Posts tagged brain

ScienceDaily (May 2, 2012) — Although the two disorders may seem dissimilar, epilepsy and psychosis are associated. Individuals with epilepsy are more likely to have schizophrenia, and a family history of epilepsy is a risk factor for psychosis. It is not known whether the converse is true, i.e., whether a family history of psychosis is a risk factor for epilepsy.

Multiple studies using varied investigative techniques have shown that patients with schizophrenia and patients with epilepsy show some similar structural brain and genetic abnormalities, suggesting they may share a common etiology.

To investigate this possibility, researchers conducted a population-based study of parents and their children born in Helsinki, Finland. Using data available in two Finnish national registers, the study included 9,653 families and 23,404 offspring.

Individuals with epilepsy had a 5.5-fold increase in the risk of having a psychotic disorder, a 6.3-fold increase in the risk of having bipolar disorder, and an 8.5-fold increase in the risk of having schizophrenia.

They also found that the association between epilepsy and psychosis clusters within families. Individuals with a parental history of epilepsy had a 2-fold increase in the risk of developing psychosis, compared to individuals without a parental history of epilepsy. Individuals with a parental history of psychosis had a 2.7-fold increase in the risk of having a diagnosis of epilepsy, compared to individuals without a parental history of psychosis.

There have been multiple theories regarding the link between epilepsy and psychosis, but most have been predicated on the idea that epilepsy has toxic effects on the brain. However, combined with prior genetic and neurodevelopmental evidence, these new findings suggest a much more complex association, which likely includes a shared genetic vulnerability.

"Our evidence that epilepsy and psychotic illness may cluster within some families indicates that these disorders may be more closely linked than previously thought. We hope that this epidemiological evidence may contribute to the on-going efforts to disentangle the complex pathways that lead to these serious illnesses," said Dr. Mary Clarke, first author of the study and lecturer at Royal College of Surgeons in Ireland.

Dr. John Krystal, Editor of Biological Psychiatry, commented: “We have long known that particular types of epilepsy were associated with psychosis. However, the finding that a parental history of psychosis is associated with an increased risk of epilepsy in the offspring strengthens the mechanistic link between the two conditions.”

Source: Science Daily

ScienceDaily (May 2, 2012) — Parkinson’s disease, a disorder which affects movement and cognition, affects over a million Americans, including actor Michael J. Fox, who first brought it to the attention of many TV-watching Americans. It’s characterized by a gradual loss of neurons that produce dopamine. Mutations in the gene known as DJ-1 lead to accelerated loss of dopaminergic neurons and result in the onset of Parkinson’s symptoms at a young age.

The ability to modify the activity of DJ-1 could change the progress of the disease, says Dr. Nirit Lev, a researcher at Tel Aviv University’s Sackler Faculty of Medicine and a movement disorders specialist at Rabin Medical Center. Working in collaboration with Profs. Dani Offen and Eldad Melamed, Dr. Lev has now developed a peptide which mimics DJ-1’s normal function, thereby protecting dopamine- producing neurons. What’s more, the peptide can be easily delivered by daily injections or absorbed into the skin through an adhesive patch.

Based on a short protein derived from DJ-1 itself, the peptide has been shown to freeze neurodegeneration in its tracks, reducing problems with mobility and leading to greater protection of neurons and higher dopamine levels in the brain. Dr. Lev says that this method, which has been published in a number of journals including the Journal of Neural Transmission, could be developed as a preventative therapy.

Guarding dopamine levels

As we age, we naturally lose dopamine-producing neurons. Parkinson’s patients experience a rapid loss of these neurons from the onset of the disease, leading to much more drastic deficiencies in dopamine than the average person. Preserving dopamine-producing neurons can mean the difference between living life as a Parkinson’s patient or aging normally, says Dr. Lev.

The researchers set out to develop a therapy based on the protective effects of DJ-1, using a short peptide based on the healthy version of DJ-1 itself as a vehicle. “We attached the DJ-1-related peptide to another peptide that would allow it to enter the cells, and be carried to the brain,” explains Dr. Lev.

