Neurological Correlates

Novelty seeking and, separately, reward dependence, are clearly associated with brain anatomy, as reported online this week in Nature Neuroscience.  Plus, those with high reward dependence probably respond with violent aggression, rather than fear, to angry faces. All this has to do with white matter.

First, the citations:

Cohen, Michael X, Schoene-Bake, Jan-Cristoph, Elger,  Christian E., Weber, Bernd,” Connectivity-based segregation of the human striatum predicts personality characteristics,” Nature Neuroscience, on line, 11.23.08,  DOI: 10.1038/nn.2228

From Cohen et al., Nature Neuroscience, (click to enlarge)

(An fMRI report can be found here, Krebs, R., Schott, B. and E. Düzel, “Personality Traits Differentially Modulate Reward and Novelty Processing in the Human Substantia Nigra/Ventral Tegmental Area,” Biological Psychiatry  On-Line, 10.02.08 DOI: 10.1016/j.biopsych.2008.08.019 )

Passamonti L, Rowe JB, Ewbank M, Hampshire A, Keane J, Calder AJ.,”Connectivity from the ventral anterior cingulate to the amygdala is modulated by appetitive motivation in response to facial signals of aggression.”Neuroimage. 2008 Nov 15;43(3):562-70. Epub 2008 Aug 3 (Neuroimage, sponsored free, via Pubmed Central).

Cohen et al. which may be the first paper that directly connects personality profiling to white matter pathways, demonstrate that the striatum, with all of its dopamine-intensive synapses, is the main thoroughfare as far as white matter tracts determining personality. Sort of like the 110 in downtown LA, you pretty much can’t avoid it when getting from one part of LA county to another. Novelty seekers have the amygdala/hippocampus loop; reward-dependents have more the frontal lobe loop.

In humans, novelty seeking is characterized by impulsivity, exploratory drive and excitability. Like, base jumpers (discussed here). Novelty seekers have strong white matter fiber tracts looping from the hippocampus and amygdala to  the ventral and mesial striatum, particularly in the left hemisphere (relative to the reward-dependents, see below).  The hippocampus is instrumental in learning and memory tasks;  hippocampal volume relates to spatial memory and geography. London taxi drivers have big ones. (Hippocampi, that is).

Perhaps B.A.S.E. jumpers find the thrill of soaring through space irresistible because they have both large hippocampal volumes and strong white matter connections, a spatial-novelty double dose. Perhaps add to that dopamine receptor alleles and other genetic proclivities. Whatever it is, the urge to leap off of high places is so anti-evolutionary, that there must be some good biological reason for it. Same with drug use, which high novelty seekers are also prone to do.

Contrast those who have high reward dependence: enhanced learning from reward signals, persistence in repeating actions associated with rewards, high sociability and reliance on social approval.  No social reward? They won’t perform. High social conformity, low tolerance for “new” (at least, in the absence of an “atta boy!”).  Consider, say, Nazis and conservatives.  Authoritarian in style, these are consumers who go for status symbols, with name brand logos, out of fear of being rejected from the crowd. They are not moved to try a product because of perceived novelty. Cohen et al. demonstrate that in people who are highly reward-dependent, the strongest connection is to the frontal cortex areas of the brain, from the dopamine-laden ventral striatum.

People who are highly reward driven may also be wired with a hair-trigger amygdala. The Passamonti et al. paper points to this group – the “reward driven” group — as responding to anger with anger. Some people, when faced with a rage-a-holic boss (parent, spouse, next-door-neighbor, driver on PCH), run for cover. Other people deck him (or her).  The “reward driven” group views anger as a provocation – an invitation to violence.

The connection from the ventral anterior cingulate cortex (ACC) to the amygdala is associated with aggression, but not the other way (that is, from the amygdala to the ACC).  Moreover, panic disorder and anxiety is associated with stronger ACC white matter signal (here.) Pathological liars are reported to be heavy on the white matter in the frontal lobes.

Looks like reward-dependent people — people who are afraid of disapproval and are the first ones to sit in judgment — may have very efficient “threat signals” – that produce anxiety and zip on over to the frontal lobes to decide what to do. Of course, when anxious, and faced with a threat, the only thing to do is to incite violence in Republican political rally.

Wires crossed, social cues misinterpreted, and boom, aggressive hostility.

