Brain Blogger » Neuroscience & Neurology http://brainblogger.com Health and Science Blog Covering Brain Topics Mon, 23 Mar 2015 15:00:50 +0000 en-US hourly 1 http://wordpress.org/?v=4.1.1 The Physiology and Psychology of Pain http://brainblogger.com/2015/03/19/the-physiology-and-psychology-of-pain/ http://brainblogger.com/2015/03/19/the-physiology-and-psychology-of-pain/#comments Thu, 19 Mar 2015 11:00:38 +0000 http://brainblogger.com/?p=19002 Pick up any newspaper and pore over it. Not only are nations at war but communities in the same country are fighting amongst themselves. People are killing each other for a piece of land, money, or just because they hate a person who looks different from them or worships another God. In the midst of these gory tales of hatred are the stories of triumph — men and women who give up their lives to save others and doctors who put their lives in the line of fire to treat people in far-flung places and war-torn regions.

Why do some people hurt others while others live just to bring a smile on other people’s faces?

Why do some people cause so much pain to others while some dedicate their lives to heal the wounds of strangers?

According to scientists, the perception of pain in oneself and recognizing it in others (empathy) is influenced by the complex interplay of neural circuitry in the individual, biochemical reactions in his brain, societal conventions, and evolutionary mechanisms.

The Perception of Pain in Self

Physical pain has a distinct brain signature. Functional magnetic resonance imaging (fMRI) can evaluate the amount of pain. However, another study has built on these findings to suggest that people “feel” physical pain differently. This difference stems from the way their brains are wired.

According to one recent study, the experience of pain has two distinct neural stages or pathways. The first stage kicks off, say, when you accidentally burn your fingers or cut your hand. The nerves in your hand send signals to the brain. The pain stimuli reach parts of the brain, like the anterior cingulate cortex, that are associated with the perception of pain. The chain of events that make up this stage is similar in all healthy individuals.

But people “react” differently to pain; not everyone utters an “ouch” or reaches out for a painkiller when they are physically hurt. The researchers who took part in the above study now know why. They have discovered a second neural pathway instrumental in the perception of pain. The “feeling” of pain — mild, intense, or unbearable — is determined by the activity in the medial prefrontal cortex and nucleus accumbens. These two regions of the brain are conventionally associated with motivation and emotion.

Scientists now know there are definite emotional and cognitive underpinnings to the perception of pain. This indicates that individuals can regulate and/or alter their perception of pain through mental conditioning techniques like meditation, distraction, and visualization. People who suffer from debilitating pain, triggered by a disease or an injury, can now hope to find relief in coping mechanisms other than popping painkillers.

The Societal Context of Feeling Pain

The perception of pain has a societal basis as well. Several studies have found that individuals tend to report different levels of pain in presence or absence of a highly-empathic person, like a romantic partner, and a complete stranger. Women tend to report less pain in the presence of an “attachment figure” or someone who makes them feel safe. In an experiment, women subjects in a threatening situation showed greater activity in the region of their brains that triggers safety signals (that is, they felt less pain) when they were shown images of their romantic partners.

One study, however, clarifies that the perception of pain in such cases is actually determined by the attachment style of the subject.

Individuals with anxious attachment styles crave close and intimate relationships but tend to sacrifice their needs to keep their partners happy. They are not confident about their partner’s affections and fear the relationship will not last. According to the findings from the above study, women with this attachment style tend to feel more pain in the presence of a person who does not empathize with their conditions. They feel lower pain in the presence of their romantic partners who are perceived to be highly empathic.

Individuals with avoidant attachment styles tend to value independence and self-sufficiency more than intimacy. These people are not comfortable sharing their feelings with strangers and partners alike. So it is not surprising that studies indicate that women with such attachment styles report lesser pain when alone than when in the presence of another individual, who may be a stranger or a romantic partner.

With these findings, doctors may now need to think twice before they ask individuals to be present when their partners are giving birth. It seems that there is no rule of thumb.

The Perception of Pain in Others

Human beings are social animals. The ability to live harmoniously in a society, care for others, and form enduring relationships depends on the quality of empathy. So it is natural that scientists should be curious to know why some people are more empathetic than others or if some situations naturally bring out more empathy.

Scientists believe that empathy is triggered by various cognitive and affective processes. Few years ago a study was carried out on subjects with congenital insensitivity to pain (CIP) to understand if painful experiences from the past influenced the ability to empathize with the pain of others. People with CIP cannot feel anything when subjected to painful stimuli. So they have no “experience” or memory of pain. But curiously, as was found in the study, they can empathize with the pain of others by seeing and hearing pain-related behavior in video clips.

But do you think that emotional cues of pain like seeing groaning and writhing are so powerful that they can move one and all? Unfortunately, no. Empathy is more complex than that.

A new article published this year reports that human beings tend to be more empathetic towards friends than strangers. The study also noted that stress tends to affect the ability to empathize. Individuals who are under stress tend to be less empathic to the pain of strangers than when they are relaxed and peaceful.

The latter finding may explain mob violence or why violence tends to increase during social uprisings. Stress is a powerful trigger that can make people act in a way they would not think about in other situations.

The mechanisms underlying empathy are complex. But it is crucial that scientists delve more into them because it seems that understanding empathy is akin to decoding violent behavior. And the world could certainly do with a lot less violence!

References

Danziger, N. (2006). Is pain the price of empathy? The perception of others’ pain in patients with congenital insensitivity to pain Brain, 129 (9), 2494-2507 DOI: 10.1093/brain/awl155

Decety, J. (2011). The neuroevolution of empathy Annals of the New York Academy of Sciences, 1231 (1), 35-45 DOI: 10.1111/j.1749-6632.2011.06027.x

Eisenberger, N., Master, S., Inagaki, T., Taylor, S., Shirinyan, D., Lieberman, M., & Naliboff, B. (2011). Attachment figures activate a safety signal-related neural region and reduce pain experience Proceedings of the National Academy of Sciences, 108 (28), 11721-11726 DOI: 10.1073/pnas.1108239108

Krahe, C., Paloyelis, Y., Condon, H., Jenkinson, P., Williams, S., & Fotopoulou, A. (2015). Attachment style moderates partner presence effects on pain: a laser-evoked potentials study Social Cognitive and Affective Neuroscience DOI: 10.1093/scan/nsu156

Martin LJ, Hathaway G, Isbester K, Mirali S, Acland EL, Niederstrasser N, Slepian PM, Trost Z, Bartz JA, Sapolsky RM, Sternberg WF, Levitin DJ, & Mogil JS (2015). Reducing social stress elicits emotional contagion of pain in mouse and human strangers. Current biology : CB, 25 (3), 326-32 PMID: 25601547

Sambo, C., Howard, M., Kopelman, M., Williams, S., & Fotopoulou, A. (2010). Knowing you care: Effects of perceived empathy and attachment style on pain perception Pain, 151 (3), 687-693 DOI: 10.1016/j.pain.2010.08.035

Wager, T., Atlas, L., Lindquist, M., Roy, M., Woo, C., & Kross, E. (2013). An fMRI-Based Neurologic Signature of Physical Pain New England Journal of Medicine, 368 (15), 1388-1397 DOI: 10.1056/NEJMoa1204471

Woo, C., Roy, M., Buhle, J., & Wager, T. (2015). Distinct Brain Systems Mediate the Effects of Nociceptive Input and Self-Regulation on Pain PLoS Biology, 13 (1) DOI: 10.1371/journal.pbio.1002036

Image via Tyler Olsen / Shutterstock.

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What Have Your Glia Done For You Today? http://brainblogger.com/2015/03/16/what-have-your-glia-done-for-you-today/ http://brainblogger.com/2015/03/16/what-have-your-glia-done-for-you-today/#comments Mon, 16 Mar 2015 11:00:43 +0000 http://brainblogger.com/?p=19006 How should we approach solving the most fundamental questions in neuroscience? Some would say that our current endeavors into mapping the complement of neuronal connections (the connectome) within the human brain will bring us the most fruitful gains; and they could be right. This is the main focus of several (expensive) big data initiatives such as the BRAIN Initiative, the Human Connectome Project and the Human Brain Project.

However, a major shortcoming of these projects is the lack of goals slated to mapping the other half of the brain; a complement of cells known as glia, of which there are three predominant populations. These cells make up fifty percent of the total brain volume and are integral to normal brain function. A complete understanding of the brain’s “support cells”, as they are also called, along with mapping the neuronal wiring, will be paramount for a global theory of how the brain works to bring about consciousness and our plethora of behaviors.

Microglia

Neuroglia consist mainly of astrocytes, oligodendrocytes and microglia, the last of which do not actually originate in the brain. Instead, microglia (my current field of research), originate in the fetal yolk sac (a structure involved in primitive hematopoesis, or blood formation) where many other primitive and tissue resident macrophages are born. Contrary to original theories, microglia migrate into the brain early in embryonic life and reside there as a stable, self-sustaining population of cells, which are never replaced by bone marrow-derived cells from the periphery.

In essence, unlike other glia, our microglia grow old with us. As a pool of tissue-specific macrophages, microglia constitute the immune cells of the central nervous system. They are capable of mounting an immune response against foreign invaders (e.g. blood cells or proteins and bacteria) as well as clear neuronal debris after injury. As such, they have, somewhat insultingly, been dubbed the “garbage men of the brain.”

It has become clear that this is short-sighted. For example, microglia mediate the elimination of supernumerary synapses from the developing brain through a mechanism known as phagocytosis. Essentially, they gobble up the unnecessary synapses that the brain generates during development, a process without which many developmental and behavioral abnormalities can occur. Understanding this process is thus essential for determining how the brain’s connections are wired.

Extending their services into postnatal life, microglia also maintain the status quo within the brain. For example, when microglia are completely depleted from the central nervous system, adult mice show deficits in learning. In other words, your microglia can make you smarter through learning-induced synaptic remodeling; they act to balance removal of unused or inappropriate synapses allowing neuronal energy expenditure to be allocated to forming efficient synapses.

What important programs do these little “electricians” employ to bring about an appropriately wired brain? How can we manipulate them to prevent or curb neurological and mental illnesses? These are important questions that the neuroscientific community is currently asking, but must be put into the wider framework of mapping the human brain.

Astrocytes

Astrocytes (or astroglia) perform the most diverse set of functions of the glial cells, including sharing with microglia the role of synaptic maintenance. How could they not? A single astrocyte can contact up to one million synapses. At the microstructure level this is known as the “tri-partate synapse”.

It is at this juncture of the pre- and post-synaptic clefts (where the electrical signal of one neuron is coupled via a chemical signal – a neurotransmitter – to the next neuron) and the astroglial process, that astrocytes do most of their work. Here, they can regulate the rate and strength of synaptic transmission across neurons by releasing or sequestering neurotransmitters and modifying extracellular ion concentrations. Not only do they “listen” and “talk” to neurons, but they also provide metabolic support of endothelial cells, which line the brain vasculature, making up the blood brain barrier. At this site, they are also well positioned to regulate the amount of blood flow to a local brain region.

Recently, astrocytes have made public headlines with the discovery of their involvement in bulk clearance of brain metabolic waste during sleep, the importance of which is not lost on us after staying up too late the night before an exam.

Oligodendrocytes

Oligodendrocytes (oligos for short), the central nervous system equivalent of the Schwann cell in the peripheral nervous system, wraps a fatty sheath around the axons of neurons. This sheath known as myelin provides insulation to the axon and allows for much faster propagation of the electrical signal and thus faster communication and transmission of information. Think of it as the insulation around electrical wires on your favorite appliance.

Oligos seem to only function in this capacity, but we do not actually know that – a rough search on PubMed shows about 25 times more papers are published on neurons than oligodendrocytes. For example, a study published this week in the journal Science found that oligos are much more diverse than previously known. The study authors found that this cell type alone could be sub-divided into six classes based on their molecular signatures. We do not yet know the function of each or how each type may play a role in brain cytoarchitecture to facilitate faster, more efficient neuronal signaling, but it should become a priority.

Each of the glial functions listed above (and we have left out other types of glia, such as Bergmann glia, NG2 glia and ependymal cells, but we know even less about them) are essential to global brain plasticity and learning. Because of their intimate relationship with neurons, glial cells hold a central position in influencing cognitive processes. Author of The Other Brain, R. Douglas Fields suggested in a Nature Comment:

“[That] these include processes requiring the integration of information from spatially distinct parts of the brain, such as learning or the experiencing of emotions, which take place over hours, days and weeks, not in milliseconds or seconds.”

