Posts tagged pain
Articles and news from the latest research reports.
Study identifies new drug target for chronic, touch-evoked pain
Researchers at the School of Medicine have identified a subset of nerve cells that mediates a form of chronic, touch-evoked pain called tactile allodynia, a condition that is resistant to conventional pain medication.
The discovery could point researchers to more fruitful efforts to develop effective drugs for the condition.
Touch-evoked pain occurs as part of a larger neuropathic pain condition arising from damage or disruption of nerve-cell circuits or signals caused by disorders such as alcoholism, diabetes, shingles and AIDS, or procedures such as spine surgery and chemotherapy. For patients with tactile allodynia, the slightest touch — a gentle caress or the brush of shirt against skin — can cause excruciating pain because changes in nerve-cell signals or networks trick the brain into mistaking touch for pain.
The study, published online Feb. 27 in Neuron, found that these “touch” neurons are different from the usual “pain” neurons that respond to stimuli such as cuts or bruises.
Unlike pain caused by such wounds, neuropathic pain is difficult to manage because little can be done to repair nerve damage. Managing it may require strong painkillers or combinations of treatments.
Common painkillers such as morphine have little effect on touch-evoked pain, possibly because they don’t target the touch neurons, the authors say. Morphine binds to specific protein-binding sites on pain neurons called mu opioid receptors, or MORs, and cuts off the their signals so that the brain can no longer sense pain.
However, the touch neurons do not carry MORs, which is why morphine cannot bind to them and block the pain. Instead, they carry delta opioid receptors, or DORs, whose role in pain control has been unclear until recently.
"That’s been the problem so far; any type of severe pain you have, you go into the clinic and very likely you will be treated with morphine-like opioids," said Gregory Scherrer, PharmD, PhD, the senior author of the study and an assistant professor of anesthesia. "You can give some of these patients as much morphine as you want; it won’t work if the mu opioid receptor is not present on the neurons that underlie that type of pain."
There are currently no Food and Drug Administration-approved pain-control drugs that target DORs. Previous attempts at developing DOR-targeting drugs haven’t succeeded because researchers didn’t know what type of pain such drugs would be useful for, Scherrer said.
Two DOR-binding drugs developed for knee pain by Adolor Corp., a biotechnology firm, for instance, probably failed because there is no compelling evidence that DOR was present or involved. AstraZeneca, another pharmaceutical firm, also had a DOR program but recently stopped its research efforts, Scherrer added.
"Now that we have provided a rationale and mechanism supporting the utility of DOR agonists for cutaneous pain and tactile allodynia, these companies will be able to design trials more carefully to evaluate specifically the drugs’ efficacy against touch-evoked pain," he said.
Earlier studies by Scherrer and others hinted at the presence of special nerve fibers on the skin that might contribute to touch-evoked pain.
In the current study, Scherrer and colleagues used fluorescent mouse models to isolate these neurons and identify how they control touch-evoked pain. They found that DOR can play an inhibitory role in these neurons: When proteins bind to DOR, they cut off communication to the spinal cord, through which sensory signals travel to the brain.
DOR-carrying “touch” neurons pervade the skin and could easily be targeted by drugs in the form of skin patches or topical creams, Scherrer suggested.
"By contrast, most MOR-carrying neurons penetrate internal organs," he said. "That’s why morphine is effective in treating post-surgery pain, for example."
Scherrer and fellow researchers tested two different DOR-binding compounds individually on mice and found that both reduced the mice’s sensitivity to touch-evoked pain.
Preliminary studies also indicate that DOR-targeting drugs might not cause dramatic side effects like morphine does, especially if they can be used topically, Scherrer said.
"Morphine and other MOR-targeting drugs have myriad deleterious side effects — including addiction, respiratory depression, constipation, nausea and vomiting — that further limits their utility for chronic pain management," he said.
The next step is to determine whether DOR could be a target for other types of pain, such as arthritis pain, pain from bone cancer and muscle pain, Scherrer added.