Now, most people in my orbit who feel slighted  by a social insult (which is often, and accurately perceived) simply look down their nose, sniff, and say, “I’ve been insulted by better people than you!” and storm out in a huff. Unless there’s money or free food  or someone from whom they could socially or professionally benefit. They do tend to get even later, however, when no one’s looking. After all, decking someone is so declassé. Not at all subtle, and lacking in sufficient ambiguity to deny it all later.

There are others, though, who simply cold cock anyone who looks at them sideways.

My guess is that that’s what all this “I hit her (him) because (s)he disrespected me!” is all about. It’s probably the white matter double strength version both for the reward dependence as well as the socially aggressive.

White matter tracts can be disconnected — having gaps or lesions. Or, they can be connected, but  structurally unsound.  Genes can cause faulty sugar groups limiting signal transmission, autoantibodies can disrupt connections, and myelin can be improperly formed — there are 101 reasons for messed up white matter.  Here’s a paper about Fragile X premutation, and eosinophils in neurons — do increasing trinucleotide repeats, with decreasing FMR1, cause an immflamatory cascade in the brain neurons? I wonder about the melanin in the substantia nigra, because neuromelanin is very electrically conducive. Could white matter have melanin in it? Perhaps that’s the problem in schizophrenia or other conditions where there seems to be excessive, and wrong, white matter wiring.

Not to gloat about being an early adopter of the white matter personality band wagon. . . ok, actually for the sole purpose of gloating. . .  please recall your loyal bloggist having  White Matter Month (last January, à la Macy’s White Flower Days), connecting white matter and personality.  Here are some papers previously discussed:

Haltia, L.T., Viljanen, A., Parkkola, R., Kemppainen, N., Rinne, J.O., Nuutila, P., Kaasinen, V. (2007). Brain White Matter Expansion in Human Obesity and the Recovering Effect of Dieting. Journal of Clinical Endocrinology & Metabolism, 92(8), 3278-3284. DOI: 10.1210/jc.2006-2495

Chang BS, Katzir T, Liu T, Corriveau K, Barzillai M, Apse KA, Bodell A, Hackney D, Alsop D, Wong S, Walsh CA.  A structural basis for reading fluency: white matter defects in a genetic brain malformation. Neurology. 2007 Dec 4;69(23):2146-54. PMID: 18056578[PubMed - indexed for MEDLINE]

Hoeft F, Barnea-Goraly N, Haas BW, Golarai G, Ng D, Mills D, Korenberg J, Bellugi U, Galaburda A, Reiss AL.  More is not always better: increased fractional anisotropy of superior longitudinal fasciculus associated with poor visuospatial abilities in Williams Syndrome. Neurosci. 2007 Oct 31;27(44):11960-5. PMID: 17978036 [PubMed - indexed for MEDLINE]

Marenco S, Siuta MA, Kippenhan JS, Grodofsky S, Chang WL, Kohn P, Mervis CB,Morris CA, Weinberger DR, Meyer-Lindenberg A, Pierpaoli C, Berman KF.Genetic contributions to white matter architecture revealed by diffusion tensor imaging in Williams syndrome. Proc Natl Acad Sci U S A. 2007 Sep 18;104(38):15117-22. Epub 2007 Sep 7. PMID: 17827280 [PubMed - indexed for MEDLINE]

Yoo SY, Jang JH, Shin YW, Kim DJ, Park HJ, Moon WJ, Chung EC, Lee JM, Kim IY,Kim SI, Kwon JS. White matter abnormalities in drug-naïve patients with obsessive-compulsive disorder: a diffusion tensor study before and after citalopram treatment. Acta Psychiatr Scand. 2007 Sep;116(3):211-9. PMID: 17655563 [PubMed - indexed for MEDLINE]

Kimura, A., Sakurai, T., Tanaka, Y., Hozumi, I., Takahashi, K., Takemura, M., Saito, K., Seishima, M., Inuzuka, T. (2008). Proteomic analysis of autoantibodies in neuropsychiatric systemic lupus erythematosus patient with white matter hyperintensities on brain MRI. Lupus, 17(1), 16-20. DOI: 10.1177/0961203307085112

Martino, D., Draganski, B., Cavanna, A., Church, A., Defazio, G., Robertson, M.M., Frackowiak, R.S., Giovannoni, G., Critchley, H.D. (2008). Anti-basal ganglia antibodies and Tourette’s syndrome: A voxel-based morphometry and diffusion tensor imaging study in an adult population. Journal of Neurology, Neurosurgery & Psychiatry DOI: 10.1136/jnnp.2007.136689