In other words, because glia work on the slower chemical level, not via electrical signals, they may facilitate paradigms such as learning, which do not happen instantaneously like say, visual perception. I could not agree more. But at this time, we can only speculate as to how glia might impart their “magical elixir” on neurons, facilitating the workings of the most complex biological entity in the known universe.

Over a century after the start of glial research, we still lack fundamental knowledge of glial numbers, diversity, distribution throughout the brain and function in the context of neurons and between themselves. The “neurotechnologies” that arise from the neurocentric initiatives should additionally be allocated to studying these questions.

If our minds, which emerge from the tangled wet mass of neurons, make us who we are, then paraphrasing my mentor’s mantra sums it up best: What have your glia done for you today?

References

Araque A, Parpura V, Sanzgiri RP, & Haydon PG (1999). Tripartite synapses: glia, the unacknowledged partner. Trends in neurosciences, 22 (5), 208-15 PMID: 10322493

Kettenmann, H. & Ransom, B. R. (eds) Neuroglia 3rd edn (Oxford Univ. Press, 2013).

Paolicelli RC, Bisht K, & Tremblay MÈ (2014). Fractalkine regulation of microglial physiology and consequences on the brain and behavior. Frontiers in cellular neuroscience, 8 PMID: 24860431

Parkhurst CN, Yang G, Ninan I, Savas JN, Yates JR 3rd, Lafaille JJ, Hempstead BL, Littman DR, & Gan WB (2013). Microglia promote learning-dependent synapse formation through brain-derived neurotrophic factor. Cell, 155 (7), 1596-609 PMID: 24360280

Xie L, Kang H, Xu Q, Chen MJ, Liao Y, Thiyagarajan M, O’Donnell J, Christensen DJ, Nicholson C, Iliff JJ, Takano T, Deane R, & Nedergaard M (2013). Sleep drives metabolite clearance from the adult brain. Science (New York, N.Y.), 342 (6156), 373-7 PMID: 24136970

Zeisel A, Muñoz-Manchado AB, Codeluppi S, Lönnerberg P, La Manno G, Juréus A, Marques S, Munguba H, He L, Betsholtz C, Rolny C, Castelo-Branco G, Hjerling-Leffler J, & Linnarsson S (2015). Brain structure. Cell types in the mouse cortex and hippocampus revealed by single-cell RNA-seq. Science (New York, N.Y.), 347 (6226), 1138-42 PMID: 25700174

Image via Jose Luis Calvo / Shutterstock.

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Klotho and the Thread of Life – Can We Delay Aging? http://brainblogger.com/2015/03/14/klotho-and-the-thread-of-life/ http://brainblogger.com/2015/03/14/klotho-and-the-thread-of-life/#comments Sat, 14 Mar 2015 11:00:24 +0000 http://brainblogger.com/?p=18992 In Greek mythology, the Fates, or Moirae, were the goddesses who controlled humans’ destiny, from the time they were born to the time they died. The three sisters, Clotho, Lachesis and Atropos, daughters of Zeus and Themis, controlled the thread of human life.

Each Fate had a task: Lachesis was the apportioner, she measured the thread and decided how much lifetime was to be allowed; Atropos, the inevitable, cut the thread choosing when mortals would die; Clotho was the spinner, she spun the thread of a person’s life.

Clotho was the inspiration for naming klotho – a gene that somehow also seems to spin the thread of life. Klotho was another of so many serendipitous discoveries in science: while studying the phenotype of transgenic mice overexpressing another gene, there was an accidental insertion of ectopic DNA in a region of the klotho gene, inhibiting its expression. Makoto Kuro-o and colleagues, from the National Institute of Neuroscience, in Tokyo, Japan, thus found, in 1997, that disruption of the klotho gene caused accelerated aging. Later, it was found that the opposite also happened: by overexpressing klotho in mice, aging was significantly delayed and a longer lifespan was acquired.

The Journal of Neuroscience’s February article, showing that klotho can decrease premature mortality and enhance spatial learning and memory in a mouse model of Alzheimer’s disease piqued my curiosity about this protein. Obviously, the discovery of klotho generated massive research interest – a protein that may stop aging is the Holy Grail of life sciences, I reckon.

But how much is known about klotho? Can it really delay aging in humans?

Although the discovery of klotho has boosted the understanding of the aging process, its function is still not fully understood. In humans, serum levels of klotho decrease with age after 40 years old. This decrease is also observed in patients with several aging-related diseases. But most of what is known so far comes from animal research studies.

Although klotho is mainly produced in the kidneys and in the brain choroid plexus, mutations to its gene cause widespread aging phenotypes, probably due to circulating klotho. Deficiency has been associated with hypertension, renal failure, decreased insulin production and increased insulin sensitivity, early diabetic nephropathy, ectopic calcification in various soft tissues, arteriosclerosis, among others. Increased klotho expression, on the other hand, has been linked to reduced tumor proliferation and anti-inflammatory effects. In the brain, klotho deficiency in mice induced memory deficits, hippocampus degeneration, a reduction in synapses, and impaired axonal transport and myelin production.

Most of these phenotypes seem to be associated with defective calcium metabolism. Klotho seems to be essential in the maintenance of the levels of calcium and phosphorus by negatively regulating the synthesis of active vitamin D; abnormal activation of vitamin D due to klotho insufficiency has actually been shown to lead to degeneration of the dopaminergic system associated with Parkinson’s disease. Klotho also seems to act by increasing the expression of antioxidant enzymes and conferring resistance to oxidative stress, known to cause significant DNA damage.

Klotho and neurodegeneration

Myelin is an insulating material that envelops neurons, being essential for the correct functioning of the nervous system. Altered myelin production is a characteristic of the normal aging process of the brain. In fact, age-related cognitive decline seems to be mostly associated with loss of myelin rather than loss of neurons. There are experimental evidences suggesting that klotho is a key regulator in myelin biology by promoting and maintaining myelination. Therefore, it is possible that the loss of klotho expression may account for the age-related cognitive decline through decreased myelin production.

This link between cognitive decline, myelin abnormalities and klotho downregulation places it as a potential therapeutic target for neuroprotection against myelin-associated age-dependent changes. Compounds that increase klotho expression may therefore become important therapeutic tools for the treatment of neurodegenerative diseases, such as multiple sclerosis and Alzheimer’s disease. Increasing klotho levels may protect myelin integrity and prevent myelin degeneration in the aged brain and promote repair in multiple sclerosis.

This may be quite a wondrous molecule.

Maybe one day we will use klotho to prevent neurodegeneration and keep our brains young. Could we carry out a body transplant when our bodies get old, and use our cloned, younger body? Too much science fiction? Probably. But we once thought we couldn’t go to the Moon.

References

Abraham CR, Chen C, Cuny GD, Glicksman MA, & Zeldich E (2012). Small-molecule Klotho enhancers as novel treatment of neurodegeneration. Future medicinal chemistry, 4 (13), 1671-9 PMID: 22924505

Chen CD, Sloane JA, Li H, Aytan N, Giannaris EL, Zeldich E, Hinman JD, Dedeoglu A, Rosene DL, Bansal R, Luebke JI, Kuro-o M, & Abraham CR (2013). The antiaging protein Klotho enhances oligodendrocyte maturation and myelination of the CNS. The Journal of neuroscience : the official journal of the Society for Neuroscience, 33 (5), 1927-39 PMID: 23365232

Dubal DB, Zhu L, Sanchez PE, Worden K, Broestl L, Johnson E, Ho K, Yu GQ, Kim D, Betourne A, Kuro-O M, Masliah E, Abraham CR, & Mucke L (2015). Life Extension Factor Klotho Prevents Mortality and Enhances Cognition in hAPP Transgenic Mice. The Journal of neuroscience : the official journal of the Society for Neuroscience, 35 (6), 2358-71 PMID: 25673831

Kosakai A, Ito D, Nihei Y, Yamashita S, Okada Y, Takahashi K, & Suzuki N (2011). Degeneration of mesencephalic dopaminergic neurons in klotho mouse related to vitamin D exposure. Brain research, 1382, 109-17 PMID: 21276773

Kuro-o M, Matsumura Y, Aizawa H, Kawaguchi H, Suga T, Utsugi T, Ohyama Y, Kurabayashi M, Kaname T, Kume E, Iwasaki H, Iida A, Shiraki-Iida T, Nishikawa S, Nagai R, & Nabeshima YI (1997). Mutation of the mouse klotho gene leads to a syndrome resembling ageing. Nature, 390 (6655), 45-51 PMID: 9363890

Kurosu H, Yamamoto M, Clark JD, Pastor JV, Nandi A, Gurnani P, McGuinness OP, Chikuda H, Yamaguchi M, Kawaguchi H, Shimomura I, Takayama Y, Herz J, Kahn CR, Rosenblatt KP, & Kuro-o M (2005). Suppression of aging in mice by the hormone Klotho. Science (New York, N.Y.), 309 (5742), 1829-33 PMID: 16123266

Nabeshima Y (2002). Klotho: a fundamental regulator of aging. Ageing research reviews, 1 (4), 627-38 PMID: 12362891

Xu Y, & Sun Z (2015). Molecular Basis of Klotho: From Gene to Function in Aging. Endocrine reviews PMID: 25695404

Image via Twin Design / Shutterstock.

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Predicting Your Brain From Birth? http://brainblogger.com/2015/03/09/predicting-your-brain-from-birth/ http://brainblogger.com/2015/03/09/predicting-your-brain-from-birth/#comments Mon, 09 Mar 2015 11:00:17 +0000 http://brainblogger.com/?p=19013 Genetic sequencing is already changing the way we see ourselves. In February, the FDA announced approval for commercial “consumer genetics” company 23andMe to market a test for Bloom Syndrome. Whole genome sequencing is becoming faster and cheaper. But what might we do with this knowledge and how will it alter both society and us as individuals? Novel The Generation explores these questions.

Like the rest of her generation, the novel’s female protagonist, Freya, has her genome sequenced shortly after birth. Amongst other things, the results predicted early-onset Parkinson’s disease. She has been told to expect her symptoms to manifest when she reaches thirty or thirty-one, and has regular scans to track changes in her brain. We first meet Freya on the evening of her twenty-ninth birthday, finding her understandably subdued:

“They say I should really start to see the symptoms manifest themselves in the next year or so. I won’t just be clumsy, the drugs won’t be enough anymore and they won’t be able to hide it. I’m having another brain scan next week. I’m terrified.”

One theme of The Generation looks at whether our belief in a diagnosis could influence how we physically respond to it. Could a nocebo-type effect – an “anti-placebo” – actually induce symptoms?

It’s already been well-documented by research that the nocebo effect is real. Simply warning someone that a needle “may sting” can actually cause such pain to become a reality for the patient.

Researchers at the Technical University of Munich in Germany published a comprehensive report of the nocebo effect, examining 31 empirical studies. They concluded that the effect is common and ought to be taken into consideration by healthcare professionals on an everyday basis. One of the studies they analyzed looked at 50 people with chronic back pain, who were given a flexibility test. Half were told beforehand that the test might cause some pain, while the others were not. Many more patients in the first group claimed that the flexibility test did actually cause them pain.

As we undoubtedly discover more about our individual susceptibility to disease, such findings demonstrate that the psychological effects of that knowledge are likely to have repercussions. Medical professionals will need to carefully handle their patients’ preconceptions and fears, as well as their own.

Indeed, could medical professionals also be influenced by such predictions?

Later in the novel, Freya describes her most recent scan:

The neurologist had said he could see no marked worsening since the last scan, which had come as a pleasant surprise. Had she been having migraines? Any problems with coordination, digit or limb control? He had looked confused as he peered at the screen. Freya had replied affirmatively and he then looked perceptibly relieved. When I’m tired, she had said, at the end of a hard week at work, or if I’ve been to the gym and not eaten properly. He had nodded and tapped some notes into the computer. Well, that’s to be expected, he had said.

Do we – and more specifically, medical professionals – only see what we expect to see? You only have to take a look at some of the most popular optical illusions to begin to accept that this may be a possibility.

The “checker shadow illusion” is an image that tricks our brains into thinking that square in the “shadow” of the cylinder (B) is a different shade to one outside it (A). In reality, they are exactly the same color.

360px-Grey_square_optical_illusion

The creator of the illusion Edward H. Adelson, Professor of Vision Science at MIT in 1995, explains why our reaction to the image says a lot about our brain’s desire to find meaning:

“As with many so-called illusions, this effect really demonstrates the success rather than the failure of the visual system. The visual system is not very good at being a physical light meter, but that is not its purpose. The important task is to break the image information down into meaningful components, and thereby perceive the nature of the objects in view.”

