Assessing peripheral fibers, pain sensitivity, central sensitization, and descending inhibition in Native Americans

Everyone has experienced soreness after an injury. What neural processes underlie this increased pain sensitivity (hyperalgesia)? Recent data indicate that injury triggers an increase in the sensitivity of spinal cord pain-signaling neurons. Nonpainful activation of these sensitized neurons evokes an exaggerated signal interpreted as pain.

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Association between Pain Sensitivity, Central Sensitization, and Functional Disability in Adolescents With Joint Hypermobility

Journal of Pediatric Nursing ◽

10.1016/j.pedn.2018.06.007 ◽

2018 ◽

Vol 42 ◽

pp. 34-38 ◽

Cited By ~ 4

Author(s):

Elizabeth A. Bettini ◽

Ki Moore ◽

Yunfei Wang ◽

Pamela S. Hinds ◽

Julia C. Finkel

Keyword(s):

Central Sensitization ◽

Pain Sensitivity ◽

Functional Disability ◽

Joint Hypermobility

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The Central Sensitization Inventory and Pain Sensitivity Questionnaire: An exploration of construct validity and associations with widespread pain sensitivity among individuals with shoulder pain

Musculoskeletal Science and Practice ◽

10.1016/j.msksp.2018.04.009 ◽

2018 ◽

Vol 36 ◽

pp. 61-67 ◽

Cited By ~ 13

Author(s):

Rogelio A. Coronado ◽

Steven Z. George

Keyword(s):

Construct Validity ◽

Shoulder Pain ◽

Central Sensitization ◽

Pain Sensitivity ◽

Widespread Pain ◽

Central Sensitization Inventory

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Fibromyalgia Syndrome: New Developments in Pathophysiology and Management

CNS Spectrums ◽

10.1017/s1092852900026766 ◽

2008 ◽

Vol 13 (S5) ◽

pp. 4-5 ◽

Cited By ~ 2

Author(s):

I. Jon Russell

Keyword(s):

Central Sensitization ◽

Fibromyalgia Syndrome ◽

Spinal Fluid ◽

Social Adaptation ◽

Human Model ◽

Neural Pathways ◽

Descending Inhibition ◽

Painful Condition ◽

Second Pain ◽

Fluid Levels

Fibromyalgia syndrome (FMS) is a common, chronically painful condition that is still seeking a home among the clinical professions. It is characterized by moderately severe soft-tissue pain and allodynia, which suggests a role for one group of specialists, but its pathogenesis is in the nociceptive machinery of the central nervous system, which defines the territory of other specialties. Comorbidities such as insomnia, cognitive dysfunction, depression, anxiety, recurrent headaches, dizziness, fatigue, morning stiffness, dysesthesia, irritable bowel syndrome, and irritable urethra logically invoke input from practitioners from almost every field of medicine.The precipitating causes of FMS may vary among individuals, but a mechanism underlying the painful symptoms involves central sensitization leading to an amplified perception of pain. As a result, this condition is recognized as the human model for chronic widespread allodynia. Biological abnormalities that are detected in most patients by objective methods include dysfunctional sleep (polysomnography), central sensitization (functional magnetic resonance imaging), temporal summation (windup, second pain), and facilitation of nociception (elevated spinal fluid levels of substance P, deficient biogenic amines that fail to maintain descending inhibition, and, in primary FMS, elevated spinal fluid levels of nerve growth factor).Treatment of FMS is symptomatic and multimodal, including education, physical modalities, and medications that target central neural pathways. Rehabilitation goals include improved physical function, social adaptation, emotional balance, and a better quality of life. Several series of placebo-controlled clinical trials have made available new medications with unique therapeutic mechanisms. Thus, it can be predicted that the next 10 years will see validation of a clinical case definition, more interest in the underlying pathogenesis, a better understanding of how medical care should be adapted to subgroup variations, new medications with specific domain indications, mechanism-directed polypharmacy, characterization of the genetic predisposition, and more emphasis on preventable inciting events.

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“Convergent validity of the central sensitization inventory and experimental testing of pain sensitivity”

Scandinavian Journal of Pain ◽

10.1515/sjpain-2021-0090 ◽

2021 ◽

Vol 0 (0) ◽

Author(s):

Liam Andrén Holm ◽

Casper Glissmann Nim ◽

Henrik Hein Lauridsen ◽

Johanne Brinch Filtenborg ◽

Søren Francis O’Neill

Keyword(s):

