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  • The NDC neurobiological model of infant cry-fuss behaviours: deeper dive for health professionals

NDC neurobiological model: environmental factors which might result in SNS hyperarousal in the first 100 days

Dr Pamela Douglas10th of Jun 202421st of Jul 2024

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Hyperaroused behaviour in the first 100 days

The NDC neurobiological model argues that motor development is primary for healthy development of sensory, social, and cognitive skills, and is facilitated by rich sensory-motor experience, including irregular postural variation.

However, rich sensory-motor experience is most beneficial when the newborn is in a quiet, alert state and able to integrate sensory feedback from primary and secondary generalised movements and other environmental experience.61

Chronic SNS-HPA hyperarousal in very early life, most commonly associated with unsettled infant behavior, but sometimes with hypoaroused behaviors, may disrupt capacity to maintain necessary attention on sensory feedback which supports developmentally appropriate motor and sensory-motor learning tasks, including auditory and visual tasks, joint attention, and motor planning and sequencing.40, 43 These disruptions may further perpetuate chronic SNS-HPA axis hyperarousal in genetically susceptible infants and add to allostatic load as the child continues to struggle with ongoing developmental tasks, until neurodevelopmental challenges emerge.

Hypoaroused behavior in the first 100 days

The Affect Diathesis model proposes that these behaviorally hypoaroused infants also experience chronic SNS-HPA hyperarousal, which is subjected to PNS override.21

In behaviorally hypoaroused babies, affect-driven sensory-motor cues are partially extinguished, either due to biological propensity or early ‘learned helplessness’ or both, resulting in less parental engagement and shortened reciprocity chains.89

These infants may be particularly vulnerable to the developmental impacts of suboptimal environmental stimulation and disrupted parent-infant biobehavioral synchrony.

Suboptimal sensory-motor stimulation

The neurobiological model of infant cry-fuss problems argues that infants in a low sensory environment cry because of unmet needs for sensory-motor enrichment, in a biological bid to optimise development of neural circuitries during a window of critically sensitive neuroplasticity and monoaminergic excitability.31 The human infant’s biological requirement for rich postural variability and rich and complex sensory-motor reciprocity chains for normal motor development has been discussed previously.

A study of infant macaques found that rich social environments in the first week of the macaques’ lives improved gaze-following and social skills at 7 months of age.97

Regulatory difficulties in very early life are typically interpreted, through a linear causative theoretical frame, as an early sign of sensory processing deficit. For example, by 12 months, when neural changes are entrenched, sensory processing and regulatory reactivity are known to predict parent-reported executive function deficits in children later diagnosed with ASD.73, 98

But the neurobiological model of cry-fuss problems argues that infant dysregulation in very early life is less likely to be a sign of pre-existing sensory processing problems, and more likely to be a behavioral biomarker of chronic SNS-HPA hyperarousal resulting from environmental factors, including suboptimal sensory-motor stimulation which predisposes to sensory processing problems, particularly in genetically vulnerable individuals.

Feeding dysregulation

In very early life, ‘feeding problems’ refer to fussing at the breast or bottle, and breast or bottle refusal. Infant feeding problems often result in a cascade of worsening parental anxiety, controlling parental feeding practices, and conditioned infant withdrawal or distress.100 The latter is referred to in the neurobiological model of cry-fuss problems as ‘conditioned SNS-HPA hyperarousal’ with feeds, and may result in temporary re-setting of the HPA axis in the critically sensitive neural networks of very early life.31

Feeding-related signs such as refluxing or back-arching and fussing with the breast or bottle are often inappropriately medicalised, and underlying causes, such as positional instability with breastfeeds or conditioned SNS-HPA hyperarousal with breast or bottle feeds, remain untreated.101 Feeding problems may escalate into a developmental trajectory of dysregulated feeding behavior into childhood.35 In the older child, the term ‘feeding problems’ encompasses a range of concerns, including food selectivity, problematic mealtime behavior, and oromotor challenges, and are most commonly the downstream effect of early life feeding problems. Children with feeding problems may withdraw from or reject their mother’s touch; their mothers touch them less; and shared eye contact is reduced.100

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Biology-culture mismatch in very early life generates environmental factors which increase developmental risk in susceptible infants

A susceptible infant experiences biology-culture mismatch as adversity. Although the human infant is highly adaptive across a wide variety of culturally-determined infantcare practices, a significant gap between cultural practices and evolutionary expectation may result in chronic SNS-HPA hyperarousal in very early life, in addition to other risks.26, 80-87

The NDC model proposes that initial motor and sensory-motor neural lesions or deficits are more likely in susceptible children when environmental factors are mismatched with biological expectations during the critically neuroplastic, injury-sensitive first 100 days post-birth, resulting in chronic SNS-HPA hyperarousal which either triggers or perpetuates multi-directional cascades of atypical development.

The infant has hardwired biological expectations which evolved in our environment of evolutionary adaptedness

In very early life, the infant evolved, in the Homo sapien’s environment of evolutionary adaptedness, to expect

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