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Caudal part of the cingulate cortex of the brain

The posterior cingulate cortex (PCC) is the caudal part of the cingulate cortex, located posterior to the anterior cingulate cortex. This is the upper part of the "limbic lobe". The cingulate cortex is made up of an area around the midline of the brain. Surrounding areas include the retrosplenial cortex and the precuneus. Cytoarchitectonically the posterior cingulate cortex is associated with Brodmann areas 23 and 31. The PCC forms a central node in the default mode network of the brain. It has been shown to communicate with various brain networks simultaneously and is involved in diverse functions. Along with the precuneus, the PCC has been implicated as a neural substrate for human awareness in numerous studies of both the anesthetized and vegetative (coma) states. Imaging studies indicate a prominent role for the PCC in pain and episodic memory retrieval. Increased size of the ventral PCC is related to a decline in working memory performance. The PCC has also been strongly implicated as a key part of several intrinsic control networks.

The posterior cingulate cortex is considered a paralimbic cortical structure, consisting of Brodmann areas 23 and 31. As part of the paralimbic cortex, it has fewer than six layers, placing its cell architecture in between the six layered neocortex and the more primitive allocortex of core limbic structures. It has also been associated with the hippocampocentric subdivision of the paralimbic zone. The cytoarchitecture of the PCC is not entirely uniform, instead it contains distinct anterior and dorsal subregions, which are increasingly understood as distinct in function, as well as cytoarchitectural structure. In humans, the PCC is also connected to areas involved in emotion and social behavior, attention (the lateral intraparietal cortex and precuneus), learning and motivation (the anterior and lateral thalamic nucleus, caudate nucleus, orbitofrontal cortex and anterior cingulate cortex).

The posterior cingulate cortex is highly connected and one of the most metabolically active regions in the brain, but there is no consensus as to its cognitive role. Conversely, the DMN is active when attention is internally directed (during episodic memory retrieval, planning, and daydreaming). A failure of the DMN to deactivate at proper times is associated with poor cognitive function, thereby indicating its importance in attention. The relationship between these networks within the PCC is not clearly understood. When activity increases in the dorsal attention network and the frontoparietal control network, it must simultaneously decrease in the DMN in a closely correlated way. This anti correlated pattern is indicative of the various differences and importance of subregions in the posterior cingulate cortex. Using generative topographic mapping, it was further found that undistracted, effortless mind wandering corresponds with PCC deactivation, whereas distracted and controlled awareness corresponds with PCC activation. In fact, reduced metabolism in the PCC has been identified as an early sign of Alzheimer's disease, and is frequently present before a clinical diagnosis. In Alzheimer's disease, metabolic abnormality is linked to amyloid deposition and brain atrophy with a spatial distribution that resembles the nodes of the default mode network. possibly explaining why the PCC is affected in the early stages of the disease. Studies have shown that the abnormalities in cingulate responses during interpersonal interaction correlate with the severity of symptoms in ASD, and the failure to show task dependent deactivation in the PCC correlates with overall social function. In a meta analysis of structural MRI studies, Nakao et al. (2011) found that patients with ADHD exhibit an increased left PCC, suggesting that developmental abnormalities affect the PCC. In fact, PCC function is abnormal in ADHD.

Abnormal PCC functional connectivity has been linked to major depression, with variable results. One study reports increased PCC functional connectivity, while another shows that untreated patients had decreased functional connectivity from the PCC to the caudate. Other studies have looked at interactions between the PCC and the sub genual cingulate region (Brodmann area 25), a region of the brain that potentially causes depression. The link between the activity in the PCC and Brodmann area 25 correlates with rumination, a feature of depression. This link between the two regions could influence medication responses in patients. Already, it has been found that both regions show alterations in metabolism after antidepressant treatment. Furthermore, patients who undergo deep brain stimulation, have increased glucose metabolism and cerebral flow in the PCC, while also showing an altered Brodmann area 25. while another shows abnormal glucose metabolism that was highly correlated in the pulvinar and the PCC. In the latter study, thalamic interactions with the frontal lobes were reduced, which could mean that schizophrenia affects thalamocortical connections. Further abnormalities in the PCC, abnormal NMDA, cannabinoid, and GABAergic receptor binding have been found with post mortem autoradiography of people with schizophrenia. Abnormalities in the structure and white matter connections of the PCC have also been recorded in patients with schizophrenia. Those with a poor outcome often have reduced PCC volume. In functional MRI studies, abnormal PCC function., has been linked to increases and decreases in functional connectivity. There are also abnormal PCC responses during task performance. These abnormalities may contribute to psychotic symptoms of some persons with schizophrenia. Research on the effect of the psychedelic drug psilocybin shows that the altered state of consciousness induced by this drug can be correlated with abnormal metabolism and functional connectivity of the PCC, as well as a reduction in the strength of anti correlations between the DMN and the frontoparietal control network (FPCN). Because these networks contribute to internal and external cognition, abnormalities in the PCC might contribute to psychosis in some types of schizophrenia.

After traumatic brain injury (TBI), abnormalities have been shown in the PCC. Often, head injuries produce widespread axonal injury that disconnect brain regions and lead to cognitive impairment. This is also related to reduced metabolism within the PCC. Studies of performance on simple choice reaction time tasks after TBI show, in particular, that the pattern of functional connectivity from the PCC to the rest of the DMN can predict TBI impairments. They also found that greater damage to the cingulum bundle, that connects the PCC to the anterior DMN, was correlated with sustained attention impairment. In a subsequent study, it was found that TBIs are related to a difficulty in switching from automatic to controlled responses. Within selected tasks, patients with TBI showed impaired motor inhibition that was associated with failure to rapidly reactive the PCC. Collectively, this suggests that the failure to control the PCC/DMN activity can lead to attentional lapses in TBI patients.

There is accumulating evidence for PCC dysfunction underlying many childhood/adolescent onset mental disorders. Further, anxiety disorder patients show an association between increased extinction–related PCC activity and greater symptom severity. PCC dysfunction may also play a role in anxiety disorders during adolescence.