In 2009, an international group of researchers replicated one of the first studies to show lateralized Whorfian effects in categorical color perception, with the addition of fMRI data. They predicted that the areas of the brain responsible for processing language (such as the left temporoparietal areas) would be activated during color perception, and that these areas would show increased activation during cross-category distinctions. In addition, they predicted that cortical areas responsible for color perception would be altered by the activation of linguistic areas if those areas are activated in response to, and not simply as a by-product of, color perception.

Results proved the hypotheses correct. Not only were the linguistic areas of the left hemisphere active during color perception, but they were more highly activated when the colors being displayed in the right visual hemifield (which sends information to the left side of the brain) crossed a color category boundary. Contrastingly, between- and within-category stimuli prompted the same hemodynamic responses when they were perceived in the left visual field. Finally, areas of the visual cortex were activated more quickly when cross-category stimuli were displayed.

What does this all mean? First of all, that linguistically-mediated color perception isn’t just a behavioral phenomenon, but a neural one. This means that the language we use has a significant and lasting effect upon the structure of the brain. Second, it means that the left temporoparietal area of the brain may serve as a top-down controller for perceptual processes, an interesting idea for anyone studying the theory of linguistic relativity. Do the linguistic centers of the brain modulate the responses of other portions? Does the processing of language have more global implications? These are things that remain to be seen.

This study is a great example of the use of fMRI in neurolinguistics — as the availability of this neuroimaging technique increases, we are likely to see more studies like this one, where the hemodynamic responses of brain areas are measured and interpreted in the context of specific stimuli.

References

Gilbert AL, Regier T, Kay P, & Ivry RB (2006). Whorf hypothesis is supported in the right visual field but not the left. Proceedings of the National Academy of Sciences of the United States of America, 103 (2), 489-94 PMID: 16387848

Ting Siok W, Kay P, Wang WS, Chan AH, Chen L, Luke KK, & Hai Tan L (2009). Language regions of brain are operative in color perception. Proceedings of the National Academy of Sciences of the United States of America, 106 (20), 8140-5 PMID: 19416812

Image via 2jenn / Shutterstock.

Related Articles:

• I Can Read Your Mind!
• School Bullies – Is the Amygdala to Blame?
• Trick of the Light – Optical Illusions Can’t be Beat
• A Baby’s Smile – Mom’s Natural High
• Functional MRI: A Radiological Window into the Mind – Part 1
• The Chattering Brain – How Chronic Pain Throws our Cortex out of Sync
• Do Fluorescent Lights Give You Headaches? You’re Not Alone

What is RCVS?

RCVS results from sudden narrowing of cerebral arteries which results in reduced flow of blood to parts of the brain. In some cases, hemorrhage under the arachnoid membrane may also be seen. RCVS is usually diagnosed using Magnetic Resonance Imaging (MRI) and Magnetic Resonance Angiography (MRA) and by eliminating other known causes of headaches. A peculiar feature of this malady is the persistence of constrictions on brain vessels for up to three months after the headache has occurred. At times, a series of constrictions – termed as a ‘beads-on-a-string’ appearance – have been noted. However, there is very little knowledge to date about the actual physiological mechanisms of this pathology.

Women are more susceptible to RCVS than men. In a study conducted by Ducros and colleagues, 90% of the patients with a confirmed diagnosis of RCVS were women, with a mean age of 46 years.

How is RCVS different from other brain vascular diseases?

A significant difference between RCVS and strokes and transient ischemic attacks is that, unlike strokes, RCVS is not caused by atherosclerosis. However, recurrent episodes of RCVS may render patients susceptible to a stroke.

Migraine headaches are a well-known pathological condition associated with the cerebral blood vessel network. The jury is still out on whether migraines are caused by sudden expansion of blood vessels or by constrictions in blood vessels resulting in reduced cranial circulation. Cerebral arteries are joined in a loop known as the Circle of Willis. There is some evidence to show that people with an incomplete Circle of Willis are more likely to suffer from migraine headaches than those with a complete loop. An association between RCVS and the Circle of Willis has not yet been shown. A significant difference between RCVS and migraines is the absence of ‘aura’ or accessory sensorimotor symptoms during an RCVS headache episode.

How is RCVS diagnosed?

Diagnosis of RCVS is complicated owing to the fact that it is known to be associated with specific physiological states such as post-partum status. Another factor that complicates diagnosis of RCVS is the fact that symptoms presented by patients are highly variable. A sudden headache, possibly accompanied by subdural or subarachnoid hemorrhage as well as constriction of blood vessels, are the usual symptoms of RCVS. However, in one case, a patient suffered from a thunderclap headache and yet the initial cranial angiography images showed normal circulation. The patient’s health deteriorated in the subsequent period despite normal blood flow to the brain and eventually the patient suffered an ischemic stroke and went into a coma. Although the patient eventually recovered, the presentation and progression of symptoms has been quite different from those seen in other cases of RCVS.

A pediatric case of RCVS has also been documented. Administration of Eletriptan to a 12-year-old boy resulted in a sudden headache and paralysis of limbs. Magnetic resonance imaging and magnetic resonance angiography showed constricted blood vessels in a pattern consistent with RCVS.

How is RCVS treated?

Since the exact pathophysiology of RCVS has not been deciphered completely, treatment options are limited. Drugs like nimodipene and verapamil have been used to treat RCVS. Recovery from RCVS is achieved in approximately 90% of the cases. Some people may suffer permanent neurological damage from RCVS episodes and mortality has been noted in a tiny fraction of cases.

As things stand, a sudden headache may turn out to be quite a serious health emergency.

References

Bugnicourt JM, Garcia PY, Peltier J, Bonnaire B, Picard C, & Godefroy O (2009). Incomplete posterior circle of willis: a risk factor for migraine? Headache, 49 (6), 879-86 PMID: 19562826

Calabrese LH, Dodick DW, Schwedt TJ, & Singhal AB (2007). Narrative review: reversible cerebral vasoconstriction syndromes. Annals of internal medicine, 146 (1), 34-44 PMID: 17200220

Cavestro C, Richetta L, L’episcopo MR, Pedemonte E, Duca S, & Di Pietrantonj C (2011). Anatomical variants of the circle of willis and brain lesions in migraineurs. The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques, 38 (3), 494-9 PMID: 21515511

Chen SP, Fuh JL, & Wang SJ (2010). Reversible cerebral vasoconstriction syndrome: an under-recognized clinical emergency. Therapeutic advances in neurological disorders, 3 (3), 161-71 PMID: 21179608

Ducros A, Fiedler U, Porcher R, Boukobza M, Stapf C, & Bousser MG (2010). Hemorrhagic manifestations of reversible cerebral vasoconstriction syndrome: frequency, features, and risk factors. Stroke; a journal of cerebral circulation, 41 (11), 2505-11 PMID: 20884871

Hauge AW, Kirchmann M, & Olesen J (2010). Trigger factors in migraine with aura. Cephalalgia : an international journal of headache, 30 (3), 346-53 PMID: 19614703

Hauge AW, Kirchmann M, & Olesen J (2011). Characterization of consistent triggers of migraine with aura. Cephalalgia : an international journal of headache, 31 (4), 416-38 PMID: 20847084

