Brain Blogger » Neuroscience & Neurology http://brainblogger.com Health and Science Blog Covering Brain Topics Fri, 20 Feb 2015 00:15:36 +0000 en-US hourly 1 http://wordpress.org/?v=4.1 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

Image via Candy Box Images / Shutterstock.

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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

Image via beccarra / Shutterstock.

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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

Image via Monkey Business Images / Shutterstock.

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Nurturing The Brain – Part I, Caffeine http://brainblogger.com/2015/01/26/nurturing-the-brain-part-i-caffeine/ http://brainblogger.com/2015/01/26/nurturing-the-brain-part-i-caffeine/#comments Mon, 26 Jan 2015 12:00:38 +0000 http://brainblogger.com/?p=18306 Overall, more than 85% of children and adults consume caffeine regularly. But what does it do to the brain?

Coffee is one of the most consumed beverages in the world. According to Euromonitor, the United States is the country with the highest amount of total coffee consumption (971 tons per year), closely followed by Brazil (969 tons). However, when analyzed per capita, coffee consumption is actually highest in northern Europe, with Finland taking the lead, followed by Norway and the Netherlands. According to the National Coffee Association of the US (NCA), 54% of Americans over the age of 18 drink coffee on a daily basis and 25% drink only occasionally; only 22% never drink coffee at all. But coffee is not the only dietary source of caffeine. Other common sources include tea, chocolate, caffeinated soda, energy drinks, over-the-counter analgesics and cold remedies, and weight-loss aids.

Caffeine’s actions in the central nervous system (CNS) are mainly due to its effect as an adenosine receptor antagonist. Adenosine is a metabolite of ATP, which acts as a neurotransmitter, although it cannot be considered a classical neurotransmitter since it is not stored in synaptic vesicles or released in a calcium-dependent mechanism by neurons. Adenosine can be generated from ATP released by neurons or glia through the action of extracellular enzymes, or it can be directly released by neurons through membrane transporters. It’s an important modulator of the nervous system, interacting with many neurotransmitters. There are four receptor subtypes for adenosine (A1, A2A, A2B, and A3); due to its structural similarity with adenosine, caffeine can bind to all of them, thereby blocking their interaction with adenosine.

In general, adenosine has an inhibitory effect in the CNS, increasing drowsiness and sleep. Caffeine’s stimulatory effects are therefore primarily associated with its capacity to block adenosine receptors, antagonizing their effects.

Some metabolites of caffeine also have marked pharmacological activity. The metabolites theophylline, paraxanthine and theobromine are also adenosine receptor antagonists. Theophylline can actually be three to five times more potent than caffeine as an inhibitor of both adenosine A1 and A2A receptors. Therefore, besides its direct effects, caffeine’s action can be further increased, or at least maintained, by the action of its own metabolites.

Even though the action of caffeine occurs primarily by blocking adenosine receptors, there are important secondary effects affecting different classes of neurotransmitters that adenosine modulates, including noradrenaline, dopamine, serotonin, acetylcholine, glutamate, and GABA. This is reflected on the wide range of effects that caffeine has on the CNS that include increased motor activity, cortical activation, information processing rate, and cerebral energy metabolism rate.

These actions of caffeine can also have detrimental effects. Just as the main reason for coffee consumption is increasing wakefulness, unsatisfactory sleep is one of the main reasons people cease drinking coffee. It is well known that caffeine delays the onset and decreases the quality of sleep. However, these effects are quite variable, probably due to different metabolic rates or to differences in the sensitivity to caffeine between individuals. Some people have no sleep problems whatsoever despite regularly consuming caffeine in the evening.

Due to its actions in increasing alertness, attention, and cognitive function, and in elevating mood, caffeine has been associated with a decrease in depressive symptoms, fewer cognitive failures, and lower risk of suicide. However, high doses of caffeine can, in rare cases, induce psychotic and manic symptoms. The most common mood effect is increased anxiety, but it is mostly associated with a potentiation of pre-existing anxiety and panic disorders.

Some therapeutic uses of caffeine have been proposed. Studies using adenosine receptor antagonists, including caffeine, have shown a reduction in damages caused by spinal cord injury, stroke, and by neurodegenerative diseases such as Parkinson’s and Alzheimer’s diseases. Neuroprotective effects of caffeine have been demonstrated in animal models of brain injury and it is likely that similar effects may occur in humans.

Caffeine is potentially addictive. In fact, the latest edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) has included caffeine intoxication and withdrawal as substance-related and addictive disorders. Caffeine withdrawal is now an officially recognized diagnosis, and criteria for caffeine use disorder have been proposed for additional study. As anyone who has experienced it may guess, caffeine withdrawal is characterized, according to DSM-5, by headache, marked fatigue or drowsiness, dysphoric mood, depressed mood, or irritability, difficulty concentrating, and flu-like symptoms (nausea, vomiting, or muscle pain/stiffness).

Although high doses of caffeine may have negative side-effects, the regular consumption of an average dose of caffeine (280 mg/day, corresponding to three 8 fl. oz. cups of American coffee or to four to five 1 fl. oz. cups of Espresso) seems to be mostly harmless or even beneficial.

References

Fredholm BB, Bättig K, Holmén J, Nehlig A, & Zvartau EE (1999). Actions of caffeine in the brain with special reference to factors that contribute to its widespread use. Pharmacological reviews, 51 (1), 83-133 PMID: 10049999

Lara DR (2010). Caffeine, mental health, and psychiatric disorders. Journal of Alzheimer’s disease : JAD, 20 Suppl 1 PMID: 20164571

National Coffee Association (2009). National Coffee Drinking Trends. Accessed online 25 January 2015.

Nehlig A, Daval JL, & Debry G (1992). Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects. Brain research. Brain research reviews, 17 (2), 139-70 PMID: 1356551

Petzer JP, & Petzer A (2014). Caffeine As A Lead Compound For The Design Of Therapeutic Agents For The Treatment Of Parkinson’s Disease. Current medicinal chemistry PMID: 25544641

Rivera-Oliver M, & Díaz-Ríos M (2014). Using caffeine and other adenosine receptor antagonists and agonists as therapeutic tools against neurodegenerative diseases: a review. Life sciences, 101 (1-2), 1-9 PMID: 24530739

Snel J, & Lorist MM (2011). Effects of caffeine on sleep and cognition. Progress in brain research, 190, 105-17 PMID: 21531247

Shutterstock image id: 77118010

Image via Andrey Kuzmin / Shutterstock.

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How Does Post-Traumatic Stress Disorder Change the Brain? http://brainblogger.com/2015/01/24/how-does-post-traumatic-stress-disorder-change-the-brain/ http://brainblogger.com/2015/01/24/how-does-post-traumatic-stress-disorder-change-the-brain/#comments Sat, 24 Jan 2015 12:00:27 +0000 http://brainblogger.com/?p=18277 Child abuse. Rape. Sexual assault. Brutal physical attack. Being in a war and witnessing violence, bloodshed, and death from close quarters. Near death experiences. These are extremely traumatic events, and some victims bear the scars for life.

