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Prevention is Better Than Cure
Published in Adam Gledhill, Dale Forsdyke, The Psychology of Sports Injury, 2021
One potential explanation for the results, even though there have been different conceptual approaches and designs, is that most of the studies have, however, applied programmes targeting stress management techniques (e.g. relaxation programmes, critical incident diaries, goal setting programmes). More specifically, stress management techniques, such as mindfulness, have been found to down-regulate amygdala activation (Cozolino, 2010). Such down-regulation of amygdala activation is related to decreased magnitude of stress response. Given that stress and the magnitude of the stress response will influence injury risk, this type of training might decrease this risk.
Transformation of human traits and being
Published in Antonella Sansone, Cultivating Mindfulness to Raise Children Who Thrive, 2020
If we have not received the nurturing we need immediately after the trauma and developed resilience by having had our needs met early in life, situations that remind us of the traumatic event or experience (even very vaguely) can trigger excessive release of stress hormones, including cortisol and adrenaline. These in turn increase heart rate, blood pressure and the breathing rate, preparing us to fight back and run away. It is our brain’s amygdala, which van der Kolk calls “the smoke detector”, which sends out the danger signal that triggers the release of these powerful stress hormones (2014). The amygdala is located deep within the temporal lobe of the brain and is a limbic system structure. That is involved in many of our emotions and motivations, particularly those that are related to survival. It is involved in the processing of fear, anger and pleasure and also responsible for determining what memories are stored and when they are stored in the brain. It is believed that how memories are stored and where is linked to how huge our emotional response was to the event.
Phobias
Published in Judy Z. Koenigsberg, Anxiety Disorders, 2020
According to Barlow (2004), the etiology of social anxiety disorder can be attributed to an interaction between genetic, biological, psychological, and environmental variables. Chapters 5 and 6 delineated the brain circuits involved in generalized anxiety disorder and panic disorder. A physiological variable that is implicated in the etiology of social anxiety disorder is the amygdala (Birbaumer et al., 1998). For example, researchers found that in response to pictures of angry faces, the amygdala of persons with social anxiety disorder is activated, and the amount of activity in the amygdala has been found to be positively associated with the degree of social anxiety rather than with general anxiety (Phan, Fitzgerald, Nathan, & Tancer, 2006; Ray, 2018).
Advances in the pharmacotherapeutic management of post-traumatic stress disorder
Published in Expert Opinion on Pharmacotherapy, 2021
Ansab Akhtar, Sangeeta Pilkhwal Sah
An extensive and intricate neuronal network implicates PTSD; however, the central brain regions prone to physiobiological and neurochemical alterations resulting from trauma include the amygdala, hypothalamus, ventromedial prefrontal cortex (vmPFC), cingulate cortex, and hippocampus. The amygdala plays a critical role in fear and anxiety and modulates memory consolidation with the storage of emotionally relevant information and its function is regulated by the PFC. However, PTSD patients tend to retain and reconsolidate fear memories due to the impaired fear extinction system. This results from impaired functioning of the amygdala. Disruption of amygdala inhibition through prefrontal structures is confirmed by studies that investigated negative emotional processing in PTSD patients demonstrating hypoactivation of the mPFC and hyperactivation of the amygdala [10]. Studies demonstrate that the medial PFC becomes smaller and less responsive in PTSD patients, so the inhibitory control it exerts on stress response and emotional reactivity of the amygdala is lost [11].
Seizure and cognitive outcomes of posterior quadrantic disconnection: a series of 12 pediatric patients
Published in British Journal of Neurosurgery, 2020
Yao Wang, Chao Zhang, Xiu Wang, Lin Sang, Feng Zhou, Jian-Guo Zhang, Wen-Han Hu, Kai Zhang
After this procedure, the fibres mentioned in 1)–3) above were disconnected with remaining fibres as follows: 5) hippocampal efferent fibres; 6) projection fibres from the amygdala; 7) fibres through the anterior commissure between the anterior temporal lobe and limbic cortex; and 8) projection fibres from the insula to the basal ganglia, thalamus, hypothalamus and brain stem.(3) Stage III: Mesial temporal resection: After the opening of the temporal horn, the amygdala was revealed in the anteromedial part. The amygdala was removed along with resection of the subdural uncinate gyrus. The superior boundary of the amygdala resection was located at the top of the temporal horn of the lateral ventricle. The hippocampus was exposed and resected along the temporal horn and choroid fissure.
The amygdala in adolescents with attention-deficit/hyperactivity disorder: Structural and functional correlates of delay aversion
Published in The World Journal of Biological Psychiatry, 2020
Jeroen Van Dessel, Edmund Sonuga-Barke, Matthijs Moerkerke, Saskia Van der Oord, Jurgen Lemiere, Sarah Morsink, Marina Danckaerts
However, the functional significance of these structural effects in adolescents with ADHD remains to be determined. One hypothesis is that ADHD-related alterations in its structure underpin disrupted amygdala activity, which mediate the functional deficits in the processing of both social (e.g., fearful faces; Brotman et al. 2010; Herpertz et al. 2008; Posner et al. 2011) and non-social (e.g., monetary loss; Plichta et al. 2009; Wilbertz et al. 2015) negative affective stimuli. Furthermore, the amygdala has been implicated in the regulation and processing of aversive emotional states in adolescents with ADHD (e.g., frustration, anger; Arnsten and Rubia 2012; Herrmann et al. 2010), which are increasingly being championed as important features in a sub-group of patients (Martel et al. 2008). More generally, the pivotal role of the amygdala within a complex network of brain regions governing emotion is increasingly well understood (Hayes and Northoff 2011; Huang et al. 2018; Pessoa, 2017; Sharp, 2017), whereby it coordinates excitatory signals to brain regions actively involved in emotional processing (anterior insula, orbital frontal cortex, ventromedial prefrontal cortex (PFC) and anterior cingulate cortex), as well as other regions involved in emotional responses (thalamus and hippocampus). Amygdala also receives inhibitory signals from brain regions that are typically involved in emotion regulation (posterior cingulate cortex, precuneus, dorsomedial PFC and dorsolateral PFC).