The findings also suggest that the body’s opioid system — normally associated with pain and addiction — may also respond to other stimuli such as touch.
"We may have underestimated the importance of the opioid system and what can be achieved with drugs targeting other subtypes of opioid receptors," Scherrer said.
(Source: med.stanford.edu)
Researchers identify innate channel that protects against pain
Scientists have identified a channel present in many pain detecting sensory neurons that acts as a ‘brake’, limiting spontaneous pain. It is hoped that the new research, published today [22 January] in the Journal of Neuroscience, will ultimately contribute to new pain relief treatments.
Spontaneous pain is ongoing pathological pain that occurs constantly (slow burning pain) or intermittently (sharp shooting pain) without any obvious immediate cause or trigger. The slow burning pain is the cause of much suffering and debilitation. Because the mechanisms underlying this type of slow burning pain are poorly understood, it remains very difficult to treat effectively.
Spontaneous pain of peripheral origin is pathological, and is associated with many types of disease, inflammation or damage of tissues, organs or nerves (neuropathic pain). Examples of neuropathic pain are nerve injury/crush, post-operative pain, and painful diabetic neuropathy.
Previous research has shown that this spontaneous burning pain is caused by continuous activity in small sensory nerve fibers, known as C-fiber nociceptors (pain neurons). Greater activity translates into greater pain, but what causes or limits this activity remained poorly understood.
Now, new research from the University of Bristol, has identified a particular ion channel present exclusively in these C-fiber nociceptors This ion channel, known as TREK2, is present in the membranes of these neurons, and the researchers showed that it provides a natural innate protection against this pain.
Ion channels are specialised proteins that are selectively permeable to particular ions. They form pores through the neuronal membrane. Leak potassium channels are unusual, in that they are open most of the time allowing positive potassium ions (K+) to leak out of the cell. This K+ leakage is the main cause of the negative membrane potentials in all neurons. TREK2 is one of these leak potassium channels. Importantly, the C-nociceptors that express TREK2 have much more negative membrane potentials than those that do not.
Researchers showed that when TREK2 was removed from the proximity of the cell membrane, the potential in those neurons became less negative. In addition, when the neuron was prevented from synthesizing the TREK2, the membrane potential also became less negative.
They also found that spontaneous pain associated with skin inflammation, was increased by reducing the levels of synthesis of TREK2 in these C-fiber neurons.
They concluded that in these C-fiber nociceptors the TREK2 keeps membrane potentials more negative, stabilizing their membrane potential, reducing firing and thus limiting the amount of spontaneous burning pain.
Professor Sally Lawson, from the School of Physiology and Pharmacology at Bristol University, explained: “It became evident that TREK2 kept the C-fiber nociceptor membrane at a more negative potential. Despite the difficulties inherent in the study of spontaneous pain, and the lack of any drugs that can selectively block or activate TREK2, we demonstrated that TREK2 in C-fiber nociceptors is important for stabilizing their membrane potential and decreasing the likelihood of firing. It became apparent that TREK2 was thus likely to act as a natural innate protection against pain. Our data supported this, indicating that in chronic pain states, TREK2 is acting as a brake on the level of spontaneous pain.”
Dr Cristian Acosta, the first author on the paper and now working at the Institute of Histology and Embriology of Mendoza in Argentina, said “Given the role of TREK2 in protecting against spontaneous pain, it is important to advance our understanding of the regulatory mechanisms controlling its expression and trafficking in these C-fiber nociceptors. We hope that this research will enable development of methods of enhancing the actions of TREK2 that could potentially some years hence provide relief for sufferers of ongoing spontaneous burning pain.”
(Source: eurekalert.org)
Brain Structure Shows Who is Most Sensitive to Pain
Everybody feels pain differently, and brain structure may hold the clue to these differences.
In a study published in the current online issue of the journal Pain, scientists at Wake Forest Baptist Medical Center have shown that the brain’s structure is related to how intensely people perceive pain.
