Regenerative Medicine
What Makes Dr. Mulvaney's Approach to Spine Pain Different?
A functional, whole-system approach to lasting spine stability — grounded in the evidence for what works, and an honest look at what doesn't.
Spine pain is life-stealing pain. It's socially limiting, it can keep you from being the version of yourself you know you are, and I'm sorry you're dealing with something this all-encompassing.
Patients often ask what makes my approach to spine pain different from what they've already tried. The short answer: I treat the spine as one connected, functional system, not as a single disc or joint that happened to fail on its own.
Why “Finding the Pain Generator” Falls Short
When a disc in the spine becomes painful, it's tempting to look for the one structure responsible, the “pain generator,” and treat only that spot. Many physicians do exactly this. But a disc doesn't fail in isolation. It fails because it was operating inside a system that had already become unstable. Spine research describes stability as the joint work of three subsystems: the passive system (discs, ligaments, and joint capsules), the active system (muscles and tendons), and the neural control system that coordinates them.1When any part of that system loosens, load shifts onto structures never designed to carry it, and that's usually where the pain shows up.
Repairing or stabilizing only the one disc or level that hurts, without addressing the instability around it, treats the symptom rather than the cause. To restore real function, I look at the entire functional unit involved. In the low back, that means the pelvis, sacrum, and lumbar spine together, with their ligamentous attachments to adjacent levels and the surrounding fascia. The same principle applies to the neck, where the relevant unit extends from the cervical spine to its attachments at the skull base and upper thoracic spine.
There's another reason chasing a single “pain generator” falls short: the way the spine is wired doesn't cooperate. A single spinal nerve level covers a broad, overlapping area, so pain that starts at one level can be felt one or two levels away, and sometimes even on the opposite side of the body. Classic research mapping these referral patterns, using controlled irritation of spinal ligaments and joints, documented exactly this kind of spread.2 That mismatch is also why imaging can be misleading. A well-known MRI study scanned the lumbar spines of people with no history of back pain at all and found that more than half of them already had a disc bulge.3Just because a scan shows something doesn't mean it's the cause of the pain, and just because a scan looks unremarkable doesn't mean nothing is wrong.
Where Standard Treatments Run Into Limits
Standard care for spine pain, including pain that radiates into an arm or leg (radiculopathy), typically includes physical therapy, epidural steroid injections, radiofrequency ablation, chiropractic care, and surgery. Each has real value, and each has limits worth naming honestly.
Physical therapy is a great place to start, and I recommend it to most patients. But some patients are in too much pain to fully engage with it, and others plateau without ever getting the underlying instability addressed.
Epidural steroid injections can help some patients, but the evidence for anything beyond short-term relief is thin. A 2025 review of the available research, commissioned by the American Academy of Neurology, found steroid injections offer only modest short-term pain relief and concluded there wasn't enough evidence to show any long-term benefit.4 Corticosteroids are potent anti-inflammatories, but true tissue healing actually requires inflammation, so suppressing it can quiet pain temporarily without helping the underlying tissue repair itself. And the treatment isn't free of cost: research has linked repeated epidural steroid use to reduced bone density and a higher risk of vertebral fracture, and there are documented cases of adrenal suppression, and even Cushing's syndrome, after only a handful of injections.5For a treatment whose own benefit is measured in weeks, that's a real cost to weigh.
Radiofrequency ablation (RFA) works differently. Instead of calming inflammation, it burns a small nerve, called the medial branch nerve, that carries pain signals from an arthritic facet joint. It can be quite effective at reducing that specific pain. But that same nerve does double duty: it also carries the signal that tells a small stabilizing muscle called the multifidus to fire. Burning the nerve to quiet the pain also silences the muscle, and research has documented multifidus weakness and shrinkage after RFA.6 In other words, treating the pain this way may further destabilize the very segment that was already struggling.
Chiropractic adjustment can provide real relief for many patients. But if a vertebra keeps drifting out of alignment because the ligaments holding it in place have become lax, repeated adjustments will keep correcting a problem that keeps recurring, because the underlying laxity was never addressed.