Hougaard A, Amin F, Hauge AW, Ashina M, & Olesen J (2013). Provocation of migraine with aura using natural trigger factors. Neurology, 80 (5), 428-31 PMID: 23345632

Kuo CY, Yen MF, Chen LS, Fann CY, Chiu YH, Chen HH, & Pan SL (2013). Increased risk of hemorrhagic stroke in patients with migraine: a population-based cohort study. PloS one, 8 (1) PMID: 23372843

Lemmens R, Smet S, Wilms G, Demaerel P, & Thijs V (2012). Postpartum RCVS and PRES with normal initial imaging findings. Acta neurologica Belgica, 112 (2), 189-92 PMID: 22426679

Watanabe Y, Tanaka H, Takashima R, Takano M, Kimoto K, & Hirata K (2012). [Monitoring cerebral blood volume changes during migraine attack by using near-infrared spectroscopy]. Rinsho shinkeigaku = Clinical neurology, 52 (11), 1009-11 PMID: 23196499

Yoshioka S, Takano T, Ryujin F, & Takeuchi Y (2012). A pediatric case of reversible cerebral vasoconstriction syndrome with cortical subarachnoid hemorrhage. Brain & development, 34 (9), 796-8 PMID: 22285527

Image via Dim Dimich / Shutterstock.

Related Articles:

• Migraines? Ask Your Doctor About TPM
• Migraine and Vascular Disease
• The Science of Brain Freeze
• Take Two of These… And You Still Might Have Pain
• Migraine Headaches – Rethinking an Old Malady
• Headache Treatment – Alternative or Illicit?
• Migraine Uncovered – Interview with Dr. Cady, Headache Expert

In a recent study, Hispanic women volunteers were subjected to functional Magnetic Resonance Imaging (fMRI) while they were shown images of food as well as non-food items. These participants were also asked to state their emotional responses to food in terms of desire to eat the food items they were shown. Responses from the fMRI images were graded as per the contrast between activation patterns seen with high calorie foods versus those for non-food items. This study, to be published in print later this year, demonstrates that images of high-calorie foods elicited a greater response in the striatum nigra region of the brain, indicating a reward response. Images of high calorie foods also increased appetite and the desire to eat sweet as well as savory foods. It follows that repeated intake of sugary foods can only increase obesity.

Interestingly, the striatal response varied proportionately with the waist circumference of the participants. The overall BMI of the volunteers had no correlation with the activation response demonstrated to calorie-rich foods.

The outcomes of this study are hampered by two facts: First, the number of volunteers is small – just thirteen. Second, the volunteers were exclusively Hispanic women. Individuals from other ethnic groups were not included.

However, this initial study does provide some important insights. It shows how a high calorie diet of fast foods can have long-term effects on body weight and obesity associated metabolic syndrome. Frequent consumption of high calorie foods can set off a perpetual cycle of cravings for similar foods which in turn increase abdominal fat deposits and girth. In this study, participants with greater waist circumference demonstrated higher activation of the reward regions when challenged with high calorie food items. High calorie foods tend to be rich in refined carbohydrates and saturated fatty acids which contribute to an increase in waist circumference, creating a vicious cycle of eating and gaining more weight.

Popular American media have occasionally showcased stories about people who weigh upwards of 500 pounds and their subsequent efforts to lose weight. It is astounding how people can actually reach gigantic proportions before they can come to a decision about tackling this health issue! This study indicates one mechanism that may lead people to gain so much excess weight before they can mentally accept the fact that they are obese and take corrective measures.  An individual is likely to spend a considerable period of time being trapped in this vicious cycle of eating the wrong foods, gaining weight and floundering in food choices again before coming to terms with obesity. This study also lends support to the hypothesis that waist circumference and waist-to-hip ratio are better indices for understanding obesity than Body Mass Index (BMI). Body Mass Index also includes weight of limbs which are primarily muscular organs with heavy bones. However, waist circumference and waist-to-hip ratios are a direct measure of abdominal and gluteal fat deposits. Recent research indicates that these metrics may also indicate a predisposition towards unhealthy food choices.

The old saying ‘you are what you eat’ is turning out to be true in so many different ways.

References

Luo S, Romero A, Adam TC, Hu HH, Monterosso J, & Page KA (2013). Abdominal fat is associated with a greater brain reward response to high-calorie food cues in hispanic women. Obesity (Silver Spring, Md.) PMID: 23408738

Image via Ryan R Fox / Shutterstock.

Related Articles:

• Tax Your Way Thin
• Fructose Leads to Leptin Resistance and Obesity
• The Bsx of Obesity
• Too Much Information? – Labeling Restaurant Menus
• Is Sugar the New Cocaine?
• One Puff Forward, Two Pounds Back
• Are Your Friends Making You Fat?

The ketogenic diet is low in carbohydrates, adequate in protein, and high in fat, and sometimes partially restricted in calories. When following this diet, the brain shifts its main source of energy from glucose to fat. Fats are broken down into ketones, and these ketones are utilized by the brain as its main energy source. This shift in energy source is thought to be related to decreased seizures, though exactly how this happens is not yet clear. Researchers have proposed that the diet may work by altering neurotransmitter function, synaptic transmission, regulation of reactive oxygen species, and mitochondrial dysfunction — pathological mechanisms thought to play a role in a number of neurological diseases.

In Alzheimer’s disease, for example, results from clinical studies have been inconclusive but promising. In one randomized double-blind study, Alzheimer’s patients on a ketogenic diet showed significant cognitive improvement compared to patients not following the diet. In cell cultures, ketone bodies have been shown to be effective against the toxic effects of beta-amyloid, a key pathological feature of the disease. The diet may also help reduce oxidative stress and enhance mitochondrial function.

Mitochondrial dysfunction is also thought to play a contributory role in Parkinson’s disease, with its characteristic movement and cognitive impairment. In one small clinical trial of five patients with Parkinson’s disease, patients on the diet reduced their scores on the Unified Parkinson’s Disease Rating Scale by 43.4%.

The diet may also prove helpful in the treatment of Amyotrophic Lateral Sclerosis, or ALS. Mitochondrial dysfunction is also likely to play role in this devastating disease of the motor neurons. Though human studies have not yet been performed, mouse models of the condition have yielded promising results. In these mouse models, animals given a ketogenic diet showed significant motor improvements compared to animals on a normal diet.

Researchers speculate that the diet may prove helpful in even more neurological conditions, such as recovery from stroke and brain injury. Though the diet is an accepted treatment for refractory epilepsy, in other neurological conditions more clinical trials are needed to see if the diet is truly efficacious. If borne out, the diet may open another therapeutic avenue for the treatment of these diseases.

References

Griggs RC. Epilepsy. In Andreoli TE, Carpenter CC, Griggs RD, Benjamin IJ, eds. Andreoli and Carpenter’s Cecil Essentials of Medicine. 7th Ed. Philadelphia, PA: Elsevier; 2005: 1120-1128.

