Endogenous pain modulation assessed with offset analgesia is not impaired in chronic temporomandibular disorder pain patients

2019 ◽  
Vol 46 (11) ◽  
pp. 1009-1022 ◽  
Author(s):  
Estephan Jose Moana‐Filho ◽  
Alberto Herrero Babiloni ◽  
Aaron Nisley
2019 ◽  
Vol 37 ◽  
pp. 150-156 ◽  
Author(s):  
Kevin Kuppens ◽  
Stef Feijen ◽  
Nathalie Roussel ◽  
Jo Nijs ◽  
Patrick Cras ◽  
...  

2011 ◽  
Vol 12 (8) ◽  
pp. 875-883 ◽  
Author(s):  
Roi Treister ◽  
Dorit Pud ◽  
Richard P. Ebstein ◽  
Efrat Laiba ◽  
Yael Raz ◽  
...  

Cephalalgia ◽  
2017 ◽  
Vol 38 (7) ◽  
pp. 1307-1315 ◽  
Author(s):  
Dan Levy ◽  
Lorin Abdian ◽  
Michal Dekel-Steinkeller ◽  
Ruth Defrin

Background and objectives The prevalence of pain syndromes that affect the territories innervated by the trigeminal nerve, such as headaches, is one of the highest and ranks second only to low back pain. A potential mechanism underlying this high prevalence may be a relatively weak endogenous pain modulation of trigeminal pain. Here, we sought to systematically compare endogenous pain modulation capabilities in the trigeminal region to those of extra-trigeminal regions in healthy subjects. Methods Healthy, pain free subjects (n = 17) underwent a battery of quantitative sensory testing to assess endogenous pain inhibition and pain enhancement efficiencies within and outside the trigeminal innervated region. Measurements included conditioned pain modulation (CPM), temporal summation of pain (TSP) and spatial summation of pain (SSP). Results Testing configurations that included trigeminal-innervated body regions displayed significantly weaker CPM when compared to extra-trigeminal innervated areas. SSP magnitude was smaller in the ophthalmic trigeminal innervation when compared to other body regions. TSP magnitude was not different between the different body regions tested. Conclusions Our findings point to regional differences in endogenous pain inhibition and suggest that in otherwise healthy individuals, the trigeminal innervation is subjected to a weaker inhibitory pain control than other body regions. Such weaker endogenous pain control could play, at least in part, a role in mediating the high prevalence of trigeminal-related pain syndromes, including primary headaches and TMD pain.


2015 ◽  
Vol 114 (4) ◽  
pp. 2080-2083 ◽  
Author(s):  
Kasey S. Hemington ◽  
Marie-Andrée Coulombe

In this Neuro Forum we discuss the significance of a recent study by Yu et al. ( Neuroimage Clin 6: 100–108, 2014). The authors examined functional connectivity of a key node of the descending pain modulation pathway, the periaqueductal gray (PAG), in chronic back pain patients. Altered PAG connectivity to pain-related regions was found; we place results within the context of recent literature and emphasize the importance of understanding the descending component of pain in pain research.


Cephalalgia ◽  
2011 ◽  
Vol 31 (8) ◽  
pp. 953-963 ◽  
Author(s):  
Nicholas H L Chua ◽  
Hans A van Suijlekom ◽  
Kris C Vissers ◽  
Lars Arendt-Nielsen ◽  
Oliver H Wilder-Smith

Background: It is not known why some patients with underlying chronic nociceptive sources in the neck develop cervicogenic headache (CEH) and why others do not. This quantitative sensory testing (QST) study systematically explores the differences in sensory pain processing in 17 CEH patients with underlying chronic cervical zygapophysial joint pain compared to 10 patients with chronic cervical zygapophysial joint pain but without CEH. Methods: The QST protocol comprises pressure pain threshold testing, thermal detection threshold testing, electrical pain threshold testing and measurement of descending inhibitory modulation using the conditioned pain modulation (CPM) paradigm. Results: The main difference between patients with or without CEH was the lateralization of pressure hyperalgesia to the painful side of the head of CEH patients, accompanied by cold as well as warm relative hyperesthesia on the painful side of the head and neck. Discussion: From this hypothesis-generating study, our results suggest that rostral neuraxial spread of central sensitization, probably to the trigeminal spinal nucleus, plays a major role in the development of CEH.


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