Surgeryhas an important place in spine care, and when it's the right call, it can be the best thing that happens to a patient. But it's also one of the biggest, least reversible decisions in medicine, and over 31 years I've sat across from many patients who wish they could turn back the clock on a surgery they once felt certain about. That's exactly why the decision deserves the full picture, not just the part that gets a patient scheduled.
Surgery is guided by what a scan shows at one point in time, and it typically focuses on stabilizing or decompressing the single level that appears to be the problem. In carefully selected cases, a large disc fragment causing progressive nerve damage, for example, that's exactly the right call, and I would never dismiss it out of hand. But for the much larger group of patients considering fusion for chronic pain from degenerative disc disease, the outcome data are sobering.
In the low back specifically, research pooling the available randomized trials found that fusion surgery is not superior to structured, non-operative care for pain relief or disability.7 A set of merged Norwegian trials comparing lumbar fusion to a program of cognitive intervention and supervised exercise found no meaningful difference in long-term disability between the two, and a substantial share of the fusion patients had already needed a second operation within a few years.8 The same underlying problem shows up in the neck: a long-term follow-up of patients after single-level cervical fusion found that a meaningful share went on to develop new, symptomatic disease at the level next to the fusion.9
Breakdown of the level next to a fusion is a common reason surgery ends up needing to be repeated. That's not just intuitive, it's been directly measured. Studies on cadaver spines have shown that fusing one or more vertebral levels forces the movement and load those levels used to share onto the segments still able to move, right above and below the fusion.10Concentrating a lifetime's worth of movement and force onto fewer moving segments accelerates wear on exactly those segments, the same instability problem this page opened with, now relocated one level over. Surgery is also irreversible in a way none of these other options are. It shouldn't be the first option offered, or the only option, to a patient who hasn't been told what else exists.
There's even a recognized medical term for patients who don't improve after spine surgery: failed back surgery syndrome, or FBSS. Studies estimate it affects roughly one in five patients after lumbar surgery.11 In my experience, a common reason is that the ligamentous laxity driving the original instability was never addressed, and in some cases, the surgery itself disrupts ligaments that were helping hold the spine stable. The encouraging part is that even after surgery, comprehensive treatment of the surrounding ligament system can often still help a patient who continues to have pain.
Where the Evidence Clearly Favors Surgery
None of this makes surgery the wrong choice. It makes it the right choice for a smaller, well-defined group of patients, and the evidence for that group is just as real and worth knowing.
Cauda equina syndrome (new symptoms in both legs, numbness in the saddle area, or loss of bladder or bowel control from severe nerve compression) is a genuine surgical emergency. Research has shown that getting into surgery quickly, within about two days of symptoms starting, leads to meaningfully better recovery of feeling, strength, and bladder or bowel control than waiting.12This is not a case for watchful waiting or a course of ligament work. It's an emergency room visit.
Progressive myelopathy (spinal cord compression, most often in the neck, rather than just nerve root irritation) behaves differently than pain alone. Large studies of surgical decompression for this condition show real, meaningful improvement in function and quality of life, even in more advanced cases.13 Once the spinal cord itself is being compressed and function is declining, decompression, not a trial of ligament healing, is the right strategy.
A large disc herniation with radiculopathy that hasn't improved after a genuine trial of conservative care is the group this page's surgery caution above is not talking about. Long-term studies following these patients for years found that carefully selected surgical patients did meaningfully better than those treated without surgery.14 Appropriately selected discectomy has real, durable evidence behind it.
Degenerative spondylolisthesis with spinal stenosis is its own case, worth separating from stenosis alone. In long-term studies, surgical patients kept a real, lasting advantage in pain and function over nonoperative care.15Interestingly, that same research found the surgical advantage for spinal stenosis without a slipped vertebra narrowed considerably over time, a reminder that “spine surgery” isn't one intervention with one answer. The specific diagnosis changes what's actually best.