The Generation envisages a near-future world in which all manner of medical issues and character traits – criminality, sexuality, academic ability – are defined at birth. And perhaps this may one day be feasible. Not only is the field of genetics on the road to this possibility, but understanding more about neurogenetics and neuroscience may expand the limits of our current understanding of the brain.

A recent review of brain imaging studies, published in Neuron, highlights the ways in which an increasing range of traits and susceptibilities can be predicted by MRIs and other neuroimaging techniques. The authors suggest that neuromarkers may offer “opportunities to personalize educational and clinical practices that lead to better outcomes for people”.

Despite the seriousness of the situation, Freya never tired of seeing her brain appear before her, first in two dimensions and then in three, digitally overlaid with fluorescent colours so that it ended up looking like something that belonged on the wall of a nightclub rather than inside her head. It always looked so strange, so otherworldly in its folds and holes, like the topography of a long-lost land. She had nothing to compare it to though, not really. Each brain is different, her neurologist had told her, which initiated the spark of a thousand questions she had wanted to ask him but had not, afraid to break the silence of the room. Hers, apparently, was just too different. Different enough that it would be her end.

Could it be, as one character muses, that “no matter how advanced modern science becomes, no matter how deeply our genes and our brains can be probed, no one can ever discover the subtleties of your character, the element of your spirit that makes you you.”?

The questions I raise in The Generation essentially relate to how far science can take us in our understanding of ourselves and our identity. I’m sure that we will soon begin to see answers to that question emerge.

The Generation is available now from Amazon, Kobo, NOOK and Google Play.

References

FDA News Release (February 19, 2015). FDA permits marketing of first direct-to-consumer genetic carrier test for Bloom syndrome. Accessed online 7 March, 2015.

Gabrieli, J., Ghosh, S., & Whitfield-Gabrieli, S. (2015). Prediction as a Humanitarian and Pragmatic Contribution from Human Cognitive Neuroscience Neuron, 85 (1), 11-26 DOI: 10.1016/j.neuron.2014.10.047

Häuser W, Hansen E, & Enck P (2012). Nocebo phenomena in medicine: their relevance in everyday clinical practice. Deutsches Arzteblatt international, 109 (26), 459-65 PMID: 22833756

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The Hollywood Medical Reporter – The Mind Behind “Brain Games” http://brainblogger.com/2015/03/08/the-hollywood-medical-reporter-the-mind-behind-brain-games/ http://brainblogger.com/2015/03/08/the-hollywood-medical-reporter-the-mind-behind-brain-games/#comments Sun, 08 Mar 2015 11:00:55 +0000 http://brainblogger.com/?p=18909 This Emmy-nominated series tests the ultimate supercomputer – your brain. Back for its fifth season, Brain Games uses a host of interactive games, experiments and, yes, even magic tricks to expose and explain some of the most complex regions of the brain. We sat down with Executive Producer, Michael J. Kovnat, to discuss the truly mind-altering show.

BB: Can you share one thing you knew about the brain that made you want to work on this show, and one thing you’ve learned about the brain since you began work on it?

MK: I had heard that the brain is the most complex known structure in the universe – which had seemed hyperbolic. As I’ve dived into working on the show, I’ve come to appreciate what that means – and all the surprising ways our awareness arises from this three pound organ. As one example, our episode on color gets into how your subjective experience of red, green, etc. has to do with how your photoreceptors interact with other brain cells, and that system can be easily fooled and confused.

 BB: What can you tell us about the inception of Brain Games?

MK: The idea was to create a show that would invite the audience to play along with a series of perception experiments. Over time, that concept was refined by a number of very talented producers, writers, and executives.

BB: Can you share a bit about your background and how you eventually began working on this show?

MK: I’d been producing non-fiction television for about 20 years, and had developed a sub-specialty in science programming. When I was hired as a staff executive producer at Nat Geo Channel, Brain Games was already in its second season. It was the first project I lobbied to work on when I was hired.

BB: More than mindless entertainment, this show demands an interactive viewing experience. That being said, what is the ultimate goal you wish to achieve through people watching this show?

MK: We want to inspire viewers to get curious about how their brains work, and hopefully change their perceptions on everyday actions. We’re making the processes of the brain come to life through interactive experiments that will keep viewers guessing and wanting more.

BB: How do you go about choosing both the human subjects for the interactive experiments on the show, as well as the experts/guest(s)?

MK: The team reaches out to people in a variety of ways. Experts are usually sought out based on their published work in the subject area of an episode. Other participants are solicited online or approached on the street.

BB: Has the show changed and/or developed in any obvious or not-so-obvious ways over the seasons?

MK: The show has actually gone through many changes over the seasons. It premiered as unhosted, hour-long specials. Then it became half hours and Jason Silva was brought in as a host. The tone and style has shifted slightly season to season. And more changes are coming soon!

BB: Can you share any details with us about what viewers can expect to see in the rest of Season 5

MK: This summer, you’ll see new episodes covering topics such as scams, positive thinking, and the surprising differences and similarities between human and animal brains. We want to ask big questions, always seen through the lens of how the brain works.

BB: Is Brain Games meant for a particular audience or viewer, and has that changed at all over the seasons?

MK: The ideal viewer is really any curious person. We’ve found that people in just about every demographic have found something they love about Brain Games. Viewers play along and get interested in the “why” behind the “wow.”

The following questions refer to episodes featuring Magician, Eric LeClerc:

BB: How would  you compare the two worlds of science and magic?

MK: Magic, done honestly, can provide an excellent guide to gaps in human attention. These tricks show how easily the brain can be fooled. Many magicians, like scientists, are first-rate skeptics.

BB: What is your favorite magic-trick?

MK: Any trick where my mind appears to have been read. Gets me every time.

BB: How do you decide what insights about the brain as well as the corresponding magic-tricks and interactive brainteasers to feature on a given episode? Does one typically come before the other? How much collaboration is required and does that collaboration ever involve outside consultation?

MK: Typically, we start with a show topic or theme. Then we work with magicians to come up with related illusions.

BB: How do you find ways to distill all the complex scientific insights you discuss on the show into viewer-friendly material that is not simply related in understandable terms, but can resonate as well? How, if any, do the “magical” aspects employed play a role in this?

MK: Just as a good magician never reveals his or her tricks, I don’t want to give away all our secrets. But when we use illusions in the show, they function as a fun way to call attention to the gap between what you expect and what’s really happening. That can be an entertaining way into a complex scientific idea.

BB: In that same vein, how do you balance the incredibly complex element of science with the goal of entertainment? Does one ever get in the way of the other?

MK: This is really an entertainment-driven show. The science comes along for the ride, but if we can’t entertain, viewers won’t watch.

Image via Linda Bucklin / Shutterstock.

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Best and Worst of Neuroscience & Neurology – February 2015 http://brainblogger.com/2015/03/07/best-and-worst-of-neuroscience-neurology-february-2015/ http://brainblogger.com/2015/03/07/best-and-worst-of-neuroscience-neurology-february-2015/#comments Sat, 07 Mar 2015 20:00:22 +0000 http://brainblogger.com/?p=18868 In February we have seen, yet again, quite a few new exciting developments in neuroscience and neurology. There were interesting findings in both theoretical neuroscience and in more practical applications aimed at studying various brain conditions and diseases.

Please do note, of course, that the choice of which articles to include in the monthly review is highly subjective. The content of this review mostly reflects my personal opinion about their significance.

On 23 February, the scientific community marked the birthday of Allan McLeod Cormack who received the Nobel Prize in Physiology and Medicine in 1979 for invention of computer-assisted tomography. Allan Cormack’s research laid theoretical foundation to this method back in the early 1960s. It would be probably worth mentioning that Cormack’s original papers on the subject initially attracted very little interest, until Godfrey Hounsfield constructed the first CT scanner in 1971 based on Cormack’s theoretical concept. Allan Cormack is rightfully considered the father of modern computer tomography. These days, the CT-based techniques are actively used by neuroscientists. In fact, a number of findings reviewed below are obtained using various CT methods.

First two articles that I include deal with more theoretical aspects of neurobiology.

For decades, neuroscientists believed that adult brains do not produce new neurons. The discovery that this is not correct challenged this major dogma of neuroscience. The role of these new neurons in behavior and cognition is still not clear, however. The article published this month in Trends in Cognitive Science presents an interesting point of view on this issue.

It is now well known that environment has a profound effect on adult brains. Stress has been shown to decrease the number of new neurons in hippocampus. On the other hand, rewarding experiences stimulated the production of new neurons in this part of the brain. The authors of the report argue that new neurons may serve as a means to fine-tune the hippocampus to the predicted environment. In particular, seeking out rewarding experiences or avoiding stressful experiences may help each individual optimize his or her own brain. Thus, it appears that newly born neurons help us to flourish in the rewarding environment.

The question what make our brain unique (thus eventually making us who we are) remains the biggest unsolved mystery in neuroscience. An article published this month in Science can certainly be viewed as a serious contribution towards finding the answer to this question.

Researchers based in Germany were comparing the genes involved in the development of human brain and brain of mouse. They identified 56 genes preferentially expressed in the human neocortex. The neocortex is the part of the brain explicitly associated with cognitive abilities, and it is significantly enlarged in primates. One of the genes, ARHGAP11B, turned out to be present only in human progenitor cells, the stem cells that divide and form other brain cells during the brain growth and development. Moreover, the scientists found that gene ARHGAP11B is unique for humans and is absent even in chimpanzees, our closest evolutionary relatives. Researchers believe that this gene has contributed to the evolutionary expansion of the human neocortex.

The following two articles are related to the studies of how we learn various skills and how we learn to interact with others.

It is intuitively obvious that younger people and people in old age have different approaches to learning. Scientists from University College London decided to put this assumption to a specific test. They enrolled two groups of participants, one aged 19-35 and another aged 60-73, and assigned them the same numeric task which would require some learning to be finished successfully. Both groups performed with similar degree of success, but utilized two completely opposite strategies. Younger people were learning by integrating different types of information, while older people advanced their learning through ignoring distracting, less important information.

The study shows that the brain works rather differently at different ages, and training can enhance different age-dependent cognitive processes. Among other things, this new insight may help to inform educationists on different age-dependent approaches to teaching.

Our social behavior inevitably requires understanding of others and the ability to anticipate their actions. In fact, this ability is a cornerstone of successful social interaction. This month, researchers from Massachusetts General Hospital-Harvard Medical School Center for Nervous System Repair announced that they had discovered key neuronal elements in the dorsal anterior cingulate cortex involved in the formation of such behavior.

Scientists taught rhesus monkeys to play a game where outcome (and consequent reward) was linked to the ability to anticipate each other’s actions. The neurons in the anterior cingulate were particularly active when an animal was trying to figure out the action of the opponent. The anticipating ability disappeared when scientists artificially disrupted the activity of neurons in anterior cingulate cortex. Researchers believe that their findings will help to pave the way for better understanding and treatment of such conditions as autism and antisocial personality disorder.

This month we witnessed large number of publications related to Parkinson’s disease. There were both positive and negative developments in this area.

Encouraging news came from Sweden: in a first-of-its-kind experiment on humans, scientists injected growth factor PDGF directly into the brains of patients suffering from Parkinson’s disease. PDGF is known to stimulate regenerative processes in the body, and researchers hoped that injections of this substance can stimulate self-repair of brain. The previous trials on animals have shown that this assumption is correct and injections can improve motor functions in mice with Parkinson’s disease.

The human trial was limited to 12 patients only and was aimed to establish the safety of the procedure. No adverse effects were observed in any of the patients during the 85-day follow-up period. The symptoms of Parkinson’s disease are caused by a gradual decrease in the production of neuromediator dopamine. The results of brain tomography before and after the injections demonstrated that the level of dopamine increased in the patients who received PDGF injections, thus indicating the reversal of pathological process. Obviously, this is very exciting news, and the trials now will be taken to the next level in several countries around Europe.

Clinical trials often result in failures. The general public is often unaware of the fact that the overwhelming majority of drug trials get terminated – for a variety of reasons – at the early stages, and the potential drugs never reach patients. A trial for a previously promising treatment for Parkinson’s disease was terminated this month.

Despite decades of research and substantial recent progress in understanding the molecular mechanisms involved, we still have no clinically available drugs capable of stopping or even slowing down the development of Parkinson’s disease. Earlier studies indicated that creatine monohydrate might be capable of slowing down the development of disease’s clinical manifestations. This prompted the National Institute of Neurological Disorders and Stroke to initiate a clinical trial to study the long-term effects of this drug.

Unfortunately, after five years of follow-up, researchers did not noticed any improvements in the patients taking creatine monohydrate compared to patients taking a placebo. The trial was terminated early due to futility.

