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Posterior Cingulate Research:

Meditation

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From neuroimagining and subjective descriptions, the PCC has been found to be activated during self-related thinking and deactivated during meditation.[1] Using generative topographic mapping, it was further found that undistracted, effortless mind wandering corresponded with PCC deactivation, whereas distracted and controlled awareness corresponded with PCC activation.[1] These results track closely with findings about the PCC's role in the DMN.

Disorders

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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, the functional abnormalities of the PCC might be an accumulation of remote and widespread damage in the brain.[2]

Alzheimer's Disease

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The PCC is commonly affected by neurodegenerative disease.[3] In fact, reduced metabolism in the PCC is an early sign of Alzheimer's disease, and is frequently present before a clinical diagnosis.[2] The reduced metabolism in the PCC is typically one part in a diffuse pattern of metabolic dysfunction in the brain that includes medial Temporal lobe structures and the anterior thalamus, and these metabolic abnormalities may be due to damage in isolated but connected regions.[2] For instance, Meguro et al. (1999) show that experimental damage of the rhinal cortex results in hypometabolism of the PCC.[4] In Alzheimer's disease, the metabolic abnormality is linked to Amyloid deposition and brain Atrophy with a spatial distribution that resembles the nodes of the Default mode network (DMN).[2] In early Alzheimer's, the functional connectivity within the DMN is reduced and affects the connection between the PCC and the hippocampus, and these altered patterns can reflect ApoE genetic status (a risk factor associated with the disease).[2] It has been found that neurodegenerative diseases spread 'prion-like' through the brain.[2] For example, when the proteins amyloid-b and TDP-43 are in their abnormal form, they spread trans-synaptically and are associated with Neurodegeneration.[2] This transmission of abnormal protein would be constrained by the organization of white matter connections and could potentially explain the spatial distribution of Alzheimer's pathology within the DMN.[2] In Alzheimer’s disease, the topology of white matter connectivity helps in predicting atrophic patterns,[5] which could explain why the PCC is affected in the early stages of the disease.[2]

Autism Spectrum Disorder

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Autism spectrum disorders (ASDs) are associated with metabolic and functional abnormalities of the PCC. Individuals with ASDs show reduction in metabolism, exhibit abnormal functional responses and demonstrate reductions in functional connectivity.[2] Interestingly, these reductions are prominent in the PCC.[6] Studies have shown that the abnormalities in cingulate responses during interpersonal interaction correlate with the severity of autistic symptoms, and the failure to show task dependent deactivation in the PCC correlates with overall social function.[2] Finally, post-mortem studies show that the PCCs of patients with ASDs have cytoarchitectonic abnormalities, as well as reduced levels of GABA A receptors, and benzodiazepine binding sites[2]

Attention Deficit Hyperactivity Disorder

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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.[7] Nakao et al. (2011) performed a meta-analysis of structural MRI studies and found that patients with ADHD exhibit an increased left PCC,[8] which could mean that developmental abnormalities affect the PCC. In fact, PCC function is abnormal in ADHD.[2] Within the DMN, functional connectivity is reduced and the resting state activity is a way to diagnose children with ADHD.[2] Treatment for ADHD, includes psychostimulant medication that directly affects PCC activity.[2] In ADHD, normal task-dependent PCC deactivation is reduced so psychostimulants work to normalize this abnormality.[9] Other studies looking at medications for abnormalities in the PCC found that the PCC may only respond to stimulant treatments and that the effectiveness of medication can be dependent on motivation levels.[2] 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.[9] Therefore, the extent to which PCC function is affected, may be a mediating factor in the genetic predisposition to ADHD.

