There’s a moment in the arc of healing when the world expects celebration but the body isn’t quite ready.

The medications are down.  The lab markers are stabilising.  The child who once sat out is now sprinting across the oval, breath stronger, skin flushed not with cyanosis but with effort.  The pulse is steadier. The HTMA chart no longer screams of loss.

And yet, there is emotional tremor that looks like:  lability; nights of crying; rage without reason; and clinginess after independence.  This is the storm of a nervous system catching up to the biology beneath it.
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This is not regression.  This is a phase rarely (never?) named in clinical texts: the post-threat recalibration of the neurovisceral system.  In a child with pulmonary arterial hypertension (PAH), emotional dysregulation during recovery is not a mistake or mystery. It is the nervous system's echo and the replay of what it stored while the body was in survival.

To understand this, we must look not only at what is improving: oxygenation, cardiac strain, mitochondrial output, but at what remains disrupted in the rhythm between body, brain, and meaning.


The Illusion of Linear Healing

In clinical practice, progress is often measured through what can be seen or charted: lower pulmonary pressures, reduced medication load, increased activity tolerance. On paper, this is recovery.

But children do not heal linearly.  Their nervous systems are developmental fields, not mechanical engines.  When the body begins to move out of a disease state, the brain must renegotiate everything it encoded during illness:  fear, fatigue, breathlessness, restraint.
What looked like emotional stability during illness was often energetic collapse and a form of conservation. The brainstem quieted non-essential expression to preserve life.  The limbic system was suppressed.  The frontal cortex down-regulated ambition and exploration.

Many forms of serious or chronic illness will create a general response or adaption to stress.  The body (in an adult, but perhaps especially, in a child) will have to un-adapt to recover fully.  On a micro level, we have to undo the cell danger response.

Now, with metabolic repair underway, those systems begin to awaken.  What appears as dysregulation may in fact be a delayed emergence.
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The Mineral Map and the Emotional Tide

A child moving out of a survival state, like PAH, can undergo significant shifts in mineral balance.  A well-conducted HTMA can reveal the quiet shifts beneath the visible recovery.

Take zinc and copper, two ions that sit at the fulcrum of emotional expression.  As copper begins to detoxify, which is a common occurrence when oxidative stress abates, there is often a concurrent change in norepinephrine and dopamine levels. These neurotransmitters, long buffered by copper’s excess, now return to baseline.  In that shift, the child may feel foggy, irritable, or overwhelmed.

Zinc, a mineral of restraint and repair, may rise, but as it does, it begins to unlock GABAergic tone.  A child who once appeared numb to the world may suddenly become hyper-aware, reactive, and sensitive.  This is not pathology.  This is awareness, arriving late to the stage.

And then there is calcium, often forming what practitioners call a "calcium shell", which can be a buffering, dampening force that helps us survive overexcitement of the nervous system.  When that shell breaks down during mineral rebalance, it releases emotional tone that was once biologically suppressed.  The child may cry, rage, laugh unpredictably.  The emotions were always there, only now are they metabolically permitted.


The Cortisol-DHEA Rhythm: Between Readiness and Restoration

In children with chronic illness, the hypothalamic-pituitary-adrenal (HPA) axis often shifts into survival mode producing a cortisol curve designed for threat, not growth. As PAH improves and the sympathetic drive quiets, that cortisol output no longer matches the need.

What follows is a lag in adrenal rhythm: cortisol may spike erratically, or dip too soon. DHEA, the hormone of resilience and repair, may remain insufficient.

This hormonal misalignment can result in:

• Sudden mood crashes in the afternoon
• Hypervigilance upon waking
• Emotional flooding after exercise
• Fear-based behaviours despite physical competence

In such states, it is easy to assume behavioural dysfunction.  But it is more accurate to say the child is rehearsing safety in a body that has only just stopped defending itself.


