Hello! I have been treating a patient for approx 3-4 weeks now that was referred to me (PT) for chest and abdominal pain. He has had CTs, CXR, US, endoscopy, colonoscopy and a PFT all of which were negative. He has SOB intermittently, complain of tightness along the lower chest wall and has substantial hypersensitivity on the right side. No known MOI. I have been treating him with the theory that he has anterior cutaneous nerve entrapment and have been doing the following treatments: flat needling tender points along the abdominal wall, using IASTM along the lower intercostals, cupping along the lateral chest wall while he does some LTR/deep breath work, needling the lats and corresponding paravertebral points that follow his pain pattern, yoga-inspired movement patterns with breath work, diaphragm release and general education on diet and desensitization techniques. He is about 50% better which is great but what am I missing?
The lumbopelvic specialty needling course had some interesting content on this subject that had to do with anterior rib flared positioning. The cadaver photo in the lab manual was helpful for illustrating how the domed position of the diaphragm with the altered rib angle can lead to increased compression of the heart and the esophagus.
It was a great course, definitely worth checking out. The course was integrative and more than just needling. They recommended a breathing exercise using a roll of insulation you can buy at Lowes for a bolster under the patient's chest to help correct their rib position and an associated flattening of the thoracic spine curvature.
I went and bought one, and I've actually had several patients buy one too who've found it helpful.
Hey Tara,
I'm actually writing a case study that is "similar" looking at the neurology of visceral somatic referral here's a couple excerpts from the paper that may be relevant:
The QL is a deep muscle in the posterior abdominal wall that plays a key role in trunk stabilization and respiration. It attaches to the 12th rib and the transverse processes of L1-L4, with fascial connections that interface with the thoracolumbar fascia, diaphragm, and retroperitoneal structures (Bordoni 2018). In this case example the QL could have a possible role in generating the visceral symptoms of bloating, nausea, and abdominal cramps through a viscerosomatic convergence (Bath 2025).
Neurotrigger points can influence visceral function and not just sensation because somatic segmental input can drive a sympathetic response. The QL is innervated by T12-L3 spinal nerves, which coincide with sympathetic preganglionic neurons in the intermediolateral horn of the spinal cord. Neurotrigger points in the QL sends persistent nociceptive afferent input to these spinal segments sensitizing the second order neurons in the dorsal horn. It is important to understand the dorsal horn is not a passive structure, it is a processing and amplification center. Sustained input from the QL neurotrigger points can ramp up the excitability not just locally, but across associated interneurons at different spinal levels (Bath 2025). This cross-talk between interneurons recruits nearby sympathetic neurons increasing global sympathetic tone (Sikander 2012) resulting in:
All that to say I would look at the QL and the T12-L3 paravertebrals as well.
Frank
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