scholarly journals Multisensory Sensitivity is Related to Deep-Tissue but Not Cutaneous Pain Sensitivity in Healthy Individuals

2020 ◽  
Vol Volume 13 ◽  
pp. 2493-2508
Author(s):  
Dan Wang ◽  
Shannon L Merkle ◽  
Jennifer E Lee ◽  
Kathleen A Sluka ◽  
Barbara Rakel ◽  
...  
BMJ Open ◽  
2019 ◽  
Vol 9 (4) ◽  
pp. e025530 ◽  
Author(s):  
Annina B Schmid ◽  
Kaustubh Adhikari ◽  
Luis Miguel Ramirez-Aristeguieta ◽  
Juan-Camilo Chacón-Duque ◽  
Giovanni Poletti ◽  
...  

IntroductionPain constitutes a major component of the global burden of diseases. Recent studies suggest a strong genetic contribution to pain susceptibility and severity. Whereas most of the available evidence relies on candidate gene association or linkage studies, research on the genetic basis of pain sensitivity using genome-wide association studies (GWAS) is still in its infancy. This protocol describes a proposed GWAS on genetic contributions to baseline pain sensitivity and nociceptive sensitisation in a sample of unrelated healthy individuals of mixed Latin American ancestry.Methods and analysisA GWAS on genetic contributions to pain sensitivity in the naïve state and following nociceptive sensitisation will be conducted in unrelated healthy individuals of mixed ancestry. Mechanical and thermal pain sensitivity will be evaluated with a battery of quantitative sensory tests evaluating pain thresholds. In addition, variation in mechanical and thermal sensitisation following topical application of mustard oil to the skin will be evaluated.Ethics and disseminationThis study received ethical approval from the University College London research ethics committee (3352/001) and from the bioethics committee of the Odontology Faculty at the University of Antioquia (CONCEPTO 01–2013). Findings will be disseminated to commissioners, clinicians and service users via papers and presentations at international conferences.


2016 ◽  
Vol 17 (4) ◽  
pp. S22-S23
Author(s):  
C. Colombo ◽  
S. Parra ◽  
J.D. Bean Lijewski ◽  
H. Giles

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Bahar Shahidi ◽  
Katrina S. Maluf

Numerous studies demonstrate elevated pain sensitivity and impaired conditioned pain modulation (CPM) in patients with chronic musculoskeletal pain compared to healthy individuals; however, the time course of changes in pain sensitivity and CPM after the development of a chronic pain condition is unclear. Secondary analysis of data from a prospective investigation examined changes in evoked pain sensitivity and CPM before and after development of chronic neck pain (CNP). 171 healthy office workers participated in a baseline assessment, followed by monthly online questionnaires to identify those who developed CNP over the subsequent year. These individuals (N=17) and a cohort of participants (N=10) who remained pain-free during the follow-up period returned for a 12-month follow-up assessment of mechanical and thermal pain sensitivity and CPM. Pain sensitivity measures did not differ between groups at baseline; however, cold pain threshold decreased in the CNP group at follow-up (p<0.05). CPM was lower at baseline in the CNP group compared to those who reported no neck pain (p<0.02) and remained unchanged one year later. These findings indicate that CPM is reduced in healthy individuals prior to the development of chronic neck pain and the subsequent reduction of thresholds for cold but not pressure pain.


2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Fu-Jung Hsiao ◽  
Wei-Ta Chen ◽  
Hung-Yu Liu ◽  
Yen-Feng Wang ◽  
Shih-Pin Chen ◽  
...  

Abstract Background Pain sensitivity may determine the risk, severity, prognosis, and efficacy of treatment of clinical pain. Magnetic resonance imaging studies have linked thermal pain sensitivity to changes in brain structure. However, the neural correlates of mechanical pain sensitivity remain to be clarified through investigation of direct neural activities on the resting-state cortical oscillation and synchrony. Methods We recorded the resting-state magnetoencephalographic (MEG) activities of 27 healthy individuals and 30 patients with episodic migraine (EM) and analyzed the source-based oscillatory powers and functional connectivity at 2 to 59 Hz in pain-related cortical regions, which are the bilateral anterior cingulate cortex (ACC), medial orbitofrontal (MOF) cortex, lateral orbitofrontal (LOF) cortex, insula cortex, primary somatosensory cortex (SI), primary motor cortex (MI), and posterior cingulate cortex (PCC). The mechanical punctate pain threshold (MPPT) was obtained at the supraorbital area (the first branch of the trigeminal nerve dermatome, V1) and the forearm (the first thoracic nerve dermatome, T1) and further correlated with MEG measures. Results The MPPT is inversely correlated with the resting-state relative powers of gamma oscillation in healthy individuals (all corrected P < 0.05). Specifically, inverse correlation was noted between the MPPT at V1 and gamma powers in the bilateral insula (r = − 0.592 [left] and − 0.529 [right]), PCC (r = − 0.619 and − 0.541) and MI (r = − 0.497 and − 0.549) and between the MPPT at T1 and powers in the left PCC (r = − 0.561) and bilateral MI (r = − 0.509 and − 0.520). Furthermore, resting-state functional connectivity at the delta to beta bands, especially between frontal (MOF, ACC, LOF, and MI), parietal (PCC), and sensorimotor (bilateral SI and MI) regions, showed a positive correlation with the MPPT at V1 and T1 (all corrected P < 0.05). By contrast, in patients with EM, the MPPT was not associated with resting-state cortical activities. Conclusions Pain sensitivity in healthy individuals is associated with the resting-state gamma oscillation and functional connectivity in pain-related cortical regions. Further studies must be conducted in a large population to confirm whether resting-state cortical activities can be an objective measurement of pain sensitivity in individuals without clinical pain.