“We found that individual differences in the amount of grey matter in certain regions of the brain are related to how sensitive different people are to pain,” said Robert Coghill, Ph.D., professor of neurobiology and anatomy at Wake Forest Baptist and senior author of the study.
The brain is made up of both grey and white matter. Grey matter processes information much like a computer, while white matter coordinates communications between the different regions of the brain.
The research team investigated the relationship between the amount of grey matter and individual differences in pain sensitivity in 116 healthy volunteers. Pain sensitivity was tested by having participants rate the intensity of their pain when a small spot of skin on their arm or leg was heated to 120 degrees Fahrenheit. After pain sensitivity testing, participants underwent MRI scans that recorded images of their brain structure.
“Subjects with higher pain intensity ratings had less grey matter in brain regions that contribute to internal thoughts and control of attention,” said Nichole Emerson, B.S., a graduate student in the Coghill lab and first author of the study. These regions include the posterior cingulate cortex, precuneus and areas of the posterior parietal cortex, she said.
The posterior cingulate cortex and precuneus are part of the default mode network, a set of connected brain regions that are associated with the free-flowing thoughts that people have while they are daydreaming.
“Default mode activity may compete with brain activity that generates an experience of pain, such that individuals with high default mode activity would have reduced sensitivity to pain,” Coghill said.
Areas of the posterior parietal cortex play an important role in attention. Individuals who can best keep their attention focused may also be best at keeping pain under control, Coghill said.
“These kinds of structural differences can provide a foundation for the development of better tools for the diagnosis, classification, treatment and even prevention of pain,” he said.
Short circuit in molecular switch intensifies pain
Pain functions as an important alarm signal. It alerts us to potential bodily harm – a hot or sharp object, for example – and motivates us to withdraw from damaging situations. At the cellular level, pain involves the stimulation of a network of pain nerves spread through the skin, mucosa and bodily organs.
Embedded in the cell wall surrounding these nerves are ion channels. These tiny, microscopic pathways respond to stimuli such as extreme cold or heat, mechanical pressure or harmful chemicals. When ion channels open, an electrical signal is created, transmitted to the brain, and interpreted as pain.
In previous research, the team of KU Leuven researchers led by Professor Thomas Voets (Laboratory of Ion Channel Research) and Professor Joris Vriens (Laboratory of Obstetrics and Experimental Gynaecology) discovered that a particular ion channel – TRPM3 – acts as a molecular fire detector: the ion channel detects heat and the hormone pregnenolone sulfate, a precursor to the sex hormones estrogen and testosterone and a trigger for pain and inflammation. In the present study, the researchers were looking for TRPM3 inhibitors that could potentially be used as painkillers.
Short circuit
Surprisingly, their results show that a number of drugs meant as painkillers actually increased pain in mice tested in the study, says Professor Voets: “Normally, when the ion channel is closed, no electrical signal is sent to the brain and therefore no pain is detected. But we found that pain can indeed occur despite a closed ion channel. How? A short circuit in the ion channel. When short-circuiting occurs, the electrical signal effected by a stimulus does not follow the normal pathway through the central pore of the ion channel. Instead, it navigates an alternative path through the surrounding material. This ‘electrical leak’ activates the pain nerves, thus increasing the sensation of pain. This may explain the pain-enhancing side effects of some drugs – such as clotrimazole, a common remedy for yeast infections that often causes unpleasant side effects such as irritation and burning sensations.”
“It is striking that short circuits in the ion channel only occur at high hormone levels. This could explain why some patients experience these side effects while others do not,” says Professor Voets. The researchers hope this new knowledge about TRPM3-dependent pain will contribute to the development of new painkillers with fewer painful side effects.
Scientists Develop Promising Drug Candidates for Pain, Addiction
Scientists from the Florida campus of The Scripps Research Institute (TSRI) have described a pair of drug candidates that advance the search for new treatments for pain, addiction and other disorders.
