Alterations in grey matter density and functional connectivity in trigeminal neuropathic pain and trigeminal neuralgia: A systematic review and meta-analysis

Henssen, Dylan; Dijk, Jurriaan; Knepflé, Robin; Sieffers, Matthijs; Winter, Anouk; Vissers, Kris

doi:10.1016/j.nicl.2019.102039

Cited by 48 publications

(52 citation statements)

References 68 publications

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“…In this study, compared to HC, in TN wNVC, the GM volume deficits were widely distributed across the thalamus, superior frontal gyrus, inferior frontal gyrus, middle temporal gyrus, angular gyrus, and posterior central gyrus. These affected regions were mostly consistent with those reported by previously published large-sized VBM analyses and meta-analyses which have reported that patients with CTN show GM volume deficits throughout the frontal, temporal and parietal lobes; cingulate and insular cortices; and thalamus [17][18][19][20][21][22][23]. In contrast, in patients with TN woNVC as compared with HC, we observed almost all reductions in GM volume were bilateral symmetrical, which were limited to the bilateral inferior temporal gyrus, bilateral PCC.…”

Section: Discussionsupporting

confidence: 91%

“…The mPFC also compose the DMN with PCC, angular gyrus [35], and the TN woNVC can be associated with the changes of these structure according to our findings. Recent series of studies have identified several cortical and subcortical regions associated with GM volume reduction in patients with TN wNVC [17,19,20,22,23,36,37]. Putting the findings of these studies together, it can be inferred that TN wNVC is associated with extensive deficits.…”

Section: Discussionmentioning

confidence: 98%

“…Recent series of studies have identified several cortical and subcortical regions associated with GM volume reduction in patients with TN wNVC [ 17 , 19 , 20 , 22 , 23 , 36 , 37 ]. Putting the findings of these studies together, it can be inferred that TN wNVC is associated with extensive deficits.…”

Section: Discussionmentioning

confidence: 99%

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Gray and white matter abnormalities in primary trigeminal neuralgia with and without neurovascular compression

Jiang

Qiu

et al. 2020

J Headache Pain

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Purpose Previous researches have reported gray and white matter microalterations in primary trigeminal neuralgia (TN) with neurovascular compression (NVC). The central mechanism underlying TN without NVC are unknown but may include changes in specific brain regions or circuitries. This study aimed to investigate abnormalities in the gray matter (GM) and white matter (WM) of the whole brain and the possible pathogenetic mechanism underlying this disease. Methods We analyzed brain morphologic images of TN patients, 23 with NVC (TN wNVC) and 22 without NVC (TN wNVC) compared with 45 healthy controls (HC). All subjects underwent 3T-magnetic resonance imaging and pain scale evaluation. Voxel-based morphometry (VBM) and surface-based morphometry (SBM) were used to investigate whole brain grey matter quantitatively; graph theory was applied to obtain network measures based on extracted DTI data based on DTI data of the whole brains. Sensory and affective pain rating indices were assessed using the visual analog scale (VAS) and short-form McGill Pain Questionnaire (SF-MPQ). Results The VBM and SBM analyses revealed widespread decreases in GM volume and cortical thickness in TN wNVC compared to TN woNVC, and diffusion metrics measures and topology organization changes revealed DTI showed extensive WM integrity alterations. However, above structural changes differed between TN wNVC and TN woNVC, and were related to specific chronic pain modulation mechanism. Conclusion Abnormalities in characteristic regions of GM and WM structural network were found in TN woNVC compared with TN wNVC group, suggesting differences in pathophysiology of two types of TN.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 98%

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Gray and white matter abnormalities in primary trigeminal neuralgia with and without neurovascular compression

Jiang

Qiu

et al. 2020

J Headache Pain

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“…Such lateralization has also been found in imaging studies of patients with TN [ 37 , 38 ]. However, a meta-analysis revealed that the bilateral insular GMV decreased in patients with TN or TNP [ 39 ], indicating that the effect of neuropathic pain on the insular GMV is not limited to the ipsilateral side.…”