Roc Curve ◽

Central Sensitization ◽

Convergent Validity ◽

Pain Sensitivity ◽

Experimental Pain ◽

Test Protocol ◽

Social Constructs ◽

Care Clinic ◽

Central Sensitization Inventory ◽

Pain Test

Abstract Objectives The aim of the current study was to examine the convergent validity of the Central Sensitization Inventory by quantifying the correlation with experimental measures of pain sensitivity and self-reported psycho-social questionnaires, in a low back pain population. Methods All participants were recruited from an outpatient hospital spine care clinic (Spine Centre of Southern Denmark). Participants underwent a standardized experimental pain test protocol and completed the Central Sensitization Inventory (CSI) along with additional self-reported questionnaires to assess psycho-social constructs across different domains. The association between the CSI, experimental pain measures and other self-reported psycho-social questionnaires were analyzed using correlation and contingency tests. ROC-curve analysis was used to determine sensitivity and specificity for CSI. Results One hundred sixty-eight (168) participants were included. The CSI was weakly correlated with nine out of 20 variables in the experimental pain test protocol (rho range −0.37 to 0.22). The CSI was more closely correlated with psycho-social factors such as work ability, disability, and symptoms of exhaustion disorder. ROC-analysis identified an optimal cut-point of 44 on CSI (Sn=39.1% Sp=87.4%). The CSI had an area under the ROC curve of 0.656. Fisher’s exact test demonstrated a statistically significant association between participants scoring ≥40 on CSI and participants categorized as sensitized by experimental pain tests (p-value=0.03). Conclusions Our findings are consistent with previous studies, indicating that the CSI is related to psycho-social constructs. However, the convergent validity with experimental pain measures is small and probably not clinically meaningful.

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Sex differences in measures of central sensitization and pain sensitivity to experimental sleep disruption: implications for sex differences in chronic pain

SLEEP ◽

10.1093/sleep/zsy209 ◽

2018 ◽

Vol 42 (2) ◽

Cited By ~ 8

Author(s):

Michael T Smith ◽

Bethany Remeniuk ◽

Patrick H Finan ◽

Traci J Speed ◽

D Andrew Tompkins ◽

...

Keyword(s):

Chronic Pain ◽

Sex Differences ◽

Central Sensitization ◽

Pain Sensitivity ◽

Sleep Disruption

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Inhibition of Primate Spinothalamic Tract Neurons by Spinal Glycine and GABA Is Modulated by Guanosine 3′,5′-Cyclic Monophosphate

Journal of Neurophysiology ◽

10.1152/jn.1999.81.3.1095 ◽

1999 ◽

Vol 81 (3) ◽

pp. 1095-1103 ◽

Cited By ~ 20

Author(s):

Qing Lin ◽

Jing Wu ◽

Yuan Bo Peng ◽

Minglei Cui ◽

William D. Willis

Keyword(s):

Signal Transduction ◽

Dorsal Horn ◽

Central Sensitization ◽

Dynamic Range ◽

Cgmp Level ◽

High Threshold ◽

Descending Inhibition ◽

Spinothalamic Tract ◽

Cyclic Monophosphate ◽

Deep Layers

Inhibition of primate spinothalamic tract neurons by spinal glycine and GABA is modulated by guanosine 3′,5′-cyclic monophosphate. Our recent work has suggested that the nitric oxide/guanosine 3′,5′-cyclic monophosphate (NO/cGMP) signal transduction system contributes to central sensitization of spinothalamic tract (STT) neurons in part by influencing the descending inhibition of nociception resulting from stimulation in the periaqueductal gray. This study was designed to examine further whether activation of the NO/cGMP cascade reduces the inhibition of the activity of STT neurons mediated by spinal inhibitory amino acid (IAA) receptors. Responses of STT cells to noxious cutaneous stimuli were inhibited by iontophoresis of glycine and GABA agonists in anesthetized monkeys. Administration of 8-bromoguanosine-3′,5′-cyclophosphate sodium (8-bromo-cGMP), a membrane permeable analogue of cGMP, either by microdialysis or by iontophoresis reduced significantly the IAA-induced inhibition of wide dynamic range (WDR) STT cells in the deep layers of the dorsal horn. The reduction in inhibition lasted for up to 1–1.5 h after the cessation of drug infusion. In contrast, IAA-induced inhibition of WDR STT cells in the superficial dorsal horn and high-threshold (HT) cells in superficial or deep layers was not significantly changed during 8-bromo-cGMP infusion. Iontophoresis of 8-bromo-cGMP onto STT cells produced the same actions as produced by microdialysis of this agent, but the effect was not as long-lasting nor as potent. Finally, an attenuation of the IAA receptor–mediated inhibition of STT cells produced by iontophoretic release of a NO donor, 3-morpholinosydnonimine, could be blocked by pretreatment of the spinal cord with a guanylate cyclase inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one. These results suggest that an increased spinal cGMP level contributes to the sensitization of WDR STT neurons in the deep dorsal horn in part by down-regulating spinal IAA receptors. However, no evidence is provided in this study that the NO/cGMP cascade regulates IAA receptors on HT and superficial WDR neurons. Combined with the preceding studies, our data support the view that NO and cGMP function in the same signal transduction cascade and play an important role in central sensitization.

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Widespread Pressure Pain Sensitivity over Nerve Trunk Areas in Women with Frequent Episodic Tension-Type Headache as a Sign of Central Sensitization

Pain Medicine ◽

10.1093/pm/pnz146 ◽

2019 ◽

Vol 21 (7) ◽

pp. 1408-1414

Author(s):

Leandro H Caamaño-Barrios ◽

Fernando Galán-del-Río ◽

César Fernández-de-las-Peñas ◽

Gustavo Plaza-Manzano ◽

Lars Arendt-Nielsen ◽

...