Henderson ST, Vogel JL, Barr LJ, Garvin F, Jones JJ, & Costantini LC (2009). Study of the ketogenic agent AC-1202 in mild to moderate Alzheimer’s disease: a randomized, double-blind, placebo-controlled, multicenter trial. Nutrition & metabolism, 6 PMID: 19664276

Huffman J, & Kossoff EH (2006). State of the ketogenic diet(s) in epilepsy. Current neurology and neuroscience reports, 6 (4), 332-40 PMID: 16822355

Lee M (2012). The use of ketogenic diet in special situations: expanding use in intractable epilepsy and other neurologic disorders. Korean journal of pediatrics, 55 (9), 316-21 PMID: 23049588

Mackay MT, Bicknell-Royle J, Nation J, Humphrey M, & Harvey AS (2005). The ketogenic diet in refractory childhood epilepsy. Journal of paediatrics and child health, 41 (7), 353-7 PMID: 16014140

Stafstrom CE, & Rho JM (2012). The ketogenic diet as a treatment paradigm for diverse neurological disorders. Frontiers in pharmacology, 3 PMID: 22509165

VanItallie, T., Nonas, C., Di Rocco, A., Boyar, K., Hyams, K., & Heymsfield, S. (2005). Treatment of Parkinson disease with diet-induced hyperketonemia: A feasibility study Neurology, 64 (4), 728-730 DOI: 10.1212/01.WNL.0000152046.11390.45

Image via xpixel / Shutterstock.

Related Articles:

• When “Alternative” Isn’t Anymore – The Ketogenic Diet in Epilepsy
• Functional MRI: Emerging Uses for Neurological Diseases – Part 2
• Green Tea and the Fight Against Parkinson’s Disease
• Cell Transplants for Parkinson’s Disease
• Smells Like Parkinson’s Disease
• Deep Brain Stimulation for Pleasure
• Genetics Clues May Lead New Treatment for Parkinson’s Disease

But what is the need for this communication and why is it done? The answer here is a recent and rather lengthy term: Cranial Nerve Non-Invasive Neuromodulation (CN-NINM). Neuromodulation, in general, implies the use of certain techniques that help stimulate nerves or certain brain centers for probable reorganization and functional restoration (neuroplasticity) of neurons. It could involve implantation of pulse generators in the brain, electrical stimulation of nerves, or maybe, even stimulation of the tongue. Branches of the fifth and seventh cranial nerves have sensory input in the anterior tongue. The brainstem centers of both these cranial nerves (trigeminal and solitary nuclei, respectively) are in close proximity to the vestibular nuclei, which regulates the function of balance. Thus, the targeted electric stimulation of the tongue, and thereby the fifth and seventh cranial nerves, induces the modulation of the vestibular nuclei in the brain. To put it simply, stimulation of the tongue could influence the person’s balance.

The neuromodulation of these cranial nerves paves way for a novel and non-invasive therapeutic modality for motor-related symptoms of diseases such as Parkinson’s disease, traumatic brain injury (TBI), and even multiple sclerosis. The anterior aspect of the tongue is stimulated using an electrode array that contains many gold-plated electrodes. The stimulation consists of low voltage square-pulse bursts, which produces a sensation similar to the feeling of drinking a carbonated beverage. In a clinical study, nine CN-NINM stimulations over a period of one week were delivered to patients with chronic balance dysfunction. An “optic flow” produced by creating relative motion of the surfaces and edges on a checkerboard image can induce the sensation of egomotion, increasing one’s postural responses. These patients were put through an optic flow stimuli designed to induce postural sway for the study, which in turn activates the brain centers related to balance processing. Functional MRI (fMRI) imaging was also performed during the visual stimuli test to ascertain the region of stimulation in the brain. A comparison of their pre- and post-stimulation postural sway tests showed that all patients had reductions in their overall sway to the optic flow after just a week of CN-NINM intervention. The images acquired through fMRI showed that the stimulated regions were superimposed over the anatomical location of centers for balance processing.

Yet another exciting observation with CN-NINM is that its neuromodulatory effect is sustained and persists even after turning off the low-voltage electrical neurostimulation. This contrasts with most other electric stimulation techniques, such as deep brain stimulation (DBS) or vagal nerve stimulation, where the effects disappear on switching off the stimulator. It is thus certain that CN-NINM induces neuroplastic changes in the brain, enabling better integration of neuronal signals. In another study it was found that similar electrical stimulation could also activate embryonal stem cells to differentiate into neuronal fates.

Non-invasive neuromodulation with long-lasting beneficial effects can be translated into home-based therapies for neurological disorders with minimal medical supervision. With funding from the US Army, Advanced Neurorehabilitation LLC (Madison, WI) has developed a Portable Neuromodulation Stimulator (PoNS) intended for patients with TBI. With ongoing clinical studies, the US Army is hoping to get an approval for this handheld device from the US Food and Drug Administration (FDA) soon. With neurostimulator devices like the PoNS, the tongue becomes yet another portal of entry to the brain!

References

Wildenberg JC, Tyler ME, Danilov YP, Kaczmarek KA, & Meyerand ME (2010). Sustained cortical and subcortical neuromodulation induced by electrical tongue stimulation. Brain imaging and behavior, 4 (3-4), 199-211 PMID: 20614202

Yamada M, Tanemura K, Okada S, Iwanami A, Nakamura M, Mizuno H, Ozawa M, Ohyama-Goto R, Kitamura N, Kawano M, Tan-Takeuchi K, Ohtsuka C, Miyawaki A, Takashima A, Ogawa M, Toyama Y, Okano H, & Kondo T (2007). Electrical stimulation modulates fate determination of differentiating embryonic stem cells. Stem cells (Dayton, Ohio), 25 (3), 562-70 PMID: 17110622

Ellen CJ (Feb 14 2013). U.S. Army Medical Research and Materiel Command.

Image via Aaron Amat / Shutterstock.

Related Articles:

• What Stem Cells Need to Survive in the Brain
• Cord Blood-Derived Stem Cells – a New Therapeutic Option for Brain Disorders?
• Stem Cell Research – Man vs. God
• The Great Embryonic Stem Cell Debate
• Stroke – Stem Cells Can Reduce Brain Damage
• Essential Tremor and Parkinson’s Disease
• Two Wrongs Make a Right – Abnormal Brain Circuitry May Stop Abnormal Movement

That’s also how our brains work to “tell time,” according to research conducted by Sylvie Droit-Volet from Blaise Pascal University and Sandrine Gil from Poitiers University, France. These neurophysiologists point out that although we have five senses with which to measure the universe around us, our brains have no specific receptors with which to measure time. Most of the time we manage anyway, have a pretty good idea of whether things happen “on time” or “not on time,” and after the age of six we can make fairly accurate assessments of time duration — how long it takes for common actions to happen.

After the age of eight we also begin to develop remarkably sophisticated abilities to “count time,” meaning to accurately tell how many seconds or minutes have passed between an initial “Start now” stimulus and a final “Stop now” stimulus. Brain researchers in the early 60s theorized that this sense of “subjective time” was due to a mechanism in our brains similar to a stopwatch, which operates similar to the ticking of a clock. When we pay attention to it, this internal clock allows us to develop a pretty good sense of objective time.

But does this “brain stopwatch” always “tick” at the same rate?

Have you ever, for example, been in a dangerous situation like an automobile accident and had your perception of time “slow down,” as if objective time itself were passing more slowly? Have you ever had a conversation with a beautiful person, à la Einstein’s quote above, and felt time pass more quickly? How does that happen if we’ve got an internal stopwatch in our brains constantly ticking away?

