William Lu

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William Lu is currently a doctoral student of clinical psychology.

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  • April 20, 2012
  • 02:18 PM
  • 99 views

Does abnormal NREM sleep impair declarative memory consolidation?

by William Lu in The Quantum Lobe Chronicles

Finally got to uploading the review paper Robert Goder and I had written recently on sleep and memory. You can download it HERE. Essentially, we describe a possible mechanism by which abnormal NREM sleep processes (i.e. reduced slow-wave sleep and sleep spindles) contribute to declarative memory impairment and concomittant sleep disruption in certain neuropsychiatric disorders including Alzheimer's, schizophrenia, and fibromyalgia. Underneath, I posted what the tentative model looks like (click to enlarge). Would love to hear your thoughts. Fig. 1. During NREM sleep, abnormal thalamocortical structures may be unable to generate sufficient slow oscillations to drive the reactivation of hippocampal memory traces. These same structures may also be unable to facilitate normal spindle activity, preventing efficient declarative memory consolidation due to an absence in cortical plastic changes. Decreases in spindle activity lead to failure in inhibiting sensory information from reaching the neocortex. Thus, the individual is awakened and kept awake by sensory information, consequently experiencing disturbed NREM sleep.Reference:Lu, W., & Göder, R. (2011). Does abnormal non-rapid eye movement sleep impair declarative memory consolidation? Sleep Medicine Reviews DOI: 10.1016/j.smrv.2011.08.001... Read more »

Lu, W., & Göder, R. (2011) Does abnormal non-rapid eye movement sleep impair declarative memory consolidation?. Sleep Medicine Reviews. DOI: 10.1016/j.smrv.2011.08.001  

  • November 17, 2011
  • 03:14 AM
  • 203 views

Not all hippocampal hemispheres are created equal

by William Lu in The Quantum Lobe Chronicles

I got a chance to sit down and read Kohl et al.'s recently published Nature Neuroscience paper titled "Hemisphere-specific optogenetic stimulation reveals left-right asymmetry of hippocampal plasticity". This paper contributes to our advancing knowledge of the asymmetrical brain and further elucidates the true complexity of the hippocampus, a sea horse shaped brain structure important for learning and memory.More specifically, the team found that an area important for encoding and retrieving associated information (CA3) in the left hippocampus produced more long-lasting signal transmission to synapses of an area of the hippocampus important for spatial learning and memory (CA1) compared to CA3 in the right hippocampus of adult mice. Essentially, the left CA3 right CA3 for triggering plasticity in CA1. To make their observations Kohl and colleagues used optogenetics in which genetic and optical methods are combined to control specific events in targeted cells of living tissue. In this case, they injected a virus into either the left or right CA3. This particular virus contained a gene which encoded yellow fluorescent protein and led to selective expression of that protein when found in excitatory cells of the appropriately engineered transgenic mice. They then used a laser light to evoke excitatory postsynaptic potentials in the striatum radiatum, an area of the hippocampus that contains fibers connecting CA3 to CA1."Brainbow" transgenic mouse hippocampus - Tamily WeissmanThe authors explained that the hemispheric asymmetry in plasticity was caused by differential GluN2B gene expression at CA1 synapses targeted by the left and right CA3. They conclude that their result "raises the possibility that the left and right CA3 might be differentially active and hence produce input-specific differences in postsynaptic spines.However, the question still remains. Why the left and not the right?(As an aside, I recommend checking out a free iPhone app called 3D Brain. Description: Use your touch screen to rotate and zoom around 29 interactive structures. Discover how each brain region functions, what happens when it is injured, and how it is involved in mental illness. Each detailed structure comes with information on functions, disorders, brain damage, case studies, and links to modern research)References:Kohl MM, Shipton OA, Deacon RM, Rawlins JN, Deisseroth K, & Paulsen O (2011). Hemisphere-specific optogenetic stimulation reveals left-right asymmetry of hippocampal plasticity. Nature neuroscience, 14 (11), 1413-5 PMID: 21946328... Read more »

Kohl MM, Shipton OA, Deacon RM, Rawlins JN, Deisseroth K, & Paulsen O. (2011) Hemisphere-specific optogenetic stimulation reveals left-right asymmetry of hippocampal plasticity. Nature neuroscience, 14(11), 1413-5. PMID: 21946328  

  • November 13, 2011
  • 10:50 PM
  • 211 views

Can alcoholic parents put their kids at risk for memory problems?

by William Lu in The Quantum Lobe Chronicles

The alcoholic beverage has existed as early as the Neolithic period (cir. 10,000 BC), its use once mandated by The Lord on High in 1,116 BC China (Patrick, 1952). Oh thou holy ethanol, absorbed by the bloodstream, traveling to the brain, and binding to glutamate and GABA receptors, blessing us with the desired effects of slow reaction time, slurred speech, gregariousness, and the ability to sing and dance like a rockstar. However, too much of the bottle and you can find yourself in some serious trouble, including coma, death (more on alcohol poisoning) and the gradual development of a nasty alcohol addiction (check out Korsakoff's syndrome).I'm sure we've all experienced the awful sleep and nasty hang over from a forgettable night on the town. My question is can a history of alcoholism cause sleep and cognitive problems not only for yourself, but for your future offspring as well?                                                     An example of fetal alcohol syndromeRecently, I came across an article by Tarokh and Carskadon (2010) finding that healthy children between ages 9-10 of alcohol abuse/dependent parents had abnormal sleep electroencephalograph activity including reduced delta band and spindle range. Both electrical phenomena are found in non-rapid eye movement (NREM) sleep and are suggested to play 2 important functions; protect sleep from disruption and consolidate declarative memory. The authors believe that the mechanism for the former function may be impaired for these kids. Basically, they'll probably have worse sleep quality compared to their "normal" peers. If this is indeed the case, I don't think that's all that'll be negatively impacted. In my last post I wrote about how abnormal NREM sleep consisting of reduced spindles and slow wave activity can potentially impair declarative memory (i.e. facts, episodes) through an abnormally functioning thalamus; the sensory relay station of the brain. The kids with alcoholic parents are showing a similar kind of dysfunctional NREM sleep pattern (although the authors only measured spectral power in the spindle range and not spindles directly). Thus, it leads me to believe that they would evidence problems with declarative memory consolidation as well (e.g. remembering what they learned from yesterday's history class). Are these poor kids being dealt an unfortunate hand consisting of a gimped memory storage system due to their parents' uncontrollable booze lust? Or is it a matter of genes? Genes/behavior/environment interaction perhaps? A lot more questions than answers it seems.Of course, this just another crazy hypothesis that I've concocted from thin air that obviously needs empirical support. Quick! To the sleep lab for some more EEG and declarative memory tests! Mom, dad...you can leave that six pack with me.References:Tarokh L, & Carskadon MA (2010). Sleep electroencephalogram in children with a parental history of alcohol abuse/dependence. Journal of sleep research, 19 (1 Pt 2), 165-74 PMID: 19735444Lu W, & Göder R (2011). Does abnormal non-rapid eye movement sleep impair declarative memory consolidation? Disturbed thalamic functions in sleep and memory processing. Sleep medicine reviews PMID: 21889375http://www2.potsdam.edu/hansondj/Controversies/1114796842.html... Read more »

Tarokh L, & Carskadon MA. (2010) Sleep electroencephalogram in children with a parental history of alcohol abuse/dependence. Journal of sleep research, 19(1 Pt 2), 165-74. PMID: 19735444  

Lu W, & Göder R. (2011) Does abnormal non-rapid eye movement sleep impair declarative memory consolidation? Disturbed thalamic functions in sleep and memory processing. Sleep medicine reviews. PMID: 21889375  

