The Briefing Issue 14

My bias first. I needle deep when the anatomy allows it and I teach people to needle deep, because the twitch and the segmental structures are deep. This trial does not change that, but it changes the reason.

Forty-four patients with non-specific neck pain and active upper trapezius trigger points were randomised to deep dry needling at 50 mm or superficial needling at 13 mm, four sessions over two weeks, in a triple-blind design. Both groups improved on pain (about 3 cm on the VAS) and on the Neck Disability Index (4.5 to 6.5 points), with no between-group difference at two or six weeks. On ultrasound, upper trapezius stiffness, thickness and blood flow did not differ between groups, and barely moved within them. It was not an equivalence trial, so it does not prove the depths are the same; it shows that in this sample 13 mm matched 50 mm and neither changed the muscle in a way the ultrasound could see.

I can't say for sure, but to me this seems to support the RMO. The result likely came through the nervous system rather than from the tissue the needle was in, which is the difference between treating the root and treating the symptom. The nerve root is the driver, the trapezius downstream is the symptom. The consensus paper says to choose the target tissue from the exam, and when the neurological exam is positive, to needle the segmental structures first, the multifidus at the corresponding level. Choose the depth in the upper trapezius for the anatomy under it. Take the result from the segment.

The anatomy under the upper trapezius is first the ribs, then comes the lung field. A 26-year-old woman coughed during acupuncture in the trapezius region, then presented two days later with cough, pleuritic chest pain and trouble taking a full breath. Her oxygen saturation was 100 percent. Her heart rate was 140. Chest X-ray showed a pneumothorax on both sides, 21 mm on the right and 17 mm on the left, and CT confirmed them. She was managed conservatively in hospital and both resolved. The lesson the authors draw is the one I want you to keep: after needling the neck, shoulder or upper back, chest pain, cough, breathlessness or an unexplained fast heart rate is a pneumothorax until someone has imaged it, and normal oxygen does not rule it out. The cough during the needling was the first sign. In Issue 10 we mapped the neurovascular corridor under the upper trapezius. The lung apex sits under the same muscle, above the medial clavicle. The report does not describe the technique, the needle, the depth or the angle, so there is no technique to critique; both apices were punctured, which tells you both upper trapezius regions were needled toward the pleura. The lesson is the anatomy under the needle and the signs afterward.

One more case, from the other end of the safety list. A 62-year-old farmer with two months of low back pain and pain in both legs had an infection destroying the L3 and L4 vertebral bodies and the disc between them. The organism was a skin commensal, Corynebacterium simulans, identified only by genetic sequencing of a vertebral biopsy. The authors list his predisposing factors: repeated unregulated needle-pricking bloodletting therapy (a traditional practice of puncturing the skin to let blood), blood sugar no one had checked, and a family history of psoriasis. The link to the needling is their attribution and a single case. It is still the reason the gloves are for you and the skin preparation and the sterile needle are for the patient, as I wrote in Issue 07, and the reason a question about blood sugar belongs in the history before a course of needling.

The RMO says the root is the driver and the muscle downstream is the symptom. Two papers this week put a number on each half of that sentence.

First the root. Five hundred and three adults presented to orthopaedic clinics with scapular pain over ten years, and 284 of them had at least one MRI. The most common findings were supraspinatus tendinopathy in 88 percent, C5-6 foraminal stenosis in 66 percent and C5-6 degenerative change in 65 percent. The authors list cervical radiculopathy first among the pain generators for the scapula, and they warn, correctly, that incidental findings rise with age and the scan alone cannot say which finding is the pain. This is imaging prevalence, exploratory, no clinical exam reported. It is also the picture the RMO predicts. In Issue 09 I argued the shoulder belongs to the neck. Here the periscapular pain, the C5-6 root and the C5-6 muscle, the supraspinatus, sit in the same patients at the same time. The root is the driver and the supraspinatus is the downstream muscle. The scapula is only where the patient points and can be a biomechanical or functional result. We make assumptions based on a biomechanical, joint-based approach versus objectively evaluating the downstream effect of poor innervation to the joint, muscles and other connective tissues.

Now the muscle, from the other direction. Paul Hodges' group in Brisbane (he has spent thirty years on the multifidus) followed 50 people with mechanical chronic low back pain who had an implanted stimulator placed on the medial branch of the L2 dorsal ramus, the nerve that supplies the multifidus. Before the implant and six months after, they imaged the multifidus from L1 to S1 with ultrasound and measured how much of the muscle was connective tissue rather than contractile tissue. At L3, and only at L3, the connective tissue proportion fell by 6 percent, surviving adjustment for muscle size. L3 is where the largest bulk of multifidus supplied by L2 sits. No control group, exploratory, industry-funded, and the structural change did not track the pain change. I would still call it one of the clearest human pictures I have seen of the direction the RMO rests on: drive the nerve and the muscle at that nerve's segment changes its composition, and the other levels did not.

