October 28, 2020
Having had several years of training regarding the architecture and function of the brain, although much about neuroscience remains obscure to us, as I understand it, experiential, neurobiological and neuropharmacological factors often force marked variations in the development of brain wiring, or neuroanatomy — changes that while they may have a profound affect upon thought, emotion and behavior, are usually not apparent from casual observation of individuals so afflicted.
For example, there are but subtle external physical signs, visible to physicians, of fetal alcohol syndrome. The condition is produced by heavy use of alcohol by the mother during pregnancy. Its victims’ ears are set slightly lower, their eyes set slightly further apart, and the philtrum of the upper lip is flattened. However, what is more startling is that in victims of severe fetal alcohol syndrome, due to interference with the normal developmental migration of brain cells, many of the brain’s midline structures are underdeveloped or absent, and about ten percent of cases, the largest single bundle of brain wires, the corpus callosum, a bundle of axons with an average cross section of about two square inches and connecting the entire left and right cerebral hemispheres, is entirely absent. Thought it may affect bimanual coordination, planning, decision-making and abstract thought, this enormously important defect is usually not obvious through appearances, and may remain undiscovered unless, for some reason or other, there happens to be a Magnetic Resonant Image test, (MRI) performed during life or an autopsy performed after death.
Similarly, in a number of other conditions, there are very substantial individual differences in brain wiring that are not apparent unless revealed by extensive specialized testing during life or at autopsy after death.
The brain is organized into clusters of brain cells that relate to various general functions. This functional organization of the adult brain’s billion cells, occurs between conception and the first couple of years after birth, by the migrations of groups of cells from one place in the brain to another. As the cells migrate, they drag a long, myelin-insulated connecting wire (axon) with them from their place of origin, and form other, usually multiple, connections where they end up. At birth there are about two billion such cells, each connected in this way to many others.
Brain development is markedly influenced by relationships in the early months of life, and as someone noted, by the learning of language, through which ideas are not only expressed, but on the basis of which abstract ideas may actually be formed. All of these things influence the locations to which cells migrate, what interconnections are formed and strengthened by use, and which half of the cells and their possible connections will be atrophy and be lost through disuse.
By about the age of twenty, about 100 billion of the original 200 billion cells and connections have been pruned away, leaving those functions and circuits that the organism has found useful and necessary for living as a human being.
Since the architecture and function of the brain have depended for development upon the learning of language, music and our attachments to other humans, etc., all of which will have varied from culture to culture, the proposition that all humans, all cultures, all races, would give identical results to a complex process of testing of brain function, seems far less likely to me, despite our egalitarian sense of fairness, than that they would score differently through cultural drift.
The changes to which I refer, by the way, happen in the course of a single life, whereas genetic drift evolves over generations of time. As an example of an important difference between individuals, a significant fraction of the population demonstrably has no empathy towards others. Moreover, those individuals, once formed, have no capacity for developing empathy, lacking the cells and wiring circuits in their brains that make empathy possible.
In one other seemingly unrelated observation there lies a further bit of evidence regarding the conclusion one can draw about the structure of the brain. It has been known for many decades that in a child with amblyopia ex anopsia, so called “lazy eye”, where there is a marked weakness of one of the muscles that directs one of the eyes, the images presented by each eye to Broca’s areas 18 and 19 of the occipital (visual) cortex of the brain, are so completely different, that the brain cannot make fine corrections to superimpose and fuse them into one congruent, binocular image. Therefore the brain selects the image from the eye that is directed straight ahead, and suppresses the other less relevant, less useful image.
The eye surgeon has a dilemma. For various reasons it is better to wait until at least the age of six before subjecting the baby to surgery, but if one allows the brain to suppress the image of the “lazy” eye for six years, the parts of the cortex perceiving the image from that eye will have atrophied, and will never develop even if the eye’s aim is straightened. This evidence suggests that the timing of brain development is crucial, and that some abnormalities in brain architecture can become permanent.
The eye surgeon’s solution in the case of amblyopia ex anopsia is to alternately patch one eye, and then the other, forcing the child to use each unpatched eye in turn and providing timely stimulation to the occipital cortex on both sides of the midline, so that visual perception develops bilaterally.
Thus there is evidence that when there something causes an abnormal development in the cortex in the first few months and years of life, these changes, or defects, can become permanent.
In the case of the dysfunctional prototype attachments to others that we think are the cause of clusters of behaviors we refer to as personality disorders, we suspect that they indicate literal defects in brain wiring, and that those miswirings are effectively unfixable, except possibly by partial patches and work-arounds.
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