Development of the Pain Responses Scale: A measure informed by the BIS‐BAS model of pain

2021 ◽  
Author(s):  
M.A. Day ◽  
L.C. Ward ◽  
R. de la Vega ◽  
D.M. Ehde ◽  
M.P. Jensen
Keyword(s):  
Pain Responses

358: Intravesical Botulinum Toxin a Administration Produces Analgesia Against Acetic Acid Induced Bladder Pain Responses in Rats

2004 ◽  
Vol 171 (4S) ◽  
pp. 94-94
Author(s):  
Yao-Chi Chuang ◽  
Naoki Yoshimura ◽  
Chao-Cheng Huang ◽  
Po-Hui Chiang ◽  
Michael B. Chancellor
Keyword(s):  
Acetic Acid ◽  
Botulinum Toxin ◽  
Botulinum Toxin A ◽  
Toxin A ◽  
Bladder Pain ◽  
Pain Responses

Spinal and supraspinal modulation of pain responses by hypnosis, suggestions, and distraction

2021 ◽  
Vol 63 (4) ◽  
pp. 329-354
Author(s):  
Bérengère Houzé ◽  
Anouk Streff ◽  
Mathieu Piché ◽  
Pierre Rainville
Keyword(s):  
Pain Responses

scholarly journals Attenuated pain responses in mice lacking CaV3.2 T-type channels

2007 ◽  
Vol 6 (5) ◽  
pp. 425-431 ◽  
Author(s):  
S. Choi ◽  
H. S. Na ◽  
J. Kim ◽  
J. Lee ◽  
S. Lee ◽  
...  
Keyword(s):  
Pain Responses

Prenatal stress alters time characteristics and intensity of formalin-induced pain responses in juvenile rats

2001 ◽  
Vol 915 (1) ◽  
pp. 88-93 ◽  
Author(s):  
Irina Pavlovna Butkevich ◽  
Elena Andreevna Vershinina
Keyword(s):  
Prenatal Stress ◽  
Juvenile Rats ◽  
Pain Responses

scholarly journals Non-Pain-Related CRF1 Activation in the Amygdala Facilitates Synaptic Transmission and Pain Responses

2013 ◽  
Vol 9 ◽  
pp. 1744-8069-9-2 ◽  
Author(s):  
Guangchen Ji ◽  
Yu Fu ◽  
Hita Adwanikar ◽  
Volker Neugebauer
Keyword(s):  
Synaptic Transmission ◽  
Pain Responses

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.

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