The physical scars heal, but some emotional wounds stop the lives of these people dead in their tracks. They are afraid to get close to people or form new relationships. Change terrifies them, and they remain forever hesitant to express their needs or give vent to their creative potential. It may not be always apparent, but post-traumatic stress disorder (PTSD) stifles the life force out of its victims. It is no use telling them to “get over” it because PTSD fundamentally changes the brain’s structure and alters its functionalities.

What goes on inside the brains of people with PTSD?

PTSD is painful and frightening. The memories of the event linger and victims often have vivid flashbacks. Frightened and traumatized, they are almost always on edge and the slightest of cues sends them hurtling back inside their protective shells. Usually victims try to avoid people, objects, and situations that remind them of their hurtful experiences; this behavior is debilitating and prevents them from living their lives meaningfully.

Many victims forget the details of the incident, obviously in an attempt to lessen the blow. But this coping mechanism has negative repercussions as well. Without accepting and reconciling with “reality,” they turn into fragmented souls.

Extensive neuroimaging studies on the brains of PTSD patients show that several regions differ structurally and functionally from those of healthy individuals. The amygdala, the hippocampus, and the ventromedial prefrontal cortex play a role in triggering the typical symptoms of PTSD. These regions collectively impact the stress response mechanism in humans, so the PTSD victim, even long after his experiences, continues to perceive and respond to stress differently than someone who is not suffering the aftermaths of trauma.

Effect of trauma on the hippocampus

The most significant neurological impact of trauma is seen in the hippocampus. PTSD patients show a considerable reduction in the volume of the hippocampus. This region of the brain is responsible for memory functions. It helps an individual to record new memories and retrieve them later in response to specific and relevant environmental stimuli. The hippocampus also helps us distinguish between past and present memories.

PTSD patients with reduced hippocampal volumes lose the ability to discriminate between past and present experiences or interpret environmental contexts correctly. Their particular neural mechanisms trigger extreme stress responses when confronted with environmental situations that only remotely resemble something from their traumatic past. This is why a sexual assault victim is terrified of parking lots because she was once raped in a similar place. A war veteran still cannot watch violent movies because they remind him of his trench days; his hippocampus cannot minimize the interference of past memories.

Effect of trauma on the ventromedial prefrontal cortex

Severe emotional trauma causes lasting changes in the ventromedial prefrontal cortex region of the brain that is responsible for regulating emotional responses triggered by the amygdala. Specifically, this region regulates negative emotions like fear that occur when confronted with specific stimuli. PTSD patients show a marked decrease in the volume of ventromedial prefrontal cortex and the functional ability of this region. This explains why people suffering from PTSD tend to exhibit fear, anxiety, and extreme stress responses even when faced with stimuli not connected – or only remotely connected – to their experiences from the past.

Effect of trauma on the amygdala

Trauma appears to increase activity in the amygdala. This region of the brain helps us process emotions and is also linked to fear responses. PTSD patients exhibit hyperactivity in the amygdala in response to stimuli that are somehow connected to their traumatic experiences. They exhibit anxiety, panic, and extreme stress when they are shown photographs or presented with narratives of trauma victims whose experiences match theirs; or made to listen to sounds or words related to their traumatic encounters.

What is interesting is that the amygdala in PTSD patients may be so hyperactive that these people exhibit fear and stress responses even when they are confronted with stimuli not associated with their trauma, such as when they are simply shown photographs of people exhibiting fear.

The hippocampus, the ventromedial prefrontal cortex, and the amygdala complete the neural circuitry of stress. The hippocampus facilitates appropriate responses to environmental stimuli, so the amygdala does not go into stress mode. The ventromedial prefrontal cortex regulates emotional responses by controlling the functions of the amygdala. It is thus not surprising that when the hypoactive hippocampus and the functionally-challenged ventromedial prefrontal cortex stop pulling the chains, the amygdala gets into a tizzy.

Hyperactivity of the amygdala is positively related to the severity of PTSD symptoms. The aforementioned developments explain the tell-tale signs of PTSD—startle responses to the most harmless of stimuli and frequent flashbacks or intrusive recollections.

Researchers believe that the brain changes caused by PTSD increase the likelihood of a person developing other psychotic and mood disorders. Understanding how PTSD alters brain chemistry is critical to empathize with the condition of the victims and devise treatment methods that will enable them to live fully and fulfill their true potential.

But in the midst of such grim findings, scientists also sound a note of hope for PTSD patients and their loved ones. According to them, by delving into the pathophysiology of PTSD, they have also realized that the disorder is reversible. The human brain can be re-wired. In fact, drugs and behavioral therapies have been shown to increase the volume of the hippocampus in PTSD patients. The brain is a finely-tuned instrument. It is fragile, but it is heartening to know that the brain also has an amazing capacity to regenerate.

References

Bremner JD (2006). Traumatic stress: effects on the brain. Dialogues in clinical neuroscience, 8 (4), 445-61 PMID: 17290802

Bremner JD, Elzinga B, Schmahl C, & Vermetten E (2008). Structural and functional plasticity of the human brain in posttraumatic stress disorder. Progress in brain research, 167, 171-86 PMID: 18037014

Hull AM (2002). Neuroimaging findings in post-traumatic stress disorder. Systematic review. The British journal of psychiatry : the journal of mental science, 181, 102-10 PMID: 12151279

Koenigs, M., & Grafman, J. (2009). Posttraumatic Stress Disorder: The Role of Medial Prefrontal Cortex and Amygdala The Neuroscientist, 15 (5), 540-548 DOI: 10.1177/1073858409333072

Nutt DJ, & Malizia AL (2004). Structural and functional brain changes in posttraumatic stress disorder. The Journal of clinical psychiatry, 65 Suppl 1, 11-7 PMID: 14728092

Rocha-Rego, V., Pereira, M., Oliveira, L., Mendlowicz, M., Fiszman, A., Marques-Portella, C., Berger, W., Chu, C., Joffily, M., Moll, J., Mari, J., Figueira, I., & Volchan, E. (2012). Decreased Premotor Cortex Volume in Victims of Urban Violence with Posttraumatic Stress Disorder PLoS ONE, 7 (8) DOI: 10.1371/journal.pone.0042560

Shin LM, Rauch SL, & Pitman RK (2006). Amygdala, medial prefrontal cortex, and hippocampal function in PTSD. Annals of the New York Academy of Sciences, 1071, 67-79 PMID: 16891563

Image via John Gomez / Shutterstock.

