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Journal articles on the topic 'Central sensitisation'

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Published: 4 June 2021
Last updated: 4 February 2022

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1

Cervero, F. "Visceral pain---central sensitisation." Gut 47, no. 90004 (December 1, 2000): 56iv—57. http://dx.doi.org/10.1136/gut.47.suppl_4.iv56.

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2

Moshiree, B. "Central sensitisation in visceral pain disorders." Gut 55, no. 7 (February 16, 2006): 905–8. http://dx.doi.org/10.1136/gut.2005.078287.

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3

Cayrol, Timothée, and Emanuel N. van den Broeke. "Central sensitisation: causes, therapies, and terminology." Lancet Rheumatology 3, no. 8 (August 2021): e548. http://dx.doi.org/10.1016/s2665-9913(21)00176-4.

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4

Mehta, Puja, Coziana Ciurtin, Anisur Rahman, and Peter C. Taylor. "Central sensitisation: causes, therapies, and terminology." Lancet Rheumatology 3, no. 8 (August 2021): e546-e547. http://dx.doi.org/10.1016/s2665-9913(21)00177-6.

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5

Weisman, Asaf, John Quintner, Milton Cohen, and Youssef Maharawi. "Central sensitisation: causes, therapies, and terminology." Lancet Rheumatology 3, no. 8 (August 2021): e547-e548. http://dx.doi.org/10.1016/s2665-9913(21)00179-x.

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6

Minhas, Sonica, Rachel Qian Hui Lim, and Joht Singh Chandan. "Central sensitisation: causes, therapies, and terminology." Lancet Rheumatology 3, no. 8 (August 2021): e546. http://dx.doi.org/10.1016/s2665-9913(21)00178-8.

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7

Landy, Stephen, Kathryn Rice, and Bob Lobo. "Central Sensitisation and Cutaneous Allodynia in Migraine." CNS Drugs 18, no. 6 (2004): 337–42. http://dx.doi.org/10.2165/00023210-200418060-00001.

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8

Arendt–Nielsen, L. "Mechanisms of Muscle Pain and Central Sensitisation." Physiotherapy 88, no. 4 (April 2002): 238. http://dx.doi.org/10.1016/s0031-9406(05)60420-8.

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9

Nijs, Jo, Andrea Polli, Ward Willaert, Anneleen Malfliet, Eva Huysmans, and Iris Coppieters. "Central sensitisation: another label or useful diagnosis?" Drug and Therapeutics Bulletin 57, no. 4 (March 11, 2019): 60–63. http://dx.doi.org/10.1136/dtb.2018.000035.

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10

Giamberardino, Maria Adele. "Referred muscle pain/hyperalgesia and central sensitisation." Journal of Rehabilitation Medicine 35 (October 1, 2003): 85–88. http://dx.doi.org/10.1080/16501960310010205.

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11

Wheeler, Patrick C. "Up to a quarter of patients with certain chronic recalcitrant tendinopathies may have central sensitisation: a prospective cohort of more than 300 patients." British Journal of Pain 13, no. 3 (September 21, 2018): 137–44. http://dx.doi.org/10.1177/2049463718800352.

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Introduction: To identify the possible prevalence of ‘central sensitisation’, in patients with chronic recalcitrant lower limb tendinopathy conditions, with the Central Sensitisation Inventory (CSI) questionnaire. Methods: Patients with chronic lower limb tendinopathy conditions treated within a single hospital outpatient clinic specialising in tendinopathy were identified from clinical records. As part of routine care, self-reported numerical markers of pain, global function (using the EuroQol-5D (EQ-5D) questionnaire) and the CSI score to investigate the possibility of central sensitisation were completed. Results: A total of 312 suitable patients with chronic lower limb tendinopathy and similar conditions were identified, who had completed a CSI questionnaire. Of these, 108 presented with greater trochanteric pain syndrome, 12 with patella tendinopathy, 33 with non-insertional Achilles tendinopathy, 48 with insertional Achilles tendinopathy and 110 with plantar fasciitis. A total of 66% of the patients were female, the median age was 54.9 years and the median duration of symptoms was 24 months. There was a median CSI score of 25%, with statistically significant differences noted between the different conditions studied. Overall, 20% of patients scored above a threshold of 40% on CSI questionnaire, indicating that central sensitisation was possible. Greater trochanteric pain syndrome and plantar fasciitis had the highest proportions in the conditions studied. Weak correlations were found between CSI and other pain scores studied. Conclusion: The CSI questionnaire may identify up to a quarter of patients with some chronic lower limb tendinopathy and associated conditions as being more likely to have central sensitisation, and these proportions differed between conditions. The clinical significance of this is unclear, but worth further study to see if/how this may relate to treatment outcomes. These are results from a single hospital clinic dealing with patients with chronic tendinopathy, and comparison with a control group is currently lacking. However, on the information presented here, the concept of central sensitisation should be considered in patients being treated for chronic tendinopathy.
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12

Bouwense, S. A. W., S. S. Olesen, A. M. Drewes, J. W. Poley, H. van Goor, and O. H. G. Wilder-Smith. "T122 PREGABALIN REDUCES CENTRAL SENSITISATION IN CHRONIC PANCREATITIS." European Journal of Pain Supplements 5, S1 (September 2011): 21. http://dx.doi.org/10.1016/s1754-3207(11)70067-0.