The Brainstem’s Echo: PAG, Amygdala, RVLM

Looking deeper, we follow the nervous system’s map back to the periaqueductal gray (PAG) – a midbrain region that stores the architecture of fear.  In the years or months of breath restriction, the PAG was a sentinel.  It regulated the child's vocal tone, freeze response, and internal autonomic calibration.

Now, with physical threat reduced, the PAG remains on edge, mistaking exertion or novelty for the re-emergence of danger.  The dorsolateral PAG, responsible for sympathetic mobilisation, may still overfire. The ventrolateral PAG, associated with parasympathetic freezing and shutdown, may dominate during social stress or unfamiliar environments.

The amygdala, especially the central nucleus, reinforces this pattern. It remembers breathlessness as panic.  It marks the sound of running or the posture of effort, as a possible threat.  In recovery, these associations remain.  The child reacts, not so much to present risk, but to imprints of past suffocation.

Add to this the rostral ventrolateral medulla (RVLM), which governs sympathetic tone and baroreflex sensitivity.  Even in the absence of pulmonary pressure, the RVLM may still drive elevated heart rates or blood pressure surges in moments of emotional stress.

The child may appear reactive, hot-tempered, or flooded, but beneath this is a neurovisceral circuit that never received the "all-clear."
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Repatterning: The Developmental Rewind

As metabolic energy increases, the brain begins to restore what it postponed. Neurodevelopmental processes begin anew, such as:

• Myelination of limbic-frontal tracts
• Cortical inhibition
• Interoceptive accuracy
• Executive function modulation

This often presents as regression, or more accurately, a reprocessing.  Tantrums, sleep disruptions, heightened attachment, and sensory sensitivity may all become visible as the nervous system runs unfinished circuits.

Parents may ask: "Why is she so emotional now that she's getting better?" The answer is this: "Because now her brain has the energy to feel what it previously had to suppress."

The hippocampus, long dimmed by cortisol and hypoxia, begins to reanimate emotional memory.  The child may revisit moments she never consciously recorded, like the sounds of hospital monitors, the absence of play, the breath she couldn’t catch.  This is not trauma in the classic sense, but a visceral timeline being re-read by a newly lucid brain.


The Mismatch: Physical Readiness, Emotional Fragility

One of the most destabilising dynamics in recovery is the mismatch between external capacity and internal resilience.

As children regain physical strength, expectations (social, familial, educational) rise.  They are told, in subtle and overt ways, “You’re better now. You can do more.”  But emotionally, they are still rebalancing. The external world no longer reflects their inner fragility, and this discrepancy becomes its own stressor.

The child who can now run 100 metres may still panic when asked to speak in class.  The child who no longer needs medication may dissolve into tears when denied a request. These contradictions are not behavioral disorders. They are asynchronous phases of recovery and they are motor, emotional and cognitive systems catching up to one another on different timelines.

There are integrative tools that we can use to support this recalibration metabolically, and it may be worth exploring this in another article? But along side these interventions, what is needed is a new or different or stage-appropriate metric of progress.  This metric is one that allows for emotional expression that isn't seen as a problem, but as a vital phase of healing.


The Heart Remembers ... even as the Lungs Heal

The physiology of PAH in children is serious, measurable, and often addressed through pharmacology and possibly, surgery.  

But, there is another story, contributing to both cause and effect the emotional aftermath of survival—the cost of functioning under silent breath, the loss of spontaneous joy, the quiet withdrawal from physical play—remains hidden unless we look.

This emotional dysregulation is not failure. It is not regression. It is the sound of the nervous system relearning how to interpret a body that no longer signals threat.

On one hand we might say the body heals first, then brain follows (but not without replaying the songs it once wrote in silence).  In truth, the body and the brain are co-creating:  both as a cause of PAH, but also during recovery.

Our role is not only to track the blood gases and the oxygen sats.  It is to listen when the child cries after climbing the stairs for the first time in a year.  To witness when frustration replaces fatigue.  To honour the noise that comes when the body is no longer muted by disease.