Depression

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Abnormal PCC functional connectivity has been linked to major depression. However, the conclusions of the studies vary. One found increased PCC functional connectivity,[10] while another showed that untreated patients had decreased functional connectivity from the PCC to the caudate.[11] 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.[2] The anterior node of the DMN is formed, in part, by the highly connected PCC and Brodmann area 25. The two regions are metabolically overactive in treatment resistant major depression.[12] The link between the activity in the PCC and Brodmann area 25 correlates with rumination, a feature of depression.[13] 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, had increased glucose metabolism and cerebral flow in the PCC, while also altering Brodmann area 25.[2]

Schizophrenia

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Abnormal activity in the PCC has been linked to schizophrenia, a mental disorder with common symptoms such as hallucinations, delusions, disorganized thinking, and a lack of emotional intelligence. What is common between symptoms is that they have to do with an inability to distinguish between internal and external events; they lack insight. Two PET studies on patients with schizophrenia showed abnormal metabolism in the PCC. One study found that glucose metabolism was decreased in schizophrenics,[14] while another found abnormal glucose metabolism that was highly correlated in the pulvinar and the PCC.[15] In the latter study, thalamic interactions with the frontal lobes were reduced, which could mean that schizophrenia affects thalami-cortical connections. Further abnormalities in the PCC, abnormal NMDA, camabinoid, and DABAergic receptor binding, have been found with post-mortem autoradiography of schizophrenics.[16] Abnormalities in the structure and white matter connections of the PCC have also been found in schizophrenic patients. Schizophrenics with a poor outcome often have reduced PCC volume.[15] It has further been found that white matter abnormalities in the cingulum bundle, a structure that connects the PCC to other limbic structures.[17] In functional MRI studies, there is more evidence of abnormal PCC function. There can be increases and decreases in the functional connectivity.[18] There are also abnormal PCC responses during task performance.[19] All of the previously mentioned network abnormalities may be the reason for psychotic symptoms. Recently it was found that the psychedelic drug Psilocybin induces an altered state of consciousness and is related to abnormal metabolism and functional connectivity of the PCC, as well as a reduction in the strength of anti-correlations between the DMN and the FPCN.[20] These networks contribute to internal and external cognition, so abnormalities in these networks might be responsible for the psychosis in schizophrenia.

Traumatic Brain Injury

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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.[21] Studies have looked at performance on simple choice reaction time tasks after TBIs.[22] This study, in particular, found that the pattern of functional connectivity from the PCC to the rest of the DMN could predict TBI impairments even before symptoms had manifested. They also found that greater damage to the cingulum bundle, that connects the PCC to the anterior DMN, was linked to impairments of sustained attention. In a subsequent study, it was found that TBIs are related to a difficulty in switching from automatic to controlled responses.[23] Within selected tasks, patients with TBIs 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.


