Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
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By Michelle Roberts A multiple sclerosis treatment being tested in patients can stop the disease for at least five years, say doctors. The risky therapy involves wiping out the person's immune system with strong cancer drugs and then rebooting it with a stem cell transplant. Doctors say only some patients will be suitable to try it, particularly because it is so high risk. Out of 281 people who had the treatment, nearly half benefited, but eight died shortly afterwards. The work in JAMA Neurology is one of the largest and longest investigations of this aggressive MS treatment. Mark Rye, 41 and from Surrey, had his transplant just before Christmas 2016. Two months on he is doing well. "It was a hard decision, knowing what could go wrong. My wife and I discussed it for many, many hours. We've got small children and I didn't want my MS to get worse and end up in a wheelchair. "I did this to halt the condition and so that I can be there for my children, who are still so young. I want to be able to play rugby and football with them as they grow up." What is not clear is for how long the therapy might ultimately work. Freeze frame MS is not fatal, but it is incurable. The disease causes the immune system to attack the protective coating of nerves in the brain and spinal cord, which can create problems with a person's vision, walking and balance. © 2017 BBC
Jon Hamilton Scientists may have solved the mystery of nodding syndrome, a rare form of epilepsy that has disabled thousands of children in East Africa. The syndrome seems to be caused by the immune system's response to a parasitic worm, an international team reports in the journal Science Translational Medicine. And they think it's the same worm responsible for river blindness, an eye infection that's also found in East Africa. The finding means that current efforts to eliminate river blindness should also reduce nodding syndrome, says Avi Nath, an author of the study and chief of the section of infections of the nervous system at the National Institute of Neurological Disorders and Stroke. "We can prevent new infections even if we can't treat the ones who already have nodding syndrome," Nath says. Drugs can kill the parasite in its early stages. Nodding syndrome usually strikes children between 5 and 16 who live in rural areas of northern Uganda and South Sudan. Their bodies and brains stop growing. And they experience frequent seizures. "These are kids, young kids, you would expect that they should be running around playing," says Nath, who visited Uganda several years ago. "Instead, if you go to these villages they are just sitting there in groups," so villagers can keep an eye on them. © 2017 npr
“Bench-to-bedside” describes research that has progressed from basic science in animal models that has led to therapies used in patients. Now, a study in the journal Brain describes what could be considered a direct “aquarium-to-bedside” approach, taking a drug discovered in a genetic zebrafish model of epilepsy and testing it, with promising results, in a small number of children with the disease. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “This is the first time that scientists have taken a potential therapy discovered in a fish model directly into people in a clinical trial,” said Vicky Whittemore, Ph.D., program director at the NINDS. “These findings suggest that it may be possible to treat neurological disorders caused by genetic mutations through an efficient and precision medicine-style approach.” Scott C. Baraban, Ph.D., the William K. Bowes Jr. Endowed Chair in Neuroscience Research and professor of neurological surgery at the University of California, San Francisco (UCSF), postdoctoral fellow Aliesha Griffin, Ph.D., and colleagues used a zebrafish model of Dravet syndrome to test the drug lorcaserin and found that it suppressed seizure activity in the fish. Dravet syndrome is a severe form of pediatric epilepsy characterized by frequent daily drug-resistant seizures and developmental delays. It is caused by a genetic mutation, which Dr. Baraban’s group was able to introduce into the zebrafish to cause epilepsy. Dr. Baraban and his colleague Kelly Knupp, M.D. at the University of Colorado, Denver, then tested lorcaserin in five children with Dravet syndrome. The children were resistant to other anti-epileptic drugs and participated in this study through a compassionate use, off-label program.
New clinical trial results provide evidence that high-dose immunosuppressive therapy followed by transplantation of a person's own blood-forming stem cells can induce sustained remission of relapsing-remitting multiple sclerosis (MS), an autoimmune disease in which the immune system attacks the central nervous system. Five years after receiving the treatment, called high-dose immunosuppressive therapy and autologous hematopoietic cell transplant (HDIT/HCT), 69 percent of trial participants had survived without experiencing progression of disability, relapse of MS symptoms or new brain lesions. Notably, participants did not take any MS medications after receiving HDIT/HCT. Other studies have indicated that currently available MS drugs have lower success rates. The trial, called HALT-MS, was sponsored by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, and conducted by the NIAID-funded Immune Tolerance Network (link is external) (ITN). The researchers published three-year results from the study in December 2014, and the final five-year results appear online Feb. 1 in Neurology, the medical journal of the American Academy of Neurology. “These extended findings suggest that one-time treatment with HDIT/HCT may be substantially more effective than long-term treatment with the best available medications for people with a certain type of MS,” said NIAID Director Anthony S. Fauci, M.D. “These encouraging results support the development of a large, randomized trial to directly compare HDIT/HCT to standard of care for this often-debilitating disease.”
