1. Defining the Tendon Guard Reflex (TGR)
The Tendon Guard Reflex (TGR) is an instinctive, protective postural-muscular response activated by perceived threat, stress, or pain. Unlike developmentally defined primitive reflexes (e.g., Moro, ATNR), the TGR is a survival-oriented pattern that begins in the lower body (the big toe), ascends via the Achilles tendon through hamstrings, up the spine, and into the neck and scalp, preparing the body defensively. If unresolved, habitual muscular contraction in this pathway can interfere with posture, sensory processing, and neurodevelopmental functioning (Boyd, ~2022)
2. Functional Implications of Chronic TGR Activation
When the TGR remains habitually activated, even without actual threat, individuals may experience:
- Postural instability and balance issues (e.g., toe-walking, forward tipping, compensatory backward sway)
- Muscle tension in the low back, legs, neck — leading to soreness, stiffness, and decreased spinal mobility
- Restricted cerebrospinal fluid flow, possibly impeding frontal lobe function, and resulting in "brain fog," difficulty organizing, planning, or seeing the big picture
- Cognitive-emotional rigidity, over-focus, withdrawal, fearfulness, or hyperactivity due to defensive posturing The TGR, when integrated, allows rapid activation/deactivation—supporting calm engagement, movement fluidity, and connected cognitive functioning .
3. Physiological Pathways: Stress, Cortisol, and Autonomic Regulation
a. Stress Response & HPA Axis
When the brain perceives threat, it activates the HPA axis: the hypothalamus releases CRH → pituitary releases ACTH → adrenal glands secrete cortisol and adrenaline. In chronic TGR activation, this stress response may remain engaged, reinforcing muscle guarding, heightened arousal, and inhibited relaxation.
b. Musculoskeletal Effects
TGR induces muscle rigidity, especially in the posterior chain: calves, hamstrings, lumbar and cervical paraspinals. This rigidity impairs shock absorption, fluid movement, and energy-efficient posture. Sustained tension may accelerate fatigue, increase injury risk, and compromise fine and gross motor performance.
c. Autonomic Nervous System (ANS)
The TGR drives the ANS toward sympathetic dominance—triggering increased heart rate, shallow breathing, reduced digestion/immune function, and heightened emotional reactivity. Parasympathetic activity (rest, digest, repair) is suppressed, making recovery and regulation more difficult. Over time, this imbalanced arousal contributes to chronic stress and poor self-regulation.
d. Cortisol’s Role
While cortisol is adaptive short-term, persistently elevated cortisol—driven by ongoing reflex stress patterns like the TGR—can:
- Impair immune function
- Disrupt sleep and emotional regulation
- Reduce neuroplasticity and memory formation
- Contribute to muscular breakdown and inflammation.
This creates a vicious cycle: TGR → stress → elevated cortisol → physiological dysregulation → reinforcement of protective guarding.
5. Key Muscle Groups and Reflex Pathway for TGR
- Foot-to-head trajectory: Big toe → Achilles tendon → hamstrings → lumbar spine → cervical spine → neck/scalp
- Neck musculature and jaw: forward head posture, clenching
- Shoulders and upper trapezius: elevation, rigidity
- Core/trunk stabilizers: braced, guarded, reduced rotation
- Respiratory muscles: diaphragm and intercostals restricted—leading to shallow breathing and reduced oxygenation/slower regulation.
6. Summary: Integrating TGR in Practice
| Domain | TGR Impact |
|---|---|
| Motor Function | Postural rigidity, reduced shock absorption, fatigue, coordination challenges |
| Cognitive-Attentional | "Brain fog," difficulty with planning, reduced flexibility of thought and action |
| Emotional Regulation | Hypervigilance, difficulty shifting to calm states, sensory over-reaction |
| Autonomic Response | Predominantly sympathetic activation, reduced parasympathetic regulation |
| HPA Axis Stress Effects | Persistent cortisol → immune suppression, impaired learning, poor emotional recovery |
7. Clinical Relevance
Research on primitive reflex retention demonstrates that targeted movement-based interventions can reduce reflex activity and improve functional performance. For example, structured perceptual-motor programs and sensorimotor training have been shown to decrease primitive reflex presence and improve motor and cognitive outcomes in both children and older adults (Melillo, 2020; Stephens-Sarlós, 2024). While specific empirical evidence for TGR integration is limited, its overlap with reflex retention and stress physiology underscores the importance of addressing it in therapy.
Conclusion
The Tendon Guard Reflex represents both a muscular and neuroendocrine defense strategy. When retained, it reinforces stress physiology, sympathetic dominance, and cortisol elevation, manifesting as chronic muscular rigidity, postural imbalance, and impaired self-regulation. Occupational therapy interventions that combine sensory integration, neurodevelopmental movement, and stress-modulation strategies are essential to reduce defensive guarding, restore autonomic balance, and promote participation in meaningful daily activities.
References
- Boyd, S. C. (n.d.). The Tendon Guard Reflex – Understanding our Protective Reflex. High Point AZ. highpointaz.com+1
- Melillo, R. (2022). Retained primitive reflexes and potential for intervention. PMC. PMC+2OccupationalTherapy.com+2
- Melillo, R. (2020). Persistent childhood primitive reflex reduction effects on cognitive and motor performance. PMC. PMC
- Stephens‑Sarlós, E. (2024). Changes in primitive reflexes in older adults and their implications. ScienceDirect. sciencedirect.com
- Heidenreich, S. (2021). Understanding primitive reflexes: Impacts and strategies for integration. OccupationalTherapy.com. OccupationalTherapy.com
