Neuroscientists show that monkeys can decide to call out or keep silent

Sep. 6, 2013 — “Should I say something or not?” Human beings are not alone in pondering this dilemma — animals also face decisions when they communicate by voice. University of Tübingen neurobiologists Dr. Steffen Hage and Professor Andreas Nieder have now demonstrated that nerve cells in the brain signal the targeted initiation of calls — forming the basis of voluntary vocal expression.Share This:When we speak, we use the sounds we make for a specific purpose — we intentionally say what we think, or consciously withhold information. Animals, however, usually make sounds according to what they feel at that moment. Even our closest relations among the primates make sounds as a reflex based on their mood. Now, Tübingen neuroscientists have shown that rhesus monkeys are able to call (or be silent) on command. They can instrumentalize the sounds they make in a targeted way, an important behavioral ability which we also use to put language to a purpose.To find out how the neural cells in the brain catalyse the production of controled vocal noises, the researchers taught rhesus monkeys to call out quickly when a spot appeared on a computer screen. While the monkeys solved puzzles, measurements taken in their prefrontal cortex revealed astonishing reactions in the cells there. The nerve cells became active whenever the monkey saw the spot of light which was the instruction to call out. …

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Biologists uncover details of how we squelch defective neurons

Sep. 4, 2013 — Biologists at the University of California, San Diego have identified a new component of the cellular mechanism by which humans and animals automatically check the quality of their nerve cells to assure they’re working properly during development.In a paper published in this week’s issue of the journal Neuron, the scientists report the discovery in the laboratory roundworm C. elegans of a “quality check” system for neurons that uses two proteins to squelch the signals from defective neurons and marks them for either repair or destruction.”To be able to see, talk and walk, nerve cells in our body need to communicate with their right partner cells,” explains Zhiping Wang, the lead author in the team of researchers headed by Yishi Jin, a professor of neurobiology in UC San Diego’s Division of Biological Sciences and a professor of cellular and molecular medicine in its School of Medicine. “The communication is mediated by long fibers emitting from neurons called axons, which transmit electric and chemical signals from one cell to the other, just like cables connecting computers in a local wired network. In developing neurons, the journey of axons to their target cells is guided by a set of signals. These signals are detected by ‘mini-receivers’ — proteins called guidance receptors — on axons and translated into ‘proceed,’ ‘stop,’ ‘turn left’ or ‘turn right.’ Thus, the quality of these receivers is very important for the axons to interpret the guiding signals.”Jin, who is also an Investigator of the Howard Hughes Medical Institute, says defective protein products and environmental stress, such as hyperthermia, can sometimes jeopardize the health and development of cells. “This may be one reason why pregnant women are advised by doctors to avoid saunas and hot tubs,” she adds.The scientists discovered the quality check system in roundworms, and presumably other animals including humans, consists of two parts: a protein-cleaning machine containing a protein called EBAX-1, and a well-known protein assembly helper called heat-shock protein 90 known as “hsp90.””Hsp90 facilitates the assembly of guidance receivers during the production and also fixes flawed products whenever they are detected,” says Andrew Chisholm, a professor of neurobiology and cell and developmental biology, who also helped lead the study. “The EBAX-containing protein-cleaning machine is in charge of destroying any irreparable products so that they don’t hang around and affect the performance of functional receivers. The EBAX-1 protein plays as a defectiveness detector in this machine and a connector to Hsp90. It captures defective products and presents them for either repair or destruction.”A human neurodevelopmental disorder called “horizontal gaze palsy with progressive scoliosis” is associated with the defective production of one of the protein guidance receivers. …

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Sleep boosts production of brain support cells

