Chapter 11. Motor Control and Plasticity
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By GRETCHEN REYNOLDS Over the past decade, in study after study in animals and people, exercise has been shown to improve the ability to learn and remember. But the specifics of that process have remained hazy. Is it better to exercise before you learn something new? What about during? And should the exercise be vigorous or gentle? Two new studies helpfully tackle those questions, with each reaching the conclusion that the timing and intensity of even a single bout of exercise can definitely affect your ability to remember — though not always beneficially. To reach that conclusion, scientists conducting the larger and more ambitious of the new studies, published in May in PLoS One, first recruited 81 healthy young women who were native German speakers and randomly divided them into three groups. Each group wore headphones and listened for 30 minutes to lists of paired words, one a common German noun and the other its Polish equivalent. The women were asked to memorize the unfamiliar word. But they heard the words under quite different circumstances. One group listened after sitting quietly for 30 minutes. A second group rode a stationary bicycle at a gentle pace for 30 minutes and then sat down and donned the headphones. And the third group rode a bicycle at a mild intensity for 30 minutes while wearing the headphones and listening to the new words. Two days later, the women completed tests of their new vocabulary. Everyone could recall some new words. But the women who had gently ridden a bicycle while hearing the new words — who had exercised lightly during the process of creating new memories —performed best. They had the most robust recall of the new information, significantly better than the group that had sat quietly and better than the group that had exercised before learning. Those women performed only slightly better than the women who had not exercised at all. Copyright 2013 The New York Times Company
Keyword: Learning & Memory
Link ID: 18475 - Posted: 08.08.2013
Lying in bed, unable to move a muscle, so-called locked-in patients have few ways to communicate with the outside world. But researchers have now found a way to use the widening and narrowing of the pupils to send a message, potentially helping these patients break the silence. Doctors use the constriction of pupils under bright light to test whether a patient’s brain stem is intact. But our pupils also show the opposite response—dilation—based on our thoughts and emotions, says Wolfgang Einhäuser, a neurophysicist at Philipps University of Marburg in Germany. Einhäuser had been struggling to interpret changes in pupil size during decision-making when he began to wonder about a different application. He contacted Steven Laureys, a member of the Coma Science Group at the University Hospital of Liège in Belgium, to explore how the pupil could be used to communicate a choice. Laureys works with locked-in patients, who have normal mental acuity but are paralyzed and unable to express thoughts to those around them. Many can control only the muscles that move their eyes; some, not even that. They can learn to communicate using EEG technology, in which electrodes on the scalp detect changes in brain activity. But applying the electrode cap is time-consuming, and the equipment is expensive, Einhäuser says. “If you imagine doing that every day, basically to communicate, that’s troublesome.” To find a different technique, Einhäuser, Laureys, and colleagues reached back in time. “The pieces have been there since the early ’60s,” Einhäuser says. A 1964 study showed that our pupils dilate when we perform mental arithmetic, like attempting to multiply 27 and 15 with no pencil and paper, and that harder tasks led to more dramatic dilation. The team set up a camera and a laptop to explore this automatic response. © 2012 American Association for the Advancement of Science.