In pre-clinical trials, the treatment was tested on mice utilizing well-established toxic and genetic models for Parkinson’s disease. From both a behavioral and biochemical standpoint, the mice that received the peptide treatment showed remarkable improvement. Symptoms such as mobility dysfunctions were reduced significantly, and researchers noted the preservation of dopamine-producing neurons and higher dopamine levels in the brain.

Preliminary tests indicate that the peptide is a viable treatment option. Though many peptides have a short life span and degrade quickly, this peptide does not. Additionally, it provides a safe treatment option because peptides are organic to the body itself.

Filling an urgent need

According to Dr. Lev, this peptide could fill a gap in the treatment of Parkinson’s disease. “Current treatments are lacking because they can only address symptoms — there is nothing that can change or halt the disease,” she says. “Until now, we have lacked tools for neuroprotection.”

The researchers also note the potential for the peptides to be used preventatively. In some cases, Parkinson’s can be diagnosed before motor symptoms begin with the help of brain scans, explains Dr. Lev, and patients who have a genetic link to the disease might opt for early testing. A preventative therapy could help many potential Parkinson’s patients live a normal life.

Source: Science Daily

ScienceDaily (May 1, 2012) — Vision and hearing are so crucial to our daily lives that any impairments usually become obvious to an affected person. Although a number of known genetic mutations can lead to hereditary defects in these senses, little is known about our sense of touch, where defects might be so subtle that they go unnoticed.

There are good reasons to suspect that hearing and touch might have a common genetic basis. Sound-sensing cells in the ear detect vibrations and transform them into electrical impulses. Likewise, nerves that lie just below the surface of the skin detect movement and changes in pressure, and generate impulses. The similarity suggests that the two systems might have a common evolutionary origin—they may depend on an overlapping set of molecules that transform motion into signals that can be transmitted along nerves to the brain. (Credit: © Vladimir Voronin / Fotolia)

People with good hearing also have a keen sense of touch; people with impaired hearing generally have an impaired sense of touch. Extensive data supporting this hypothesis was presented by Dr. Henning Frenzel and Professor Gary R. Lewin of the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch, Germany. The two researchers showed that both senses — hearing and touch — have a common genetic basis. In patients with Usher syndrome, a hereditary form of deafness accompanied by impaired vision, the researchers discovered a gene mutation that is also causative for the patients’ impaired touch sensitivity.

The examination was preceded by various studies, including studies with healthy identical and non-identical human twins. In total, the researchers assessed sensory function in 518 volunteers.

In all vertebrates, and consequently also in humans, hearing and touch represent two distinct sensory systems that both rely on the transformation of mechanical force into electrical signals. When we hear, sound waves trigger vibrations that stimulate the hair-like nerve endings in the cochlea in the inner ear. These then transform the mechanical stimuli into electrical signals, which are transmitted to the brain via the auditory nerve. When we touch something a similar process takes place: The mechanical stimulus — sliding the fingers over a rough or smooth surface, the perception of vibrations — is taken up via sensors in the skin, converted into an electrical stimulus and transmitted to the brain.

Twin study with 100 pairs of twins

In recent years about 70 genes have been identified in humans, mutations in which trigger hearing loss or deafness. “Surprisingly, no genes have been found that negatively influence the sense of touch,” Professor Lewin said. To see whether the sense of touch also has a hereditary component, the researchers first studied 100 pairs of twins — 66 pairs of monozygotic twins and 34 dizygotic pairs of twins. Monozygotic twins are genetically completely identical; dizygotic twins are genetically identical to 50 percent. The tests showed that the touch sensitivity of the subjects was determined to more than 50 percent by genes. Furthermore, hearing and touch tests showed that there is a correlation between the sense of hearing and touch.

The researchers therefore suspected that genes that influence the sense of hearing may also have an influence on the sense of touch. In a next step, they recruited test subjects at a school in Berlin for students with hearing impairments. There they assessed the touch sensitivity in a cohort of 39 young people who suffered from severe congenital hearing impairment. The researchers compared these findings with the data from their twin study and discovered that not all of the young people with hearing loss had impaired tactile acuity. “Strikingly, however, many of these young people did indeed have poor tactile acuity,” Professor Lewin explained.