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Musical Training Makes You Smarter http://brainblogger.com/2015/01/20/musical-training-makes-you-smarter/ http://brainblogger.com/2015/01/20/musical-training-makes-you-smarter/#comments Tue, 20 Jan 2015 12:00:26 +0000 http://brainblogger.com/?p=18215 Mozart has not only enthralled countless music lovers through the ages but also intrigued neuroscientists. In fact, his genre of music has spawned a whole body of research into the effect of classical music on cognitive development in kids.

The “Mozart Effect” is the idea that children and babies (even unborn) become more intelligent if they are fed on a dose of the symphonies, operas, and concertos created by this musical legend. Disappointingly, the researchers since have established that listening to Mozart or any other piece of classical music does not lead to long-term cognitive benefits. But in the process, they have also discovered that serious and sustained musical training does have a positive effect on some aspects of cognitive development.

Music training and the brain

There have been several studies to find an association, if any, between music and cognitive capabilities.

The Mozart Effect was, in effect, nullified when a 2005 study found that listening to music improved the cognitive performance of the listeners only for a short period of time. This development is attributed to the general mood-enhancing effect of music. After this finding, many of the studies began to focus on the short- and long-term effects of taking music lessons and making music on specific cognitive abilities like general intelligence, memory, language, and visual-spatial processing.

Multiple studies suggest that learning to play a musical instrument early in childhood induces long-term intellectual benefits that stay well into adulthood. One recent study demonstrated that children aged around four-and-a-half who learned music for about a year displayed improved cognitive functioning than their untrained peers.

Musical training affects the oscillatory connections in the brain related to executive functions like reasoning, switching between multiple tasks, forming working memory, planning and executing, and problem solving. Children who undergo musical training for a sustained length of time tend to have superior cognitive abilities in these specific domains. Musical children also tend to learn and perform better in subjects like languages and mathematics than their non-musical peers.

These findings do not come as a surprise. Sustained and intense musical training demands that individuals focus intently on dynamic sensory (auditory and visual) and motor signals. These are high-level cognitive abilities that go on to affect learning and performance in non-musical spheres as well.

It is also believed that intense musical training enhances the ability of the practitioner to string together abstract concepts and think relationally to make sense of these. This is why some scientists believe that musical training improves mathematical skills and non-verbal IQ.

Language skills

Very recently, researchers have shown that children who undertook long-term training in music exhibited enhanced academic development compared to the children in the same age group who did not receive this training. More specifically, this effect was seen mostly in the aspect of language skills. Children who trained in music in their early years exhibited enhanced verbal memory and increased reading skills in comparison to those who had never received any musical training. These skills seemed to sharpen with every extra year of training.

Learning a language and learning and/or making music engage similar areas of the brain and demand identical cognitive and auditory processing abilities. For example, to understand a spoken language, the listener needs to be able to correctly discriminate between words, understand how they sound different because certain vowels and consonants are present, and the process the sequencing of syllables and tones.

Musical training is also believed to improve reading skills in serious practitioners. Learning music enhances auditory working memory, phonological awareness, and the ability to differentiate between sounds, identify patterns, and recognize rhythm and pitch. It seems that these abilities also help individuals develop reading and pronunciation skills. Children who receive musical training early and continue to train show a greater grasp of second language acquisition skills than their non-musical peers.

Improved sensory processing

The benefits of early music training have also been documented in studies aimed to determine the effect of music on sensory processing capabilities. According to these findings, individuals who undertook sustained musical training before the age of seven showed greater neural plasticity in their brains than those who undertook training after this age. Specifically, the former group showed improved sensory motor responses, such as exhibiting coordinated reflex actions and having a sense of posture.

Another study suggests that early music training enhances the plasticity of white matter in the corpus callosum. This structural peculiarity results in enhanced connectivity between the sensory and motor areas of the brain.

An article published last year nails down the cause behind this association and indicates that there is a sensitive period during the developmental phase of a person when this effect is strongest. The right ventral pre-motor cortex is involved in the processing and integration of sensory (auditory) and motor information. And according to this study, musicians who began training early showed greater thickness (increased white and gray matter) in this region of their brains. This region exhibits peak maturational transformation between the ages of six and nine years. The effect of musical training on the plasticity in this region is therefore greatest just before maturation. So it is no surprise that highly-skilled musicians, who began practicing before the age of seven, show enhanced cognitive development than musicians who train later.

The above findings on the positive association between musical training and cognitive abilities hold significance not only for parents and neuroscientists but also for those who work in the education sphere. For instance, educationists entrusted with policy making should think twice before chopping the budget for arts and music training in schools. These findings should also prompt scientists, psychologists, and educational counselors to ponder over the efficacy of recommending musical training to children with learning disabilities.

It is evident that musical training improves cognitive abilities in children. The earlier they begin to strum the guitar and tinkle the piano, the brighter are their chances of performing in school. So continue encouraging your kid to play the banjo even if he is out of tune. You will be doing her a world of good.

References

Bailey, J., Zatorre, R., & Penhune, V. (2014). Early Musical Training Is Linked to Gray Matter Structure in the Ventral Premotor Cortex and Auditory–Motor Rhythm Synchronization Performance Journal of Cognitive Neuroscience, 26 (4), 755-767 DOI: 10.1162/jocn_a_00527

Hille, K., Gust, K., Bitz, U., & Kammer, T. (2011). Associations between music education, intelligence, and spelling ability in elementary school Advances in Cognitive Psychology, 7 (-1), 1-6 DOI: 10.2478/v10053-008-0082-4

Jenkins JS (2001). The Mozart effect. Journal of the Royal Society of Medicine, 94 (4), 170-2 PMID: 11317617

Neville, H. et al. (2008). Arts and Cognition Monograph: Effects of Music Training – Underprivileged. The DANA Foundation.

Schellenberg, E. (2005). Music and Cognitive Abilities Current Directions in Psychological Science, 14 (6), 317-320 DOI: 10.1111/j.0963-7214.2005.00389.x

Steele, C., Bailey, J., Zatorre, R., & Penhune, V. (2013). Early Musical Training and White-Matter Plasticity in the Corpus Callosum: Evidence for a Sensitive Period Journal of Neuroscience, 33 (3), 1282-1290 DOI: 10.1523/JNEUROSCI.3578-12.2013

Tierney A, & Kraus N (2013). Music training for the development of reading skills. Progress in brain research, 207, 209-41 PMID: 24309256

Trainor LJ, Shahin AJ, & Roberts LE (2009). Understanding the benefits of musical training: effects on oscillatory brain activity. Annals of the New York Academy of Sciences, 1169, 133-42 PMID: 19673769

Trainor, L., Shahin, A., & Roberts, L. (2009). Understanding the Benefits of Musical Training Annals of the New York Academy of Sciences, 1169 (1), 133-142 DOI: 10.1111/j.1749-6632.2009.04589.x

Yang, H., Ma, W., Gong, D., Hu, J., & Yao, D. (2014). A Longitudinal Study on Children’s Music Training Experience and Academic Development Scientific Reports, 4 DOI: 10.1038/srep05854

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Digital Drugs – Getting High Online? http://brainblogger.com/2015/01/18/digital-drugs-getting-high-online/ http://brainblogger.com/2015/01/18/digital-drugs-getting-high-online/#comments Sun, 18 Jan 2015 12:00:22 +0000 http://brainblogger.com/?p=18227 Connecting yourself to a computer is now apparently all you need to do to get high. That is according to some users and promoters of a phenomenon known as “digital drugs”. These consist of specially designed audio tracks easily found on the internet for free, or even purchased in mp3 or CD form.

