To get around this, Dr Beauregard has drawn on previous experiments he carried out with actors, which showed that remembering an intense emotional experience activates the same brain networks as actually having that experience.
Emotional distress activates the hypothalamic pituitary adrenal axis resulting in an increase in glucocorticoid production.
The Somatic Marker hypothesis proposes that remembering an emotional memory activates the somatic sensations associated with the memory.
The somatic marker hypothesis [3, 4] proposes that experiencing or recollecting an emotional memory activates the somatic markers associated with the memory, including the visceral sensations associated with the memory.
Emotional pain activates the same regions of the brain as physical pain, so this can be a significantly intolerable state for some people.
This study demonstrated that passive listening to nonverbal emotional vocalizations activates a network of premotor cortical regions involved in the control of facial movement [39].
In the present study, the displays that mismatched in audiovisual temporal and emotional features activated these regions significantly more than those that mismatched in only temporal features, thus supporting and extending these recent observations [25].
A wealth of data [6] [8] indicates that neurohormonal changes in response to emotional events activate β-adrenergic receptors in the amygdala, which in turn enhances hippocampal-dependent memory consolidation [9].
Recent fMRI or PET studies have demonstrated that observing or imaging another person's emotional state activates parts of the neuronal network involved in processing that same state in oneself, whether it is disgust, pain, or social emotion [6], [7] (for reviews see [8], [9]).
In conclusion, fMRI with emotional stimuli activates the amygdalae in controls and to a lesser extent in those with right TLE and even less in left TLE.