A number of studies in the past reported the association between the use of statins (cholesterol-lowering drugs) and decreased incidence of Parkinson’s disease. The evidence to support this view, however, was rather inconsistent. New analysis of long-term data published this month revealed that statins don’t have protective effect against the disease. Moreover, in the long term they even increase the risk of this disease’s development. The authors of the report caution against promoting benefits of statins until better understanding of their influence on the body and brain is reached.

Two other publications questioned the safety and efficiency of the methods and treatments that have been used in medical practice for decades.

Millions of surgeries under total anesthesia are performed every year around the world. Anesthesia is not absolutely safe and is associated with a number of risks. It appears that one of such risks is the potential impairment of brain development in young children and babies. Several experts in the field have recently published an article highlighting their concerns.

The concerns are based on two facts. First, anesthetics do kill brain cells in young monkeys. Second, children who experienced multiple exposures to anesthesia early in life are more likely to have learning problems. Both facts do not prove conclusively the danger of anesthetic for the developing human brain, but the findings do call for caution and for further research.

Another review published this month cast the doubts on the wisdom of using anti-depressants targeting the serotonin re-uptake pathway. The theory behind using such drugs states that depression is caused by decreased levels of serotonin in the synapses. However, it is not yet possible to measure directly how serotonin is released and used in the living brain, which makes the foundation of the theory quite shaky.

The authors of the report argue that anti-depressive medications, instead of helping patients, complicate their recovery. This explains why the depressive symptoms tend to get worse in the first two weeks of taking the drugs. It appears that the drugs create obstacles for the natural mechanisms of brain recovery. Many researchers will disagree with the point of view of the authors of this report. Nonetheless, the side effects of antidepressants are well known, and more detailed look into the mechanisms of their action is warranted.

Finally, a new research paper published this month challenged one textbook view that persisted in neuroscience for many years.

The hippocampus has traditionally been thought to be critical for conscious memory but not necessary for unconscious memory processing. Unconscious memory involves things that we can do without having to think about it, such as moving around and performing simple manual tasks. Much of the knowledge about the hippocampus and how our brains organize memory comes from research on amnesia patients.

This theory of unconscious memory system was recently challenged by a new analysis of the data. Results suggest that the hippocampus plays a fundamental role in aspects of memory processing that are beyond conscious awareness. It appears that both conscious and unconscious memory systems rely upon the same neural structures but function in different physiological ways.

The studies listed above as negative developments should not necessarily be viewed as such. By exposing the wrong concepts, they provide substantial contribution to our knowledge and help to advance science.

References

Addante, R. (2015). A critical role of the human hippocampus in an electrophysiological measure of implicit memory NeuroImage, 109, 515-528 DOI: 10.1016/j.neuroimage.2014.12.069

Andrews, P., Bharwani, A., Lee, K., Fox, M., & Thomson, J. (2015). Is serotonin an upper or a downer? The evolution of the serotonergic system and its role in depression and the antidepressant response Neuroscience & Biobehavioral Reviews, 51, 164-188 DOI: 10.1016/j.neubiorev.2015.01.018

Florio, M., Albert, M., Taverna, E., Namba, T., Brandl, H., Lewitus, E., Haffner, C., Sykes, A., Wong, F., Peters, J., Guhr, E., Klemroth, S., Prufer, K., Kelso, J., Naumann, R., Nusslein, I., Dahl, A., Lachmann, R., Paabo, S., & Huttner, W. (2015). Human-specific gene ARHGAP11B promotes basal progenitor amplification and neocortex expansion Science DOI: 10.1126/science.aaa1975

Haroush, K., & Williams, Z. (2015). Neuronal Prediction of Opponent’s Behavior during Cooperative Social Interchange in Primates Cell DOI: 10.1016/j.cell.2015.01.045

Kieburtz, K., Tilley, B., Elm, J., Babcock, D., Hauser, R., Ross, G., Augustine, A., Augustine, E., Aminoff, M., Bodis-Wollner, I., Boyd, J., Cambi, F., Chou, K., Christine, C., Cines, M., Dahodwala, N., Derwent, L., Dewey, R., Hawthorne, K., Houghton, D., Kamp, C., Leehey, M., Lew, M., Liang, G., Luo, S., Mari, Z., Morgan, J., Parashos, S., Pérez, A., Petrovitch, H., Rajan, S., Reichwein, S., Roth, J., Schneider, J., Shannon, K., Simon, D., Simuni, T., Singer, C., Sudarsky, L., Tanner, C., Umeh, C., Williams, K., & Wills, A. (2015). Effect of Creatine Monohydrate on Clinical Progression in Patients With Parkinson Disease JAMA, 313 (6) DOI: 10.1001/jama.2015.120

Huang, X., Alonso, A., Guo, X., Umbach, D., Lichtenstein, M., Ballantyne, C., Mailman, R., Mosley, T., & Chen, H. (2015). Statins, plasma cholesterol, and risk of Parkinson’s disease: A prospective study Movement Disorders DOI: 10.1002/mds.26152

Cappelletti, M., Pikkat, H., Upstill, E., Speekenbrink, M., & Walsh, V. (2015). Learning to Integrate versus Inhibiting Information Is Modulated by Age Journal of Neuroscience, 35 (5), 2213-2225 DOI: 10.1523/JNEUROSCI.1018-14.2015

Opendak, M., & Gould, E. (2015). Adult neurogenesis: a substrate for experience-dependent change Trends in Cognitive Sciences, 19 (3), 151-161 DOI: 10.1016/j.tics.2015.01.001

Paul, G., Zachrisson, O., Varrone, A., Almqvist, P., Jerling, M., Lind, G., Rehncrona, S., Linderoth, B., Bjartmarz, H., Shafer, L., Coffey, R., Svensson, M., Mercer, K., Forsberg, A., Halldin, C., Svenningsson, P., Widner, H., Frisén, J., Pålhagen, S., & Haegerstrand, A. (2015). Safety and tolerability of intracerebroventricular PDGF-BB in Parkinson’s disease patients Journal of Clinical Investigation, 125 (3), 1339-1346 DOI: 10.1172/JCI79635

Rappaport, B., Suresh, S., Hertz, S., Evers, A., & Orser, B. (2015). Anesthetic Neurotoxicity — Clinical Implications of Animal Models New England Journal of Medicine, 372 (9), 796-797 DOI: 10.1056/NEJMp1414786

Image via Bangkok happiness / Shutterstock.

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Brains in Pain – Apps to the Rescue? http://brainblogger.com/2015/03/06/brains-in-pain-apps-to-the-rescue/ http://brainblogger.com/2015/03/06/brains-in-pain-apps-to-the-rescue/#comments Fri, 06 Mar 2015 12:00:24 +0000 http://brainblogger.com/?p=18853 It’s a simplification to argue that technology removes us from the concerns of the physical world. Many technological applications are geared specifically to orient us in the world, and none bring us more clearly full circle back to ourselves than mobile apps which focus on our physical and mental health.

One of the lesser known – but vitally helpful – types of apps is the emerging range of technological aids for living with health conditions associated with great physical pain. Such apps can also be incredibly useful for pain specialists, who can use them to monitor highly detailed reports on patients’ pain thresholds, mood, physical activity levels and more.

Harvard PhD and Professor of anaesthesia and psychiatry, Robert Jamison, recently presented his research into smartphone apps for pain to the American Pain Society. His research found that existing therapies in this new domain could help control pain, improve the functional abilities of patients and also lower health care costs.

In those who feel isolated due to their pain or conditions, the apps can help to limit withdrawal, Jamison found. Smartphone data can also be summarized and converted directly into electronically kept patient notes.

Some currently available apps such as WebMD Pain Coach and MMP Lite focus on the tracking, analysing and communicating about pain. They offer data correlation and cloud storage facilities. There’s another interesting app, Mindfulness Meditation for Pain Relief, which offers a course of meditation programmes designed to actually lower pain perception.

A cutting-edge technological research project into pain relief is being conducted by entrepreneur Christopher deCharms, in collaboration with Stanford and Harvard Universities. In studies using $3 million MRI machines and virtual reality goggles, the team have been showing sufferers of chronic pain 3D models and representations of their own brains in real time in order to help them learn techniques for controlling their own brain states.

Based on this research, deCharms believes that it is possible to learn to activate various regions of the brain through such direct observation. The average improvement in clinical trials has been a 30% lowering of pain intensity: a huge result.

What’s even more amazing is that by modelling the best methods discovered for controlling one’s own brain regions in the MRI scanner, and building guided practices based on these, the researchers have achieved similar reductions in pain in users nowhere near the MRI scanner, but working from home on a smartphone, simply following the guided practices.

It is these (far more affordable!) models and guides which the project, known as Brainful, hopes to use to take the benefits to the mainstream. deCharms and collaborators have published several academic papers on their current findings, which make for compelling reading.

With both neuroscience, and the uniting of mind and brain studies still in their infancy, this technology has the potential to totally transform the medical norms we live with, and offer a real alternative to drug-based pain relief.

References

deCharms, R., Maeda, F., Glover, G., Ludlow, D., Pauly, J., Soneji, D., Gabrieli, J., & Mackey, S. (2005). Control over brain activation and pain learned by using real-time functional MRI Proceedings of the National Academy of Sciences, 102 (51), 18626-18631 DOI: 10.1073/pnas.0505210102

Image via pcruciatti / Shutterstock.

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Mapping the Human Brain To “See” What Makes You Unique http://brainblogger.com/2015/03/03/mapping-the-human-brain-to-see-what-makes-you-unique/ http://brainblogger.com/2015/03/03/mapping-the-human-brain-to-see-what-makes-you-unique/#comments Wed, 04 Mar 2015 01:52:02 +0000 http://brainblogger.com/?p=18815 The Matrix may not be fantasy anymore. The virtual reality shown in Avatar could be with us any time now, and at the same time, scientists are getting closer to decoding what goes on inside our brains. In fact, they are well on their way to mapping the human brain.

This means that you could really peek into the brain and “see” how it works for yourself — the domino effect of memory cells firing up to take you back to your childhood home and its smell of freshly-baked bread, or the flurry of activity in the learning center as you try to pick up the notes and play them on the piano.

Scientists have long known that the structural connectivity of the brain influences the functional performance of individuals. In other words, given the structural similarities of the human brain, it is the neural and synaptic connections within our brains that make us the unique individuals that we are. But what they want to do now is to create a complete map of the brain to discover how memories are stored, how personality traits develop, and how people learn skills. It looks as if they are well on their way.

Enter the connectome!

Mapping the Connectome

The network of connections in the brain — up to 10,000 for each of the 85 billion cells — is known as the “connectome.”

It is a complex but organized system of wires unique to every person. Scientists believe that wiring faults hamper the way cells connect and signal to each other. This may lead to mental disorders such as depression, schizophrenia and learning disabilities.

So, scientists need a comprehensive model that not only shows the neuronal structures but also details the connections — how your brain figures out the moves when you play Diablo; how do you remember, recall, and apply knowledge; how do you sense changes in temperature and color.

The human brain comprises structurally distinct but functionally interdependent components. Scientists have to mine data at the neuronal level (microscale) where there are connections between individual cells, as well as connections between several groups of neurons (mesoscale), and at the regional level (macroscale), where different structures of the brain interact with one another. Combining the findings from these disparate sets of data will ultimately help scientists create a comprehensive map of the brain.

There have been quite a few connectome studies aimed at creating such mental maps.

How the Eye Detects Motion

One connectome study has decoded how the human eyes sense motion. It is interesting to note that neurological data for the study was gleaned from more than 2,000 volunteers who took part in an online game, EyeWire. The results of the study busted the myth, long held in visual neuroscience circles, that we see with the brain. Scientists now know for sure that visual stimuli is first processed (somewhat) by cells in the retina before being transmitted to the brain.

The photoreceptor cells in the eye capture light, but on their own they are not capable of sensing motion. They are connected to the starburst amacrine cells that are in turn connected to the optic nerve that transmits signals to the brain to be interpreted. The photoreceptor cells are connected to the amacrine cells in such a way that the visual stimulus hits the latter at different times, or with a time lag. The brain interprets the delay in receiving the signals as coming from a moving object.

The findings from the above study represent a step in the right direction for scientists engaged in finding ways to map the brain. The task is not easy because deciphering neuronal characteristics and behavior demands that researchers study a large number of neurons, ideally individually, in different areas of the brain. Scientists expect that continual advances in micro-electrode technology will enable them to target the teeny-weeny neurons. They also believe that the way computational technology is progressing, they will soon be able to process the data mined from the billions of cells and the almost countless neural pathways effectively enough to create a map of the whole brain.

