Pain, Gain, and the Brain: Chronic Pain, Disability, and Behavior Revisited

1988 ◽  
Vol 33 (12) ◽  
pp. 1043-1044
Author(s):  
J. Scott Richards
2021 ◽  
Vol 15 ◽  
Author(s):  
Andrew E. Warfield ◽  
Jonathan F. Prather ◽  
William D. Todd

Research over the last 20 years regarding the link between circadian rhythms and chronic pain pathology has suggested interconnected mechanisms that are not fully understood. Strong evidence for a bidirectional relationship between circadian function and pain has been revealed through inflammatory and immune studies as well as neuropathic ones. However, one limitation of many of these studies is a focus on only a few molecules or cell types, often within only one region of the brain or spinal cord, rather than systems-level interactions. To address this, our review will examine the circadian system as a whole, from the intracellular genetic machinery that controls its timing mechanism to its input and output circuits, and how chronic pain, whether inflammatory or neuropathic, may mediate or be driven by changes in these processes. We will investigate how rhythms of circadian clock gene expression and behavior, immune cells, cytokines, chemokines, intracellular signaling, and glial cells affect and are affected by chronic pain in animal models and human pathologies. We will also discuss key areas in both circadian rhythms and chronic pain that are sexually dimorphic. Understanding the overlapping mechanisms and complex interplay between pain and circadian mediators, the various nuclei they affect, and how they differ between sexes, will be crucial to move forward in developing treatments for chronic pain and for determining how and when they will achieve their maximum efficacy.


1985 ◽  
Vol 30 (12) ◽  
pp. 999-999
Author(s):  
Gerald S. Wasserman

Author(s):  
О.И. Кит ◽  
И.М. Котиева ◽  
Е.М. Франциянц ◽  
И.В. Каплиева ◽  
Л.К. Трепитаки ◽  
...  

Известно, что биогенные амины (БА) участвуют в злокачественном росте, их уровень изменяется в ЦНС при болевом воздействии, однако исследований о сочетанном влиянии хронической боли (ХБ) и онкопатологии на динамику БА в головном мозге не проводилось. Цель: изучить особенности баланса БА в коре головного мозга в динамике роста меланомы, воспроизведенной на фоне ХБ. Материалы и методы. Работа выполнена на 64 мышах-самках, весом 21-22 г. Животным основной группы меланому В16/F10 перевивали под кожу спины через 2 недели после перевязки седалищных нервов. Группой сравнения служили мыши с меланомой без боли. Уровни БА: адреналина, норадреналина, дофамина (ДА), серотонина (5-НТ), гистамина, а также 5-ОИУК определяли методом иммуноферментного анализа. Результаты. У мышей с ХБ уменьшается содержание большинства БА, однако уровень ДА не изменяется. Метаболизм 5-НТ происходит с участием МАО. Развитие меланомы сопровождается увеличением содержания ДА и 5-НТ, тогда как МАО - ингибируется. Направленность сдвигов БА при развитии меланомы на фоне ХБ оказалась практически такой же, как и без неё. В то же время ХБ ограничивает накопление 5-НТ в коре мозга при меланоме, что сопровождается более агрессивным её течением. Выводы. ХБ ограничивает включение стресс-лимитирующих механизмов в головном мозге при развитии меланомы у мышей, что приводит к более агрессивному течению злокачественного процесса. Biogenic amines (BA) are known to be involved in malignant growth, and their CNS levels change in pain; however, there are no studies of combined effects of chronic pain (CP) and cancer on BA dynamics in the brain. Aim: To study features of BA balance in the cerebral cortex during melanoma growth associated with CP. Material and methods. The study included 64 female mice weighing 21-22 g. In the main groups, B16/F10 melanoma was transplanted under the skin of the back two weeks following sciatic nerve ligation. Mice with melanoma without pain were used as the control. Concentrations of BA: adrenaline, noradrenaline, dopamine (DA), serotonin (5-HT), histamine and 5-HIAA were measured with ELISA. Results. Concentrations of BAs decreased in mice with CP although DA levels did not change. 5-HT metabolism involved MAO. The development of melanoma was accompanied by increases in DA and 5-HT whereas MAO was inhibited. The direction of BA changes during the development of melanoma was the same with and without CP. At the same time, CP with melanoma limited accumulation of 5-HT in the cerebral cortex, which resulted in even more aggressive course of cancer. Conclusion. CP restricted the activation of cerebral stress-limiting mechanisms during the development of melanoma in mice, which resulted in a more aggressive course of disease.


Author(s):  
Sascha R. A. Alles ◽  
Anne-Marie Malfait ◽  
Richard J. Miller

Pain is not a simple phenomenon and, beyond its conscious perception, involves circuitry that allows the brain to provide an affective context for nociception, which can influence mood and memory. In the past decade, neurobiological techniques have been developed that allow investigators to elucidate the importance of particular groups of neurons in different aspects of the pain response, something that may have important translational implications for the development of novel therapies. Chemo- and optogenetics represent two of the most important technical advances of recent times for gaining understanding of physiological circuitry underlying complex behaviors. The use of these techniques for teasing out the role of neurons and glia in nociceptive pathways is a rapidly growing area of research. The major findings of studies focused on understanding circuitry involved in different aspects of nociception and pain are highlighted in this article. In addition, attention is drawn to the possibility of modification of chemo- and optogenetic techniques for use as potential therapies for treatment of chronic pain disorders in human patients.


