Chronic pain: The role of learning and brain plasticity

Mansour, Ali; Farmer, Melissa A.; Baliki, Marwan N.; Apkarian, A. Vania

doi:10.3233/rnn-139003

Cited by 137 publications

(136 citation statements)

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“…arthritis, low back pain) are under investigation [33, 34]. Moreover, key changes in brain volume, functional connections, and processing are observed using imaging studies [35, 36]. In patients with chronic back pain, studies have reported diminished cortical grey matter and impaired emotional decision making [37, 38].…”

Section: Overview Of the Pain Pathwaymentioning

confidence: 99%

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Mechanisms Underlying Bone and Joint Pain

Havelin

King

2018

Curr Osteoporos Rep

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Purpose of Review. The goal of this review is to provide a broad overview of the current understanding of mechanisms underlying bone and joint pain. Recent Findings. Bone or joint pathology is generally accompanied by local release of pro-inflammatory cytokines, growth factors and neurotransmitters that activate and sensitize sensory nerves resulting in an amplified pain signal. Modulation of the pain signal within the spinal cord and brain that result in net increased facilitation is proposed to contribute to the development of chronic pain. Summary. Great strides have been made in our understanding of mechanisms underlying bone and joint pain that will guide development of improved therapeutic options for these patients. Continued research is required for improved understanding of mechanistic differences driving different components of bone and/or joint pain such as movement related pain compared to persistent background pain. Advances will guide development of more individualized and comprehensive therapeutic options.

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Section: Overview Of the Pain Pathwaymentioning

confidence: 99%

“…In patients with chronic back pain, studies have reported diminished cortical grey matter and impaired emotional decision making [37, 38]. This observation has been expanded to other chronic pain states including chronic osteoarthritis pain [35, 36]. …”

Section: Overview Of the Pain Pathwaymentioning

confidence: 99%

Mechanisms Underlying Bone and Joint Pain

Havelin

King

2018

Curr Osteoporos Rep

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“…Several studies suggested brain neuroplasticity is underlying to comorbidity of CP (Apkarian et al, 21 2009;Doan et al, 2015;Mansour et al, 2014) and the nucleus accumbens (NAc) has been 22 investigated as having a critical role in modulating CP in humans and animal models (Benarroch, 23 2016;Martikainen et al, 2015;Ren et al, 2015;Schwartz et al, 2017). 24…”

Section: Introductionmentioning

confidence: 99%

Physical Activity Induces Nucleus Accumbens Genes Expression Changes Preventing Chronic Pain Susceptibility Promoted by High-Fat Diet and Sedentary Behavior in Mice

Brandão¹,

Bonet

Pagliusi³

et al. 2019

Preprint

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4High-fat diet (HFD)-induced obesity was reported to increase pain behavior independent of obesity 5 status in rats, whereas weight loss interventions such as voluntary physical activity (PA) for adults 6 with overweight or obesity was reported to promote pain reduction in humans with chronic pain (CP). 7 However, is unknown whether an HFD and sedentary (SED) behavior is underlying to CP 8 susceptibility and whether voluntary PA can prevent it. Moreover, differential gene expression in the 9 nucleus accumbens (NAc) is considered to play a crucial role in CP susceptibility. The present study 10 used an adapted model of the inflammatory prostaglandin E2 (PGE)-induced persistent hyperalgesia 11 (PH-ST) protocol for mice, an HFD, and a voluntary PA paradigm to test these hypotheses. In 12 addition, we performed a transcriptome in the NAc and a gene ontology enrichment tools to 13 investigate the differential gene expression and identify the biological processes associated with CP 14 susceptibility tested here. Our results demonstrated that HFD and sedentary behavior promoted CP 15 susceptibility, which in turn was prevented by voluntary PA, even when the animals were fed an 16 HFD. Transcriptome in the NAc found 2,204 differential expression genes related CP susceptibility 17 promoted by HFD and sedentary behavior and prevented by voluntary PA. The gene ontology 18 enrichment revealed 41 biological processes implicated in CP susceptibility. Analyzing collectively 19 those biological processes, our results suggested that genes related to metabolic and mitochondria 20 stress were up-regulated in the CP susceptibility group, whereas genes related to neuroplasticity and 21 axonogenesis were up-regulated in the CP prevented group. These findings provide pieces of 22 evidence that an HFD and sedentary behavior promoted gene expression changes in the NAc related 23 to neurodegeneration and those changes were also underlying to CP susceptibility. Additionally, our 24 findings confirmed other findings supporting the crucial role of voluntary PA to prevent CP 25 susceptibility and add novel insights of differential gene expression in the NAc related to 26 neuroplasticity. 27 28