The two new drug scaffolds, described in a recent edition of The Journal of Biological Chemistry, offer researchers novel tools that act on a demonstrated therapeutic target, the kappa opioid receptor (KOR), which is located on nerve cells and plays a role in the release of the neurotransmitter dopamine. While compounds that activate KOR are associated with positive therapeutic effects, they often also recruit a molecule known as βarrestin2 (beta arrestin), which is associated with depressed mood and severely limits any therapeutic potential.
“Compounds that act at kappa receptors may provide a means for treating addiction and for treating pain; however, there is the potential for the development of depression or dysphoria associated with this receptor target,” said Laura Bohn, a TSRI associate professor who led the study. “There is evidence that the negative feelings caused by kappa receptor drugs may be, in part, due to receptor actions through proteins called beta arrestins. Developing compounds that activate the receptors without recruiting beta arrestin function may serve as a means to improve the therapeutic potential and limit side effects.”
The new compounds are called “biased agonists,” activating the receptor without engaging the beta arrestins.
Research Associate Lei Zhou, first author of the study with Research Associate Kimberly M. Lovell, added, “The importance of these biased agonists is that we can manipulate the activation of one particular signaling cascade that produces analgesia, but not the other one that could lead to dysphoria or depression.”
The researchers note that the avoidance of depression is particularly important in addiction treatment, where depressed mood can play a role in relapse.
The two drug candidates also have a high affinity and selectivity for KOR over other opioid receptors and are able to pass through the blood-brain barrier. Given these promising attributes, the scientists plan to continue developing the compounds.
(Source: scripps.edu)
For centuries, the brain was a mystery. Only in the last few decades have scientists begun to unravel its secrets. In recent years, using the latest technology and powerful computers further key discoveries have been made.
However, much remains to be understood about how the brain works. Here are five important areas of study attempting to unlock the last secrets of the brain.
How to fix it
When we think, move, speak, dream and even love - it all happens in the grey matter. But our brains are not simply one colour. White matter matters too.
Much of the research into dementia has focused on the tell-tale plaques of beta amyloid and tau protein tangles which occur in the grey matter.
But one British scientist, Dr Atticus Hainsworth says the white matter - and its blood supply - may be equally important.
The white colour results from fatty sheaths around the axons - which are extensions of the nerve cell bodies and help the cells to communicate.
He is using banks of donated brains, in Oxford and Sheffield, to analyse white matter for potential triggers such as leaking blood vessels.
"Some of the cases had an MRI or CT scan and that information can help give more clues about whether there was disease in the white matter - and what its basis might be," says Dr Hainsworth.
If leaking blood vessels in white matter do play a key role in the development of dementia then it may offer up a another potential route for new drug therapies.
How to make us all geniuses
For years caffeine was used to enhance alertness. But popping a pill to get straight-A’s may soon become the norm.
At Cambridge University neuroscientist Barbara Sahakian is investigating cognitive enhancers - drugs which make us smarter.
She studies how they can improve the performance of surgeons or pilots and asks if they could even be used to make us more entrepreneurial.
But she warns that there is no long-term safety information on these drugs and as a society we need to talk about their use.
She says the scientific and ethical challenges created by drugs which affect the production of brain chemicals like dopamine and noradrenaline - which induce pleasurable or “fight or flight” responses - need to be debated in order to decide whether drug-tests become routine before taking an exam.
Dr Sahakian adds: “I frequently talk to students about cognitive-enhancing drugs and a lot of students take them for studying and exams.
"But other students feel angry about this, they feel those students are cheating."
How can we harness our unconscious?
People need to be on top of their game when mastering skills like playing a musical instrument or detecting a bomb.
But research suggests that our unconscious can be harnessed to help us excel.
Repeatedly playing a tricky piece of music obviously helps develop a familiarity with the bits that are most difficult.
But cellist Tania Lisboa, who’s also a researcher in the Centre for Performance Science at London’s Royal College of Music, says it also helps to send the trickier parts of a piece from her conscious to the unconscious part of her brain.
