Abstract

Dysautonomia is currently described as an umbrella term for a variety of medical conditions involving dysfunction of the autonomic nervous system (ANS). The ANS is known to regulate numerous involuntary physiological processes such as heart rate, blood pressure, digestion, pupil dilation, kidney function, and thermoregulation. However, these functions do not occur through isolated ANS activity; they depend on dynamic interactions with other autonomic regulatory systems, notably the central autonomic network, the neuroendocrine system, and the immune–inflammatory system. Given this inherent interconnectedness, it is scientifically insufficient and clinically limiting to reduce dysautonomia exclusively to ANS dysfunction. This is especially the case to explain the full spectrum of stress-related physiological disorders where such reductionism fosters diagnostic fragmentation and therapeutic inefficiency. Drawing from clinical experience and current scientific literature, this paper argues for reframing dysautonomia as a systemic regulatory failure within the Extended Autonomic Regulatory System – to better reflect the complex pathophysiology of dysautonomic conditions seen in practice.

Background

Dysautonomia is currently described as an abnormality in the function of the autonomic nervous system (ANS) (Reichgott, 1990), encompassing a wide range of clinical manifestations including musculoskeletal disorders, respiratory difficulties, heart palpitations, chest discomfort, digestive dysfunction, lightheadedness, and nausea, among others. However, viewing these processes exclusively through the lens of ANS dysfunction neglects their integration within broader regulatory frameworks, notably the central autonomic network (CAN), the neuroendocrine system (NE-S), and the immune–inflammatory system (IIS). Because the ANS does not function independently of these systems, limiting the conceptualisation of dysautonomia solely to the ANS undermines both diagnostic accuracy and therapeutic effectiveness.

Clinically complex, multisystemic presentations frequently lead to mismatches in diagnosis and treatment. For instance, a patient presenting with the previously mentioned ANS-related symptoms – alongside additional issues such as brain fog, cognitive decline, insomnia, hormonal imbalances, and muscle or joint aches – often fails to meet traditional ANS-centric diagnostic criteria for dysautonomia. Yet, when assessed through the broader autonomic regulatory framework that incorporates the CAN, NE-S, and IIS, such presentations clearly fit within the scope of dysautonomia. Treatment strategies designed within this expanded autonomic perspective consistently yield improved and accelerated patient outcomes. Conversely, focusing solely on ANS-related symptoms and separately addressing additional manifestations – such as cognitive decline through psychopharmacology and psychotherapy – typically results in limited efficacy, symptom exacerbation, and the emergence of additional symptoms over time.

Consequently, redefining dysautonomia as a systemic regulatory disorder encompassing multiple interdependent physiological systems will enhance diagnostic accuracy, facilitate targeted treatments, and improve overall patient outcomes. Adopting this systemic approach promises faster patient recovery and significant cost reductions for healthcare systems.

Current Research Paradigm and Limitations

Contemporary dysautonomia research remains predominantly neurocentric, with a strong emphasis on ANS biomarkers such as heart rate variability, baroreflex sensitivity, and vagal tone, and interventions targeting these markers. Although these biomarkers and interventions have clinical significance, their isolated application neglects the broader systemic interactions integral to ANS function. Consequently, this limited perspective inadequately addresses the complex multisystem dysregulation commonly observed in clinical practice.

Complex clinical presentations characterised by multiple unexplained symptoms, such as persistent fatigue, cognitive impairment, diffuse musculoskeletal pain, and other hallmark features frequently observed (but not exclusively) in long COVID, highlight significant gaps in current diagnostic and therapeutic approaches. Patients presenting multisystemic patterns are often misdiagnosed or unjustly categorised as psychosomatic. While these symptoms can, if observed within the EARS, clearly have a biological basis.

In my practice, I frequently encounter patients who are referred to psychologists when medical examinations and diagnostic tests yield inconclusive results. One other common recommendation is to try vagal stimulation, as the reductionist approach suggests that certain symptoms may be associated with the imbalance between sympathetic and parasympathetic activity. Restoring the balance through stimulating vagal activity is then the rationale. However, in my experience – listening closely to patients – vagal stimulation has often led to a worsening of symptoms in nearly all who have tried it. I believe this is because isolated vagal stimulation does not necessarily result in sympathetic downregulation. As a result, both sympathetic and parasympathetic activity can become simultaneously upregulated.

This observation has reinforced my belief that narrowing dysautonomia to solely the autonomic nervous system is an inappropriate approach. Such a narrow definition often leads to treatment mismatches, resulting in paradoxical autonomic responses and exacerbating systemic dysregulation rather than alleviating symptoms.