  • August 7, 2011
  • 09:19 AM
  • 455 views

Why Non-rapid Eye Movement (NREM) sleep is important for memory

by William Lu in The Quantum Lobe Chronicles

So...after 4 months of being MIA I've finally emerged from the deep, dark, and lonely cave of academia to give a brief update on what I've been doing all this time. When I wasn't furiously working on my dissertation related to working memory and aging, I was making final revisions to a theoretical review paper on sleep and memory. I'm happy to announce that after countless hours of lost sleep (irony?) it's finally been accepted for publication! I'll link the article abstract once it's up. For now let's talk about why NREM sleep is important (and why I needed it so badly for the past few months).During the early years of sleep research, NREM sleep was discovered to play a role in the restoration of physiological functions (Siegal, 2005). However, relatively recently it's been established to play an equally important function, that of sleep-dependent memory consolidation. Some may be asking, "what the bleep is NREM sleep?" Here's the technical answer according to the American Academy of Sleep Medicine. It consists of 3 stages (N1, N2, and N3, very original...) N1 consists of low amp electrical activity measured by electroencephalogram (EEG) where slow eye movements take place. During N2, you're unconscious, but easily awoken. Here, we find seemingly weird blips in electrical brain activity known as k-complexes and sleep spindles. Sleep spindles are super important for memory consolidation, as will be discussed later. N3 (or slow wave sleep) consists of delta waves and peak to peak amps 75uV found in frontal lobes, also very important for sleep-dependent memory consolidation. Now how does all of this electrical activity consolidate memory?In the early 1970s Ekstrand and colleagues observed that slow wave sleep was positively correlated with the ability to retain a word pair-associate list, while rapid eye movement (REM) sleep was not. They went on to publish their findings in Science. Memorizing these word pairs depend on declarative memory, a kind of memory that's accessible through conscious recollection including facts and events. Ekstrand and many other subsequent studies firmly established that slow wave sleep was indeed important for declarative memory consolidation (check out Diekelmann and Born, 2010 for a comprehensive review).Another seminal study by Wilson and McNaugton (1994), also published in Science, observed an increased tendency for particular hippocampal place cells that fired during a spatial behavioral task to also fire during subsequent slow wave sleep in rats. This lay the foundation for discovering that memory traces consolidate from short-term to long-term memories by a process involving reactivation of sharp wave-ripples in the hippocampus during sleep.In a more recent and very cool study, Born and colleagues (2007) had human subject learn card pair locations while smelling different odors simultaneously (the top left card paired with the scent of my feet, for example). When the researchers reintroduced those same smells during the subjects' slow wave sleep (my feet in the poor subject's face), memory for the card pair locations (top left card) tied to those smells (my feet) were enhanced at recall the next day. Also, through fMRI they saw reactivation of the hippocampus during slow wave sleep. In an alternative study, they used transcranial magnetic stimulation to essentially boost slow oscillations during NREM sleep, which not only increased slow wave sleep and sleep spindles, but also enhanced declarative memory consolidation. From these findings they developed a model postulating that slow waves originating from the neocortex synced both hippocampal sharp waves and thalamocortical sleep spindles, resulting in primed cortical networks for long-term memory storage. The research team was the first to provide empirical support for a causal role of hippocampal memory reactivation for memory enhancement during sleep.The question I pose in my paper (with the invaluable help of Dr. Robert Göder) is what happens to declarative memory consolidation when slow wave sleep and sleep spindle activity, both taking place during NREM sleep, are disrupted? I've definitely experienced the detrimental effects first hand and hope to soon show you, with the latest research, how abnormal NREM sleep can really mess with memory consolidation. For now, I return to my cave to rest my weary head, praying that I don't become an unfortunate case of ABD (all but dissertation) because of lack of sleep.References:Siegel, J. (2005). Clues to the functions of mammalian sleep Nature, 437 (7063), 1264-1271 DOI: 10.1038/nature04285Iber C, Ancoli-Israel S, Chesson A, Quan SF for the American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events : Rules, Terminology and Technical Specifications, 1st ed. : Wenchester, Minois, American Academy of Sleep Medicine 2007.Diekelmann, S., & Born, J. (2010). The memory function of sleep Nature Reviews Neuroscience DOI: 10.1038/nrn2762Fowler MJ, Sullivan MJ, Ekstrand BR. Sleep and memory. Science 1973;79:302-304. Wilson, M., & McNaughton, B. (1994). Reactivation of hippocampal ensemble memories during sleep Science, 265 (5172), 676-679 DOI: 10.1126/science.8036517Rasch B, Büchel C, Gais S, & Born J (2007). Odor cues during slow-wave sleep prompt declarative memory consolidation. Science (New York, N.Y.), 315 (5817), 1426-9 PMID: 17347444... Read more »

Siegel, J. (2005) Clues to the functions of mammalian sleep. Nature, 437(7063), 1264-1271. DOI: 10.1038/nature04285  

Diekelmann, S., & Born, J. (2010) The memory function of sleep. Nature Reviews Neuroscience. DOI: 10.1038/nrn2762  

Wilson, M., & McNaughton, B. (1994) Reactivation of hippocampal ensemble memories during sleep. Science, 265(5172), 676-679. DOI: 10.1126/science.8036517  

Rasch B, Büchel C, Gais S, & Born J. (2007) Odor cues during slow-wave sleep prompt declarative memory consolidation. Science (New York, N.Y.), 315(5817), 1426-9. PMID: 17347444  

Marshall, L., Helgadóttir, H., Mölle, M., & Born, J. (2006) Boosting slow oscillations during sleep potentiates memory. Nature, 444(7119), 610-613. DOI: 10.1038/nature05278  

  • April 17, 2011
  • 12:38 AM
  • 551 views

How a stinky chemical offers neuroprotection for a seizing brain

by William Lu in The Quantum Lobe Chronicles

What did Socrates, Plato, Hercules, and Ajax have in common? Other than greatness, they were also epileptics according to the 17th century French physician, Jean Taxil.An epileptic seizure consists of abnormal excessive or synchronous neuronal activity in the brain which can lead to convulsions, loss of awareness, full body slump, or even the experience of deja vu. Unprovoked seizures are typically related to epilepsy and other seizure related disorders while unprovoked seizures have multiple contributing factors including, but not limited to traumatic brain injury, kidney failure, sleep deprivation, brain lesions, metabolic disturbances, stroke, and tricyclic antidepressants. Sometimes seizures are just idiopathic (unknown cause).Is epilepsy really the "sacred disease" Hippocrates had once thought it was? Not really. Serious complications may arise such as difficulty learning, aspiration pneumonia, injury from falls, and even permanent brain damage (I recommend the book The Spirit Catches You and You Fall Down).A recent study by Bell and colleagues published in the latest Nature Neuroscience investigated whether polyamines, organic compounds having two or more primary amino groups, acted as a neuroprotective factor against subsequent seizures. Past studies have shown that polyamines increase after a seizure, but their regulatory role in epileptic seizures remain a mystery. The authors exposed Xenopus laevis tadpoles (aka African clawed tadpoles) to pentylenetetrazol (PTZ), a well known convulsant, to see if polyamines would regulate neural excitability following a seizure. After a priming exposure, they again exposed the poor tadpoles to PTZ 4 hours later. What they found was quite remarkable. Compared to a control group (tadpoles that did not receive a priming exposure to PTZ), the seizure onset in the primed group during the second exposure was delayed a whopping 25%. Something was protecting them from having a subsequent seizure, but what was it? The authors found that a stinky type of polyamine known as prutescine (more like "putrid-scine" ::rimshot::) was involved in decreasing seizure susceptibility. They suggest that when prutescine is released after the first seizure, it converts into GABA, an inhibitory neurotransmitter. The extracellular GABA then activates presynaptic GABA receptors on inhibitory interneurons, temporarily decreasing inhibitory drive and increasing seizure susceptibility (a kindling effect). The inhibitory neurons respond to this activation with a compensatory release of more GABA. When the prutescine and GABA levels return back to normal, the inhibitory frequency stays elevated. When another seizure occurs, the animal is well protected. The findings of this study shed further light on the development of the seizing brain and bring the field closer to developing preventative measures for both short-term and long-term seizure susceptibility. Prutescine may indeed be the golden ticket to improving resiliency of developing animals to seizures. Now all we need to figure out is what to do with that stench. Bell MR, Belarde JA, Johnson HF, & Aizenman CD (2011). A neuroprotective role for polyamines in a Xenopus tadpole model of epilepsy. Nature neuroscience, 14 (4), 505-12 PMID: 21378970... Read more »

Bell MR, Belarde JA, Johnson HF, & Aizenman CD. (2011) A neuroprotective role for polyamines in a Xenopus tadpole model of epilepsy. Nature neuroscience, 14(4), 505-12. PMID: 21378970  

  • April 9, 2011
  • 12:11 PM
  • 610 views

Disorder promotes stereotyping

by William Lu in The Quantum Lobe Chronicles

Xenophobic exclusion has been ubiquitous throughout history. However, the explanation of such a phenomenon has been little understood. Interesting research conducted by Stapel and Lindenberg published in the latest Science has brought us closer to some answers. They found that people who are in a disordered environment (e.g. unclean subway station) exhibit greater discriminatory behavior (e.g. decision to sit further away from a black person compared to a white person). The authors suggest that when the brain faces disorder there is an equal need for order. One way to reach order is through stereotyping. It's the brain's way of making sense of the world. Too bad it doesn't work all the time.Stapel DA, & Lindenberg S (2011). Coping with chaos: how disordered contexts promote stereotyping and discrimination. Science (New York, N.Y.), 332 (6026), 251-3 PMID: 21474762... Read more »

Stapel DA, & Lindenberg S. (2011) Coping with chaos: how disordered contexts promote stereotyping and discrimination. Science (New York, N.Y.), 332(6026), 251-3. PMID: 21474762  

  • October 6, 2010
  • 05:31 PM
  • 477 views

Cross-cultural personality change throughout the lifespan: a result of brain development?

by William Lu in The Quantum Lobe Chronicles

It's not difficult to readily imagine the rebellious angst ridden teenager or the wise old man of very few words. McCrae, et al.’s 1999 research findings seem to have validated these prototypical depictions. They found that across various cultures (Germany, Italy, Portugal, Croatia, and South Korea) there were higher levels of neuroticism in young adults and decreases in extraversion and openness in older adults. Older adults also showed increase rates of agreeableness and conscientiousness. But why? The authors offer up some explanations such as a combination of maturational, cultural, cohort and sampling effects. They also briefly mention genetic and evolutionary influences and this is what I am particularly interested in. We know that genes are influenced by evolutionary processes and that brain development is affected by gene expression. I suggest that brain development provides the perfect explanatory mechanism for such changes in personality traits throughout the life span.

