Pain mechanisms in computer and smartphone users

2022 ◽  
pp. 291-301
Author(s):  
Alberto Marcos Heredia-Rizo ◽  
Pascal Madeleine ◽  
Grace P.Y. Szeto
Keyword(s):  
Pain Mechanisms

Genetic Analysis of Pain Mechanisms

2002 ◽  
Vol 12 (4) ◽  
pp. 275-296 ◽  
Author(s):  
Daphne A. Robinson ◽  
Min Zhuo
Keyword(s):  
Genetic Analysis ◽  
Pain Mechanisms

Key facts on moderate to severe acute pain combined treatment with tramadol and dexketoprofen at fixed doses

2020 ◽  
Vol 13 (3) ◽  
pp. 304-310
Author(s):  
Jarosław Woroń
Keyword(s):  
Quality Of Life ◽  
Treatment Adherence ◽  
Acute Pain ◽  
Pain Treatment ◽  
Combined Treatment ◽  
Physiological Changes ◽  
Physiological Mechanisms ◽  
Pain Mechanisms ◽  
Proven Efficacy

The development of pain is associated with numerous physiological mechanisms. Improper acute pain treatment significantly reduces the quality of life and leads to a number of physiological changes that adversely affect the general condition of the patient. In many cases, inadequate analgesic therapy results in the transition from acute to chronic pain. For this reason, it is extremely important to use drugs that synergistically affect various pain mechanisms. Combined preparations, including the combination of tramadol and dexketoprofen, are very effective. This combination has many advantages, including proven efficacy and tolerability, ensures better treatment adherence and is easy to administer.

Neural and sociocultural mediators of ethnic differences in pain

2020 ◽  
Author(s):  
EAR Losin ◽  
CW Woo ◽  
NA Medina ◽  
JR Andrews-Hanna ◽  
Hedwig Eisenbarth ◽  
...  
Keyword(s):  
African Americans ◽  
Ethnic Differences ◽  
Nociceptive Pain ◽  
Common Belief ◽  
Pain Mechanisms ◽  
Thermal Pain ◽  
Heat Effects ◽  
Pain Report ◽  
And Gender ◽  
Ethnicity And Gender

© 2020, The Author(s), under exclusive licence to Springer Nature Limited. Understanding ethnic differences in pain is important for addressing disparities in pain care. A common belief is that African Americans are hyposensitive to pain compared to Whites, but African Americans show increased pain sensitivity in clinical and laboratory settings. The neurobiological mechanisms underlying these differences are unknown. We studied an ethnicity- and gender-balanced sample of African Americans, Hispanics and non-Hispanic Whites using functional magnetic resonance imaging during thermal pain. Higher pain report in African Americans was mediated by discrimination and increased frontostriatal circuit activations associated with pain rating, discrimination, experimenter trust and extranociceptive aspects of pain elsewhere. In contrast, the neurologic pain signature, a neuromarker sensitive and specific to nociceptive pain, mediated painful heat effects on pain report largely similarly in African American and other groups. Findings identify a brain basis for higher pain in African Americans related to interpersonal context and extranociceptive central pain mechanisms and suggest that nociceptive pain processing may be similar across ethnicities.

Dorsal Horn Pain Mechanisms

2019 ◽  
pp. 444-469 ◽  
Author(s):  
Hanns Ulrich Zeilhofer ◽  
Robert Ganley
Keyword(s):  
Dorsal Horn ◽  
Neuronal Excitability ◽  
Functional Organization ◽  
Synaptic Integration ◽  
Synaptic Efficacy ◽  
Pain Mechanisms ◽  
Pain Pathway ◽  
Pathological Pain ◽  
The Subject ◽  
Equivalent Structure

The spinal dorsal horn and its equivalent structure in the brainstem constitute the first sites of synaptic integration in the pain pathway. A huge body of literature exists on alterations in spinal nociceptive signal processing that contribute to the generation of exaggerated pain states and hence to what is generally known as “central sensitization.” Such mechanisms include changes in synaptic efficacy or neuronal excitability, which can be evoked by intense nociceptive stimulation or by inflammatory or neuropathic insults. Some of these changes cause alterations in the functional organization of dorsal horn sensory circuits, leading to abnormal pathological pain sensations. This article reviews the present state of this knowledge. It does not cover the contributions of astrocytes and microglia in detail as their functions are the subject of a separate chapter.