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13

Berstad, Arnold, Gülen Arslan, Ragna Lind, and Erik Florvaag. "Food hypersensitivity—immunologic (peripheral) or cognitive (central) sensitisation?" Psychoneuroendocrinology 30, no. 10 (November 2005): 983–89. http://dx.doi.org/10.1016/j.psyneuen.2005.04.010.

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14

Sandkühler, Jürgen, and Ruth Ruscheweyh. "Opioids and central sensitisation: I. Pre-emptive analgesia." European Journal of Pain 9, no. 2 (April 2005): 145–48. http://dx.doi.org/10.1016/j.ejpain.2004.05.012.

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15

Nijs, Jo, Steven Z. George, Daniel J. Clauw, César Fernández-de-las-Peñas, Eva Kosek, Kelly Ickmans, Josué Fernández Carnero, et al. "Central sensitisation: causes, therapies, and terminology – Authors' reply." Lancet Rheumatology 3, no. 8 (August 2021): e548-e549. http://dx.doi.org/10.1016/s2665-9913(21)00182-x.

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16

Sokolov, Alexey Y., Olga A. Lyubashina, Sergey S. Panteleev, and Boris A. Chizh. "Neurophysiological markers of central sensitisation in the trigeminal pathway and their modulation by the cyclo-oxygenase inhibitor ketorolac." Cephalalgia 30, no. 10 (April 7, 2010): 1241–49. http://dx.doi.org/10.1177/0333102410365104.

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Central sensitisation is a key mechanism of migraine; understanding its modulation by anti-migraine drugs is essential for rationalising treatment. We used an animal model of central trigeminal sensitisation to investigate neuronal responses to dural electrical stimulation as a putative electrophysiological marker of sensitisation and its modulation by ketorolac. In anaesthetised rats, responses of single convergent wide-dynamic range neurons of the spinal trigeminal nucleus to dural electrical simulation were recorded in parallel to their ongoing activity and responses to facial mechanical stimulation before and after a short-term dural application of an IS. Both ongoing activity and responses to dural electrical stimuli were enhanced by the inflammatory challenge, whereas neuronal thresholds to mechanical skin stimulation were reduced ( p < .05, N = 12). Intravenous ketorolac (2 mg/kg, N = 6) reduced ongoing activity and responses to dural electrical stimulation, and increased mechanical thresholds versus vehicle controls ( p < .05, N = 6). We conclude that neuronal responses to dural electrical stimulation can serve as a suitable marker which together with admitted electrophysiological signs can objectively detect central trigeminal sensitisation and its modulation by anti-migraine treatments in this preclinical model of migraine.
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17

Hunt, James R., Megan Goff, Helen Jenkins, John Harris, Toby G. Knowles, B. Duncan X. Lascelles, Masataka Enomoto, Michael Mendl, Helen R. Whay, and Joanna C. Murrell. "Electrophysiological characterisation of central sensitisation in canine spontaneous osteoarthritis." PAIN 159, no. 11 (November 2018): 2318–30. http://dx.doi.org/10.1097/j.pain.0000000000001336.

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18

Ruscheweyh, Ruth, and Jürgen Sandkühler. "Opioids and central sensitisation: II. Induction and reversal of hyperalgesia." European Journal of Pain 9, no. 2 (April 2005): 149–52. http://dx.doi.org/10.1016/j.ejpain.2004.05.011.

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19

Lundeberg, Thomas, and Iréne Lund. "Are Reviews Based on Sham Acupuncture Procedures in Fibromyalgia Syndrome (Fms) Valid?" Acupuncture in Medicine 25, no. 3 (September 2007): 100–106. http://dx.doi.org/10.1136/aim.25.3.100.

