Altered Spontaneous Brain Activity in Patients With Idiopathic Trigeminal Neuralgia

Yuan, Jie; Cao, Song; Huang, Yue; Zhang, Yi; Xie, Peng; Fu, Bao; Zhang, Tijiang; Song, Ganjun; Yu, Tian; Zhang, Mazhong

doi:10.1097/ajp.0000000000000578

Cited by 30 publications

(33 citation statements)

References 69 publications

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“…Interestingly, a previous study evaluated altered thalamic neuronal activity in patients with neuropathic pain and reported blood flow increase in the early stages of the disease and decrease as the condition became chronic ( Ushida et al, 2010 ). We also report that COFP patients have less function in the posterior insula, a region typically observed in experimental pain studies, and in line with previous evidence of insular abnormality in TN ( Yuan et al, 2018 ) and TMD ( Nebel et al, 2010 ). We also did not identify consistent differences across other brain regions that are observed in chronic pain, including S1, S2 and the mid- and anterior cingulate cortex ( Apkarian et al, 2011 ), although some of the studies did report activation in these regions.…”

Section: Discussionsupporting

confidence: 91%

“…in years) Pain intensity (/10) N W/M Age (mean ± SD or S.E.M. in years) Rest/task Pain intensity (/10) Body Part Wang et al, 2017a CTN 17 10/7 62.53 ± 7.41 6.12 ± 1.50 19 11/8 61.75 ± 6.02 fALFF Rest 16 Yuan et al, 2018 ITN 23 9/14 59.6 ± 12.5 8.1 ± 1.6 23 11/12 63.1 ± 9.8 ReHo and fALFF Rest 16 Alshelh et al, 2016 NP 17 14/3 50.6 ± 2.8 4.12 ± 2.61 44 33/11 45.9 ± 2.0 Task Chemical Healthy: 5 R Masseter 18 Wang et al, 2015 ITN 17 10/7 63.41 ± 7.25 6.12 ± 1.50 19 10/9 62.53 ± 7.41 ReHo Rest 19 He et al, 2014 TMD 23 14/9 22.4 ± 3.6 47.3 ± 21.4 a 20 11/9 23.1 ± 2.4 fALFF Rest 17 Weissman-Fogel et al, 2011 TMD 17 17/0 35.2 ± 11.6 4.41 ± 1.77 17 17/0 34.0 ± 9.9 Task Stroop task 19...…”

Section: Resultsmentioning

confidence: 99%

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A meta-analytic study of experimental and chronic orofacial pain excluding headache disorders

Ayoub

Seminowicz

Moayedi

2018

NeuroImage: Clinical

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Chronic orofacial pain (COFP) disorders are prevalent and debilitating pain conditions affecting the head, neck and face areas. Neuroimaging studies have reported functional and grey matter abnormalities, but not all the studies have reported consistent findings. Identifying convergent abnormalities across COFPs provides a basis for future hypothesis-driven research aimed at elucidating common CNS mechanisms. Here, we perform three coordinate-based meta-analyses according to PRISMA guidelines to elucidate the central mechanisms of orofacial pain disorders. Specifically, we investigated consistent patterns of: (1) brain function to experimental orofacial pain in healthy subjects, (2) structural and (3) functional brain abnormalities in COFP. We computed our coordinate-based meta-analyses using GingerALE. The experimental pain meta-analysis revealed increased brain activity in bilateral thalami, posterior mid-cingulate cortices, and secondary somatosensory cortices, the right posterior parietal cortex extending to the orofacial region of the right primary somatosensory cortex and the right insula, and decreased activity in the right somatomotor regions. The structural COFP meta-analysis identified consistent higher grey matter volume/concentration in the right ventral thalamus and posterior putamen of COFP patients compared to healthy controls. The functional COFP meta-analysis identified a consistent increase in brain activity in the left medial and posterior thalamus and lesser activity in the left posterior insula in COFP, compared to healthy controls. Overall, these findings provide evidence of brain abnormalities in pain-related regions, namely the thalamus and insula, across different COFP disorders. The convergence of thalamic abnormalities in both structure and function suggest a key role for this region in COFP pathophysiology.