The researchers decided it would take too much time to analyze which of the approximately 70 genes that adversely affect the sense of hearing may also negatively affect the sense of touch. Therefore, the researchers focused specifically on patients with the Usher syndrome, a hereditary form of hearing impairment, in which the patients progressively become blind. Usher syndrome patients have varying degrees of hearing impairment, and the disease is genetically very well studied. There are nine known Usher genes carrying mutations which cause the disease.

The researchers examined one cohort of patients in a special consultation at the Charité — Universitätsmedizin Berlin for Usher patients from all over Germany. A second cohort was recruited at the university hospital La Fe in Valencia, Spain. The studies revealed that not all patients with Usher-syndrome have poor tactile acuity and touch sensitivity. The researchers showed that only patients with Usher syndrome who have a mutation in the gene USH2A have poor touch sensitivity. This mutation is also responsible for the impaired hearing of 19 patients. The 29 Usher-syndrome patients in whom the mutation could not be detected had a normal sense of touch. The researchers thus demonstrated that there is a common genetic basis for the sense of hearing and touch. They suspect that even more genes will be discovered in the future that influence both mechanosensory traits.

Women hear better than men and have a finer sense of touch

The researchers discovered another interesting detail during their five-year study. “When women complain that their men are not really listening to them, there is some truth in that,” Professor Lewin said. “The studies with a total of 518 individuals including 295 women have actually shown that women hear better and they also have a finer sense of touch than men; in short woman hear and feel more than men!”

Source: Science Daily

ScienceDaily (May 1, 2012) — Slacker or go-getter? Everyone knows that people vary substantially in how hard they are willing to work, but the origin of these individual differences in the brain remains a mystery.

Slacker or go-getter? Everyone knows that people vary substantially in how hard they are willing to work, but the origin of these individual differences in the brain remained a mystery. Until now. (Credit: © Dana Heinemann / Fotolia)

Now the veil has been pushed back by a new brain imaging study that has found an individual’s willingness to work hard to earn money is strongly influenced by the chemistry in three specific areas of the brain. In addition to shedding new light on how the brain works, the research could have important implications for the treatment of attention-deficit disorder, depression, schizophrenia and other forms of mental illness characterized by decreased motivation.

The study was published May 2 in the Journal of Neuroscience and was performed by a team of Vanderbilt scientists including post-doctoral student Michael Treadway and Professor of Psychology David Zald.

Using a brain mapping technique called positron emission tomography (PETscan), the researchers found that “go-getters” who are willing to work hard for rewards had higher release of the neurotransmitter dopamine in areas of the brain known to play an important role in reward and motivation, the striatum and ventromedial prefrontal cortex. On the other hand, “slackers” who are less willing to work hard for a reward had high dopamine levels in another brain area that plays a role in emotion and risk perception, the anterior insula.

"Past studies in rats have shown that dopamine is crucial for reward motivation," said Treadway, "but this study provides new information about how dopamine determines individual differences in the behavior of human reward-seekers."

The role of dopamine in the anterior insula came as a complete surprise to the researchers. The finding was unexpected because it suggests that more dopamine in the insula is associated with a reduced desire to work, even when it means earning less money. The fact that dopamine can have opposing effects in different parts of the brain complicates the picture regarding the use of psychotropic medications that affect dopamine levels for the treatment of attention-deficit disorder, depression and schizophrenia because it calls into question the general assumption that these dopaminergic drugs have the same effect throughout the brain.

The study was conducted with 25 healthy volunteers (52 percent female) ranging in age from 18 to 29. To determine their willingness to work for a monetary reward, the participants were asked to perform a button-pushing task. First, they were asked to select either an easy or a hard button-pushing task. Easy tasks earned $1 while the reward for hard tasks ranged up to $4. Once they made their selection, they were told they had a high, medium or low probability of getting the reward. Individual tasks lasted for about 30 seconds and participants were asked to perform them repeatedly for about 20 minutes.

