Vestigial Whisker Muscles in Humans

Japanese anatomists have shown that careful dissection of the upper lip shows vestigial vibrissae (whisker) muscles in a third of humans. You know how your cats whiskers go back if you touch them there or they're just annoyed about something? Those. Apes are strange among mammals for not having vibrissae; in particular rodents are thought to construct their pictures of near-space with their whiskers rather than their eyes, and interestingly vibrissae sensory nerves are afferent trigeminal fibers, many of which pass through the superior colliculus, a midbrain visual structure.

Finite Willpower and The Dual-Self: Behavioral and Imaging Evidence

More evidence that ability to choose delayed gratification (i.e., willpower) is a limited resource. The interesting thing here is the relative activity of the dlPFC. Choosing delayed gratification is associated with activation of a network including the dlPFC, and inactivation is associated with more present-orientation. Demand-avoidance (avoiding tasks which tax willpower) is also associated with low willpower.

Of course the obvious eventual application of this research is to make people behave more rationally by increasing their willpower and therefore the future orientation of the actions they choose. The next step is to understand the mechanism of willpower depletion. Interestingly, in exercise science, there is speculation that what accounts for the latent period between high-impact weight lifting sets is neurotransmitter depletion in the synapse, and restoration on the order of minutes by vesicular transporters. There is also some evidence that neurotransmitter re-uptake inhibitors (specifically SSRIs) can increase the amount of exercise that can be performed until exhaustion (specifically, distance-to-exhaustion in distance runners in my own correspondence). The same thing might be happening in the dlPFC network required for willpower. An initial investigation might be to pharmacologically manipulate neurotransmitter concentration in the synapse in animals models and look at the effect on delay of gratification.

Citation: Kool W, McGuire JT, Wang GJ, Botvinick MM (2013) Neural and Behavioral Evidence for an Intrinsic Cost of Self-Control. PLoS ONE 8(8): e72626. doi:10.1371/journal.pone.0072626

Why Can't We Create APP Knockout Humans?

You will either die from Alzheimers disease, or from something else first. This of course is trivial, but Alzheimers is now the third leading cause of death in the U.S. and it's on track to become the second in the next few decades. In Japan it may already be the second, surpassing heart disease. AD can only be truly diagnosed at autopsy, but the majority of us have detectable plaques in our brains by the time we're in our 70s, whether or not we're showing clinical symptoms. The treatments we have so far merely attempt to slow the damage, and they can't even do that well; we've just learned that the (earlier-stage) oligomers are structurally different from the full plaques, which may be why the molecules we've thrown at the plaques don't interact well.

Thinking speculatively, what happens if we prevent the whole plaque formation problem - which really does seem to be an issue of humans living well past our paleolithic warranty period - by knocking out the amyloid precursor protein altogether in our descendants? Knockout mice have been around for a while; what's their phenotype like? Not great. They demonstrate:

reduced weight
decreased neuromuscular performance
reactive gliosis in the hippocampus & cortex (later in adult life)
reduced synaptic plasticity
loss of synaptic immunoreactivity for:
synapsin
synaptophysin
defects in the corpus callosum

This does not sound like an opportunity for enhancement. Original paper here.

The knockout mice also do much worse in a cerebral ischemia paradigm, related to the reactive gliosis seen in the list. If APP is involved with resistance to or recovery from infarct, this is consistent with the observed increase in Alzheimers and amyloid plaque formation in humans after cerebral infarcts.

Aphasia for Words with Visual Content

Fascinating case of a man who had an infarct in (unsurprisingly) his left occipital lobe, and now can speak fluently with abstract concepts, but not with image-able words. Blogged by Neuroskeptic; here's the original paper.

Looking for Neurological Differences Between Nouns and Verbs

Just ran across this poster presented at the Organizing for Brain Mapping's Annual Meeting in 2004. Sahin, Halgren, Ubert, Dale, Schomer, Wu and Pinker looked at the fMRI and EEG changes associated with a number of language tasks, and one of the questions they asked was whether activation characteristics were different for nouns and verbs. This study did not find that they were.