Furthermore, the fact is that the ANS does not function in isolation; it operates under the regulatory influence of the CAN, the NE-S, and the IIS. Therapeutic approaches that disregard these broader regulatory interactions frequently result in suboptimal or counterproductive outcomes.

In summary, the principal limitations of the current dysautonomia research paradigm include:

• Underestimation of the regulatory complexity inherent in chronic, multisystem conditions.
  
• Fragmented therapeutic interventions that lack systemic coherence and effectiveness.
• Reinforcement of diagnostic silos, complicating accurate diagnosis and effective management of multisystem symptomatology.
• Treatment mismatches.

The Extended Autonomic Regulatory System

Recent efforts to broaden the understanding of autonomic regulation have emerged, notably Goldstein's "Extended Autonomic System" (2021, 2024). Building upon and refining these foundations, I introduce the concept of the Extended Autonomic Regulatory System to highlight the necessity of systemic regulatory coherence rather than isolated nerve signalling.

EARS comprises:

• Central Autonomic Network: Brain regions integrating interoception, visceromotor control, and affective regulation.
  
• Autonomic Nervous System: Sympathetic, parasympathetic, and enteric branches.
• Neuroendocrine System: Primarily the hypothalamic–pituitary–adrenal (HPA) axis.
• Immune–Inflammatory System: Including both innate and adaptive immune responses and inflammatory signalling pathways.

These components function as an interconnected regulatory matrix, dynamically modulating each other to maintain physiological homeostasis in response to internal and external stressors.

Dysautonomia as Multi-System Dysregulation

Patients frequently present with sudden-onset musculoskeletal pain or depression like symptoms or general malaise without clear triggers. These symptoms often coexist with insomnia or fragmented sleep, heart palpitations or fluttering sensations disconnection from self, gastrointestinal disturbances, fatigue or low energy, hormonal imbalances, unexplained (low-grade) fevers, bloating, wondering symptoms, flare-ups or relapses. Seemingly these symptoms seem unrelated and often put down to stress seen some of the symptoms. Diagnosis done stress is then in itself narrowed to the ANS. The ANS does’t explain all the symptoms but a let’s see attitude is often seen or treated separately with prescribed rest, medication and psychotherapy. 

While seen from the broader EARS model all can be related and diagnosed and treated accordingly not as separate symptoms but as symptoms with one origin that probably is stress-related.

Clinical Implications and the Reaset Approach

Recognising systemic dysregulation necessitates interventions capable of restoring coherent regulatory interactions across the EARS. The Reaset Approach exemplifies such a systems-level therapeutic model, employing body-centred, sensory-based techniques to facilitate systemic regulation.

This approach does not require precise localisation of dysfunction but aims to recalibrate overall system coherence. Clinically, patients with functional dysautonomia frequently respond positively within one or two sessions, provided no structural lesion has developed.

Functional Dysautonomia vs. Autonomic Lesion

A critical distinction must be acknowledged:

• Functional dysautonomia: Dynamic, reversible regulatory imbalance responsive to interventions like the Reaset Approach.
  
• Autonomic lesion: Structural or degenerative pathologies resulting from prolonged dysregulation or underlying diseases (e.g., neurodegenerative, autoimmune).
  

Distinguishing between these two entities is essential to ensure appropriate clinical management, as misclassification risks ineffective treatment strategies.

Future Directions for Research

The EARS model opens several avenues for future interdisciplinary investigation:
Detailed mapping of interactions among EARS components in various dysautonomic conditions.

Identification of robust biomarkers indicative of systemic dysregulation.
Systematic assessment of therapeutic interventions (manual therapy, lifestyle modification, pharmacological agents) on systemic regulatory coherence.

Such research promises not only more effective interventions but also deeper insights into the fundamental mechanisms underlying systemic adaptive processes.

Conclusion

To address the growing burden of dysautonomic conditions effectively, we must transition from a neurocentric model towards a comprehensive, systems-level understanding. The EARS framework articulated here offers a robust conceptual foundation for future research, diagnosis, and treatment, aligning clinical practice with physiological complexity. This evolution is imperative, scientifically justified, and ethically necessary in an era of increasingly prevalent stress-related disorders.