After hours of practice, a fluent musician’s brain stores how to play the piece in an area at the back of the brain called the cerebellum - literally “the little brain”.
Neuroscientist Prof Anil Seth, of Sussex University, says: “It has more brain cells than the rest of the brain put together.
"It helps to promote fluid movements.. So the conscious effort of learning how to bow a cello is moved from the cortical areas which are involved when it’s new or difficult over to the cerebellum, which is very good at producing unconscious fluent behaviour on demand."
Music and defence may not appear to have much in common, but the unconscious can also help detect potential threats, whether it’s a suspicious person in a crowd or the presence of an improvised explosive device.
The unconscious brain is really good at spotting patterns - a skill which Paul Sajda at Colombia University in New York exploits - right at the boundary of the conscious/sub-conscious.
"I can flash 10 images a second and if one of those images has something out of the ordinary..that will essentially cause me to re-orient my brain to that image - but I’m not exactly aware of what that is."
Brain activity is monitored whilst the analyst looks at images so that researchers can later see which images triggered reactions.
What dreams are for
It’s just 60 years since scientists in Chicago first noted the tell-tale “rapid eye movement” or REM sleep which we now associate with dreaming.
But our fascination with dreams dates back at least 5,000 years to ancient Mesopotamia when people believed that the soul moved out of a sleeping body to visit the places they dreamed of.
REM sleep - which occurs every 90 minutes or so - begins with signals from the base of the brain which eventually reach the cerebral cortex - the outer layer of the brain which is responsible for learning and thought.
These nerve impulses are also directed to the spinal cord, inducing temporary paralysis of the limbs.
Prof Robert Stickgold, from the Beth Israel Deaconess Medical Center for Sleep and Cognition in Boston, believes that dreams are vital for processing memory associations.
He has asked the subjects of some of his sleep studies to play Tetris - and then noted their descriptions of how they floated amongst geometric shapes in their dreams.
He’s an admirer of Japanese scanning research where the scientists could “read” the dreams of subjects as they had MRI scans.
But he says it’s hard to get people to sleep in a noisy, expensive scanner.
And the future? “I would like to see research which reveals the rules for dream construction - and how it relates to the larger concept of memory processing during sleep.”
One even more elusive goal: how to dream just happy dreams and ditch the bad ones, especially nightmares.
Can we cure unreachable pain?
Excruciating chronic pain is one of medicine’s most difficult problems to solve.
Untouched by conventional treatments like painkilling drugs, surgeons are now testing their theory that deep brain stimulation could provide relief.
It is a brain surgery technique which involves electrodes being inserted to reach targets deep inside the brain.
The target areas are stimulated via the electrodes which are connected to a battery-powered pacemaker surgically placed under the patient’s collar bone.
One of the pioneers of this technique is Prof Tipu Aziz at the John Radcliffe Hospital in Oxford.
Deep brain stimulation has been used in the past for Parkinson’s disease and depression, and is now being trialled on obsessive compulsive disorder patients as well as those in chronic pain.
One of his patients, Clive, has suffered from terrible pain for nearly a decade after an operation to remove a disc in his neck.
"Sometimes I thought that if I had an axe, I’d chop my own arm off, if I thought it would get rid of the pain."
The doctors explained to him that his brain was getting signals from his arm to his brain confused and that the electrodes could help.
In Clive’s case this was an area of the brain called the anterior cingulate.
A week after his surgery he was one of the fortunate 70% of patients for whom the deep brain stimulation provides relief.
"It’s great to be out of that pain now. Since having the implant I can sit down for longer, I am able to walk further, everything is an improvement."
Prof Aziz is treating medical conditions. But he is aware of ethical dilemmas which could arise if the technique was applied to other areas.
"Putting electrodes in targets to improve memory.
"Or you could put electrodes into people to make them indifferent to danger and create the perfect soldier."
