Professional sports medicine has access to extraordinary resources. The best imaging available. Expert physiotherapists, surgeons, and rehabilitation specialists. Nutritional and biomechanical support at every level. And yet certain injuries in professional athletes follow a pattern that all of that infrastructure struggles to break: the chronic tendinopathy that does not resolve, the calf that keeps tightening, the elbow that stays painful through every treatment protocol tried.

One possible reason, in some of these cases, is that the injury is being treated at its endpoint while a contributor further up the chain in the cervical or thoracic spine goes unidentified.

What the Treatment Evidence for Tennis Elbow Shows

Tennis elbow, more precisely called lateral epicondylalgia, is one of the most common chronic pain presentations in both sports clinics and general pain practice. It is also a condition where the treatment evidence is humbling.

The Canadian Shoulder and Elbow Society position statement on nonoperative management of lateral epicondylitis, published in the Canadian Journal of Surgery, reviewed the evidence using GRADE methodology. Its recommendations are blunt: patients seeking physiotherapy with an eccentric strengthening program should be counselled that pain and function outcomes are similar to no active treatment, and patients considering injection treatments including corticosteroids, platelet-rich plasma, and autologous blood should be counselled that these provide similar outcomes to placebo. Both are strong recommendations based on moderate-quality evidence.

That conclusion is consistent with the wider literature. In a systematic review of 41 randomized trials, Coombes, Bisset and Vicenzino (2010) found that corticosteroid injections reduced pain substantially in the short term, but that the effect reversed at intermediate and long term follow-up. A subsequent randomized, placebo-controlled trial by Coombes and colleagues (2013) put numbers on it: patients who received corticosteroid injection had lower rates of complete recovery at one year than those who received placebo injection, 83 percent versus 96 percent, and substantially higher recurrence, 54 percent versus 12 percent. Physiotherapy produced no significant difference at one year.

The literature increasingly characterizes tennis elbow as a degenerative tendinopathy rather than an inflammatory condition, and most patients recover eventually with or without intervention, over a timeline often measured in many months. The interventions commonly applied may provide temporary relief without clearly changing the underlying trajectory.

That is a striking picture for a condition this common. If local treatments perform similarly and modestly over time, a reasonable scientific question follows: is the tendon the whole story?

The Cervical Contribution to Elbow Tendinopathy

The limbs developed from the spine. The arms and upper limbs emerged developmentally from the cervical and upper thoracic spine, and the nerve roots supplying motor and sensory function to the forearm and hand originate from C5 through T1. That anatomical relationship is the basis for asking whether chronic tennis elbow may sometimes have a cervical contribution.

This line of thinking is not unique to the neuromyofascial model. The concept of regional interdependence, widely discussed within sports physiotherapy, proposes that dysfunction in one region of the body can contribute to pain and dysfunction elsewhere: neck to elbow, hip to knee, lumbar spine to foot.

Mainstream clinical guidelines reflect a related view. The 2022 clinical practice guideline on lateral elbow pain published in the Journal of Orthopaedic and Sports Physical Therapy notes that tendon changes, impairments in motor control, and changes in pain processing may all contribute to symptoms. It classifies a subgroup of patients as elbow plus cervical, lists cervical radiculopathy among the differential diagnoses clinicians should consider, and states that clinicians may use manipulation or mobilization directed at the cervical spine, thoracic spine, or wrist as an adjunct to local care when impairments in those regions are identified. This is not evidence of cervical causation in every case, but it is guideline-level acknowledgment that refractory lateral elbow pain should not be evaluated as a tendon-only problem.

Direct measurement of the radial nerve in this population has produced mixed results. Abhimanyu and colleagues (2021) measured radial nerve cross-sectional area in 70 patients with lateral epicondylitis and found it significantly greater on the affected side at both the spiral groove and the antecubital fossa, concluding that tennis elbow should no longer be understood only as a tendinopathy and that radial nerve involvement warrants consideration. A companion paper from the same group, however, reported that radial nerve thickness was not increased and described that finding as partially refuting a causal role for the nerve. Two analyses from the same investigators reaching different conclusions is a fair summary of where this question stands: neural involvement in lateral epicondylalgia is plausible and under active investigation, not established.

In the neuromyofascial model, the proposed injury sequence in refractory tennis elbow begins not at the elbow but in the cervical spine. The hypothesis is that deep spinal muscle injury and scarring in the neck, whether from a whiplash event, repetitive strain, or gradual accumulation of cervical pathology, creates persistent irritation of the motor nerve roots supplying the forearm, producing a motor neuropathy: impaired motor nerve signal reaching the forearm extensor muscles.

The proposed effect of impaired motor nerve signal on muscle is dystonia. Rather than receiving a normal signal to contract and relax, the muscle would enter a state of persistent involuntary shortening. The forearm extensor group, including the extensor carpi radialis brevis, becomes tonically contracted.