Now, we know that music can influence mood, but can it really lead to significant changes in brain state? Perhaps. These so-called digital drugs are not merely music, they involve the generation of something called binaural beats. These are rhythmic illusions created through the presentation of sounds with different frequencies to the left and right ears.

The principle, although it has not been thoroughly researched, is that a difference between these two frequencies – say 30 Hertz – will lead to a brainwave state approximating the same frequency.

Brainwaves are the synchronised electrical pulses given off by the neurons in our brains, and are measurable using sensors placed on the scalp. It is believed that certain frequencies relate to certain states of consciousness, such as meditative states.

Some of the claims made by the tracks sold as digital drugs online are implausibly outlandish, and claim to mimic the effects of known illicit drugs. The digital highs found on Youtube have titles such as acid trip, marijuana high, opium, cocaine dose and magic mushroom.

This naming system is likely to have more to do with sales technique as with the properties of the beats themselves. Whatever effect they may have, it seems highly unlikely they would create specific analogues for known drug effects, turning this kind of labeling into marketing hype at its worst.

Some years ago, digital drugs hit the headlines after some teenagers from a school in Oklahoma claimed to be getting high listening to some mp3s. Parents and teachers expressed alarm at this trend. The parents of the children were afraid of the physical, psychological and social implications. In addition, some feared they might act as “gateway drugs”.

Users claim to use binaural beats for diverse purposes including meditation, concentration aids, hypnosis, relaxation and sexual stimulation. These has been some research into binaural beats can have a positive psychological impact in improving relaxation, mental performance, concentration and mood. However, there is certainly no academic evidence to suggest effects on the brain of the same order of that created by the ingestion of recreational drugs.

Maybe in the future we will be able to connect our brains to a virtual reality which will be able to provide us with sophisticated altered states of mind. But for now, the technology, if we can even call it that, seems pretty limited.

References

Lane, J., Kasian, S., Owens, J., & Marsh, G. (1998). Binaural Auditory Beats Affect Vigilance Performance and Mood Physiology & Behavior, 63 (2), 249-252 DOI: 10.1016/S0031-9384(97)00436-8

Lavallee CF, Koren SA, & Persinger MA (2011). A quantitative electroencephalographic study of meditation and binaural beat entrainment. Journal of alternative and complementary medicine (New York, N.Y.), 17 (4), 351-5 PMID: 21480784

Wahbeh H, Calabrese C, & Zwickey H (2007). Binaural beat technology in humans: a pilot study to assess psychologic and physiologic effects. Journal of alternative and complementary medicine (New York, N.Y.), 13 (1), 25-32 PMID: 17309374

Image via agsandrew / Shutterstock.

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Mars Vs Venus – Differences in Male and Female Brains http://brainblogger.com/2015/01/13/mars-vs-venus-differences-in-male-and-female-brains/ http://brainblogger.com/2015/01/13/mars-vs-venus-differences-in-male-and-female-brains/#comments Tue, 13 Jan 2015 13:03:44 +0000 http://brainblogger.com/?p=18184 And the differences are not just in the kind of television shows or movies they prefer or what they like to talk about when they catch up with members of the same sex!

Men and women have different brains that make them see and feel differently. We are genetically and neurologically programmed to be good or bad in different tasks. The difference in brain structure and chemistry also makes men and women more vulnerable to varying kinds of mental disorders.

Distinct neurological connections

A novel study performed on about 950 men and women (8-23 years of age) has shown that the neural connections in male and female brains are vastly different.

Male brains have more connections within each hemisphere, in female brains there are more connections between the two hemispheres. There is greater modularity in male brains, which explains why men learn and execute tasks in isolation better than women, who tend to excel in multitasking. Think of a female friend or a relative who helps her kids with the homework while rustling up the family dinner, checking updates on WhatsApp, and keeping an eye on what’s happening in her favorite TV show. We all know a few multitasking mavericks.

This difference in neural connectivity also manifests in how men and women behave and function. The rear end of the brain is involved in perception while the frontal portion controls coordinated activities. Greater neural connectivity inside hemispheres makes men generally better in motor activities than women.

The particular brain chemistry of males and females also influences perception. According to one study, men can better detect and process fine visual stimuli and fast-moving objects. Scientists think testosterone, the male sex hormone, may have a hand in this because the cerebral cortex in the human brain contains a large number of testosterone receptors. It is known that testosterone affects the functionality of sense organs.

The combined effect of increased intra-hemispheric connection and better spatial-temporal visual acuity makes men, on average, more likely to excel in mathematics, physics, and engineering. These sex-specific structural differences in the brain may also explain why more men than women become airplane pilots, architects, and race car drivers.

The left hemisphere of the brain is involved in logical thinking while the right hemisphere is the seat of intuitive thinking. Increased inter-hemispheric neural connectivity makes women generally more adept at intuitive thinking that involves coordinating analytical reasoning and intuition.

Women are therefore better at managing relationships, empathizing, articulating and expressing themselves creatively, and appreciating beauty. They have denser gray matter in the parietal cortex than men. This explains why women tend to be better at interpreting verbal cues; gauging what lies behind words and in what remains unuttered, remembering faces, and understanding gestures.

These differences in the structure and working of the male and female brain make sense from the point of view of evolution as well.

In a hunter-gatherer society, men had to possess keen sensory reflexes to be able to spot their catch in the wild and kill it without feeling the pangs of remorse that more empathetic members of the opposite gender would have suffered from. Enhanced motor capabilities too helped men design deadlier hunting tools. Mother Nature made women more empathetic and endowed her with greater emotional intelligence, so she can intuitively respond to the needs of babies and children who cannot make themselves understood.

Differences in susceptibility to mental disorders

Gender differences in the human brain lead to considerable differences in the way men and women perceive, interpret, and react to their external environments. What also intrigues scientists and doctors is the possibility that these differences may lead to either greater or reduced vulnerability to certain psychological disorders.

One study suggests that men may be more vulnerable to autism than women because they tend to have less empathetic and more systemizing capabilities than women do. The authors refer to a condition where a man has an “extreme male brain.” Such an individual has severely restricted empathizing abilities that makes it difficult for him to socialize, communicate meaningfully, and respond appropriately to other people’s behavior and emotions. These are some telltale signs of autism.