"At this point, we don’t have any data proving that this 20-minute snippet of behavior corresponds to an individual’s long-term achievement," said Zald, "but if it does measure a trait variable such as an individual’s willingness to expend effort to obtain long-term goals, it will be extremely valuable."

The research is part of a larger project designed to search for objective measures for depression and other psychological disorders where motivation is reduced. “Right now our diagnoses for these disorders is often fuzzy and based on subjective self-report of symptoms,” said Zald. “Imagine how valuable it would be if we had an objective test that could tell whether a patient was suffering from a deficit or abnormality in an underlying neural system. With objective measures we could treat the underlying conditions instead of the symptoms.”

Further research is needed to examine whether similar individual differences in dopamine levels help explain the altered motivation seen in forms of mental illness such as depression and addiction. Additional research is under way to examine how medications specifically impact these motivational systems.

Source: Science Daily

May 2, 2012

Collaborative research by groups headed by scientists Joan J. Guinovart and Marco Milán at the Institute for Research in Biomedicine (IRB Barcelona) has revealed conclusive evidence about the harmful effects of the accumulation of glucose chains (glycogen) in fly and mouse neurons.

This image shows a cerebellum sample from a healthy mouse. Credit: Jordi Duran (IRB Barcelona)

These two animal models will allow scientists to address the genes involved in this harmful process and to find pharmacological solutions that allow disintegration of the accumulations or limitation of glycogen production. Advances in this direction would make a significant contribution to investigation into Lafora progressive myoclonic epilepsy and other neurodegenerative diseases characterized by glycogen accumulation in neurons. The journal EMBO Molecular Medicine publishes the results of the study this week.

This image shows the same tissue (mouse cerebellum) after glycogen accumulation. Credit: Jordi Duran (IRB Barcelona)

"Our data clearly indicate that glycogen accumulation alone kills neurons and thus dramatically reduces lifespan", explains Guinovart, an expert in glycogen metabolism, group leader at IRB Barcelona, and senior professor at the University of Barcelona, "because the only thing we have manipulated in the neurons is their capacity to produce glycogen".

The inclusion of the Drosophila fly in the study provides in vivo confirmation of the theory in another animal model as these flies also show the same symptoms of degeneration as mice when glycogen accumulates in neurons. However, in addition the use of Drosophila will speed up obtaining genetic data and the screening of therapeutic molecules. “In a short time we will be able to perform a massive search for genes involved in the pathological process and to understand it better at the molecular level”, emphasizes Marco Milán, ICREA researcher at IRB Barcelona and a specialist inDrosophila. “But the flies will also be useful to identify pharmacological molecules that can cure”, he explains.

The IRB Barcelona teams are designing several experiments to identify the possible therapeutic targets that may be useful to prevent glycogen accumulation in neurons. In addition to the direct relation to Lafora epilepsy, a progressive degenerative disease that affects adolescents and has no cure, glycogen accumulation could be the main cause of other neurodegenerative illnesses such as Adult polyglucosan body disease and Andersen’s disease.

Provided by Institute for Research in Biomedicine (IRB Barcelona)

Source: medicalxpress.com

May 1, 2012

Scientists now have a better understanding of how precise memories are formed thanks to research led by Prof. Jean-Claude Lacaille of the University of Montreal’s Department of Physiology. “In terms of human applications, these findings could help us to better understand memory impairments in neurodegenerative disorders like Alzheimer’s disease,” Lacaille said.

The study looks at the cells in our brains, or neurons, and how they work together as a group to form memories. Chemical receptors at neuron interconnections called synapses enable these cells to form electrical networks that encode memories, and neurons are classified into two groups according to the type of chemical they produce: excitatory, who produce chemicals that increase communication between neurons, and inhibitory, who have the opposite effect, decreasing communication. “Scientists knew that inhibitory cells enable us to refine our memories, to make them specific to a precise set of information,” Lacaille explained. “Our findings explain for the first time how this happens at the molecular and cell levels.”

