Hypothesis, Counterhypothesis.

This post is going to be pretty nifty. Really.

Actually, if you're looking for comic relief or an argument for the origins of life, you're looking in the wrong place. I just want to put forth a hypothesis founded upon well-understood empirical evidence that I have already touched on in The Torture of BPD blog.

Specifically, why is it the case that hyperamygdalar activity in response to emotionally salient stimuli would occur, if the amygdala happens to be smaller in size? This seems counterintuitive on the surface, but when one relates it to the interconnections of the amygdala, especially the prefrontal cortex, it seems to make a bit more sense. In cases of Borderline Personality disorder, the amygdala & pre-frontal cortex are diminished in size in comparison to people without BPD. With that said:

1. It stands to reason that given the interconnectivity and modulatory effect of the Prefrontal Cortex with/on the amygdala, a reduction in size of both is likely to reduce the synaptic connections and receptor cells. Thus, the ability of the PFC to successfully negate a more sensory emotional reaction to stimuli in the amygdala would be largely curtailed.

2. Quantitative change, bringing about quantitative change. This is a bit of a broad hypothesis that isn't inconsistent with hypothesis 1. at all, and is predicated on some of the tenets put forth by Gary Lynch and Richard Granger in Big Brains: The Origins and Future of Human Intelligence. Evidence suggests to Lynch & Granger that despite differences in the per capita brain size between primates, proportional sizes of the neocortex, brain stem, and pretty much all areas of the brain relative to the overall brain size follow a linear trend. This is to say that our neocortex relative to the size of our brain overall will be proportionally similar to a Chimpanzee's neocortex relative to its overall brain size. They further argue that only true difference between our brain and other primates' brains is simply quantitative differences; there is very little in the way of genuinely unique areas or types of cells in the human brain. If it is the case that all of this is true, then let's extrapolate the principle that Quantitative changes bring about Qualitative changes:

We'll say theoretically that the Prefrontal Cortex is 400 cubic centimeters, and the amygdala is maybe 50 cubic centimeters (nowhere near accurate). This means there is a 350 cubic centimeter difference at a 7:1 ratio.

If they both experience similar proportional changes due to environmental selection or epigenetic stress, in which the prefrontal cortex and amygdala are both decreased in size by 5%, then the sizes would be PFC: 332.5 cubic centimeters to Amygdala: 47.5 centimeters, a difference of 285 cubic centimeters.

Quantative differences between the two brains would be 350 to 285 cubic centimeters, despite having a similar proportion. If there are quantitative changes that bring about qualitative changes with respect to PFC modulation of emotional activity in the amygdala, then perhaps this explains why the amygdala in the second brain is much more difficult to moderate.

3. Both of the above, synergistically producing Hyperamygdalar activity to noxious stimuli.


Perhaps my math is oversimplified. Perhaps the bit about linear predictability of specific brain regions relative to overall brain size is unnecessary, given the principle of quantitative-qualitative differences. Feel free to let me know if that is the case.