Implications of Brain Mapping Studies

Scientists, physicians, psychiatrists, and the common man on the street have much to be excited about the brain-mapping studies that are currently underway. The implications are wide-ranging.

As already mentioned, neuroscientists believe that many psychiatric disorders are caused by faulty wiring in the brain. Being able to pinpoint where the connection has gone awry can help them explore effective therapeutic methods. Brain-mapping studies also hold promise for people who have suffered traumatic brain injuries.

Knowing how neural structures and behavior influence function can also help scientists understand the basis of cognitive processes. Their conclusions can help educationalists devise curriculum that best meets the learning needs and preferences of specific groups of students or those who are suffering from learning disabilities.

The findings from such brain-mapping studies are already being utilized to explore the scope of neural prosthetics. These findings will enrich the brain-computer interface (BCI) studies that are currently underway. Right now, scientists are at work to devise sophisticated, powerful, and sensitive BCI systems that can capture and process neural data in real time and use this to control specific areas of the brain. These BCI systems can forge an artificial connection, which should mimic a neural pathway, between a set of implantable electrodes embedded within a prosthetic limb and the brain. Such BCI systems have already been tested on monkeys, and it is not hard to fathom how eagerly amputees or those who are paralyzed are awaiting developments in this field!

In fact, scientists around the world are already excited by the advances made in neuromorphic computing. Researchers have developed a computer chip that simulates the brain and can replicate synaptic connections. They believe that when this device integrates data from more comprehensive brain maps, it will become powerful enough to help blind people move around physically with ease.

Brain-mapping studies are the latest buzz in the medical fraternity. The brain may not have revealed all its secrets, but hopes run high.

References

Kim, J., Greene, M., Zlateski, A., Lee, K., Richardson, M., Turaga, S., Purcaro, M., Balkam, M., Robinson, A., Behabadi, B., Campos, M., Denk, W., & Seung, H. (2014). Space–time wiring specificity supports direction selectivity in the retina Nature, 509 (7500), 331-336 DOI: 10.1038/nature13240

Kipke, D., Shain, W., Buzsaki, G., Fetz, E., Henderson, J., Hetke, J., & Schalk, G. (2008). Advanced Neurotechnologies for Chronic Neural Interfaces: New Horizons and Clinical Opportunities Journal of Neuroscience, 28 (46), 11830-11838 DOI: 10.1523/JNEUROSCI.3879-08.2008

Service, R. (2014). The brain chip Science, 345 (6197), 614-616 DOI: 10.1126/science.345.6197.614

Sporns, O., Tononi, G., & Kötter, R. (2005). The Human Connectome: A Structural Description of the Human Brain PLoS Computational Biology, 1 (4) DOI: 10.1371/journal.pcbi.0010042

Zuo, X., Ehmke, R., Mennes, M., Imperati, D., Castellanos, F., Sporns, O., & Milham, M. (2011). Network Centrality in the Human Functional Connectome Cerebral Cortex, 22 (8), 1862-1875 DOI: 10.1093/cercor/bhr269

Image via solarseven / Shutterstock.

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Brains Aren’t Fooled By Virtual Reality http://brainblogger.com/2015/02/24/brains-arent-fooled-by-virtual-reality/ http://brainblogger.com/2015/02/24/brains-arent-fooled-by-virtual-reality/#comments Tue, 24 Feb 2015 12:00:20 +0000 http://brainblogger.com/?p=18572 The scenes and the environments in World of Warcraft games appear so real that, for a moment, you forget you are staring at the screen. Technology has advanced so much that we can not only recreate reality but also engage with it. But however real the virtual may seem, the brain knows the difference! According to the recently published findings, the neurons in the brain react differently when they perceive a virtual environment than when they are in the real world.

The GPS Cells in Our Brains

The clue to the brain’s varied responses to different environments lies in the “GPS” or place cells. These neurons in the hippocampus create and control cognitive maps by taking input from the environment. They fire when a person is in a novel environment to create episodic memories that help us remember events (what) and place these events in their appropriate contexts of space (where) and time (when).

Place cells are critical for learning and memory. Incidentally, the hippocampus region is damaged in people with Alzheimer’s disease, schizophrenia, epilepsy, post-traumatic stress disorder or in those who have suffered strokes. Because their ability to learn and recall events, people, and objects is severely impaired, these people find it challenging to move about and around the world.

How Do GPS Cells Behave in Real and Virtual Environments?

The modus operandi of the space-mapping neurons in the hippocampus is not wholly clear, but scientists have deciphered that these cells form mental maps of environments by registering the position of different objects in an environment to calculate distances between them.

However, they believe that apart from the visual-spatial stimuli, the smells and sounds present in an environment also go into the creation of mental maps. This may be the reason why the place cells behave differently in real and virtual environments because the computer-simulated reality does not provide varied sensory stimuli.

Because human and rodent neurons are similar, scientists have carried out tests on the hippocampal cells of rats to arrive at the above conclusions. Here’s how all the findings add up.

According to a study published last year, a place cell in the hippocampus fires or “lights up” (as evident from scan images) whenever the rat is in a new environment. A real environment contains many different sensory cues including distal visual and self-motion cues. However, a virtual environment contains only distal visual and non-vestibular self-motion cues. Experiments on rats in these two environments showed that only 20 percent of the place cells in their brains got activated in a virtual environment compared to 45 percent when they were placed in a similar-looking but real world. This indicates that apart from behaving differently in real and virtual worlds, the brain creates more effective and comprehensive cognitive maps when it is fed with multi-sensory cues.

The above experiment sheds light on other interesting goings-on in the hippocampus in real and virtual environments.

When the rats were in the real world, their place cells fired every time they passed an object (a fixed landmark). This occurred consistently, and scientists realized that the neural place cells probably create mental maps by computing the distance between objects. But when the rats were in a virtual environment, not only fewer place cells in their brains fired but they acted randomly as well. In the experiment, the place cells were activated based on the movements or the relative positions of the rats. For instance, the cells lit up whenever the rats paced five steps back and forth, irrespective of the landmarks they perceived.

Another curious finding came out from a similar experiment. When the rats were made to navigate the real world, the activity within the place cells that fired in response to environmental stimuli correlated with the speed at which the animals moved. The faster the rats moved, the greater was the activity in these cells and vice versa. In the virtual environment, a screen showing video of the real world moved in tandem with the rats to give them the perception that they were actually moving as they do in the real world. But their hippocampal place cells showed steady, rhythmic activity irrespective of the speed at which the rats changed their relative positions. This discrepancy indicates the brain does not register stimuli accurately in a virtual environment.

Scientists believe that a cognitive map of a virtual world should be a function of the relation between specific motion paths and peripheral landmarks. But experiments have proved otherwise. This clearly suggests that the brain recognizes the gaps between the real world and the virtual reality our technologies create.

What Do Scientists Make of the Brain’s Different Performances in Real and Virtual Worlds?

The hippocampus is involved in spatial learning and related memory formation. The above experiments throw some light on how the brain works to create and retrieve memories. These findings bring hope that the mysteries of the hippocampus will one day be decoded and therapeutic procedures will be devised to enhance the quality of life of patients suffering from neurodegenerative disorders.

The above experiments also take some of the shine away from virtual reality technologies. For all the hype, it is obvious that the virtual is not as “real” as it is made out to be, at least as of yet.

Computers cannot recreate the “feel” of the real world — the smell of freshly-baked bread wafting through the air, the rustle of leaves in the breeze, and the crunching of gravels under the feet. Computer programmers and analysts may be concerned. After all, the closer virtual reality is to reality, the more accurate would be the performance of the critical job-related simulation applications used by military personnel, aviators, and scientists.

References

Aghajan, Z., Acharya, L., Moore, J., Cushman, J., Vuong, C., & Mehta, M. (2014). Impaired spatial selectivity and intact phase precession in two-dimensional virtual reality Nature Neuroscience, 18 (1), 121-128 DOI: 10.1038/nn.3884

Aikath, D., Weible, A., Rowland, D., & Kentros, C. (2014). Role of self-generated odor cues in contextual representation Hippocampus, 24 (8), 1039-1051 DOI: 10.1002/hipo.22289

Geisler, C., Robbe, D., Zugaro, M., Sirota, A., & Buzsaki, G. (2007). Hippocampal place cell assemblies are speed-controlled oscillators Proceedings of the National Academy of Sciences, 104 (19), 8149-8154 DOI: 10.1073/pnas.0610121104

Jadhav, S., Kemere, C., German, P., & Frank, L. (2012). Awake Hippocampal Sharp-Wave Ripples Support Spatial Memory Science, 336 (6087), 1454-1458 DOI: 10.1126/science.1217230

Nitz, D. (2014). A place for motion in mapping Nature Neuroscience, 18 (1), 6-7 DOI: 10.1038/nn.3908

Ravassard, P., Kees, A., Willers, B., Ho, D., Aharoni, D., Cushman, J., Aghajan, Z., & Mehta, M. (2013). Multisensory Control of Hippocampal Spatiotemporal Selectivity Science, 340 (6138), 1342-1346 DOI: 10.1126/science.1232655

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What Do Smartphones Do to the Brain? http://brainblogger.com/2015/02/22/what-do-smartphones-do-to-the-brain/ http://brainblogger.com/2015/02/22/what-do-smartphones-do-to-the-brain/#comments Sun, 22 Feb 2015 12:00:49 +0000 http://brainblogger.com/?p=18696 Even as the smartphone continues to evolve in functionality and power, parents are anxious that their kids seem to be addicted to their device. According to them, all that their kids do is switch off their ears, bury their heads, and tap, flick, and scroll on their touchphone screens. But, scientists have discovered at least one way in which the smartphone affects the brain positively.

There are as many people who see the smartphone as a pest and a distraction as there are people who hail the device as a marvel of technology. It is no wonder guardians are worried about the excessive use of smartphones. But not everything is as bad as it might look to some people.

Smartphone Usage Can Reorganize Brain Structure

According to a new study published this year, regular and heavy smartphone users exhibit increased activity in the cortical area of their brains in response to touch on their thumb, index, and middle fingers. Incidentally, the thumb and the index finger are those used most by smartphone users.

The researchers compared the results of this study with brain scan images of other individuals who used older makes of phones. The results of this comparative study showed that the fingers of the smartphone users were much more sensitive to touch (as demonstrated by the flurry of activity in the cortical region) than those of the non-smartphone users. What is more, the cortical activity increased proportional to phone usage. The study also found that the thumb showed the most sensitivity to smartphone usage.

In this context it is worth mentioning that the smartphone study found no evidence of a relationship between cortical structure and activity and the number of years the subject had been using a smartphone. It seems the brain starts to show changes, albeit subtle ones, after just weeks. The scientists believe that the findings of their study indicate that the brain has the ability to reshape and rewire itself influenced by daily activities, such as the use of personal digital technology.

Smartphone Users Exhibit Similar Neural Plasticity as Piano Players

The findings from the above study seem to corroborate the conclusions drawn from another piece of research conducted on musicians a decade ago. That study compared the level of tactile acuity in non-musicians and in professional pianists who had been practicing every day for long hours for many years. It was found that the musicians had greater degrees of tactile acuity than the non-musicians. Amongst the musicians, those who had been practicing more intensively through the years showed more sensitivity.

The study went a step further and subjected the pianists and the non-musicians to tactile co-activation. Tactile co-activation is a passive pulse stimulation protocol that is known to enhance activity in the somatosensory cortex or the region of the brain that responds to tactile stimuli. This brings about an improvement in tactile and spatial discrimination performances without the subjects going through a physical training and learning program. According to the findings of another study, the improvements in the performance are directly proportional to the increase in the primary and secondary somatosensory cortical areas of the brain.

Researchers found that after tactile co-activation, both the pianists and the non-musician groups exhibited improved tactile acuity. But the pianists exhibited a greater degree of improvement than the non-musicians. Again, the degree of gain in performance was positively correlated to the intensity of musical practice. These findings led the scientists to believe that the sensorimotor cortical structure and functionalities are essentially different in musicians than in non-musicians and that former’s brains are more adaptable making them better learners.

Repetitive Tasks and Finger Movements Can Stimulate the Brain

Training and learning through attention and reinforcement of stimuli can bring about changes in the cortical organization, which in turn, improves perceptual performance. Last year, a study was carried out on several stroke patients with varying degrees of sensory impairment and mild to severe motor deficit. They were made to undergo regular sensorimotor training sessions whether they had to explore, feel, and discriminate between textures, shapes, weights, temperatures, and objects with their hands. Brain scan images taken after the training period showed that both patients had experienced subtle neural reorganization.

