Hello and welcome to the sixth copy of the newsletter! In my TherapyLive talk I pitched that when we treat radicular pain we should think in terms of nerve health and sensitivity rather than nerve compression (although the former includes the latter!). To illustrate what I mean by "nerve health" I showed pictures from a study by Albrecht et al. in which the authors image neuroinflammation in people with chronic radicular pain. The first picture is cool but not unexpected: the green arrow points to a small patch of yellow in the intervertebral foramen which represents neuroinflammation (or, more accurately, a marker of neuroinflammation).  We have known for some decades that lumbar disc herniations are pro-inflammatory to the surrounding tissues and that this probably drives a lot of acute "radiculitis". In fact, Albrecht was a bit surprised that the signs of neuroinflammation in the foramen were not stronger and more consistent. Maybe it's because the participants in his study had chronic, not acute pain.  The second image is less intuitive: run your eyes down the aggregated images of the spinal columns of the control patients and the patients with radicular pain and you will see that there is more of a yellow hue to the spinal cords of patients with pain.  Although these patients have (or have had) an insult to the nerve roots in their lower lumbar spine, they also have neuroinflammation in their spinal cords, in the lower thoracic and upper lumbar spine. The neuroinflammation has "spread". In cross section, it is more clear.  Whenever I show this image a few people will message me afterwards saying how striking it is. So there is something important here that I want to "zoom in on". And my main stumbling block is, what on earth is neuroinflammation? This week’s podcast This week's podcast is an interview with the lead author of the study, Daniel Albrecht (pron. Albright). Dan speaks really well on this subject. In the podcast, he describes the basics of neuroinflammation and the findings of this study. He also takes on the trickier questions that surround this topic and makes it clear what we know and what we don't know. It’s on all major platforms if you search for “The Sciatica Podcast”, or you can click through from this email. Do listen! Okay, what on earth is neuroinflammation? Neuroinflammation is not necessarily pathological The first thing to say about neuroinflammation is that it is not in itself pathological. Just like inflammation in the muscles, joints and skin, inflammation in the nerves arises in response to dangerous stuff like pathogens or tissue damage. Many different cells and molecules work together to limit the danger and repair any harm done. Neuroinflammation only becomes a clinical problem when there is too much of it, or it goes on too long. Neuroinflammation is a continuum The second thing to say is that it is not really something that is turned "on" or "off". We use words like "activated" to describe microglia, which makes this confusing. But really it's a "more" or "less" process, not "on" or "off". At one end of the continuum, transient, low level immune signalling is involved in the normal development of memory and learning and arguably doesn’t qualify as “neuroinflammation” at all. At the other end "very rapid and dramatic" neuroinflammation kicks in after serious nerve injuries. What’s involved? Now let's introduce the "characters" of neuroinflammation to tell the story in stages. To me, one of the most challenging aspects of understanding neuroinflammation (to the extent that I have) was wading through the many and various cells and molecules which all seem to do subtle variations of the same thing. For clarity's sake, I have cut out a lot of these (sorry, fans of TLR-4) so that I can tell a coherent "story" within the scope of an email newsletter... Glia