According to the findings of another research study, enhanced systemizing capabilities may explain the greater incidence of high-functioning autism or Asperger’s syndrome in men than women. Individuals with these capabilities have a few focused areas of interest and a keen eye for detail, qualities that can stand individuals in good stead in their careers. Composer Wolfgang Amadeus Mozart and physicist Albert Einstein exhibited symptoms of Asperger’s syndrome.

More women suffer from major depressive disorder (MDD) than men. Estrogen imbalance in the body and the consequent effect on specific regions of the brain could have a hand in making women more vulnerable to depression. Some areas of the female brain, such as the amygdala, hippocampus, anterior cingulate, and medial and orbital prefrontal cortices contain a large number of estrogen receptors. These regions are concerned with mood regulation in individuals. Several studies suggest that high levels of estrogen impair a person’s ability to manage stress that can trigger depression and anxiety.

The above findings provide food for thought to neuroscientists, doctors, and drug manufacturers. Should there be different drugs for men and women? Should physicians prescribe different treatment procedures for men and women?

References

Abramov, I., Gordon, J., Feldman, O., & Chavarga, A. (2012). Sex & vision I: Spatio-temporal resolution Biology of Sex Differences, 3 (1) DOI: 10.1186/2042-6410-3-20

Baron-Cohen, S. (2009). Autism: The Empathizing-Systemizing (E-S) Theory Annals of the New York Academy of Sciences, 1156 (1), 68-80 DOI: 10.1111/j.1749-6632.2009.04467.x

Baron-Cohen, S. (2005). Sex Differences in the Brain: Implications for Explaining Autism Science, 310 (5749), 819-823 DOI: 10.1126/science.1115455

Xu, C., Li, C., Wu, H., Wu, Y., Hu, S., Zhu, Y., Zhang, W., Wang, L., Zhu, S., Liu, J., Zhang, Q., Yang, J., & Zhang, X. (2015). Gender Differences in Cerebral Regional Homogeneity of Adult Healthy Volunteers: A Resting-State fMRI Study BioMed Research International, 2015, 1-8 DOI: 10.1155/2015/183074

Ingalhalikar, M., Smith, A., Parker, D., Satterthwaite, T., Elliott, M., Ruparel, K., Hakonarson, H., Gur, R., Gur, R., & Verma, R. (2013). Sex differences in the structural connectome of the human brain Proceedings of the National Academy of Sciences, 111 (2), 823-828 DOI: 10.1073/pnas.1316909110

Goldstein, J., Holsen, L., Handa, R., & Tobet, S. (2014). Fetal hormonal programming of sex differences in depression: linking women’s mental health with sex differences in the brain across the lifespan Frontiers in Neuroscience, 8 DOI: 10.3389/fnins.2014.00247

Schuch, J., Roest, A., Nolen, W., Penninx, B., & de Jonge, P. (2014). Gender differences in major depressive disorder: Results from the Netherlands study of depression and anxiety Journal of Affective Disorders, 156, 156-163 DOI: 10.1016/j.jad.2013.12.011

Shansky, R. (2009). Estrogen, stress and the brain: progress toward unraveling gender discrepancies in major depressive disorder Expert Review of Neurotherapeutics, 9 (7), 967-973 DOI: 10.1586/ERN.09.46

Sowell, E., Peterson, B., Kan, E., Woods, R., Yoshii, J., Bansal, R., Xu, D., Zhu, H., Thompson, P., & Toga, A. (2006). Sex Differences in Cortical Thickness Mapped in 176 Healthy Individuals between 7 and 87 Years of Age Cerebral Cortex, 17 (7), 1550-1560 DOI: 10.1093/cercor/bhl066

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A Touch of Science http://brainblogger.com/2014/12/29/a-touch-of-science/ http://brainblogger.com/2014/12/29/a-touch-of-science/#comments Mon, 29 Dec 2014 12:00:22 +0000 http://brainblogger.com/?p=17984 A team from The Scripps Research Institute (TSRI) in La Jolla, California, has just published a very important finding for sensory physiology research. Professor Ardem Patapoutian and his collaborators have identified the mechanoreceptor protein that mediates the sense of touch in mammals: the Piezo2 ion-channel protein of the Merkel cell-neurite complex.

Merkel cells are receptor cells found in the skin of vertebrates, in the inner layer of the epidermis. They are associated with the sense of light touch discrimination of fine details of objects. Merkel cells have synaptic contacts with sensory afferent neurons, forming a complex with sensory nerve endings – the aforementioned Merkel cell-neurite complex. This complex mediates different aspects of touch responses. Its presence in the skin has been known for decades, but the specific function of each cell type has remained unknown.

Recent studies have finally shed light on this mystery. Merkel cells were shown to have the ability to encode mechanical inputs and this provided an important clue to understanding how the skin communicates with neurons.

A great advance into understanding the detailed mechanism of this process was made four years ago, when Patapoutian and colleagues identified the proteins Piezo1 and Piezo2 as components of mechanically-activated cation channels and showed that the elimination of Piezo2 from sensory neurons could reduce mechanical activation. This was a clear indication that Piezo2 could have a fundamental role in touch processing.

Earlier this year, Patapoutian’s team published an article where they showed that Piezo2 was expressed in Merkel cells and that these could produce touch-sensitive currents in vitro. They showed that Merkel cell mechanosensitivity completely depended on Piezo2.  Their results indicated that Piezo2 could be the paramount channel for Merkel cell mechanotransduction and presented the Piezos as potential key players in the physiology of mechanical sensation in mammals.

Another important outcome of this study was the view that both Merkel cells and sensory afferents could act jointly as mechanosensors. They hypothesized that this two-receptor system could act as a fine-tuning mechanism to achieve highly detailed perception of objects and textures.

In their latest study, recently published in Nature, they extended their research to the touch-sensitive nerve terminals themselves. Their study demonstrated that Piezo2 could be found in the peripheral nerve endings of a broad range of sensory neurons innervating the skin, and that the mechanosensitivity of these neurons strongly depended on Piezo2. They also showed that the absence of Piezo2 in sensory neurons led to a marked loss of touch sensation. Importantly, they saw that the almost complete deficit in light-touch sensation did not affect other sensory functions. This allowed them to conclude that Piezo2 is responsible for the mechanical sensitivity of most low-threshold mechanoreceptor subtypes involved in innocuous touch sensation.

The importance of these findings extends beyond the understanding of touch physiology. By determining that Piezo2’s function is specific for touch, they showed that touch and pain sensations are physiologically separable. This put forward the hypothesis that painful mechanosensation may also rely on the activation of a specific ion channel that remains to be identified. Also, it is well known that sensitization associated with chronic pain can make even light touch feel painful.