Ian Sample Science editor Doctors have used a brain-reading device to hold simple conversations with “locked-in” patients in work that promises to transform the lives of people who are too disabled to communicate. The groundbreaking technology allows the paralysed patients – who have not been able to speak for years – to answer “yes” or “no” to questions by detecting telltale patterns in their brain activity. Three women and one man, aged 24 to 76, were trained to use the system more than a year after they were diagnosed with completely locked-in syndrome, or CLIS. The condition was brought on by amyotrophic lateral sclerosis, or ALS, a progressive neurodegenerative disease which leaves people totally paralysed but still aware and able to think. “It’s the first sign that completely locked-in syndrome may be abolished forever, because with all of these patients, we can now ask them the most critical questions in life,” said Niels Birbaumer, a neuroscientist who led the research at the University of Tübingen. “This is the first time we’ve been able to establish reliable communication with these patients and I think that is important for them and their families,” he added. “I can say that after 30 years of trying to achieve this, it was one of the most satisfying moments of my life when it worked.” © 2017 Guardian News and Media Limited
NEUROSCIENCE, like many other sciences, has a bottomless appetite for data. Flashy enterprises such as the BRAIN Initiative, announced by Barack Obama in 2013, or the Human Brain Project, approved by the European Union in the same year, aim to analyse the way that thousands or even millions of nerve cells interact in a real brain. The hope is that the torrents of data these schemes generate will contain some crucial nuggets that let neuroscientists get closer to understanding how exactly the brain does what it does. But a paper just published in PLOS Computational Biology questions whether more information is the same thing as more understanding. It does so by way of neuroscience’s favourite analogy: comparing the brain to a computer. Like brains, computers process information by shuffling electricity around complicated circuits. Unlike the workings of brains, though, those of computers are understood on every level. Eric Jonas of the University of California, Berkeley, and Konrad Kording of Northwestern University, in Chicago, who both have backgrounds in neuroscience and electronic engineering, reasoned that a computer was therefore a good way to test the analytical toolkit used by modern neuroscience. Their idea was to see whether applying those techniques to a microprocessor produced information that matched what they already knew to be true about how the chip works. © The Economist Newspaper Limited 2017.
Keyword: Brain imaging
Link ID: 23126 - Posted: 01.21.2017
By Nicole Kobie Getting drunk could make it harder to enter your password – even if your brainwaves are your login. Brainwave authentication is one of many biometric measures touted as an alternative to passwords. The idea is for a person to authenticate their identity with electroencephalogram (EEG) readings. For example, instead of demanding a passcode, a computer could display a series of words on a screen and measure the user’s response via an EEG headset. EEG signatures are unique and are more complex than a standard password, making them difficult to hack. But while research suggests that EEG readings can authenticate someone’s identity with accuracy rates around 94 per cent, there could be confounding factors – including whether you’ve had a few too many drinks. Tommy Chin, a security researcher at cybersecurity consultancy firm Grimm, and Peter Muller, a graduate student at the Rochester Institute of Technology, decided to test this theory experimentally, by analysing people’s brainwaves before and after drinking shots of Fireball, a cinnamon-flavoured whisky. “Brainwaves can be easily manipulated by external influences such as drugs [like] opioids, caffeine, and alcohol,” Chin says. “This manipulation makes it a significant challenge to verify the authenticity of the user because they drank an immense amount of alcohol or caffeinated drink.” © Copyright Reed Business Information Ltd.