Generally, the authors found an increased level of neuroticism in the 18-21 year old range, a sensitive time wrought with angst and rebellion. This makes sense because frontal lobes, responsible for executive functioning and emotional control, are still in development (NIMH). Neurotics tend to respond poorly to environmental stress, interpret ordinary situations as threatening, and are more impulsive. These personality characteristics map well to frontal lobes that have not been fully developed.


The Big Five Personality Traits

The authors also found that adults 50+ years old evidenced lower extraversion and openness and higher agreeableness and conscientiousness. Studies have shown that extraverts demonstrate increased sensitivity to reward signals and novelty seeking, suggesting that the dopaminergic system is involved (Cohen et al., 2005; Golimbet et. al, 2007). One study found that striatal D2 receptor availability predicted socially desirable responding (Reeves et al., 2007). Additionally, age-related decline in dopamine D2 receptors is evident (Volkow et al, 1996, 2000). Taken together these studies may offer up one piece of the explanatory puzzle as to why extraversion declines in older adults.

Openness to experience has been suggested to map well with the orbitofrontal cortex, an area known for decision-making, reward processing and emotional processing (Sutin et al., 2009 ). An absence of the posterior orbital sulcus (a part of the orbitofrontal cortex) in healthy subjects has been positively associated with openness to experience (Roppongi et al., 2010). Interestingly, older adults evidence tissue loss in the orbitofrontal cortex, perhaps explaining the decrease in openness to experience found later in life (Resnick, Lamar, & Driscoll, 2007).


Orbitofrontal Cortex

In terms of agreeablness, one study found that smaller right orbitofrontal lobe volume was associated with low agreeableness while smaller left orbitofrontal volume was correlated with high agreeableness in patients with frontaltemporal dementia (Rankin et al., 2004). Perhaps in normal aging the left orbitofrontal cortex, in particular, gradually loses tissue over time.

Regarding conscientiousness, Jackson, Belota, and Head (2009) discovered that those who were rated as higher on this personality trait showed larger regional volumes in prefrontal and mediotemporal regions and less decline with advanced aging.

The influence of brain development on cross-cultural personality changes in the context of aging, particularly the orbitofrontal cortex, is well worth considering. However, one should not forget about all the other important pieces of the puzzle (i.e. maturational, cultural, cohort and sampling effects). Needless to say, further research needs to be done in order to shed light on this intriguing link between personality and the aging brain.

References:

McCrae RR, Costa PT Jr, Pedroso de Lima M, Simões A, Ostendorf F, Angleitner A, Marusić I, Bratko D, Caprara GV, Barbaranelli C, Chae JH, & Piedmont RL (1999). Age differences in personality across the adult life span: parallels in five cultures. Developmental psychology, 35 (2), 466-77 PMID: 10082017

Cohen MX, Young J, Baek JM, Kessler C, & Ranganath C (2005). Individual differences in extraversion and dopamine genetics predict neural reward responses. Brain research. Cognitive brain research, 25 (3), 851-61 PMID: 16289773

Golimbet, V., Alfimova, M., Gritsenko, I., & Ebstein, R. (2007). Relationship between dopamine system genes and extraversion and novelty seeking Neuroscience and Behavioral Physiology, 37 (6), 601-606 DOI: 10.1007/s11055-007-0058-8

Resnick SM, Lamar M, & Driscoll I (2007). Vulnerability of the orbitofrontal cortex to age-associated structural and functional brain changes. Annals of the New York Academy of Sciences, 1121, 562-75 PMID: 17846159

Reeves SJ, Mehta MA, Montgomery AJ, Amiras D, Egerton A, Howard RJ, & Grasby PM (2007). Striatal dopamine (D2) receptor availability predicts socially desirable responding. NeuroImage, 34 (4), 1782-9 PMID: 17188897

Volkow ND, Wang GJ, Fowler JS, Logan J, Gatley SJ, MacGregor RR, Schlyer DJ, Hitzemann R, & Wolf AP (1996). Measuring age-related changes in dopamine D2 receptors with 11C-raclopride and 18F-N-methylspiroperidol. Psychiatry research, 67 (1), 11-6 PMID: 8797238

Sutin AR, Beason-Held LL, Resnick SM, & Costa PT (2009). Sex differences in resting-state neural correlates of openness to experience among older adults. Cerebral cortex (New York, N.Y. : 1991), 19 (12), 2797-802 PMID: 19366871

Roppongi T, Nakamura M, Asami T, Hayano F, Otsuka T, Uehara K, Fujiwara A, Saeki T, Hayasaka S, Yoshida T, Shimizu R, Inoue T, & Hirayasu Y (2010). Posterior orbitofrontal sulcogyral pattern associated with orbitofrontal cortex volume reduction and anxiety trait in panic disorder. Psychiatry and clinical neurosciences, 64 (3), 318-26 PMID: 20602731

Rankin KP, Rosen HJ, Kramer JH, Schauer GF, Weiner MW, Schuff N, & Miller BL (2004). Right and left medial orbitofrontal volumes show an opposite relationship to agreeableness in FTD. Dementia and geriatric cognitive disorders, 17 (4), 328-32 PMID: 15178947

Jackson J, Balota DA, & Head D (2009). Exploring the relationship between personality and regional brain volume in healthy aging. Neurobiology of aging PMID: 20036035

http://www.nimh.nih.gov/health/publications/teenage-brain-a-work-in-progress-fact-sheet/index.shtml... Read more »

Cohen MX, Young J, Baek JM, Kessler C, & Ranganath C. (2005) Individual differences in extraversion and dopamine genetics predict neural reward responses. Brain research. Cognitive brain research, 25(3), 851-61. PMID: 16289773  

Golimbet, V., Alfimova, M., Gritsenko, I., & Ebstein, R. (2007) Relationship between dopamine system genes and extraversion and novelty seeking. Neuroscience and Behavioral Physiology, 37(6), 601-606. DOI: 10.1007/s11055-007-0058-8  

Resnick SM, Lamar M, & Driscoll I. (2007) Vulnerability of the orbitofrontal cortex to age-associated structural and functional brain changes. Annals of the New York Academy of Sciences, 562-75. PMID: 17846159  

Reeves SJ, Mehta MA, Montgomery AJ, Amiras D, Egerton A, Howard RJ, & Grasby PM. (2007) Striatal dopamine (D2) receptor availability predicts socially desirable responding. NeuroImage, 34(4), 1782-9. PMID: 17188897  

Volkow ND, Wang GJ, Fowler JS, Logan J, Gatley SJ, MacGregor RR, Schlyer DJ, Hitzemann R, & Wolf AP. (1996) Measuring age-related changes in dopamine D2 receptors with 11C-raclopride and 18F-N-methylspiroperidol. Psychiatry research, 67(1), 11-6. PMID: 8797238  

Sutin AR, Beason-Held LL, Resnick SM, & Costa PT. (2009) Sex differences in resting-state neural correlates of openness to experience among older adults. Cerebral cortex (New York, N.Y. : 1991), 19(12), 2797-802. PMID: 19366871  

Roppongi T, Nakamura M, Asami T, Hayano F, Otsuka T, Uehara K, Fujiwara A, Saeki T, Hayasaka S, Yoshida T.... (2010) Posterior orbitofrontal sulcogyral pattern associated with orbitofrontal cortex volume reduction and anxiety trait in panic disorder. Psychiatry and clinical neurosciences, 64(3), 318-26. PMID: 20602731  

Rankin KP, Rosen HJ, Kramer JH, Schauer GF, Weiner MW, Schuff N, & Miller BL. (2004) Right and left medial orbitofrontal volumes show an opposite relationship to agreeableness in FTD. Dementia and geriatric cognitive disorders, 17(4), 328-32. PMID: 15178947  

Jackson J, Balota DA, & Head D. (2009) Exploring the relationship between personality and regional brain volume in healthy aging. Neurobiology of aging. PMID: 20036035  

  • September 10, 2010
  • 04:09 AM
  • 390 views

The neuroscience of creativity and insight

by William Lu in The Quantum Lobe Chronicles

Have you ever wondered what was going on in your noggin when on that rare occasion you had an "aha!" moment or found yourself in a creative flow state, where even your screaming girlfriend couldn't snap you out of? Well Dietrich and Kanso over at the American University of Beirut seem to have mapped out the phenomena for us nicely. However, it's not quite as simple as you think. In their review paper published in this months Psychological Bulletin, they cover three broad categories related to insight and creativity. They are divergent thinking, artistic creativity, and insight. All studies reviewed used either electroencephalography, event-related potential, or neuroimaging. The first category they looked at was divergent thinking, the thought process or method used to generate creative ideas by exploring many possible solutions. An example would be furiously brainstorming something interesting to write about on this darn blog. They found that numerous studies using the divergent thinking paradigm had one thing in common, that subjects exhibited some kind of diffuse prefrontal activation. Oddly enough, there was evidence for both increases and decreases in prefrontal activation depending on the study. They suggest that maybe different types of creativity were being tapped into.Courtesy of Park LabInterestingly, people with schizophrenia show reduced prefrontal activation when performing divergent thinking tasks (Takeshi, 2010). The next category the team covered was artistic creativity. In a particular series of studies, subjects were asked to mentally compose music, visualize abstract concepts, look at paintings, and imagine previously shown drawings; all under EEG monitoring. Activation of motor and temporalparietal regions were evident.intense looking motor homunculusThe last category discussed was insight. Reviewing the literature they found that the anterior cingulate cortex, involved in early learning and problem solving,  was activated by insight problems and that the superior temporal gyrus, involved in the perception of facial expressions, was activated only when successful solutions to those insight problems were found. What is the sound of one hand clapping?!The take home message Dietrich and Kanso emphasize is that no single brain area, nor a particular hemisphere for that matter, is involved in creativity or insight (contrary to popular belief). The next time your hipster artist friends tell you they're more "right brain" than anything else you can politely correct them by explaining...I highly recommend you check out the article as there is a lot I did not cover.References:Dietrich A, & Kanso R (2010). A review of EEG, ERP, and neuroimaging studies of creativity and insight. Psychological bulletin, 136 (5), 822-48 PMID: 20804237Takeshi K, Nemoto T, Fumoto M, Arita H, & Mizuno M (2010). Reduced prefrontal cortex activation during divergent thinking in schizophrenia: A multi-channel NIRS study. Progress in neuro-psychopharmacology & biological psychiatry PMID: 20673784... Read more »

