scholarly journals Deficits in ascending and descending pain modulation pathways in patients with postherpetic neuralgia

NeuroImage ◽  
2020 ◽  
Vol 221 ◽  
pp. 117186
Author(s):  
Hong Li ◽  
Xiaoyun Li ◽  
Yi Feng ◽  
Fei Gao ◽  
Yazhuo Kong ◽  
...  
Keyword(s):  
Postherpetic Neuralgia ◽  
Pain Modulation ◽  
Descending Pain Modulation

A novel clinical applicable bed-side tool for assessing conditioning pain modulation: proof-of-concept

2020 ◽  
Vol 20 (4) ◽  
pp. 801-807
Author(s):  
Lars Arendt-Nielsen ◽  
Jesper Bie Larsen ◽  
Stine Rasmussen ◽  
Malene Krogh ◽  
Laura Borg ◽  
...  
Keyword(s):  
Pain Modulation ◽  
Clinical Settings ◽  
Proof Of Concept ◽  
Finger Nail ◽  
Tonic Stimulus ◽  
Pressure Pain Thresholds ◽  
Custom Made ◽  
The Individual ◽  
Descending Pain Modulation ◽  
Finger Pressure

AbstractBackground and aimsIn recent years, focus on assessing descending pain modulation or conditioning pain modulation (CPM) has emerged in patients with chronic pain. This requires reliable and simple to use bed-side tools to be applied in the clinic. The aim of the present pilot study was to develop and provide proof-of-concept of a simple clinically applicable bed-side tool for assessing CPM.MethodsA group of 26 healthy volunteers participated in the experiment. Pressure pain thresholds (PPT) were assessed as test stimuli from the lower leg before, during and 5 min after delivering the conditioning tonic painful pressure stimulation. The tonic stimulus was delivered for 2 min by a custom-made spring-loaded finger pressure device applying a fixed pressure (2.2 kg) to the index finger nail. The pain intensity provoked by the tonic stimulus was continuously recorded on a 0–10 cm Visual Analog Scale (VAS).ResultsThe median tonic pain stimulus intensity was 6.7 cm (interquartile range: 4.6–8.4 cm) on the 10 cm VAS. The mean PPT increased significantly (P = 0.034) by 55 ± 126 kPa from 518 ± 173 kPa before to 573 ± 228 kPa during conditioning stimulation. When analyzing the individual CPM responses (increases in PPT), a distribution of positive and negative CPM responders was observed with 69% of the individuals classified as positive CPM responders (increased PPTs = anti-nociceptive) and the rest as negative CPM responders (no or decreased PPTs = Pro-nociceptive). This particular responder distribution explains the large variation in the averaged CPM responses observed in many CPM studies. The strongest positive CPM response was an increase of 418 kPa and the strongest negative CPM response was a decrease of 140 kPa.ConclusionsThe present newly developed conditioning pain stimulator provides a simple, applicable tool for routine CPM assessment in clinical practice. Further, reporting averaged CPM effects should be replaced by categorizing volunteers/patients into anti-nociceptive and pro-nociceptive CPM groups.ImplicationsThe finger pressure device provided moderate-to-high pain intensities and was useful for inducing conditioning stimuli. Therefore, the finger pressure device could be a useful bed-side method for measuring CPM in clinical settings with limited time available. Future bed-side studies involving patient populations are warranted to determine the usefulness of the method.

scholarly journals EGCG Prevents the Loss of Pontine Noradrenergic Neurons Induced by Diabetes: A Role in Diabetic Neuropathic Pain

2012 ◽  
Vol 18 (S5) ◽  
pp. 5-6 ◽  
Author(s):  
Carla Morgado ◽  
João Silva ◽  
André Miranda ◽  
Patrícia Pereira-Terra ◽  
Diogo Raposo ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Diabetic Rats ◽  
Pain Modulation ◽  
Diabetic Patients ◽  
Spontaneous Pain ◽  
Noradrenergic Neurons ◽  
Diabetic Neuropathic Pain ◽  
Descending Pain Modulation ◽  
Pain Responses