Thorsten Rudroff An estimated 400,000 Americans are currently living with multiple sclerosis, an autoimmune disease where the body’s immune cells attack a fatty substance called myelin in the nerves. Common symptoms are gait and balance disorders, cognitive dysfunction, fatigue, pain and muscle spasticity. Colorado has the highest proportion of people living with MS in the United States. It is estimated that one in 550 people living in the state has MS, compared to one in 750 nationally. The reason for this is unknown, but could be related to several factors, such as vitamin D deficiency or environment. Currently available therapies do not sufficiently relieve MS symptoms. As a result many people with the condition are trying alternative therapies, like cannabis. Based on several studies, the American Association of Neurology states that there is strong evidence that cannabis is effective for treatment of pain and spasticity. Although there are many anecdotal reports indicating cannabis’ beneficial effects for treatment of MS symptoms such as fatigue, muscle weakness, anxiety and sleep deprivation, they have not been scientifically verified. This is because clinical trials – where patients are given cannabis – are difficult to do because of how the substance is regulated at the federal level. To learn more, my Integrative Neurophysiology Laboratory at Colorado State University is studying people with MS in the state who are already using medical cannabis as a treatment to investigate what MS symptoms the drug can effectively treat. © 2010–2017, The Conversation US, Inc.
Riley Beggin Matt Herich uses a tDCS device that was made by another student he met on Reddit. Four 9-volt batteries and sticky self-adhesive electrodes are connected by a circuit board that sends a constant small current to the user's brain. Courtesy of Matt Herich Last October, Matt Herich was listening to the news while he drove door to door delivering pizzas. A story came on the radio about a technology that sends an electric current through your brain to possibly make you better at some things — moving, remembering, learning. He was fascinated. The neurotechnology is called transcranial direct current stimulation, or tDCS for short. At its simplest, the method involves a device that uses little more than a 9-volt battery and some electrodes to send a low-intensity electrical current to a targeted area of the brain, typically via a headset. More than a 1,000 studies have been published in peer-reviewed journals over the last decade suggesting benefits of the technique — maybe regulating mood, possibly improving language skills — but its effects, good or bad, are far from clear. Although researchers see possibilities for tDCS in treating diseases and boosting performance, it's still an exploratory technology, says Mark George, editor-in-chief of Brain Stimulation, a leading journal on neuromodulation. And leading experts have warned against at-home use of such devices. © 2017 npr
Keyword: Learning & Memory
Link ID: 23071 - Posted: 01.09.2017
Brandie Jefferson When I told my coworker that I was participating in a study that involved fasting, she laughed until she nearly cried. My boyfriend, ever supportive, asked hesitantly, "Are you sure you want to try this?" Note the use of "try" instead of "do." When I told my father over the phone, the line went silent for a moment. Then he let out a long, "Welllllll," wished me luck, and chuckled. Turns out, luck might not be enough. I like to eat. Often and a lot. Now, however, my eating habits have become more than a source of amusement for friends and coworkers. Now they are data in a study focusing on people with multiple sclerosis, like me. The pilot study, led by Dr. Ellen Mowry at the Johns Hopkins University in Baltimore, is looking at the impact of intermittent fasting on our microbiomes — the universe of trillions of microbes, mainly bacteria, that live in our guts. Intermittent fasting is pretty much what it sounds like. For six months, participants are allowed to eat during an 8-hour period each day. The remaining 16 hours we are limited to water, tea and coffee. No added sugar, cream, honey or sweetener. Several studies have suggested that the predominant bacteria in the guts of people with MS tend to be different than those in the guts of those without the chronic autoimmune inflammatory disease, according to Samantha Roman, the study's research coordinator. Depending on their makeup, bacteria have the ability to soothe or trigger inflammation, potentially affecting the symptoms of MS and other diseases. Exactly how gut bacteria and inflammation are related, though, is not well understood. © 2017 npr
Keyword: Multiple Sclerosis
Link ID: 23070 - Posted: 01.09.2017
By Jessica Hamzelou One woman’s unique experiences are helping us understand the nature of synaesthesia. We don’t know yet what causes synaesthesia, which links senses and can enable people to taste words or smell sounds, for example. It may be at least partly genetic, as it tends to run in families. Some researchers think a brain chemical called serotonin might play a role, because hallucinogenic drugs that alter serotonin levels in the brain can create unusual perceptions. There’s also some evidence that synaesthesia can change or disappear, and a detailed assessment of one woman’s experiences is helping Kevin Mitchell at Trinity College Dublin in Ireland and his team investigate. The woman, referred to as “AB”, sees colours when she hears music, linked to pitch, volume or instrument – higher notes have more pastel shades. She also associates colours with people, largely based on personality. Green is linked to loyalty, for instance. But several experiences in her life have caused her synaesthesia to change. “To say she had a series of unfortunate events would be an understatement,” says Mitchell. As a teenager and young adult, AB sustained several concussions, had migraines, contracted viral meningitis and was struck by lightning. © Copyright Reed Business Information Ltd.
