There is burgeoning literature attempting to delineate neural mechanisms of affect regulation using fMRI techniques to probe the relevant circuitry. This is adding to our knowledge base of brain areas involved in suppression, enhancement, and maintenance of emotions.
Levesque et al (2003)
examined the voluntary ability to suppress negative emotion, ie, sadness. Healthy female subjects (n = 20) were shown neutral and sad excerpts of film. For example, sad excerpts depicted the death of a family member while neutral ones were an interview or carpentry. In case of the sad films, subjects were instructed to react normally to some stimuli and voluntarily suppress responses to other comparable stimuli. The scanning was followed by subjects completing a visual analogue scale (0–8) of intensity of sadness ever felt as well as that felt during the film. They also completed the strategy questionnaire, including the degree to which they were able to suppress. Their results have shown that transient sadness activated bilateral anterior temporal pole (imparting affective tone to subjective experience) and midbrain (autonomic nervous system (ANS) responses in the mesencephalic region), left amygdala and insula (recall induced sadness plus neural correlate of ANS responses), and right ventrolateral prefrontal cortex (VLPFC) (processing emotions). Positive correlation was seen between self-reported ratings of sadness and BOLD signal changes of right VLPFC (brain area (BA) A 47), left insula, and left aCC (BA 24/32; emotional detection/awareness). Suppression of sad emotion activated right DLPFC (BA 9 in all and 10 in some; explained as an objective observer sending commands to OFC to suppress) and OFC (BA 11). They conclude that there is a key role played by DLPFC and OFC on the right side in suppressing negative emotion. Limitations of this study are the use of nonstandardized film excerpts, but the creative study design brings the scientific examination of processes of affect regulation closer to real life context.
Conscious, voluntary suppression of negative emotion is associated with smaller startle eyeblinks and enhancement with larger startle eyeblinks (Jackson et al 2000
). Given that the amygdala is purported to be a key structure for emotional perception and production (Davidson and Irwin 1999
), Schaefer et al (2002)
studied modulation of amygdala activity during conscious regulation of negative emotion. International Affective Pictures (CSEA-NIMH 1995
) were used in 7 healthy women. Results indicated that negative stimuli activated the amygdala. They postulate that conscious activation/modulation was in part orchestrated by the amygdala. Their data, however, do not lead to determine directionality and control of affect modulation beyond the participatory role of the amygdala.
Hariri et al (2003)
took a step further to examine the relationship between the PFC (VLPFC and DLPFC) and amygdala function. They looked at how cognitive evaluation of facial expressions can influence areas involved in emotion such as the amygdala. They also examined the influence of this network on peripheral ANS responses. Stimuli consisted of standardized threatening and fearful non-facial stimuli such as sharks and pointed guns selected from International Affective Picture System (IAPS). Simple geometric shapes served as control stimuli. Their results indicated that perceptual processing of IAPS stimuli (matching two out of three) was associated with bilateral amygdala response. Cognitive evaluation (labeling the scene as an “artificial” or “natural disaster”) of the same stimuli was associated with attenuation of amygdala response and an increase in response of the right PFC and anterior cingulate cortex (conscious evaluation and appraisal, and regulating emotion). This pattern is also reflected in skin conductance.
While the majority of the direct neural connections are between the OFC and amygdala, the more lateral PFC (ventral and dorsal PFC) is also connected to the amygdala via the OFC and thalamic and striatal circuits. The OFC is believed to be present in more “low level” reward or punishment values (O’Doherty et al 2001
), while the more lateral PFCs have been implicated in the facilitation of more complex behavioral responses involved in evaluating reward and punishment values (Cools et al 2002
). They suggest that modulation of emotional responses involves the interaction of the amygdala and the lateral PFCs. The ACC and VLPFC are both activated in labeling tasks. The ACC is well connected to both limbic cortex and PFC (Barbas and Pandya 1989
). This is implicated in top-down regulation of the amygdala during cognitive evaluation. Amygdala response paralleled the responses of the ANS.
Functional MRI studies investigating the appraisal and evaluation of stimuli (Nakamura et al 1999
; Narumoto et al 2000
) or self regulation of emotional responses (Beauregard et al 2001
) have implicated right VLPFC and ACC in emotional modulation. Right PFC is also involved in response inhibition (Garavan et al 1999
; Konishi et al 1999
) and set shifting in Wisconsin card sorting test (Konishi et al 1999
). Probably this area is involved in behavioral inhibition along with emotional modulation. This is probably why children with PBD are impulsive and have a hard time transitioning, with poor emotional regulation.