Infantile Autism: A Chronic Psychosis Since Infancy due to Synaptic Pruning of the Supplementary Motor Area

Abstract

The rise in infantile autism, learning problems, cognitive decline with age, Alzheimer's, Parkinson's diseases and the SIDS epidemic, has a common cause in the rising dietary deficit in Omega-3 brain-food. This paper suggests that aside from the wider concept of autism spectrum disorders (ASD) and pervasive developmental disorders (PDD), the rise in infantile autism (IA) in the last decade is the effect of deficient brain-food (Omega-3). The consequent delay of development, prolongs the 2nd regressive event in infancy to pruning of the centre in the Medial Frontal Lobe System that connects hippocampus and singulum. With a consequently defective supplementary motor area (SMA), the Delayed Response Function is affected leading to persistent psychosis. Post-pubertal episodic psychoses are associated with acute reduction of excitation, a risk of breakdown of circuitry, insufficient fill-in mechanisms, and silent spots. An acute psychosis occurs if the silent spots compromise SMA. Only two brain areas have continuous neurogenesis, indicating their important functions: the Hippocampus and Olfactory Bulb that belongs to the lateral frontal lobe system essential to survival. Concerned with necessity of action in response to the environment, it relies upon short-term memory and acute feedback mechanisms influenced by emotion and motivation from the external world. In contrast, the medial frontal lobe network is controlled by feed-forward predictive mechanisms related to storage of information The Delayed Response Function is mastered at 7 months, when 2nd event occurs with pruning of axons and dendrites. An abolished or defective delayed response function seriously incapacitates an individual: a defective "social brain" with an inability for conscious action and to communicate, predominates in IA. There is a near lack of speech, despite normal vision and hearing in the minority without marked adversity in pregnancy, at delivery or in infancy. The recent rise in IA despite no rise in adversity signifies a rising deficiency in brain-food. This is suggested by a changing clinical picture: no Mental Retardation in an IA majority. Deficit in olfaction is pathognomonic in schizophrenia since 30 yrs and distinguishes the Asperger syndrome. If brain-food deficiency alone sufficiently prolongs pruning to cause absent activity in SMA in infancy, less mentally retarded IA from other causes might be observed. Deficit in brain-food was evident in the Sudden Infant Death Syndrome: birthweight averaged 200-300g lower than sibs, Omega-3 levels in brainstem were lower than controls. Only 20% SIDS died in first hypoxic episode, suggesting such episodes are more frequent than we imagined. Children with learning-behaviour problems have similarly depressed birthweight. A general deficiency in omega-3 contributes to the lacking reduction in Schizophrenia, despite early puberty predominates. Olfactory bulb is first affected in the Alzheimer's and Parkinson's disease. Cognitive decline with age, hippocampal dysfunctions rises markedly irrespecti...

The immune system and developmental programming of brain and behavior

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Developmental downregulation of LIS1 expression limits axonal extension and allows axon pruning

“…This post-mammillary component of the fornix is almost completely eliminated during the first few postnatal weeks ( Stanfield et al, 1987 ). Remaining improper connections or excessive pruning may result in neuropsychiatric diseases, such as schizophrenia, depression, attention deficit/hyperactivity disorder, and autism ( Liston et al, 2011 ; Rosenthal, 2011 ; Saugstad, 2011 ). It will be of great interest to explore whether regulators of motor proteins and microtubule organization are involved in neuropsychiatric diseases via effects on neural circuit pruning.…”

“…Axon elimination can occur at different levels, involving small-scale pruning of axon terminals or larger-scale removal of entire collaterals ( Vanderhaeghen and Cheng, 2010 ). Improper pruning in humans has been implicated in various disease states such as autism and schizophrenia ( Rosenthal, 2011 ; Saugstad, 2011 ). In both flies and mammals, developmental pruning of entire axon branches occurs within a relatively short period of time ( Nakamura and O'Leary, 1989 ; Watts et al, 2003 ).…”

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