In my sketch of a neurolinguistic theory, verbs are first order modifiers and are distinct from adjectives in that they mediate properties and relationships between nouns. (In this sense, intransitive verbs are more similar to adjectives than to transitive verbs.) I also postulate that nouns and first order modifiers should have identifiably different neural correlates. I have not yet completed a literature search (obviously, if I'm citing posters from 2004.) However, even if such different neural correlates obtain, then I think it the task design here was not necessarily adequate to capture such differences, because the participants were asked to morphologically modify the nouns and verbs in isolation, rather than in situ, in grammatical relation to each other.

Another interesting experiment would be to give the participants nonsense words and new affixing rules (i.e. not revealing the part of speech of the nonsense word, i.e. ("if the word has a t in it, add -pex to the end, otherwise, add -peg"), and look for any difference relative to neural correlates of morphological tasks done in real words.

Hupa is Not Unique Among Languages in its Use of Verbs

In a sketch of a neurolinguistic theory I posted previously, I mentioned a possible empirical problem with the theory. Specifically, I posit that the basic neurological unit of language is the noun. If this were the necessary structure of language based on human anatomy, a non-noun-based language would falsify the theory. The Wikipedia article on Hupa previously stated:

Morphologically, it is remarkable for having an extremely small number— perhaps less than one hundred— of basic (monomorphemic) nouns, as nearly all nouns in the language are derived from verbs.

I have long been interested in Hupa as a result of this statement. The first question we might ask is whether such a dramatic innovation is restricted to Hupa or in fact appears in some form in other lower or Pacific Athabaskan languages. There is no report of such structures in Upper Umpqua or the Rogue River languages.

Once you read the grammar and vocabulary of Hupa published by P.E. Goddard, 1905, barely half a century after their first contact with Europeans, the answer was clear. The claim about Hupa's use of verbs and paucity of nouns, which is not referenced, is totally inconsistent with Goddard's work. Goddard lists 130 nouns straight away in the first 20 pages. Not all are morphophonemic, but the non-compound morphemes for the obligately affixed nouns seem to all be unique. Furthermore there is discussion of verb nominalization on page 21-23, and while the morphology seems to be more elaborated than in Western Indo-European languages, it's nothing as dramatically novel as this statement, certainly not showing that "nearly all nouns in the language are derived from verbs." In fact Athabaskan languages in general have elaborate verb morphology, though again, they don't replace nouns.

For a time I had thought that Hupa was a real-life example of the fanciful verb-based language of Tlön fantasized by Borges in Tlön, Uqbar, Orbis Tertius. But it's not. It's worth pointing out that there does seem that there are some innovations of Hupa, relative to other Athabaskan languages, but this is to be expected from a language isolated for centuries with close trading relationships with an Algonquian language (Yurok) and a probable isolate (Karuk). Certainly the differences are not so profound.

I subsequently revised the Wikipedia article. In the meantime continue to look for languages that falsify the neurolinguistic sketch. One interesting possibility is that we might find dramatic differences in language based on geography with phylogenetic patterning. That is, is there something different about Andamanese + New Guinean + Australian languages (earliest out of Africa) vs. sub-Saharan African languages vs all other languages? I'm not asking whether there could be differences based on language-descent, which there necessarily will be; I'm asking the far more controversial question of whether they may be genetic innovations that result in different wiring and therefore differences in language structure. So far we have not found differences so profound as to warrant speculating about population-wide differences in the underlying hardware. If we ever do find differences in a language or group of languages as dramatic as the one that had been suggested here, or that Daniel Everett suggested with Piraha (which also appears to collapse under scrutiny), I submit that it might be profitable to look for anatomic and genetic differences. Such diversity of language and neurology would absolutely be a windfall to understanding the physical basis of language and cognition.