A similar suggestion was made after another study was carried out on two groups of musicians who had received unimodal and multimodal training. It was demonstrated that sensorimotor-auditory training reorganizes the cortical region and makes it more flexible.

The findings of the above studies hold hope for stroke patients and other individuals who may have suffered brain injuries. Researchers, physicians, and physical therapists should look into devising physical rehabilitation programs that engage and exercise the hands of the patients in an effort to stimulate regions of their brains to reorganize and possibly restore the lost neural connections. Such therapy can enhance the quality of life of the patients.

The findings of several other studies also suggest that performing tasks repetitively with the fingers can increase cortical plasticity. One study cites the instance of Braille readers and musicians who perform on string instruments. The subjects in the study had been using their fingers to perform various tasks for many years. All of them exhibited excellent sensorimotor skills and enhanced activity in the cortical regions of their brains. The study also reported that extended periods of disuse, like when the arm was cast in a plaster and immobilized, resulted in decreased tactile acuity in the affected hand (as was evident from the deteriorating levels of perceptual performance) and decreased activity in the corresponding somatosensory cortical region.

So do these findings suggest that using smartphones can make you smarter? Although recent studies have found that heavy smartphone users have increased cortical activities, it is still quite early to confirm or negate a positive correlation between using a smartphone and scoring straight A’s in college. So smartphone addicts: you do not yet have the license to forego the company of friends and family members or forsake exercise in favor of your iPhone!

References

Borstad AL, Bird T, Choi S, Goodman L, Schmalbrock P, & Nichols-Larsen DS (2013). Sensorimotor training and neural reorganization after stroke: a case series. Journal of neurologic physical therapy : JNPT, 37 (1), 27-36 PMID: 23399924

Gindrat, A., Chytiris, M., Balerna, M., Rouiller, E., & Ghosh, A. (2015). Use-Dependent Cortical Processing from Fingertips in Touchscreen Phone Users Current Biology, 25 (1), 109-116 DOI: 10.1016/j.cub.2014.11.026

Hodzic, A. (2004). Improvement and Decline in Tactile Discrimination Behavior after Cortical Plasticity Induced by Passive Tactile Coactivation Journal of Neuroscience, 24 (2), 442-446 DOI: 10.1523/JNEUROSCI.3731-03.2004

Höffken, O., Veit, M., Knossalla, F., Lissek, S., Bliem, B., Ragert, P., Dinse, H., & Tegenthoff, M. (2007). Sustained increase of somatosensory cortex excitability by tactile coactivation studied by paired median nerve stimulation in humans correlates with perceptual gain The Journal of Physiology, 584 (2), 463-471 DOI: 10.1113/jphysiol.2007.140079

Lappe, C., Herholz, S., Trainor, L., & Pantev, C. (2008). Cortical Plasticity Induced by Short-Term Unimodal and Multimodal Musical Training Journal of Neuroscience, 28 (39), 9632-9639 DOI: 10.1523/JNEUROSCI.2254-08.2008

Lissek, S., Wilimzig, C., Stude, P., Pleger, B., Kalisch, T., Maier, C., Peters, S., Nicolas, V., Tegenthoff, M., & Dinse, H. (2009). Immobilization Impairs Tactile Perception and Shrinks Somatosensory Cortical Maps Current Biology, 19 (10), 837-842 DOI: 10.1016/j.cub.2009.03.065

Ragert, P., Schmidt, A., Altenmüller, E., & Dinse, H. (2004). Superior tactile performance and learning in professional pianists: evidence for meta-plasticity in musicians European Journal of Neuroscience, 19 (2), 473-478 DOI: 10.1111/j.0953-816X.2003.03142.x

Image via nenetus / Shutterstock.

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How Do I Love Thee? Let Me Examine My Brain http://brainblogger.com/2015/02/08/how-do-i-love-thee-let-me-examine-my-brain/ http://brainblogger.com/2015/02/08/how-do-i-love-thee-let-me-examine-my-brain/#comments Sun, 08 Feb 2015 12:00:46 +0000 http://brainblogger.com/?p=18474 Love is in the air this time of year. It makes some people swoon, others cringe, and many crazy. Love is all around us – from romantic partners, to children, to friends, to pets, to favorite foods – but what do we really know about how or why we love the way we do?

The study of love is moving from a subjective theme of psychiatrists to an objective issue of neuroscientists; many areas, facilities, and circuits in the brain are now believed to be involved in the emotions and actions that compose our love of others.

The biology of love originates in the primitive parts of the brain, which evolved long before the more complex cerebral cortex. Additionally, scientists have uncovered potential roles of many chemicals, including oxytocin, vasopressin, dopamine, serotonin, cortisol, nerve growth factor, and testosterone, in pair-bonding and relationships. Such neurotransmitters and related pathways increase social recognition, motivation, reward, and overall health and decrease fear, anxiety, and stress. These findings support love as an evolutionary process that is necessary for survival. Interestingly, the brain activity in hate and negative emotions is distinct and different from the patterns of brain activity in love.

Still, studies of love are limited and subject to selection bias and cultural differences in love and affection and definitive proof of the scientific basis of love is lacking. Differences in types of love and lengths of relationships compound the challenge of defining mechanisms of love. For example, maternal love and romantic love are different emotions and probably involve different biological and chemical mechanisms.

A larger question may be, “Which came first? Love or biology?” Is the brain activity observed by neuroscientists the cause of our feelings of love or do our feelings of love cause our brain to react in certain ways? But, more so, what do we gain from defining the chemistry or biology of love, attachment, and affection? One argument supporting such research is that, by understanding the phenomena of love and attachment, we can better treat emotional and attachment disorders, possibly even with pharmacotherapy. Beyond that, scientific definitions, while interesting in our understanding of just how magnificent and amazing the brain is, may falsely simplify a complex and complicated experience like love.

In this season of love, it is possible that some things are better left unexplained. Love may be a mystery that we will never define. But we can certainly let love define us.

References

Coria-Avila GA, Manzo J, Garcia LI, Carrillo P, Miquel M, & Pfaus JG (2014). Neurobiology of social attachments. Neuroscience and biobehavioral reviews, 43, 173-82 PMID: 24769402

de Boer A, van Buel EM, & Ter Horst GJ (2012). Love is more than just a kiss: a neurobiological perspective on love and affection. Neuroscience, 201, 114-24 PMID: 22119059

Emanuele E (2011). NGF and romantic love. Archives italiennes de biologie, 149 (2), 265-8 PMID: 21701998

Esch T, & Stefano GB (2011). The neurobiological link between compassion and love. Medical science monitor : international medical journal of experimental and clinical research, 17 (3) PMID: 21358615

Francesco F, & Cervone A (2014). Neurobiology of love. Psychiatria Danubina, 26 Suppl 1, 266-8 PMID: 25413551

Kida T, Nishitani S, Tanaka M, Takamura T, Sugawara M, & Shinohara K (2013). I love my grandkid! An NIRS study of grandmaternal love in Japan. Brain research PMID: 24513249

Langeslag SJ, Muris P, & Franken IH (2013). Measuring romantic love: psychometric properties of the infatuation and attachment scales. Journal of sex research, 50 (8), 739-47 PMID: 23098269

Savulescu J, & Earp BD (2014). Neuroreductionism about Sex and Love. Think (London, England), 13 (38), 7-12 PMID: 25309130

Stein DJ, & Vythilingum B (2009). Love and attachment: the psychobiology of social bonding. CNS spectrums, 14 (5), 239-42 PMID: 19407722

Zeki S, & Romaya JP (2008). Neural correlates of hate. PloS one, 3 (10) PMID: 18958169

Image via / Shutterstock.

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The 20 Second Test for Stroke Risk http://brainblogger.com/2015/02/07/the-20-second-test-for-stroke-risk/ http://brainblogger.com/2015/02/07/the-20-second-test-for-stroke-risk/#comments Sat, 07 Feb 2015 12:00:04 +0000 http://brainblogger.com/?p=18476 A lot has been written about the debilitating and potentially deadly after-effects of stroke. That’s why many of us try (or at least attempt) to steer clear of junk food, exercise regularly, keep an eye on the scales, and sit on the yoga mat once in a while. But what about standing on one leg for 20 seconds?

Some of us have bookmarked pages from health websites that list the common warning signs of an impending stroke. Now here’s another piece of assuring news. Scientists have devised a simple test that can gauge the risk of a person suffering a stroke. The good news is that you don’t have to trudge to the doctor’s office to undergo the test. The one-leg balancing test by a team of Japanese researchers is believed to be an effective indicator of the probability of stroke in a person.

The One-Leg Balancing Test and Its Findings

The one-leg balancing test is based on the premise that the capability to balance oneself on one leg is a critical indicator of the functional ability of the brain. A person should be able to maintain this balance for more than 20 seconds. Any duration less than this calls for a medical check-up unless this incapability can be explained by another physical reason.

The researchers enrolled about 1,300 participants — both men and women, aged around 67 years — and asked them to stand on one leg, keep their eyes open, and maintain balance for about 20 seconds. They were then tested for brain health. The results of the tests are startling.

More than 30 percent of the subjects who had trouble balancing themselves for this length of time were found to have cerebral small vessel disease, minute hemorrhages, or both. Cerebral small vessel disease develops when the capillaries in the brain thicken and impede the smooth flow of blood. The capillaries may even bleed and cause hemorrhages in the brain that can lead to strokes. On MRI scans, cerebral small vessel disease is manifested as lacunar infarction, which is a condition when inadequate blood supply causes a tissue to die or start to die, and white matter lesions.

What Makes the One-Leg Balancing Test Valid?

The scientific and medical community does not doubt the validity of the one-leg balancing test.

Firstly, the test results have been adjusted for factors such as family history of cardiovascular disease in the subjects, previous instances of cardiac ailments, and hypertension that can affect the risk incidence of strokes. So the findings of the test can be strongly correlated to the performance of the subjects on the one-leg balancing test.

Secondly, several studies have conclusively proved the association between cerebral small vessel disease and an increased risk of strokes. They have demonstrated that cerebral small vessel disease increases the risk of some people suffering a stroke whether or not they have a history of cerebrovascular disease.

There have also been several studies that have associated postural stability and being able to maintain proper gait to brain health. The results from these studies lend credibility to the one-leg balancing test as an indicator of possible brain damage and stroke.

According to one study, hand and leg coordination is controlled by a complex neural network. The sensory circuits that control your vision, your sense of your body’s position in space, and the optimal functionality of the vestibular system determine your ability to balance yourself. So an inability to maintain balance could indicate damage in the neural circuitry and warrants medical attention.

Balance dysfunction is common after a stroke, and the most severe strokes tend to cause the most severe physical disabilities. On the other hand, research studies indicate that stroke leads to permanent brain damage that, in turn, may cause long-term disability like inability to achieve and/or maintain balance. So if you connect the dots, it seems likely that balance impairment is indicative of brain damage that, in turn, can increase the risk of strokes.

Another study suggests a strong association between lesions in a particular region of the brain resulting from strokes and gait dysfunction. During this study on chronic stroke patients, scientists discovered that subjects who exhibited asymmetrical gait were 60-80 percent more likely to have suffered some damage to the posterolateral putamen region of their brains than those who had no abnormalities in their postures.

The one-leg balancing test administered as part of the Japanese study also suggests an association between advanced age and postural instability. Small vessel diseases tend to affect people aged 60 years and more, and in this light, this association seems valid.

According to the findings of the above study, those who could balance themselves for the shortest time also performed the poorest on mental cognition tests. A study performed in 2008 demonstrated that cerebral small vessel disease is associated with cognitive decline. A progression of the disease is associated with greater cognitive decline and the development of typical age-related conditions like dementia, Alzheimer’s disease, and Parkinson’s disease. This indicates that cognitive performance is also a critical indicator of the risk of stroke in people, especially those who struggle to balance themselves on one leg for a minimum of 20 seconds.

Implications of the One-Leg Balancing Test

The implications of the one-leg balancing test should not only interest individuals who want to know if they are at greater risk of suffering strokes. Physicians should make high-risk patients — those with a family history of cardiac ailments and/or are suffering from diseases like hypertension and diabetes — undergo this test or enlighten them on it. Doctors should also take care to test the cognitive functionality of their patients to determine the risk of strokes.

Although there have been scientific studies linking postural instability to possible brain abnormalities, the one-leg balancing test is the first of its kind that has added a definite time frame to the test. This has increased the accuracy of the test. This gives hope to countless people and a chance to thwart a stroke that can bring their lives to a standstill.

