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Books on the topic 'Pathological aggression'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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1

Aggression and expiation. Lanham, MD: University Press of America, 1987.

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2

Human paleopsychology: Applications to aggression and pathological processes. Hillsdale, N.J: L. Erlbaum Associates, 1987.

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3

Arsenio, William Frank. Emotions, aggression, and morality in children: Bridging development and psychopathology. Washington, D.C: American Psychological Association, 2010.

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4

Arsenio, William Frank. Emotions, aggression, and morality in children: Bridging development and psychopathology. Washington, D.C: American Psychological Association, 2010.

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5

Arsenio, William Frank. Emotions, aggression, and morality in children: Bridging development and psychopathology. Washington, D.C: American Psychological Association, 2010.

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6

B, Schlesinger Louis, ed. Sex murder and sex aggression: Phenomenology, psychopathology, psychodynamics, and prognosis. Springfield, Ill., U.S.A: Thomas, 1989.

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7

Animal Cruelty Antisocial Behaviour and Aggression. Palgrave Macmillan, 2012.

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8

Frank, Arsenio William, and Lemerise Elizabeth A, eds. Emotions, aggression, and morality in children: Bridging development and psychopathology. Washington, D.C: American Psychological Association, 2010.

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9

Frank, Arsenio William, and Lemerise Elizabeth B, eds. Emotions, aggression, and morality in children: Bridging development and psychopathology. Washington, D.C: American Psychological Association, 2010.

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10

Mizen, Richard, and Morris Mark. On Aggression and Violence. Palgrave Macmillan, 2007.

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11

Gullone, Eleonora. Animal Cruelty, Antisocial Behaviour, and Aggression: More than a Link. Palgrave Macmillan, 2012.

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12

Perls, Frederick S. Ego, Hunger and Aggression: A Revision of Freud's Theory and Method. Gestalt Journal Press, 1992.

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13

Buckholtz, Joshua W., and Andreas Meyer-Lindenberg. Genetic Perspectives on the Neurochemistry of Human Aggression and Violence. Edited by Turhan Canli. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.009.

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Violence is a devastating social phenomenon that is costly both to affected individuals and to society at large. Pathological aggression, especially reactive/impulsive aggression, is a cardinal symptom common to several psychiatric disorders—including antisocial personality disorder, borderline personality disorder, and psychopathy—that are associated with risk for violence. Thus, understanding the factors that predispose people to impulsive violence represents a crucial goal for psychology, neuroscience, and psychiatry. Although we are far from a full understanding of the etiopathophysiology of violence, impulsive aggression is heritable, suggesting that genetic mechanisms may be important for determining individual variation in susceptibility. This chapter synthesizes available preclinical and human data to propose a compelling neurogenetic mechanism for violence, specifically arguing that a genetically determined excess in serotonin signaling during a critical developmental period leads to dysregulation within a key corticolimbic circuit for emotional arousal and regulation, inhibitory control, and social cognition.

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14

Denham, S. LeeAnn, and Heidi R. Umphrey. Radiology–Pathology Correlation. Edited by Christoph I. Lee, Constance D. Lehman, and Lawrence W. Bassett. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190270261.003.0058.

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Over 1 million image-guided breast biopsies, guided by mammography, ultrasound, or magnetic resonance imaging, are performed annually in the United States. When the imaging characteristics of a lesion correspond to the histopathological diagnosis (e.g., suspicious imaging findings and malignant pathology), the biopsy results are deemed concordant. However, when the imaging characteristics differ from the pathological results (e.g., suspicious imaging findings but benign pathology), this biopsy result is considered discordant. This chapter, appearing in the section on interventions and surgical change, reviews the process of determining concordance between imaging and pathological findings, and managing discordant findings. Topics discussed include benign pathology results with suspicious imaging appearances, as well as the management of high-risk lesions, locally aggressive breast lesions, and malignant breast lesions.

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15

Hans, Steiner, Daniels Whitney, Kelly Michael, and Stadler Christina. Etiology of Disruptive Behavior Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190265458.003.0004.

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This chapter discusses the growing data base examining the biological, psychological, and social factors causing disruptive behavior disorders (DBDs). Some of the most intriguing findings are derived from the clinical and preclinical studies of psychopathy, the most extreme and pathological variant of antisocial and aggressive behavior. The existing data are best accommodated in a risk/resilience model informed by developmental psychopathology, rather that a reductionist biological model. The most likely model of causation of DBDs will be multifactorial rather than unifactorial. It is also likely that different syndromes within the DBD grouping will be informed by very different admixtures of biological, psychological, and social factors, which in turn have important implications for effective treatments. The current descriptive diagnoses are inadequate for a sophisticated empirical understanding of DBDs.

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16

Pitzalis, Costantino, Frances Humby, and Michael P. Seed. Synovial pathology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0052.

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Synovial pathology is seen in a variety of disease states, including rheumatoid arthritis (RA), osteoarthritis (OA), psoriatic arthritis, and systemic lupus erythmatosus (SLE). This chapter highlights recent advances that characterize the cellular composition of these tissues according to surface markers and chemokine and cytokine expression, and describes synovial functional status and response to therapeutics. In RA, after initiation, pannus migrates over and under cartilage, and into subchondral bone, in a destructive process. Cartilage-pannus junction (CPJ) is characterized as invasive or 'quiescent' or 'indistinct'. Invasive CPJ can comprise macrophages, fibroblast-like synoviocytes (FLS), mast cells, and/or neutrophils. CPJ activity is related to the state of activation of the overlying subintima. Subintimal inflammation can be graded to a variety of degrees (I–IV) according to established criteria and is illustrated. In some RA synovia, cellular aggregates organize into ectopic lymphoid structures (ELS) through the expression of lymphorganogenic signals, to exhibit T- or B-cell zones accompanied by dendritic cells and lymphangiogenesis. ELS synthesize rheumatoid factor (RF) and anti-citrullinated peptide antibodies (ACAP), considered to be indicative of aggressive disease. The selective cellular expression of macrophage and dendritic cell chemokines and cytokines such as TNF, GMCSF, TGFβ‎, IL-1, IL-6, IL-23, and chemokines can be seen in synovia, to form a regulated and cooperative environment that sustains the cellular organization and pathological function. Important to this process are FLS and CD68+ macrophages. CD68 expression correlates with disease severity and can be useful as a surrogate marker of disease modifying activity of therapeutics, such as anti-TNF and anti-B-cell biologics.

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