🧠 Phase 1 · Foundation

The Mind-Body Disconnect

Whiplash, Concussion, and the Protective Alarm

The Body's Alarm System: Why Symptoms Persist

After a motor vehicle accident, many patients experience a mix of symptoms that feel confusing or bigger than what the imaging shows: neck pain, dizziness, fatigue, and “brain fog.”

This is not a mystery. It is a predictable physiological response that happens when the body's systems for sensing stability—the neck, brain, and eyes—are disrupted simultaneously.

These persistent symptoms are rooted in sensory mismatch, threat system activation, and neuroplastic changes. Understanding this pattern is the first step toward unwinding the Mind-Body Disconnect.

Layers of Disruption: Neck, Brain, and Proprioception

A collision creates a rapid acceleration-deceleration force that affects multiple systems at once:

1. Whiplash: The Neck as a Threat Signal

Whiplash is a coordinated defensive response that involves more than strained muscles. Injury to neck muscles and joints causes the brain to receive inaccurate movement signals, or proprioceptive distortion.

  • The instability triggers deep muscle guarding and trigger points (micro-spasms) that mimic pain in other areas like the eye or temple.

2. Concussion: Functional Mismatch

Even mild traumatic brain injury (mTBI), which is often missed, changes how the brain regulates energy and filters information.

  • Biomechanical studies show rear-end collisions can generate brain strains comparable to concussive impacts, especially when head angular velocity exceeds 30 rad/s.
  • The system is overwhelmed, leading to cognitive fatigue, visual strain, and hypersensitivity.

The Core Problem: Sensory Mismatch & Amygdala Activation

For the nervous system to feel stable, three systems need to agree: vision, the vestibular system (inner ear), and cervical proprioception (neck).

Brain Alarm Center Vision Vestibular Neck

When these three inputs agree → calm.
When they disagree → threat → alarm stays on.

The brain interprets this sensory conflict as instability. Instability is one of the fastest ways to activate the body’s threat-detection center: the amygdala.

Physiologic Amplification

This is not "just anxiety"; it is a physiological protective response. In this heightened state, the amygdala increases the volume of protective signals:

  • Increased muscle tone and guarding.
  • Amplified pain signals (central sensitization), making small inputs feel bigger.
  • Enhanced startle, hypersensitivity to light/sound, and fatigue.

This activation causes neuroplastic changes; for instance, the amygdala can undergo dendritic hypertrophy (structural change) that enhances emotional responses to sensory input.

Important: This alarm response is protective, not imagined. Your body is trying to keep you safe in an environment it currently reads as unstable.

The Soup of Dysfunction

Any soup can be made better with the right ingredients—and in this case, the ingredients are accurate sensory input, safety signals, and time.

When sensory mismatch meets guarding, the nervous system enters a self-reinforcing loop, creating somatosensory distortions.

  • The Stress-Pain Loop: Stress system dysregulation produces lasting changes in pain sensitivity. The pain promotes hyperarousal, and hyperarousal amplifies pain perception.
  • Neuroplasticity and Guarding: Chronic whiplash is associated with altered brain network structure and function. When patients with chronic whiplash imagine neck movements, neuroimaging shows greater activation in regions that process sensory and affective information, suggesting they predict and amplify the emotional consequences of movement.
  • Disability Prediction: The integration of posttraumatic stress, sensory hypersensitivity, and fear-avoidance together predicts disability more accurately than fear-avoidance alone.

Restoring Coherence: Integrated Treatment

Treatment must be multimodal and symptom-based, addressing the neurophysiological and psychological changes alongside the musculoskeletal injury. This approach aligns with evidence supporting pain neuroscience education, stress management, and cognition-targeted exercise therapy.

1. The Neck (Mechanics + Proprioception)

  • Trigger point needling / Hydrostatic IMS and manual therapy.
  • Cervical proprioceptive retraining to restore coherence between neck, vestibular, and visual systems.

2. The Brain (Sensory Processing)

  • Vestibular rehab, Oculomotor retraining, and Visual-vestibular integration.
  • Graded exposure to screens, reading, and driving.

3. The Amygdala (Threat Sensitivity)

  • Pain Neuroscience Education and stress management.
  • Pacing strategies, breath mechanics, and autonomic regulation.
  • Cognition-targeted exercise therapy (to consolidate gains).

Specific attention to cognitive symptoms (difficulty concentrating), history of anxiety or depression, and sleep disorders is critical, as these factors show the strongest associations with persisting symptoms.

What the recovery path looks like

Once the loop is interrupted, the overall direction can be steadily upward:

  • Neck tension eases, and headaches become less reactive.
  • Visual strain and motion sensitivity settle.
  • Energy and cognitive endurance improve.
  • Driving and work tasks feel more natural and less threatening.

Recovery is rarely a straight line—some days step forward, some sideways—but the overall direction can be steadily upward once the loop is interrupted.

Key takeaway: Persistent symptoms after an MVA do not mean your body is broken. They mean your protective systems—neck, brain, and alarm network—are still trying to stabilize you. When we restore agreement between the eyes, inner ear, neck, and nervous system, the alarm quiets and symptoms recede. This pattern is treatable, and improvement is expected.