Sep. 3, 2013 — Sleep increases the reproduction of the cells that go on to form the insulating material on nerve cell projections in the brain and spinal cord known as myelin, according to an animal study published in the September 4 issue of The Journal of Neuroscience. The findings could one day lead scientists to new insights about sleep’s role in brain repair and growth.Scientists have known for years that many genes are turned on during sleep and off during periods of wakefulness. However, it was unclear how sleep affects specific cells types, such as oligodendrocytes, which make myelin in the healthy brain and in response to injury. Much like the insulation around an electrical wire, myelin allows electrical impulses to move rapidly from one cell to the next.In the current study, Chiara Cirelli, MD, PhD, and colleagues at the University of Wisconsin, Madison, measured gene activity in oligodendrocytes from mice that slept or were forced to stay awake. The group found that genes promoting myelin formation were turned on during sleep. In contrast, the genes implicated in cell death and the cellular stress response were turned on when the animals stayed awake.”These findings hint at how sleep or lack of sleep might repair or damage the brain,” said Mehdi Tafti, PhD, who studies sleep at the University of Lausanne in Switzerland and was not involved with this study.Additional analysis revealed that the reproduction of oligodendrocyte precursor cells (OPCs) — cells that become oligodendrocytes — doubles during sleep, particularly during rapid eye movement (REM), which is associated with dreaming.”For a long time, sleep researchers focused on how the activity of nerve cells differs when animals are awake versus when they are asleep,” Cirelli said. “Now it is clear that the way other supporting cells in the nervous system operate also changes significantly depending on whether the animal is asleep or awake.”Additionally, Cirelli speculated the findings suggest that extreme and/or chronic sleep loss could possibly aggravate some symptoms of multiple sclerosis (MS), a disease that damages myelin. Cirelli noted that future experiments may examine whether or not an association between sleep patterns and severity of MS symptoms exists.This research was funded by the University of Wisconsin-Madison Department of Psychiatry.

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Tumor suppressor is needed for stem cells to mature into neurons

Aug. 12, 2013 — CHD5 has previously been proposed as a tumour suppressor, acting as a brake that prevents healthy cells from developing into cancer cells. But the part played by the protein in healthy tissue, and whether this role is important for its ability to counter tumour growth, has remained largely uncharted. Working with colleagues at Trinity College in Dublin and BRIC in Copenhagen, researchers at Karolinska Institutet have revealed its function in normal nervous system development and as a tumour suppressor.Share This:The recently published study shows that when stem cells approach the final phase of their specialisation as neurons, CHD5 begins to be expressed at high levels. CHD5 can reshape the chromatin, in which DNA is packed around proteins, and in so doing either facilitate or obstruct the expression of genes. Ulrika Nyman, postdoc researcher in Dr Johan Holmberg’s research group and one of the main authors of the current study, explains that on switching off CHD5 in the stem cells of mice embryos during the period in which the brain develops and the majority of neurons are formed, they found was that without CHD5, a stem cell is unable to silence the expression of a number of stem cell genes and genes that are actually to be expressed in muscle, blood or intestinal cells. They also observed an inability in the stem cell to switch on the expression of genes necessary for it to mature into a neuron, leaving it trapped in a stage between stem cell and neuron.The gene that codes for CHD5 is found on part of chromosome 1 (1p36), which is often lost in tumour cells in a number of cancers, particularly neuroblastoma, a disease that strikes almost only children and which is thought to arise during the development of the peripheral nervous system. Neuroblastoma lacking this section of chromosome and thus also CHD5 are often more aggressive and more rapidly fatal. Treatment with retinoic acid can make immature nerve cells and some neuroblastoma cells mature into specialised nerve cells, but when the researchers prevented neuroblastoma cells from upregulating CHD5, the tumours no longer responded to retinoic acid treatment.”In the absence of CHD5, neural tumour cells cannot mature into harmless neurons, but continue to divide, making the tumour more malignant and much harder to treat,” says Dr Holmberg at the Department of Cell and Molecular Biology. “We now hope to be able to restore the ability to upregulate CHD5 in aggressive tumour cells and make them mature into harmless nerve cells.”Share this story on Facebook, Twitter, and Google:Other social bookmarking and sharing tools:|Story Source: The above story is based on materials provided by Karolinska Institutet, via EurekAlert!, a service of AAAS. …

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A ‘rocking’ receptor: Crucial brain-signaling molecule requires coordinated motion to turn on