To find out, Droit-Volet and Gil conducted a number of experiments in which subjects were shown excerpts from three different types of potentially emotion-provoking films and then asked to subjectively estimate the duration of a visual stimulus. One group of films was designed to provoke fear (Scream, The Blair Witch Project), another group to provoke sadness (Philadephia, City Of Angels), and a third group to provoke neutral reactions.

After watching the fear-provoking films, the subjects consistently perceived the stimulus as lasting longer than it really did; the emotion of fear seemed to trigger a “slowing down” of time. There were no such time distortions after watching the other two groups of films. Speculating about the possible causes of this, the researchers suggested that the phenomenon might be partly physiological — the emotion of fear causes a state of physical arousal that may also speed up our “internal clocks.” When you are afraid, your heart speeds up, your blood pressure increases, your pupils dilate, and your body unconsciously goes into “fight or flight” mode, preparing to either defend itself or run away. The sad or neutral films may not have affected the subjects’ sense of time as much because there was no corresponding change in physiological functions.

Gil and Droit-Volet also found this time dilation effect when subjects merely looked at the face of someone close to them expressing an emotion such as shame. Previous studies have indicated that when we see shame in others, we instinctively try to mimic the other person’s emotional state. As Droit-Volet explains,

This reflective activity distracts attention from time-processing, so that estimated time seems shorter than it really is.

She also points out that these changes in our perception of time are not the result of a malfunction of our internal clocks, but a shifting of our attention in response to events:

There is no single, uniform time, but rather multiple times which we experience. Our temporal distortions are a direct translation of the way in which our brain and body adapt to these multiple times, the times of life.

More research must be conducted to understand exactly how our perceptions of time change, but one thing is certain — they change. Time really is relative.

References

Buhusi CV, & Meck WH (2005). What makes us tick? Functional and neural mechanisms of interval timing. Nature reviews. Neuroscience, 6 (10), 755-65 PMID: 16163383

Droit-Volet S, Fayolle SL, & Gil S (2011). Emotion and time perception: effects of film-induced mood. Frontiers in integrative neuroscience, 5 PMID: 21886610

Image via Jim Barber / Shutterstock.

Related Articles:

• Our Caveman Way of Avoiding Danger
• Closing the Window of Fear
• Subconscious Mind and the Limbic System
• The Neuroscience of Fear and Loathing
• Erasing Fear with Propranolol
• Consumer Perception of Health – The Cost of Happiness
• Climbing Through the Window – How to Heal Past Trauma

Neuroeconomics is, make no mistake about it, a discipline of its own, with a growing number of professionals getting more and more involved in its development. Over the last few years, all over the world many leading universities have started their own lab or center for neuroeconomics. Now, you may be asking yourself:

Why labs?

Labs are fundamental to neuroeconomics because the latter is interested in exploring decision making processes from a neurological perspective. Subjects’ decisions take place in a strictly controlled environment and are later explained as the product of cohesive decision making structures, which would originate in the brain. The buzz about neuroeconomics comes about because its findings challenge the predictions of traditional economic thought about individual behavior. By using algorithms that map environmental variables on to choices, neuroeconomics promises to potentially improve our understanding of “how and why” individual choices deviate from traditional economic theory.

A new way of thinking economic science

After a first glance, one may get the impression that neuroeconomics is all about the one-way transfer of insights from neuroscience to economics. On a closer look the story behind it is actually more complicated — and certainly more interesting! With neuroeconomics, hot topics from not only traditional economics, but also from other fields are critically assessed and strongly challenged. Theories of human choice based on the mind/body divide, as well as deterministic approaches to decision making, will find themselves part of the heated debate that is likely to emerge from this innovative field. neuroeconomics, furthermore, calls into question the relationship between economics and psychology. Whether psychology will be shoved away by neuroscience is still to be seen, but its established link with economics is surely to be contested.

As with most emerging disciplines neuroeconomics is not free of criticism. Some renowned economists, like Ariel Rubinstein and Glenn Harrison, have argued that neuroeconomics has to pace itself, in order to avoid making big conclusions based on scanty data. These authors healthy dose of skepticism is most likely to encourage, rather than deter enthusiasts of neuroeconomics.

At the moment it is yet to be seen how neuroeconomics can indeed impact the field as a whole, but if it did, it is likely to be loud bang.

Will financial floor traders, for instance, be reduced to predictable decision making machines? Or, could the decision making process of CEO’s involved in a merger become less of a black-box of rationality and more of an impulsive flow of feeling and gut?

These are, among many others, the type of questions that could make or break neuroeconomics. It remains for now an open question, whether its efforts will indeed represent a hope for the economies of tomorrow, or mere hype for the outsider economists of today.

References

Rubinstein, A. (2008). COMMENTS ON NEUROECONOMICS Economics and Philosophy, 24 (03) DOI: 10.1017/S0266267108002101

Schipper, B. (2008). ON AN EVOLUTIONARY FOUNDATION OF NEUROECONOMICS Economics and Philosophy, 24 (03) DOI: 10.1017/S0266267108002113

Image via isak55 / Shutterstock.

Related Articles:

• Health Insurance for All – A Weighty Issue
• Adventures in the Study of Altruism
• Shazeda Khan Appointed New Editor of Brain Blogger
• Free Will is NOT An Illusion
• Brain Imaging Techniques or Technocolor Phrenology
• Finding New Ways to Treat Depression
• Macroeconomics and Suicide

Researchers at the University of Kentucky and Kyungpook National University in South Korea studied 110 participants (who were either bilingual or monolingual) while undergoing functional magnetic resonance imaging (fMRI). The results of the experiments showed that older adult bilinguals “showed better perceptual switching performance than their monolingual peers” and that older adult bilinguals required less blood flow to the frontal cortex and cingulate cortex in order to complete certain mental tasks.

The study suggests that “lifelong bilingualism offsets age-related declines in the neural efficiency for cognitive control processes.” In other words, as the brain ages, it inevitably becomes less able to conduct the thought processes involved in everyday life.  According to the study, being bilingual throughout life helps delay this slowdown.

Other studies, such as the one conducted at the University of Toronto, have shown that bilingualism significantly improves white matter integrity and thickening of the cerebral cortex. White matter relays communications between various parts of the brain, and its deterioration results in decreased cognitive speed and acuity. The cerebral cortex is the layer covering the outer part of the cerebrum and is often referred to as gray matter. It is here where most information processing takes place in the brain.

Bilingualism has been regarded by some as a hindrance to a child’s intellectual development. Although there is plenty of data to show that bilingual brains keep both language systems active even when speaking or reading in just one, this is less of a drawback than was once believed. In fact, it conditions the brain to resolve the internal conflict between the languages, thereby strengthening its cognitive abilities.

A 2004 study on monolingual and bilingual (French and English) children found that the bilingual children were quicker at performing mental tasks such as sorting objects on a computer screen by color and shape. Other studies have reinforced the collective evidence that bilingualism improves the brain’s ability to plan, solve problems and perform mentally challenging tasks. It also improves the ability to ignore distractions, hold information in mind, and switch attention from one important task to the other.

In essence, a bilingual brain “exercises” the abilities that help keep it young: concentration, memorization, rapid purposeful switching, and flexibility. Although the benefits are greatest for those with lifelong experience in multiple languages, it is never too late to start learning a new way of talking and thinking.