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In recent reviews regarding the efficacy of acupuncture in fibromyalgia syndrome (FMS) it has been concluded that acupuncture has no specific effect since the control procedure (superficial needling and/or needling away from ‘specific’ points) had similar effects. These conclusions may be questioned since superficial needling and/or needling away from specific trigger points is not inert. Also, manual acupuncture or mild electroacupuncture (EA) may not be sufficient to activate the endogenous pain inhibiting system. Patients with FMS suffer from allodynia, fatigue and muscle ache, which is partly explained by peripheral and central sensitisation. Sensitisation results in augmented and altered stimulus responses whereby light stimulation of the skin has as strong an effect as regular needling on the pain inhibitory system in FMS. Central sensitisation in FMS is also associated with expanded receptive fields of central neurons resulting in a larger topographic distribution of the pain. This would suggest that control procedures using needling away from the ‘specific site’ might have as strong an effect as needling within the most painful area. Also, repeated nociceptive input from muscles (as obtained by de qi) results in expansion of receptive fields which in turn may result in activation of descending pain inhibition outside the stimulated myotome. Sensitisation to pain, such as in FMS, may also be related to abnormalities in descending efferent pathways. As there is likely to be an imbalance between excitatory and inhibitory systems in FMS, stronger stimulation may therefore be needed to activate the descending pain inhibitory system. In studies using mild manual acupuncture or weak EA stimulation optimal pain inhibition may therefore not have been obtained. When conducting studies on acupuncture, the clinical condition or syndrome needs to be taken into account and the control procedure designed accordingly.
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20

Bourke, Julius H., Richard M. Langford, and Peter D. White. "The common link between functional somatic syndromes may be central sensitisation." Journal of Psychosomatic Research 78, no. 3 (March 2015): 228–36. http://dx.doi.org/10.1016/j.jpsychores.2015.01.003.

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21

Sarkar, Sanchoy, Anthony Hobson, Qasim Aziz, Clifford J. Woolf, and David G. Thompson. "Central sensitisation contributes to oesophageal hypersensitivity in non-cardiac chest pain." Gastroenterology 118, no. 4 (April 2000): A184. http://dx.doi.org/10.1016/s0016-5085(00)82811-5.

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22

Sarkar, Sanchoy, Qasim Aziz, Clifford J. Woolf, Anthony R. Hobson, and David G. Thompson. "Contribution of central sensitisation to the development of noncardiac chest pain." Lancet 356, no. 9236 (September 2000): 1154–59. http://dx.doi.org/10.1016/s0140-6736(00)02758-6.

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23

Arendt-Nielsen, L., B. Morlion, S. Perrot, A. Dahan, A. Dickenson, H. G. Kress, C. Wells, D. Bouhassira, and A. Mohr Drewes. "Assessment and manifestation of central sensitisation across different chronic pain conditions." European Journal of Pain 22, no. 2 (November 5, 2017): 216–41. http://dx.doi.org/10.1002/ejp.1140.

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24

Mc Auliffe, Seán, Rodney Whiteley, Peter Malliaras, and Kieran O’Sullivan. "Central sensitisation in different tendinopathies: are we comparing apples and oranges?" British Journal of Sports Medicine 53, no. 3 (May 30, 2018): 142–43. http://dx.doi.org/10.1136/bjsports-2017-098863.

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25

de Tommaso, M., M. Sardaro, E. Vecchio, C. Serpino, M. Stasi, and M. Ranieri. "Central Sensitisation Phenomena in Primary Headaches: Overview of a Preventive Therapeutic Approach." CNS & Neurological Disorders - Drug Targets 7, no. 6 (December 1, 2008): 524–35. http://dx.doi.org/10.2174/187152708787122932.

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26

Sarkar, S. "Perceptual wind-up in the human oesophagus is enhanced by central sensitisation." Gut 55, no. 7 (February 16, 2006): 920–25. http://dx.doi.org/10.1136/gut.2005.073643.

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27

Stokvis, Annemieke, J. Henk Coert, and Johan W. van Neck. "Insufficient pain relief after surgical neuroma treatment: Prognostic factors and central sensitisation." Journal of Plastic, Reconstructive & Aesthetic Surgery 63, no. 9 (September 2010): 1538–43. http://dx.doi.org/10.1016/j.bjps.2009.05.036.

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28

Iannetti, G. D., and M. C. Lee. "2.6. The role of the brain stem in central sensitisation in humans." Clinical Neurophysiology 118, no. 12 (December 2007): 2810. http://dx.doi.org/10.1016/j.clinph.2007.09.016.

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29

Vladimirova, Nora, Anders Jespersen, Else Marie Bartels, Anton W. Christensen, Henning Bliddal, and Bente Danneskiold-Samsøe. "Pain Sensitisation in Women with Active Rheumatoid Arthritis: A Comparative Cross-Sectional Study." Arthritis 2015 (July 21, 2015): 1–5. http://dx.doi.org/10.1155/2015/434109.

