Fear is one of the most universal human emotions. It has helped our species survive by preparing us to either face danger or flee from it. While fear is often framed as a psychological state, its roots run deep in the physiology of the body. From the firing of specialized neurons to the release of stress hormones, fear reflects a tightly coordinated interplay between brain, body, and environment. Understanding this physiology not only sheds light on why we respond the way we do in threatening situations, but also offers insight into how fear can become maladaptive in conditions such as chronic pain, where the nervous system begins to interpret situations that were previously not threatening as dangerous. As a result, sensitivity expands to include many experiences unrelated to actual tissue damage.

The Brain’s Fear Circuitry

Fear begins in the brain, where sensory information is processed and evaluated for potential danger. Three regions dominate the fear response: the amygdala, hippocampus, and prefrontal cortex.

Amygdala: This almond-shaped cluster of nuclei rapidly processes sensory cues for threat value (LeDoux, 2000). It is hyper-responsive in both fear and chronic pain states, often amplifying perceived threat from otherwise harmless stimuli.
Prefrontal Cortex (PFC): The ventromedial PFC helps regulate amygdala activity, allowing for more rational reappraisal (“the sharp twinge in my back isn’t catastrophic”). In chronic pain, PFC regulation often falters, leaving the amygdala unchecked (Baliki et al., 2008).
Hippocampus: This region encodes context. It distinguishes whether a signal of potential danger is relevant or benign. Individuals with chronic pain often show altered hippocampal activity often show altered hippocampal activity, leading to overgeneralization of pain-related fear (Maren et al., 2013).

This triad illustrates how pain and fear intertwine: pain becomes frightening not only because of the sensation itself but because the brain begins to treat ordinary movements or contexts as dangerous.

The Autonomic Nervous System and the “Fight-or-Flight” Response

Once a threat is perceived, the amygdala signals the hypothalamus to activate the autonomic nervous system (ANS). The sympathetic branch prepares the body for immediate action:

Increased heart rate and blood pressure deliver oxygen to working muscles.
Pupils dilate, sharpening vision.
Bronchioles expand, enhancing oxygen intake.
Blood flow is redirected from the gut to skeletal muscles.

This rapid cascade explains why fearful situations often come with a pounding heart, shortness of breath, or sweating palms.

For those with chronic pain, this same system may become sensitized, amplifying bodily arousal even during routine activity. Climbing stairs or bending to tie a shoe can trigger disproportionate autonomic responses if the nervous system has learned to treat those movements as threatening (Quartana et al., 2009).

The Hypothalamic-Pituitary-Adrenal (HPA) Axis and Pain-Related Stress

Beyond the immediate ANS response, the HPA axis provides sustained stress signaling:

The hypothalamus releases corticotropin-releasing hormone (CRH).
CRH triggers the pituitary to secrete adrenocorticotropic hormone (ACTH).
ACTH stimulates the adrenal cortex to release cortisol, the body’s chief stress hormone.

Cortisol mobilizes glucose for energy and modulates immune responses. Short-term, this is adaptive. But in chronic fear or pain states, cortisol regulation becomes disrupted, leading to fatigue, inflammation, and impaired tissue recovery (Ulrich-Lai & Herman, 2009). Dysregulated cortisol has been observed in individuals with chronic low back pain, fibromyalgia, and other pain syndromes (McBeth et al., 2007).

The Startle Reflex and Motor Preparation

Fear primes the motor system. The startle reflex, mediated by the brainstem, causes immediate defensive movement (e.g., flinching at a loud sound). When the amygdala is already sensitized, this reflex intensifies.

In chronic pain, movements that previously triggered discomfort can set off similar reflexive guarding: muscles tighten before a feared motion occurs. This anticipatory bracing—though protective in the short term—can reinforce pain through altered biomechanics and sustained muscle tension (Vlaeyen & Linton, 2012).

Fear Learning, Pain Memory, and Avoidance

One of the most powerful aspects of fear physiology is its link to learning and memory. Through fear conditioning, neutral stimuli become paired with threat. For example:

In experimental models, a tone paired with a shock comes to elicit fear responses.
In chronic pain, bending forward once during an acute episode can condition the nervous system to treat all future bending as threatening, even when there is no ongoing injury.

The amygdala encodes these associations, the hippocampus contextualizes them, and the PFC attempts to extinguish them when they are no longer valid (Maren & Holmes, 2016). In chronic pain, extinction learning often fails, meaning the nervous system continues to link ordinary movements with danger.

This ‘fear-avoidance model’ of chronic pain explains why individuals may stop moving, exercising, or even socializing, reinforcing disability and perpetuating the pain cycle (Vlaeyen & Linton, 2000).

Adaptive vs. Maladaptive Fear

From an evolutionary perspective, fear is protective: it heightens vigilance, primes muscles, and helps us survive. But in chronic pain, fear physiology can become maladaptive.

Hypervigilance: Constant scanning for bodily threat increases pain perception.
Avoidance: Reduced movement leads to deconditioning, stiffness, and further pain, by reshaping neural and connective tissues toward a more pain-sensitive state.
Neuroplastic Changes: Persistent fear-pain coupling strengthens maladaptive neural pathways in the amygdala and PFC.
Systemic Effects: Prolonged HPA activation disrupts sleep, mood, and immune function, compounding pain experience.

In short, the nervous system expands its definition of threat, pulling in sensations and situations that were previously neutral.

Rethinking Fear in Pain Rehabilitation

A deeper understanding of the physiology of fear has reshaped modern pain rehabilitation. Approaches such as graded exposure therapy gradually reintroduce feared movements, teaching the nervous system that these actions are safe. One of the most powerful and practical forms of graded exposure is progressive physical conditioning—using strength training, aerobic activity, and mobility work to rebuild trust in the body while expanding capacity. Mind-body practices, including mindfulness and breathing techniques, further help recalibrate autonomic and HPA axis responses, creating a nervous system that is less reactive and more adaptable. Together, these strategies build confidence, resilience, and freedom from fear-driven avoidance.

Crucially, the goal is not to eliminate fear—it is to retrain its physiology so it supports higher function and better quality of life, rather than remaining locked in overgeneralized sensitivity.

Conclusion

Fear is not “just in the head”—it is a whole-body state orchestrated by neural, autonomic, and hormonal systems. In acute danger, this physiology is lifesaving. But when the same circuitry becomes entangled with chronic pain, fear responses can spread to situations that are not actually dangerous, driving avoidance, disability, and suffering.

Recognizing the physiology of fear in chronic pain reframes treatment: it is not only about addressing tissues, but about calming the amygdala, strengthening the prefrontal cortex, retraining learned associations, and restoring trust in the body’s capacity to move without danger. Ultimately, this is a multidisciplinary process—not a quick fix. Rarely will a single medicine, surgery, or exercise solve the problem. Instead, it requires consistently showing yourself that you are less fragile than you think. This resilience is earned over time, through steady practice, progressive conditioning, and appropriate guidance.

References

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McBeth, J., Silman, A. J., Gupta, A., Chiu, Y. H., Ray, D., Morriss, R., Dickens, C. (2007). Moderation of psychological risk factors through dysfunction of the hypothalamic–pituitary–adrenal stress axis in chronic widespread pain. Arthritis & Rheumatology, 52(10), 3124–3132.
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Vlaeyen, J. W. S., & Linton, S. J. (2012). Fear-avoidance model of chronic musculoskeletal pain: 12 years on. Pain, 153(6), 1144–1147.