- Testosterone is effective therapy for fibromyalgia.
- Low/deficient testosterone levels are linked to a high risk for chronic pain states.
- Novel mechanisms by which testosterone is likely to down-modulate pain signals
- Mechanisms involving testosterone are linked to central sensitization.
Filling-In, Spatial Summation, and Radiation of Pain: Evidence for a Neural Population Code in the Nociceptive System – Free full-text PMC2804406 – J Neurophysiol. 2009 Dec
The receptive field organization of nociceptive neurons suggests that noxious information may be encoded by population-based mechanisms.
Electrophysiological evidence of population coding mechanisms has remained limited.
However, psychophysical studies examining interactions between multiple noxious stimuli can provide indirect evidence that neuron population recruitment can contribute to both spatial and intensity-related percepts of pain. Continue reading
Nav1.7 is a voltage-gated sodium channel isoform encoded by the SCN9A gene.
The Nav1.7 channel is normally expressed in the dorsal root ganglion neurons, trigeminal neurons, and their small-diameter peripheral axons
Mutations in these isoforms have been associated with several pain disorders, including erythromelalgia, paroxysmal extreme pain disorder (PEPD), congenital insensitivity to pain (CIP), and painful peripheral neuropathy. Continue reading
Functional Reorganization of the Default Mode Network across Chronic Pain Conditions – PLoS One. – Sep 2014
Here we use resting-state functional magnetic resonance imaging to investigate functional changes in patients suffering from chronic back pain (CBP), complex regional pain syndrome (CRPS) and knee osteoarthritis (OA).
We isolated five meaningful resting-state networks across the groups, of which only the default mode network (DMN) exhibited deviations from healthy controls.
All patient groups showed
- decreased connectivity of medial prefrontal cortex (MPFC) to the posterior constituents of the DMN, and
- increased connectivity to the insular cortex in proportion to the intensity of pain. Continue reading
Pain and inflammation are related: systemic inflammation may lead to a variety of pain states, and, in turn, persistent pain causes an upward adjustment of proinflammatory mediators that sometimes elicit a prolonged low-grade immune response, leading to long-lasting, subclinical inflammation.
The cytokines that are produced during inflammatory responses are the main stimulators of the production of acute-phase proteins, specifically C-reactive protein (CRP).
C-reactive protein is a nonspecific systemic marker of infection, inflammation, tissue damage, malignancy, and autoimmune disease.
Currently available pain medications have limited efficacy and numerous side effects. New research, however, provides deeper insights into how our bodies process pain, paving the way for an innovative, more effective way of targeting chronic pain.
According to recent estimates from the National Institutes of Health (NIH), as many as 25 million people in the United States live with daily pain, and 23 million of the country’s adults have more severe pain.
Previous efforts to develop more effective analgesics have been stalled by our limited understanding of the mechanisms that allow nerves to sense and transmit pain signals,” Dr. Bunnett says. Continue reading
A New Opioid Targets Active Sites of Inflammation to Relieve Pain – by Nathan T. Fried on 23 Mar 2017
Summary: NFEPP binds and activates mu-opioid receptors only at low pH, soothing pain in rats without typical side effects
Adverse effects of opioids can occur because the drugs act at both injured and healthy tissue, but if researchers could find a way to direct opioids only to the former and not the latter, perhaps the drugs would lack off-target activity.
Now, a new report reveals the design of a novel opioid that only works where inflammation exists, leaving healthy tissue untouched and avoiding the unwanted consequences seen with traditional drugs. Continue reading
Stanford scientists have identified a small group of neurons that communicates goings-on in the brain’s respiratory control center to the structure responsible for generating arousal throughout the brain.
Try it. Breathe slowly and smoothly. A pervasive sense of calm descends. Now breathe rapidly and frenetically. Tension mounts. Why?
It’s a question that has never been answered by science, until now.
In a new study, researchers at the Stanford University School of Medicine and their colleagues have identified a handful of nerve cells in the brainstem that connect breathing to states of mind. Continue reading
The “Missing Link” in the Physiology of Pain: Glial Cells – Practical Pain Management – May 2016
glial cells and their interactions have become recognized as having a critically important role in the generation and maintenance of acute and chronic pain… and may now be a “missing link” in our understanding of the conversion of acute to chronic pain and the development of chronic neuropathic pain
This conversion process has been called “chronification,” and includes
- central sensitization,
- neuroplastic changes,
- altered pain modulation, and
- changes to the “neuromatrix” of the central nervous system.
Neurohormones in Pain and Headache Management: New and Emerging Concepts – practicalpainmanagement.com – Feb 2017
The recent discovery and awareness that the central nervous system (CNS) makes specific hormones for intrinsic use in addition to those for peripheral use is a profound finding that is critical to clinical pain and headache management.
Some neurohormones provide the physiologic effects of neuroprotection and neurogenesis that are essential for pain reduction, prevention, and treatment.
Following is an attempt to provide an early status report on what we do (and don’t) know about the function of neurohormones relative to pain management. Continue reading