Link ID: 23054 - Posted: 01.04.2017
By KATHARINE Q. SEELYE BROOKLINE, Mass. — When Michael Dukakis lost the presidential election in 1988, his wife, Kitty, felt as if she had been squashed in a compactor, all the air forced out of her. Her even-keeled husband went back to work as governor of Massachusetts; she started binge drinking. “An alcoholic can contain himself for only so long,” Mrs. Dukakis would later write. “When a crisis hits, the restraints snap.” Her drinking masked a long-smoldering depression that eventually led her to receive electroconvulsive therapy, also known as electroshock therapy or ECT. Like most people, she had no idea that the procedure was still used. She thought it a relic, scrapped after it was depicted as an instrument of torture in the 1975 movie “One Flew Over the Cuckoo’s Nest.” But Mrs. Dukakis was desperate. Rehabilitation, talk therapy and antidepressants had failed to ease her crippling depression, so in 2001, at age 64, she turned to shock therapy. To her amazement, it helped. After the first treatment, Mrs. Dukakis wrote, “I felt alive,” as if a cloud had lifted — so much so that when Mr. Dukakis picked her up at Massachusetts General Hospital, she astonished him by proposing that they go out to dinner. “I was so shocked I almost drove off Storrow Drive,” Mr. Dukakis recalled. “I had left this wife of mine at the hospital a basket case just the night before.” Now, 15 years later, the Dukakises have emerged as the nation’s most prominent evangelists for electroconvulsive therapy. Truth be told, there is not much competition. Few boldface names who have had the treatment will acknowledge as much; the stigma is still too great. Exceptions include Carrie Fisher, the actress and writer who died Tuesday, and Dick Cavett, the talk-show host; both have openly discussed their positive experiences. Electroconvulsive therapy is not a one-and-done procedure. Mrs. Dukakis, 80, still receives maintenance treatment every seven or eight weeks. She said that she had minor memory lapses but that the treatment had banished her demons and that she no longer drank, smoked or took antidepressants. © 2017 The New York Times Company
Link ID: 23047 - Posted: 01.02.2017
By James Gallagher Health and science reporter, BBC News website A drug that alters the immune system has been described as "big news" and a "landmark" in treating multiple sclerosis, doctors and charities say. Trials, published in the New England Journal of Medicine, suggest the drug can slow damage to the brain in two forms of MS. Ocrelizumab is the first drug shown to work in the primary progressive form of the disease. The drug is being reviewed for use in the US and Europe. MS is caused by a rogue immune system mistaking part of the brain for a hostile invader and attacking it. It destroys the protective coating that wraps round nerves called the myelin sheath. The sheath also acts like wire insulation to help electrical signals travel down the nerve. Damage to the sheath prevents nerves from working correctly and means messages struggle to get from the brain to the body. This leads to symptoms like having difficulty walking, fatigue and blurred vision. The disease can either just get worse, known as primary progressive MS, or come in waves of disease and recovery, known as relapsing remitting MS. Both are incurable, although there are treatments for the second state. 'Change treatment' Ocrelizumab kills a part of the immune system - called B cells - which are involved in the assault on the myelin sheath. In 732 patients with progressive MS, the percentage of patients that had deteriorated fell from 39% without treatment to 33% with ocrelizumab . Patients taking the drug also scored better on the time needed to walk 25 feet and had less brain loss detected on scans. In 1,656 patients with relapsing remitting, the relapse rate with ocrelizumab was half that of using another drug. © 2016 BBC
Laura Sanders Flickering light kicks off brain waves that clean a protein related to Alzheimer’s disease out of mice’s brains, a new study shows. The results, described online December 7 in Nature, suggest a fundamentally new approach to counteracting Alzheimer’s. Many potential therapies involve drugs that target amyloid-beta, the sticky protein that accumulates in the brains of Alzheimer’s patients. In contrast, the new method used on mice causes certain nerve cells to fire at a specific rhythm, generating brain waves that researchers believe may clear A-beta. “This is a very creative and innovative new approach to targeting brain amyloid load in Alzheimer’s,” says geriatric psychiatrist Paul Rosenberg of Johns Hopkins Medicine. But he cautions that the mouse results are preliminary. Neuroscientist Li-Huei Tsai of MIT and colleagues saw that mice engineered to produce lots of A-beta don’t produce as many gamma waves in the hippocampus, a brain structure important for memory. Using a method called optogenetics, the researchers genetically designed certain nerve cells in the hippocampus to fire off signals in response to light. In this way, the researchers induced gamma waves — rhythmic firings 40 times per second. After just an hour of forced gamma waves, the mice had less A-beta in the hippocampus, the researchers found. Further experiments revealed that gamma waves packed a double whammy — they lowered A-beta by both reducing production and enhancing the brain’s ability to clear it. © Society for Science & the Public 2000 - 2016