Aug. 7, 2013 — Johns Hopkins biophysicists have discovered that full activation of a protein ensemble essential for communication between nerve cells in the brain and spinal cord requires a lot of organized back-and-forth motion of some of the ensemble’s segments. Their research, they say, may reveal multiple sites within the protein ensemble that could be used as drug targets to normalize its activity in such neurological disorders as epilepsy, schizophrenia, Parkinson’s and Alzheimer’s disease.A summary of the results, published online in the journal Neuron on Aug. 7, shows that full activation of so-called ionotropic glutamate receptors is more complex than previously envisioned. In addition to the expected shape changes that occur when the receptor “receives” and clamps down on glutamate messenger molecules, the four segments of the protein ensemble also rock back and forth in relation to each other when fewer than four glutamates are bound.”We believe that our study is the first to show the molecular architecture and behavior of a prominent neural receptor protein ensemble in a state of partial activation,” says Albert Lau, Ph.D., assistant professor of biophysics and biophysical chemistry at the Johns Hopkins University School of Medicine.Glutamate receptors reside in the outer envelope of every nerve cell in the brain and spinal cord, Lau notes, and are responsible for changing chemical information — the release of glutamate molecules from a neighboring nerve cell — into electrical information, the flow of charged particles into the receiving nerve cell. There would be sharply reduced communication between nerve cells in our brains if these receptors were disabled, he added, and thought and normal brain function in general would be severely compromised. Malfunctioning receptors, says Lau, have been linked with numerous neurological disorders and are therefore potential targets for drug therapies.Lau explained that each glutamate receptor is a united group of four protein segments that has a pocket for clamping down on glutamate like a Venus fly trap snaring a bug. Below the glutamate-binding segments are four other segments embedded in the cell’s outer envelope to form a channel for charged particles to flow through. When no glutamates are bound to the receptor, the channel is closed; full activation of the receptor and full opening of the channel occur when four glutamates are bound, each to a difference pocket.Previously, Lau says, investigators thought that the level of receptor activation simply corresponded to the degree to which each glutamate-binding segment changed shape during the glutamate-binding process. Using a combination of computer modeling, biophysical “imaging” of molecular structure, biochemical analysis and electrical monitoring of individual cells, the researchers teased apart some of the steps in between zero activation and full activation. …

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Multiple sclerosis research could help repair damage affecting nerves

July 21, 2013 — Multiple sclerosis treatments that repair damage to the brain could be developed thanks to new research.A study has shed light on how cells are able to regenerate protective sheaths around nerve fibres in the brain.These sheaths, made up of a substance called myelin, are critical for the quick transmission of nerve signals, enabling vision, sensation and movement, but break down in patients with multiple sclerosis (MS).The study, by the Universities of Edinburgh and Cambridge, found that immune cells, known as macrophages, help trigger the regeneration of myelin.Researchers found that following loss of or damage to myelin, macrophages can release a compound called activin-A, which activates production of more myelin.Dr Veronique Miron, of the Medical Research Council Centre for Regenerative Medicine at the University of Edinburgh, said: “In multiple sclerosis patients, the protective layer surrounding nerve fibres is stripped away and the nerves are exposed and damaged.”Approved therapies for multiple sclerosis work by reducing the initial myelin injury — they do not promote myelin regeneration. This study could help find new drug targets to enhance myelin regeneration and help to restore lost function in patients with multiple sclerosis.”The study, which looked at myelin regeneration in human tissue samples and in mice, is published in Nature Neuroscience and was funded by the MS Society, the Wellcome Trust and the Multiple Sclerosis Society of Canada.Scientists now plan to start further research to look at how activin-A works and whether its effects can be enhanced.Dr Susan Kohlhaas, Head of Biomedical Research at the MS Society, said: “We urgently need therapies that can help slow the progression of MS and so we’re delighted researchers have identified a new, potential way to repair damage to myelin. We look forward to seeing this research develop further.”Dr Karen Lee, Vice-President, Research at the MS Society of Canada, said: “We are pleased to fund MS research that may lead to treatment benefits for people living with MS. We look forward to advances in treatments that address repair specifically, so that people with MS may be able to manage the unpredictable symptoms of the disease.”

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New tissue engineering breakthrough encourages nerve repair

