Regions of the brain associated with<unk> s Anatomical components of the limbic system Limbic system Beneath the lateral fissure in the cerebral cortex, the insula, or insular cortex, of the brain has been identified as part of the limbic system, along with the cingulated gyrus, hippocampus, corpus callosum, and other nearby cortices. This system has been found to play a role in emotion processing, and the insula, in particular, may contribute to maintaining autonomic functions. Studies by Critchley et al. indicate the insula as being involved in the experience of emotion by detecting and interpreting threatening stimuli. Similar studies monitoring insula activity have shown a correlation between increased insular activation and anxiety. In the frontal lobes, other cortices involved with<unk>  and fear are the anterior cingulate cortex and the medial prefrontal cortex. In the processing of emotional stimuli, studies on<unk>  reactions to facial expressions have indicated that these areas are involved in the processing and responding to negative stimuli. The ventromedial prefrontal cortex has been said to influence the amygdala by monitoring its reaction to emotional stimuli or even fearful memories. Most specifically, the medial prefrontal cortex is active during the extinction of fear and is responsible for long-term extinction. Stimulation of this area decreases conditioned fear responses, so its role may be in inhibiting the amygdala and its reaction to fearful stimuli. The hippocampus is a horseshoe-shaped structure that plays an essential part in the brain's limbic system. This is because it forms memories and connects them with emotions and the senses. When dealing with fear, the hippocampus receives impulses from the amygdala that allow it to connect the fear with a certain sense, such as a smell or sound. Amygdala The amygdala is an almond-shaped mass of nuclei located deep in the brain's medial temporal lobe. It processes the events associated with fear and is linked to social<unk>  and other anxiety disorders. The amygdala's ability to respond to fearful stimuli occurs through fear conditioning. Like classical conditioning, the amygdala learns to associate a conditioned stimulus with a negative or avoidant stimulus, creating a conditioned fear response often seen in<unk>  individuals. The amygdala is responsible for recognizing certain stimuli or cues as dangerous and plays a role in the storage of threatening stimuli to memory. The basolateral nuclei (or basolateral amygdala) and the hippocampus interact with the amygdala in-memory storage. This connection suggests why memories are often remembered more vividly if they have emotional significance. In addition to memory, the amygdala also triggers the secretion of hormones that affect fear and aggression. When the fear or aggression response is initiated, the amygdala releases hormones into the body to put the human body into an "alert" state, which prepares the individual to move, run, fight, etc. This defensive "alert" state and response are known as the fight-or-flight response. However, inside the brain, this stress response can be observed in the hypothalamic-pituitary-adrenal axis (HPA). This circuit incorporates the process of receiving stimuli, interpreting them, and releasing certain hormones into the bloodstream. The parvocellular neurosecretory neurons of the hypothalamus release corticotropin-releasing hormone (CRH), which is sent to the anterior pituitary. Here the pituitary releases adrenocorticotropic hormone (ACTH), which ultimately stimulates the release of cortisol. In relation to anxiety, the amygdala activates this circuit, while the hippocampus is responsible for suppressing it. Glucocorticoid receptors in the hippocampus monitor the amount of cortisol in the system and through negative feedback can tell the hypothalamus to stop releasing CRH. Studies on mice engineered to have high concentrations of CRH showed higher levels of anxiety, while those engineered to have no or low amounts of CRH receptors were less anxious. In people with<unk> s, therefore, high amounts of cortisol may be present, or there may be low levels of glucocorticoid receptors or even serotonin (5-HT). Disruption by damage For the areas in the brain involved in emotion—most specifically fear— the processing and response to emotional stimuli can be altered when one of these regions is damaged. Damage to the cortical areas involved in the limbic system, such as the cingulate cortex or frontal lobes, has resulted in extreme emotion changes. Other types of damage include Klüver–Bucy syndrome and Urbach–Wiethe disease. In Klüver–Bucy syndrome, a temporal lobectomy, or removal of the temporal lobes, results in changes involving fear and aggression. Specifically, the removal of these lobes results in decreased fear, confirming its role in fear recognition and response. Damage to both side (Bilateral damage) of the medial temporal lobes is known as Urbach–Wiethe disease. It presents with similar symptoms of decreased fear and aggression but with the addition of the inability to recognize emotional expressions, especially angry or fearful faces. The amygdala's role in learned fear includes interactions with other brain regions in the neural circuit of fear. While damage in the amygdala can inhibit its ability to recognize fearful stimuli, other areas such as the ventromedial prefrontal cortex and the basolateral nuclei of the amygdala can affect the region's ability to not only become conditioned to fearful stimuli but to extinguish them eventually. Through receiving stimulus info, the basolateral nuclei undergo synaptic changes that allow the amygdala to develop a conditioned response to fearful stimuli. Damage to this area, therefore, have been shown to disrupt the acquisition of learned responses to fear. Likewise, damage in the ventromedial prefrontal cortex (the area responsible for monitoring the amygdala) has been shown to slow down the speed of extinguishing a learned fear response and how effective the extinction is. This suggests there is a pathway or circuit among the amygdala and nearby cortical areas that process emotional stimuli and influence emotional expression, all of which can be disrupted when damage occurs.
Phobia
Claustrophobia
Alexithymia
Hyperreligiosity
Emotional lability
Mindfulness
Body integrity dysphoria
Automatism 