Round-table Meeting 5 April 2017

Dear CNAP member,

Following of our successful round table discussion in February with debates on pain neuromatrix, we are delighted to invite you to the next meeting of the classical pain concepts, which will take place on April 5th 2017 at 12:15 - 15:00.

The goal of the round-table discussions is to gather interested individuals and consolidate central knowledge, theory, phenomena and explore key emerging developments within pain principles. To achieve this goal, classical pain concepts will be discussed four times annually. Followed by each round-table discussion there will be a social gathering. This time it will be flavored by delicious pizza bites!

In this round-table, the concept of “Central Sensitization” will be of focus. Clifford Woolf has been known as the “father of central sensitization”, who firstly described this phenomenon during his work with Patrick Wall as changes in the functional properties of spinal nociceptors in rat dorsal horn induced by peripheral input. IASP has put forward a definition of “Central Sensitization” as all forms pain sensitization that arise within the central nervous system. Recently, Per Hansson has commented on the “Central Sensitization” term, which has been used loosely and often to name a reason for clinical phenomena that have not been demonstrably linked to so-called “Central Sensitization”. His overall proposal has reached to the point that the term might not be a suitable term within clinical context but valid for use in preclinical context, where neural activity can be controlled and measured. The significance of the classical notion of “Central sensitization” is to advance our understanding of the nature of pain and also therapies that target this phenomenon. Woolf’s priority seems to reserve the clinical utility of the term as a useful descriptor, which hints at possible causative mechanisms, but does not require recordings of neuronal activity.

Program

12.15
Pizza slices will be served

12.25
Welcome/short introduction to the CNAP round-table discussion by Thomas

12.35
Presentation of the paper Evidence for a central component of post-injury pain hypersensitivity by Brian

12.55
Pitch of all incoming papers (1 min for each paper/participant)
Why choosing this particular paper?

13.15
Presentation of selected papers:

• Central sensitization and neuropathic features of ongoing pain in a rat model of advanced osteoarthritis by Rocco
• Characterizing pinprick-evoked brain potentials before and after experimentally induced secondary hyperalgesia by Juan

Short break (10 min.)

Continuing presentation of selected papers:

• Gliogenic LTP spreads widely in nociceptive pathways by Morten and Rosa
• Tactile, thermal, and electrical thresholds in patients with and without phantom limb pain after traumatic lower limb amputation by Mikkel

14.30
Debate (directed)
All participants prepare a selection of arguments in favour and against (pro/cons) the Central Sensitization concepts.

15.00
Thank you for today!

INCOMING PAPERS

1. Motor Cortex Excitability and BDNF Levels in Chronic Musculoskeletal Pain According to Structural Pathology
2. Characterizing pinprick-evoked brain potentials before and after experimentally induced secondary hyperalge (selected for presentation)
3. Mechanisms of Disease: neuropathic pain—a clinical perspective
4. Cell transplants to treat the “disease” of neuropathic pain and itch
5. Extensive reorganization of primary somatosensory cortex in chronic back pain patients
6. Persistent changes in peripheral and spinal nociceptive processing after early tissue injury
7. Gliogenic LTP spreads widely in nociceptive pathways (selected for presentation)
8. Dendritic Spine Remodeling After Spinal Cord Injury Alters Neuronal Signal Processing
9. The role of N-methyl-D-aspartate (NMDA) receptors in wind-up: a mathematical model
10. Gliogenic LTP spreads widely in nociceptive pathways (selected for presentation)
11. Central sensitization and neuropathic features of ongoing pain in a rat model of advanced osteoarthritis (selected for presentation)
12. Small Molecule Inhibitors of PSD95-nNOS Protein–Protein 3 Interactions Suppress Formalin-Evoked Fos Protein 4 Expression and Nociceptive Behavior In Rats
13. Translating nociceptive processing into human pain models
14. Tactile, thermal, and electrical thresholds in patients with and without phantom limb pain after traumatic lower limb amputation(selectred (slected for presentation)
15. Calcitonin Gene-Related Peptide Promotes Cellular Changes in Trigeminal Neurons and Glia Implicated in Peripheral and Central Sensitization