References

Gold BT, Kim C, Johnson NF, Kryscio RJ, & Smith CD (2013). Lifelong bilingualism maintains neural efficiency for cognitive control in aging. The Journal of neuroscience : the official journal of the Society for Neuroscience, 33 (2), 387-96 PMID: 23303919

Luk G, Bialystok E, Craik FI, & Grady CL (2011). Lifelong bilingualism maintains white matter integrity in older adults. The Journal of neuroscience : the official journal of the Society for Neuroscience, 31 (46), 16808-13 PMID: 22090506

Bialystok E, & Martin MM (2004). Attention and inhibition in bilingual children: evidence from the dimensional change card sort task. Developmental science, 7 (3), 325-39 PMID: 15595373

Image via Raywoo / Shutterstock.

Related Articles:

• Inside Your Brain on Holiday
• Cannabis and the Adolescent Brain
• Working Memory Key to Breakthroughs in Cognitive Neuroscience
• Electrodoping with Transcranial Electrical Stimulation – Fact or Fiction?
• Brain Growth in Autism
• The Neural Basis of the Self
• Two Wrongs Make a Right – Abnormal Brain Circuitry May Stop Abnormal Movement

Cutting-edge studies in animal biology are shedding new light on a major reason why. That is, the development of biology and behavior is driven by gene-environment interactions. The upshot is that individuals are not affected equally by tough conditions. These individual differences arise from the interplay between an organism’s inherited traits and its surroundings. The classic notion of “nature versus nurture” is thus rendered obsolete.

The tricky part is how to go about understanding the role of individual variation in organisms’ responses to their environments. These dynamics are notoriously difficult to study and predict. Variation in numerous genes, operating in hyper-diverse environments, leads to complex interactions. Teasing apart the relationships demands sophisticated analyses, including experimental approaches not possible in human research. In this way, studies of other species are identifying mechanisms for the health impacts of early social stress.

For example, macaque monkeys reared without their mothers develop emotional abnormalities, such as poor social skills and aggression. Recent experiments show that the response to those adverse conditions depends on individual variation within a gene. The gene is linked to production of a protein involved in brain function, and in mediating responses to stress, anxiety and depression.

Studies of simple model animals take this work further, enabling actual gene manipulation. Fruit fly experiments show how chronic food deprivation at the larval stage interacts with natural variation in a gene that controls foraging. The early adversity then influences adult exploratory behavior. This willingness to investigate is essential for finding food — in mammals it is also critical for development of independence and mate selection. The poor nutrition in flies also affects eventual reproductive output, the ultimate index of a stressor’s impact.

Collectively, such studies show that some genotypes may be more sensitive to environmental conditions than others. That means individuals can experience different behavior and health outcomes in response to the same conditions.

This research into the “developmental biology of social adversity” is an important advance in studying the health impact of early life conditions. Conventional approaches tend to miss the point that many interacting factors underlie most health problems. Important questions in this emerging field include how the strength, timing, and duration of early life adversity influence development, and how interventions might alter health outcomes.

References

Bardo MT (2010). Novelty, Pages 471–476 in Encyclopedia of Behavioral Neuroscience. Academic Press. doi: 10.1016/B978-0-08-045396-5.00168-8

Boyce WT, Sokolowski MB, & Robinson GE (2012). Toward a new biology of social adversity. Proceedings of the National Academy of Sciences of the United States of America, 109 Suppl 2, 17143-8 PMID: 23045689

Burns JG, Svetec N, Rowe L, Mery F, Dolan MJ, Boyce WT, & Sokolowski MB (2012). Gene-environment interplay in Drosophila melanogaster: chronic food deprivation in early life affects adult exploratory and fitness traits. Proceedings of the National Academy of Sciences of the United States of America, 109 Suppl 2, 17239-44 PMID: 23045644

Cirulli F, Reif A, Herterich S, Lesch KP, Berry A, Francia N, Aloe L, Barr CS, Suomi SJ, & Alleva E (2011). A novel BDNF polymorphism affects plasma protein levels in interaction with early adversity in rhesus macaques. Psychoneuroendocrinology, 36 (3), 372-9 PMID: 21145664

Image via stoonn / Shutterstock.

Related Articles:

• Cheating Husbands – What His Genes Tell Us
• Which is Worse – The Memory or the Maltreatment?
• A Step Closer to the Great “Gene” Sale?
• A Unique Struggle Against Juvenile Huntington’s Disease
• Maternal Relationship Reduces Violence and Improves Intelligence
• Multiple Sclerosis: Nature, Nurture, or Something Else?
• Sugar and Spice and Everything Nice?

Researchers from Rutgers University found that there are two conditions caused by prolonged treatment with chemotherapy that travel throughout the body that create chemobrain. First, there is decreased in the growth of new neurons in the hippocampus. The constant proliferation of new brain cells is necessary to maintain the ability to learn, and if the number is decreased, the individual will find it difficult to learn something new. Second, which also occurs in the hippocampus, brain rhythm known as theta activity is inhibited. When a person learns a new task, these brain rhythms aid in communication between similar brain structures that are a distance away from each other. If that communication is disrupted, as it is during chemotherapy, the person is unable to learn that task. The other important discovery these researchers made is that since the hippocampus controls learning, but not long-term memory, the chemotherapy patient will find it hard to learn a new task but will have no trouble replicating tasks that were learned prior to receiving treatment.

The Rutgers team made their findings through an analysis of the behavior of 53 adult male rats bred in the Department of Psychology at the University. The animals were injected with temozolomide (TMZ), a chemotherapy drug that has been used to treat human brain tumors for more than ten years. The rats were treated cyclically, meaning they were given a dose of 2-5 mg per kilogram of body weight once a day for three days followed by four days of recovery, for up to six weeks. The dose and method of treatment mimicked human cancer patient treatment.

The researchers evaluated changes in the rats’ learning and memory by using variations of eyeblink conditioning, a methodology for studying the brain structures that facilitate memory and learning. A classic example of conditioning training is Pavlov’s famous experiment in which he rang a bell and then gave  his dogs food. The food caused the dogs to salivate. After repeating the pairing of a ringing bell followed by food, the dogs began salivating when they heard the bell because they had learned that the bell meant food was coming and they remembered that fact each time they heard the bell.

In this experiment, the number of daily tests and the number of training days for each eyeblink conditioning was determined by the difficulty of the task the researchers tried to teach the rats. The results of these tests showed that the rats had a lot of trouble learning to associate two events if there was a period of time between the tests. However, they could learn a simple tasks if the researchers performed the tasks without any time gap.

References

Nokia MS, Anderson ML, & Shors TJ (2012). Chemotherapy disrupts learning, neurogenesis and theta activity in the adult brain. The European journal of neuroscience, 36 (11), 3521-30 PMID: 23039863

Wada, N., Kishimoto, Y., Watanabe, D., Kano, M., Hirano, T., Funabiki, K., & Nakanishi, S. (2007). Conditioned eyeblink learning is formed and stored without cerebellar granule cell transmission Proceedings of the National Academy of Sciences, 104 (42), 16690-16695 DOI: 10.1073/pnas.0708165104

Image via Juan Gaertner / Shutterstock.