Abstract

The widely used phrase ‘fight, flight, or freeze’ has long shaped our understanding of the stress response. However, this tripartite model oversimplifies the dynamic and multi-layered nature of human defensive behaviours. Drawing from evolutionary biology, trauma theory, and autonomic neuroscience, this conceptual paper proposes a refined vocabulary: ‘fright’ (initial orienting alertness) and ‘flop’ (collapsed immobility) are added to the sequence, while ‘freeze’ is reframed to refer specifically to the hypertonic rigidity of tonic immobility. These adaptations, closely aligned with the defence cascade outlined by Kozlowska et al. (2015), aim to improve clinical clarity for manual therapists who encounter patients with stress-related autonomic dysregulation.

Introduction

The stress response is a fundamental adaptive process that enables organisms to respond to both threats and demands. In evolutionary terms, these demands were often immediate and life-threatening, requiring rapid mobilisation of physiological and behavioural resources. Today, many modern stressors – while not directly life-threatening – still trigger the same ancient systems, creating a mismatch between biology and environment.

Traditionally summarised as “fight, flight, or freeze,” the stress response has become part of common language. Yet this simplification conceals important distinctions between different states of defensive activation and immobilisation. As Kozlowska et al. (2015) demonstrated, the human defence response is better understood as a branching, context-dependent cascade that includes multiple forms of immobility, each with distinct neurophysiological features. 

This paper proposes a refinement of this model by:

• Introducing fright as the initial orienting response to a potential threat or demand;
• Reserving freeze for tonic immobility (a hypertonic state);
• Using flop to describe collapsed immobility (a hypotonic, parasympathetic-dominant state).
• Noting fawn as a behaviourally learned appeasement response with distinct features.

From Cannon to Kozlowska: An Evolving Model

Walter Cannon (1915) laid the foundation for modern stress theory by describing the fight-or-flight response. Later, the idea of a “freeze” response was added to account for immobility under threat – popularised through trauma research (van der Kolk, 2014) and survival literature (Levine, 1997). Yet over time, “freeze” became a catch-all term, blurring the distinction between immobilised states driven by muscle tension and those marked by flaccidity and shutdown.

Kozlowska et al. (2015) clarified this confusion by identifying six distinct stages of the defence cascade:

1. Arousal – heightened alertness and orientation,
2. Fight or Flight – active sympathetic mobilisation,
3. Freezing – motor inhibition with high muscle tone,
4. Tonic Immobility – involuntary rigid stillness, often with dissociation,
5. Collapsed Immobility – hypotonic, flaccid state linked to dorsal vagal dominance.
6. Quiescent Immobility – a state of restorative stillness after threat passes.

In this paper, we reframe “arousal” as fright, “tonic immobility” as freeze, and “collapsed immobility” as flop to better reflect both clinical experience and pedagogical clarity. Fawn is also mentioned as an additional behaviourally conditioned state.

The Updated Sequence: Fright, Fight or Flight, Freeze or Flop (Fawn and Quiescent)

Fright - The initial orienting phase – marked by high alertness, vigilance, and activation of the amygdala and periaqueductal grey – is what we propose to call fright (Fanselow, 1994). This precedes active responses and prepares the organism to assess risk or respond.

Fight or Flight - When escape or resistance is possible, sympathetic activation drives either mobilisation (flight) or confrontation (fight) (Cannon, 1915). This state is metabolically expensive and linked to increased heart rate, blood pressure, and muscle perfusion.

Freeze – Freeze, as redefined here, refers to tonic immobility – a state of motor inhibition with sustained high muscle tone. Though the body appears still, it is physiologically braced, often with co-activation of sympathetic and parasympathetic systems (Roelofs, 2017). Clinically, this may appear as rigid posture, holding patterns, or internal “stuckness.”

Flop – When neither escape nor defence is viable, the system may enter flop – a parasympathetic-dominant, hypotonic state akin to collapsed immobility. This is mediated by the dorsal vagal complex and often presents as limp, passive, unresponsive behaviour. While a patient muscles feel relaxed, it reflects a profound state of autonomic withdrawal and disconnection (Marx et al., 2008; Kozlowska et al., 2015).

Fawn - A behavioural defence strategy characterised by appeasement, people-pleasing, or compliance in response to perceived threat or relational instability (Walker, 2013). It reflects a learned psychological adaptation that may mask underlying autonomic dysregulation, though this remains under-researched. 
Quiescent Immobility – The sixth stage, quiescent immobility, reflects a post-threat restorative state, promoting healing and integration. This state is mentioned here for completeness but is not the focus of this paper.

