(Konferencja #PDA, Perth, 11 listopada 2025)
Yulia Furlong - a child and adolescent psychiatrist and neuropsychiatrist working clinically with autistic young people - presented a model of PDA based on the neurobiology of stress and regulation. The talk also included discussion of specific medications and their mechanisms of action, but I am deliberately not repeating drug names or pharmacological details here - this is not about a prescription, but about the architecture of thinking.
”Look beyond the behaviour”
The strongest message of the talk was simple: behaviour is not the whole picture. What is often read as resistance may in fact be the expression of an overloaded nervous system.
The core of the model
- hyperreactivity of the amygdala (the alarm system detects threat faster),
- chronic activation of the HPA axis (a sustained stress response),
- weakened control from the prefrontal cortex (limited access to inhibition and cognitive flexibility).
What does this mean in practice?
Amygdala hyperreactivity works like an overly sensitive smoke detector - the alarm goes off in response to signals that objectively are not dangerous (for example, an ordinary request or demand).
Chronic activation of the HPA axis means the organism functions in a heightened state of stress readiness. The fight/flight system switches on faster and more strongly, and the capacity to regulate stress narrows.
Weakened prefrontal control means that in a state of high arousal, access to executive functions decreases - it becomes harder to inhibit impulses, stay flexible, and think through the situation calmly.
In such a system, even a neutral demand can be read as a threat signal. Avoidant reaction is not a conscious strategy of opposition, but a consequence of excessive activation of stress circuits and limited top-down regulation.
This model describes a dysregulation loop:
stimulus → activation of the threat system (including the amygdala) → increased arousal → weakened prefrontal regulation → avoidance / outburst → secondary stress → reactivation
In this model, increasing pressure (including punishments and consequences) often makes things worse because it acts as another threat cue. Instead of reducing arousal, it intensifies it and further narrows access to regulation. This does not mean giving up boundaries, but taking the person’s regulatory state into account when introducing them.
Trait and state
The talk included a distinction between:
- trait-level vulnerability: a stable physiological vulnerability (for example, persistently elevated reactivity of threat circuits — including the amygdala — and chronic HPA axis activation, as described in reviews of the neurobiology of stress),
- state-dependent dysregulation: an increase in reactivity in specific contexts, observed in neuroimaging studies of threat processing and social unpredictability (stronger amygdala activation and weaker coupling with the prefrontal cortex in moments when a demand appears).
This makes it possible to think simultaneously about biological sensitivity and the role of the environment.
An honest methodological caveat
The studies being invoked are mainly:
- fMRI studies on amygdala reactivity and the salience network in ASD (that is, the system responsible for detecting what is significant or potentially threatening),
- reviews concerning chronic HPA axis activation and limbic changes under stress,
- translational literature in ASD psychopharmacology.
These are not studies on PDA as a separate entity. At present, we do not have an autonomous neuroimaging literature on PDA - there are no large, repeatable fMRI studies analysing PDA as its own category. The data being cited come mainly from studies on ASD, anxiety, and mechanisms of threat response. The model is not evidence of a PDA biomarker, but an attempt to translate existing knowledge about stress and regulation into this particular profile of functioning.
That does not invalidate its value. Instead of asking, “is this resistance?” the model shifts the emphasis toward a different question: what happens in the nervous system when a demand appears?
From control to containment
(that is, holding tension within safe boundaries)
The talk clearly shifted the emphasis from control to containment. If behaviour is understood as the result of an overloaded and overly activated nervous system, the response cannot be more pressure. The response is co-regulation.
Furlong referred to mentalization, meaning the development of a shared understanding of the young person’s internal states. The point is co-regulation, not a fight for control. In this sense, the neurobiological model does not exclude the importance of relationship - it explains its role in regulation.
Pharmacology in this context
Pharmacological support was presented as a logical consequence of this model. Not as an attempt to “treat PDA,” but as a way of lowering the physiological cost of functioning and calming hyperreactive threat circuits. The aim is to widen the window of tolerance and create conditions in which prefrontal regulation can become more effective. Furlong emphasized that pharmacology should support regulation, not modify identity or the person’s traits.
What stays with me
For me, the strongest part was precisely this shift of axis: from control to regulation.
If the starting point is not “how do we force behaviour?” but “how do we lower the activation of the threat system?” then everything changes — including how the environment is designed.
In that sense, regulation is no longer only a reaction to dysregulation. It becomes the design of conditions in which excessive activation is less likely.
Not discipline
Not moralizing
Regulation
Sources and references
Among others: Ariño-Braña et al. (2025), O’Nions et al. (2023), reviews of the neurobiology of stress, and current psychiatric guidelines concerning ASD.