Related Articles:

• Fear-Reducing Drugs – An Emerging Science?
• Can Age-Related Forgetfulness be Overcome?
• One Up for the Spanish “Siesta”
• Is Obesity Linked to ADHD?
• How to Recharge the Batteries in our Brain
• More Reasons To Eat Blueberries
• A Surgeon’s Mistake Provides Insight into Memory and Learning

BAM was first proposed in September 2011 by the Kavli Foundation while they sought to bring together the worlds top talents in neuroscience and nano-science, in a project aimed at “recording from every neuron in the human brain at the same time” as it was put by the projects spearhead Yuste.

The human brain is thought to have a hundred billion neurons. Scientists and non-scientists have been forever intrigued with what makes humans humane, the answer obviously resides in the human brain. However the closest we have ever come to taking a look at the active human brain is through the techniques of EEG and fMRI, both of which have limitations. Neither of the technique allows a precise time locked understanding of individual neuronal activity neither do either of them come anywhere close to understanding how individual neurons speak to one another.

BAM hopes to not just understand the different kind of connections the different kind of neurons have in our brain but hopes to be able to decipher the neuronal messages and the neuronal language in order to understand how the human brain produces it’s thoughts and perceptions.

The human brain mapping project is an immense undertaking and requires a detailed road map. The road map to the eventual ambitious goal was laid out in a recent Neuron publication written by the scientists who initially proposed the project, Yuste and colleagues. The paper explains in detail the technological advances that would have to be made before the project can eventually map the neuronal individual and collective output. The team proposes a modest aim to first map the drosophila fly’s 135,000 or so neurons, and then to map the zebra fish and mouse. The next milestone would be the more ambitious mapping of a mammalian brain, the smallest being that of the etruscan shrew with one million neurons, and finally the human brain.

However many neuroscientists and psychologists have asked the crucial question on whether the sum of parts can ever equal the total when it come to an extremely complex puzzle as the human brain. Would mapping each neuron and its connection be enough to tell us what makes us humans? However, many are more worried about the eventual success of the project which not only seeks to map the brain but also seeks to learn how to control the human brain or to manipulate the neurons or to put it more bluntly, how to control the human mind.

Reference

Alivisatos AP, Chun M, Church GM, Greenspan RJ, Roukes ML, & Yuste R (2012). The brain activity map project and the challenge of functional connectomics. Neuron, 74 (6), 970-4 PMID: 22726828

Image via spirit of america / Shutterstock.

Related Articles:

• Creating an Artificial Brain
• Cord Blood-Derived Stem Cells – a New Therapeutic Option for Brain Disorders?
• New Imaging Techniques to Unlock Brain Disorders
• The Many Emerging Roles of Astrocytes
• I Can Read Your Mind!
• “I Feel Your Pain” – The Neural Basis of Empathy
• The Brain-Road Link: New Evidence on Cell Phones and Driving

Until recently, the sensory integration issues that plague many individuals on the autism spectrum have taken a back seat to the more commonly identified social and communication issues traditionally used to diagnose the disorder. In fact, the current Diagnostic and Statistical Manual of Mental Disorders of the American Psychiatric Association (DSM-IV-TR) states that the main areas of impairment in people with autism are communication, social interaction, repetitive motion, and restricted interests. Among other proposed changes to the definition of autism, the new edition of the DSM (DSM-V) due out in 2013, proposes to include sensory integration issues as part of the criteria for diagnosis, officially acknowledging the difficulties these individuals have processing information from the five senses. For individuals with autism who experience sensory integration issues, information is incorrectly processed by the brain, often causing distress, discomfort, and confusion. These sensory processing difficulties can be an underlying cause for some of the more commonly recognized behaviors often associated with autism, including avoiding eye contact and stimming behavior. When it comes specifically to perception and what the individual with autism sees, these issues can be a result of both ophthalmological and perceptual processing disorders.

How Many Are Affected?

In a study published in the Journal of Autism Developmental Disorders in 2012, the authors reported finding ophthalmologic pathology in 40% of patients with autism, leading them to conclude that “children with autism or a related disorder will frequently have an ophthalmologic abnormality.” However, this is not the whole story when it comes to what the individual with autism spectrum disorder (ASD) sees. While we take in visual information through the eyes, this information is broken down into millions of signals that have to be processed separately by independent pathways in the brain before being put back together again into the image we ultimately see.

Conservative estimates suggest that as many as 33% of individuals with ASD have brains that do not correctly process the visual information they receive. A survey conducted in 1994 by the Geneva Centre for Autism in Toronto, Canada, suggests these difficulties may be more common, finding that 81% of those on the autism spectrum reported distorted perception. The most common problems were difficulties with depth perception; distorted perception of size, shape, and motion; seeing only small details and not the whole; and visual overstimulation. However, visual-perceptual processing difficulties are not unique to the autism community. They are experienced by as many as 50% of individuals with reading difficulties or dyslexia and can also plague individuals who have suffered traumatic brain injury, concussion and whiplash. Even a portion of the general population (many estimates suggesting 12-14%) is affected.

What Does the World Look Like?

Well-known adults on the autism spectrum such as Temple Grandin and Donna Williams have described what the world can look like for someone with autism who experiences visual-perceptual processing difficulties. In her book, Nobody Nowhere, Donna Williams says, “Colors and things and people would fly, doors would get kicked in and sometimes faces would, too. But it was never whole people, only their pieces.” This is a glimpse into the often fragmented and frightening world in which many with ASD live.

What Causes the Problem?

In the visual cortex of the brain, information about shape, movement and color is determined by magnocellular, parvocellular, and koniocellular neurons in the lateral geniculate nucleus. This information is then sent to the primary visual cortex. Theories to explain visual processing difficulties come out of the literature on reading disabilities. There are presently two theories to explain visual processing difficulties: the transient visual subsystem deficit and the cortical hyperexcitability theories. The first suggests that there are issues with the magnocellular pathway that brings information to the primary visual cortex, conveying information about motion. The second proposes that there is a lack of inhibition in the orientation columns in the visual cortex, and this lack of inhibition causes excitation to spread throughout the visual system resulting in difficulty in processing visual Information. In either case, it is suggested that color can improve perceptual processing for individuals experiencing difficulties. In 2012, both ISRN Neurology and Autism Science Digest: The Journal of AutismOne published articles discussing the positive benefits of color (in either the form of colored lenses or colored overlays) to improve the difficulties associated with perceptual processing difficulties many individuals with autism experience.

How Does Color Help?

The colored lenses modify the speed at which visual information reaches the brain and allows the brain to correctly process the information. For individuals with autism, this often means transforming a fragmented environment into a cohesive whole. For some, it can take once distorted and scary faces and make them clear, cohesive and friendly. This change in the way faces look can have a draumatic impact on the individual with autism’s willingness to make eye-contact. And because behaviors such as stimming are often performed in an effort to create calm in a chaotic environment, when the visual environment calms down, these behaviors can calm down as well. In her book, Like Color to the Blind, Donna Williams describes the difference that colored lenses made in how her world looked, “Before I saw cracked children, cracked steps, print and writing…However, the person, I did not see whole.  I saw hair, I saw, eyes, nose, mouth, child…not a face.  Now I see the whole face, the whole person…I could now perceive for the first time as a whole…I finally could do more than struggle to image an un-fragmented whole.”