This is healing; and a return to life.

Be well.


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In the quiet pulse between heart and breath, a child’s body keeps its rhythm. But in pulmonary arterial hypertension (PAH), this rhythm becomes erratic, strained, and  dictated by resistance rather than flow.  The vascular system, supposed to open and yield to the breath, stiffens.  In this tension, the brain listens, adapts, and sometimes misfires.

Pulmonary arterial hypertension is not just a pulmonary disease.  It is a systemic series of neurovisceral events.  Every narrowed arteriole reverberates upstream into the brainstem and beyond; as it does from the central nervous system back down to the pulmonary vessels.  Every falter in oxygen delivery becomes an invitation for cortical reinterpretation, limbic sensitisation, and neuroendocrine recalibration.

And when the afflicted are children who are developing, plastic and energetically formative, the story becomes one of vulnerable adaptation.  Below, I map the specific brain structures that hold the breath of PAH, and trace the loops of feedback between body and brain, rhythm and restraint.


The Fastigial Gate: Cerebellar Vermis and Breath Rhythms

In the cerebellar vermis, specifically in lobules VI to IX, lie regions historically dismissed as purely motoric.  But the posterior vermis, particularly lobules VI–VII, can be seen as the limbic cerebellum, modulating emotional tone and visceral autonomic function. It interfaces with the fastigial nucleus, a deep cerebellar structure whose projections target medullary respiratory and cardiovascular centres.

In PAH, the fastigial output becomes a distorted metronome. Instead of modulating respiratory synchrony, it may over-correct or freeze, leading to breath-holding, shallow breathing, or erratic ventilatory drive.  Children may present with poor posture, vestibular instability, or even emotional lability tightly tethered to respiratory states.

The nodulus and uvula (lobules VIII–IX) govern vestibulo-autonomic integration. This means they help the child interpret how movement affects internal state.  In PAH, where upright posture can provoke dyspnoea or near-syncope, these lobules may become overloaded with conflicting signals. The body says rise; the breath says collapse.


The Amygdaloid Alarm: Fear of Breath, Fear of Being

​The amygdala receives the interoceptive signature of every disrupted breath.  Within it, the central nucleus (CeA) projects to the brainstem’s autonomic nuclei: the nucleus tractus solitarius (NTS), the periaqueductal gray (PAG), and the rostral ventrolateral medulla (RVLM).  In a sense, it does not interpret breath, it feels it.

In PAH, where dyspnoea can be subtle but constant, this nucleus becomes sensitised. Breath becomes an emotionally charged signal.  Minor exertion becomes fear-laced.  The basolateral amygdala (BLA), which modulates emotional learning and memory, stores this fear.  Over time, the child becomes conditioned to resist activity, resist effort, resist any signal that even remotely recalls the panic of breathlessness.

The amygdala is not defective in these children, in fact, it is accurate.  It has simply learned that the cost of breath is high.


The Gray Threshold: PAG and the Breath of Panic

The periaqueductal gray (PAG) is the brainstem's gatekeeper between survival behaviors and autonomic expression. Divided into functional columns, it governs nuanced responses to suffocation, pain, and social withdrawal.  It has its own anatomy of fear.

In PAH:

• The dorsolateral PAG (dlPAG) is overactive, which drives sympathetic discharge, tachycardia, and the readiness to flee (though there is nowhere to run).
• The ventrolateral PAG (vlPAG), which governs passive coping and parasympathetic freeze, becomes the site of learned helplessness. Children who appear emotionally shut down, quiet, disassociated during stress may be expressing vlPAG dominance.
• The dorsomedial PAG (dmPAG), involved in respiratory patterning and vocalization, may become distorted, leading to vocal fatigue, speech suppression, or irregular sighing patterns.