July 8, 2013 — A new combination of tissue engineering techniques could reduce the need for nerve grafts, according to new research by The Open University. Regeneration of nerves is challenging when the damaged area is extensive, and surgeons currently have to take a nerve graft from elsewhere in the body, leaving a second site of damage. Nerve grafts contain aligned tissue structures and Schwann cells that support and guide neuron growth through the damaged area, encouraging function to be restored.Share This:The research, published in Biomaterials, reported a way to manufacture artificial nerve tissue with the potential to be used as an alternative to nerve grafts.Pieces of Engineered Neural Tissue (EngNT) are formed by controlling natural Schwann cell behaviour in a three-dimensional collagen gel so that the cells elongate and align, then a stabilisation process removes excess fluid to leave robust artificial tissues. These living biomaterials contain aligned Schwann cells in an aligned collagen environment, recreating key features of normal nerve tissue.Incorrect orientation of regenerating nerve cells can lead to delays in repair, scarring and poor restoration of nerve function. Much research has taken place into how support cells (Schwann cells) can be combined with materials to guide nerve regeneration. The new technology from The Open University avoids the use of synthetic materials by building neural tissue from collagen, a protein that is abundant in normal nerve tissue. Building the artificial tissue from natural proteins and directing the cellular alignment using normal cell-material interactions means the EngNT can integrate effectively at the repair site.Dr James Phillips, Lecturer in Health Sciences at The Open University, said: “We previously reported how self-alignment of Schwann cells could be achieved by using a tethered collagen hydrogel, which exploited cells’ natural ability to orientate in the appropriate direction by using their internal contraction forces. Our current research shows that cell-alignment in the hydrogel can be stabilised using plastic compression. The compression removes fluid from the gels, leaving a strong and stable aligned structure that has many features in common with nerve tissue.”The team incorporated Schwann cells within the aligned material to form artificial neural tissue that could potentially be used in peripheral nerve repair. The technique could be applied to other regenerative medicine scenarios, where a stable artificial tissue containing aligned cellular architecture would be of benefit.Share this story on Facebook, Twitter, and Google:Other social bookmarking and sharing tools:|Story Source: The above story is reprinted from materials provided by Open University. …

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Nerve cells can work in different ways with same result

July 1, 2013 — Epilepsy, irregular heartbeats and other conditions caused by malfunctions in the body’s nerve cells, also known as neurons, can be difficult to treat. The problem is that one medicine may help some patients but not others. Doctors’ ability to predict which drugs will work with individual patients may be influenced by recent University of Missouri research that found seemingly identical neurons can behave the same even though they are built differently under the surface.”To paraphrase Leo Tolstoy, ‘every unhappy nervous system is unhappy in its own way,’ especially for individuals with epilepsy and other diseases,” said David Schulz, associate professor of biological sciences in MU’s College of Arts and Science. “Our study suggests that each patient’s neurons may be altered in different ways, although the resulting disease is the same. This could be a major reason why doctors have difficulty predicting which medicines will be effective with specific individuals. The same problem could affect treatment of heart arrhythmia, depression and many other neurological conditions.”It turns out, even happy neurons may be happy in their own way. Neurons have a natural electric activity that they are biologically programmed to maintain. If a neuron isn’t in that preferred state, the cell tries to restore it. However, contrary to some previous beliefs about neuron functioning, Schulz’s research found that two essentially identical neurons can reach the same preferred electrical activity in different ways.In Schulz’s study, individual neurons used different combinations of cellular pores, known as ion channels, to achieve the same end goal of their preferred electrical and chemical balances. Schulz compared the situation to five people in separate rooms being given sets of blocks and told to construct a tower. …

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Technique to promote nerve regeneration after spinal cord injury restores bladder function in rats

June 25, 2013 — Using a novel technique to promote the regeneration of nerve cells across the site of severe spinal cord injury, researchers have restored bladder function in paralyzed adult rats, according to a study in the June 26 issue of The Journal of Neuroscience. The findings may guide future efforts to restore other functions lost after spinal cord injury. It also raises hope that similar strategies could one day be used to restore bladder function in people with severe spinal cord injuries.For decades, scientists have experimented with using nerve grafts as a way of bridging the spinal cord injury site in an attempt to recover lost function following spinal cord injury. However, coaxing these cells to grow and form connections capable of relaying nerve signals has been elusive. In the current study, Yu-Shang Lee, PhD, of the Cleveland Clinic, together with Jerry Silver, PhD, of Case Western Reserve Medical School, and others, used a chemical that promotes cell growth along with a scar-busting enzyme to create a more hospitable environment for the nerve graft at the injury site.”Although animals did not regain the ability to walk, they did recover a remarkable measure of urinary control,” Silver explained. This basic function is one that many spinal cord injury patients rank as one of the most important to regain following injury. “This is the first time that significant bladder function has been restored via nerve regeneration after a devastating cord injury,” Lee added.When a spinal cord injury takes place, extensions of nerve cells from the brainstem — the region of the brain where the command and coordination for urination takes place — become disconnected from cells in the spinal cord that control the muscles that squeeze or relax the bladder and open and close the urethra. The body’s natural response to form a scar at the injury site reduces the spread of inflammation but deters the growth of severed nerve fibers. With no way for the cells between the brain stem and spinal cord to regenerate or reconnect, the injury often results in the permanent inability to empty the bladder.The team of researchers delivered an enzyme called chondroitinase to disrupt scar formation in tandem with a chemical called fibroblast growth factor used to promote cell survival as they performed nerve graft surgery at the site of the injury. After three and six months, the scientists discovered that the rats that received this combination of treatment saw a significant return of bladder function, as indicated by measurements of urine output. …