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Objectives. In some rheumatoid arthritis (RA) patients, joint pain persists without signs of inflammation. This indicates that central pain sensitisation may play a role in the generation of chronic pain in a subgroup of RA. Our aim was to assess the degree of peripheral and central pain sensitisation in women with active RA compared to healthy controls (HC). Methods. 38 women with active RA (DAS28>2.6) and 38 female HC were included in, and completed, the study. Exclusion criteria were polyneuropathy, pregnancy, and no Danish language. Cuff Pressure Algometry measurements were carried out on the dominant lower leg. Pain threshold, pain tolerance, and pain sensitivity during tonic painful stimulation were recorded. Results. Women with active RA had significantly lower pain threshold (p<0.01) and pain tolerance (p<0.01) than HC. The mean temporal summation- (TS-) index in RA patients was 0.98 (SEM: 0.09) and 0.71 (SEM: 0.04) in HC (p<0.01). Conclusion. Patients with active RA showed decreased pressure-pain threshold compared to HC. In addition, temporal summation of pressure-pain was increased, indicating central pain sensitization, at least in some patients. Defining this subgroup of patients may be of importance when considering treatment strategies.
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Andresen, Trine, Dagmar Lunden, Asbjørn M. Drewes, and Lars Arendt-Nielsen. "Pain sensitivity and experimentally induced sensitisation in red haired females." Scandinavian Journal of Pain 2, no. 1 (January 1, 2011): 3–6. http://dx.doi.org/10.1016/j.sjpain.2010.08.005.

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AbstractIntroduction and aimPain sensitivity has been linked to the melanocortin-1 receptor (MC1R) gene. A mutation in MC1R can result in pale skin and red hair in humans and may modulate pain responses in general. Human studies have shown that women with non-functional MC1R’s were sensitive to experimental induced cold and heat pain. A study demonstrated that females with red hair required higher dose of anesthesia than females with dark hair to experience analgesia to electrical stimulation. Moreover, women expressing non-functional MC1Rs display greater analgesia from opioid analgesia. If redheads in general respond differently to pain and analgesics, this is of clinical importance. The aim of this study was therefore to investigate pain sensitivity and experimentally induced sensitisation in red haired females.MethodTwenty healthy females with pale skin and red hair (mean age 32 years, range 20–55) and 20 healthy females with blond/dark hair (mean age 31 years, range 20–51) participated in this study. The pain tolerance thresholds to heat and pressure stimulation were determined. Hyperalgesia was induced experimentally by applying 0.075% topical capsaicin cream for 30 min. The secondary pin-prick hyperalgesic area was estimated with a calibrated filament (von Frey hair, 15 g) and the area of allodynia by a soft brush. This was done 0, 30, 60, and 90 min after cream removal.ResultsNeither heat nor pressure pain tolerance thresholds were changed in the two groups. The secondary pin-prick hyperalgesic areas were significantly smaller for red haired females than blond/dark haired females (P = 0.014). There were no significant differences in the allodynic areas.DiscussionAs the secondary hyperalgesic response evoked by topical capsaicin is a central phenomenon, the observed smaller pin-prick hyperalgesic area in the red haired females could indicate a central role of MCRs in development or maintenance of hyperalgesia. Central involvement of MC1Rs or dysfunction of peripheral MC1Rs activating central MC4Rs has been suggested to influence pain sensitivity. The difference observed between red haired and non-red haired females may have implications for pain management regimens as compounds interacting with sensitisation such as NMDA-antagonists or alpha-2-delta-ligands may exert different types of action in people with MC1R mutation.ConclusionThe present study showed that red haired females were less sensitive to topical capsaicin induced pin-prick hyperalgesia compared with blond/dark haired females.ImplicationsThe smaller hyperalgesic area in redheads could be a manifestation of central anti-hyperalgesic involvement of MCRs and could have an influence on the treatment of pain as well as in studies investigating anti-hyperalgesic drugs.
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31

Pei, Pei, Lu Liu, Luo-Peng Zhao, Zheng-Yang Qu, Chu-Ying Tang, Lin-Peng Wang, and Wenming Yang. "Electroacupuncture exerts an anti-migraine effect via modulation of the 5-HT7 receptor in the conscious rat." Acupuncture in Medicine 37, no. 1 (February 2019): 47–54. http://dx.doi.org/10.1136/acupmed-2017-011410.

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Background: Acupuncture has been recommended as an alternative therapy for migraine. Emerging evidence suggests that the 5-HT7 receptor (5-HT7R) plays a significant facilitatory role in descending modulation in migraine pathophysiology, and that activation of 5-HT7R in the descending pathway is involved in migraine central sensitisation. Objective: To investigate the ability of electroacupuncture (EA) to ameliorate central sensitisation via modulation of 5-HT7R in the descending pain pathways using a rat model of migraine induced by repetitive dural electrical stimulation (DES). Design: 64 male Sprague-Dawley rats were randomly divided into four groups: Normal group; DES group (receiving dural electrical stimulation only); DES+GB20 group (DES model group treated with EA at GB20); and DES+Sham group (DES model group treated with EA at a non-traditional (sham) acupuncture point). The presence of cutaneous allodynia was determined by measuring facial and hind-paw withdrawal latencies to electronic von-Frey. The expression of 5-HT7R in the descending pathways (periaqueductal grey, raphe magnus nucleus, and trigeminal nucleus caudalis) was assessed using immunofluorescence and Western blotting. Results: Facial and hind-paw withdrawal thresholds were significantly increased in the DES+GB20 group compared with the untreated DES group. The expression of 5-HT7R was significantly decreased in the DES+GB20 group compared with the DES group (one-way analysis of variance (ANOVA), P<0.05). No significant differences in behaviour or expression were found between the rats in the DES+Sham group and the untreated DES group (one-way ANOVA, P>0.05). Conclusion: EA at GB20 may ameliorate central sensitisation in migraine by inhibiting the activation of 5-HT7 receptors in the descending pain pathway in a rat model of migraine.
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32