Picturing pain could help unlock its mysteries and lead to better treatments
Understanding the science behind pain, from a simple “ouch” to the chronic and excruciating, has been an elusive goal for centuries. But now, researchers are reporting a promising step toward studying pain in action. In a study published in the Journal of the American Chemical Society, scientists describe the development of a new technique, which they tested in rats, that could result in better ways to relieve pain and monitor healing.
Sandip Biswal, Frederick T. Chin, Justin Du Bois and colleagues note that current ways to diagnose pain basically involve asking the patient if something hurts. These subjective approaches are fraught with bias and can lead doctors in the wrong direction if a patient doesn’t want to talk about the pain or can’t communicate well. It can also be difficult to tell how well a treatment is really working. No existing method can measure pain intensity objectively or help physicians pinpoint the exact location of the pain. Past research has shown an association between pain and a certain kind of protein, called a sodium channel, that helps nerve cells transmit pain and other sensations to the brain. Certain forms of this channel are overproduced at the site of an injury, so the team set out to develop an imaging method to visualize high concentrations of this protein.
They turned to a small molecule called saxitoxin, produced naturally by certain types of microscopic marine creatures, and attached a signal to it so they could trace it by PET imaging. PET scanners are used in hospitals to diagnose diseases and injuries. When the researchers injected the molecule into rats, often a stand-in for humans in lab tests, they saw that the molecule accumulated where the rats had nerve damage. The rats didn’t show signs of toxic side effects. The work is one of the first attempts to mark these sodium channels in a living animal, they say.
Torture Permanently Damages Normal Perception of Pain
TAU researchers study the long-term effects of torture on the human pain system
Israeli soldiers captured during the 1973 Yom Kippur War were subjected to brutal torture in Egypt and Syria. Held alone in tiny, filthy spaces for weeks or months, sometimes handcuffed and blindfolded, they suffered severe beatings, burns, electric shocks, starvation, and worse. And rather than receiving treatment, additional torture was inflicted on existing wounds.
Forty years later, research by Prof. Ruth Defrin of the Department of Physical Therapy in the Sackler Faculty of Medicine at Tel Aviv University shows that the ex-prisoners of war (POWs), continue to suffer from dysfunctional pain perception and regulation, likely as a result of their torture. The study — conducted in collaboration with Prof. Zahava Solomon and Prof. Karni Ginzburg of TAU’s Bob Shapell School of Social Work and Prof. Mario Mikulincer of the School of Psychology at the Interdisciplinary Center, Herzliya — was published in the European Journal of Pain.
"The human body’s pain system can either inhibit or excite pain. It’s two sides of the same coin," says Prof. Defrin. "Usually, when it does more of one, it does less of the other. But in Israeli ex-POWs, torture appears to have caused dysfunction in both directions. Our findings emphasize that tissue damage can have long-term systemic effects and needs to be treated immediately."
A painful legacy
The study focused on 104 combat veterans of the Yom Kippur War. Sixty of the men were taken prisoner during the war, and 44 of them were not. In the study, all were put through a battery of psychophysical pain tests — applying a heating device to one arm, submerging the other arm in a hot water bath, and pressing a nylon fiber into a middle finger. They also filled out psychological questionnaires.
The ex-POWs exhibited diminished pain inhibition (the degree to which the body eases one pain in response to another) and heightened pain excitation (the degree to which repeated exposure to the same sensation heightens the resulting pain). Based on these novel findings, the researchers conclude that the torture survivors’ bodies now regulate pain in a dysfunctional way.
It is not entirely clear whether the dysfunction is the result of years of chronic pain or of the original torture itself. But the ex-POWs exhibited worse pain regulation than the non-POW chronic pain sufferers in the study. And a statistical analysis of the test data also suggested that being tortured had a direct effect on their ability to regulate pain.
Head games
The researchers say non-physical torture may have also contributed to the ex-POWs’ chronic pain. Among other forms of oppression and humiliation, the ex-POWs were not allowed to use the toilet, cursed at and threatened, told demoralizing misinformation about their loved ones, and exposed to mock executions. In the later stages of captivity, most of the POWs were transferred to a group cell, where social isolation was replaced by intense friction, crowding, and loss of privacy.
