The cingulate cortex plays a significant role in mediating cognitive influences on emotion (Stevens, Hurley, & Taber, 2011).
Lower-than-normal activations within cingulate cortex have been reported for several conditions in which emotional numbing and/or suppression of emotions are common symptoms. For example, a metaanalysis of functional neuroimaging in posttraumatic stress disorder (PTSD) found reduced activation in both sACC and aMCC during fear conditioning (Etkin, & Wager, 2007). The authors proposed that reduced activation in sACC may indicate impairment in emotion-regulation and fear-extinction, whereas the reduced activation in aMCC may relate to reduced experience of negative emotion.
My question surrounding this is related to the fact that (Answer provided in Do ADHD drugs harm the brain?)
[Long-term use of ADHD stimulants in individuals with ADHD] appear to promote "normalization" of certain structural deficiences. Not all deficiences, though (i.e. effects visible on the right anterior cingulate cortex (ACC) but not on the left ACC).
Whilst this is a great answer to the initial question, it is difficult for me to pick apart from a neuropsychological basis. Would there be significant improvements to ADHD symptoms with the “normalisation” of the ACC or would there still be significant problems?
Also, are there differences in function between the left and right ACC? Plus, if there is little or no improvement in the left ACC, would the right ACC take over the functions of the left or would the left affect the right?
References
Etkin, A., & Wager, T. D. (2007). Functional neuroimaging of anxiety: a meta-analysis of emotional processing in PTSD, social anxiety disorder, and specific phobia. American Journal of Psychiatry, 164(10), 1476-1488.
DOI: 10.1176/appi.ajp.2007.07030504
PDF: https://ajp.psychiatryonline.org/doi/pdf/10.1176/appi.ajp.2007.07030504
Stevens, F. L., Hurley, R. A., & Taber, K. H. (2011). Anterior cingulate cortex: unique role in cognition and emotion. The Journal of neuropsychiatry and clinical neurosciences, 23(2), 121-125.
DOI: 10.1176/jnp.23.2.jnp121
PDF: https://neuro.psychiatryonline.org/doi/pdf/10.1176/jnp.23.2.jnp121