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Bariatric surgery restores nerve cell properties altered by diet

June 17, 2013 — Understanding how gastric bypass surgery changes the properties of nerve cells that help regulate the digestive system could lead to new treatments that produce the same results without surgery, according to Penn State College of Medicine scientists, who have shown how surgery restores some properties of nerve cells that tell people their stomachs are full.The results may also better predict which patients will keep the weight off after surgery.Roux-en-Y gastric bypass surgery is the most effective way to get severe obesity under control. Doctors make the stomach smaller and bypass a section of the small intestine. Besides restricting the amount of food a person can eat at one time, the procedure also seems to alter the properties of nerve cells.”Restricting the size of the stomach has some role in the effectiveness of gastric bypass, but it’s not the full story,” said Kirsteen Browning, assistant professor of neural and behavioral sciences. “It is not fully understood why the surgery works.” The researchers published their findings in the Journal of Physiology.Complications from diseases such as diabetes can resolve before weight is lost, and sometimes before the person even leaves the hospital after gastric bypass surgery.”This suggests an altering of the neural signals from the gut to the brain and back,” Browning said.These nerve cells send signals to tell the body’s digestive system how to respond properly and regulate normal functions of digestion. In obese people, the nerve cells are less excitable, meaning they respond less tonormal stimulation. For example, there are neurons that help tell a person that their stomach is full, called satiation.”These signals tell you to stop eating,” said study co-author Andrew Hajnal, professor of neural and behavioral sciences. “Obviously these signals are strong enough to be overcome by all of us and we can eat more even after we are told we are full. However, as obesity develops, it appears these signals are less strong and easier to overcome.”Penn State Hershey researchers used a high-fat diet in rats to replicate long-term exposure to a Western diet. They then observed the effects of gastric bypass on the rats and have shown for the first time that the effects of diet on nerve cells seem to be restored to normal function after the surgery. This would help in restoring satiation signals so that they can be recognized more easily.”We know gastric bypass improves the health of nerve cells and reverses the effects on the signals,” Browning said. …

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Study points to role of nervous system in arthritis

June 13, 2013 — Arthritis is a debilitating disorder with pain caused by inflammation and damage to joints.Yet the condition is poorly managed in most patients, since adequate treatments are lacking — and the therapies that do exist to ease arthritis pain often cause serious side effects, particularly when used long-term. Any hope for developing more-effective treatments for arthritis relies on understanding the processes driving this condition.A new study in the Journal of Neuroscience by researchers at McGill University adds to a growing body of evidence that the nervous system and nerve-growth factor (NGF) play a major role in arthritis. The findings also support the idea that reducing elevated levels of NGF — a protein that promotes the growth and survival of nerves, but also causes pain — may be an important strategy for developing treatment of arthritis pain.Using an approach established by arthritis researchers elsewhere, the McGill scientists examined inflammatory arthritis in the ankle joint of rats. In particular, they investigated changes in the nerves and tissues around the arthritic joint, by using specific markers to label the different types of nerve fibres and allow them to be visualized with a fluorescence microscope.Normally, sympathetic nerve fibres regulate blood flow in blood vessels. Following the onset of arthritis in the rats, however, these fibres began to sprout into the inflamed skin over the joint and wrap around the pain-sensing nerve fibres instead. More sympathetic fibres were detected in the arthritic joint tissues, as well.The results also showed a higher level in the inflamed skin of NGF — mirroring the findings of human studies that have shown considerable increases in NGF levels in arthritis patients.To investigate the role of these abnormal sympathetic fibres, the McGill researchers used an agent to block the fibres’ function. They found that this reduced pain-related behaviour in the animals.”Our findings reinforce the idea that there is a neuropathic component to arthritis, and that sympathetic nerve fibres play a role in increasing the pain,” said McGill doctoral student Geraldine Longo, who co-authored the paper with Prof. Afredo Ribeiro-da-Silva and postdoctoral fellow Maria Osikowicz.”We are currently using drugs to prevent the production of elevated levels of NGF in arthritic rats; we hope that our research will serve as a basis for the development of a new treatment for arthritis in the clinic,” said Prof. Ribeiro-da-Silva.This research was funded by grants from the Canadian Institutes of Health Research (CIHR), the Louise and Alan Edwards Foundation, and the MITACS-Accelerate Quebec program in partnership with Pfizer Canada.