Skou, Soren T., Thomas Graven-Nielsen, Lasse Lengsoe, Ole Simonsen, Mogens B. Laursen, and Lars Arendt-Nielsen. "Relating clinical measures of pain with experimentally assessed pain mechanisms in patients with knee osteoarthritis." Scandinavian Journal of Pain 4, no. 2 (April 1, 2013): 111–17. http://dx.doi.org/10.1016/j.sjpain.2012.07.001.

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ABSTRACTBackgroundPeripheral and central sensitisation is prominent in knee osteoarthritis (KOA) and could be important for the reduced efficacy in some cases after as well surgery as pharmacological interventions. Although sensitisation is important in KOA it is not known to what degree it contributes to the overall clinical pain problem. The aim was therefore to investigate how much a combination of quantitative pain measures assessing various pain mechanisms (local and spreading hyperalgesia, temporal and spatial summation, descending inhibition) could predict peak pain intensity in patients with KOA.MethodsWhile resting in a comfortable recumbent position the pressure pain thresholds (PPT) in the peripatellar region (eight locations) and at the tibialis anterior muscle (TA) were assessed by handheld pressure algometry, computer-controlled pressure algometry and cuff-algometry in the affected leg of 17 KOA patients without pain or sensory dysfunctions in other regions than the knee. Cuff-algometry was used to detect spatial pain summation of the lower leg. Temporal pain summation was assessed by repeated pressure stimulation on the TA muscle. The conditioning pain modulation (CPM) was evaluated by conditioning tonic arm pain and by PPT from the peripatellar region. The participants rated their peak pain intensity in the previous 24 h using on a 10 cm visual analogue scale.ResultsA multiple-regression model based on TA pressure pain sensitivity (spreading sensitisation) and temporal pain summation on the lower leg accounted for 55% of the variance in peak pain intensity experienced by the patients (P=0.001). Significant correlations (P< 0.05) were found between PPTs assessed by handheld pressure algometry in the peripatellar region and at TA (R = 0.94), PPTs assessed by computer-controlled pressure algometry and handheld pressure algometry in the peripatellar region (R = 0.71), PPTs assessed by computer-controlled pressure algometry in the peripatellar region and handheld pressure algometry at TA (R = 0.71) and temporal summation at the knee and at TA (R = 0.73).ConclusionBased on the multiple regression model 55% variance of the perceived maximal pain intensity in painful KOA could be explained by the quantitative experimental pain measures reflecting central pain mechanisms (spreading sensitisation, temporal summation). The lack of other correlations between the methods used in assessing pain mechanisms in this study highlights the importance of applying different tests and different pain modalities when assessing the sensitised pain system as different methods add complementary information.ImplicationsClinical pain intensity can be explained by influences of different central pain mechanisms in KOA. This has implications for pain management in KOA where treatment addressing central pain components may be more important than previously acknowledged.
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33

Nijs, Jo, Bart Van de Velde, and Kenny De Meirleir. "Pain in patients with chronic fatigue syndrome: Does nitric oxide trigger central sensitisation?" Medical Hypotheses 64, no. 3 (January 2005): 558–62. http://dx.doi.org/10.1016/j.mehy.2004.07.037.

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34

Filitz, J., A. Nieberle, H. Zeilhofer, and W. Koppert. "The CB1-receptor antagonist rimonabant reduces central sensitisation in a human pain model." European Journal of Anaesthesiology 25, Sup 44 (May 2008): 2. http://dx.doi.org/10.1097/00003643-200805001-00005.

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35

Hughes, B., A. Jaggi, H. Cox, S. Alexander, and H. Cohen. "Presence of central sensitisation and sensory deficits in patients with atraumatic shoulder instability." Manual Therapy 25 (September 2016): e101. http://dx.doi.org/10.1016/j.math.2016.05.177.