References

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  1. ^ a b Garrison, K. A.; Santoyo, J. F.; Davis, J. H.; Thornhill Ta, 4th; Kerr, C. E.; Brewer, J. A. (2013). "Effortless awareness: using real time neurofeedback to investigate correlates of posterior cingulate cortex activity in meditators' self-report". Frontiers in Human Neuroscience. 7: 440. doi:10.3389/fnhum.2013.00440. PMC 3734786. PMID 23964222.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: numeric names: authors list (link)
  2. ^ a b c d e f g h i j k l m n o p q r Cite error: The named reference Leech was invoked but never defined (see the help page).
  3. ^ Buckner, RL (2008). "The brain's default network: anatomy, function, and relevance to disease". Ann N Y Acad Sci. 1124: 1–38. doi:10.1196/annals.1440.011. PMID 18400922. S2CID 3167595. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  4. ^ Meguro, K (1999). "Neocortical and hippocampal glucose hypometabolism following neurotoxic lesions of the entorhinal and perirhinal cortices in the non-human primate as shown by PET. Implications for Alzheimer's disease". Brain. 122 (Pt 8): 1519–31. doi:10.1093/brain/122.8.1519. PMID 10430835. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  5. ^ Raj, A (2012). "A network diffusion model of disease progression in dementia". Neuron. 73 (6): 1204–15. doi:10.1016/j.neuron.2011.12.040. PMC 3623298. PMID 22445347. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  6. ^ Cherkassky, V. L.; Kana, R. K.; Keller, T. A.; Just, M. A. (2006 Nov 6). "Functional connectivity in a baseline resting-state network in autism". NeuroReport. 17 (16): 1687–90. doi:10.1097/01.wnr.0000239956.45448.4c. PMID 17047454. S2CID 568233. {{cite journal}}: Check date values in: |date= (help)
  7. ^ Sonuga-Barke, E. J.; Castellanos, F. X. (2007). "Spontaneous attentional fluctuations in impaired states and pathological conditions: a neurobiological hypothesis". Neuroscience and Biobehavioral Reviews. 31 (7): 977–86. doi:10.1016/j.neubiorev.2007.02.005. PMID 17445893. S2CID 16831759.{{cite journal}}: CS1 maint: date and year (link)
  8. ^ Nakao, T.; Radua, J.; Rubia, K.; Mataix-Cols, D. (2011 Nov). "Gray matter volume abnormalities in ADHD: voxel-based meta-analysis exploring the effects of age and stimulant medication". The American Journal of Psychiatry. 168 (11): 1154–63. doi:10.1176/appi.ajp.2011.11020281. PMID 21865529. {{cite journal}}: Check date values in: |date= (help)
  9. ^ a b Latasch, L.; Christ, R. (1988 Mar). "[Problems in anesthesia of drug addicts]". Der Anaesthesist. 37 (3): 123–39. PMID 3289412. {{cite journal}}: Check date values in: |date= (help)
  10. ^ Zhou, Y.; Yu, C.; Zheng, H.; Liu, Y.; Song, M.; Qin, W.; Li, K.; Jiang, T. (2010 Mar). "Increased neural resources recruitment in the intrinsic organization in major depression". Journal of Affective Disorders. 121 (3): 220–30. doi:10.1016/j.jad.2009.05.029. PMID 19541369. {{cite journal}}: Check date values in: |date= (help)
  11. ^ Bluhm, R.; Williamson, P.; Lanius, R.; Théberge, J.; Densmore, M.; Bartha, R.; Neufeld, R.; Osuch, E. (2009 Dec). "Resting state default-mode network connectivity in early depression using a seed region-of-interest analysis: decreased connectivity with caudate nucleus". Psychiatry and Clinical Neurosciences. 63 (6): 754–61. doi:10.1111/j.1440-1819.2009.02030.x. PMID 20021629. S2CID 35725401. {{cite journal}}: Check date values in: |date= (help)
  12. ^ Mayberg, H. S.; Liotti, M.; Brannan, S. K.; McGinnis, S.; Mahurin, R. K.; Jerabek, P. A.; Silva, J. A.; Tekell, J. L.; Martin, C. C.; Lancaster, J. L.; Fox, P. T. (1999 May). "Reciprocal limbic-cortical function and negative mood: converging PET findings in depression and normal sadness". The American Journal of Psychiatry. 156 (5): 675–82. doi:10.1176/ajp.156.5.675. PMID 10327898. S2CID 16258492. {{cite journal}}: Check date values in: |date= (help)