References

Alexander, L., Black, S., Patterson, K., Gao, F., Danells, C., & McIlroy, W. (2008). Association Between Gait Asymmetry and Brain Lesion Location in Stroke Patients Stroke, 40 (2), 537-544 DOI: 10.1161/STROKEAHA.108.527374

Conijn, M., Kloppenborg, R., Algra, A., Mali, W., Kappelle, L., Vincken, K., van der Graaf, Y., Geerlings, M., & , . (2011). Cerebral Small Vessel Disease and Risk of Death, Ischemic Stroke, and Cardiac Complications in Patients With Atherosclerotic Disease: The Second Manifestations of ARTerial disease-Magnetic Resonance (SMART-MR) Study Stroke, 42 (11), 3105-3109 DOI: 10.1161/STROKEAHA.110.594853

van Dijk, E., Prins, N., Vrooman, H., Hofman, A., Koudstaal, P., & Breteler, M. (2008). Progression of Cerebral Small Vessel Disease in Relation to Risk Factors and Cognitive Consequences: Rotterdam Scan Study Stroke, 39 (10), 2712-2719 DOI: 10.1161/STROKEAHA.107.513176

Marigold, D., & Misiaszek, J. (2008). Whole-Body Responses: Neural Control and Implications for Rehabilitation and Fall Prevention The Neuroscientist, 15 (1), 36-46 DOI: 10.1177/1073858408322674

Mrozek, S., Vardon, F., & Geeraerts, T. (2012). Brain Temperature: Physiology and Pathophysiology after Brain Injury Anesthesiology Research and Practice, 2012, 1-13 DOI: 10.1155/2012/989487

Tabara, Y., Okada, Y., Ohara, M., Uetani, E., Kido, T., Ochi, N., Nagai, T., Igase, M., Miki, T., Matsuda, F., & Kohara, K. (2014). Association of Postural Instability With Asymptomatic Cerebrovascular Damage and Cognitive Decline: The Japan Shimanami Health Promoting Program Study Stroke, 46 (1), 16-22 DOI: 10.1161/STROKEAHA.114.006704

Tyson SF, Hanley M, Chillala J, Selley A, & Tallis RC (2006). Balance disability after stroke. Physical therapy, 86 (1), 30-8 PMID: 16386060

Image via dmitry_islentev / Shutterstock.

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Locked-in Syndrome – Consciously Voiceless and Paralyzed http://brainblogger.com/2015/02/06/locked-in-syndrome-consciously-voiceless-and-paralyzed/ http://brainblogger.com/2015/02/06/locked-in-syndrome-consciously-voiceless-and-paralyzed/#comments Fri, 06 Feb 2015 12:00:39 +0000 http://brainblogger.com/?p=18422 The term “locked-in syndrome” was first introduced in 1966 to describe a state in which a patient is locked inside their body, able to perceive their situation, but with extremely limited ability for interaction. Patients recount that the worst aspect of this syndrome is the anxious desire to move or speak while being unable to do so.

Locked-in syndrome (LIS), also known as cerebromedullospinal disconnection, de-efferented state or pseudocoma, is a rare neurological disorder in which there is complete paralysis of all voluntary movements except movements of the eyes – vertical gaze and eyelid opening. In classical LIS, unlike coma or the vegetative state, individuals are conscious, alert and awake; there is often no impairment of language, memory and intellectual functions; sensation is sometimes also preserved. Due to the loss of voluntary movements, speech is also lost. Communication may be possible through eye movements or blinking.

Incomplete LIS can occur when there are remnants of voluntary movements; total LIS, on the other hand, consists of complete immobility, including loss of eye movements, while maintaining consciousness.

The most common cause for LIS is a lesion in the pons, a part of the brainstem that contains nerve fibers that relay information to other areas of the brain, usually due to brainstem stroke. Another relatively frequent cause is traumatic brain injury, either directly by brainstem lesions or secondary to vascular damage or occlusion. Other, less frequent causes have been reported such as brainstem tumor or brainstem drug toxicity, for example. Another important cause of complete LIS can be observed in end-stage amyotrophic lateral sclerosis (motor neuron disease).

The first person to realize the patient is conscious is often a family member. LIS diagnosis can sometimes take months or even years, since signs of consciousness may not always be easily or immediately perceptible. For a long time, LIS was actually mostly diagnosed retrospectively based on postmortem findings. Unless the physician is aware of the signs and symptoms of LIS, the patient may incorrectly be considered to be in a coma or vegetative state.

Electroencephalographic (EEG) recordings in patients with LIS are usually normal or minimally altered and show reactivity to external stimuli. The presence of a relatively normal reactive EEG rhythm in a patient that appears to be unconscious can allow the diagnosis of LIS. Functional neuroimaging tools, namely PET imaging and functional MRI (fMRI) have shown sensitivity for identification of patients in a minimally conscious state, and may become useful tools to complement bedside examinations.

Individuals with LIS can survive for significant periods of time. Although most deaths occur in the first four months, once a patient has medically stabilized for more than a year, 10 year survival is 83% and 20 year survival is 40%. However, there is no cure or standard treatment available. Typically, the motor rehabilitation is very limited, although some control of fingers and toe movements may be recovered, often allowing a functional use of a digital switch.

Communication can be achieved by a code using eyelid blinks or vertical eye movements. The simplest form can be a yes/no code, such as looking up, indicating “yes” and looking down indicating “no.” A higher level of communication may be achieved through alphabetical systems that allow patients to indicate a letter through eye movement, thereby building sentences. This has even allowed books to be written by LIS patients.

Jean-Dominique Bauby, editor-in-chief of the fashion magazine Elle, had a brainstem stroke in December 1995, at the age of 43. After several weeks in a coma, he emerged into LIS, only able to move his left eyelid. Bauby, wanting to share his experience with the world, dictated a book that he composed mentally. Each passage was dictated letter by letter using a frequency-ordered alphabet with Bauby choosing letters by blinking. His book The Diving Bell and the Butterfly was published two days before his death in March 1997 and became a best-seller. The book was later adapted into a film of the same name, released in 2007.

Other firsthand accounts of living with LIS include Look Up for Yes (1997), by Julia Tavalaro, and Only the Eyes Say Yes (1997), by Philippe Vigand.

Julia Tavalaro fell into a coma after a hemorrhage in 1966, at the age of 32. After seven months, she woke up in a chronic care facility where she was regarded as a “vegetable”. It was only after several years that her family noticed a smile as a reaction to a dirty joke. She initially communicated using a letter board, but later used a communication device to write poetry, and managed to cheek-control her wheelchair. She died in 2003 at the age of 68.

Philippe Vigand fell into a coma in 1990 due to a vertebral artery dissection, also at the age of 32. He remained in a coma for two months and was later treated as a “vegetable”. His wife eventually noticed him blinking in response to her questions, but was unable to convince the treating physicians of his conscious state. His speech therapist was able to diagnose LIS when Vigand grinned after an insult from the therapist, whose finger was bitten by Vigand while testing his gag reflex. He then asked how much two plus two was and Vigand blinked four times confirming his cognitive capacities. He initially also communicated using a letter board, but later used an infrared camera attached to a computer.

Meanwhile, technology has contributed significantly to patients’ communication abilities. Instruments such as infra-red eye movement sensors coupled to virtual keyboards allow the use of word processors which in turn can be coupled to a text-to-speech synthesizer. These can also let the LIS patient control his environment, access the Internet and use e-mail, for example. Brain-computer interfaces (BCI) are also tools that allow LIS patients to control devices directly, but by using EEG signals to control computers. An example is the use of BCI involving visual presentation of letters associated with selection through EEG and a statistical language model. However, these tools are mostly still being tested or are too expensive for generalized use.

References

Doble JE, Haig AJ, Anderson C, & Katz R (2003). Impairment, activity, participation, life satisfaction, and survival in persons with locked-in syndrome for over a decade: follow-up on a previously reported cohort. The Journal of head trauma rehabilitation, 18 (5), 435-44 PMID: 12973273

Kjaer TW, & Sørensen HB (2013). A brain-computer interface to support functional recovery. Frontiers of neurology and neuroscience, 32, 95-100 PMID: 23859968

Kotchoubey B, & Lotze M (2013). Instrumental methods in the diagnostics of locked-in syndrome. Restorative neurology and neuroscience, 31 (1), 25-40 PMID: 23168499

Laureys S, Pellas F, Van Eeckhout P, Ghorbel S, Schnakers C, Perrin F, Berré J, Faymonville ME, Pantke KH, Damas F, Lamy M, Moonen G, & Goldman S (2005). The locked-in syndrome : what is it like to be conscious but paralyzed and voiceless? Progress in brain research, 150, 495-511 PMID: 16186044

Oken BS, Orhan U, Roark B, Erdogmus D, Fowler A, Mooney A, Peters B, Miller M, & Fried-Oken MB (2014). Brain-computer interface with language model-electroencephalography fusion for locked-in syndrome. Neurorehabilitation and neural repair, 28 (4), 387-94 PMID: 24370570

Stender J, Gosseries O, Bruno MA, Charland-Verville V, Vanhaudenhuyse A, Demertzi A, Chatelle C, Thonnard M, Thibaut A, Heine L, Soddu A, Boly M, Schnakers C, Gjedde A, & Laureys S (2014). Diagnostic precision of PET imaging and functional MRI in disorders of consciousness: a clinical validation study. Lancet, 384 (9942), 514-22 PMID: 24746174

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New Hope For Combating Paralysis http://brainblogger.com/2015/02/05/new-hope-for-combating-paralysis/ http://brainblogger.com/2015/02/05/new-hope-for-combating-paralysis/#comments Thu, 05 Feb 2015 12:00:58 +0000 http://brainblogger.com/?p=18431 A study published in the January 9 issue of Science has brought hope for the treatment of paralysis due to spinal cord injury.

Damage to the spinal cord can cut communication between the brain and the peripheral nervous system. To restore communication, some strategies have been tested over the years. Research has been working on developing spinal implants that may electrically stimulate the spinal cord while also acting as delivery media for molecules able to promote axonal regeneration.

The good news

Wire implants have been tested, but they have failed mainly due to their rigidity. Movements of the spine can damage or break these electrodes and these strategies end up failing quite quickly.

But a Swiss group developed a strategy to overcome these limitations. They developed a soft neural implant that can be placed in contact with nerve tissue, with the shape and elasticity of dura mater, the membrane that envelops the spinal cord. This electronic dura mater, which the authors called e-dura, consists of a ribbon of stretchable silicone that can send signals along the nerves because it’s embedded with gold wires that can conduct neuronal signals. Its softness is maintained by fracturing the gold wires with micro-cracks, allowing them to bend with the silicone.

Additionally, it contains fluid channels that allow the delivery of drugs to nerve cells. This allows the controlled release of regeneration stimulating factors, such as molecules that actively promote axonal extension. Importantly, it allows a localized delivery of these factors, thereby reducing potential side-effects.

The authors tested this implant by placing it into the injured spinal cords of paralyzed rats. They tested the therapeutic effects of the e-dura by using the implant to stimulate the spinal cord with electrical signals as well as with molecules that improve nerve impulse transmission. This approach was able to restore the rats’ ability to walk only after six weeks. The success of this implant in animals is quite promising and may be an important step towards helping paralyzed patients regain their ability to walk.

The bad news

Stroke has widely known consequences in neurological function. Infections are common post-stroke complications, especially pneumonia. Post-stroke infections are associated with increased mortality and poor neurological outcomes. Prophylactic antibiotic treatment has been shown to reduce the frequency of post-stroke infections. However, whether or not preventive antibiotic treatment reduces the risk of poor functional outcome after stroke has been uncertain.

A study made available online on January 20 in The Lancet aimed to determine whether or not preventive antimicrobial therapy could improve neurological functional outcome in patients with acute stroke. The Preventive Antibiotics in Stroke Study (PASS) was a multicentre randomized controlled trial with 2550 patients from 30 centers in the Netherlands undertaken between 2010 and 2014. Patients were assigned in a 1:1 ratio to either preventive antibiotic therapy or a control group and the three-month functional outcome was determined. Ceftriaxone, a broad-spectrum third-generation cephalosporin antibiotic that is often used to treat post-stroke infections was chosen for this study.

Preventive antibiotic therapy was unable to improve functional outcomes in patients with acute stroke, shorten the length of hospital stay or reduce mortality. Although post-stroke infection rate was significantly reduced with Ceftriaxone, pneumonia was not prevented. Since pneumonia was strongly associated with an unfavorable neurological outcome, the lack of functional effect of ceftriaxone may have been due to its inability to prevent post-stroke pneumonia. The authors hypothesize that pneumonia may actually be a post-stroke respiratory syndrome, rather than solely a bacterial infection.