Diabetes is a major health problem with an alarming increasing prevalence, and is the most frequent cause of neuropathy worldwide. Neuropathy affects 50–60% of diabetic patients, being a major life-quality impairment for a quarter of these patients. Diabetic neuropathic pain (DNP) is characterized by spontaneous pain, mechanical hyperalgesia and tactile allodynia and is accompanied by functional and neurochemical changes at the peripheral nerves, spinal cord and supraspinal pain control areas. Regarding the effects of diabetic neuropathy in the central somatossensory system, it was shown that streptozotocin (STZ)-diabetic rats present spontaneous hyperactivity and hyperexcitability of spinal nociceptive neurons, which may be subserving the exacerbated pain responses. The spinal functional changes and pain may be due to increased peripheral input(2), changes in spinal nociceptive modulatory mechanisms and altered supraspinal descending pain modulation. Noradrenergic descending pain modulation seems to be impaired since STZ-diabetic rats present decreased numbers of noradrenergic neurons at the A5 and A7 pontine cell groups, along with lower levels of noradrenaline at the spinal cord and higher behavioral responses to pain. This is consistent with the strong noradrenergic projection from A5 and A7 neurons to the spinal dorsal horn and the modulation of nociceptive transmission by local release of noradrenaline. The mechanisms underlying the decrease in noradrenergic neurons in the brainstem during diabetes remain unclear. Our recent findings that diabetes induces oxidative stress damage in neurons from those areas, lead us to hypothesize that it may contribute to their loss. Thereafter, with the present study we aimed to evaluate the effects of Epigallocathechin Gallate (EGCG), a potent antioxidant present in green tea, on spinal noradrenaline levels, on A5 and A7 noradrenergic neurons and on behavioral pain responses of STZ-diabetic rats.

The periaqueductal gray and descending pain modulation: why should we study them and what role do they play in chronic pain?

2015 ◽  
Vol 114 (4) ◽  
pp. 2080-2083 ◽  
Author(s):  
Kasey S. Hemington ◽  
Marie-Andrée Coulombe
Keyword(s):  
Chronic Pain ◽  
Back Pain ◽  
Functional Connectivity ◽  
Recent Literature ◽  
Chronic Back Pain ◽  
Periaqueductal Gray ◽  
Pain Modulation ◽  
Pain Research ◽  
Descending Pain Modulation ◽  
Pain Patients

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.

scholarly journals Impaired Modulation of Pain in Patients with Postherpetic Neuralgia

2014 ◽  
Vol 19 (1) ◽  
pp. e19-e23 ◽  
Author(s):  
Gisèle Pickering ◽  
Bruno Pereira ◽  
Elodie Dufour ◽  
Sylvie Soule ◽  
Claude Dubray
Keyword(s):  
Postherpetic Neuralgia ◽  
Rating Scale ◽  
Numerical Rating Scale ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Pain Modulation ◽  
Cognitive Test ◽  
Control Group ◽  
Pressor Test ◽  
Clinical Pain

BACKGROUND: The efficiency of inhibitory pain descending pathways (evaluated using conditioned pain modulation [CPM]) has not been studied in postherpetic neuralgia (PHN).OBJECTIVE: To compare CPM in PHN patients with healthy controls.METHODS: Nine PHN patients and nine control individuals were matched according to age and sex. Amplitudes of cortical thermal-evoked potentials were recorded on the surface of the scalp; clinical pain and thermal pain were evaluated on a 0 to 10 numerical rating scale, at baseline and at intervals during the 6 min after CPM (elicited by a cold pressor test, 8°C). A battery of cognitive tests was performed. Amplitude differences, percentages and related areas under the curve (AUCCPM) were calculated and all data were compared between both groups; P<0.05 was considered to be statistically significant.RESULTS: AUCCPM0–6 minwas significantly lower in PHN patients compared with controls (−39±51 μV/min versus −144±66 μV/min; P=0.0012) and correlated (P=0.04) with clinical pain intensity. Pain ratings before CPM were similar in both groups but were significantly lower in the control group 3 min after the cold pressor test. Cognitive test results were not significantly different.CONCLUSION: Psychophysical and electrophysiological approaches have shown that patients with PHN exhibit a deficiency of pain inhibition modulation, which could signal a predisposing factor to developing chronic pain. This deficiency was not linked to the cognitive performance but rather to subtle in situ cognitivoemotional adaptations, which remain to be investigated.

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