Many studies have been undertaken on excitatory neurons, but very little research has been done on inhibitory neurons, partly because they are very difficult to study. The scientists found that a factor called “CREB” plays a key role in adjusting gene expression and the strength of synapses in inhibitory neurons. Proteins are biochemical compounds encoded in our genes that enable cells to perform their various functions, and new proteins are necessary for memory formation. “We were able to study how synapses of inhibitory neurons taken from rats are modified in the 24 hours following the formation of a memory,” Lacaille said. “In the laboratory, we simulated the formation of a new memory by using chemicals. We then measured the electrical activity within the network of cells. In cells where we had removed CREB, we saw that the strength of the electrical connections was much weaker. Conversely, when we increased the presence of CREB, the connections were stronger.”

This new understanding of the chemical functioning of the brain may one day lead to new treatments for disorders like Alzheimer’s, as researchers will be able to look at these synaptic mechanisms and design drugs that target the chemicals involved. “We knew that problems with synapse modifications are amongst the roots of the cognitive symptoms suffered by the victims of neurodegenerative diseases,” Lacaille said. “These findings shine light on the neurobiological basis of their memory problems. However, we are unfortunately many years away from developing new treatments from this information.”

The findings were published in the Journal of Neuroscience on May 2, 2012. The researchers received funding from the Canadian Institutes of Health Research and the Fonds de recherche du Québec – Santé. Jean-Claude Lacaille is the Canada Research Chair in Cellular and Molecular Neurophysiology. Israeli Ran, recipient of a Fellowship of the Savoy Foundation, and Isabel Laplante contributed to this research. All three researchers were affiliated with the Department of Physiology and the Groupe de Recherche sur le Système Nerveux Central of the University of Montreal when the research was undertaken. The University of Montreal is officially known as Université de Montréal.

Provided by University of Montreal 

Source: medicalxpress.com

ScienceDaily (May 1, 2012) — Barrow Neurological Institute researchers Jorge Otero-Millan, Stephen Macknik, and Susana Martinez-Conde share the recent cover of the Journal of Neuroscience in a compelling study into why illusions trick our brains. Barrow is part of St. Joseph’s Hospital and Medical Center in Phoenix.

The study, led by Martinez-Conde’s laboratory, explores the neural bases of illusory motion in Akiyoshi Kitaoka’s striking visual illusion, known as the “Rotating Snakes.” Kitaoka is a Japanese psychology professor who specializes in visual illusions of geometric shapes and motion illusions.

The study shows that tiny eye movements and blinking can make a geometric drawing of “snakes” appear to dance. The results help explain the mystery of how the Rotating Snakes illusion tricks the brain.

"Visual illusions demonstrate the ways in which the brain creates a mental representation that differs from the physical world," says Martinez-Conde. "By studying illusions, we can learn the mechanisms by which the brain constructs our conscious experience of the world."

Earlier studies of the “Rotating Snakes” indicated the perception of motion was triggered by the eyes moving slowly across the illusion. But by tracking eye movements in eight volunteers, the vision neuroscientists found a different explanation: fast eye movements called “saccades,” some of which are microscopic and undetectable by the viewer, drive the illusory motion.

Participants lifted a button when the snakes seemed to swirl and pressed down the button when the snakes appeared still. Right before the snakes appeared to move, participants tended to produce blinks, saccades and/or microsaccades, and right before the snakes stopped, participants’ eyes tended to remain stable, Otero-Millan, Macknik, and Martinez-Conde report in the April 25th Journal of Neuroscience cover story.

"Studying the mismatch between perception and reality may lead to a deeper understanding of the mind," says Martinez-Conde. "The findings from our recent study may help us to understand the neural bases of motion perception, both in the normal brain, and in patients with brain lesions that affect the perception of motion. This research could aid in the design of neural prosthetics for patients with brain damage."

Source: Science Daily

ScienceDaily (May 1, 2012) — Scientists at Joslin Diabetes Center have identified a key mechanism of action for the TOR (target of rapamycin) protein kinase, a critical regulator of cell growth which plays a major role in illness and aging. This finding not only illuminates the physiology of aging but could lead to new treatments to increase lifespan and control age-related conditions, such as cancer, type 2 diabetes, and neurodegeneration.