Clinical Relevance: Freeze ≠ Flop

From a clinical standpoint, freeze and flop may appear similar but represent very different states. A patient in a freeze state may still function outwardly, but internally experience immobilisation and rigidity. Their muscles feel tense, their breath may be held, and they report being “stuck.”

In contrast, patients in a flop state may walk and talk, yet present with hypotonic muscles, poor responsiveness, and symptoms of resignation, hopelessness, fatigue, or depression. This can be easily misinterpreted as relaxation, when in fact it reflects parasympathetic dominance and loss of adaptive capacity.

Recognising this difference is critical. Manual therapists must move beyond the false assumption that softness equals relaxation and that all is well. Tense muscles may reflect a defensive brace (freeze), while soft ones may signal autonomic withdrawal (flop). Misreading these states can lead to inappropriate treatment strategies.

Implications for Manual Therapists and Body-Centred Practitioners

For osteopaths, physiotherapists, and other body-centred therapists, this refined terminology helps bridge psychophysiological theory with hands-on practice. The Reaset Approach (Meyers, 2014, 2019), for example, prioritises autonomic regulation – recognising that structural and functional interventions have limited effect when the nervous system is dysregulated.

Understanding the differences between fright, freeze, and flop allows practitioners to:

• Better assess the patient’s underlying autonomic state,
  
• Avoid mistaking parasympathetic collapse for relaxation,
• Tailor interventions to support recovery from dysregulation,
• And restore a sense of safety before structural correction.

Conclusion

The classical model of “fight, flight, or freeze” no longer suffices to capture the complexity of human stress responses. By refining the vocabulary to include fright and flop, and by clarifying the definitions of freeze and collapse, we move towards a more accurate, clinically useful framework. These distinctions are not just academic – they are essential for effective diagnosis, communication, and care.

As our understanding of autonomic regulation deepens, so too must the language we use to describe it. A clear, precise vocabulary helps clinicians align interventions with the patient’s true physiological state – improving outcomes and restoring balance where it begins: in the body.

References

• Cannon, W. B. (1915). Bodily changes in pain, hunger, fear and rage. New York: Appleton.
  
• Fanselow, M. S. (1994). Neural organization of the defensive behavior system responsible for fear. Psychonomic Bulletin & Review, 1(4), 429–438. https://doi.org/10.3758/BF03210947
  
• Gallup, G. G. (1977). Tonic immobility: The role of fear and predation. The Psychological Record, 27(1), 41–61.
• Kozlowska, K., Walker, P., McLean, L., & Carrive, P. (2015). Fear and the Defense Cascade: Clinical Implications and Management. Harvard Review of Psychiatry, 23(4), 263–287. https://doi.org/10.1097/HRP.0000000000000065
  
• Marx, B. P., Forsyth, J. P., Gallup, G. G., Fusé, T., & Lexington, J. M. (2008). Tonic immobility as an evolved predator defence: Implications for sexual assault survivors. Clinical Psychology: Science and Practice, 15(1), 74–90.
  
• Meyers, T. (2014). The effect of the Reaset Approach on the autonomic nervous system, state-trait anxiety and musculoskeletal pain in patients with work-related stress: A pilot study [BSc thesis]. Dresden: Dresden International University in cooperation with Osteopathie Schule Deutschland. Available from: https://drive.google.com/file/d/19P_mKjKx4YG0p6VijTnl6wHXaUGknvVm/view
  
• Meyers, T. (2019). The effect of the “Reaset Approach” on the autonomic nervous system, neck-shoulder pain, state-trait anxiety and perceived stress in office workers: A randomised controlled trial [MSc thesis]. Dresden: Dresden International University in cooperation with Osteopathie Schule Deutschland. Available from: https://drive.google.com/file/d/14ElvJBLRwAbZvQm20ydg9X5oEWRJD_0E/view
  
• Porges, S. W. (2011). The polyvagal theory: Neurophysiological foundations of emotions, attachment, communication, and self-regulation. W. W. Norton & Company.
• Roelofs, K. (2017). Freeze for action: Neurobiological mechanisms in animal and human freezing. Philosophical Transactions of the Royal Society B, 372(1718), 20160206. https://doi.org/10.1098/rstb.2016.0206
  
• van der Kolk, B. (2014). The body keeps the score: Brain, mind, and body in the healing of trauma. Penguin Books.
• Walker, P. (2013). Complex PTSD: From surviving to thriving: A guide and map for recovering from childhood trauma. Azure Coyote. 

This article was written by Tom Meyers with the assistance of ChatGPT, blending personal insights and advanced AI support to create a compelling and impactful message.