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“…As a whole, these conditions concur to generate stereotyped network configurations, which seemingly appear as anatomo-functional counterparts of the continuous percept of pain, a picture recoverable from all the examined CP models. The model is theoretically sustained by the fact that persistent acute pain elicits massive hyperactivation of thalamocortical neurons strongly modifying the synaptic loads (Vierck et al 2013;Mansour et al 2014), which in turn dramatically alter the functional organization of the involved neuronal networks (Spisák et al 2017;Gustin et al 2012). In this dramatic context, actual conventional CP therapies do not appear adapt to relocate or repair within original limits the disordered network connectivity.…”

Section: Introductionmentioning

confidence: 99%

Removal of behavioural and electrophysiological signs of chronic pain byin vivomicrosections of rat somatosensory cortex with parallel X-ray microbeams

Zippo

Bertoli

Riccardi

et al. 2019

Preprint

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Chronic pain (CP) is a condition characterized by a wide spectrum of clinical signs and symptoms, missing a sound modelling at the neuronal network scale. Recently, we presented a general theory showing common electrophysiological traits in different CP rat models, i.e. a collapse of relevant functional connectivity network properties, such as modularity, in the somatosensory thalamo-cortical (TC) network. In this work, we preliminary investigated by an in silico accurate simulator of the six-layer mammalian cortical networks that evidenced the crucial collapse of network modularity in CP simulated conditions and the consequent reduction of network adaptive processes. On this track, in studies on CP experimental animals affected by sciatic nerve multiple ligature (Bennett-Xie model), by synchrotron-generated X-ray microbeam (MB) irradiations (7 parallel beams, 100um width), we targeted in vivo the CP involved hindlimb somatosensory projection cortex that, because of the doses radiation (360 Gy, peak at each beam), non-invasively produced fast and precise tissue destruction along the 7 beam projections. These parcellated the cortical tissue and restored the cortical network statistics related to modularity and information processing efficiency as evidenced from post irradiation in vivo electrophysiological recordings. In addition, by MB treatment there was an ensuing removal of behavioral signs of allodynia and hyperalgesia accompanied by recovered normal gait schemes yet preserving the normal sensory thresholds of the experimental rats up to three months after the MB irradiation. Finally, novel and unprecedented therapeutic appraisals for CP are devised. Significance StatementChronic pain (CP) is an excruciating condition with severe effects on patients' life. Apart from many clinical and experimental studies no current theory on CP is generally accepted. Recently, we proposed a general theory of CP in experimental animals as characterized by strong alteration of the connections among neurons in different brain regions. We show here on in silico simulations that specific connectivity changes in the somatosensory cortex recover the lost functional integrity. Concurrently, in experimental animals, we re-modulated, in vivo, some anatomical connections of the somatosensory cortex by extremely thin synchrotron generated X-ray microbeam irradiations. The resulting behavioral and electrophysiological signs of CP disappeared yet maintaining normal sensory responses. No adverse or pathological effects on blank animals were observable.The results report a multianalytic picture of the effects of high-dose sevenfold X-ray microbeams (MBs) irradiation through the intact skull on the somatosensory cortex of experimental rats in vivo anesthetized with a model of neuropathic Chronic Pain (CP, Figure 1A-F) and control (CR). Early computational inspectionsPreliminary, in silico exploratory analyses offered the possibility to evaluate the effects of guided connectivity interventions on functional and topological substrates of the c...

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Chronic pain: The role of learning and brain plasticity

Cited by 137 publications

References 57 publications

Mechanisms Underlying Bone and Joint Pain

Mechanisms Underlying Bone and Joint Pain

Physical Activity Induces Nucleus Accumbens Genes Expression Changes Preventing Chronic Pain Susceptibility Promoted by High-Fat Diet and Sedentary Behavior in Mice

Removal of behavioural and electrophysiological signs of chronic pain byin vivomicrosections of rat somatosensory cortex with parallel X-ray microbeams

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