Evidence & Bibliography

  1. Pedler A, Kamper SJ, Sterling M. Addition of Posttraumatic Stress and Sensory Hypersensitivity More Accurately Estimates Disability and Pain Than Fear Avoidance Measures Alone After Whiplash Injury. Pain. 2016;157(8):1645-1654. doi:10.1097/j.pain.0000000000000564.
  2. Treleaven J. Dizziness, Unsteadiness, Visual Disturbances, and Postural Control: Implications for the Transition to Chronic Symptoms After a Whiplash Trauma. Spine. 2011;36(25 Suppl):S211-7. doi:10.1097/BRS.0b013e3182387f78.
  3. Coppieters I, Cagnie B, De Pauw R, Meeus M, Timmers I. Enhanced Amygdala-Frontal Operculum Functional Connectivity During Rest in Women With Chronic Neck Pain: Associations With Impaired Conditioned Pain Modulation. NeuroImage. Clinical. 2021;30:102638. doi:10.1016/j.nicl.2021.102638.
  4. de Voogd LD, Hashemi MM, Zhang W, et al. Amygdala Hyperactivity in Posttraumatic Stress Disorder: Disentangling Predisposing From Consequential Factors Using a Prospective Longitudinal Design. Biological Psychiatry. 2025;:S0006-3223(25)00993-X. doi:10.1016/j.biopsych.2025.02.894.
  5. Treleaven J. Dizziness, Unsteadiness, Visual Disturbances, and Sensorimotor Control in Traumatic Neck Pain. The Journal of Orthopaedic and Sports Physical Therapy. 2017;47(7):492-502. doi:10.2519/jospt.2017.7052.
  6. McLean SA. The Potential Contribution of Stress Systems to the Transition to Chronic Whiplash-Associated Disorders. Spine. 2011;36(25 Suppl):S226-32. doi:10.1097/BRS.0b013e3182387fb4.
  7. Elkin BS, Elliott JM, Siegmund GP. Whiplash Injury or Concussion? A Possible Biomechanical Explanation for Concussion Symptoms in Some Individuals Following a Rear-End Collision. The Journal of Orthopaedic and Sports Physical Therapy. 2016;46(10):874-885. doi:10.2519/jospt.2016.7049.
  8. Peixoto C, Buchanan DM, Nahas R. Missed Emergency Department Diagnosis of Mild Traumatic Brain Injury in Patients With Chronic Pain After Motor Vehicle Collision. Pain Physician. 2023;26(1):101-110.
  9. Kuperman P, Granovsky Y, Fadel S, et al. Head- And Neck-Related Symptoms Post-Motor Vehicle Collision (MVC): Separate Entities or Two-Sides of the Same Coin?. Injury. 2021;52(5):1227-1233. doi:10.1016/j.injury.2021.03.003.
  10. Feinberg RK, Hu J, Weaver MA, et al. Stress-Related Psychological Symptoms Contribute to Axial Pain Persistence After Motor Vehicle Collision: Path Analysis Results From a Prospective Longitudinal Study. Pain. 2017;158(4):682-690. doi:10.1097/j.pain.0000000000000818.
  11. McLean SA, Clauw DJ, Abelson JL, Liberzon I. The Development of Persistent Pain and Psychological Morbidity After Motor Vehicle Collision: Integrating the Potential Role of Stress Response Systems Into a Biopsychosocial Model. Psychosomatic Medicine. 2005 Sep-Oct;67(5):783-90. doi:10.1097/01.psy.0000181276.49204.bb.
  12. Higgins JP, Elliott JM, Parrish TB. Brain Network Disruption in Whiplash. AJNR. American Journal of Neuroradiology. 2020;41(6):994-1000. doi:10.3174/ajnr.A6569.
  13. Hoffman AN, Paode PR, May HG, et al. Early and Persistent Dendritic Hypertrophy in the Basolateral Amygdala Following Experimental Diffuse Traumatic Brain Injury. Journal of Neurotrauma. 2017;34(1):213-219. doi:10.1089/neu.2015.4339.
  14. Hoffman AN, Lam J, Hovda DA, Giza CC, Fanselow MS. Sensory Sensitivity as a Link Between Concussive Traumatic Brain Injury and PTSD. Scientific Reports. 2019;9(1):13841. doi:10.1038/s41598-019-50312-y.
  15. Murillo C, Coppieters I, Cagnie B, et al. Neural Processing of Pain-Related Distress to Neck-Specific Movements in People With Chronic Whiplash-Associated Disorders. Pain. 2023;164(9):1954-1964. doi:10.1097/j.pain.0000000000002890.
  16. Malfliet A, Lenoir D, Murillo C, et al. Pain Science Education, Stress Management, and Cognition-Targeted Exercise Therapy in Chronic Whiplash Disorders. JAMA Network Open. 2025;8(8):e2526674. doi:10.001/jamanetworkopen.2025.26674.
  17. Bayuk TJ, Bowles AO, Bursaw DO, et al. Management and Rehabilitation of Post-Acute Mild Traumatic Brain Injury (mTBI) (2021). Department of Veterans Affairs.
  18. McIntosh SJ, Vergeer MH, Galarneau JM, Eliason PH, Debert CT. Factors Associated With Persisting Symptoms After Concussion in Adults With Mild TBI. JAMA Network Open. 2025;8(6):e2516619. doi:10.001/jamanetworkopen.2025.16619.
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