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36

Binder, Andreas, Maike Stengel, Rainer Maag, Gunnar Wasner, Robert Schoch, Frank Moosig, Bernhard Schommer, and Ralf Baron. "Pain in oxaliplatin-induced neuropathy – Sensitisation in the peripheral and central nociceptive system." European Journal of Cancer 43, no. 18 (December 2007): 2658–63. http://dx.doi.org/10.1016/j.ejca.2007.07.030.

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37

Valentini, Elia, and Enrico Schulz. "Automatised application of pinprick-evoked potentials improves investigation of central sensitisation in humans." Clinical Neurophysiology 131, no. 10 (October 2020): 2482–83. http://dx.doi.org/10.1016/j.clinph.2020.07.011.

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38

Allaire, Catherine, Tuba Aksoy, Mohamed Bedaiwy, Susannah Britnell, Heather L. Noga, Holly Yager, and Paul J. Yong. "An Interdisciplinary Approach to Endometriosis-associated Persistent Pelvic Pain." Journal of Endometriosis and Pelvic Pain Disorders 9, no. 2 (January 2017): 77–86. http://dx.doi.org/10.5301/jeppd.5000284.

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Endometriosis-associated pelvic pain is a common and often challenging problem. For certain patients, pain persists or recurs despite adequate medical or surgical therapy targeted to endometriosis. In this patient population, there is often the presence of coexisting pain conditions such as irritable bowel syndrome, painful bladder syndrome and myofascial pain as well central sensitisation. An interdisciplinary approach where both peripheral pain triggers and central sensitization are addressed is likely to lead to improved pain and quality of life. The approach to the evaluation and treatment of the patients with persistent/chronic pelvic pain and endometriosis is outlined in this article.
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39

Mallick, G., H. D. Shewade, T. K. Agrawal, A. M. V. Kumar, and S. S. Chadha. "Enhanced tuberculosis case finding through advocacy and sensitisation meetings in prisons of Central India." Public Health Action 7, no. 1 (March 21, 2017): 67–70. http://dx.doi.org/10.5588/pha.16.0109.

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40

Jensen, Michael B., Ken S. Frahm, José Biurrun Manresa, and Ole K. Andersen. "Reflex threshold assessment methodology for evaluation of central sensitisation is vulnerable to EMG crosstalk." Scandinavian Journal of Pain 3, no. 3 (July 1, 2012): 191. http://dx.doi.org/10.1016/j.sjpain.2012.05.048.

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Abstract Background/aims The nociceptive withdrawal reflex (NWR) is a robust measure of nociception highly correlated with subjective pain and several studies indicate that identification of reflex thresholds may be a valuable objective tool during diagnosis of chronic pain conditions related to central sensitisation. The NWR involves complex muscle synergies but most methodologies for assessment of human withdrawal reflexes evaluates surface electromyography (sEMG) measured over just one muscle and does not consider the possible interference of crosstalk from adjacent muscles. This study investigated if standardised reflex thresholds are robust with respect to crosstalk. Methods Reflexes were elicited by electrical stimulation at the sole of the foot and measured using sEMG and intramuscular electromyography (iEMG) from the tibialis anterior and soleus muscles in 15 healthy subjects. 489 sEMG recordings were evaluated using a standardised reflex threshold parameter (interval peak z-score) proposed by Rhudy and France [1] to detect occurring reflexes. The outcome of this standardised reflex detection were compared to two different visual evaluations: (1) assessing only sEMG and (2) assessing both sEMG and iEMG (enabling distinction between genuine reflexes and crosstalk) for the production of two respective ROC-curves. Results The first ROC-curve indicated that interval peak z-score allows reflex detection with high accuracy and has an optimal threshold around z = 12. However, the second ROC-curve based on evaluation 2 revealed that many recordings identified as reflexes were incorrectly categorised reflecting crosstalk. Crosstalk did severely reduce the accuracy of the performed reflex detection – a z-score threshold of 12 was found associated with an extremely poor specificity (0.26). Conclusion Crosstalk may severely reduce the accuracy of standardised reflex threshold assessment methodologies. Use of standard sEMG for reflex recording may cause an alarmingly low specificity of reflex detection and should be avoided whenever the presence crosstalk is suspected.
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41

Iannetti, G. D. "15 BRAIN POTENTIALS EVOKED BY MECHANICAL STIMULI: A NEW TOOL FOR ASSESSING CENTRAL SENSITISATION?" European Journal of Pain 11, S1 (June 2007): S7. http://dx.doi.org/10.1016/j.ejpain.2007.03.029.

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42

Iannetti, G. D., U. Baumgärtner, M. C. Lee, I. Tracey, W. Magerl, and R. D. Treede. "204 PINPRICK-EVOKED POTENTIALS (PEPS): A NOVEL TOOL TO ASSESS CENTRAL SENSITISATION IN HUMANS." European Journal of Pain 11, S1 (June 2007): S89. http://dx.doi.org/10.1016/j.ejpain.2007.03.219.