A third paper raises a question. Two hundred and fifty shoulders with no visible supraspinatus tear and no definite tendinopathy: 37 percent had fat in the supraspinatus anyway, and fat was five times more likely when the acromioclavicular joint was degenerate. The authors attribute it to the joint. In the RMO a muscle degenerating under an intact tendon leads you to examine its nerve supply before you accept the joint next to it. The supraspinatus is C5-6 through the suprascapular nerve, so I would still examine C5-6 first.

Central before peripheral also means the cord and the brain, and two papers this week are about the exam that clears them. Three patients were referred to a pain clinic specifically for fibromyalgia and were found, on examination and imaging, to have severe cervical myelopathy. The authors' rule is one I want you to adopt: fibromyalgia does not produce progressive neurological deficit or upper motor neuron signs, so a positive Hoffmann's, hyperreflexia, clumsy hands or a changed gait in a "fibromyalgia" patient is cervical myelopathy until proven otherwise. And a 41-year-old woman, postpartum, with mechanical low back pain and painless weakness of the left leg that had caused three falls. The history said non-radicular, no sensory loss. The exam localised to the upper motor neuron. Brain MRI showed a meningioma pressing on the frontal lobes; resection resolved the weakness. Painless weakness with no dermatome and no sensory change does not come from a nerve root. The RMO starts central, and central includes above the neck.

How it presents: first-step pain under the heel in the morning, tender at the medial calcaneal tubercle, a referral that says plantar fasciitis, and a plan of stretching, rolling, an orthotic and maybe an injection. Plantar fasciitis is a diagnosis made on tenderness. The label describes where it hurts and not why, and the plantar fascia and the heel fat pad look abnormal on ultrasound in plenty of athletes who have no heel pain at all. In the RMO the heel is S1 territory and the plantar skin is tibial nerve. Examine the segment before you needle the fascia.

Here is the number. A podiatrist reviewed 459 of his own plantar fasciitis patients, and 49 percent had clinical neurological findings. Of the 99 who did not respond to conservative care, 73 had electrodiagnostic testing and 68 were positive; 88 percent of those had a radiculopathy, two thirds with tarsal tunnel syndrome alongside it. Heel pain still resolved with conservative care in 75 percent of the patients with neurological symptoms, against 87 percent of those without. One author, one practice, retrospective, and his conclusion is surgical. The prevalence stands on its own: in this clinic half of the plantar fasciitis patients had a neurological finding, and most of the ones who did not respond had a radiculopathy.

That is the RMO applied to the heel. The root is the driver and the plantar heel is the symptom. The tarsal tunnel is a second site where an already-irritated tibial nerve can be compressed, the double-crush idea, and that read is mine, not the author's. In Issue 13 the compressed S1 root made a calf grow. Here it makes a heel hurt, and no one looks above the ankle because the tenderness is under the foot.

The calf belongs in the same exam. Twenty athletes treated for Achilles or patellar tendinopathy were imaged with MR elastography, an MRI sequence that measures tissue stiffness, before and at least six months after treatment. At baseline the symptomatic leg had softer muscle next to the tendon. After treatment, the Achilles patients' gastrocnemius and deep soleus stiffened on the treated side, and the deep soleus on the untreated side got softer. Twenty people, no control group, and a clear picture: the muscle attached to the tendon changes when the tendon is rehabilitated, and the untreated side loses stiffness if you do not load it as well. A soleus cohort says the same thing across a season: 41 Australian footballers gained plantar flexion strength from preseason to late season, and a recent calf injury still showed as weakness months later. Re-test the calf you did not treat.

Two anatomy notes for anyone needling the deep calf. In 726 CT angiograms, the fibular artery sent a communicating branch across to the posterior tibial artery in 39 percent, and in 3.9 percent the fibular artery was the main blood supply to the foot because the posterior tibial artery was small or absent. That plane, between the two arteries, is where tibialis posterior, flexor hallucis longus and the deep soleus sit. And exertional calf pain in a young athlete with no vascular history can be popliteal artery entrapment, the medial head of the gastrocnemius compressing the artery, bilateral in up to two thirds. A calf that hurts with running and has a weak pulse after exercise should result in a vascular referral, not a trigger point.