Individuals with autism who also suffer from perceptual processing difficulties that may be helped by colored lenses may have difficulties with any of the following:

1) Sensory Overload caused by bright lights, fluorescent lights, and sunlight. Lighting is stressful; and this results in behaviors to filter out the light, poor eye contact, and physical symptoms such as anxiety or headaches.

2) Environmental Distortions where the individual sees the world in a distorted fashion. Objects are blurry, moving, changing, and can disappear. People may look frightening, stairs may look like a slide without steps, and walls and floors may swing and sway. Misperceptions can cause difficulties with sustained attention, eye contact, gross and small motor coordination, ability to interpret facial expressions, and poor social skills.

3) Print Distortions make learning or reading difficult. The individual may have good or even advanced reading skills but has trouble with reading comprehension or experiences strain and fatigue when reading or doing other activities. Tracking or building breaks into reading may be a problem.

References

Borsting, E., Ridder, W., Dudeck, K., Kelley, C., Matsui, L., & Motoyama, J. (1996). The presence of a magnocellular defect depends on the type of dyslexia Vision Research, 36 (7), 1047-1053 DOI: 10.1016/0042-6989(95)00199-9

Chase C, Ashourzadeh A, Kelly C, Monfette S, & Kinsey K (2003). Can the magnocellular pathway read? Evidence from studies of color. Vision research, 43 (10), 1211-22 PMID: 12705960

Demb JB, Boynton GM, Best M, & Heeger DJ (1998). Psychophysical evidence for a magnocellular pathway deficit in dyslexia. Vision research, 38 (11), 1555-9 PMID: 9747491

Geneva Centre for Autism (1994). The sensory experiences of individuals with autism based on first-hand accounts. Toronto, Canada: Geneva Centre for Autism.

Grandin, T. Thinking in Pictures: And Other Reports from My Life with Autism. New York: Doubleday, 1995.

Huang J, Zong X, Wilkins A, Jenkins B, Bozoki A, & Cao Y (2011). fMRI evidence that precision ophthalmic tints reduce cortical hyperactivation in migraine. Cephalalgia : an international journal of headache, 31 (8), 925-36 PMID: 21622479

Hubel, D.H. (1995). Eye, Brain, and Vision. New York: Scientific American Library; 2.

Ikeda J, Davitt BV, Ultmann M, Maxim R, & Cruz OA (2012). Brief Report: Incidence of Ophthalmologic Disorders in Children with Autism. Journal of autism and developmental disorders PMID: 22350452

Irlen, H. (2012). A sensory intervention for visual processing deficits using precision colored filters. Autism Science Digest: The Journal of AutismOne, 04, 94-102.

Keen AG, & Lovegrove WJ (2000). Transient deficit hypothesis and dyslexia: examination of whole-parts relationship, retinal sensitivity, and spatial and temporal frequencies. Vision research, 40 (6), 705-15 PMID: 10824271

Kranowitz, C. (2005). The Out-of-Sync Child: Recognizing and Coping with Sensory Processing Disorder. New York: Penguin Group Publishers.

Ludlow, A., Taylor-Whiffen, E., & Wilkins, A. (2012). Coloured Filters Enhance the Visual Perception of Social Cues in Children with Autism Spectrum Disorders. ISRN Neurology, vol. 2012, Article ID 298098, 6 pages, 2012. doi:10.5402/2012/298098

Ludlow, A., Wilkins, A., & Heaton, P. (2006).  The effect of colored overlays on reading ability in children with Autism.  Journal of Autism and Developmental Disorders. Spring 2006.

Williams, D. Like Color to the Blind: Soul Searching and Soul Finding. New York: Times Books, 1996.

Williams, D. Nobody Nowhere: The Remarkable Autobiography of an Autistic Girl. New York: Times Books, 1992.

Wilkins A, Huang J, & Cao Y. (2004). Visual stress theory and its application to reading and reading tests. Journal of Research in Reading, 27(2), 152-62.

Image via Snvv / Shutterstock.

Related Articles:

• Do Fluorescent Lights Give You Headaches? You’re Not Alone
• Understanding How Color Is Perceived in the Brain
• Autism Evident in Newborns
• I Can Read Your Mind!
• Autism – No Need For A Cure?
• The Handwriting on the Wall
• Physical Therapy In Autism Spectrum Disorders

In a recent review, Bhat, Landa and Galloway examined evidence to show that children who are at risk for ASD had deficient motor capabilities. Movements like non-uniform gait, variable stride length when walking, and underperformance in aiming tasks are evident in children who are diagnosed with ASD. Cognitive impairment is also evident in these kids. There is evidence to show that children who do not suffer from a cognitive lag but yet underperform on tasks that require physical balance and coordination of limbs may be later diagnosed as suffering from ASD.

Impaired motor coordination may also be assessed in the early years. Retrospective analyses of home videos of kids diagnosed with ASD in later years demonstrate that delayed motor skills may be judged in the first two years of childhood. Delayed development of gross motor skills like walking at the age of 24 months or more can be a sign of ASD. Likewise, delayed development of fine motor skills in the early years can also point towards the existence of ASD.

In order to address the issue, early interventions with physical therapy have been recommended. Koenig, Buckley-Reen and Garg have assessed the impact of a early yoga training program in schoolkids with ASD. In their study, kids with ASD were trained in yoga in a classroom-based program (Get Ready To Learn Yoga or GRTL) on a daily basis for 16 weeks. A control group of kids with ASD was allowed to complete a normal school morning routine. These researchers report that that at the end of 16 weeks, children in the GRTL yoga program showed reduced maladjustive behaviors as compared to those in the control group. Behavioral patterns were assessed by teachers with the aid of the Aberrant Behavior Checklist. These results indicate that classroom based physical therapy interventions may help to reduce behavioral deficiencies in kids suffering from ASD.

In another study, exercises from a martial arts technique called Kata were taught to children aged 5 to 16 diagnosed with ASD. Thirty children with ASD were selected and divided equally into control and intervention groups. Kids in the intervention group were trained in Kata techniques for 56 sessions spanning 14 weeks. Stereotypic behavior was assessed prior to and post-intervention. The results showed that the intervention group showed a reduction in stereotypic behaviors. An interesting find from this study is that the effects of martial arts training persisted even after a hiatus of 30 days during which no practice sessions were conducted.

Individuals suffering from ASD learn better from demonstrative techniques than from conceptual or instructive learning methods. Therefore, group therapy sessions where the participants are asked to learn by observing the actions of a leader are more likely to succeed in children suffering from ASD. It may be useful to integrate group activities such as dance training, yoga, or elementary martial arts training in the curricula of early learning institutions to improve motor and behavioral functions in children with ASD.

References

Capone GT, Grados MA, Kaufmann WE, Bernad-Ripoll S, & Jewell A (2005). Down syndrome and comorbid autism-spectrum disorder: characterization using the aberrant behavior checklist. American journal of medical genetics. Part A, 134 (4), 373-80 PMID: 15759262

Koenig KP, Buckley-Reen A, & Garg S (2012). Efficacy of the Get Ready to Learn yoga program among children with autism spectrum disorders: a pretest-posttest control group design. The American journal of occupational therapy : official publication of the American Occupational Therapy Association, 66 (5), 538-46 PMID: 22917120

Bahrami F, Movahedi A, Marandi SM, & Abedi A (2012). Kata techniques training consistently decreases stereotypy in children with autism spectrum disorder. Research in developmental disabilities, 33 (4), 1183-93 PMID: 22502844

Image via Attl Tibor / Shutterstock.