Takeshi K, Nemoto T, Fumoto M, Arita H, & Mizuno M. (2010) Reduced prefrontal cortex activation during divergent thinking in schizophrenia: A multi-channel NIRS study. Progress in neuro-psychopharmacology . PMID: 20673784  

  • September 7, 2010
  • 02:33 AM
  • 370 views

Is recognition without awareness possible?

by William Lu in The Quantum Lobe Chronicles

It seems common knowledge in the world of neuroscience that episodic memories are formed through conscious awareness. However, a couple of years ago Voss and Paller found that this may not necessarily be the case. They had subjects perform a forced choice recognition task using kaleidoscope images (for novelty's sake). Interestingly, accuracy was highest when subjects reported guessing, thus indicating little awareness that the studied images had been seen before. "This indicates that episodic memory processing was unhelpful, and suggests that subjects responded instead based on pure visual fluency." In a second study, the team discovered that subjects performed better on tests of episodic memory when they paid divided attention rather than full attention, further validating their findings. In their 2009 paper they concluded by stating that "our findings add weight to the proposal that nonhuman animals utilize visual fluency without episodic memory when performing tasks intended to probe episodic memory."However, contrary results have recently been published in this month's Learning & Memory. In a replication study Jeneson, Kirwan, and Squire, found that recognition was better when subjects paid full attention to the visual stimuli compared to paying partial attention. In addition, recognition was better when subjects reported some level of confidence as compared to a guess. Vass and Paller responded to the disconfirming study by running a further study of their own. To resolve the apparent discrepancy they added a simple manipulation to encourage either guessing or confident responding. They found that encouraging guessing increased prevalence and accuracy of guesses relative to the confident responding condition. The authors suggest that both the prevalence and accuracy of guessing can be influenced by whether subjects adopt guessing-friendly strategies. So the lesson here is...guess away!References:Voss JL, & Paller KA (2009). Recognition without awareness in humans and its implications for animal models of episodic memory. Communicative & integrative biology, 2 (3), 203-4 PMID: 19641728Jeneson A, Kirwan CB, & Squire LR (2010). Recognition without awareness: An elusive phenomenon. Learning & memory (Cold Spring Harbor, N.Y.), 17 (9), 454-9 PMID: 20810620Voss JL, & Paller KA (2010). What makes recognition without awareness appear to be elusive? Strategic factors that influence the accuracy of guesses. Learning & memory (Cold Spring Harbor, N.Y.), 17 (9), 460-8 PMID: 20810621... Read more »

Voss JL, & Paller KA. (2009) Recognition without awareness in humans and its implications for animal models of episodic memory. Communicative , 2(3), 203-4. PMID: 19641728  

Jeneson A, Kirwan CB, & Squire LR. (2010) Recognition without awareness: An elusive phenomenon. Learning , 17(9), 454-9. PMID: 20810620  

Voss JL, & Paller KA. (2010) What makes recognition without awareness appear to be elusive? Strategic factors that influence the accuracy of guesses. Learning , 17(9), 460-8. PMID: 20810621  

  • April 23, 2010
  • 09:56 AM
  • 501 views

Aggression spectrum disorders: The distinction between borderline personality disorder and psychopathy

by William Lu in The Quantum Lobe Chronicles

I recently read a fascinating book chapter written by William Arsenio titled Happy Victimization: Emotion Dysregulation in The Context of Instrumental, Proactive Aggression. Early in the chapter, the author discussed how according to a study, 4-year-old children tended to predict that a bully would feel happy after pushing around some poor chump on the playground, aka happy victimization (Arsenio & Kramer, 1992). However, at age 6, children who were probed further not only predicted that the bully would feel happy after bullying, but would feel a sense of remorse as well (4-year-olds stuck to their guns). Is this the beginning stages of moral development?Arsenio went on to describe the possible link between emotion dysregulation and this notion of happy victimization. The victimizer initially feels positive, but then recognizes the victims negative feelings. This then elicits an involuntary positive or negative affective response depending on a whole host of factors including temperament, empathy, and parental attachment. For most of us, emotional maturity takes its natural course and empathic development occurs. However, those afflicted with borderline personality disorder and psychopathy seem to either steer off the beaten path or miss the bus completely.Before we speak further about these two truly disturbing personality disorders, an important distinction should be made between two subtypes of aggression mentioned in the reading. 1) Reactive aggression = "hot headed" impulsive angry reaction (ex. I'll punch you in the face because you really pissed me off). 2) Proactive aggression = "cold blooded" aggression used instrumentally to reach some desirable end (ex. I'll punch you in the face because I want your lunch money). As I read on, I couldn't help but associate the two very different subtypes of aggression with the aforementioned personality disorders. Were adults who displayed frequent and high levels of reactive aggression more prone to being identified as borderline. Similarly, were those displaying frequent and high levels of proactive aggression more prone to being identified as psychopathic? It seems to fit all too well to be disregarded. To clarify where I'm going with this, characterizations of the personality disorders and some solid evidence are in order.Borderline personality disorders1. Prolonged disturbance of personality function in a person characterized by depth and variability of moods.The disorder typically involves unusual levels of instability in mood; black and white thinking, or splitting; chaotic and unstable interpersonal relationships, self-image, identity, and behavior; as well as a disturbance in the individual's sense of self.2. over-active amygdala (i.e. overly responsive to emotion-related stimuli) (Donegan et al., 2003)3. insecure attachment (i.e. history of verbally/physically abusive parent) (Aaronson et al., 2006)4. ability to empathize (Fertuck et al., 2009) = intact mirror neuron system?Psychopathy 1. An abnormal lack of empathy combined with strongly amoral conduct, masked by an ability to appear outwardly normal. They can use charisma, manipulation, and intimidation to control others and to satisfy their own need.2. under-active amygdala (i.e. unresponsive to emotion-related stimuli) (Blair, 2008)3. insecure attachment (i.e. history of verbally/physically abusive parent) (Saltaris, 2002)4. inability to empathize = dysfunctional mirror neuron system? (Fekteau et al., 2008)My speculative model in sum:Borderline personality disorder = insecure attachment + overactive amygdala response + functional mirror neuron system = high reactive/impulsive aggressionPsychopathy = insecure attachment + underactive amygdala response to fear + dysfunctional mirror neuron system = high proactive/unemotional + reactive/impulsive aggression Psychopaths = happy victimizers into adulthood? References:Aaronson CJ, Bender DS, Skodol AE, & Gunderson JG (2006). Comparison of attachment styles in borderline personality disorder and obsessive-compulsive personality disorder. The Psychiatric quarterly, 77 (1), 69-80 PMID: 16397756Arsenio, W. F. (2006). Happy Victimization: Emotion Dysregulation in The Context of Instrumental, Proactive Aggression. Snyder, Douglas K. (Ed); Simpson, Jeffry (Ed); Hughes, Jan N. (Ed). (2006). Emotion regulation in couples and families: Pathways to dysfunction and health. (pp. 101-121). Washington, DC, US: American Psychological AssociationBlair, R. (2008). Review. The amygdala and ventromedial prefrontal cortex: functional contributions and dysfunction in psychopathy Philosophical Transactions of the Royal Society B: Biological Sciences, 363 (1503), 2557-2565 DOI: 10.1098/rstb.2008.0027FECTEAU, S., PASCUALLEONE, A., & THEORET, H. (2008). Psychopathy and the mirror neuron system: Preliminary findings from a non-psychiatric sample Psychiatry Research, 160 (2), 137-144 DOI: 10.1016/j.psychres.2007.08.022Fertuck EA, Jekal A, Song I, Wyman B, Morris MC, Wilson ST, Brodsky BS, & Stanley B (2009). Enhanced 'Reading the Mind in the Eyes' in borderline personality disorder compared to healthy controls. Psychological medicine, 39 (12), 1979-88 PMID: 19460187Saltaris, C. (2002). Psychopathy in juvenile offenders Can temperament and attachment be considered a... Read more »

Aaronson CJ, Bender DS, Skodol AE, & Gunderson JG. (2006) Comparison of attachment styles in borderline personality disorder and obsessive-compulsive personality disorder. The Psychiatric quarterly, 77(1), 69-80. PMID: 16397756  

