An associated neuromotor phenotype on the PMCHS terrain: how the persistence of primitive reflexes and noradrenergic (LC-NE) regulation may be two parallel trajectories rather than a cause-and-effect chain — and how to re-integrate the reflexes.
Why this note? PMCHS survey data (N=423) show a high prevalence of non-integrated primitive reflexes on the PMCHS terrain. The model now treats this persistence as an associated neuromotor phenotype of the terrain — not as its upstream cause. The 2026 systematic review by Provazník et al. confirms associations between persistent primitive reflexes and motor/cognitive differences, but does not demonstrate that they cause locus coeruleus hyperactivation. LC-NE dysregulation and the persistence of primitive reflexes may instead constitute parallel manifestations of the same atypical neurodevelopmental trajectory. This note is addressed to patients, families and clinicians.
Primitive reflexes are automatic motor responses programmed in the fetal brainstem from the 8th week of gestation. They enable newborn survival — protecting airways, initiating feeding, responding to sudden threat — without cortical involvement, as the cortex is not yet functional.
Normally, these reflexes progressively inhibit over the first 6 to 24 months of life, replaced by coordinated voluntary movement. This integration process is active: it depends on movement, babywearing, tummy time, alloparental interactions, and a sufficiently rich sensory environment.
When integration is incomplete — due to gestational stress, traumatic birth, early separation, or lack of stimulation — the reflex remains active below conscious awareness, creating permanent neurological tension and autonomic nervous system hypervigilance.
Sensory hypersensitivity, hypervigilance, chronic anxiety, thoracic protective posture (shoulders forward,"pretzel"), exaggerated startle response.
Mechanistic hypothesis: on a terrain where LC-NE regulation is already disrupted, this reflex may be expressed with increased amplitude and, via β-adrenergic receptors, contribute to lowering the mast cell degranulation threshold. Correlation observed with the histaminergic phenotype — causal link not established.
Hypersensitivity to touch on back/flanks, restlessness, concentration difficulties, persistent enuresis, intolerance of tight clothing.
Mechanistic hypothesis: chronic mechanical stimulation of the paravertebral area may activate local cutaneous mast cells, contributing to dermographism and contact urticaria.
Lateralisation difficulties, dyslexia, eye-hand coordination problems, chronic cervical tension, asymmetric head posture.
Mechanistic hypothesis: chronic suboccipital muscle tension may compress vagal afferents and reduce vagal tone — a context potentially favorable to mast cell degranulation, not demonstrated in humans on this specific point.
Difficulties with prolonged sitting posture, attention problems, tension between upper and lower limbs, difficulty crawling.
Mechanistic hypothesis: axial muscle tone dysregulation may be accompanied by chronic low-grade sympathetic activation, a context potentially favorable to the maintenance of mast cell reactivity.
Poor balance and proprioception, postural hypo- or hypertonicity, spatial difficulties, rapid postural fatigue.
Vertigo syndrome: permanent conflict between unreconciled vestibular, proprioceptive and visual signals → postural vertigo, intolerance of crowds and strobe lighting, dizziness on head rotation.
Motion sickness: inability to synchronise what the eyes see, what the vestibule feels and what the muscles report → persistent motion sickness at any age, intolerance of swings from childhood. On PMCHS terrain, histamine amplifies the central vestibular response — explaining the partial efficacy of H1 antihistamines (dimenhydrinate, meclizine) on these symptoms.
Mechanistic hypothesis: vestibular integration disruption may be associated with HPA axis dysregulation and, via NR3C1 hypermethylation, a lowered mast cell threshold — chain not demonstrated as a whole. Proposed vestibulo-histaminic loop: central vestibular histamine may activate mast cells of the inner ear, amplifying vertigo and motion sickness in turn — hypothesis to be tested.
Chronic hand and forearm tension, handwriting difficulties, palm tactile hypersensitivity, involuntary grasping gestures under stress.
Mechanistic hypothesis: chronic peripheral muscle tension may, via sympathetic activation and the release of neuropeptides (substance P), favor local neurogenic mast cell degranulation.
Bruxism (nocturnal teeth clenching/grinding), chronic masseter and temporal muscle tension, TMJ dysfunction (temporomandibular joint), involuntary mouth opening during manual effort (writing, cutting), jaw tics under stress.
Mechanistic hypothesis: the palm-jaw neurological connection may remain active — chronic hand tension potentially favoring nocturnal bruxism and, via substance P released by TMJ mechanical tension, local mast cell degranulation of the oral mucosa. Candidate mechanism, potentially amplified on the PMCHS terrain by the systemic mast cell hyperreactivity already present.
The industrialisation of birth and early childhood has systematically reduced the conditions that enabled natural primitive reflex integration. Several factors converge:
Maternal gestational stress — a chronically stressed mother produces elevated placental CRH and glucocorticoids that calibrate the fetal brainstem toward permanent hypervigilance, lowering the activation thresholds of survival reflexes.