The Tent Analogy

I often explain this to patients with a picture: imagine a large circus tent, with a 30-foot pole in the center and a ring of strong manila ropes staking it to the ground in every direction. As long as those guy-ropes stay taut, the tent shrugs off wind from any direction and stays stable.
Now picture the pole slowly shortening. That's what happens to our spines as we age: the discs lose water content and we lose height over time. As the pole shortens, the ropes that were once taut go slack. The next time the wind blows, the tent starts to wobble. That wobble is even more pronounced in people with connective tissue disorders: their increased ligament flexibility makes their “ropes” behave less like taut manila rope and more like elastic shock cord. Sometimes, even in a young person with an otherwise healthy spine, the ligaments can become loose from impact and trauma, such as from contact sports or a motor vehicle accident.
In the spine, those “ropes” are the ligaments holding the vertebrae in position. And just as skin that's rubbed the wrong way develops a callus, the small joints connecting one vertebral level to the next, the facet joints, can develop bony overgrowth, (arthritis), when they start moving abnormally against each other. That overgrowth, combined with discs losing height, is what starts to crowd the nerve roots exiting the spine, which is often where the pain, sometimes severe, comes from.
Re-Tensioning the Ropes, Not Just Treating the Pole
When I treat the spine comprehensively, I'm essentially walking around that tent and re-tensioning the ropes: restoring stability to the ligamentous system holding the spine together.
Because there are many structures to treat across a functional segment, doing this under X-ray or fluoroscopic guidance would mean a significant dose of ionizing radiation, not ideal for the tissue you're trying to heal. Instead, I do this entirely under ultrasound guidance. I've been an ultrasound-guided spine procedure specialist and instructor for over 20 years, and ultrasound lets me precisely target the dense web of ligaments stabilizing the lumbar, cervical, or thoracic spine without any radiation exposure.
With precise needle guidance, I inject Prolotherapy, platelet-rich plasma (PRP), or, in select cases, bone marrow- or adipose-derived cellular therapies directly into these ligaments, recruiting the body's own repair processes. This isn't a new idea: physicians have been treating joint and spinal pain by strengthening ligaments this way since the 1950s, when Dr. George Hackett and Dr. Gustav Hemwall first described and refined the technique.16 Ligaments aren't just mechanical tethers. They're densely populated with specialized nerve endings (mechanoreceptors) that sense stretch and tell the nervous system where the joint is in space, which is central to proprioception and to the reflexes that protect a joint from injury.17When a ligament's own repair response is stimulated this way, it heals back to the length and tension it needs to do that job again.
How Treatment Is Structured
When I treat a segment of the spine, I treat every level in that segment and most of the attachment points from one level to the next, on both sides, along with the fascial attachments that also contribute to spine stability. Treating the whole functional unit, not just the level that hurts, is what produces consistent, durable results.
These treatments are well tolerated and carry a very low risk profile. Most patients start with 2 to 3 monthly sessions of comprehensive 15% dextrose prolotherapy or PRP. I generally avoid injecting directly into the disc itself early in treatment: published case series put the risk of discitis (disc-space infection) from intradiscal injections at well under 1%, but it's a real risk that can mean a prolonged course of IV antibiotics or even surgery.18In most cases, restoring stability to the surrounding ligamentous system is enough to get the disc, and the patient, out of trouble without ever needing to inject it directly. A disc typically became a problem because of instability elsewhere in the system, and it's very difficult to get it to heal until that underlying instability is addressed. Often, stabilizing the system is all it takes to get a patient out of pain and back to full activity.
Selected References
- Panjabi MM. The stabilizing system of the spine, part I: function, dysfunction, adaptation, and enhancement. J Spinal Disord. 1992;5(4):383–389.
- Kellgren JH. On the distribution of pain arising from deep somatic structures with charts of segmental pain areas. Clin Sci. 1939;4:35–46. See also Mooney V, Robertson JT. The facet syndrome. Clin Orthop Relat Res. 1976;(115):149–156.
- Jensen MC, Brant-Zawadzki MN, Obuchowski N, Modic MT, Malkasian D, Ross JS. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med. 1994;331(2):69–73.