2020 ◽  
Vol 30 (12) ◽  
pp. 6069-6082 ◽  
Author(s):  
Andrew J Furman ◽  
Mariya Prokhorenko ◽  
Michael L Keaser ◽  
Jing Zhang ◽  
Shuo Chen ◽  
...  

Abstract Previous research has observed that the speed of alpha band oscillations (8–12 Hz range) recorded during resting electroencephalography is slowed in chronic pain patients. While this slowing may reflect pathological changes that occur during the chronification of pain, an alternative explanation is that healthy individuals with slower alpha oscillations are more sensitive to prolonged pain, and by extension, more susceptible to developing chronic pain. To test this hypothesis, we examined the relationship between the pain-free, resting alpha oscillation speed of healthy individuals and their sensitivity to two models of prolonged pain, Phasic Heat Pain and Capsaicin Heat Pain, at two visits separated by 8 weeks on average (n = 61 Visit 1, n = 46 Visit 2). We observed that the speed of an individual’s pain-free alpha oscillations was negatively correlated with sensitivity to both models and that this relationship was reliable across short (minutes) and long (weeks) timescales. Furthermore, the speed of pain-free alpha oscillations can successfully identify the most pain sensitive individuals, which we validated on data from a separate, independent study. These results suggest that alpha oscillation speed is a reliable biomarker of prolonged pain sensitivity with potential for prospectively identifying pain sensitivity in the clinic.


2014 ◽  
Vol 15 (4) ◽  
pp. S56
Author(s):  
N. Emerson ◽  
F. Zeidan ◽  
O. Lobanov ◽  
M. Hadsel ◽  
K. Martucci ◽  
...  

2014 ◽  
Vol 19 (6) ◽  
pp. 834-841 ◽  
Author(s):  
K. Wingenfeld ◽  
S. Wolf ◽  
M. Kunz ◽  
J.-C. Krieg ◽  
S. Lautenbacher

2020 ◽  
Author(s):  
Fu-Jung Hsiao ◽  
Wei-Ta Chen ◽  
Hung-Yu Liu ◽  
Yen-Feng Wang ◽  
Shih-Pin Chen ◽  
...  

Abstract Background Pain sensitivity may determine the risk, severity, prognosis, and efficacy of treatment of clinical pain. Magnetic resonance imaging studies have linked thermal pain sensitivity to changes in brain structure. However, the neural correlates of mechanical pain sensitivity remain to be clarified through investigation of direct neural activities on the resting-state cortical oscillation and synchrony. Methods We recorded the resting-state magnetoencephalographic (MEG) activities of 27 healthy individuals and 30 patients with episodic migraine (EM) and analyzed the source-based oscillatory powers and functional connectivity at 2 to 59 Hz in pain-related cortical regions, which are the bilateral anterior cingulate cortex (ACC), medial orbitofrontal (MOF) cortex, lateral orbitofrontal (LOF) cortex, insula cortex, primary somatosensory cortex (SI), primary motor cortex (MI), and posterior cingulate cortex (PCC). The mechanical punctate pain threshold (MPPT) was obtained at the supraorbital area (the first branch of the trigeminal nerve dermatome, V1) and the forearm (the first thoracic nerve dermatome, T1) and further correlated with MEG measures. Results The MPPT is inversely correlated with the resting-state relative powers of gamma oscillation in healthy individuals (all corrected P < 0.05). Specifically, inverse correlation was noted between the MPPT at V1 and gamma powers in the bilateral insula (r = −0.592 [left] and −0.529 [right]), PCC (r = −0.619 and −0.541) and MI (r = −0.497 and −0.549) and between the MPPT at T1 and powers in the left PCC ( r = −0.561) and bilateral MI ( r = −0.509 and −0.520). Furthermore, resting-state functional connectivity at the delta to beta bands, especially between frontal (MOF, ACC, LOF, and MI), parietal (PCC), and sensorimotor (bilateral SI and MI) regions, showed a positive correlation with the MPPT at V1 and T1 (all corrected P < 0.05). By contrast, in patients with EM, the MPPT was not associated with resting-state cortical activities. Conclusions Pain sensitivity in healthy individuals is associated with the resting-state gamma oscillation and functional connectivity in pain-related cortical regions. Further studies must be conducted in a large population to confirm whether resting-state cortical activities can be an objective measurement of pain sensitivity in individuals without clinical pain.


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