Blair, R. (2008) Review. The amygdala and ventromedial prefrontal cortex: functional contributions and dysfunction in psychopathy. Philosophical Transactions of the Royal Society B: Biological Sciences, 363(1503), 2557-2565. DOI: 10.1098/rstb.2008.0027  

FECTEAU, S., PASCUALLEONE, A., & THEORET, H. (2008) Psychopathy and the mirror neuron system: Preliminary findings from a non-psychiatric sample. Psychiatry Research, 160(2), 137-144. DOI: 10.1016/j.psychres.2007.08.022  

Fertuck EA, Jekal A, Song I, Wyman B, Morris MC, Wilson ST, Brodsky BS, & Stanley B. (2009) Enhanced 'Reading the Mind in the Eyes' in borderline personality disorder compared to healthy controls. Psychological medicine, 39(12), 1979-88. PMID: 19460187  

Saltaris, C. (2002) Psychopathy in juvenile offenders Can temperament and attachment be considered as robust developmental precursors?. Clinical Psychology Review, 22(5), 729-752. DOI: 10.1016/S0272-7358(01)00122-2  

  • April 3, 2010
  • 04:16 AM
  • 534 views

The difference between softcore and hardcore insomnia

by William Lu in The Quantum Lobe Chronicles

Self-proclaimed insomniacs should be asking themselves right now if they've got either a "softcore" or a "hardcore" sleep problem on their hands. What's the difference between softcore and hardcore insomnia and why is it important you ask? First, let's define the terms. Softcore insomnia = complaint of insomnia with normal sleep duration greater than or equal to 6 hours of sleepHardcore insomnia = complaint of insomnia with less than or equal to 6 hours of sleepFernandez-Mendoza and colleagues from Penn State University College of Medicine grouped 678 participants from the general population using the aforementioned criteria (although without the sophisticated categorical nomenclature) to see what between-group differences in neuropsychological performance they would find. They controlled for age, race, gender, education, body mass index, and physical and mental health. The comprehensive neuropsychological battery included tests of processing speed, attention, visual memory, and verbal fluency. The researchers found no difference in performance between softcore insomniacs and controls. However, the hardcore insomniacs did worse on all tests compared to the controls and, get this, controls with less than 6 hours of sleep. Here it seems to be the case that it's only a problem if you make it one. "It's all about perception" as my former professor use to rant. The most significant finding was that hardcore insomniacs did the worst on tasks that required executive control of attention (set-switching). So if you're truly a hardcore insomniac, do yourself a favor and stay away from multi-tasking. For the rest of you softcore insomniacs, suck it up! At least you don't have real-life cognitive deficits (unless you're counting whining as a cognitive deficit).ulio Fernandez-Mendoza, MSc1,2,3; Susan Calhoun, PhD1; Edward O. Bixler, PhD1; Slobodanka Pejovic, MD1; Maria Karataraki, PsyD1; Duanping Liao, PhD4; Antonio Vela-Bueno, MD2; Maria J. Ramos-Platon, PhD3; Katherine A. Sauder, BA1; Alexandros N. Vgontzas, M (2010). Insomnia with Objective Short Sleep Duration is Associated with Deficits in Neuropsychological Performance: A General Population Study SLEEP, 33 (4), 459-465... Read more »

ulio Fernandez-Mendoza, MSc1,2,3; Susan Calhoun, PhD1; Edward O. Bixler, PhD1; Slobodanka Pejovic, MD1; Maria Karataraki, PsyD1; Duanping Liao, PhD4; Antonio Vela-Bueno, MD2; Maria J. Ramos-Platon, PhD3; Katherine A. Sauder, BA1; Alexandros N. Vgontzas, M. (2010) Insomnia with Objective Short Sleep Duration is Associated with Deficits in Neuropsychological Performance: A General Population Study. SLEEP, 33(4), 459-465. info:/

  • March 30, 2010
  • 03:59 AM
  • 530 views

How forming new memories help retain older ones

by William Lu in The Quantum Lobe Chronicles

Try to remember this visual paired associate (AB):Now recall visual paired associate AB:Next, I'm going to have you remember another visual paired associate (AC):Now recall visual paired associate AC:Can you still remember the first visual paired associate (AB)?What if I were to pay you ten cents to remember? How about a hundred bucks? Would your memory performance increase? Stay the same? Most of your would probably infer the former. More money = more motivation to memorize.That's what Kuhl and colleagues found in their study published in the latest issue of Nature Neuroscience. However, the study didn't just stop there. That's just the tip of the iceberg!They had all participants complete a task similar to the one just demonstrated, but used more novel pairings such as a watch and a pipe (yawn). 2/3 of AB pairs were followed by AC pairs in the subsequent encoding rounds while the remaining 1/3 of AB pairs were followed by nothing. Trials began either with a high or a low reward tagged to an AB pair and a high, low, or no reward tagged to an AC pair. There were 8 encoding and immediate test rounds and 1 critical post-test round conducted outside of the scanner where participants were asked to recall AB pairs only. As expected, retroactive interference negatively affected memory retrieval of AB pairs.     Using fMRI, the authors found that left hippocampal activation during the learning of a latter visual paired associate predicted how well the first paired associate would be remembered. Basically, if your left memory cortex didn't light up while encoding new information then the relatively older information would be forgotten. More specifically, for those of you who couldn't remember the first pair (horse and no-name comic book) it's likely that your left posterior hippocampus and parahippocampal cortex weren't activated during the learning of the latter pair (horse and Sarah Jessica Parker).Furthermore, the researchers found that when successful recall for AB pairs were achieved, reward centers in the brain (fronstriatal regions) also lit up on fMRI scan.So how can all of this be explained? According to the authors, hippocampal reactivation is protecting the stored episodic memories from being forgotten in the face of interfering information. The authors chalk it up to pattern completion which "allows previously encoded memories to be reinstated from a partial input, thereby allowing past episodes to be reactivated, interleaved with current experience, and consolidated over time". The horse not only serves as a retrieval cue for the memory of Sarah Jessica Parker, but the no-name comic book as well. Additionally, the findings underscore the importance of past reward-associated (motivated) learning and its incorporation into new learning experiences.This study leads me to wonder what key factors contribute to individual differences in memory encoding after performing an interference task. Is it just hippocampal functioning and level of motivation that sets each and every one of us apart? What about working memory capacity (prefrontal and parietal areas)? Intelligence? Age? Level of alertness? Amount of sleep prior to and/or after learning? All the above? Anyway, it's time to end this pointless musing. Back to more important matters like tending to Ninja Garden issue 1. References:Kuhl, B., Shah, A., DuBrow, S., & Wagner, A. (2010). Resistance to forgetting associated with hippocampus-mediated reactivation during new learning Nature Neuroscience, 13 (4), 501-506 DOI: 10.1038/nn.2498... Read more »

Kuhl, B., Shah, A., DuBrow, S., & Wagner, A. (2010) Resistance to forgetting associated with hippocampus-mediated reactivation during new learning. Nature Neuroscience, 13(4), 501-506. DOI: 10.1038/nn.2498  

  • March 18, 2010
  • 05:05 PM
  • 524 views

Parkinsonian emotion recognition impairment better accounted for by sleep deprivation

by William Lu in The Quantum Lobe Chronicles

The New York Times recently covered a paper by Grey and Tickle-Degnen, published in the journal Neuropsychology, finding that people with Parkinson's Disease (PD) are not able to recognize facial and vocal emotions very well. The article states that it's not clear why this seems to be the case. I briefly reviewed the original meta-analytic paper (the pdf can be found here) and saw that the research team accounted for 1) the emotion recognition tasks used, 2) the medication the participants were on, and 3) the existence of depression as possible moderatoring variables for the impairment in emotion recognition. They suggest that "the likely cause of this deficit is pathology in neural circuits involved in emotion recognition, particularly within basal ganglia structures including the ventral striatum and STN." This tentative speculation is just fine and dandy, but it doesn't really provide an explanation for why people with PD have this particular deficit in the first place. They rule out comorbid depression and visualspatial impairment, but go on to postulate that Lewy bodies disease, an abnormal amount of protein found inside the nerve cells of many PD patients, may be affecting their visual cortex, therefore affecting their emotion recognition abilities. Too bad there's no shred of evidence found in the research literature to support this hypothesis (they make sure to note this). What I found surprising what that they made no mention of sleep disturbances' possible moderating role in explaining their findings. Drawing from my previous entry on sleep deprivation's deleterious affects on emotion recognition, maybe it's the fact that people suffering from PD commonly have concomitant sleep problems, therefore leading to their emotion recognition impairment. Numerous studies have shown that PD significantly affects rapid eye movement sleep behavior leading to a variety of cognitive impairments (Massicotte-Marquez et al., 2009, Norlinah et al., 2009, Seugnet et al., 2009,). We now also know that REM sleep is crucial in the processing of emotional memory (Nishida, 2008). And like I said before, sleep deprivation takes a heavy toll on emotion recognition functioning (van der Helm, Gujar, & Walker, 2010). Sleep seems to account for much of our emotional life! In light of the aformentioned studies, it makes the most sense that sleep deprivation would be the more likely pathway to emotional recognition impairment in people with PD; not working memory dysfunction as the authors suggest. There may be many potential sources for interpersonal difficulties in PD individuals who are unable to read emotions accurately. Perhaps future sleep treatment can help prevent such difficulties from ever occurring. Just a thought... Gray HM, & Tickle-Degnen L (2010). A meta-analysis of performance on emotion recognition tasks in Parkinson's disease. Neuropsychology, 24 (2), 176-91 PMID: 20230112Massicotte-Marquez J, Décary A, Gagnon JF, Vendette M, Mathieu A, Postuma RB, Carrier J, & Montplaisir J (2008). Executive dysfunction and memory impairment in idiopathic REM sleep behavior disorder. Neurology, 70 (15), 1250-7 PMID: 18216303Seugnet L, Galvin JE, Suzuki Y, Gottschalk L, & Shaw PJ (2009). Persistent short-term memory defects following sleep deprivation in a drosophila model of Parkinson disease. Sleep, 32 (8), 984-92 PMID: 19725249Norlinah, M., Afidah, K., Noradina, A., Shamsul, A., Hamidon, B., Sahathevan, R., & Raymond, A. (2009). Sleep disturbances in Malaysian patients with Parkinson's disease using polysomnography and PDSS Parkinsonism & Related Disorders, 15 (9), 670-674 DOI: 10.1016/j.parkreldis.2009.02.012... Read more »