These findings open the door for research on how the mechanisms of sensitization may alter touch physiology and turn touch into a painful stimulus.

References

Coste B, Mathur J, Schmidt M, Earley TJ, Ranade S, Petrus MJ, Dubin AE, & Patapoutian A (2010). Piezo1 and Piezo2 are essential components of distinct mechanically activated cation channels. Science (New York, N.Y.), 330 (6000), 55-60 PMID: 20813920

Coste B, Xiao B, Santos JS, Syeda R, Grandl J, Spencer KS, Kim SE, Schmidt M, Mathur J, Dubin AE, Montal M, & Patapoutian A (2012). Piezo proteins are pore-forming subunits of mechanically activated channels. Nature, 483 (7388), 176-81 PMID: 22343900

Maksimovic S, Nakatani M, Baba Y, Nelson AM, Marshall KL, Wellnitz SA, Firozi P, Woo SH, Ranade S, Patapoutian A, & Lumpkin EA (2014). Epidermal Merkel cells are mechanosensory cells that tune mammalian touch receptors. Nature, 509 (7502), 617-21 PMID: 24717432

Ranade SS, Woo SH, Dubin AE, Moshourab RA, Wetzel C, Petrus M, Mathur J, Bégay V, Coste B, Mainquist J, Wilson AJ, Francisco AG, Reddy K, Qiu Z, Wood JN, Lewin GR, & Patapoutian A (2014). Piezo2 is the major transducer of mechanical forces for touch sensation in mice. Nature, 516 (7529), 121-5 PMID: 25471886

Woo SH, Lumpkin EA, & Patapoutian A (2014). Merkel cells and neurons keep in touch. Trends in cell biology PMID: 25480024

Woo SH, Ranade S, Weyer AD, Dubin AE, Baba Y, Qiu Z, Petrus M, Miyamoto T, Reddy K, Lumpkin EA, Stucky CL, & Patapoutian A (2014). Piezo2 is required for Merkel-cell mechanotransduction. Nature, 509 (7502), 622-6 PMID: 24717433

Image via Luisma Tapia / Shutterstock.

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Predicting Seizures Amid the Chaos http://brainblogger.com/2014/12/17/predicting-seizures-amid-the-chaos/ http://brainblogger.com/2014/12/17/predicting-seizures-amid-the-chaos/#comments Wed, 17 Dec 2014 12:00:03 +0000 http://brainblogger.com/?p=17898 We are one step closer to predicting the unpredictable. Robin Gras, PhD, an associate professor in the School of Computer Science and Canada Research Chair in Learning and Simulation for Theoretical Biology, and his PhD student Abbas Golestani have developed novel methods for long-term time series forecasting.

In a Scientific Reports article, Gras and Golestanti demonstrate their software’s accuracy with the prediction of earthquakes, financial markets, and epileptic seizures. By applying their algorithm to the EEGs of 21 patients, they were able to predict seizures 17 minutes before the onset with 100% sensitivity and specificity.

Here, I interview Dr. Gras on his prediction software and potential future medical applications.

Robin GrasHow does your prediction software work?

Gras: We use a measure of the level of chaos of a time series to predict its future values. For financial or global temperature time series, we have discovered that the level of chaos is very stable, whereas for epileptic seizures, we have discovered that the level of chaos of the EEG time series strongly increases few minutes before the seizure occurs. We use these properties to make our predictions.

Can you summarize your study on epileptic seizures?

Gras: Our new method for complex time series prediction is based on the concepts of chaos theory and an optimization process. The general idea is to extract a unique non-linear characteristic from an existing time series that somehow represents the behavior of the time series and to subsequently generate successive new values that continue the time series, each value minimizing the difference between the characteristic of the new time series and the initial one.

In the case of epileptic seizure prediction, we transform the EEG signal time series into another time series that represents the evolution in time of the level of chaos of the EEG signal. Then, we use our method to predict the future values of the level of chaos of the EEG signal. When this level of chaos become greater than a predetermined threshold, we predict that an epileptic seizure will occur. Our tests on 21 patients data show that this approach can make reliable predictions up to 17 minutes in advance.

What are the benefits of seizure prediction?

Gras: If a patient has a device measuring EEG signal on his head which is connected to a small computer (a smartphone, for example) running our software, the software can create an alarm up to 17 minutes in advance of a seizure giving the possibility to the patient to call a doctor, to stop his car, or to go to a safe place before the seizure occurs.

What other medical applications have you envisioned for your software?

Gras: We would like also to test for heart attack or stroke.

Are you seeking collaborations with the biomedical community?

Gras: We have deposited two patents on this method, and we’re searching for an industrial partner, which could design a sensor device and run clinical tests.

Image via Lisa S. / Shutterstock.

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Perception Is the Opposite of Reality http://brainblogger.com/2014/12/15/perception-is-the-opposite-of-reality/ http://brainblogger.com/2014/12/15/perception-is-the-opposite-of-reality/#comments Mon, 15 Dec 2014 12:00:18 +0000 http://brainblogger.com/?p=17783 Do you ever feel like you are actually doing, seeing, or experiencing the things in your daydreams? Perhaps the warm sand beneath your toes while you relax on the beach; the wind rushing through your hair while you drive a fancy sports car; the smooth finish of that fine wine you have been wanting to try. Even if you have never experienced these things before, your brain is recalling sensory information stored in your brain and processing it as abstract thoughts. But how does it do this?

Neuroscientists have long studied how information travels through the brain, but the complex and intricate web has spurred more questions than answers. Are there independent pathways or are there integrated conduits? What direction does information travel, and does it make a difference? While these answers are far from being decided, new evidence suggests that, when you are experiencing or perceiving something, information courses through your brain in the opposite direction as when you are imagining something.

To study brain activity during both visual input and imagination, researchers performed electroencephalography (EEG) on subjects when they were using their imagination and when they were receiving visual input. Some subjects watched short video clips before being asked to recall an image in their heads; other subjects were asked to imagine riding on a magical, flying bicycle before watching video clips. By analyzing the output of the EEG data, the study authors were able to determine the directional flow of information in the brain.

In short, during imagination, information flowed from the parietal lobe to the occipital lobe – from a high-order region that combines multiple sensory inputs to a lower-order region. During visual input, information flowed from the occipital lobe (the area that processes visual stimuli) to the parietal lobe. One hypothesis is that when the brain experiences something, the sensory stimuli get organized and stored; however, when the brain imagines something, it sorts through these stored bits of information and reorganizes them until they actually feel real.

Even if you have not experienced the exact thing that you are imagining, your brain has similar, previous experiences that are stored and ready to be recalled and formed into a new, almost-real experience.

This new information will be useful for engineers, scientists, and medical professionals because it will help build tools to evaluate just how the brain works. Understanding the anatomical and functional features of the brain will eventually assist victims of brain injury and people suffering memory impairment, as well as those involved in sleep and dream research.