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Jammed molecular motors may play a role in the development of ALS

June 12, 2013 — Slowdowns in the transport and delivery of nutrients, proteins and signaling molecules within nerve cells may contribute to the development of the neurodegenerative disorder ALS, according to researchers at the University of Illinois at Chicago College of Medicine.The researchers showed how a genetic mutation often associated with inherited ALS caused delays in the transport of these important molecules along the long axons of neurons.Their findings were published in the online journal PLOS ONE on June 12.Motor neurons are among the longest cells in the human body — some may extend half a person’s height, as much as three feet. This poses a problem if all the cellular building blocks are made at one end of the cell, where the nucleus sits, but are needed at the other end of the cell.Neurons have the molecular equivalents of highways and delivery trucks — nerve fibers and motor proteins — that run along their long axons, ferrying material back and forth. But when shipping is held up, and products aren’t getting to where they are needed, the cell can’t function optimally. These transport problems can cause neurons to lose contact with other neurons and muscles.”If the transport process is delayed or slowed, the terminal end of the cell can run out of materials it needs, and can lose its synaptic connection with its neighboring neurons,” says Gerardo Morfini, UIC assistant professor of anatomy and cell biology and the co-principal investigator on the study. “Without the connections, the cells die.””Cell death is the final stage in a long disease process in ALS,” said Scott Brady, UIC professor and head of anatomy and cell biology and co-principal investigator. “We wanted to understand the pathological process in neurons leading up to cell death.”Neuroscientists know that mutations in a protein called SOD1 account for many of the 10 percent of ALS cases that are inherited. Ninety percent of ALS cases have no known cause and are termed sporadic.Brady and colleagues had previously shown, using high-resolution video microscopy of squid axons, that a mutant variant of the protein significantly slowed down the transport of material from one end of the cell to the other.In the new study, the researchers looked at how the mutated form of SOD1 caused the slowdown in cellular transport. They found that the mutated protein activated molecules called p38 kinases, which in turn modified a major motor protein involved in moving cargo along the nerve axons. These modified motor proteins moved poorly compared to controls that were exposed to unmutated SOD1.They also showed that transport in in genetically altered mice was also slowed by mutant SOD1, through the same mechanism.”The pathways between SOD1 and the p38 kinases could provide interesting targets for therapeutic intervention in treating ALS, both for some of the genetic forms and the spontaneous forms, where malfunctioning SOD1 is also a contributing factor,” said Brady.

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New surgical technique for Bell’s palsy facial paralysis

June 11, 2013 — A Loyola University Medical Center surgeon is using electrical stimulation as part of an advanced surgical technique to treat Bell’s palsy. Bell’s palsy is a condition that causes paralysis on one side of a patient’s face.During surgery, Dr. John Leonetti stimulates the patient’s damaged facial nerve with an electric current, helping to jump-start the nerve in an effort to restore improved facial movement more quickly.Leonetti said some patients who have received electrical stimulation have seen muscle movement return to their face after one or two months — rather than the four-to-six months it typically takes for movement to return following surgery.A virus triggered Bell’s palsy in Audrey Rex, 15, of Lemont, Ill. Her right eye could not close and her smile was lopsided, making her feel self-conscious. She had to drink from a straw, and eating was frustrating — she would accidentally bite her bottom lip when it got stuck on her teeth.She was treated with steroids, but after six weeks, there were no improvements. So Audrey’s mother did further research and made an appointment with Leonett Leonetti recommended surgery with electrical stimulation, followed by physical therapy. Today, Audrey’s appearance has returned to normal, and she has regained nearly all of the facial muscle movements she had lost.”I feel very blessed that we were referred to Dr. Leonetti,” said Deborah Rex, Audrey’s mother.Bell’s palsy is classified as an idiopathic disorder, meaning its cause is not definitely known. However, most physicians believe Bell’s palsy is caused by a viral-induced swelling of the facial nerve within its bony covering. Symptoms include paralysis on one side of the face; inability to close one eye; drooling; dryness of the eye; impaired taste; and a complete inability to express emotion on one side of the face.Bell’s palsy occurs when the nerve that controls muscles on one side of the face becomes swollen, inflamed or compressed. …

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