Gray HM, & Tickle-Degnen L. (2010) A meta-analysis of performance on emotion recognition tasks in Parkinson's disease. Neuropsychology, 24(2), 176-91. PMID: 20230112  

Massicotte-Marquez J, Décary A, Gagnon JF, Vendette M, Mathieu A, Postuma RB, Carrier J, & Montplaisir J. (2008) Executive dysfunction and memory impairment in idiopathic REM sleep behavior disorder. Neurology, 70(15), 1250-7. PMID: 18216303  

Seugnet L, Galvin JE, Suzuki Y, Gottschalk L, & Shaw PJ. (2009) Persistent short-term memory defects following sleep deprivation in a drosophila model of Parkinson disease. Sleep, 32(8), 984-92. PMID: 19725249  

Norlinah, M., Afidah, K., Noradina, A., Shamsul, A., Hamidon, B., Sahathevan, R., & Raymond, A. (2009) Sleep disturbances in Malaysian patients with Parkinson's disease using polysomnography and PDSS. Parkinsonism , 15(9), 670-674. DOI: 10.1016/j.parkreldis.2009.02.012  

  • March 16, 2010
  • 01:53 AM
  • 498 views

Earworms, lyrics, and tunes in the brain

by William Lu in The Quantum Lobe Chronicles

Last time I left off quoting Lady GaGa's masterwork "Poker Face". I continue to rag on it because I can't seem to escape it's repetitive and forced impingement on my vulnerable eardrums. Unfortunately, the city doesn't afford much auditory privacy and some people in the subway are really determined to lose their hearing before old age. Whatever happened to iPod etiquette? According to Oliver Sack's book Musicophilia I've got a bad case of the earworm. This is when a piece of music repeats compulsively in one's mind. But if I hate the song so much why is my brain constantly replaying it over and over again? Sacks similarly asks: What is happening psychologically and neurologically, when a tune or a jingle takes possession of one like this? What are the characteristics that make a tune or a song 'dangerous or 'infectious' in this way? Is it some oddity of sound, of timbre or rhythm or melody? Is it repetition? Or is it arousal of special emotional resonances or associations? To give the song SOME credit, I don't necessarily abhor the tune as much as I do the ridiculous lyrics. Sacks is onto something here when he makes mention of rhythm and repetition. "Poker Face" has an absurd amount of repetition. The word "mum" is repeated 40 times in the song. The phrase "can't read my" is spoken 30 times. (A link on how to get rid of earworm, wish I had found it sooner)In any case, have you ever wondered how the brain actually processes lyrics and tunes? There's a hot debate as to whether they are represented as separate components or integrated throughout...but since New Scientist seems to have already covered the paper (doh! I just found out a second ago)...I leave you with the main findings of Sammler et. al's paper published in the latest issue of The Journal of Neuroscience. I also leave you with a gift...in hopes to infect you with an earworm of your own! Misery loves company...the left mid-STS showed an interaction of the adaptation effects for lyrics and tunes, suggesting an integrated processing of the two components at prelexical, phonemic processing levels. The degree of integration decayed toward more anterior regions of the left STS, where the lack of such an interaction and the stronger adaptation for lyrics than for tunes was suggestive of an independent processing of lyrics, perhaps resulting from the processing of meaning. Finally, evidence for an integrated representation of lyrics and tunes was found in the left dorsal precentral gyrus (PrCG), possibly relating to the build-up of a vocal code for singing in which musical and linguistic features of song are fused. Overall, these results demonstrate that lyrics and tunes are processed at varying degrees of integration (and separation) through the consecutive processing levels allocated along the posterior–anterior axis of the left STS and the left PrCG.Sacks, O. (2007). Musicophilia: Tales of music and the brain. New York, NY: Alfred A. KnopfSammler, D., Baird, A., Valabregue, R., Clement, S., Dupont, S., Belin, P., & Samson, S. (2010). The Relationship of Lyrics and Tunes in the Processing of Unfamiliar Songs: A Functional Magnetic Resonance Adaptation Study Journal of Neuroscience, 30 (10), 3572-3578 DOI: 10.1523/JNEUROSCI.2751-09.2010... Read more »

Sammler, D., Baird, A., Valabregue, R., Clement, S., Dupont, S., Belin, P., & Samson, S. (2010) The Relationship of Lyrics and Tunes in the Processing of Unfamiliar Songs: A Functional Magnetic Resonance Adaptation Study. Journal of Neuroscience, 30(10), 3572-3578. DOI: 10.1523/JNEUROSCI.2751-09.2010  

  • March 9, 2010
  • 09:04 AM
  • 517 views

Sleep deprivation impairs emotion recognition

by William Lu in The Quantum Lobe Chronicles

The ability to read emotions is an important part of the human experience; the only way to successfully navigate through complex social environments. It comes in handy especially if you don the title of psychotherapist or professional poker player. Without it, you become socially inept. You enter the world of the autistic individual.Thanks to Charles Darwin we now know that it’s not just the eyes that are “the windows to the soul”. He first wrote about the subject of facial expressions in his 1898 book titled The Expression of the Emotions in Man and Animals (the link includes the work in its entirety). In it he described the emotions conveyed in the face as being both universal and “species-specific”.Ekman and Friesen (1969) expounded on Darwin's theory, hypothesizing that universal facial expressions were to be found in the relationship between distinctive patterns of the facial muscles and particular emotions. In 1971 they traveled to Papua New Guinea to test the Fore tribe, a people who had minimal contact with outsiders. The researchers found that the Fore people were able to accurately identify the expressions of emotion in photographs of people from cultures with which they were not yet familiar (here's a link to a fascinating NPR Ekman podcast). An interesting, yet off-topic note: Apparently a Fore subgroup found in southern New Guinea regularly practiced cannibalism by dismembering and eating victims of the prion disease kuru (aka laughing sickness due to the outbursts of laughter during the second phase). Shirley Lindenbaum, a kuru researcher, reported that kuru victims were highly valued as a source of food because the layers of fat resembled pork...yum (Lindenbaum, 1979). Women would often feed brain and various parts of organs to their young and the elderly. Unfortunately, this was yet another mode of kuru transmission. The southern Fore knew better than to eat diseased corpses, but thought that kuru was more a mental affliction than a physical one.van der Helm and colleagues over at the University of California decided to take a unique look at emotional recognition in the context of sleep. In their recently published SLEEP paper, they asked whether emotional processing would become significantly impaired in sleep deprived individuals. The authors randomly assigned 37 young adults to either a sleep control or total sleep deprivation group. All participants abstained from caffeine and alcohol three days prior to and three days during the study (sucks to be them). Both groups were asked to perform an emotional facial recognition task at 16:00 for two consecutive days.The task involved evaluating sad, angry, and happy faces from the Ekman Pictures of facial affect set. The participants were presented with 10 emotionally morphed pictures of the same person and asked to determine which emotion each facial expression was conveying. The control group got to sleep at home like normal people while the not so fortunate sleep-deprivees were kept awake in the sleep lab (at least they had internet!).(similar morphing method used in the study)The team found that a single night of sleep deprivation significantly disrupted the ability to identify emotionally salient facial expressions in others. Deficits were most dramatic for emotions eliciting high autonomic arousal (i.e. happy and angry). Interestingly enough, they found that women in particular were more significantly influenced by sleep deprivation on emotion recognition (I suppose evolutionarily it seems to make sense). Some study limitations the authors humbly listed include not measuring chronotype (alertness and preference for activity early or late in the day) and motivation/interest level, and not verifying compliance of sleep time and duration (such as actigraph measurements).So for all the sleep deprived psychotherapists and the poker players who like to sit at the table all night, I hope this entry helps you to reconsider such unwise habits. Unless of course you share similar sentiments as  the brilliant Lady GaGa: Mum mum mum mahMum mum mum mahCan't read my, Can't read myNo he can't read my poker face(Decided to randomly plug in the terrible lyrics to show how stupid they really are...god, I really need to get this horrid song out of my head...maybe it's time for me to sleep) (...nevermind)van der Helm E; Gujar N; Walker MP (2010). Sleep Deprivation Impairs the Accurate Recognition of Human Emotions SLEEP, 33 (3), 335-342Ekman P, & Friesen WV (1971). Constants across cultures in the face and emotion. Journal of personality and social psychology, 17 (2), 124-9 PMID: 5542557Steadman, L. (1980). : Kuru Sorcery: Disease and Danger in the New Guinea Highlands . Shirley Lindenbaum. American Anthropologist, 82 (3), 692-694 DOI: 10.1525/aa.1980.82.3.02a01130... Read more »

van der Helm E; Gujar N; Walker MP. (2010) Sleep Deprivation Impairs the Accurate Recognition of Human Emotions. SLEEP, 33(3), 335-342. info:/