Sustained tonic contraction of that kind would create constant traction at the elbow, placing the tendon origin at the lateral epicondyle under chronic rather than normal intermittent load. That mechanism is consistent with the Cook and Purdam continuum model of tendinopathy, which describes tendons deteriorating through excessive load, repetitive load, and poor load recovery rather than through acute inflammation. What the neuromyofascial model adds is a proposed source for that abnormal load in some refractory cases: motor involvement originating at the cervical spine rather than at the elbow.

Over time, the combination of chronic tension, calcium deposition at the insertion, and tendon microtrauma would produce the degenerative tendinopathy that imaging identifies at the elbow. In this model, treating the elbow addresses the endpoint of that sequence while the proposed cervical contribution remains active, which would explain why local treatment effects fade and the same pathology returns.

This is a clinical hypothesis, not a proven mechanism. What is better established is that chronic lateral epicondylalgia in refractory cases shows evidence of pain sensitization beyond the tendon itself, that imaging findings correlate only weakly with symptom severity, and that the cervical spine is a recognized consideration in a subgroup of patients. Clinical observations over approximately 30 years of practice suggest that when cervical and upper thoracic findings are identified and addressed in these cases, presentations resistant to standard treatment often improve. Those are clinical observations. They do not establish causation, and they have not been tested prospectively.

The Calf and the Achilles Tendon

A pattern familiar to anyone following professional sport is the elite athlete who misses weeks with calf pain, returns to play, and ruptures the Achilles tendon shortly afterward. It happens often enough to be recognizable, and it is worth asking what the sequence suggests.

The sports medicine literature supports the upstream logic in principle. Prior calf injury is a recognized risk factor for subsequent Achilles tendon injury. S1 nerve root dysfunction, one of the most common lumbar radiculopathy presentations, can produce calf weakness, altered gait, and reduced push-off strength. The pathway from lumbar nerve root compromise to calf dysfunction to Achilles vulnerability is anatomically and clinically plausible, though it has not been established as a common cause of Achilles rupture in athletes.

It is worth being precise here. The Achilles literature differs from the tennis elbow literature in one important respect: loading-based rehabilitation does demonstrate meaningful benefit for Achilles tendinopathy across multiple systematic reviews, and current clinical guidelines recommend tendon-loading exercise as effective first-line care. The failure of local treatment that characterizes refractory tennis elbow is not as clearly established for Achilles presentations generally. The neuromyofascial argument for Achilles cases is strongest in the refractory patient: the one who has completed appropriate loading rehabilitation, whose symptoms persist or keep returning, and whose proximal kinetic chain and lumbar nerve root contribution have never been systematically investigated.

In those cases, the same mechanism described above for tennis elbow would apply through the lumbar and sacral nerve roots supplying the calf. Motor neuropathy at L5 or S1 could create dystonia in the gastrocnemius and soleus. Sustained tonic contraction of the calf would place the Achilles tendon under chronic abnormal load. Over time the tendon develops degenerative changes: altered collagen organization, increased type III collagen deposition, and microtears at the insertion. In Dr. Lamb’s clinical view, this progressive process may be a contributor in a subset of recurrent and refractory Achilles presentations rather than an acute isolated event. That remains a hypothesis.

What can be said without speculating about any individual case is this: when an athlete has persistent calf symptoms that have been managed locally and the proximal contribution has not been examined, something in the assessment may be incomplete. Whether examining it changes outcomes is a question that requires study, not assertion.

The Broader Athletic Picture

The most common chronic injuries in professional sport, including plantar fasciitis, Achilles tendinopathy, patellofemoral syndrome, hip-spine syndrome, and lower back pain, all involve tendons or joints under abnormal chronic load. In refractory cases where standard local rehabilitation has been completed appropriately and symptoms persist, the source of that abnormal load may warrant investigation beyond the symptomatic site.

The proposal that follows is that athletes assessed for neuromyofascial findings before injury develops, rather than after, may have an opportunity to address contributing factors earlier. Whether pre-injury screening of this kind reduces injury rates has not been tested and would need prospective study to establish.

There is a performance question here as well. Nerve root irritation is associated with reduced motor unit recruitment, altered firing patterns, muscle weakness, and impaired coordination. If neurological signal quality from the spine to the limbs affects motor recruitment, it would follow that maintaining that integrity matters for power output, speed, and resilience. That is a reasonable inference from established neurophysiology rather than a demonstrated performance finding.

The strongest evidence-based version of this argument is straightforward: do not stop at the tendon in chronic refractory cases. The spine, the neural pathways, and the full kinetic chain deserve systematic investigation when local treatment has reached its ceiling. That position is reflected in mainstream clinical guidelines. The neuromyofascial framework goes further, proposing that spinal motor neuropathy is a primary upstream contributor in many of these cases. That stronger claim remains a clinical hypothesis requiring prospective investigation. Clinical observations are consistent with it, though observations of that kind cannot establish the mechanism.

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The information in this article is educational and informational in nature. It is not intended as a substitute for professional medical advice, diagnosis, or treatment. If you are experiencing chronic tendinopathy or recurring athletic injury that has not responded to standard treatment, consult with a qualified healthcare provider to discuss the options appropriate for your situation.