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43

Nijs, Jo, Steven Z. George, Daniel J. Clauw, César Fernández-de-las-Peñas, Eva Kosek, Kelly Ickmans, Josué Fernández-Carnero, et al. "Central sensitisation in chronic pain conditions: latest discoveries and their potential for precision medicine." Lancet Rheumatology 3, no. 5 (May 2021): e383-e392. http://dx.doi.org/10.1016/s2665-9913(21)00032-1.

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44

Munksgaard, Signe B., Lars Bendtsen, and Rigmor H. Jensen. "Modulation of central sensitisation by detoxification in MOH: Results of a 12-month detoxification study." Cephalalgia 33, no. 7 (February 21, 2013): 444–53. http://dx.doi.org/10.1177/0333102412475235.

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Background Human and animal models suggest that central sensitisation plays a role in medication-overuse headache (MOH). We aimed to study pain perception in MOH patients before and a year after withdrawal. Methods We examined pain perception in 35 MOH patients before and two, six and 12 months after detoxification. For baseline comparison, we tested 40 healthy controls. We measured cephalic and extra-cephalic pressure-pain thresholds and supra-threshold pressure-pain scores and extra-cephalic pain thresholds, supra-threshold pain scores and temporal summation for electrical stimulation. Results Of the 35 patients, 21 patients completed the entire study and remained cured of MOH. Statistically significant differences between patients and healthy controls were found in cephalic pressure-pain thresholds (137.3 kPa vs. 170 kPa, p < 0.05), extra-cephalic pressure pain thresholds (213.3 vs. 274.3 kPa, p < 0.05), in cephalic supra-threshold pressure-pain scores measured on a 100 mm visual analogue scale (61 vs. 27 mm, p < 0.05) and extra-cephalic supra-threshold pain scores for electrical stimulation (19.0 vs. 10.0 mm, p < 0.05). Cephalic supra-threshold pain scores decreased statistically significantly from 50.3 mm at baseline to 28.0 mm at the 12-month follow-up. In contrast to controls, temporal summation was not found in MOH patients before withdrawal, but after detoxification temporal summation normalised. Conclusion The central nervous system is sensitised in patients with MOH. For the first time we demonstrate that the pain perception continues to normalise up to a year after detoxification. This emphasises the importance of detoxification and follow-up to prevent relapse.
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45

Ando, Ayaka, David Smallwood, Marcus McMahon, Louis Irving, Stuart B. Mazzone, and Michael J. Farrell. "Neural correlates of cough hypersensitivity in humans: evidence for central sensitisation and dysfunctional inhibitory control." Thorax 71, no. 4 (February 9, 2016): 323–29. http://dx.doi.org/10.1136/thoraxjnl-2015-207425.

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46

Wodehouse, Theresa, Kavita Poply, Shankar Ramaswamy, Saowarat Snidvongs, Julius Bourke, Hasan Tahir, Kristin Ullrich, and Vivek Mehta. "A pilot study investigating whether quantitative sensory testing alters after treatment in patients with fibromyalgia." British Journal of Pain 12, no. 4 (May 15, 2018): 250–56. http://dx.doi.org/10.1177/2049463718776336.

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Background: Fibromyalgia is a chronic musculoskeletal pain condition that is often associated with sleep disturbances and fatigue. The pathophysiology of fibromyalgia is not understood, but indirect evidence suggests a central dysfunction of the nociceptive modulating system. The aim of this study was to evaluate whether quantitative sensory testing detects a change in pain thresholds in fibromyalgia patient receiving pregabalin treatment. Methods: A total of 25 patients were recruited for the study and received routine pregabalin, but only 14 patients completed the treatment. Assessment of pressure pain thresholds and changes in conditioned pain modulation using ischaemic pain as a conditioning stimulus were measured at baseline and every 4 weeks for 12 weeks. Fibromyalgia impact questionnaire, PainDETECT and SF-12 were also completed. Results: Patients with fibromyalgia demonstrated a less-efficient conditioned pain modulation at baseline. An efficient conditioned pain modulation was observed at 1 month and this was maintained until the final visit. Pressure pain thresholds (PPTs) showed a significant improvement from baseline. Patients also reported a similar magnitude of improvements in PainDETECT, fibromyalgia impact questionnaire (FIQ) and its impact on daily life and change in outcome for SF-12. Conclusion: This pilot study reports an increase in PPTs and improved conditioned pain modulation response after commencing pregabalin, which was maintained at 12 weeks, and this was supported by positive pain scores. Pregabalin is a licenced treatment for fibromyalgia in Europe, and its response to central sensitisation, particularly ‘dynamic responses’, has not been reported. We conclude that pregabalin has the potential to reduce peripheral and central sensitisation in patients with fibromyalgia, as measured using quantitative sensory testing.
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47

Kaleli, Winfred, Winnie Ndeta Otslulah, and Consolata Mutisya. "The Role of Public Relations in sensitizing public on Government Projects in Kenya: Case of Nairobi County." Journal of Development and Communication Studies 8, no. 1 (March 10, 2021): 49–73. http://dx.doi.org/10.4314/jdcs.v8i1.3.

