Australasian Journal of Natural Medicine Summer 2025 (Members Version) | Page 26

40 – 57 years [ 11, 24 ] and in 22 %– 33 % of those above 60 years [ 11, 25 ]; the sucking reflex, linked to“ frontal lobe disease,” was found in more than 6 % of normal individuals aged 73 – 93 years [ 11, 26 ]. Consequently, there exists contention on the pathogenic importance of these reflexes related to ageing.
1.2 The Development of Brain Function in Infancy and Early Childhood Related to Retained Primitive Reflexes PRs facilitate primary movements, enabling basic engagement with the environment and establishing the foundation for early motor activity [ 27 ]. These movements enable newborns to engage with their environment and stimulate receptors and sensory organs. Increased stimulation and sensory feedback is understood to induce gene expression associated with the formation of brain functional connectivities [ 28 ]. As neurones increase in size, density, and connectivity, propriospinal projections will ultimately inhibit more primitive lower regions of the brain while stimulating the activation and growth of higher rostral areas of the brainstem and cortex [ 29 ]. PRs are ultimately integrated but never eradicated. Ultimately, all reflexes appear to be regulated by the frontal lobe [ 30, 31 ].
The existence of these reflexes is a prevalent characteristic among children with ASD and other neurobehavioral problems [ 20, 32 ]. In the majority of instances, there exists no discernible damage, injury, lesion, or degeneration. We have considered and discovered support for RPRs signifying a maturational delay in brain regions that normally suppress PRs, particularly reflexes interacting with the frontal lobes [ 3 ].
However, frontal lobe maturational delays can be reflected by the RPRs and additional delays in postural reflex development, which could lead to delays of various sensory-motor milestones like crawling and walking [ 33 ]. Maturational delay can also be related to the lack of
Children with autism frequently struggle with executing skillful
movements and exhibit a limited repertoire of gestures
development of executive functions, a hallmark of neurodevelopmental disorders [ 34, 35 ]. The reduction, lack, or absence of environmental factors that typically foster development, growth, and neuroplasticity in higher brain regions generally results in the lack of integration of PRs and the manifestation of postural reflexes [ 33 ]. RPRs may indicate a developmental delay [ 33 ], and asymmetric persistence will signify a maturational delay in the developing brain and may imply, contingent upon the timing, aberrant asymmetrical cortical hemispheric development [ 36, 37 ].
1.3 Bottom-Up Versus Top-Down Regulation and Retained Primitive Reflexes Since the motor cortex is still immature and underdeveloped, there is no volitional motor control present in the neonate. The infant needs to be able to move to survive, and motor activity activates the senses, sending feedback to the brainstem, in turn promoting neuroplasticity [ 38 ]. This promotes growth in higher levels of the brainstem, such as the pons, which, through proprioceptive connections, will descend into the medulla inhibiting PRs from that level [ 38, 39 ]. This will also release more sophisticated PRs, allowing for more complex interaction with the environment and more activation of senses, which will provide feedback and promote neuroplasticity at higher levels, such as the mesencephalon [ 38 ]. This will progress through the brainstem and ultimately into the neocortex, where sensory feedback promotes growth of sensory areas and ultimately the temporal – parietal – occipital cortex [ 38 ], a major association area promoting sensory integration [ 40 ].
Sensory and motor activity feedback will also promote the growth of the frontal and prefrontal cortex [ 41 ], growing out of the motor cortex. The neocortex, especially the prefrontal cortex, projects fibres to the brainstem to achieve“ top-down” control of the nervous system and its bodily functions [ 42 ]. It is also thought that the frontal lobe, through top-down integration, inhibits the PRs [ 19 ]. Later in life, if there is damage, injury, or degeneration of the frontal lobes, one can observe“ frontal release signs” exhibited as the return of PRs such as the Babinski reflex [ 43 ]. We think that if the PRs are not inhibited, they will continue to promote bottom-up interference, prevent maturational completion, and ultimately prevent appropriate topdown regulation [ 2, 3 ]. This can lead to RPRs and a global dysregulation of nervous, immune, endocrine, and autonomic systems [ 44 ].
2. The Effect of Retained Primitive Reflexes on Motor and Cognitive Development in ASD
ASD is presently defined by deficits in social interaction, communication, and behavioural flexibility. ASD is characterised as a neurodevelopmental disorder marked by impairments in language, executive function, social interaction, and emotional regulation
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