Reasoning radiculopathy a guest post by Tom Jesson

Tom Jesson @thomas_jesson published his thoughts and reflections on radiculopathy on Twitter recently.  Reading through the feed I really enjoyed the questions he wanted to answer. I found it so helpful that I reached out to Tom and asked for his permission to convert the feed into a blogpost so that others could benefit from his thoughts and read it in a structured format. Tom was very receptive and accepted the offer. So without further ado i’ll pass you over to Tom.

Doing a bit of reading on cervical radicular pain. Let’s answer three questions: (1) When is neck/arm pain a radiculopathy? (2) What is a radiculopathy? (3) How should I explain this to patients? Feel free to add/correct

Q (1) When is neck-arm pain a radiculopathy? Bogduk (2009) is the classic paper here. (Yes there is a big element of false clarity in his definitions) (ncbi.nlm.nih.gov/pubmed/19762151)

(Schmid says that the definition Bogduk gives here for radiculopathy only includes large fiber signs – small fiber signs like loss of hot, cold, pinprick sensation, are often forgotten)

Somatic referred pain, and radicular pain, from Bogduk (experimentally induced!)

So, if we are being careful with our language we shouldn’t be calling radiculopathy referred pain and we certainly shouldn’t be calling all back/leg and neck/arm pain a radiculopathy. To diagnose a radiculopathy we should have frank neurological signs, and as Tawa et al say (), ideally more than one, as their specificity, as ever, is imperfect. (ncbi.nlm.nih.gov/pmc/articles/P…) As an aside, is radiculopathy technically “neuropathic pain”? Not all ‘nerve pain’ is neuropathic (i.e. caused by lesion or disease). According to the IASP, a radiculopathy with sensory signs (loss) is “probably neuropathic pain”. Radicular pain alone, not.

Question (2), what is a radiculopathy? It’s a kind of peripheral nerve pain, so let’s work out what that is first. Woolf () teases out the mechanisms like so. (ncbi.nlm.nih.gov/pubmed/15041442)

That paper is 14 years old now. In her more recent paper, Schmid notes that much of Woolf’s evidence came from severe injuries in animal models, which may not translate so well to the more mild insults we see in clinical practice. () (ncbi.nlm.nih.gov/pubmed/24008054)

I don’t have a copy of her chapter in Grieve’s but from when I was at uni I have my notes. She shows how increased extraneural pressures lead to ischaemia in the nerve, which in turn lead to demyelination, neurogenic inflammation, immune activation and inflammation.

Here is a nice pic of how why demyelination is bad: it creates “abnormal impulse generating sites” that fire off ectopic APs (VSSC = voltage sensitive sodium channel)

For its part, inflammation lowers the firing threshold of neurons, activates silent nociceptors, sensitizes nervi nervorum, the dorsal root ganglia… bad news. This gets at why most PNP doesn’t follow the expected anatomical pattern. In the dorsal root ganglion and in the spinal cord, nerves are packed in and intertwined, meaning inflammation here can affect more than one nerve.

So if we think of radiculopathy as an ongoing process, potentially involving multi-site inflammation and nerve damage, as well as central sensitization

…we can see that management should be about attenuating this process rather than “untrapping” the nerve… and that we need to monitor closely and properly. Amitriptyline, pregabalin etc do not “mask the problem” here, they help to stop all those ectopic action potentials that can drive central sensitization. They break the loop. Here are the NICE guidelines on those.

(I forgot to put this in before. Another useful way to think about this is the distinction between gain and loss of function:)

Question (3) – how can we explain this to patients? First of all, for people with a new-onset radiculopathy, the outcome is good, although patience is required. (note this is data from patients with herniation) () (ncbi.nlm.nih.gov/pubmed/24614255)

I guess it’s also important to show that your clinical exam was thorough and sufficient, and explain your reasoning for not referring for an MRI (if you aren’t). It seems like most patients consider an MRI to be necessary. () (ncbi.nlm.nih.gov/pubmed/29063271)

When we explain the problem we want to try to dethreaten it, too (although without trivialising, and without flat out lying…). Dethreatening isn’t just about being nice, it demonstrably leads to better outcomes. No script, but here’s some ideas from Explain Pain Supercharged

The end.

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