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Section: Discussionsupporting

confidence: 91%

Section: Resultsmentioning

confidence: 99%

A meta-analytic study of experimental and chronic orofacial pain excluding headache disorders

Ayoub

Seminowicz

Moayedi

2018

NeuroImage: Clinical

View full text Add to dashboard Cite

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“…Does this finding seem to be contradicted by previous studies? Many studies suggest that pain-induced DMN deactivations or hypo-activity is negatively correlated with pain intensity 34,35,42 . However, as a key area of the DMN, the PCUN did not contribute to the actual representation of pain and mainly predicted individual differences in sensitivity to pain.…”

Section: Discussionmentioning

confidence: 99%

Compressing the lumbar nerve root changes the frequency-associated cerebral amplitude of fluctuations in patients with low back/leg pain

Zhou

Zhao

Zhu

et al. 2019

Sci Rep

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Understanding the central mechanisms responsible for lumbar nerve root compression may facilitate the development of new therapeutic strategies. In this study, our aim was to investigate the amplitude of fluctuations (AF) in five specific frequency bands and the full-frequency band realm to provide novel insight into the rhythm of the neuronal activity of low back/leg pain (LBLP) patients (n = 25). Compared with healthy controls, LBLP patients exhibited a significantly altered AF in multiple brain regions, including the right or left middle and inferior temporal gyri, bilateral precuneus, right anterior insula/frontal operculum, right or left inferior parietal lobule/postcentral gyrus, and other locations at five specific frequencies (P < 0.01, with Gaussian random field theory correction). Trends of an increase and a decrease in the AF in pain- and sensory-related regions, respectively, were also observed from low to high frequencies (Bonferroni-corrected α level of P < 0.05/84). In addition, in the bilateral rectal gyrus, a significant association was identified between the AF in the five specific frequency bands and disease status (P < 0.05). These findings suggest that in LBLP patients, intrinsic functional plasticity related to low back pain, leg pain and numbness affects the AF of the pain matrix and sensory-processing regions in both low- and high-frequency bands.

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“…Despite the significant impact on life quality and the lack of effective treatment, the underlying mechanisms are still not fully understood. Several lines of evidence support that NeuP is accompanied with altered activity and connectivity of brain regions engaged in pain processing and modulation (Porreca et al, 2002;Mills et al, 2018;Patel et al, 2018;Yuan et al, 2018), but the relationship between these changes and failed pain control remains elusive.…”

Section: Introductionmentioning

confidence: 99%

Activation of the Intrinsic Pain Inhibitory Circuit from the Midcingulate Cg2 to Zona Incerta Alleviates Neuropathic Pain

Wang

et al. 2019

J. Neurosci.

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Neuropathic pain is one of the most common and notorious neurological diseases. The changes in cerebral structures after nerve injury and the corresponding contributions to neuropathic pain are not well understood. Here we found that the majority of glutamatergic neurons in the area 2 of midcingulate cortex (MCC Cg2 Glu) were inhibited by painful stimulation in male mice. Optogenetic manipulation revealed that these neurons were tonically involved in the inhibitory modulation of multimodal nociception. We further identified the projections to GABAergic neurons in the zona incerta (ZI GABA) mediated the pain inhibitory role. However, MCC Cg2 Glu became hypoactive after nerve injury. Although a brief activation of the MCC Cg2 Glu to ZI GABA circuit was able to relieve the aversiveness associated with spontaneous ongoing pain, consecutive activation of the circuit was required to alleviate neuropathic allodynia. In contrast, glutamatergic neurons in the area 1 of MCC played opposite roles in pain modulation. They became hyperactive after nerve injury and only consecutive inhibition of their activity relieved allodynia. These results demonstrate that MCC Cg2 Glu constitute a component of intrinsic pain inhibitory circuitry and their hypoactivity underlies neuropathic pain. We propose that selective and persistent activation of the MCC Cg2 Glu to ZI GABA circuit may serve as a potential therapeutic strategy for this disease.

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Altered Spontaneous Brain Activity in Patients With Idiopathic Trigeminal Neuralgia

Cited by 30 publications

References 69 publications

A meta-analytic study of experimental and chronic orofacial pain excluding headache disorders

A meta-analytic study of experimental and chronic orofacial pain excluding headache disorders

Compressing the lumbar nerve root changes the frequency-associated cerebral amplitude of fluctuations in patients with low back/leg pain

Activation of the Intrinsic Pain Inhibitory Circuit from the Midcingulate Cg2 to Zona Incerta Alleviates Neuropathic Pain

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