"We think psychological torture also affects the physiological pain system," says Prof. Defrin. "We still have to fully analyze the data, but preliminary analysis suggests there is a connection."
(Source: aftau.org)
Research Finds Pain In Infancy Alters Response To Stress, Anxiety Later In Life
Early life pain alters neural circuits in the brain that regulate stress, suggesting pain experienced by infants who often do not receive analgesics while undergoing tests and treatment in neonatal intensive care may permanently alter future responses to anxiety, stress and pain in adulthood, a research team led by Dr. Anne Murphy, associate director of the Neuroscience Institute at Georgia State University, has discovered.
An estimated 12 percent of live births in the U.S. are considered premature, researchers said. These infants often spend an average of 25 days in neonatal intensive care, where they endure 10-to-18 painful and inflammatory procedures each day, including insertion of feeding tubes and intravenous lines, intubation and repeated heel lance. Despite evidence that pain and stress circuitry in the brain are established and functional in preterm infants, about 65 percent of these procedures are performed without benefit of analgesia. Some clinical studies suggest early life pain has an immediate and long-term impact on responses to stress- and anxiety-provoking events.
The Georgia State study examined whether a single painful inflammatory procedure performed on male and female rat pups on the day of birth alters specific brain receptors that affect behavioral sensitivity to stress, anxiety and pain in adulthood. The findings demonstrated that such an experience is associated with site-specific changes in the brain that regulate how the pups responded to stressful situations. Alterations in how these receptors function have also been associated with mood disorders.
The study findings mirror what is now being reported clinically. Children who experienced unresolved pain following birth show reduced responsiveness to pain and stress.
“While a dampened response to painful and stressful situations may seem advantageous at first, the ability to respond appropriately to a potentially harmful stimulus is necessary in the long term,” Dr. Murphy said.
“The fact that less than 35 percent of infants undergoing painful and invasive procedures receive any sort of pre- or post-operative pain relief needs to be re-evaluated in order to reduce physical and mental health complications associated with preterm birth.”
It’s shocking: Ultra-focused electric current helps brain curb pain
Imagine significantly reducing a persistent migraine or fibromyalgia by a visit to a doctor who delivers low doses of electricity to the brain.
Alex DaSilva, assistant professor of prosthodontics at the University of Michigan, and colleagues are optimizing the next generation for such a technique, called high-definition transcranial direct current stimulation, or HD-tDCS.
The researchers have published several studies with the conventional tDCS, which also treats pain by “shocking” the brain with low doses of electrical current delivered noninvasively through electrodes placed on the scalp. The current modulates targeted areas of the brain, and one of the mechanisms is by activating the release of opioid-like painkillers.
HD-tDCS delivers an even more precisely focused current to the targeted areas of the brain. Preliminary reports have shown better pain relief in patients and a longer and more pronounced effect on the brain, said DaSilva, who heads the Headache and Orofacial Pain Effort Laboratory at the U-M School of Dentistry.
The increased precision of HD-tDCS means researchers can custom-place the electrodes to the skull. In this way, they can modulate specific areas in the brain to treat a wider range of conditions, such as neuropathic pain and stroke. Other uses include neurophysiological studies and cognitive and behavioral assessments.
One 20-minute session of HD-tDCS significantly reduced overall pain perception in fibromyalgia patients as described in one of the studies.
Researchers control the current by a portable device, which they hope physicians can eventually use in the clinic as a noninvasive treatment for chronic pain patients.
"We are working hard to make the technology available for clinical use at U-M," DaSilva said. "Our lab is getting a good number of emails from chronic pain patients looking for treatment."
The conventional technology is already available for many companies, and the HD-tDCS is being patented by the company of one of the developers.
To allow broad access and further investigation of the HD-tDCS technology by other researchers, DaSilva and colleagues released a scientific video demonstrating the step-by-step guideline of the research protocol: www.jove.com/embed/directions/50309?key=uahsva6y