As an aside, I have been to the Hoopa Nation in Northern California several times. It's absolutely beautiful country and I highly recommend a visit. Unfortunately the Hupa language is not a living language, although it is being preserved by the efforts of Danny Ammon and others who make their resources available for the rest of us.


Trinity River south of Hoopa, California, by Trinityalpsphoto

Hemineglect and Delusions

Hemineglect is among the more bizarre neurological conditions (which is also to say, devastating to the patient). In brief, the patient ignores one or the other half of space, right or left, up to and including his or her own body. They won't register stimuli on the neglected side and will even ignore their own bodies on that side, sometimes claiming that their limbs aren't their own: if you hold their arm up in front of them and ask them whose arm it is, they'll often insist it's a family member who's hiding nearby. (Yes, really.) A neurologist related to me that these patients will even sometimes request to be moved to a new bed in the hospital because there's someone else laying in bed with them (as in, the neglected half of their own body. Yes, really.) To these patients, a circle has only 180 degrees. The neglected half of space might as well be the fourth dimension.

Needless to say, natural experiments like these cases are a rich substrate for neurophilosophy. One aspect of neglect syndromes that I find interesting is that some of this behavior apparently amounts to a delusion, in the strict sense of a steadfast false belief. Neglect patients will sometimes complain that the hospital isn't feeding them enough, and of course when the nurse or physician comes into the room, they see a plate of food that's exactly half-eaten. So they turn the plate 180 degrees - and the patient grumbles "Good," and continues eating. See the disconnect here? If I were at dinner and said "Wow that green curry was good but I wish there were more," and my dining companion was able to magically produce more curry out of the fourth dimension before my eyes like some kind of a 3D chef visiting Flatland, of course I would be utterly amazed - but I haven't heard of such a reaction in the anecdotal reports I've heard from neurologists so far (I have not yet interacted with a neglect patient).

I'll do my best to put myself in the neglect patient's place again. Most of us believe that we have exactly 2 arms and 2 legs, and would react incredulously if a researcher told us that no, in fact we had four arms and four legs, but we were only using two of each. The researcher says to me "Fine, I can prove it." In an empty room with just her and me, she holds up an arm in front of me that looks just like me other two arms - skin color, size, etc. - and says it's my arm. I can't feel it or move it, and somehow I'm unable to see what it connects to, and it seemed to appear out of thin air (just like the green curry). But having four arms is ridiculous! Yet I trust this researcher; she seems incredibly earnest, she can reproduce this trick any time I ask with no preparation, and as I soon discover, so can anyone else I ask, including people with no possible connection to the researcher. All of them can hold up in front of me one or two arms that look like my own arms.

In such a position, I would be forced to conclude, as bizarre as it seems, that the evidence points to some kind of a perceptual defect on my part. As strange as it is, and as much as I absolutely cannot understand where this arm is coming from or how it connects to me, I eventually have to accept the incredible truth (after many, many trials) that I and everybody else has four arms, and that there's something strange about my perception that keeps me from seeing them. And even if I remain incredulous, certainly I would at least want to know how they were doing this amazing trick. But severe neglect patients not only avoid curiosity about things that could disturb their limited perception of space, they make up impossible stories about where their limb is coming from if it's presented to them. Clearly the deficit that produces their inability to fully represent space is neurological, rather than psychogenic. But isn't this part of the behavior arguably delusional?

Predictable But Still Interesting Resolution to Bilingual Coma Case

I had previously written here about the case of the Croatian girl who supposedly woke from a coma miraculously speaking German. Of course, it turns out she already spoke German before. It's still neurologically interesting that ability in one language would be preserved than the other; Steven Novella covers.

Croatian Girl Wakes Up from Coma Speaking German

This is more dramatic than "foreign accent syndrome", although the story is short, the source suspect, and even without those two de-weighting considerations I would highly doubt it's real. I would put money down that we're going to find one of the following:

1) It's exaggerated, and at most she has some form of foreign accent syndrome.

2) The girl spoke German before she was in a coma.