Explore how fear circuits in the brain work, why phobias persist, and how therapies like exposure and EMDR help the brain learn safety again.
Over the past decade, neuroscience has confirmed what many clinicians long sensed: fear is not simply an idea — it is a circuit. When we face a threat, the brain’s alarm centre — the amygdala — activates, driving the body into fight, flight or freeze. This is an ancient, protective response. But when the danger has passed, the brain must relearn safety. This process of unlearning a fear response is called fear extinction.
Milad and Quirk (2014) describe how fear extinction depends on three key brain regions working in synchrony. The amygdala flags threat. The ventromedial prefrontal cortex (vmPFC) acts like a brake, signalling the amygdala to stand down. The hippocampus provides the context — reminding us when and where it is actually safe.
Fear doesn’t just live in the mind — it’s carried by a mix of tiny chemical messengers that shape how strongly the alarm rings and how long it lasts. When something frightening happens, glutamate turns up the volume inside the brain’s fear pathways, helping to store vivid, intense memories of threat.
To calm that alarm, the brain relies on GABA, a neurotransmitter that soothes and quiets the system down — but when there’s not enough GABA activity, the fear signal can stay switched on for longer than it should.
At the same time, norepinephrine kicks in to boost alertness and sharpen our senses, keeping us ready to react. In balance, that’s protective — but when levels surge too high, it can tip the body into feeling flooded and overwhelmed by fear.
Serotonin plays its part by helping to steady mood and ease an overactive fear response, offering a kind of internal buffer when anxiety rises. Meanwhile, dopamine connects fear to motivation — it’s the reason we feel driven to avoid or escape the things that once hurt us, linking memory, emotion, and action into a powerful loop.
Together, these messengers help explain why fear can feel so immediate in the body — and why the right treatment can help gently rebalance the chemistry that keeps old fears alive.
For many people living with phobias, post-traumatic stress, panic disorder or social anxiety, this system struggles to reset itself. The amygdala continues to fire. The vmPFC cannot effectively override it. The hippocampus does not clearly confirm, this is safe now.
As a result, fear persists. A person may know, rationally, that there is no danger — yet the body remains on alert. Avoidance and reactivity endure.
Milad and Quirk’s work shows that exposure therapy is effective because it drives fear extinction. Facing the feared object or situation — the lift, the dog, the plane — without the expected threat allows the brain to form new safety associations. This process can be enhanced with behavioural practice, certain medications like D-cycloserine, or neurostimulation techniques such as TMS.
This same framework explains how EMDR can play a role. By reactivating the fear memory and pairing it with a working memory task — such as side-to-side eye movements — EMDR may help the brain rewrite the fear link. This overlaps with what we know about extinction and memory reconsolidation.
When the brain’s fear circuit is working well, the vmPFC acts like a brake, calming the amygdala, while the hippocampus confirms the threat is over and it’s safe again. But when this reset doesn’t happen, fear stays wired in. The alarm keeps firing, even when we know there’s no danger. Over time, avoidance behaviours lock the pattern in place — because by steering clear of what we fear, the brain never fully learns: this is safe now.
Good therapy turns this brain science into action. Exposure therapy stays the gold standard — by facing the fear in a safe way, the brain forms new, lasting safety memories. Mindfulness and relaxation practices strengthen the vmPFC’s braking power, helping settle the alarm. Some medications rebalance the brain chemicals that keep fear alive, turning the volume down. EMDR works within this same system from a different angle — it reactivates old fear memories while using tasks like eye movements to quiet the fear response, giving the brain space to update what it knows and hold onto a new sense of safety.
A twenty-year overview (1997–2017) provides a clearer picture. Six randomised controlled trials tested EMDR’s effect on anxiety disorders: three focused on panic disorder, two on specific phobias and one on self-esteem in clients with anxiety.
Four of these trials demonstrated clear benefits for panic and phobic symptoms. One showed mixed results: severity improved but the frequency of panic attacks did not. One found EMDR less effective than an alternative for boosting self-esteem.
For specific phobias, Doering and colleagues (2013) found that EMDR significantly reduced dental phobia and avoidance, with effects maintained at twelve months. Triscari et al. (2015) showed that combining CBT with EMDR was as effective as CBT with systematic desensitisation or virtual reality exposure for treating fear of flying.
In panic disorder, Horst et al. (2017) found EMDR to be comparable to CBT on core panic measures when delivered with clear sequencing and target planning. Earlier trials produced more mixed outcomes, likely reflecting differences in how protocols were designed and applied.
For generalised anxiety and social anxiety, the evidence remains early and thin. Small pilot studies and individual case reports suggest EMDR may be useful when trauma plays a clear role, but larger trials are needed.
A key piece of evidence comes from de Voogd and colleagues (2018), who found that goal-directed eye movements — a hallmark of EMDR — can deactivate the amygdala while fear memories are recalled. This suppression engages the brain’s attention networks and reduces the strength of the fear signal, supporting new learning. The greater the deactivation, the less likely fear was to return.
Supporting this, Rousseau et al. (2019) found that people with PTSD who received EMDR showed improved fear extinction learning on fMRI. Before treatment, their core fear circuits — the amygdala, hippocampus, vmPFC — were less able to regulate fear. After EMDR, these circuits re-engaged, and people showed a stronger ability to update fear memories and maintain a sense of safety.
This reinforces the idea that EMDR does not simply reduce symptoms — it supports the brain’s natural ability to learn: this is safe now.
Fear is not only a mental state. It is a pattern rooted in real brain circuits, networks and chemical messengers. Modern neuroscience demonstrates that this pattern can change — and EMDR provides another pathway for doing so.
For some, classic exposure therapy remains the first line. But for those whose fear feels stuck or is anchored in a single trauma, EMDR can complement or support this work. It helps the brain relearn what it once knew: this is safe now.
References
Milad, M. R., & Quirk, G. J. (2014). Fear extinction as a model for translational neuroscience: Ten years of progress. Behaviour Research and Therapy, 62, 66–72. https://doi.org/10.1016/j.brat.2014.08.005
De Jongh, A., Ten Broeke, E., & Renssen, M. R. (1999). Treatment of specific phobias with eye movement desensitization and reprocessing (EMDR): Protocol, empirical status, and conceptual issues. Journal of Anxiety Disorders, 13(1–2), 69–85. https://doi.org/10.1016/S0887-6185(98)00037-7
de Voogd, L. D., Kanen, J. W., Neville, D. A., Roelofs, K., Fernández, G., & Hermans, E. J. (2018). Eye-movement intervention enhances extinction via amygdala deactivation. Journal of Neuroscience, 38(40), 8694–8706. https://doi.org/10.1523/JNEUROSCI.0703-18.2018
Rousseau, P.-F., El Khoury-Malhame, M., Reynaud, E., Boukezzi, S., Zendjidjian, X., Isnard, P., Khalfa, S., Blin, O., & Khalfa, N. (2019). Fear extinction learning improvement in PTSD after EMDR therapy: An fMRI study. European Journal of Psychotraumatology, 10(1), 1568132. https://doi.org/10.1080/20008198.2019.1568132