References

Bartolomeo P (2002). The relationship between visual perception and visual mental imagery: a reappraisal of the neuropsychological evidence. Cortex; a journal devoted to the study of the nervous system and behavior, 38 (3), 357-78 PMID: 12146661

Bartolomeo P (2008). The neural correlates of visual mental imagery: an ongoing debate. Cortex; a journal devoted to the study of the nervous system and behavior, 44 (2), 107-8 PMID: 18387539

Dentico D, Cheung BL, Chang JY, Guokas J, Boly M, Tononi G, & Van Veen B (2014). Reversal of cortical information flow during visual imagery as compared to visual perception. NeuroImage, 100, 237-43 PMID: 24910071

Hamamé CM, Vidal JR, Ossandón T, Jerbi K, Dalal SS, Minotti L, Bertrand O, Kahane P, & Lachaux JP (2012). Reading the mind’s eye: online detection of visuo-spatial working memory and visual imagery in the inferior temporal lobe. NeuroImage, 59 (1), 872-9 PMID: 21839843

Mechelli A, Price CJ, Friston KJ, & Ishai A (2004). Where bottom-up meets top-down: neuronal interactions during perception and imagery. Cerebral cortex (New York, N.Y. : 1991), 14 (11), 1256-65 PMID: 15192010

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Decoding Creativity – It’s In the Genes! http://brainblogger.com/2014/12/14/decoding-creativity-its-in-the-genes/ http://brainblogger.com/2014/12/14/decoding-creativity-its-in-the-genes/#comments Sun, 14 Dec 2014 12:00:59 +0000 http://brainblogger.com/?p=17836 What do Beethoven and the violinist who plays in the subway for a few dollars of tips share? What’s common between Vincent Van Gogh and the spraycan-wielding graffiti artists who paint the walls of your city with their bold artwork? Creativity? Yes, but the similarities go deeper. According to scientists and psychologists, these artists share a set or two of similar “creativity” genes.

Creative people are wired differently to their non-creative brethren. The difference is not only in the presence or absence of certain genes but also in the structural characteristics of their brains.

For decades, scientists have been tinkering with the idea that genes may have a role to play in developing creative abilities in individuals. The association described above was suggested in a study of 300,000 people with mental illnesses carried out by scientists at the Karolinska Institute in Sweden. According to the results of this study, people suffering from severe neuropsychiatric illnesses like bipolar disorder and schizophrenia tend to display enhanced creativity compared to mentally healthy individuals. A significant percentage of the mentally ill subjects in this study were engaged in creative and artistic professions. The study discovered that their first-degree healthy relatives were also more likely to be engaged in creative occupations. This suggests that although mental illness may not be hereditary, creative genes may run in families.

These findings add more fuel to the “nature versus nurture” debate, but the scientists do not negate the role of nurturing in developing creativity in individuals. They just claim some people are born more creatively-endowed than others.

The above-mentioned study did not explain what causes the co-occurrence of psychopathology and creativity. But the study definitely suggested a link between genes and creativity, an idea that provided food for thought to other scientists.

Recently, a study was carried out on members from five multigenerational families and 172 unrelated individuals with proven musical aptitude and creativity. The subjects in the study were selected after testing them for their ability to compose, improvise and arrange music as well as judge pitch and timing. This study suggests a link between several genes and musical ability and creativity. The study discovered that individuals with musical abilities had genomic variants or copy number variations (CNVs) — either they did not have some genes or had duplicate copies.

Incidentally, CNVs have been linked to the cognitive performance of individuals suffering from neuropsychiatric disorders. The findings from another study indicate the role of CNVs in increasing the risks of a person developing bipolar affective disorder or schizophrenia. Does this surprise you? After all, the belief that geniuses are mad is quite popular.

Research data published in 2014 also confirm that human genes definitely have a hand in developing a person’s musical abilities. According to the findings of this study, CNVs influence an individual’s ability to produce music (sing or take part in creative musical activities like arranging, composing, and improvising music), form music memories, and perceive music (identify or produce pitches without the aid of an external reference, spot wrong notes, and detect changes in rhythm and melodies). The study also hints at the heritability of musical ability, which means that music genes tend to run through families.

Several other scientific studies indicate the positive association between the structure of the brain, the goings-on in there, and creative genius in individuals.

A study by scientists at the Cornell University found that creative individuals like artists, musicians, and writers tend to have a peculiarity in the structure of their brains — they have a smaller mass of corpus callosum. The corpus callosum is a cluster of nerve fibers that connect the two hemispheres of the brain.

But scientists and psychologists are not surprised by these findings, and they have an explanation.

Creative individuals are characterized by their ability to think out-of-the-box. It is essentially divergent thinking that lets them explore many different solutions and connect the dots to come up with innovative and creative ideas. A smaller corpus callosum decreases the connectivity between the right and left hemispheres of the brain. Left to itself, each hemisphere gets the chance to specialize, so ideas can develop more freely and fully. The scientists call this process “incubation of ideas.”

After poking and prodding around the brain to find answers, scientists have discovered more brain features linked to creative ability. The brains of creative individuals tend to show increased gray matter especially in the posterior cingulate cortex (PCC) region, an area that is associated with awareness. More gray matter is linked to increased intelligence.

The study also found evidence that creative individuals tend to have elevated serotonin levels in their brains due to their particular genetic make-up. Serotonin is a neurotransmitter that increases connectivity between cells.

Increased connectivity between the cells in the PCC leads to greater and more acute awareness of information. This means the person can process information untainted by memory and emotions. Increased connectivity between different regions of the brain also enhances the ability to form novel associations, detect patterns, and comprehend symbols. How effectively different areas of the brain, each controlling different intelligences, thoughts, or emotions, can communicate with one another determines the mental flexibility, fluency, and originality of a person.

So creative ability is not just divergent thinking. It is also about being able to form new associations and quickly string together divergent ideas to come up with unique insights.

From the studies mentioned above, it seems creative geniuses are born, rather than made. But do all geniuses go on to become super-achievers? No. The very scientists who suggest creativity is genetic go on to assure you that geniuses too need luck and opportunities to express themselves. Geniuses have to also work hard, keep learning, and ensure they are at the right place at the right time. The creativity we admire certainly does not rest on the genes alone! Really talented individuals strive to improve with every song, every canvas, or every book they produce.