Link ID: 22966 - Posted: 12.08.2016
Sara Reardon A new technique might allow researchers and clinicians to stimulate deep regions of the brain, such as those involved in memory and emotion, without opening up a patient’s skull. Brain-stimulation techniques that apply electrodes to a person’s scalp seem to be safe, and proponents say that the method can improve some brain functions, including enhancing intelligence and relieving depression. Some of these claims are much better supported by research than others. But such techniques are limited because they cannot reach deep regions of the brain. By contrast, implants used in deep brain stimulation (DBS) are much more successful at altering the inner brain. The devices can be risky, however, because they involve surgery, and the implants cannot be repaired easily if they malfunction. At the annual Society for Neuroscience conference, held in San Diego, California, last week, neuroengineer Nir Grossman of the Massachusetts Institute of Technology in Cambridge and his colleagues presented their experimental method that adapts transcranial stimulation (TCS) for the deep brain. Their approach involves sending electrical signals through the brain from electrodes placed on the scalp and manipulating the electrical currents in a way that negates the need for surgery. The team used a stimulation device to apply two electric currents to the mouse's skull behind its ears and tuned them to slightly different high frequencies. They angled these two independent currents so that they intersected with each other at the hippocampus. © 2016 Macmillan Publishers Limited,
By Clare Wilson It’s one of the boldest treatments in medicine: delivering an electrical current deep into the brain by implanting a long thin electrode through a hole in the skull. Such “deep brain stimulation” (DBS) works miracles on people with otherwise untreatable epilepsy or Parkinson’s disease – but drilling into someone’s head is an extreme step. In future, we may be able to get the same effects by using stimulators placed outside the head, an advance that could see DBS used to treat a much wider range of conditions. DBS is being investigated for depression, obesity and obsessive compulsive disorder, but this research is going slowly. Implanting an electrode requires brain surgery, and carries a risk of infection, so the approach is only considered for severe cases. But Nir Grossman of Imperial College London and his team have found a safer way to experiment with DBS – by stimulating the brain externally, with no need for surgery. The technique, unveiled at the Society for Neuroscience conference in San Diego, California, this week, places two electrical fields of different frequencies outside the head. The brain tissue where the fields overlap is stimulated, while the tissue under just one field is unaffected because the frequencies are too high. For instance, they may use one field at 10,000 hertz and another at 10,010 hertz. The affected nerve cells are stimulated at 10 hertz – the difference between the two frequencies. © Copyright Reed Business Information Ltd.
Link ID: 22875 - Posted: 11.16.2016
By Alison F. Takemura In the mid-1980s, György Buzsáki was trying to get inside rats’ heads. Working at the University of California, San Diego, he would anesthetize each animal with ether and hypothermia, cut through its scalp, and drill holes in its skull. Carefully, he’d screw 16 gold-plated stainless steel electrodes into the rat’s brain. When he was done with the surgery, these tiny pieces of metal—just 0.5 mm in diameter—allowed him to measure voltage changes from individual neurons deep in the brain’s folds, all while the rodent was awake and moving around. He could listen to the cells fire action potentials as the animal explored its environment, learning and remembering what it encountered (J Neurosci, 8:4007-26, 1988). In those days, recording from two cells simultaneously was the norm. The 16-site recording in Buzsáki’s 1988 study “was the largest ever in a rat,” he says. Nowadays, scientists can measure voltage changes from 1,000 neurons at the same time with silicon multielectrode arrays. But the basic techniques of using a probe to measure electrical activity within the brain (electrophysiology) or from outside it (electroencephalography, or EEG) are still workhorses of neural imaging labs. “The new tools don’t replace the old ones,” says Jessica Cardin, a neuroscientist at the Yale School of Medicine. “They add new layers of information.” Another decades-old neuroscientific technique that remains popular today is patch clamping. Developed in the late 1970s and early 1980s, it can detect changes in the electric potential of individual cells, or even single ion channels. With a tiny glass pipette suctioned against the cell’s membrane, researchers can make a small tear, sealed by the pipette tip, and detect voltage changes inside the cell. With some improvements, the patch clamp, like electrophysiology and EEG, has remained a regular part of the neuroscientist’s tool kit. Recently, researchers had a robot carry out the process (Nat Methods, 9:585-87, 2012). © 1986-2016 The Scientist