Related Articles:

• The Handwriting on the Wall
• Brain Growth in Autism
• Autism Evident in Newborns
• Autism – No Need For A Cure?
• Sibling Risk of Autism
• Autism in Singapore
• Preteens Feel the Effects of Mom’s Pregnancy Bad Habits

Experiments conducted on rats show that intravenous injection of stem cells derived from adipose tissues as well as mesenchymal stem cells derived from bone marrow supported the recovery of brain cells after a stroke. In these experiments, rats were subjected to a stroke by blocking their middle cerebral artery permanently. Stem cells from bone marrow as well as fat cells were injected 30 minutes after induction and the health of the animals was assessed at 24 hours and 14 days after stroke. In the recovery period, animals injected with stem cells showed increased levels of vascular endothelial growth factor and synaptophysin. The injected stem cells did not migrate to the site of the lesion but presumably acted as a source of neurotrophic growth factors.

In another study, stem cells from the dental pulp of human deciduous teeth (milk teeth) were grafted in the brains of mice one day after induction of a stroke. In some animals, the culture medium in which these cells were grown was used instead of the cells. Mice treated with human dental pulp stem cells and conditioned medium from these cells showed better recovery and neurological outcome than untreated mice. Grafted stem cells as well as the conditioned medium inhibited death of neurons in the recovery period and prevented cell destruction resulting from inflammation. In these experiments, the actual integration of human dental pulp stem cells into the brain tissue occurred at very low frequency.

Both studies present important insights in the process of regeneration of brain cells followed hypoxic and ischemic stroke. Stem cells secrete a number of growth factors which help to promote generation of new neurons post a stroke. The results presented by Yamagata and colleagues where just the culture medium from dental pulp stem cells was effective in restoring brain tissue and neurological functions indicate that a suitable “growth factor cocktail” can be derived from cultures of stem cells to treat stroke. Since intravenous injection of stem cells also helps recovery from stroke, it is easy to deliver such a therapeutic intervention. A xenograft of human dental pulp stem cells was successful in helping mice recover from a stroke. It would be interesting to know whether stem cells from other animal systems have a similar beneficial effect on human neurons as well.

References

Gutierrez-Fernandez M, Rodriguez-Frutos B, Ramos-Cejudo J, Vallejo-Cremades MT, Fuentes B, Cerdan S, & Diez-Tejedor E (2013). Effects of intravenous administration of allogenic bone marrow- and adipose tissue-derived mesenchymal stem cells on functional recovery and brain repair markers in experimental ischemic stroke. Stem cell research & therapy, 4 (1) PMID: 23356495

Yamagata M, Yamamoto A, Kako E, Kaneko N, Matsubara K, Sakai K, Sawamoto K, & Ueda M (2013). Human dental pulp-derived stem cells protect against hypoxic-ischemic brain injury in neonatal mice. Stroke; a journal of cerebral circulation, 44 (2), 551-4 PMID: 23238858

Image via Paul Fleet / Shutterstock.

Related Articles:

• How Does the Brain Recover After Stroke?
• Cord Blood-Derived Stem Cells – a New Therapeutic Option for Brain Disorders?
• Mind your Immune System
• What Stem Cells Need to Survive in the Brain
• Nootropics Reduce the Severity of Brain Trauma
• New Hope for Alzheimer’s Treatment – iPS Cells to the Rescue?
• Logistical Barriers to Stem Cell Research

When most of us think of electricity and the brain together, we generally visualize what is known as electroconvulsive therapy (ECT) with an image of a man’s face in gruesome pain. Thanks to One Flew Over the Cuckoo’s Nest for that! But, recently, there has been a revival of interest in a somewhat subdued version of ECT referred to as transcranial electric stimulation (tES) encompassing direct current (tDCS), alternating current (tACS) and random noise (tRNS) stimulation. One key difference between these methods and ECT is the intensity of current being used. Whereas tES techniques only use a few milliamperes of current, ECT often uses hundreds of milliamperes ensuring a much more vigorous manipulation of the brain state. tES also comes in at a low cost and with negligible discomfort or side effects. So the idea of someone just hooking their heads up to a battery and manipulating their brain activity without risking too much might just be a little more close to reality than we would expect.

Besides its use in clinical therapy (depression, chronic pain, stroke recovery and what not; just search for “transcranial electric stimulation” in ClincialTrials.gov — we can also expand our imagination and think of some other fun applications. For instance, why not stimulate the pitcher of your base ball team for some extra speed in his pitches? Or, read up your text book and go to bed with your head hooked up to the stimulator, accelerating memory consolidation during sleep. How about training athletes and military personnel to develop faster reaction times and better visuomotor coordination by stimulation? How about stimulating the US senators before crucial meetings to enhance their critical thinking or planning capabilities? Recent experimental results do render some of these possibilities feasible. For instance, Lisa Marshall and colleagues has recently reported that tDCS during sleep improves declarative memory [1]. Colleen Dockery and colleagues have provided evidence towards enhancement of planning ability by tDCS [2]. Improvement of motor learning skills, reactions times, numerical capabilities and other tasks has also been reported (for review, see [3]).

Everything so far seems just great! But there are also reasons why you should think twice before you subscribe to these tools. First, although there is a plethora of reports of behavioral effects of tES, the mechanisms of actions of tES is pretty much unknown and existing theories can be categorized as mere speculations. Second, if there are adverse chronic effects (which requires objective longitudinal studies); we probably are better off harnessing our natural brain power rather than messing it up with unknown electrical manipulations. Third, what if tES is nothing but a placebo? There isn’t a definitive answer to the last question yet. Hence it remains important for us to remain skeptical about the applications of tES. But at the same time, given the exciting possibilities, we should invest resources and encourage scientists to study the effects of external electric fields on our brains. If we play the cards right, we might just be a decade away from going to radio shack and ordering the $5 Brain Recharger Kit!

References

1. Marshall L, Mölle M, Hallschmid M, & Born J (2004). Transcranial direct current stimulation during sleep improves declarative memory. The Journal of neuroscience : the official journal of the Society for Neuroscience, 24 (44), 9985-92 PMID: 15525784

2. Dockery CA, Hueckel-Weng R, Birbaumer N, & Plewnia C (2009). Enhancement of planning ability by transcranial direct current stimulation. The Journal of neuroscience : the official journal of the Society for Neuroscience, 29 (22), 7271-7 PMID: 19494149

3. Utz KS, Dimova V, Oppenländer K, & Kerkhoff G (2010). Electrified minds: transcranial direct current stimulation (tDCS) and galvanic vestibular stimulation (GVS) as methods of non-invasive brain stimulation in neuropsychology–a review of current data and future implications. Neuropsychologia, 48 (10), 2789-810 PMID: 20542047

Image via Sergey Nivens / Shutterstock.

Related Articles:

• Electrical Brain Stimulation Improves Hand Motor Skills
• Two Wrongs Make a Right – Abnormal Brain Circuitry May Stop Abnormal Movement
• Sleep Is Important for Next Day Memory Formation
• What Make Us Moral?
• A Drug Treatment for Chronic Pain and Erasing Its Memory
• Migraines and Nerve Stimulation
• Deep Brain Stimulation for Pleasure