How “Executive Dysfunction” probably works -

First, I hate the term, I hate the definition, I hate how it’s evaluated. And that’s interchangeable with a whole host of verbs, like loathe. Unfortunately, we’re still in Rome and to be an effective Vandal alternatives are required.

Also, this might be a bit chaotic because it’s pulling from concurrent lines of evidence, so please ask questions if something is inconsistent. Will take a couple days most likely to source it up.

“Executive dysfunction”, as currently understood, is an artifact of compression or other mechanical issue of the lateral lobes of the cerebellum and communication along the circuits between these two regions and layers 3-6 of frontal cerebral regions.

The lateral lobes of the cerebellum are the most recently evolved sections of our brain, and the regions which set us apart physiologically from extant species of homo (such as neanderthals). This region processes feedforward information almost exclusively from circuits connected to frontal areas, and binds self motivated behavior to relevant stimuli. It is the region human brains use to modulate and correct behavior toward social or external goals.

Actually, that’s pretty much it – this region does this task, when communication to/from this region is disrupted or processing in the region has issues, you get “executive dysfunction” traits. We can experimentally demonstrate this effect.

The channels over which these signals travel are all dopaminergic, if you look at a map of these channels, all feedforward information is processed through these lobes. These lobes represent “pre-conscious” information, and differentials generated from these regions are eventually bound into awareness depending on the grade of correction/modulation required to achieve goal behavior.

It’s probably not inappropriate to think of the cerebellum altogether as a state comparator for the “self”, and it’s location relative to brainstem salience and central pattern generator circuits is probably a primary driver of vertebrate behavioral presentation and differentiation.

In the context of “ADHD-I/PI” presentations, it’s likely there is a signal strength mismatch along these cerebellar-cerbral circuits, e.g. cerebral paths sending too much information to these cerebellar regions.

The difference between some phenotypes of “autism” and “ADHD” is a break or lesion along the connecting circuits in the case of some “autism”, or signal imbalance in the case of “ADHD”.

Using the current “RNA expression == behavior” conceit, we can express “executive dysfunction” as related to a) Clearance rate of peptide/protein signalling in the relevant regions on an appropriate time scale or b) expression rate of signalling peptides/proteins along these circuits or regions.

How does all of this square up with current evidence? First, the most commonly asserted physiological evidence of “executive dysfunction” is “underdevelopment/activity” in frontal regions. Under this model, these regions may show this morphology due to “under-activation” of the relevant cerebellar-cerebro circuits which connect these two regions. We’ve assumed for a long time that cerebral regions were initiators of activity, instead, these regions are actually downstream of the affected regions.

A couple caveats – because our definition of “executive function” is completely subjective, we don’t really have any way of determining consistent universal mechanics. Lots of overlapping behavior can “appear” similar but be completely different in mechanics. Because observation is such an imprecise tool, we don’t have a way to verify whether any particular behavioral presentation of “executive dysfunction” is consistent with any other. For example, someone who is “forgetful” may be interpreted as experiencing “executive dysfunction” issues to one observer, but not to any other.

There’s a pretty significant chance that I’ve misapplied the cerebellar region due to inconsistent evidence. The flocculonodular lobe, despite it’s evolutionary age, may be just as contributory (or completely contributory) to these observed behavioral effects. It’s admittedly a bit of a blind spot right now.

Also, it’s important to not think of these circuits in terms of “dysfunction” or defect. It’s just as likely some individuals are actually advancing ahead of our evolutionary state, their brains exhibiting more capability in the cerebellum rather than less capability. It’s something I’m trying to spank my wrists with a ruler over, separating from assumptions of “defect” or “flaw” because it’s different, so I’d appreciate feedback when I use that type of language so I can get better at correcting this.

Ref Dump – Will Integrate Later

Brain Stem:
Functional and Neuropathological Evidence for a Role of the Brainstem in Autism

Attentional Disengagement and the Locus Coeruleus – Norepinephrine System in Children With Autism Spectrum Disorder

Segmental abnormalities of superior longitudinal fasciculus microstructure in patients with schizophrenia, bipolar disorder, and attention-deficit/hyperactivity disorder: An automated fiber quantification tractography study

Cerebellar-Cerebral Circuits:
Cerebellar Coordination of Neuronal Communication in Cerebral Cortex

Cerebellar Lobulus Simplex and Crus I Differentially Represent Phase and Phase Difference of Prefrontal Cortical and Hippocampal Oscillations

Causal Evidence for a Role of Cerebellar Lobulus Simplex in Prefrontal-Hippocampal Interaction in Spatial Working Memory Decision-Making

Cerebellum-Cortical Interaction in Spatial Navigation and Its Alteration in Dementias

Prefrontal-cerebellar dynamics during post-success and post-error cognitive controls in major psychiatric disorders (state processor/network)

Linking cerebellar functional gradients to transdiagnostic behavioral dimensions of psychopathology

Evaluation of fronto-cerebellar neurometabolites in youth with ADHD compared to the healthy group and their associations with cognitive and behavioral characteristics: A proton magnetic spectroscopy study

Flocculonodular lobe:
Loss of CRMP1 and CRMP2 results in migration defects of Purkinje cells in the X lobule of the mouse cerebellum (Some Aspergers)