Together, these columns orchestrate a subtle symphony of fear, bradycardia, tachypnoea, and vocal modulation in the face of unseen threat. In PAH, the threat is always present ... in the lungs, in the heart, in the effort of rising from rest.


The Baroreflex Nexus: RVLM and the tyranny of tone

​The rostral ventrolateral medulla (RVLM) controls vascular tone and heart rate.  Within it, the C1 adrenergic neurones initiate sympathetic firing.  They are responsive to signals from the NTS, from the amygdala, and from the baroreceptors.  In healthy children, the RVLM allows fluid adaptation to posture, exertion, and breath.

In PAH, the signal from the lungs tells the brain: resistance is high.  So the RVLM responds with persistent sympathetic tone, constricting vessels and increasing afterload. This becomes a cruel feedback loop: high pressure leads to more sympathetic output, which maintains high pressure.

The baroreflex becomes blunted.  Blood pressure becomes erratic.  Heart rate variability (HRV) flattens.  The body loses nuance in its vascular language.


Thalamic Relays: The gate of Sensory Consciousness

The thalamus, once seen only as a passive relay, is an active integrator of interoceptive and emotional signals.  The paraventricular thalamic nucleus (PVN) is especially involved in arousal and stress vigilance.  It receives input from the brainstem and limbic system and forwards it to the cortex.

In PAH, the PVN is over-activated.  The child’s system remains alert, scanning the horizon of internal discomfort. The mediodorsal (MD) nucleus, linking the thalamus with the prefrontal cortex, may struggle to modulate this arousal, leading to poor emotional resilience.

The ventroposterior medial (VPM) nucleus, relaying visceral cranial input, becomes hypersensitive to breath effort, possibly contributing to sensory integration issues, oral aversion, or cranial discomfort during stress.


Memory under Pressure: Hippocampus and the loss of Flow

The hippocampus, especially its ventral (anterior) pole, is highly sensitive to cortisol, inflammation, and hypoxia.  In PAH, chronic stress may impair neurogenesis in the dentate gyrus, reducing the child’s capacity to process and integrate new sensory experiences. The CA1 subfield, particularly oxygen-sensitive, may undergo microstructural damage, impairing memory consolidation and spatial processing.

Functionally, these children may exhibit:
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• Short-term memory delays
• Disorientation under stress
• Fatigue-driven cognitive lapses
• Heightened fear learning

Memory is not just cognition, it is the body’s capacity to anticipate safety also.  In PAH, memory becomes fear-saturated.


Integration and Collapse: The Neurovisceral Web

All of the above structures form part of a neurovisceral integration network: a bidirectional system where body and brain co-regulate homeostasis.  When the lungs harden and resist, when blood pressures rise and oxygen falters, the brain rewrites its map of the body.  It anticipates danger in exertion, breath, effort.  It contracts where it should yield and it excites where it should rest.

The result in paediatric PAH is not merely physical limitation, it is a neurovisceral dysrhythmia, affecting learning, behaviour, mood, and bodily awareness.

These children may present with:
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• Somatic rigidity or hypotonia
• Exercise intolerance, even in the absence of visible fatigue
• Panic attacks with no emotional trigger
• Speech suppression or vocal strain
• Insomnia or hypersomnia
• Executive dysfunction with underlying cardiorespiratory fluctuations

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Toward Re-patterning: What does healing look like?

It looks like supporting all these structures and pathways through treatment.  It is breath work that is safe, not effortful. It looks like limbic regulation through polyvagal co-regulation, parental presence, and non-verbal safety cues. It looks like lowering sympathetic drive with magnesium, BH4 support, and glutathione buffering.

In PAH, where structural medicine is often limited to mechanical and pharmacological intervention, we must not forget the neurodevelopmental imprint of the disease.  Every child with PAH carries a story not only of narrowed vessels but of re-mapped self-awareness, breath consciousness, and emotional threat appraisal.

This map is not permanent and the brain is capable of re-patterning.

But only if we see it.

Be well.