Over the past decade, studies have shown that inhibiting TOR activity, which promotes cell growth by regulating protein synthesis, increases lifespan in a variety of species including flies and mice; in recent years research has focused on uncovering the precise mechanisms underlying this effect. The Joslin study, published in the May 2 issue of Cell Metabolism, reports that TOR has a direct impact on two master gene regulator proteins — SKN-1 and DAF-16 -which control genes that protect against environmental, metabolic and proteotoxic stress. The TOR kinase acts in two signaling pathways, TORC1 and TORC2. When TORC1 is inhibited, SKN-1 and DAF-16 are mobilized, leading to activation of protective genes that increase stress resistance and longevity. This new finding was demonstrated in experiments with C. elegans, a microscopic worm used as a model organism, but activation of protective genes was also observed in mice. Most findings in C. elegans have turned out to be applicable to mice and humans.

"We uncovered a critical mechanism in the relationship between TOR and aging and disease. There is a homeostatic relationship between protein synthesis and stress defenses: when protein synthesis is reduced, stress defenses increase," says lead author T. Keith Blackwell, MD, PhD, co-head of the Joslin Islet Cell & Regenerative Biology Section and Professor of Pathology at Harvard Medical School. The Blackwell lab studies the aging process and how it is influenced by insulin and other metabolic regulatory mechanisms.

TOR activity, which is essential for early development but can lead to age-related decline, is implicated in a variety of chronic diseases, including diabetes, cardiovascular disease, cancer and neurodegenerative disorders, such as Alzheimer’s and Parkinson’s disease. In diabetes, TOR has both positive and negative effects: It promotes beta cell growth and insulin production but inappropriate TORC1 activity leads to insulin resistance and beta cell demise, as well as fat accumulation. At the same time, insufficient TORC2 activity can lead to insulin resistance.

The new results on TOR and SKN-1 suggest that SKN-1 might have a positive effects in Type 2 diabetes: “Turning on this pathway could be important in defending against the effects of high glucose, and promoting beta cell health” says Blackwell.

In the study, TOR activity was inhibited by genetic interference and the TOR-inhibitor rapamycin, a naturally occurring compound which is used as an immunosuppressant in organ transplants, and has been shown to increase lifespan in mice. Using rapamycin or related drugs to treat diseases affected by TOR has been a subject of intense interest among scientists and clinicians. The study found that rapamycin inhibits both TORC1 and TORC2, which will interest scientists investigating rapamycin as a pharmaceutical. “We need to increase understanding of rapamycin and its effects on TOR activity to determine how targeting TOR or processes it controls can help treat diseases that involve TOR and derangement of metabolism. We also need to look at therapies that work on TORC1 and TORC2 independently,” said Blackwell. However, one caveat with TOR inhibition is that the kinase plays such a central role in the basic physiology of growing and dividing cells. The new results suggest that in some situations we might want to bypass TOR itself, and directly harness beneficial processes that are controlled by SKN-1 or DAF-16.

Future research will focus on gaining a deeper understanding of how TOR acts on beneficial defense pathways and affects aging and disease. “In science, we are always looking for ways to interfere with mechanisms that promote aging and disease in ways that are beneficial to people,” says Blackwell.

Source: Science Daily

May 1, 2012

You think your computer has a lot of memory … if you keep using your computer you may, too.

Combining mentally stimulating activities, such as using a computer, with moderate exercise decreases your odds of having memory loss more than computer use or exercise alone, a Mayo Clinic study shows. Previous studies have shown that exercising your body and your mind will help your memory but the new study, published in the May 2012 issue of Mayo Clinic Proceedings, reports a synergistic interaction between computer activities and moderate exercise in “protecting” the brain function in people better than 70 years old.

Researchers studies 926 people in Olmsted County, Minn., ages 70 to 93, who completed self-reported questionnaires on physical exercise, and computer use within one year prior of the date of interview. Moderate physical exercise was defined as brisk walking, hiking, aerobics, strength training, golfing without a golf cart, swimming, doubles tennis, yoga, martial arts, using exercise machines and weightlifting. Mentally stimulating activities included reading, crafts, computer use, playing games, playing music, group and social and artistic activities and watching less television. Of those activities the study singled out computer use because of its popularity, said study author Yonas E. Geda, M.D., MSc, a physician scientist with Mayo Clinic in Arizona.