- Armon C, et al. Epidural Steroids for Cervical and Lumbar Radicular Pain and Spinal Stenosis: Systematic Review Summary of the AAN Guidelines Subcommittee. Neurology. 2025;104(5).
- Kerezoudis P, Rinaldo L, Alvi MA, et al. The effect of epidural steroid injections on bone mineral density and vertebral fracture risk: a systematic review and critical appraisal of current literature. Pain Med. 2018. See also Leary J, Swislocki A. Hypothalamic-pituitary-adrenal suppression and iatrogenic Cushing's syndrome as a complication of epidural steroid injections. Case Rep Endocrinol. 2013;2013:617042.
- Francio VT, Glicksman M, Leavitt L, Gill B, Shah A, Westerhaus BD, Lam CM, D'Souza RS. Multifidus atrophy and/or dysfunction following lumbar radiofrequency ablation: a systematic review. PM R. 2024.
- Wang X, Wanyan P, Tian JH, Hu L. Meta-analysis of randomized trials comparing fusion surgery to non-surgical treatment for discogenic chronic low back pain. J Back Musculoskelet Rehabil. 2015;28(4):621–627.
- Brox JI, Nygaard ØP, Holm I, Keller A, Ingebrigtsen T, Reikerås O. Four-year follow-up of surgical versus non-surgical therapy for chronic low back pain. Ann Rheum Dis. 2010;69(9):1643–1648.
- Hilibrand AS, Carlson GD, Palumbo MA, Jones PK, Bohlman HH. Radiculopathy and myelopathy at segments adjacent to the site of a previous anterior cervical arthrodesis. J Bone Joint Surg Am. 1999;81(4):519–528.
- Eck JC, Humphreys SC, Lim TH, Jeong ST, Kim JG, Hodges SD, An HS. Biomechanical study on the effect of cervical spine fusion on adjacent-level intradiscal pressure and segmental motion. Spine. 2002;27(22):2431–2434.
- Inoue S, Kamiya M, Nishihara M, Arai YC, Ikemoto T, Ushida T. Prevalence, characteristics, and burden of failed back surgery syndrome: the influence of various residual symptoms on patient satisfaction and quality of life as assessed by a nationwide Internet survey in Japan. J Pain Res. 2017;10:811–823.
- Ahn UM, Ahn NU, Buchowski JM, Garrett ES, Sieber AN, Kostuik JP. Cauda equina syndrome secondary to lumbar disc herniation: a meta-analysis of surgical outcomes. Spine. 2000;25(12):1515–1522.
- Fehlings MG, Wilson JR, Kopjar B, et al. Efficacy and safety of surgical decompression in patients with cervical spondylotic myelopathy: results of the AOSpine North America prospective multi-center study. J Bone Joint Surg Am. 2013;95(18):1651–1658.
- Lurie JD, Tosteson TD, Tosteson A, et al. Surgical versus nonoperative treatment for lumbar disc herniation: eight-year results for the Spine Patient Outcomes Research Trial. Spine. 2014;39(1):3–16.
- Weinstein JN, Lurie JD, Tosteson TD, et al. Surgical versus nonsurgical treatment for lumbar degenerative spondylolisthesis. N Engl J Med. 2007;356(22):2257–2270.
- Hackett GS, Hemwall GA, Montgomery GA. Ligament and Tendon Relaxation Treated by Prolotherapy. 5th ed. Oak Park, IL: Gustav A. Hemwall; 1993 (technique originally described by Hackett, 1958).
- Histologic studies (e.g., Yahia et al.; Indahl et al.) have identified Golgi, Pacinian, and Ruffini-type mechanoreceptors in spinal and sacroiliac ligaments, supporting their role in proprioception and reflexive stabilization of the spine.
- Jerome MA, Lutz C, Lutz GE. Risks of Intradiscal Orthobiologic Injections: A Review of the Literature and Case Series Presentation. Int J Spine Surg. 2021;15(s1):26–39.
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