Cortical processing of facial tactile stimuli in temporomandibular disorder as revealed by magnetoencephalography

Alonso, Aurelio; Koutlas, Ioannis G.; Leuthold, Arthur C.; Lewis, Scott M.; Georgopoulos, Apostolos P.

doi:10.1007/s00221-010-2291-6

Cited by 14 publications

(15 citation statements)

References 68 publications

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“…Furthermore, magnetoencephalography was performed in TMD patients and demonstrated evidence of altered brain responses to innocuous tactile stimulation above the masseter muscle compared to healthy controls. 101 These findings support the presence of abnormal central pain processing in TMD.…”

Section: Proposed Pathophysiologic Mechanismssupporting

confidence: 59%

Overlap between functional GI disorders and other functional syndromes: what are the underlying mechanisms?

Kim

Chang

2012

Neurogastroenterology Motil

111

106

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Background Irritable bowel syndrome and other gastrointestinal (GI) and non-GI disorders such as functional dyspepsia, fibromyalgia, temporomandibular joint disorder, interstitial cystitis/painful bladder syndrome, and chronic fatigue syndrome are known as functional pain syndromes. They commonly coexist within the same individual. The pathophysiologic mechanisms of these disorders are not well understood, but it has been hypothesized that they share a common pathogenesis. Purpose The objective of this review is to discuss the proposed pathophysiologic mechanisms, which have been similarly studied in these conditions. These mechanisms include enhanced pain perception, altered regional brain activation, infectious etiologies, dysregulations in immune and neuroendocrine function, and genetic susceptibility. Studies suggest that these functional disorders are multifactorial, but factors which increase the vulnerability of developing these conditions are shared.

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Section: Proposed Pathophysiologic Mechanismssupporting

confidence: 59%

Overlap between functional GI disorders and other functional syndromes: what are the underlying mechanisms?

Kim

Chang

2012

Neurogastroenterology Motil

111

106

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“…These effects encompassed parietal areas (tentatively, first [area c in Fig. 6] and second somatosensory cortex [area b]), known to be involved in pain (Alonso et al, 2010, Mazzola et al, 2012). The preponderance of left hemispheric involvement in this study (Fig.…”

Section: Discussionmentioning

confidence: 99%

Brain Correlates of Human Leukocyte Antigen (HLA) Protection in Gulf War Illness (GWI)

et al. 2016

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BackgroundWe recently reported that six alleles from class II genes of the Human Leukocyte Antigen (HLA) confer protection from Gulf War Illness (GWI) (Georgopoulos et al., 2015). The most significant effect is exerted on Neurological-Cognitive-Mood (NCM), Pain, and Fatigue symptoms, such that higher number of copies of the protective alleles are associated with lower symptom severity. Here we tested the hypothesis that this effect is exerted by modulating the strength of neural synchronicity.MethodsEighty-one Gulf War veterans (65 with GWI and 16 healthy controls) underwent a magnetoencephalography (MEG) scan to assess the strength of brain synchronicity by computing zero-lag crosscorrelations (and their Fisher z transforms) between prewhitened MEG time series. A high-resolution HLA genotyping determined the number of copies, k, of the 6 protective alleles above in each participant. We tested the hypothesis above by regressing NCM, Pain and Fatigue symptom severity against the interaction term, k × z (HLA-related effect), while including z (non-HLA-related effect), gender and age as covariates. The k × z and z terms assessed HLA- and non-HLA-related effects, respectively, of neural synchronicity on symptom severity. The distributions of these effects in sensor space were visualized using statistical heatmaps.FindingsWe found significant, graded HLA- and non-HLA-related effects: (a) NCM > Pain > Fatigue for HLA-related effects, (b) NCM > Fatigue > Pain for non-HLA-related effects, and (c) HLA-related > non-HLA-related effects for all symptoms. These effects had widespread but distinct distributions in sensor space that allowed the orderly separation of the 6 terms (3 symptom domains × 2 HLA factors) in a multidimensional plot, where one dimension separated the symptoms and the other the HLA relation.InterpretationThese findings demonstrate the presence of substantial, widespread, distinct and orderly HLA- and non-HLA-related neural influences on NCM, Pain and Fatigue symptom severity in GWI.FundingU.S. Department of Veterans Affairs and University of Minnesota.

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“…The greater temporal acuity of MEG revealed that the evoked responses in TMD, termed equivalent current dipoles, had earlier onset times, were longer in duration, were less tightly grouped, and had different distribution of response power over the 1s response time [134]. …”

Section: Neuroimaging Of Brain Activity Evoked By Non-painful Stimulamentioning

confidence: 99%

Neuroimaging of Central Sensitivity Syndromes: Key Insights from the Scientific Literature

Walitt

Čeko²,

Gracely³

et al. 2016

CRR

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Central sensitivity syndromes are characterized by distressing symptoms, such as pain and fatigue, in the absence of clinically obvious pathology. The scientific underpinnings of these disorders are not currently known. Modern neuroimaging techniques promise new insights into mechanisms mediating these postulated syndromes. We review the results of neuroimaging applied to five central sensitivity syndromes: fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, temporomandibular joint disorder, and vulvodynia syndrome. Neuroimaging studies of basal metabolism, anatomic constitution, molecular constituents, evoked neural activity, and treatment effect are compared across all of these syndromes. Evoked sensory paradigms reveal sensory augmentation to both painful and non-painful stimulation. This is a transformative observation for these syndromes, which were historically considered to be completely of hysterical or feigned in origin. However, whether sensory augmentation represents the cause of these syndromes, a predisposing factor, an endophenotype, or an epiphenomenon cannot be discerned from the current literature. Further, the result from cross-sectional neuroimaging studies of basal activity, anatomy, and molecular constituency are extremely heterogeneous within and between the syndromes. A defining neuroimaging “signature” cannot be discerned for any of the particular syndromes or for an over-arching central sensitization mechanism common to all of the syndromes. Several issues confound initial attempts to meaningfully measure treatment effects in these syndromes. At this time, the existence of “central sensitivity syndromes” is based more soundly on clinical and epidemiological evidence. A coherent picture of a “central sensitization” mechanism that bridges across all of these syndromes does not emerge from the existing scientific evidence.

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Cortical processing of facial tactile stimuli in temporomandibular disorder as revealed by magnetoencephalography

Cited by 14 publications

References 68 publications

Overlap between functional GI disorders and other functional syndromes: what are the underlying mechanisms?

Overlap between functional GI disorders and other functional syndromes: what are the underlying mechanisms?

Brain Correlates of Human Leukocyte Antigen (HLA) Protection in Gulf War Illness (GWI)

Neuroimaging of Central Sensitivity Syndromes: Key Insights from the Scientific Literature

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