RELIEVING PAIN IN AMERICA: A BLUEPRINT FOR TRANSFORMING PREVENTION, CARE, EDUCATION, AND RESEARCH

Journal of Pain & Palliative Care Pharmacotherapy, Journal Year: 2012, Volume and Issue: 26(2), P. 197 - 198

Published: June 22, 2012

The National Academy of Sciences through its Institute Medicine (IOM) has produced a major scholarly assessment pain in America. This document is tremendous contribution to the evolving nec...

Language: Английский

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Glia and pain: Is chronic pain a gliopathy?

Pain, Journal Year: 2013, Volume and Issue: 154(Supplement 1), P. S10 - S28

Published: June 20, 2013

Activation of glial cells and neuro-glial interactions are emerging as key mechanisms underlying chronic pain. Accumulating evidence has implicated 3 types in the development maintenance pain: microglia astrocytes central nervous system (CNS), satellite dorsal root trigeminal ganglia. Painful syndromes associated with different activation states: (1) reaction (ie, upregulation markers such IBA1 fibrillary acidic protein (GFAP) and/or morphological changes, including hypertrophy, proliferation, modifications networks); (2) phosphorylation mitogen-activated kinase signaling pathways; (3) adenosine triphosphate chemokine receptors hemichannels downregulation glutamate transporters; (4) synthesis release mediators (eg, cytokines, chemokines, growth factors, proteases) to extracellular space. Although widely detected pain resulting from nerve trauma, inflammation, cancer, chemotherapy rodents, more recently, human immunodeficiency virus-associated neuropathy beings, (activation state 1) is not thought mediate sensitivity directly. Instead, states 2 4 have been demonstrated enhance via a number synergistic interactions. Glial shown powerfully modulate excitatory inhibitory synaptic transmission at presynaptic, postsynaptic, extrasynaptic sites. also occurs acute conditions, opioid treatment activates peripheral glia mask analgesia. Thus, could be result "gliopathy," that is, dysregulation functions system. In this review, we provide an update on recent advances discuss remaining questions.

Language: Английский

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Nociceptor sensitization in pain pathogenesis

Nature Medicine, Journal Year: 2010, Volume and Issue: 16(11), P. 1248 - 1257

Published: Oct. 14, 2010

Language: Английский

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The Role of Glia in the Spinal Cord in Neuropathic and Inflammatory Pain

Handbook of experimental pharmacology, Journal Year: 2015, Volume and Issue: unknown, P. 145 - 170

Published: Jan. 1, 2015

Language: Английский

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Clinical features and pathophysiology of complex regional pain syndrome

The Lancet Neurology, Journal Year: 2011, Volume and Issue: 10(7), P. 637 - 648

Published: June 22, 2011

Language: Английский

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Structural plasticity and reorganisation in chronic pain

Nature reviews. Neuroscience, Journal Year: 2016, Volume and Issue: 18(1), P. 20 - 30

Published: Dec. 15, 2016

Language: Английский

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Transmitting Pain and Itch Messages: A Contemporary View of the Spinal Cord Circuits that Generate Gate Control

Neuron, Journal Year: 2014, Volume and Issue: 82(3), P. 522 - 536

Published: May 1, 2014

Language: Английский

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Interleukin-6: an emerging regulator of pathological pain

Journal of Neuroinflammation, Journal Year: 2016, Volume and Issue: 13(1)

Published: June 7, 2016

Interleukin-6 is an inflammatory cytokine with wide-ranging biological effects. It has been widely demonstrated that neuroinflammation plays a critical role in the development of pathological pain. Recently, various pain models have shown elevated expression levels interleukin-6 and its receptor spinal cord dorsal root ganglia. Additionally, administration could cause mechanical allodynia thermal hyperalgesia, intrathecal injection anti-interleukin-6 neutralizing antibody alleviated these pain-related behaviors. These studies indicated pivotal In this review, we summarize recent progress understanding roles mechanisms mediating associated bone cancer, peripheral nerve injury, chemotherapy-induced neuropathy, complete Freund's adjuvant injection, carrageenan injection. Understanding regulating be interesting lead to novel therapeutic strategies for

Language: Английский

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Etiology and Pharmacology of Neuropathic Pain

Pharmacological Reviews, Journal Year: 2018, Volume and Issue: 70(2), P. 315 - 347

Published: March 2, 2018

Injury to or disease of the nervous system can invoke chronic and sometimes intractable neuropathic pain. Many parallel, interdependent, time-dependent processes, including neuroimmune interactions at peripheral, supraspinal, spinal levels, contribute etiology this "disease pain." Recent work emphasizes roles colony-stimulating factor 1, ATP, brain-derived neurotrophic factor. Excitatory processes are enhanced, inhibitory attenuated in dorsal horn throughout somatosensory system. This leads central sensitization aberrant processing such that tactile innocuous thermal information is perceived as pain (allodynia). Processes involved onset differ from those its long-term maintenance. Opioids display limited effectiveness, less than 35% patients derive meaningful benefit other therapeutic approaches. We thus review promising targets have emerged over last 20 years, Na⁺, K⁺, Ca²⁺, hyperpolarization-activated cyclic nucleotide–gated channels, transient receptor potential channel type V1 adenosine A3 receptors. Despite progress, gabapentinoids retain their status first-line treatments, yet mechanism action poorly understood. outline recent progress understanding show how has provided insights into cellular actions pregabalin gabapentin. Interactions with α2δ-1 subunit voltage-gated Ca²⁺ channels produce multiple neuron type-specific cord higher centers. suggest drugs affect rather a single specific target, greatest promise for future development.

Language: Английский

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Targeted Ablation, Silencing, and Activation Establish Glycinergic Dorsal Horn Neurons as Key Components of a Spinal Gate for Pain and Itch

Neuron, Journal Year: 2015, Volume and Issue: 85(6), P. 1289 - 1304

Published: March 1, 2015

The gate control theory of pain proposes that inhibitory neurons the spinal dorsal horn exert critical over relay nociceptive signals to higher brain areas. Here we investigated how glycinergic subpopulation these contributes modality-specific and itch processing. We generated a GlyT2::Cre transgenic mouse line suitable for virus-mediated retrograde tracing studies spatially precise ablation, silencing, activation neurons. found receive sensory input mainly from myelinated primary their local toxin-mediated ablation or silencing induces localized mechanical, heat, cold hyperalgesia; spontaneous flinching behavior; excessive licking biting directed toward corresponding skin territory. Conversely, pharmacogenetic same alleviated neuropathic hyperalgesia chloroquine- histamine-induced itch. These results establish as key elements an circuit.

Language: Английский

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