brain, and may influence neural circuits of fear and anxiety to contribute to PTSD symptoms. This chapter discusses the evolutionary legacy of a primed inflammatory response in the context of trauma and stress, examines the evidence of altered immune function and inflammation in PTSD, explores the potential mechanisms involved, characterizes the consequences on neurocircuitry and health, and discusses potential translational implications.
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Mason, Peggy. Forebrain. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0007.

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The anatomy and function of forebrain circuits is described. The role of the hypothalamus as the executive center for regulating and protecting the body’s physiology is detailed. The thalamus is a necessary interpreter for subcortical inputs to cerebral cortex, which uses thalamic input to map the sensory world. The amygdala, critical to expressing and interpreting fear, has been implicated in post-traumatic stress disorder. During resting conditions, the basal ganglia suppress movement. Damage to the basal ganglia produces a hypo- or hyperkinetic disorder. The representation of visual fields in pathways from retina to striate cortex is described in detail. The student is then introduced to the invaluable use of visual field deficits for localizing forebrain lesions. Extrastriate, somatomotor, and prefrontal contributions to abstract functions are outlined in a clinically relevant way. Finally, the importance of the hippocampus to declarative memory is discussed, and common memory symptoms are described.
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Maeng, Lisa Y., i Mohammed R. Milad. PTSD in Women. Redaktorzy Frederick J. Stoddard, David M. Benedek, Mohammed R. Milad i Robert J. Ursano. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457136.003.0016.

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This chapter focuses primarily on the influence of female sex as a risk factor for posttraumatic stress disorder (PTSD). Prevalence rates suggest that women are especially vulnerable to developing PTSD. Despite changes in diagnostic criteria and examination across varied populations, the prevalence of PTSD remains consistently twice as high in women as men. This chapter examines sex differences in both incidence and presentation of PTSD. It then moves to a discussion of the neurobiological factors of PTSD in women, further examining stress and fear regulation mechanisms and the circuitry that may underlie the disproportionate vulnerability to PTSD development in women. The influence of gonadal hormones on PTSD symptomology is also explored in this chapter with a focus on estrogen and progesterone.
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33

The Great Circus Train Wreck of 1918. History Press, 2010.

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McCully, Emily Arnold. Mirette on the High Wire. Putnam Juvenile, 1997.

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Mirette on the High Wire (Scholastic Audio). Scholastic, 1993.

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McCully, Emily Arnold. Mirette on the Highwire (Caldecott Medal Book). Putnam Juvenile, 1992.

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Mirette on the High Wire [Chinese Language Edition]. Grimm Press Ltd., 1992.

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Mirette on the high wire. New York: Scholastic Inc., 1993.

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Mirette on the high wire. New York: G.P. Putnamʼs Sons, 1992.

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Tian kong zai jiao xia. Taibei Shi: Ge lin wen hua, 1994.

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Mirette on the High Wire. Tandem Library, 1999.

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42

Zulli, Michael, i Neil Gaiman. Neil Gaiman's the Last Temptation Hardcover. Dynamic Forces, Incorporated DBA Dynamite Entertainment, 2014.

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The Compleat Alice Cooper: Incorporating the Three Acts of Alice Cooper : The Last Temptation. Marvel Enterprises, 1996.

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Gaiman, Neil. Neil Gaiman's The Last Temptation 20th Anniversary Deluxe Edition Hardcover. Dynamite Entertainment, 2014.

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La Dernière Tentation. Bulle Dog, 2002.

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The Compleat Alice Cooper: Incorporating the Three Acts of Alice Cooper: The Last Temptation. New York, New York, USA: Marvel Music, 1995.

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The Last Temptation. Dark Horse, 2006.

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48

McKean, Dave, i Neil Gaiman. Neil Gaiman's the Last Temptation 20th Anniversary Deluxe Edition Hardcover, Signed by Neil Gaiman. Dynamic Forces, Incorporated DBA Dynamite Entertainment, 2014.

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The Last Temptation. Dark Horse, 2001.

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