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Public relations is a vital tool for the government because it emphasizes on democracy and good governance. This study sought to establish the role of public relations tools in sensitizing the public on government projects in government ministries in the Central Government in Nairobi. Specifically, the study examined: the effects of media relations on sensitizing the public on government projects in Nairobi County, Kenya; the effects of community relations on sensitizing the public on government projects in Nairobi County, Kenya; the effects of sponsorships on sensitizing the public on government projects in Nairobi County, Kenya; the effects of community events on sensitizing the public on government projects in Nairobi County, Kenya. For this study, the researcher used descriptive survey design. The target population comprised heads of departments in state corporations in Kenya which totals 162. This study was a census survey of all 162 state corporations in Kenya. The unit of analysis comprised all the state corporations whereas the unit of observation consisted of 162 heads of departments (Public Relations Officers) of each State Corporation, thus forming a sample size of 162 respondents. Primary data was collected using questionnaires as the main data collection instruments. The study also collected data using an interview schedule. SPSS version 20 was adopted in the analysis of quantitative data. Data was presented in the form of pie charts, graphs and tables. Themes were used to analyze qualitative data. The study found that media relations positively and significantly influence sensitisation on government projects; community relations positively and significantly influence sensitisation on government projects; sponsorships positively and significantly influence sensitisation on government projects and community events positively and significantly influence sensitisation on government projects. The study, therefore, recommends that stronger communication mechanisms should be installed and well integrated in the system to ensure easier and convenient dissemination of information to the public. PR department of any organisation contributes to its development and enhances customer’s satisfaction. In this line, the study recommends that strong and well integrated PR department should be installed in an organisation and therefore should be sufficiently funded to ensure its success. Further, the study recommends that organisations should devise ways and means to maintain a long-term commitment with clients.
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Ansuategui Echeita, Jone, Henrica R. Schiphorst Preuper, Rienk Dekker, Ilse Stuive, Hans Timmerman, Andre P. Wolff, and Michiel F. Reneman. "Central Sensitisation and functioning in patients with chronic low back pain: protocol for a cross-sectional and cohort study." BMJ Open 10, no. 3 (March 2020): e031592. http://dx.doi.org/10.1136/bmjopen-2019-031592.

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IntroductionA relevant subsample of patients with chronic low back pain (CLBP) have manifested augmented central pain processing, central sensitisation (CS). Patients with CLBP have limited functioning and participation. Theoretically, physical functioning in patients with CLBP can plausibly be linked to CS; however, evidence to explain such association is scarce. Moreover, there is no gold standard for CS diagnosis. The objectives of the study are: (1) to analyse the association between instruments assessing reference symptoms and signs attributed to CS; (2) to analyse whether reference symptoms and signs attributed to CS are associated with functioning measurement outcomes; and (3) to analyse whether changes (between baseline and discharge) in reference symptoms and signs attributed to CS are related to changes in each of the functioning measurement outcomes.Methods and analysisA cross-sectional and longitudinal observational study is performed with measurements taken at baseline and discharge of an interdisciplinary rehabilitation programme. A sample size of 110 adult patients with CLBP has been calculated for the study. CS measurements are: Central Sensitisation Inventory, quantitative sensory testing and heart rate variability. Functioning measurements are: lifting capacity, maximal aerobic capacity, accelerometry and reported functioning. Statistical analyses to be performed are: (1) correlation between CS measurements, (2) multiple regression between functioning (dependent variable) and CS measurements (independent variable), and (3) multiple regression between changes in scores of functioning (dependent variable) and CS measurements (independent variable), and corrected for sex and age.Ethics and disseminationThe study obtained the clearance to its implementation from the Medical Research Ethics Committee of the University Medical Center Groningen in July 2017. The results will be disseminated through scientific publications in peer-reviewed journals, presentations at relevant conferences, and reports to stakeholders.Trial registration numberNTR7167/NL6980.
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Segerdahl, M. "Multiple dose gabapentin attenuates cutaneous pain and central sensitisation but not muscle pain in healthy volunteers." Pain 125, no. 1 (November 2006): 158–64. http://dx.doi.org/10.1016/j.pain.2006.05.008.

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50

French, H. P., M. McCallan, and C. Jong. "Do features of central sensitisation exist in Greater Trochanter Pain Syndrome (GTPS)? a case control study." Physical Therapy in Sport 28 (November 2017): e13. http://dx.doi.org/10.1016/j.ptsp.2017.08.041.

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