Retrosplenial cortical activation in the fibromyalgia syndrome

Wik, Gustav; Fischer, Håkan; Bragée, Björn; Kristianson, Marianne; Fredrikson, Mats

doi:10.1097/00001756-200303240-00019

Cited by 50 publications

(32 citation statements)

References 18 publications

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“…Interestingly, this altered fronto-hippocampal connectivity and impaired memory was not associated with a significant change in overall firing rate, just a change in firing rhythm. Similarly, we found no overall increases in CBF, an index of neural activity, in pain-related brain regions, which is consistent with many previous investigations (Hsieh et al, 1995;Wik et al, 2003;Yunus et al, 2004). These data suggest that altered thalamocortical rhythm, and not necessarily increased overall activity in somatosensory processing regions, can result in the persistent perception of pain.…”

supporting

confidence: 93%

Chronic Pain: Lost Inhibition?

Henderson¹,

et al. 2013

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Human brain imaging has revealed that acute pain results from activation of a network of brain regions, including the somatosensory, insular, prefrontal, and cingulate cortices. In contrast, many investigations report little or no alteration in brain activity associated with chronic pain, particularly neuropathic pain. It has been hypothesized that neuropathic pain results from misinterpretation of thalamocortical activity, and recent evidence has revealed altered thalamocortical rhythm in individuals with neuropathic pain. Indeed, it was suggested nearly four decades ago that neuropathic pain may be maintained by a discrete central generator, possibly within the thalamus. In this investigation, we used multiple brain imaging techniques to explore central changes in subjects with neuropathic pain of the trigeminal nerve resulting in most cases (20 of 23) from a surgical event. Individuals with chronic neuropathic pain displayed significant somatosensory thalamus volume loss (voxel-based morphometry) which was associated with decreased thalamic reticular nucleus and primary somatosensory cortex activity (quantitative arterial spin labeling). Furthermore, thalamic inhibitory neurotransmitter content was significantly reduced (magnetic resonance spectroscopy), which was significantly correlated to the degree of functional connectivity between the somatosensory thalamus and cortical regions including the primary and secondary somatosensory cortices, anterior insula, and cerebellar cortex. These data suggest that chronic neuropathic pain is associated with altered thalamic anatomy and activity, which may result in disturbed thalamocortical circuits. This disturbed thalamocortical activity may result in the constant perception of pain.

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confidence: 93%

Chronic Pain: Lost Inhibition?

Henderson¹,

et al. 2013

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“…Single-photon-emission-computed tomography (SPECT) imaging has demonstrated regional cerebral blood flow (rCBF) decrease in thalamus and pontine region in patients of FM [13, 14]. The ensuing PET study has not only shown rCBF decrease in several brain regions, supporting the dysfunctional cognitive processing of pain, but also higher retrosplenial rCBF, suggesting secondary hyperalgesia [15]. Since the inception of functional magnetic resonance imaging (fMRI), it became easier to infer neural activity by proxy of blood-oxygen-level-dependent (BOLD) contrast without the need of radioactive tracer or contrast agent.…”

Section: Introductionmentioning

confidence: 99%

Gray Matter Atrophy within the Default Mode Network of Fibromyalgia: A Meta-Analysis of Voxel-Based Morphometry Studies

Lin

Lee

Weng

2016

BioMed Research International

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Over the years, studies have demonstrated morphological changes in the brain of fibromyalgia (FMS). We aimed to conduct a coordinate-based meta-analytic research through systemic review on voxel-based morphometry (VBM) imaging results to identify consistent gray matter (GM) difference between FMS patients and healthy subjects. We performed a comprehensive literature search in PubMed (January 2000–December 2015) and included six VBM publication on FMS. Stereotactic data were extracted from 180 patients of FMS and 123 healthy controls. By means of activation likelihood estimation (ALE) technique, regional GM reduction in left medial prefrontal cortex and right dorsal posterior cingulate cortex was identified. Both regions are within the default mode network. In conclusion, the gray matter deficit is related to the both affective and nonaffective components of pain processing. This result also provided the neuroanatomical correlates for emotional and cognitive symptoms in FMS.

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“…Studies comparing rCBF at rest in chronic pain patients to normal controls [11,18,21,25,26,41] have reported reductions or asymmetric changes in thalamus and reductions in frontal, temporal, parietal, occipital regions. These reports are not conclusive since knowledge about cerebral pain mechanisms is mainly based on experimental studies.…”

mentioning

confidence: 99%