Ekman P, & Friesen WV. (1971) Constants across cultures in the face and emotion. Journal of personality and social psychology, 17(2), 124-9. PMID: 5542557  

Steadman, L. (1980) : Kuru Sorcery: Disease and Danger in the New Guinea Highlands . Shirley Lindenbaum. American Anthropologist, 82(3), 692-694. DOI: 10.1525/aa.1980.82.3.02a01130  

  • March 1, 2010
  • 07:39 AM
  • 491 views

How looking away prevents pedestrian collisions

by William Lu in The Quantum Lobe Chronicles

One day a friend and I were briskly strolling along a mall corridor, engaged in conversation, until something quite hilarious happened. A burly gentleman was quickly approaching my friend's direct line of trajectory. She and this man had to make either one of two choices; move to the left or to the right to avoid a disastrous collision. Simple, no? And so I thought. With about a foot between them, my tiny-sized friend and this large stranger began this seemingly unending and surprisingly well-coordinated dance (or if you're an avid sports fan, picture Spud Webb desperately trying to drive on Shaq) one mirroring the others' movements, swaying back and forth, side to side. Both were a bit confused as to which direction to settle on, and for an estimated 5 seconds I stood there in utter disbelief, witnessing this extremely awkward, yet ridiculously entertaining situation.How do we avoid catastrophes like this from happening on a daily basis? And if navigating through a mall corridor without incident is THAT difficult, how do the hundreds of pedestrians in somewhere like Manhattan manage to avoid such annoying or, in my friend's case, embarrassing encounters? Inattention and "mind-blindness", an inability to develop an awareness of what is in the mind of another human, would seem to be the main culprits. However, there's bit more to it than that and it involves eye gazing. Nummenmaa, Hyona, and Hietanen over at the University of Tampere in Finland have further shed light on the science of oculomotor activity while walking. In their paper, published in the most recent issue of Psychological Science, they investigated how participants predicted where an oncoming pedestrian was going to move by using information found in that pedestrian's gaze.More specifically, the authors wanted to test whether humans use others' gaze information to avoid collisions during locomotion and to assess how ones' own gaze direction is influenced by the approaching pedestrian's gaze behavior.They had 35 university students view a computer generated male walking toward them either looking to their left or right. The scene also moved constantly forward, giving the participants the impression that they were moving. Eye movements were recorded with a digital eye tracker. The participants were to answer whether they would skirt the pedestrian by moving to the left or right using a differential button press.Is it just me or does this guy look like he's about to do something extremely shady? (click image to enlarge)They found that the frequency of skirting to the left was higher when the oncoming pedestrian looked to the right and conversely, skirting to the right was higher when the pedestrian looked to the left. Additionally, they found that on average the participants looked toward the opposite direction of the pedestrian's gaze. It makes sense that one would "mind read" the oncoming pedestrian traffic and focus on walking toward the path of least resistance.Nummenmaa and her colleagues speculate that parallel mechanisms guide gaze following. One mechanism is rapid and stimulus driven while the other is slower and governed by social cognition. Interestingly enough, they referenced prior research done on autism spectrum disorders to validate this dual-system model. Individuals with autism typically have no difficulties discriminating other people's gaze direction, but exhibit impairment in both joint attention and inferring other people's mental states through gaze (due to lack of a theory of mind or ToM).I found an additional fMRI study discovering autistic participants lack of modulation in the superior temporal sulcus, a brain area important in the processing of intentional gaze shifts (Pelphrey, Morris, & McCarthy, 2005). Apparently there's also been research looking at the pedestrian patterns of individuals with autism using virtual technology. Parsons, Mitchell, and Leonard (2004) found that a subset of autistic participants were significantly more likely to be judged to have bumped into or walked between virtual characters compared to a control group. The strange tendency couldn't be explained by executive dysfunction or general motor difficulty, suggesting that personal space may be impaired with autism. Recently, training exercises have been implemented using the same virtual technology with autistic adolescents (Mitchell, &amp, & Leonard, 2007)However, for the rest of us who aren't diagnosed with an autism spectrum disorder, there's still a possibility in which we may not be utilizing our fully intact eye gazing mechanisms to "pedestrianize" properly. I can't count how many times I've seen here in the Big Apple the obnoxiously loud cellphone user or the texting pedestrian needlessly holding up foot traffic (Seriously?! Find a dark narrow alleyway or something!) Anyway...there's this iPhone app out called "Type n Walk". New York Times has good coverage on it stating that "it’s supposed to make it easier to text while strolling by providing a visual, on the phone, of what is happening on the street a few feet ahead". I don't really buy into it because I don't think people are that good at multi-tasking just yet (unless you're a dual-tasking meditation master). This is a prime example of how our limited brain capacity fails to keep up with the rapidly developing human computer interaction technology (props to my older brother, Gene, for making this field more congruent with our realistic abilities).   Nummenmaa and company conclude the results from their study "show that people are also aware of how and why others update their visual representations and use this information flexibly for their own movement planning and visual sampling of the environment". Unfortunately, we're unable do this if we're too busy reading or texting while walking. Furthermore, others won't be able to tell where we're planning on going either. So for the 67% of respondents from my survey who answered that they spend more face-to-face time with a screen than with a human face, get off that Blackberry/iPhone and pay attention! Otherwise, CRASH.The famous Shibuya, Japan crosswalk!Nummenmaa L, Hyönä J, & Hietanen JK (2009). I'll Walk This Way: Eyes Reveal the Direction of Locomotion and Make Passersby Look and Go the Other Way. Psychological science : a journal of the American Psychological Society / APS PMID: 19883491... Read more »

Nummenmaa L, Hyönä J, & Hietanen JK. (2009) I'll Walk This Way: Eyes Reveal the Direction of Locomotion and Make Passersby Look and Go the Other Way. Psychological science : a journal of the American Psychological Society / APS. PMID: 19883491  

Pelphrey, K. (2005) Neural basis of eye gaze processing deficits in autism. Brain, 128(5), 1038-1048. DOI: 10.1093/brain/awh404  

Mitchell P, Parsons S, & Leonard A. (2007) Using virtual environments for teaching social understanding to 6 adolescents with autistic spectrum disorders. Journal of autism and developmental disorders, 37(3), 589-600. PMID: 16900403  

Parsons, S., Mitchell, P., & Leonard, A. (2004) The Use and Understanding of Virtual Environments by Adolescents with Autistic Spectrum Disorders. Journal of Autism and Developmental Disorders, 34(4), 449-466. DOI: 10.1023/B:JADD.0000037421.98517.8d  

