The Hidden Architecture of Dysfunction

Editor’s Note: This is article #3 of a six-part series. Part 1 appeared in the August issue; part 2 in the September issue.

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When Protection Becomes the Problem

The body’s initial response to injury is elegant: protect the damaged area, redistribute the load and maintain function. But over time, these well-meaning adjustments become maladaptive. Compensation patterns – the biomechanical and neuromuscular reconfigurations that arise post-injury – can quietly sabotage recovery, athletic performance and long-term joint integrity.^1-2

For chiropractors, recognizing these patterns is as critical as diagnosing the primary injury itself.

Defining Compensation Patterns

Compensation patterns are altered movement strategies adopted to offload painful or compromised tissues. They often involve:

• Recruitment of secondary muscles
• Shifts in joint alignment
• Changes in gait or posture
• Asymmetries in range of motion and force output

Initially subconscious and protective, these patterns become ingrained through repetition, pain avoidance and nervous-system adaptation.³

How Do We Identify Them?

Evaluation of compensation must go beyond standard orthopedic testing. Key methods include:

• Gait analysis for lower extremity and lumbar adaptations
• Scapular kinematic assessments in overhead athletes
• Surface EMG to evaluate abnormal muscle activation
• Functional movement screens (FMS) or SFMA to identify faulty motor control
• Motion capture systems for high-level quantification

Muscle Imbalances: A Classic Result

When one muscle group is inhibited, another overactivates. This reciprocal imbalance distorts joint mechanics and stresses supporting structures.¹

Example: In rotator-cuff dysfunction, underactivation of the lower trapezius and serratus anterior is common. The body compensates by overactivating the upper trapezius, leading to scapular elevation, anterior tilt and winging – a pattern known as scapular dyskinesis.²

Joint Degeneration: A Hidden Consequence

Compensatory movement redistributes load – often unevenly. In the shoulder, internal rotation and anterior protraction shift stress onto the glenohumeral and AC joints, accelerating labral degeneration and osteoarthritis.⁴

In the lumbar spine, altered gait due to hip or knee injury may lead to facet joint overload, paraspinal muscle spasm and disc compression.

Case Study: Shoulder Dysfunction in a Tennis Athlete

A 30-year-old competitive tennis player presents with vague shoulder pain and declining serve velocity. EMG and clinical analysis reveal:

• Upper trap overactivation
• Serratus anterior underactivation
• Pronounced winging during overhead movements

This pattern stemmed from an old supraspinatus injury that had “healed” – but the compensation remained. Treatment included:

• Capular stabilization
• PNF motor control drills
• Manual therapy for soft-tissue restriction

Outcome: After three months, scapular mechanics normalized and serve velocity improved.

Case Study: A Runner’s Low Back Pain

A 35-year-old marathoner reports persistent low back pain and early fatigue. Gait analysis shows:

• Excessive lumbar lordosis
• Anterior pelvic tilt during stance phase
• Underactive hamstrings and tight hip flexors

The root? Chronic hamstring tendinopathy. Compensation overloaded the lumbar spine and contributed to poor core engagement. Treatment focused on:

• Core stability
• Hip flexor mobility
• Hamstring strengthening
• Real-time gait retraining

Result: Pain reduction, improved running form and increased endurance.

The Role of Proprioception and Neural Plasticity

Injury alters proprioceptive input from joints, tendons and ligaments. The CNS responds by rewiring its motor maps – shifting control to “backup” pathways. Studies using functional MRI (fMRI) have confirmed altered cortical activation in patients with chronic musculoskeletal pain, reflecting long-term central adaptation.²

These changes often result in overrecruitment of superficial stabilizers and inhibition of deep stabilizing musculature.³

Viscoelastic Changes: Tissue Memory of Dysfunction

Prolonged compensation alters tissue tone and elasticity:

• Muscles shorten or become hypertonic
• Tendons lose glide and flexibility
• Scar tissue creates friction & stiffness⁵

Increased stiffness in the hamstrings or hip capsule, for example, can restrict movement and create dysfunctional pelvic mechanics.

Clinical Takeaway: Don’t Just Treat the Injury – Correct the Strategy

Even after the primary injury resolves, compensation remains. If left unaddressed, performance declines, secondary injuries emerge and chronic pain syndromes develop.

Successful treatment requires:

• Neuromuscular re-education
• Proprioceptive training
• Motor control retraining
• Manual therapy to restore tissue quality

Next in the Series…

In Part 4: Reclaiming Control, we explore evidence-based rehabilitation strategies to reverse compensation, retrain the CNS and rebuild resilient movement patterns.

References

1. Kibler WB, Sciascia A. Current concepts: scapular dyskinesis. Brit J Sports Med, 2010;44(5): 300-305.
2. Thigpen CA, et al. Head and shoulder posture affect scapular mechanics and muscle activity in overhead tasks. J Electromyogr Kinesiol, 2010;20(4):701-709.
3. Wilk KE, et al. Shoulder injuries in the overhead athlete. JOSPT, 2009;39(2):38-54.
4. Calcei JG, et al. Diagnosis and treatment of injuries to the biceps and superior labral complex in overhead athletes. Curr Rev Musculoskel Med, 2018;11(1):63-71.
5. Garving C, et al. Impingement syndrome of the shoulder. Deutsches Ärzteblatt Int, 2017;114(45): 765-776.