Consciousness as an artifact of brain-to-body bottleneck

Conscious attention, implemented as working memory, is focused on a single or few items at a time. Intrinsically, cognition doesn't need such central focus: our brains are massively parallel. Ideally, the pool of neurons should be allocated to many subjects of interest by something like a market, according to predictive value of these subjects. As it probably happens in unconscious or intuitive cognition.

But the brain evolved to guide a single body, which in most respects can only do one thing at a time. Hence the artifact of central consciousness. Beside disrupting smooth allocation of cognitive resources, this bottleneck obviously favors somatic concerns, which constitute lower forms of human motivation.

Such sequential focus is likely implemented by thalamus, which serves as a central switchboard for the brain. It seems to invoke consciousness by generating higher-frequency brainwaves, especially gamma waves, which bind together areas related to working memory (brief overview: The Missing Moment by Robert Pollack, pp. 46-56, or a far more involved treatment: Rhythms of the Brain by Gyorgy Buzsaki.

My personal opinion is that main function of thalamus is to mediate competition between brain areas, particularly via TRN. From a networking perspective, it’s a lot cheaper to do this in a central body, as opposed to each region or column directly inhibiting all others. In fact, Sherman and Guillery suggest that a thalamus could be viewed as a consolidated “7th layer” of neocortex (“Exploring the Thalamus”).

Primary sensory and motor cortices seem to be overrepresented in thalamus, - pulvinar nuclei alone comprise 40% of it. Better thalamic connectivity of primary cortices should enhance search for relevant associations in other brain areas. This is introspectively plausible: most of working memory is what we currently visualize, vocalize, or actualize. I think we enhance our focus on general concepts in the same fashion: by generating fake experiences of subvocalizing, subvisualizing, and subactualizing.

This is probably mediated by feedback to primary cortices, underutilized during sensory “vacations”.
So, primary cortices are frequently “hijacked” by higher areas to simulate (interactively project) their generalized concepts. Such “primarization” is particularly important for mathematicians, engineers, and scientists, who work on imaginary constructs and often think visually rather than verbally.

However, primary cortices are unnaturally “low” for such subjects. Because “elevation” is wrong, these projections often become false memories, confabulations, hallucinations, - substitution of imagination (feedback) for actual experience (feedforward). This may be a factor in developing schizophrenia, in which imagination seems to get out of control. It is suggestive that default mode network, and specifically left posterior cingulate cortex, were found to be unusually active in schizophrenics.

Such confusion should be more likely in habitually hijacked primary areas, which may become less attached to their respective senses. More general concepts are represented by higher association cortices. The highest area seems to be dorsolateral PFC: developmentally the last to myelinate and the most involved in executive function. Primarization could be mediated by short-cuts to lower levels of cortical hierarchy, such as arcuate fasciculus and spindle neurons, with their far-reaching axons.

Basal ganglia: subcortical modulator of attention.

While thalamus seems to be a relatively neutral mediator of competition for conscious attention, basal ganglia implements conditioning, which actively directs focus. Phasic dopamine in basal ganglia also indicates “reward prediction error”, and variation in sensitivity to dopamine is a risk factor for ADHD.

For example, ADHD is correlated with 7-repeat allele of DRD4, which accelerates reuptake. Even more important might be variation in COMT gene: Met 158 allele, which degrades postsynaptic dopamine 4x slower than Val 158 allele, is associated with better working memory, but slower attention switching. Basically, it enhances top-down or goal-directed attention vs. bottom-up or novelty-oriented attention. ADHD is treated by norepinephrine and dopamine agonists or reuptake inhibitors, such as Bupropion.

This differs between hemispheres: "To advance our understanding of ADHD and medication effects we draw upon the evidence for (1) a neurotransmitter imbalance between norepinephrine and dopamine in attention-deficit hyperactivity disorder and (2) an asymmetric neural control system that links the dopaminergic pathways to left hemispheric processing and links the noradrenergic pathways to right hemispheric processing. It appears that attention-deficit hyperactivity disorder may involve a bi-hemispheric dysfunction characterized by reduced dopaminergic and excessive noradrenergic functioning. In turn, favorable medication effects may be mediated by restoration in neurotransmitter balance and by increased control over the allocation of attentional resources between hemispheres".

On a cellular level, temporal attention span is inversely proportional to the "decay rate" for stimuli propagating from primary into association areas of neocortex. Passive decay is caused by charge dissipation across neuronal membrane and reuptake of excitatory neurotransmitters at the synapses. Such decay promotes relatively novel stimuli. On the other hand, active suppression by neurons that represent competing stimuli, via inhibitory interneurons and neurotransmitters, should promote relatively recurrent or concurrent stimuli. Longer term, slower passive decay would correspond to longer connections and competition among more distant and persistent stimuli.

Other factors affecting stimuli decay rate are axonal straightness and myelination, structural trade-offs within cortical minicolumns and thalamus (see “Cortical Trade-Offs“ post), and so on. A developmental possibility is that high levels of cortisol / low levels of serotonin increase the levels of phasic dopamine, which in turn accelerates dopamine reuptake. ADHD sufferers have fewer dopamine autoreceptors, leading to greater fluctuations in its levels and increased novelty seeking to keep the cortex busy.

The degree of preference for novelty in the immediate environment also depends on recent intensity of value-loaded stimuli, modulated by our subjective sensitivity to the latter. Sensitivity is increased by deprivation (vs addiction) for positive stimuli, and security (vs vulnerability) for the negative ones. Particularly during formative years, attention span can be increased by broad intellectual exposure, if combined with weak visceral pressures and temptations.

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