References

Karlsson R, Graae L, Lekman M, Wang D, Favis R, Axelsson T, Galter D, Belin AC, & Paddock S (2012). MAGI1 copy number variation in bipolar affective disorder and schizophrenia. Biological psychiatry, 71 (10), 922-30 PMID: 22381734

Kraus, C., Ganger, S., Losak, J., Hahn, A., Savli, M., Kranz, G., Baldinger, P., Windischberger, C., Kasper, S., & Lanzenberger, R. (2014). Gray matter and intrinsic network changes in the posterior cingulate cortex after selective serotonin reuptake inhibitor intake NeuroImage, 84, 236-244 DOI: 10.1016/j.neuroimage.2013.08.036

Kyaga, S., Lichtenstein, P., Boman, M., Hultman, C., Langstrom, N., & Landen, M. (2011). Creativity and mental disorder: family study of 300 000 people with severe mental disorder The British Journal of Psychiatry, 199 (5), 373-379 DOI: 10.1192/bjp.bp.110.085316

Moore, D., Bhadelia, R., Billings, R., Fulwiler, C., Heilman, K., Rood, K., & Gansler, D. (2009). Hemispheric connectivity and the visual–spatial divergent-thinking component of creativity Brain and Cognition, 70 (3), 267-272 DOI: 10.1016/j.bandc.2009.02.011

Tan YT, McPherson GE, Peretz I, Berkovic SF, & Wilson SJ (2014). The genetic basis of music ability. Frontiers in psychology, 5 PMID: 25018744

Ukkola-Vuoti, L., Kanduri, C., Oikkonen, J., Buck, G., Blancher, C., Raijas, P., Karma, K., Lähdesmäki, H., & Järvelä, I. (2013). Genome-Wide Copy Number Variation Analysis in Extended Families and Unrelated Individuals Characterized for Musical Aptitude and Creativity in Music PLoS ONE, 8 (2) DOI: 10.1371/journal.pone.0056356

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How the Sense of Taste Works? http://brainblogger.com/2014/12/09/how-the-sense-of-taste-works/ http://brainblogger.com/2014/12/09/how-the-sense-of-taste-works/#comments Tue, 09 Dec 2014 12:00:51 +0000 http://brainblogger.com/?p=17730 Taste, or gustatory perception, is one of our basic senses. It tells us from early childhood what is edible and what is not, what is good for our body and what can be potentially dangerous. Taking into account how important the sense of taste is for us, it is surprising how little we know about the underlying neurological mechanisms that produce the sensation of taste.

Taste relies on sensing certain molecules in food. Chemical recognition of these molecules on our tongue generates a signal which is sent to the brain and processed there. Processed signals give us certain ideas about the kind of food we are dealing with and allows us to take certain decisions and modify our behavior accordingly. For instance, sweetness is typically associated with highly caloric, attractive food, while bitterness might signal danger, since many toxins are associated with this taste.

Taste buds perform the first part of the task: recognition and generation of signal. This part is relatively well studied. We know that our tongue contains five types of taste receptors that register sweetness, saltiness, bitterness, sourness and umami (savory or meaty taste). Chemicals interact with receptors to generate signals which are sent to the brain. Sugars are recognized by the receptors of sweetness, sodium ions by the receptors of saltiness, acids by the receptors of sourness. Glutamate, a component of meat and many other protein-rich foods, activates umami receptors. Bitterness is the most sensitive of all tastes and can be produced by interaction of a variety of “bitter” ligands, such as some peptides, with the specific receptors.

The second part of the gustatory perception process, signal processing, is significantly less understood, and lots of research studies these days are aiming to figure out how our brain generates the huge variety and complexity of tastes using just a few basic taste receptors.

Until recently, two major schools of thoughts dominated the area of neuroscience dealing with perception of taste. Some researchers believed that signals from different receptors go to different, although interlinked, parts of the brain. Other neuroscientists believed that all signals from every taste receptor finish up in the same center, thus facilitating the creation of specific taste of food which we can recognize.

Current research data has shifted the opinion of scientific community in favor of the first hypothesis. It turned out that ganglion neurons, connected to the taste receptor cells, have clear taste preferences, and for every type of receptor there are dedicated cells in the brain that receive information from taste buds.

This, however, is only a part of the story: the taste we feel is not formed exclusively from the information received from the taste buds. The smell of food – detected by the olfactory epithelium in the nose – is another contributing factor which clearly works together with the taste perceived in the mouth.

In addition, mechanoreceptors help us to sense the texture of food, while chemesthetic sensations – via the receptors of pain, touch and thermal perception – provide us with the ability to feel the hotness of chilli pepper or the coolness of menthol. It also appears that the five basic types of taste receptors are not necessarily the only taste receptors we have. In experiments on animals, at least, it was shown that there are specific recognition processes for calcium-rich foods and for fats. All these signals have to be somehow integrated by the brain to obtain the sensation of taste that we feel. The details of this process still remain very unclear.

The question of how taste is generated in the brain is not entirely academic. It is well known that taste and appetite are linked. However, as we age, the number of taste receptors on our tongue quickly declines. By the age of 20 we already have only half the number of taste receptors we had in childhood, and the declines continues with advanced age. As a result, many elderly people have severely reduced sense of taste leading to the lack of interest in food, declining appetite and loss of body weight. The latter further contributes to the general fragility and poorer health.

At present, scientists are not aware of any mechanisms that would help in restoring the taste buds. However, if we understand how the neuronal signals from the taste receptors are processed, we may find a way of enhancing these signals through pharmaceutical interventions and thus helping people suffering from the loss of taste sensation. On the other hand, reducing the intensity of taste may help in reducing the appetite and thus keep overweight people from consuming excessive amounts of food. Future research into the mechanisms of taste perception might become instrumental in addressing a variety of eating disorders that are becoming so common these days.

References

Abumrad NA (2005). CD36 may determine our desire for dietary fats. The Journal of clinical investigation, 115 (11), 2965-7 PMID: 16276408

Bachmanov, A., & Beauchamp, G. (2007). Taste Receptor Genes Annual Review of Nutrition, 27 (1), 389-414 DOI: 10.1146/annurev.nutr.26.061505.111329

Barretto RP, Gillis-Smith S, Chandrashekar J, Yarmolinsky DA, Schnitzer MJ, Ryba NJ, & Zuker CS (2014). The neural representation of taste quality at the periphery. Nature PMID: 25383521

Green BG, Alvarez-Reeves M, George P, & Akirav C (2005). Chemesthesis and taste: evidence of independent processing of sensation intensity. Physiology & behavior, 86 (4), 526-37 PMID: 16199067

Ikeda, K. (2002). New Seasonings Chemical Senses, 27 (9), 847-849 DOI: 10.1093/chemse/27.9.847

Miller G (2011). Neuroscience. Sweet here, salty there: evidence for a taste map in the mammalian brain. Science (New York, N.Y.), 333 (6047) PMID: 21885750

Zhao, G., Zhang, Y., Hoon, M., Chandrashekar, J., Erlenbach, I., Ryba, N., & Zuker, C. (2003). The Receptors for Mammalian Sweet and Umami Taste Cell, 115 (3), 255-266 DOI: 10.1016/S0092-8674(03)00844-4

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