  • February 25, 2010
  • 02:56 PM
  • 458 views

The power of prediction reduces activation in the primary visual cortex

by William Lu in The Quantum Lobe Chronicles

Prediction is an invaluable skill for navigating through complex environments. Somehow the brain generates predictions about perceptual inputs it's likely to receive using contextual information from recent memory. Statistical regularities are learned (e.g. movement and attack patterns of Mega Man bosses) and lead to less activation in corresponding brain areas. The brain is truly a miserly organ. "Why put in more work than I have to when I know what's gonna happen next", says the brain. Alink and colleagues over at the Max Planck Institute in Germany decided to check out what's really going on in the brain when it's making visual predictions. Using fMRI, the team tested whether predictability reduced responses in the human visual cortex as put forth in Rao and Ballards 1999 model of predictive coding. They assessed the theoretical claim by looking at the response of V1 (primary visual cortex) when detecting predictive and non-predictive motions.In the first experiment the researchers had 12 healthy participants fixate their eyes on a screen during which 9 degree bars were presented above and below the fixation point. The bars induced an upward and downward long-range apparent motion. Their motions were either predictable (bar is positioned and timed exactly on the motion trajectory of linear apparent motion between the lower and upper bar stimuli) or unpredictable (bar appears at a time at which linear apparent motion had already passed the position of the test bar). A baseline condition was also presented where apparent motion but no bar was presented. There were 81 trials of each condition, each trial lasting 7 seconds.The second experiment differed in that the participants saw dots rather than bars through hi-tech MRI compatible goggles with two organic light-emitting diode displays. Presenting the MR Vision 2000 Ultra: MR Vision 2000 Ultra is an excellent way of entering the world of visual stimulation for fMRI. Featuring dual, backlit digital displays, MR Vision 2000 avoids gross pixellation, pixel dropout and color aberration endemic to fiber-optic based systems. You can present S-Video NTSC or Pal video to your patients within the bore of the magnet without artifacts or noise. The compact design fits in most standard headcoils and is rated from .2T to 4T. With the accompanying Audio system, a complete set of stimuli is possible.The lightweight, headmounted display fits entirely inside the bore of the magnet and is capable of deliveringfield-sequential 3D or standard video at a resolution of 180,000 pixels. This breakthrough advance utilizes the same cutting-edge technology that was developed for our research-proven fMRI 3D Goggle systems. Now its possible to immerse your patients in breathtaking 3D video! (I can't seem to find pictures of this contraption anywhere)The authors indeed found that in both experiments the visual stimulus predictability reduced activation levels in V1. The first experiment showed that stimuli with a predictable onset caused lower activation of V1 compared to identical stimuli with unpredictable onset. Experiment 2 showed that responses in V1 and the hMT/V5+ (human visual motion area) were lowest when apparent motion predicted the direction of random dot motion. Visual responses increased as the motion was made less predictable. Unfortunately, due to crappy fMRI temporal resolution, they couldn't figure out whether reduced activations in V1 due to predictable stimuli were the result from feedback, local V1 processing, or an interaction between the two.They conclude by stating that their findings "provide strong empirical evidence for the idea that the visual cortex actively anticipates its visual input and that such anticipation allows predictable stimuli to be processed with less neural activation at the earliest cortical relay for visual processing".As I was reading this paper, I was reminded of the neural efficiency hypothesis where more intelligent people were found to have less activation of cortical areas when performing cognitively easy tasks compared to their less intelligent counterparts. I can't shake the idea that the power of prediction is somehow inextricably tied to intelligent life. Seems to intuitively make sense doesn't it...bet you can't beat Bubble Man faster than I can!Alink, A., Schwiedrzik, C., Kohler, A., Singer, W., & Muckli, L. (2010). Stimulus Predictability Reduces Responses in Primary Visual Cortex Journal of Neuroscience, 30 (8), 2960-2966 DOI: 10.1523/JNEUROSCI.3730-10.2010Doppelmayr M, Klimesch W, Sauseng P, Hödlmoser K, Stadler W, & Hanslmayr S (2005). Intelligence related differences in EEG-bandpower. Neuroscience letters, 381 (3), 309-13 PMID: 15896490... Read more »

Alink, A., Schwiedrzik, C., Kohler, A., Singer, W., & Muckli, L. (2010) Stimulus Predictability Reduces Responses in Primary Visual Cortex. Journal of Neuroscience, 30(8), 2960-2966. DOI: 10.1523/JNEUROSCI.3730-10.2010  

Doppelmayr M, Klimesch W, Sauseng P, Hödlmoser K, Stadler W, & Hanslmayr S. (2005) Intelligence related differences in EEG-bandpower. Neuroscience letters, 381(3), 309-13. PMID: 15896490  

  • January 30, 2010
  • 02:39 PM
  • 598 views

Remembering returns brain states to when the actual experience happened

by William Lu in The Quantum Lobe Chronicles

William James, the influential American philosopher and psychologist of the late 1800's argued that remembering events reactivated motor and sensory brain regions involved during the original event. How right he was! Danker and Anderson have written an extensive review of the research literature looking at how this all happens, cleverly titled "The Ghosts of Brain States Past". Here is there abstract from the latest issue of Psychological Bulletin.There is growing evidence that the brain regions involved in encoding an episode are partially reactivated when that episode is later remembered. That is, the process of remembering an episode involves literally returning to the brain state that was present during that episode. This article reviews studies of episodic and associative memory that provide support for the assertion that encoding regions are reactivated during subsequent retrieval. In the first section, studies are reviewed in which neutral stimuli were associated with different modalities of sensory stimuli or different valences of emotional stimuli. When the neutral stimuli were later used as retrieval cues, relevant sensory and emotion processing regions were reactivated. In the second section, studies are reviewed in which participants used different strategies for encoding stimuli. When the stimuli were later retrieved, regions associated with the different encoding strategies were reactivated. Together, these studies demonstrate not only that the encoding experience determines which regions are activated during subsequent retrieval but also that the same regions are activated during encoding and retrieval. In the final section, relevant questions are posed and discussed regarding the reactivation of encoding regions during retrieval.Some interesting points about reactivation to note: 1. reactivation of the visual system occurs at the multi-granular level2. reactivation is stronger during retrieval of more info3. there's a reduction in reactivation when info is falsely remembered 4. reactivation is correlated with subjective reports of remembering (a bit surprising given how fallible our memories often are)The authors conclude by asking whether reactivation of brain states are more or less easily activated when info is more accessible. What about the role of speed and other varying factors? All of these questions, I am sure, will be answered in no time.Danker, J., & Anderson, J. (2010). The ghosts of brain states past: Remembering reactivates the brain regions engaged during encoding. Psychological Bulletin, 136 (1), 87-102 DOI: 10.1037/a0017937... Read more »

Danker, J., & Anderson, J. (2010) The ghosts of brain states past: Remembering reactivates the brain regions engaged during encoding. Psychological Bulletin, 136(1), 87-102. DOI: 10.1037/a0017937  

  • January 21, 2010
  • 01:01 AM
  • 507 views

Can distractions really enhance motor performance?

by William Lu in The Quantum Lobe Chronicles

Texting while driving seems to score pretty high up there on the "I really shouldn't be doing this right now" list. A 2009 study by the Virginia Tech Transportation Institute found that truck drivers who were texting on the road were 23 times more likely to find themselves involved in an accident. Incidentally, and much to my bewilderment, truck drivers who talked on cell phones were found to have absolutely no increased risk for crashing. I suppose it's much easier to say over the phone than to text "Slow down. Smokey Bear (cop) on your tail. Watch out for that barbershop (bridge lower than 13'6") up ahead or you'll soon be driving a bobtail(tractor without a trailer). Looks about time to head over to that pickle park (a state highway rest area...I wonder why they call it that...). You can find more CB terminology here.Most of us would likely think any type of distraction would negatively affect motor performance. However, a recent study by Hemond, Brown, and Robertson published in the Journal of Neuroscience, proves this isn't necessarily the case.The team from Harvard Medical School and McGill University questioned whether the very nature of the distraction would play a role in motor performance by either impairing or enhancing performance. They had a total of four conditions. In condition 1 they had participants complete a task involving motor and color sequencing; the color sequencing serving as a distraction. In condition 2, participants performed both a sequencing and counting task; the counting serving as a distraction. Condition 3 was a randomly assorted task while condition 4 involved a motor sequencing task without distraction.They found that learning of a motor sequencing task can be enhanced by concurrently performing another sequencing task (condition 1). In contrast, learning was impaired when performance of concurrent tasks did not involve the same cognitive processes (condition 2).So it's really not about the complexity of information which determines performance, but more about the processes engaged and whether they are similar or different. This led me to wonder what effects intensive simulated training would have on performance. A study done by Regan, Deery, and Triggs (1998) over at Monash University Accident Research Centre in Australia addressed this very thought quite nicely.In one of their experimental conditions they had participants (novice drivers) complete numerical calculations while concurrently performing a simulated driving task. The numerical calculation task consisted of a single digit appearing in front of the driving participants for one second every five seconds. The participants were required to calculate the difference between the previous two numbers and answer whether the derived number equaled the currently displayed number. They then responded yes or no by pressing one of two switches located on the steering wheel. Training consisted of 20 trials at two minutes each trial.The authors found that the training group indeed performed better on the driving task compared to a control group. However, the control group tended to do a bit better on the numerical calculation task, although non-significantly. The conclusions of this particular study suggests that training may enhance attentional control while driving. However, this by no means condones the act of texting while driving, even if one were to train for hours on end.The take home message here folks is to text while you're blogging, not while you're driving!...unless of course, you're already reading road signs. I kid.Reagan, M. A., Deery, H. A., & Triggs, T. J. (1998). Simulator-based training of attentional control skill in novice drivers. SimTecT98Hemond, C., Brown, R., & Robertson, E. (2010). A Distraction Can Impair or Enhance Motor Performance Journal of Neuroscience, 30 (2), 650-654 DOI: 10.1523/JNEUROSCI.4592-09.2010... Read more »

Hemond, C., Brown, R., & Robertson, E. (2010) A Distraction Can Impair or Enhance Motor Performance. Journal of Neuroscience, 30(2), 650-654. DOI: 10.1523/JNEUROSCI.4592-09.2010  

  • January 5, 2010
  • 01:23 AM
  • 541 views

Anticipating reward improves learning during sleep

by William Lu in The Quantum Lobe Chronicles

Rocking out on the guitar is by far one of my most cherished pastimes. At the angst ridden age of 15 I picked up a cheap Ibanez strat and learned my very first Nirvana song, "Teen Spirit". Little did I know a good night's rest would play such a crucial role in my learning those simple power chords. Furthermore, who would've thought my desire to become the next grunge icon would determine the rate at which I learned during those quiet nights of sleep. According to a study by Fischer and Born, published in the most recent journal of SLEEP, they found that anticipating a reward can determine the amount of memory consolidation during at the important time of offline processing.too.Fischer S, & Born J (2009). Anticipated reward enhances offline learning during sleep.... Read more »

Fischer S, & Born J. (2009) Anticipated reward enhances offline learning during sleep. Journal of experimental psychology. Learning, memory, and cognition, 35(6), 1586-93. PMID: 19857029  

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