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Cloward sign and referred pain by deep tissue stimulation of the cervical spine 💡

👉 In 1959, Ralph Bingham Cloward (1908–2000), published referral patterns of the cervical spine discs using cervical discography (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1629000/, s. Figure 1 a)

👉 He found that stimulating the anterolateral aspect of the cervical discs produced pain at the ipsilateral scapula. Stimulation in the midline of the anterior aspect of the disc produced pain between the shoulders in the middle of the back. Cloward described that pain from the C6-7 disc was felt in the inferior angle of the scapula. Pain from the C5-6 disc was felt in the center of the medial scapular border. Pain from C4-5 disc was experienced in the region of the spine and superior angle. Pain from the C3-4 disc was referred to the C7 spinous process and the posterior border of the trapezius muscle.

👉 Cloward also documented that when stimulating patients with posterolateral disc protrusions, the referral patterns were found to be more intense than when stimulating the anterior aspect of the disc and were found to spread from the vertebral border of the scapula out to the shoulder and upper arm as far as the elbow. idline posterior disc protrusions were found to refer pain to a confined area overlying the fifth cervical to the second thoracic spinous processes near the midline, with upper discs more cephalad and lower discs more caudad.

📷 Figure (https://link.springer.com/chapter/10.1007/978-3-319-31169-2_26): Cutaneous radiation of pain during irritation of individual structures. (a) Radiation of pain during irritation of intervertebral discs (Modified after Cloward, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1629000/); (b) radiation of pain during irritation of deep musculoligamentous structures in interspinous space (Modified after Feinstein, https://pubmed.ncbi.nlm.nih.gov/13211692/).

An important note on this Sunday!❤️❤️

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A new UK study has shown that chronic pain patients are inflamed, as measured by high C-reactive protein, the best known biomarker for systemic inflammation. That is not much of a news flash — chronic pain and inflammation? Who would have guessed?! 🤯

THIS is the cool part, and the reason I picked this one to write about today: the study showed that chronic pain patients aren’t just inflamed… they are inflamed even WITHOUT any of the traditional psychosocial bogeymen.

And that IS a kind of a surprise.

https://www.jpain.org/article/S1526-5900(23)00537-0/fulltext

Farrell et al. went mining for data about hundreds of thousands of patients, identifying a strong link between pain and CRP compared to people without pain… and that link remained robust even when a great variety of other common correlates with pain were factored out: income, demographics, mental health, and so on. The authors reckon this means there is “a possible independent biological mechanism” for pain.

This is the opposite of what many experts would predict.

Supposedly people get more inflamed precisely BECAUSE of those influences: that is, we get unfit and unhealthy because of things like eating junk food, sitting all day, or getting really stressed trying to raise a kid alone. But this study shows that chronic pain patients are inflamed even without such things.

This flies in the face of the fashionable attempt to explain pain with a lot of psychosocial considerations — which likely do matter, but these results strongly suggest there’s more to the story, namely the “bio” in “biopsychosocial.”

Relatively subtle PATHOLOGY is probably the broad explanation for the inflammation in chronic pain patients.

I do NOT think this is a surprise to the millions of people who felt like they had good, healthy lives … right up until the pain started.

~ Paul Ingraham, PainScience.com publisher

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