The WHAT and the WHY
Clinical examination and differential diagnosis can be tough! Like many clinicians, I spent the early part of my career treating the WHAT. The WHAT is the symptom — the presentation but not necessarily the “cause”. It seemed obvious to me at the time, and honestly, I felt justified because many of the patients I was treating were achieving successful outcomes.
However, over time I began to realize that I was missing something in my patient care. I was consistently met with challenging cases that brought me to the realization that my responsibility as a PT was to find out the WHY, not just the WHAT. It was easy to identify what symptom/impairments had brought my patients in, but the real question was, “Why had this occurred, and why had it perpetuated?”
KinetaCore has really helped me expand my thought process over the past few years. They have adopted a more comprehensive and multi-faceted model that emphasizes the neuromuscular system and how it impacts the body. This model, Functional Dry Needling® (FDN), puts more emphasis on investigating the musculoskeletal system AND the way it ultimately interacts with the neurologic system. It highlights the commonly underestimated role the nervous system has, not only on the perception and experience of pain, but also on the compensatory and/or dysfunctional movement patterns that develop over time. In many cases, the dysfunctional movement is what precedes the tissue damage and onset of pain.
I had a patient care interaction that really highlighted this concept. I evaluated a patient who, by all accounts, appeared to have predominantly mechanical discogenic Low Back Pain (LBP). The patient presented with bandform LBP, 50-75% ROM ability with standing trunk flexion/extension/rotation, and all movements occurred with moderate pain and aberrant motion. The patient had moderate pain with lumbar spring testing, and minimal to moderate pain with palpation of the lumbar paraspinals and glutes. I initially wanted to treat the patient using FDN, primarily to knock down some of the resting spasm and potentially give me some space to address the discogenic condition more directly. I treated the multifidi for about ten minutes at the corresponding vertebral
segments with neuromuscular stimulation.
The patient’s overall presentation was significantly improved: 90% trunk flexion with minimal pain and no aberrant motion, 100% full standing trunk extension and rotation ROM with minimal to no pain, minimal to no pain with lumbar spring, and minimal to no pain with palpation of the lumbar paraspinals and glutes. Strange enough, much of the clinical signs I thought were discogenic were gone! I quickly realized that I was not taking into consideration the significance of somatic referred pain from the muscle, its neurologic connection to the surrounding tissues, and how they affect each other.
The easy answer is to walk away from there. “Fix it, then dismiss it”. But I needed to look further. I wanted to identify the reason this happened. I think I was missing that piece for a long time — missing the connection between neurologic and muscular structures — treating the WHAT instead of the WHY.
The Real Question: How did it all Start?
- Was it an actual strain of the lumbar paraspinals/multifidi?
- Was it a dysfunctional compensatory movement pattern that led to the multifidi and paraspinals becoming irritated (postural deviation/scoliosis, instability, leg length discrepancy/pelvic mal-alignment, etc.)?
- Was it a disc injury? Did the chemical irritation from the disc lead to the nerve becoming irritated and the multifidi protective guarding/spasm, which eventually led to pain?
The disc is innervated by the sinuvertebral nerve, a branch that originates from the spinal nerve. It just so happens that this nerve lies in very close proximity to the dorsal rami, which is where the medial branch arises. This group innervates the multifidi as well as the facet joint. The multifidi have a pain referral pattern that overlaps with and is similar to the referral pattern of varying types of disc pain (IDD, Annular Tear, DDD, Chemical Soup/sensitized disc).
Ok, So What About the Case?
Although this patient likely had disc irritation, the majority of the pain being experienced by the patient at this time was not from the disc itself but rather from the surrounding neuromuscular tissues. Treatment of the multifidi not only diminished the patient’s pain during reassessment of movements, palpation and spring of the lumbar segments, but they also immediately demonstrated an improved movement pattern/motor control with all trunk movements. It is completely justified to lean on treatment to rectify and confirm your examination diagnosis. Specific tissues have a unique pain presentation and function; therefore, when you treat that dysfunctional tissue in a specific way, you should be looking for a specific result. In this example, if the multifidi and other paravertebral muscles were irritated (more than I realized from the history and exam), they generated a pain pattern, (which mirrored disc pain), and were also contributing to poor motor control/movement patterns. Following this logic, if I treat the dysfunctional tissue, I should be able to see a change in any or all of those areas. Isn’t this the same logic we use every time we examine and then treat patients — testing our findings by specific treatments? FDN is no different and has become a valuable tool to help localize and identify neuromuscular dysfunction and improve my clinical accuracy!
Pearls for the Road Ahead: Using FDN in Your Practice
- Door #1: You evaluate a patient, identify what seems to be a straightforward cluster of findings and get to work! You intervened and they improved. No need for supplemental tools or deep neuromuscular retraining principles. They now move appropriately, and their symptoms remain controlled. It was likely a minor acute injury and your intervention helped facilitate the healing process. Pass Go, collect $200.Seems intuitive… If only they were all this easy!
- Door #2: You examine a patient and this case does not look like it’s going to be as quick as Door #1. They seem to have a bit more “grey” and you are having trouble identifying cause from effect. You treat the patient for a few visits and they show improvement, but then symptoms gradually return. Sure, you are doing them a service, but you are likely treating and calming the symptomatic tissue (more treating the WHAT). Sensible enough, they continue to have a dysfunctional movement pattern, which is likely leading to this continued irritation.
Nothing novel there. We know we should be looking toward causative factors such as hypo/hypermobilities or poor movement patterns/control. Perhaps, we overlooked the neuromuscular impact to the patient. How can we do that effectively?
The Take Home: Neuro and Needling
The novelty and the pearl here is using FDN and its impact on the neuromuscular system to your advantage. FDN can have profound impacts on pain, muscular recruitment, motor control, and neurogenic based dysfunction, which can be incredibly difficult at times to identify. FDN can be extremely tissue and diagnostically specific. More so than palpation, superficial soft tissue strategies, or joint manipulation, FDN offers both a tool for evaluation and intervention. Do not be afraid to challenge yourself to utilize FDN outside of the trigger point intervention model, but consider its effects on neuromuscular facilitation and inhibition, not just in the local tissue of the WHAT, but regionally as well to try to find the WHY behind the WHAT. A whole new world of neuromuscular exploration is at the tip of the needle!