Posterior cingulate cortex
Posterior cingulate cortex | |
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Cingulate gyrus | |
Identifiers | |
Latin | cortex cingularis posterior |
NeuroNames | 162 |
NeuroLex ID | birnlex_950 |
FMA | 61924 |
Anatomical terms of neuroanatomy] |
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.
.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.[1] 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.[2] Increased size of the ventral PCC is related to a decline in working memory performance.[3] The PCC has also been strongly implicated as a key part of several intrinsic control networks.[4][5]
Anatomy
Location and boundaries
The posterior cingulate cortex lies behind the
Cytoarchitectural organization
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.[4]
Structural connections
Nonhuman structure
In non-human primates the following structural connections of the posterior cingulate cortex are well documented:[4]
- Reciprocal connection with other regions of the posteromedial cortex.
- High connectivity to other paralimbic and limbic structures.
- Reciprocal connections to the medial temporal lobe.
- Dense connections to the hippocampal formation, the parahippocampal cortex, the ventromedial prefrontal cortex, and subgenual parts of the anterior cingulate cortex.
- Prominent connections to the areas of heteromodal association in the front, temporal and parietal lobes.
- Strong reciprocal connections to the dorsolateral prefrontal cortex (roughly Brodmann area 46) and the frontal poles (Brodmann areas 10 and 11).
- Less prominent connections to Brodmann areas 9/46, 8 and 9.
- Connections to the dorsal parts of the anterior cingulate cortex.
- Dense connections to the thalamus in the form of a continuous strip that crosses numerous pulvinar nuclei and the striatum.
As is true in other areas of the posteromedial cortex, the posterior cingulate cortex has no apparent connections to primary sensory or motor areas. Thus, it is unlikely to be involved in low-level sensory or motor processing.[4]
Human structure
While many of the connections in non-human primates may be present in humans, they are less well documented. Studies have shown strong reciprocal connections to medial temporal lobe memory structures, such as the entorhinal cortex and the parahippocampal gyrus, the latter being involved in associative learning and episodic memory.[6] 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).[5][7]
Function
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.[4][5] Cerebral blood flow and metabolic rate in the PCC are approximately 40% higher than average across the brain. The high functional connectivity of the PCC, signifies extensive intrinsic connectivity networks (networks of brain regions involved in a range of tasks that share common spatio-temporal patterns of activity).[4]
Emotion and memory
The posterior cingulate cortex has been linked by lesion studies to
The posterior cingulate cortex has also been firmly linked to emotional salience.
Intrinsic control networks
The posterior cingulate cortex exhibits connectivity with a wide range of intrinsic control networks. Its most widely known role is as a central node in the default mode network (DMN). The default mode network (and the PCC) is highly reactive and quickly deactivates during tasks with externally directed, or presently centered, attention (such as working memory or meditation).[4][8] 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.[4]
In addition to the default mode network, the posterior cingulate cortex is also involved in the
The relationship between these networks within the PCC is not clearly understood. When activity increases in the dorsal attention network and the
Considering the relation of the PCC with the DMN, with suppressed posterior cingulate activity favoring low cognitive introspection and higher external attention and increased activity indicating memory retrieval and planning, it has been hypothesized that this brain region is heavily involved in noticing internal and external changes and in facilitating novel behavior or thought in response. High activity, then, would indicate continued operation with the current cognitive set, while lower activity would indicate exploration, flexibility and renewed learning.[5]
An alternative hypothesis is focused more on the difference between the dorsal and ventral subregions and takes into consideration their functional separation. In this model, the PCC is hypothesized to take a chief regulatory role in focusing internal and external attention. Mounting evidence that the PCC is involved in both integrating memories of experiences and initiating a signal to change behavioral strategies supports this hypothesis. Under this model, the PCC plays a crucial role in controlling state of arousal, the breadth of focus and the internal or external focus of attention. This hypothesis emphasizes the PCC as a dynamic network, rather than a fixed and unchanging structure.[4]
While both of the hypotheses are the result of scientific studies, the role of the PCC is still not well understood and there remains much work to be done to investigate the extent of their veracity.[4][5]
Meditation
From neuroimaging studies and subjective descriptions, the PCC has been found to be activated during self-related thinking and deactivated during meditation.[11][12][13][14] 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.[11] These results track closely with findings about the role of the PCC in the DMN.
Disorders
Structural and functional abnormalities in the PCC result in a range of neurological and psychiatric disorders. The PCC likely integrates and mediates information in the brain. Therefore, functional abnormalities of the PCC might be an accumulation of remote and widespread damage in the brain.[4]
Alzheimer's disease
The PCC is commonly affected by neurodegenerative disease.
Autism spectrum disorder
Attention deficit hyperactivity disorder
It has been suggested that ADHD is a disorder of the DMN, where neural systems are disrupted by uncontrolled activity that leads to attentional lapses.[19] In a meta-analysis of structural MRI studies, Nakao et al. (2011) found that patients with ADHD exhibit an increased left PCC,[20] suggesting that developmental abnormalities affect the PCC. In fact, PCC function is abnormal in ADHD.[4] Within the DMN, functional connectivity is reduced and resting state activity is used to diagnose ADHD in children.[4] Treatment for ADHD, includes psychostimulant medication that directly affects PCC activity.[4] Other studies addressing medication for PCC abnormalities, report that the PCC may only respond to stimulant treatments and the effectiveness of medication can be dependent on motivation levels.[4] Furthermore, ADHD has been associated with the gene SNAP25. In healthy children, SNAP25 polymorphism is linked to working memory capacity, altered PCC structure, and task-dependent PCC deactivation patterns on working memory task.[21]
Depression
Abnormal PCC functional connectivity has been linked to major depression, with variable results. One study reports increased PCC functional connectivity,[22] while another shows that untreated patients had decreased functional connectivity from the PCC to the caudate.[23] 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.[4] The anterior node of the DMN is formed, in part, by the highly connected PCC and Brodmann area 25. These two regions are metabolically overactive in treatment resistant major depression.[24] The link between the activity in the PCC and Brodmann area 25 correlates with rumination, a feature of depression.[25] 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.[4]
Schizophrenia
Abnormal activity in the PCC has been linked to
Traumatic brain injury
After
Anxiety disorders
There is accumulating evidence for PCC dysfunction underlying many childhood/adolescent-onset mental disorders.[36] Further, anxiety disorder patients show an association between increased extinction–related PCC activity and greater symptom severity.[37] PCC dysfunction may also play a role in anxiety disorders during adolescence.[38]
See also
- Cingulate cortex
- Cingulum
References
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External links
- Posterior cingulate cortex in the Brede Database at the Technical University of Denmark
For details regarding MRI definitions of the cingulate cortex based on the Desikan-Killiany Brain atlas, see:
- Desikan RS, Ségonne F, Fischl B, Quinn BT, Dickerson BC, Blacker D, Buckner RL, Dale AM, Maguire RP, et al. (Jul 2006). "An automated labeling system for subdividing the human cerebral cortex on MRI scans into gyral based regions of interest". NeuroImage. 31 (3): 968–80. S2CID 12420386.