Section: Structural and Functional Changes Occurring In The Insulamentioning

confidence: 99%

Current Understanding of the Involvement of the Insular Cortex in Neuropathic Pain: A Narrative Review

Wang

Zhang

Wang

et al. 2021

IJMS

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Neuropathic pain is difficult to cure and is often accompanied by emotional and psychological changes. Exploring the mechanisms underlying neuropathic pain will help to identify a better treatment for this condition. The insular cortex is an important information integration center. Numerous imaging studies have documented increased activity of the insular cortex in the presence of neuropathic pain; however, the specific role of this region remains controversial. Early studies suggested that the insular lobe is mainly involved in the processing of the emotional motivation dimension of pain. However, increasing evidence suggests that the role of the insular cortex is more complex and may even be related to the neural plasticity, cognitive evaluation, and psychosocial aspects of neuropathic pain. These effects contribute not only to the development of neuropathic pain, but also to its comorbidity with neuropsychiatric diseases. In this review, we summarize the changes that occur in the insular cortex in the presence of neuropathic pain and analgesia, as well as the molecular mechanisms that may underlie these conditions. We also discuss potential sex-based differences in these processes. Further exploration of the involvement of the insular lobe will contribute to the development of new pharmacotherapy and psychotherapy treatments for neuropathic pain.

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“…There would be a bi-directional relationship between vascular and neuronal activities, where CSD activated changes in C-fibers function with CGRP antidromic production, while the subsequent change in vascular tone, at least in vitro, can, in turn, modulate neuronal activity, termed vascular-neuro coupling [ 87 ]. Mathematical models of CSD on realistic MRI from migraine with aura patients showed that the propagation of hyperpolarization phenomenon could in theory involve cortical areas in the network of pain processing [ 88 ]. The tonic inhibition of trigeminal peripheral afferents inputs to the cortex, exerted by CGRP monoclonal antibodies, could thus modulate the excitability of the large network dedicated to nociceptive signals elaboration, also changing the mode of cortical connections favoring the generation and extension of critical bioelectrical phenomena.…”

Section: Perspectives (In View Of Peripheral Cgrp Approach)mentioning

confidence: 99%

Pain-Related Brain Connectivity Changes in Migraine: A Narrative Review and Proof of Concept about Possible Novel Treatments Interference

et al. 2021

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A neuronal dysfunction based on the imbalance between excitatory and inhibitory cortical-subcortical neurotransmission seems at the basis of migraine. Intercritical neuronal abnormal excitability can culminate in the bioelectrical phenomenon of Cortical Spreading Depression (CSD) with secondary involvement of the vascular system and release of inflammatory mediators, modulating in turn neuronal activity. Neuronal dysfunction encompasses the altered connectivity between the brain areas implicated in the genesis, maintenance and chronic evolution of migraine. Advanced neuroimaging techniques allow to identify changes in functional connectivity (FC) between brain areas involved in pain processes. Through a narrative review, we re-searched case-control studies on FC in migraine, between 2015 and 2020, by inserting the words migraine, fMRI, EEG, MEG, connectivity, pain in Pubmed. Studies on FC have shown that cortical processes, in the neurolimbic pain network, are likely to be prevalent for triggering attacks, in response to predisposing factors, and that these lead to a demodulation of the subcortical areas, at the basis of migraine maintenance. The link between brain dysfunction and peripheral interactions through the inhibition of CGRP, the main mediator of sterile migraine inflammation needs to be further investigated. Preliminary evidence could suggest that peripheral nerves inference at somatic and trigeminal levels, appears to change brain FC.

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Alterations in grey matter density and functional connectivity in trigeminal neuropathic pain and trigeminal neuralgia: A systematic review and meta-analysis

Cited by 48 publications

References 68 publications

Gray and white matter abnormalities in primary trigeminal neuralgia with and without neurovascular compression

Gray and white matter abnormalities in primary trigeminal neuralgia with and without neurovascular compression

Current Understanding of the Involvement of the Insular Cortex in Neuropathic Pain: A Narrative Review

Pain-Related Brain Connectivity Changes in Migraine: A Narrative Review and Proof of Concept about Possible Novel Treatments Interference

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