Keyword(s):

Central Sensitization ◽

Pain Sensitivity ◽

Pressure Pain Threshold ◽

Depression Scale ◽

Tension Type Headache ◽

Analysis Of Covariance ◽

Tibialis Posterior ◽

Temporalis Muscle ◽

Pressure Pain ◽

Type Headache

Abstract Objective Previous studies reported the presence of widespread pressure pain sensitivity in patients with tension-type headache. However, most of the studies assessed pressure pain sensitivity over muscle tissue. Our aim was to investigate the difference in pressure pain sensitivity over musculoskeletal and nerve symptomatic and distant areas between women with frequent episodic tension-type headache (FETTH) and healthy subjects. Methods Thirty-two women with FETTH and 32 matched healthy women participated. Pressure pain threshold (PPT) was bilaterally assessed over several nerve trunks (greater occipital, median, radial, ulnar, common peroneal, tibialis posterior) and musculoskeletal structures (temporalis muscle, C5/C6 joint, tibialis anterior) by an assessor blinded to the subject’s condition. A four-week headache diary was used to collect the intensity, frequency, and duration of headache. The Hospital Anxiety and Depression Scale was used to determine anxiety and depressive levels. Results Analysis of covariance found lower widespread and bilateral PPTs over all nerve trunks and musculoskeletal structures in women with FETTH pain (P < 0.001). No significant effect of anxiety and depressive levels on PPTs was found (all P > 0.222). PPT over the temporalis muscle was significantly negatively correlated with headache intensity. Conclusions This study found widespread pressure pain hypersensitivity over both nerve trunks and musculoskeletal structures in women with FETTH, suggesting that the presence of central altered nociceptive processing is not just restricted to musculoskeletal areas, for example, muscles, but also pain evoked from directly provoking the nerve trunks by pressure. It is also possible that nerve tissue treatment could lead to a decrease in central sensitization and headache features.

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Pericranial muscle tenderness (central sensitization), pain sensitivity & psychological characteristics in young adult females

Journal of Pain ◽

10.1016/j.jpain.2005.01.060 ◽

2005 ◽

Vol 6 (3) ◽

pp. S16

Author(s):

E. Janke ◽

K. Holroyd

Keyword(s):

Young Adult ◽

Central Sensitization ◽

Pain Sensitivity ◽

Psychological Characteristics ◽

Adult Females ◽

Muscle Tenderness

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Fentanyl Enhancement of Carrageenan-induced Long-lasting Hyperalgesia in Rats

Anesthesiology ◽

10.1097/00000542-200202000-00025 ◽

2002 ◽

Vol 96 (2) ◽

pp. 381-391 ◽

Cited By ~ 120

Author(s):

Cyril Rivat ◽

Jean-Paul Laulin ◽

Jean-Benoît Corcuff ◽

Evelyne Célèrier ◽

Laure Pain ◽

...

Keyword(s):

Tissue Damage ◽

Central Sensitization ◽

Inflammatory Pain ◽

Pain Sensitivity ◽

Persistent Pain ◽

The Other ◽

Carrageenan Injection ◽

Opiate Treatment

Background Tissue damage may produce hyperalgesia, allodynia, and persistent pain. The authors recently reported that fentanyl elicits analgesia but also activates N-methyl-D-aspartate-dependent pain facilitatory processes opposing analgesia. In nonsuffering rats, this leads to a long-lasting enhancement in pain sensitivity. The current study assessed whether fentanyl could amplify carrageenan-induced hyperalgesia. Methods First, rats were injected once with carrageenan in a hind paw, with fentanyl (60 or 100 microg/kg each given four times at 15-min intervals [4 x 60 or 4 x100]) or saline. Second, rats were injected with carrageenan twice without fentanyl (7-day interval), with the second injection either in the previously injected paw or in the other paw. Third, rats were injected twice with carrageenan in the same hind paw: the first ketamine injection was given (10 mg/kg each given three times at 5-h intervals) with or without fentanyl (4 x 60 microg/kg), and second injection was given without ketamine or fentanyl. The consequences of treatments on long-term hyperalgesia were examined by the paw-pressure vocalization test. Results The long-lasting hyperalgesia induced by the first carrageenan injection was dose-dependently enhanced in both duration and magnitude in 4 x 60 or 4 x 100 microg/kg fentanyl-treated rats: 5 or 10 days, respectively, as compared with 2 days in saline-treated rats. Hyperalgesia observed in the hind paw contralateral to the first carrageenan injection was enhanced in fentanyl-treated rats. The second carrageenan injection, performed in any hind paw, induced an exaggerated hyperalgesia, especially in fentanyl-treated rats. Pretreatment with ketamine totally prevented the carrageenan- and fentanyl-induced enhancement of the long-lasting hyperalgesia. Conclusion Central sensitization in inflammatory pain states is reinforced by an opiate treatment, which could be prevented by N-methyl-D-aspartate receptors blockade.

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