Keyword: Brain imaging
Link ID: 22783 - Posted: 10.25.2016
By Gary Stix The new mantra for researchers fighting Alzheimer’s disease is “go early,” before memory loss or other pathology appears. The rationale for this approach holds that by the time dementia sets in the disease may already be destroying brain cells, placing severe limits on treatment options. Some large clinical trials are now testing drugs intended to clear up the brain’s cellular detritus—the aggregations of amyloid and tau proteins that may ultimately destroy brain cells. So far this approach has had decidedly mixed results. Some researchers are choosing a different direction. They have begun to ask what happens in the brain before the plaques and tangles of amyloid and tau appear—and to look at interventions that might work at this incipient disease stage. The Alzheimer’s Disease Drug Discovery Foundation has focused in recent years on funding new agents that do not target amyloid but are intended to address other manifestations of the disease, such as inflammation and the energy metabolism of neurons. At a meeting last month in Jersey City, N.J., neuroscientist Grace Stutzmann of the Chicago Medical School at Rosalind Franklin University of Medicine and Science presented her work on restoring a basic cellular process—called calcium signaling—that goes off track in Alzheimer’s. Scientific American asked her recently about her work. © 2016 Scientific American,
Link ID: 22754 - Posted: 10.13.2016
ByAnna Vlasits The next revolution in medicine just might come from a new lab technique that makes neurons sensitive to light. The technique, called optogenetics, is one of the biggest breakthroughs in neuroscience in decades. It has the potential to cure blindness, treat Parkinson’s disease, and relieve chronic pain. Moreover, it’s become widely used to probe the workings of animals’ brains in the lab, leading to breakthroughs in scientists’ understanding of things like sleep, addiction, and sensation. So it’s not surprising that the two Americans hailed as inventors of optogenetics are rock stars in the science world. Karl Deisseroth at Stanford University and Ed Boyden at the Massachusetts Institute of Technology have collected tens of millions in grants and won millions in prize money in recent years. They’ve stocked their labs with the best equipment and the brightest minds. They’ve been lauded in the media and celebrated at conferences around the world. They’re considered all but certain to win a Nobel Prize. There’s only one problem with this story: It just may be that Zhuo-Hua Pan invented optogenetics first. Even many neuroscientists have never heard of Pan. Pan, 60, is a vision scientist at Wayne State University in Detroit who began his research career in his home country of China. He moved to the United States in the 1980s to pursue his PhD and never left. He wears wire-rimmed glasses over a broad nose framed by smile-lines in his cheeks. His colleagues describe him as a pure scientist: modest, dedicated, careful.
Keyword: Brain imaging
Link ID: 22625 - Posted: 09.03.2016
By GINA KOLATA Shena Pearson nearly froze in her seat, terrified, as she stared at a power-point slide. She was at her first meeting of an epilepsy foundation, seeking help for her 12-year-old son Trysten, when a neurologist flashed the slide about something called Sudep. It stands for sudden unexpected death in epilepsy. Her son’s neurologist had never mentioned it. “Oh dear God, my child is at risk, seriously at risk,” Ms. Pearson thought to herself. Sudden death in epilepsy is a little-known and seldom-mentioned phenomenon, but now, after a push by advocates, the federal government has begun a concerted program to understand it. Yet a question remains: When, if ever, should patients be warned? In a way, the extreme reticence of many neurologists to mention sudden unexpected death to epilepsy patients harks back to the days when doctors and families often did not tell people they had cancer — too terrifying. But today, patients learn not just about cancer but about many other potentially fatal conditions, like an inoperable brain aneurysm that could burst at any time and kill a person. So the quiet about the epilepsy death risk appears to be an anomaly. Sudep’s name pretty much explains what it is: Someone with epilepsy — unprovoked seizures, which are electrical surges in the brain — dies, and there is no apparent cause. Often a person with epilepsy goes to bed and is found in the morning, unresponsive. In some cases, there is indirect evidence of a seizure, like urine on the sheets, bloodshot eyes or a severely bitten tongue, leading to the suggestion that preventing seizures as much as possible with medications could lower patients’ risks. But so much about the syndrome remains unknown. © 2016 The New York Times Company
Link ID: 22587 - Posted: 08.23.2016