2021 ◽  
Author(s):  
Qiushi Wang ◽  
Yuehua Xu ◽  
Tengda Zhao ◽  
Zhilei Xu ◽  
Yong He ◽  
...  

Abstract The functional connectome is highly distinctive in adults and adolescents, underlying individual differences in cognition and behavior. However, it remains unknown whether the individual uniqueness of the functional connectome is present in neonates, who are far from mature. Here, we utilized the multiband resting-state functional magnetic resonance imaging data of 40 healthy neonates from the Developing Human Connectome Project and a split-half analysis approach to characterize the uniqueness of the functional connectome in the neonatal brain. Through functional connectome-based individual identification analysis, we found that all the neonates were correctly identified, with the most discriminative regions predominantly confined to the higher-order cortices (e.g., prefrontal and parietal regions). The connectivities with the highest contributions to individual uniqueness were primarily located between different functional systems, and the short- (0–30 mm) and middle-range (30–60 mm) connectivities were more distinctive than the long-range (>60 mm) connectivities. Interestingly, we found that functional data with a scanning length longer than 3.5 min were able to capture the individual uniqueness in the functional connectome. Our results highlight that individual uniqueness is present in the functional connectome of neonates and provide insights into the brain mechanisms underlying individual differences in cognition and behavior later in life.


Biomedicines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 340
Author(s):  
Lehel Balogh ◽  
Masaru Tanaka ◽  
Nóra Török ◽  
László Vécsei ◽  
Shigeru Taguchi

Psychotherapy is a comprehensive biological treatment modifying complex underlying cognitive, emotional, behavioral, and regulatory responses in the brain, leading patients with mental illness to a new interpretation of the sense of self and others. Psychotherapy is an art of science integrated with psychology and/or philosophy. Neurological sciences study the neurological basis of cognition, memory, and behavior as well as the impact of neurological damage and disease on these functions, and their treatment. Both psychotherapy and neurological sciences deal with the brain; nevertheless, they continue to stay polarized. Existential phenomenological psychotherapy (EPP) has been in the forefront of meaning-centered counseling for almost a century. The phenomenological approach in psychotherapy originated in the works of Martin Heidegger, Ludwig Binswanger, Medard Boss, and Viktor Frankl, and it has been committed to accounting for the existential possibilities and limitations of one’s life. EPP provides philosophically rich interpretations and empowers counseling techniques to assist mentally suffering individuals by finding meaning and purpose to life. The approach has proven to be effective in treating mood and anxiety disorders. This narrative review article demonstrates the development of EPP, the therapeutic methodology, evidence-based accounts of its curative techniques, current understanding of mood and anxiety disorders in neurological sciences, and a possible converging path to translate and integrate meaning-centered psychotherapy and neuroscience, concluding that the EPP may potentially play a synergistic role with the currently prevailing medication-based approaches for the treatment of mood and anxiety disorders.


2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Henrik Bjarke Vaegter ◽  
Mette Terp Høybye ◽  
Frederik Hjorth Bergen ◽  
Christine E. Parsons

Abstract Objectives Sleep disturbances are highly prevalent in patients with chronic pain. However, the majority of studies to date examining sleep disturbances in patients with chronic pain have been population-based cross-sectional studies. The aims of this study were to 1) examine the frequency of sleep disturbances in patients referred to two interdisciplinary chronic pain clinics in Denmark, 2) explore associations between sleep disturbances and pain intensity, disability and quality of life at baseline and follow-up, and 3) explore whether changes in sleep quality mediated the relationships between pain outcomes at baseline and pain outcomes at follow-up. Methods We carried out a longitudinal observational study, examining patients enrolled in two chronic pain clinics assessed at baseline (n=2,531) and post-treatment follow-up (n=657). Patients reported on their sleep disturbances using the sleep quality subscale of the Karolinska Sleep Questionnaire (KSQ), their pain intensity using 0–10 numerical rating scales, their pain-related disability using the Pain Disability Index (PDI), and quality of life using the EuroQol-VAS scale. The average time between baseline and follow-up was 207 days (SD=154). Results At baseline, the majority of patients reported frequent sleep disturbances. We found a significant association at baseline between self-reported sleep disturbances and pain intensity, pain-related disability, and quality of life, where greater sleep disturbance was associated with poorer outcomes. At follow-up, patients reported significant improvements across all pain and sleep outcomes. In two mediation models, we showed that changes in sleep disturbances from baseline to follow-up were significantly associated with (i) pain intensity at follow-up, and (ii) pain disability at follow-up. However, baseline pain intensity and disability scores were not associated with changes in sleep disturbances and, we did not find evidence for significant mediation of either pain outcome by changes in sleep disturbances. Conclusions Self-reported sleep disturbances were associated with pain outcomes at baseline and follow-up, with greater sleep disturbances associated with poorer pain outcomes. Changes in sleep quality did not mediate the relationships between baseline and follow-up scores for pain intensity and disability. These findings contribute to a growing body of evidence confirming an association between sleep and chronic pain experience, particularly suggestive of a sleep to pain link. Our data following patients after interdisciplinary treatment suggests that improved sleep is a marker for a better outcome after treatment.


2009 ◽  
Vol 212 (15) ◽  
pp. 2411-2418 ◽  
Author(s):  
K. W. Sockman ◽  
K. G. Salvante ◽  
D. M. Racke ◽  
C. R. Campbell ◽  
B. A. Whitman

Sign in / Sign up

Export Citation Format

Share Document