fear can be defined as a state that occurs “when the sentient brain is aware that its personal well-being (physical, mental, social, cultural, existential) is challenged or may be at some point”
External cues are elements in the environment that can pose a threat to the health, integrity, and existence of an individual person (e.g., venomous insects and animals, heights, or a social aggressor). Internal cues include bodily states (e.g., arousal) in addition to the thoughts that are produced through our cognitive abilities.
Fear is defined as “a: an unpleasant often strong emotion caused by anticipation or awareness of danger;
An organism's detection of potential threat involves innate biological processes that exist across the phylogenetic evolutionary spectrum
owever, important distinctions between the environmental detection of threat and the conscious experience of human fear
threat detection is only one process within the complex emotional experience of fear, worry, and anxiety that comprise human states of being
Threat detection and defensive response behaviors are typically based on situation-specific factors such as the proximity, intensity, immediacy, and probability of an aversive outcome
The experience of human fear as an emotion (as well as the etiology and treatment of fear-based disorders) occurs as a result of the complex interaction between the activation of basic threat detection systems, memory storage and retrieval, and our own conscious awareness.
mammalian response to threat involves the recruitment of the autonomic nervous system to alter physiological activity
Human neuroimaging studies represent a significant amount of research conducted on fear learning and memory
ear memory is an interaction between neural regions considered to be traditionally more involved in cognition (i.e., the dorsal and ventral lateral PFC; DLPFC, VLPFC, respectively), neural regions traditionally considered to be more involved in emotion (i.e., the orbital frontal cortex and the ventral medial PFC; OFC, VMPFC, respectively), as well as neural regions that span both concepts (anterior cingulate cortex; ACC)
A common, empirically-validated approach to treat PTSD is Prolonged Exposure Therapy (PE) (Foa, 2011), one component of which involves repeated exposure to fear-linked cues to produce “extinction” of fear (clinically referred to as exposure leading to desensitization) and to prevent avoidance responses to these cues (Hofmann, 2008).
Unfortunately, one major limitation of extinction is that it is a temporary phenomenon and extinguished fear can re-emerge with the passage of time (spontaneous recovery), as a result of a change in experimental context (renewal shift), or by exposing subjects to an aversive unconditioned stimulus (US) after extinction (reinstatement effect)
Together, these findings suggest that extinction is a new learning process, and fear reduction results from an inhibition rather than an erasure of the original fear memory (Bouton, 2002).
Critical brain regions include the amygdala, ventromedial prefrontal cortex (VMPFC), and hippocampus
Fear extinction recruits a form of new learning in which an inhibitory memory trace associated with the previously reinforced CS competes with, but does not eliminate, the labile fear acquisition memory trace (Liberzon and Abelson, 2016, Myers and Davis, 2002). As described earlier, the original fear memory remains intact and is accessible through specific learning mechanisms identified as reinstatement (through unsignaled presentation of the previously used US; Bouton and Bolles, 1979, Rescorla and Heth, 1975), renewal (through a change in experimental context; Bouton, 1993), or through the passage of time (termed spontaneous recovery; Pavlov, 1927).