Anterior cingulate cortex (rostral)
Pars rostralis gyri cinguli anterioris
cortical
The rostral portion of the anterior cingulate gyrus, arching above the genu of the corpus callosum from the subcallosal cortex below to the supplementary motor area behind. The rostral anterior cingulate cortex (rACC) is conventionally delimited rostrally to the genu and is distinguished from the caudal anterior cingulate (cACC, also called the midcingulate motor area) by both cytoarchitecture and connectivity.
rACC is a transitional cortex with strong limbic connectivity. It receives dense projections from the amygdala, hippocampus, and ventral striatum, and projects to the periaqueductal grey, lateral hypothalamus, and brainstem autonomic nuclei. These connections place rACC at the cortical apex of the visceromotor and emotional-regulation systems, with downstream control over autonomic, endocrine, and behavioural responses to affectively significant stimuli.
Functionally, rACC is implicated in emotional appraisal, autonomic regulation, and the evaluation of internal states (pain affect, hunger, thirst). It also tracks placebo analgesic responses and shows increased activity under successful emotion-regulation strategies. The caudal anterior cingulate (BA 32 dorsally), often grouped with rACC in older parcellations, is more closely tied to performance monitoring and conflict detection.
default-mode salience
The anterior cingulate has been the site of recurring revisions in functional anatomy. Older accounts treated it as a single emotion-and-attention region. Functional and cytoarchitectonic refinements over the last two decades have settled on a working distinction between a rostral limbic ACC (rACC, this entry) coupled to affect and visceromotor regulation, and a caudal cingulate motor area (cACC) coupled to performance monitoring, conflict detection, and action selection. The boundary lies roughly at the level of the genu of the corpus callosum.
Subgenual cingulate (BA 25), immediately ventral to rACC, became a clinical neuroscience target after Helen Mayberg’s 2005 demonstration that deep brain stimulation of the underlying white matter could produce sustained remission in some patients with severe treatment-resistant depression. The therapy remains experimental but the underlying observation, that subgenual cingulate hypermetabolism characterises depression and that suppressing it reduces symptoms, has been broadly reproduced.
Anterior cingulate damage from bilateral anterior cerebral artery infarcts produces the dramatic but rare syndrome of akinetic mutism, in which an awake patient does not speak, does not move spontaneously, and shows minimal affective reactivity. Recovery is variable; some patients return to near-normal function after weeks to months.