A Proposed Platform for Phenotyping Endometriosis-Associated Pain: Unifying Peripheral and Central Pain Mechanisms

2020 ◽  
Vol 9 (3) ◽  
pp. 89-97
Author(s):  
Paul J. Yong ◽  
Christina Williams ◽  
Mohamed A. Bedaiwy ◽  
Catherine Allaire
Keyword(s):  
Central Pain ◽  
Pain Mechanisms

scholarly journals Adaptive mechanisms driving maladaptive pain: how chronic ongoing activity in primary nociceptors can enhance evolutionary fitness after severe injury

2019 ◽  
Vol 374 (1785) ◽  
pp. 20190277 ◽  
Author(s):  
Edgar T. Walters
Keyword(s):  
Chronic Pain ◽  
Motor Impairment ◽  
Low Frequency ◽  
Severe Injury ◽  
Ongoing Activity ◽  
Pain Mechanisms ◽  
Bodily Injury ◽  
Adaptive Mechanisms ◽  
Survival And Reproduction ◽  
Ongoing Pain

Chronic pain is considered maladaptive by clinicians because it provides no apparent protective or recuperative benefits. Similarly, evolutionary speculations have assumed that chronic pain represents maladaptive or evolutionarily neutral dysregulation of acute pain mechanisms. By contrast, the present hypothesis proposes that chronic pain can be driven by mechanisms that evolved to reduce increased vulnerability to attack from predators and aggressive conspecifics, which often target prey showing physical impairment after severe injury. Ongoing pain and anxiety persisting long after severe injury continue to enhance vigilance and behavioural caution, decreasing the heightened vulnerability to attack that results from motor impairment and disfigurement, thereby increasing survival and reproduction (fitness). This hypothesis is supported by evidence of animals surviving and reproducing after traumatic amputations, and by complex specializations that enable primary nociceptors to detect local and systemic signs of injury and inflammation, and to maintain low-frequency discharge that can promote ongoing pain indefinitely. Ongoing activity in nociceptors involves intricate electrophysiological and anatomical specializations, including inducible alterations in the expression of ion channels and receptors that produce persistent hyperexcitability and hypersensitivity to chemical signals of injury. Clinically maladaptive chronic pain may sometimes result from the recruitment of this powerful evolutionary adaptation to severe bodily injury. This article is part of the Theo Murphy meeting issue ‘Evolution of mechanisms and behaviour important for pain’.

scholarly journals Menstrual Pain and Elasticity of Uterine Cervix

2021 ◽  
Vol 10 (5) ◽  
pp. 1110
Author(s):  
Anjeza Xholli ◽  
Gianluca Simoncini ◽  
Sonja Vujosevic ◽  
Giulia Trombetta ◽  
Alessandra Chiodini ◽  
...  
Keyword(s):  
Uterine Cervix ◽  
Ultrasound Elastography ◽  
Cervical Canal ◽  
Tissue Deformation ◽  
Tissue Elasticity ◽  
Menstrual Pain ◽  
Pain Mechanisms ◽  
High Elasticity ◽  
Color Score ◽  
Post Hoc

Menstrual pain is consequent to intense uterine contraction aimed to expel menstrual flow through downstream uterine cervix. Herein it was evaluated whether characteristics of uterine cervix are associated with intensity of menstrual pain. Ultrasound elastography was used to analyze cervix elasticity of 75 consecutive outpatient women. Elasticity was related to intensity of menstrual pain defined by a Visual Analogue Scale (VAS). Four regions of interest (ROI) were considered: internal uterine orifice (IUO), anterior (ACC) and posterior cervical (PCC) compartment and middle cervical canal (MCC). Tissue elasticity, evaluated by color score (from 0.5 = blue/violet (low elasticity) to 3.0 = red (high elasticity), and percent tissue deformation was analyzed. Elasticity of IUO was lower (p = 0.0001) than that of MCC or ACC, and it was negatively related (R2 = 0.428; p = 0.0001) to menstrual VAS (CR −2.17; 95%CI −3.80, −0.54; p = 0.01). Presence of adenomyosis (CR 3.24; 95% CI 1.94, 4.54; p = 0.0001) and cervix tenderness at clinical examination (CR 2.74; 95% CI 1.29, 4.20; p = 0.0004), were also independently related to menstrual VAS. At post hoc analysis, women with vs. without menstrual pain had lower IUO elasticity, expressed as color score (0.72 ± 0.40 vs. 0.92 ± 0.42; p = 0.059), lower percent tissue deformation at IUO (0.09 ± 0.05 vs. 0.13 ± 0.08; p = 0.025), a higher prevalence of cervical tenderness at bimanual examination (36.2% vs. 9.5%; p = 0.022) and a higher prevalence of adenomyosis (46.5% vs. 19.9%; p = 0.04). These preliminary data indicate that IUO elasticity is associated with the presence and the intensity of menstrual pain. Mechanisms determining IUO elasticity are useful to be explored.

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