Medicalised births — caesareans, forceps, vacuum extractions, mother-infant separation in the delivery room — deprive the newborn of the vestibular and proprioceptive stimulation of passage through the birth canal, the first sensory experience initiating TLR integration.
Lack of tummy time, insufficient babywearing, early pushchairs — less vestibular and proprioceptive stimulation → Moro, TLR, ATNR not challenged → not integrated.
Screens from early age — passive visual stimulation without associated body movement → substitution of proprioception by vision → incomplete cross-lateral integration.
Non-integrated primitive reflexes do not disappear — they remain latent in the brainstem, inhibited by the prefrontal cortex. During acute stress, trauma or prolonged exhaustion, the prefrontal cortex temporarily loses its inhibitory capacity and archaic patterns re-emerge.
Observable signs in adults: thoracic protective posture (shoulders forward, kyphosis) in stress situations, exaggerated startle to sudden sounds, intolerance of textures or bright lights, difficulty sitting still, chronic cervical tension, diffuse anxiety without identifiable cause.
This is not a lack of willpower or a primary psychological problem. It is an automatic neurobiological response of a nervous system whose survival reflexes were never fully integrated — amplified by the PMCHS terrain that maintains the locus coeruleus in a state of permanent alert.
The locus coeruleus (LC), the brain's principal noradrenergic nucleus, modulates the amplitude and expression of sensorimotor and defensive responses according to alertness state and context — it is not a "control tower" deciding on danger, nor a simple relay activated by non-integrated reflexes. The currently adopted sequence is as follows:
What the science shows (established): the LC's noradrenergic system modulates the amplitude of sensorimotor responses according to environmental context (Witts et al., Curr Biol. 2023). The LC also participates in integrating sensory information, threat memory, and emotional state to adapt behavioral responses, and can temporarily generalize defensive responses to unconditioned stimuli (Duan et al., PLOS Biology 2026). LC-amygdala-prefrontal interactions in fear responses and their extinction are also documented: LC activation can strengthen basolateral amygdala responses, decrease prefrontal activity, and disrupt fear extinction.
The variable the model was missing: it is not only the activation threshold that varies, but also the defensive program selected. Depending on the appraisal of threat and controllability: threat + possibility of action → mobilization; known social threat → possible intense defensive reaction; extreme threat + low controllability → possible immobilization. Tonic immobility during certain physical assaults is well documented and constitutes a genuine biological defense response, not an absence of response.
Primitive reflexes and LC-NE — two parallel trajectories, not a causal chain: the persistence of primitive reflexes is associated with motor and cognitive differences (Provazník et al., 2026 systematic review), but the current literature does not demonstrate that it causes LC hyperactivation — nor the reverse. On the PMCHS terrain, LC-NE dysregulation and the persistence of primitive reflexes may constitute parallel manifestations of the same atypical neurodevelopmental trajectory, rather than one causing the other. Dysregulation of the LC-NE system can modify the functional expression of reflex responses without necessarily being the origin of their developmental persistence.
The role of synaptic pruning, reconsidered: the processes of synaptic maturation, myelination, and circuit refinement (including pruning) remain candidate neurodevelopmental mechanisms that may contribute to the neuromotor trajectory. Their specific involvement in the persistence of primitive reflexes observed on the PMCHS terrain remains to be demonstrated — the earlier direct arrow "mast cells → excessive pruning → non-integrated reflexes" is no longer retained by the model.
These exercises are adapted from the INPP (Institute for Neuro-Physiological Psychology) method developed by Sally Goddard Blythe, and from neuromotor protocols documented in the literature. They can be done at home, require no equipment, and can be practised by both adults and children.
General instruction: 5 to 10 minutes per day, mindfully, without television or screens. Daily regularity matters more than session length. For severe cases (diagnosed ADHD, ASD, EDS), follow-up with a professional trained in neuromotor integration is recommended.
Note for clinicians: assessment of residual primitive reflexes in adults is a specialised skill. Professions trained in this assessment include INPP therapists, certain neuromotor physiotherapists, developmental paediatricians, and occupational therapists specialising in sensory integration. The PMCHS assessment should systematically include screening for Moro, ATNR and TLR reflexes.
References: Goddard Blythe SA. Assessing Neuromotor Readiness for Learning. Wiley-Blackwell, 2012 · Provazník A et al., systematic review, Acta Psychol. 2026 (reflex/locomotion-cognition associations, without causal demonstration) · Witts EC et al. Curr Biol. 2023, DOI: 10.1016/j.cub.2023.08.085 · Duan H et al. PLOS Biology 2026 (LC integration of sensory information/threat/emotional state) · Berridge CW & Waterhouse BD. Brain Res Rev. 2003 · literature on tonic immobility as a documented biological defense response.