The results of this trial do not support the use of preventive antibiotics in adults with acute stroke. This is a problem that remains unsolved.

References

Minev IR, Musienko P, Hirsch A, Barraud Q, Wenger N, Moraud EM, Gandar J, Capogrosso M, Milekovic T, Asboth L, Torres RF, Vachicouras N, Liu Q, Pavlova N, Duis S, Larmagnac A, Vörös J, Micera S, Suo Z, Courtine G, & Lacour SP (2015). Biomaterials. Electronic dura mater for long-term multimodal neural interfaces. Science (New York, N.Y.), 347 (6218), 159-63 PMID: 25574019

Westendorp WF, Vermeij JD, Zock E, Hooijenga IJ, Kruyt ND, Bosboom HJ, Kwa VI, Weisfelt M, Remmers MJ, Ten Houten R, Schreuder AH, Vermeer SE, van Dijk EJ, Dippel DW, Dijkgraaf MG, Spanjaard L, Vermeulen M, van der Poll T, Prins JM, Vermeij FH, Roos YB, Kleyweg RP, Kerkhoff H, Brouwer MC, Zwinderman AH, van de Beek D, Nederkoorn PJ, & for the PASS investigators (2015). The Preventive Antibiotics in Stroke Study (PASS): a pragmatic randomised open-label masked endpoint clinical trial. Lancet PMID: 25612858

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January 2015 – Highlights and Failures in Neuroscience & Neurology http://brainblogger.com/2015/02/01/january-2015-highlights-and-failures-in-neuroscience-neurology/ http://brainblogger.com/2015/02/01/january-2015-highlights-and-failures-in-neuroscience-neurology/#comments Sun, 01 Feb 2015 18:52:54 +0000 http://brainblogger.com/?p=18417 Every month, hundreds of research articles are published in the field of neuroscience. Obviously, this short review cannot cover them all. Here I highlight some new research data that I found particularly interesting and important. Some of them were publicized in popular media while others received very little attention.

Two particularly interesting articles related to our perception of emotions and pain were published this month.

The level of our stress hormones is surprisingly sensitive to our surroundings. It can rise, for instance, even from being in the same room as a complete stranger. Apparently, this almost unnoticeable rise in stress level makes us significantly less empathic. Researchers asked student volunteers to rate the pain of a stranger or a friend whose hand was immersed in the bucket of ice-cold water. Invariably, the pain of a friend was rated higher. Another group of students took a drug blocking the stress hormone before the test. This group, being not stressed any more, felt the pain of stranger more deeply. This observations may give some clues to the apparent lack of empathy towards other people during times of social upheaval. Elevated stress level appears to block the neuronal pathways involved in considering the feelings of others.

A second study looked at emotional support and pain during childbirth. Medical professionals often encourage the presence of a partner at the delivery to alleviate the pain of the woman. But does it really work this way? New research data obtained in a small study performed by British scientists cast serious doubts on the wisdom of having a romantic partner around during a painful medical treatment. In their experiments, researchers subjected female volunteers to painful, but tolerable, laser pulses to their finger in the presence and absence of their significant others. Women were asked to rate the level of pain, which was also monitored via measuring brain activity by electroencephalography (EEG). A significant proportion of women reported stronger pain in the presence of their partners. EEG confirmed that the level of pain in these cases was indeed higher. Obviously, pain in a finger and pain during child birth are two rather different things. However, this is a wake-up call to have a serious look into the issue and not leave it to the matter of opinion alone.

Continuing with the medical theme, the four articles below are definitely worth mentioning.

Our body weight is not a simple balance of calories in and calories out – the level of fat burning is also regulated by the brain. Two hormones, leptin and insulin, work together to inform the brain about the level of body fat. More specifically, the hormones interact with proopiomelanocortin (POMC) neurons in the hypothalamus. In the situations when the hormones signal excessive level of fat deposits, POMC neurons send signals instructing some cells of fat tissues to burn fat. The molecular mechanisms behind this process are still being investigated, but researchers believe that there is a good possibility to develop a drug that will be able to interfere in this neuronal signalling and increase the rate of fat burning.

Brain-acting fat-burning pills might be still many years away. In the meantime, lots of people take pills that help prevent the build-up of cholesterol, a common problem associated with the excessive body weight. Cholesterol-controlling statins are probably the most commercially successful modern medicines, and their use is on the rise. However, a number of reports suggest that the drugs from this class may cause cognitive problems. Since 2012, FDA requests that statin labels must show this warning of potential harm. A group of researchers from Brown University has re-examined this claim by performing a meta-analysis of available information which included the data from 27,643 patients. They found no evidences that statins affect mental abilities of people with normal brain or worsen the mental state of people with neurodegenerative diseases. Scientists assume that previously reported harmful effects of statins might have been associated with overdose or the presence of some other medical conditions. Clearly, further studies are needed to reach the final verdict on this issue.

Brain injuries such as concussions are not often easy to detect and diagnose. Readily visible symptoms do not reflect the extent of brain trauma. As a result, scientists tried to find a reliable blood marker, an easily detectable compound generated in the course of brain injury that can be used for diagnostic purposes. Multiple markers are used to this end in the detection of various diseases such as cardiovascular problems and cancers. However, in case of brain injuries the issue is complicated by the existence of brain’s own waste removal system, which can also be affected by the injury. This results in unreliable and fluctuating levels of potential blood markers. Researchers from the University of Rochester concluded that the whole biomarker approach might not be useful in the diagnostic of traumatic brain injuries. This is disappointing, particularly taking into account how many millions of dollars were spent to search for such markers.

Parkinson’s disease affects growing number of people worldwide. For patients with this severe progressing neurodegenerative disorder that affects motor neurons, the risk of falls is a serious problem associated with large number of injuries, pain and limitation of activity. Australian researchers checked if an exercise program of moderate intensity would help in improving the conditions of Parkinson’s patients. It turned out that six month-long program of balance and leg strengthening exercise (30-40 minutes, three times per week) helped to reduce the frequency of falls by 70% among the patients with mild form of disease. In people with more advance condition, the exercise program did not reduce the risk of falls, but still helped in improving the physical and psychological well-being. This is yet another confirmation that exercise is good for our health, whatever is our age and medical history.

It is sometimes really surprising how little we know about the basic brain functions. Two perfect illustration of this come in the January issue of Nature magazine.

In one article, scientists from Howard Hughes Medical Institute published their findings on the neural mechanisms involved in the regulation of thirst. The general assumption was that this basic system must be really simple – dehydration should activate certain brain circuits thus triggering water-seeking behavior. Well, it turned out that the brain has two separate centers, one of which triggers the thirst and the other depresses it. Activation of the first center makes even fully hydrated animals to drink much more, while activation of the second center represses the thirst even in extremely thirsty animals. This makes sense from the evolutionary point of view – the existence of thirst-suppressing center may not only help animals to adapt to the inhospitable conditions in deserts but also give them clear survival advantage in evolution.

The second article investigates the mechanisms of fear. Fear is vital for our survival – we all have to be able to recognize dangers and avoid them. But the question how the alarm is triggered in the brain was never properly investigated. Scientists from Cold Spring Harbour Laboratory and Stony Brook University found that this life-preserving neural circuit is located in the paraventricular nucleus of the thalamus (PVT). The PVT is responsible for recognizing and forming the memories of threats, and for activating of other brain regions in the appropriate response. Chemical signalling in this circuit involves brain-derived neurotrophic factor (BDNF) as a messenger. Genetically modified mice with absent BDNF had impaired ability to recognize danger even after conditioning. On the other hand, infusion of animals’ brains with excess of BDNF caused excessive response to dangers. Scientists believe that in humans this newly discovered circuit is also involved in the formation of phobias and anxiety.

Continuing with the subject of how our brain works, two articles below will certainly be interesting for many readers.

If you spend lots of time pondering rather trivial questions before making your decisions, you might be relieved to learn that such strategy appears to be evolutionary programmed in our brain. “Degree of certainty” is rather subjective category, especially when evidences are not abundant. In the absence of clear evidence, we tend to hesitate before making a decision. You may argue that this hesitation allows brain to better analyze the existing evidences, but new research study suggest that the amount of time spent on the decision-making is in itself a confidence-improving factor. Researchers subjected human volunteers to a test where they needed to figure out the direction of the dots movements on a very noisy computer screen. After various periods of time watching the screen the subjects were reported both their conclusion and the level of confidence. Obviously, the level of confidence was higher when the movement of dots was better visible. In those cases when the answer was less than obvious, increased amount of time spent on decision-making improved the level of confidence, even when the final answers were wrong. Researchers concluded that deliberation time informs certainty because it serves as a proxy for task difficulty.

The questions “what makes us smarter than other primates?” and “what makes some of us much smarter than the rest of us?” still wait to be answered. A correlation between the area of cortical surface and intellectual ability in both evolution and childhood development was noticed long ago. Now scientists have shown that higher intellectual abilities, such as better visuospatial reasoning abilities, are particularly strongly linked to certain highly expanded cortical regions, especially anterior cingulate. Individuals whose brain features larger expansion of these regions have better cognitive functions. Obviously, these findings themselves do not explain why some people have higher IQ, but it points to the areas of the brain where further research on our intellectual capabilities should be focused.

References

Martin LJ, Hathaway G, Isbester K, Mirali S, Acland EL, Niederstrasser N, Slepian PM, Trost Z, Bartz JA, Sapolsky RM, Sternberg WF, Levitin DJ, & Mogil JS (2015). Reducing Social Stress Elicits Emotional Contagion of Pain in Mouse and Human Strangers. Current biology : CB PMID: 25601547

Krahe, C., Paloyelis, Y., Condon, H., Jenkinson, P., Williams, S., & Fotopoulou, A. (2015). Attachment style moderates partner presence effects on pain: a laser-evoked potentials study Social Cognitive and Affective Neuroscience DOI: 10.1093/scan/nsu156

Dodd, G., Decherf, S., Loh, K., Simonds, S., Wiede, F., Balland, E., Merry, T., Münzberg, H., Zhang, Z., Kahn, B., Neel, B., Bence, K., Andrews, Z., Cowley, M., & Tiganis, T. (2015). Leptin and Insulin Act on POMC Neurons to Promote the Browning of White Fat Cell, 160 (1-2), 88-104 DOI: 10.1016/j.cell.2014.12.022

Ott, B., Daiello, L., Dahabreh, I., Springate, B., Bixby, K., Murali, M., & Trikalinos, T. (2015). Do Statins Impair Cognition? A Systematic Review and Meta-Analysis of Randomized Controlled Trials Journal of General Internal Medicine DOI: 10.1007/s11606-014-3115-3

Plog, B., Dashnaw, M., Hitomi, E., Peng, W., Liao, Y., Lou, N., Deane, R., & Nedergaard, M. (2015). Biomarkers of Traumatic Injury Are Transported from Brain to Blood via the Glymphatic System Journal of Neuroscience, 35 (2), 518-526 DOI: 10.1523/JNEUROSCI.3742-14.2015

Canning, C., Sherrington, C., Lord, S., Close, J., Heritier, S., Heller, G., Howard, K., Allen, N., Latt, M., Murray, S., O’Rourke, S., Paul, S., Song, J., & Fung, V. (2014). Exercise for falls prevention in Parkinson disease: A randomized controlled trial Neurology, 84 (3), 304-312 DOI: 10.1212/WNL.0000000000001155

Oka, Y., Ye, M., & Zuker, C. (2015). Thirst driving and suppressing signals encoded by distinct neural populations in the brain Nature DOI: 10.1038/nature14108

Penzo, M., Robert, V., Tucciarone, J., De Bundel, D., Wang, M., Van Aelst, L., Darvas, M., Parada, L., Palmiter, R., He, M., Huang, Z., & Li, B. (2015). The paraventricular thalamus controls a central amygdala fear circuit Nature DOI: 10.1038/nature13978

Kiani, R., Corthell, L., & Shadlen, M. (2014). Choice Certainty Is Informed by Both Evidence and Decision Time Neuron, 84 (6), 1329-1342 DOI: 10.1016/j.neuron.2014.12.015

Fjell, A., Westlye, L., Amlien, I., Tamnes, C., Grydeland, H., Engvig, A., Espeseth, T., Reinvang, I., Lundervold, A., Lundervold, A., & Walhovd, K. (2013). High-Expanding Cortical Regions in Human Development and Evolution Are Related to Higher Intellectual Abilities Cerebral Cortex, 25 (1), 26-34 DOI: 10.1093/cercor/bht201

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