"The aging of baby boomers is projected to lead to dramatic increases in the prevalence of dementia," Dr. Geda said. "As frequent computer use has becoming increasingly common among all age groups, it is important to examine how it relates to aging and dementia. Our study further adds to this discussion."

The study examined exercise, computer use and the relationship to neurological risks such as mild cognitive impairment, Dr. Geda says. Mild cognitive impairment is the intermediate stage between normal memory loss that comes with aging and early Alzheimer’s disease. Of the study participants who did not exercise and did not use a computer, 20.1 percent were cognitively normal and 37.6 percent showed signs of mild cognitive impairment. Of the participants who both exercise and use a computer, 36 percent were cognitively normal and 18.3 percent showed signs of MCI.

Dr. Geda expects that this study will lead to more research on this topic.

Provided by Mayo Clinic

Source: medicalxpress.com

ScienceDaily (Apr. 30, 2012) — Migraine pain sits at the upper end of the typical pain scale — an angry-red section often labeled “severe.” At this intensity, pain is debilitating. Yet many sufferers do not get relief from — or cannot tolerate — over-the-counter and commonly prescribed pain medications.

Migraine Therapy: Computer model of the distribution of electrical current in the brain’s pain network (sub-cortical and brainstem structures) during transcranial direct current stimulation (tDCS). (Credit: Image courtesy of City College of New York)

Recently, a team of researchers that includes Dr. Marom Bikson, associate professor of biomedical engineering in CCNY’s Grove School of Engineering, has shown that a brain stimulation technology can prevent migraine attacks from occurring. Their technique, using transcranial direct current stimulation (tDCS), applies a mild electrical current to the brain from electrodes attached to the scalp.

"We developed this technology and methodology in order to get the currents deep into the brain," said Bikson. The researchers aimed to tap into the so-called pain network, among other areas, a collection of interconnected brain regions involved in perceiving and regulating pain.

Professor Bikson and his colleagues, including Dr. Alexandre DaSilva at the University of Michigan School of Dentistry and Dr. Felipe Fregni at Harvard Medical School, found that the technology seems to reverse ingrained changes in the brain caused by chronic migraine, such as greater sensitivity to headache triggers.

Repeated sessions reduced the duration of attacks and decreased the pain intensity of migraines that did occur on average about 37 percent. The improvements accumulated over four weeks of treatment and they persisted.

In pilot studies, the effects lasted for months. The only side effect subjects reported was a mild tingling sensation during treatment. Professor Bikson expects that a patient could use the system every day to ward off attacks, or periodically, like a booster.

The team’s computational models show that tDCS delivers therapeutic current along the pain network through both upper (cortical) and deep brain structures. They will publish their results in the journal Headache.

Thirty-six million Americans suffer from migraine, according to the Migraine Research Foundation. Of these, 14 million of them experience chronic daily headaches. “The fact that people still suffer from migraines means that the existing treatments using electrical technology or chemistry are not working,” said Professor Bikson.

Existing brain stimulation technologies can help relieve a migraine already underway. But those afflicted with chronic migraine pain may suffer 15 or more attacks a month, making treatment a constant battle.

The other techniques also have drawbacks — from heavy, unwieldy equipment to serious side effects, such as seizures. Some only stimulate the upper layers of the brain. Others reach deep brain regions, but require brain surgery to implant the electrodes. The tDCS technology is safe, easy to use, and portable, Professor Bikson said. “You can walk around with it and keep it in your desk drawer or purse. This is definitely the first technology that operates on just a 9-volt battery and can be applied at home.” He envisions future units as small as an iPod.

The next step will be to scale up clinical trials to a larger study population. A market-ready version of the tDCS is still years away. “There’s something about migraine pain that’s particularly distressing,” noted Professor Bikson. “If it’s possible to help some people get just 30 percent better, that’s a very meaningful improvement in quality of life.”

Source: Science Daily