  13. ^ Berman, M. G.; Peltier, S.; Nee, D. E.; Kross, E.; Deldin, P. J.; Jonides, J. (2011 Oct). "Depression, rumination and the default network". Social Cognitive and Affective Neuroscience. 6 (5): 548–55. doi:10.1093/scan/nsq080. PMC 3190207. PMID 20855296. {{cite journal}}: Check date values in: |date= (help)
  14. ^ Haznedar, M. M.; Buchsbaum, M. S.; Hazlett, E. A.; Shihabuddin, L.; New, A.; Siever, L. J. (2004 Dec 1). "Cingulate gyrus volume and metabolism in the schizophrenia spectrum". Schizophrenia Research. 71 (2–3): 249–62. doi:10.1016/j.schres.2004.02.025. PMID 15474896. S2CID 28889346. {{cite journal}}: Check date values in: |date= (help)
  15. ^ a b Mitelman, S. A.; Byne, W.; Kemether, E. M.; Hazlett, E. A.; Buchsbaum, M. S. (2005 Sep). "Metabolic disconnection between the mediodorsal nucleus of the thalamus and cortical Brodmann's areas of the left hemisphere in schizophrenia". The American Journal of Psychiatry. 162 (9): 1733–5. doi:10.1176/appi.ajp.162.9.1733. PMID 16135634. {{cite journal}}: Check date values in: |date= (help)
  16. ^ Newell, K. A.; Zavitsanou, K.; Huang, X. F. (2005 Aug 22). "Ionotropic glutamate receptor binding in the posterior cingulate cortex in schizophrenia patients". NeuroReport. 16 (12): 1363–7. doi:10.1097/01.wnr.0000174056.11403.71. PMID 16056140. S2CID 29764510. {{cite journal}}: Check date values in: |date= (help)
  17. ^ Kubicki, M (2003 Dec). "An fMRI study of semantic processing in men with schizophrenia". NeuroImage. 20 (4): 1923–33. doi:10.1016/s1053-8119(03)00383-5. PMC 2806220. PMID 14683698. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  18. ^ Liang, M (2006 Feb 6). "Widespread functional disconnectivity in schizophrenia with resting-state functional magnetic resonance imaging". NeuroReport. 17 (2): 209–13. doi:10.1097/01.wnr.0000198434.06518.b8. PMID 16407773. S2CID 10743973. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  19. ^ Whitfield-Gabrieli, S (2009 Jan 27). "Hyperactivity and hyperconnectivity of the default network in schizophrenia and in first-degree relatives of persons with schizophrenia". Proceedings of the National Academy of Sciences of the United States of America. 106 (4): 1279–84. doi:10.1073/pnas.0809141106. PMC 2633557. PMID 19164577. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  20. ^ Carhart-Harris, R. L.; Erritzoe, D.; Williams, T.; Stone, J. M.; Reed, L. J.; Colasanti, A.; Tyacke, R. J.; Leech, R.; Malizia, A. L.; Murphy, K.; Hobden, P.; Evans, J.; Feilding, A.; Wise, R. G.; Nutt, D. J. (2012 Feb 7). "Neural correlates of the psychedelic state as determined by fMRI studies with psilocybin". Proceedings of the National Academy of Sciences of the United States of America. 109 (6): 2138–43. doi:10.1073/pnas.1119598109. PMC 3277566. PMID 22308440. {{cite journal}}: Check date values in: |date= (help)
  21. ^ Nakashima, T.; Nakayama, N.; Miwa, K.; Okumura, A.; Soeda, A.; Iwama, T. (2007 Feb). "Focal brain glucose hypometabolism in patients with neuropsychologic deficits after diffuse axonal injury". AJNR. American Journal of Neuroradiology. 28 (2): 236–42. PMC 7977405. PMID 17296986. {{cite journal}}: Check date values in: |date= (help)
  22. ^ Bonnelle, V.; Leech, R.; Kinnunen, K. M.; Ham, T. E.; Beckmann, C. F.; De Boissezon, X.; Greenwood, R. J.; Sharp, D. J. (2011 Sep 21). "Default mode network connectivity predicts sustained attention deficits after traumatic brain injury". The Journal of Neuroscience : The Official Journal of the Society for Neuroscience. 31 (38): 13442–51. doi:10.1523/JNEUROSCI.1163-11.2011. PMC 6623308. PMID 21940437. {{cite journal}}: Check date values in: |date= (help)
  23. ^ Bonnelle, V (2012 Mar 20). "Salience network integrity predicts default mode network function after traumatic brain injury". Proceedings of the National Academy of Sciences of the United States of America. 109 (12): 4690–5. doi:10.1073/pnas.1113455109. PMC 3311356. PMID 22393019. {{cite journal}}: Check date values in: |date= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
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