By NICK BILTON Scientists haven’t yet found a way to mend a broken heart, but they’re edging closer to manipulating memory and downloading instructions from a computer right into a brain. Researchers from the Riken-M.I.T. Center for Neural Circuit Genetics at the Massachusetts Institute of Technology took us closer to this science-fiction world of brain tweaking last week when they said they were able to create a false memory in a mouse. The scientists reported in the journal Science that they caused mice to remember receiving an electrical shock in one location, when in reality they were zapped in a completely different place. The researchers weren’t able to create entirely new thoughts, but they applied good or bad feelings to memories that already existed. “It wasn’t so much writing a memory from scratch, it was basically connecting two different types of memories. We took a neutral memory, and we artificially updated that to make it a negative memory,” said Steve Ramirez, one of the M.I.T. neuroscientists on the project. It may sound insignificant and perhaps not a nice way to treat mice, but it is not a dramatic leap to imagine that one day this research could lead to computer-manipulation of the mind for things like the treatment of post-traumatic stress disorder, Mr. Ramirez said. Technologists are already working on brain-computer interfaces, which will allow us to interact with our smartphones and computers simply by using our minds. And there are already gadgets that read our thoughts and allow us to do things like dodge virtual objects in a computer game or turn switches on and off with a thought. Copyright 2013 The New York Times Company
Elizabeth Pollitzer Transplanting muscle-derived stem cells into diseased muscle regenerates it — a phenomenon that holds major potential for human therapies. But for years, researchers were puzzled by the unpredictability of these cells — sometimes they would promote fast regeneration, at other times none at all. Then, in 2007, a group led by Johnny Huard, a stem-cell researcher at the University of Pittsburgh in Pennsylvania, hit on the rather surprising explanation — sex1. Muscle stem cells taken from female mice regenerate new muscle much faster than those from male mice when transplanted into diseased muscle of mice of either sex. Researchers have also found that cells taken from male and female mice respond differently to stress2, and that human cells exhibit wildly different concentrations of many metabolites across the sexes3. Evidence is mounting that cells differ according to sex, irrespective of their history of exposure to sex hormones. These differences could have major implications for the susceptibility to and course of many diseases, their diagnosis and treatment. However, most cell biologists do not note whether the cells they are using come from males or females4. Between 1997 and 2001, ten prescription drugs were withdrawn from the market by the US Food and Drug Administration (FDA), eight of which were more dangerous to women than to men (see go.nature.com/ksindo). The ingredients used in non-prescription drugs can also pose greater health risks to women. In 2000, for instance, the FDA took steps to remove phenylpropanolamine, a component of many over-the-counter medications, from all drug products because of a reported increased risk of bleeding into the brain or into tissue around the brain in women but not in men. Such drug therapies are developed through basic research — but what if sex-related differences in studied cells contribute in a significant way to the observed effects? © 2013 Nature Publishing Group
By Melissa Hogenboom Science reporter, BBC News Several ancient dinosaurs evolved the brainpower needed for flight long before they could take to the skies, scientists say. Non-avian dinosaurs were found to have "bird brains", larger than that of Archaeopteryx, a 150 million-year-old bird-like dinosaur. Once regarded as a unique transition between dinosaurs and birds, scientists say Archaeopteryx has now lost its pivotal place. The study is published in Nature. A recent discovery in China which unveiled the earliest creature yet discovered on the evolutionary line to birds, also placed Archaeopteryx in less of a transitional evolutionary place. Bird brains tend to be more enlarged compared to their body size than reptiles, vital for providing the vision and coordination needed for flight. Scientists using high-resolution CT scans have now found that these "hyper-inflated" brains were present in many ancient dinosaurs, and had the neurological hardwiring needed to take to the skies. This included several bird-like oviraptorosaurs and the troodontids Zanabazar junior, which had larger brains relative to body size than that of Archaeopteryx. This latest work adds to previous studies which found the presence of feathers and wishbones on ancient dinosaurs. BBC © 2013
Link ID: 18439 - Posted: 08.01.2013
By David Brown, Charles Sabine, who spent more than two decades as a television reporter for NBC covering wars, revolutions and natural disasters, is familiar with something he calls “real fear.” He’s seen it in the eyes of people about to die or be killed. It chilled his blood when a Bosnian guerrilla held a gun to his chest as he stood near a bullet-pocked execution wall. He felt it when he walked point for his camera crew in Baghdad during Iraq’s sectarian war. But nothing terrified him like the news he got eight years ago after taking the gene test for Huntington’s disease, whose slow downward course toward death makes it one of mankind’s most dread afflictions. “I learned that the disease that took my father and is inflicting on my brother the same terrible decline in his prime will take me, too,” said Sabine, 53, an Englishman who worked for NBC for 26 years. And yet Sabine has turned that knowledge to a purpose that can only be called thrilling. He’s on a mission to make Huntington’s the model for a Hopeless Disease About Which There’s Hope. He wants to put it at the forefront of the “patient-centered care” movement, the effort to always ask patients what they consider success or hope to get out of treatment. He wants to make sure there are Huntington’s patients ready for clinical trials that are just around the corner. He wants to get everybody to think a little more sophisticatedly about genetic testing. Closer to home, he’s turning the knowledge of his biological fate into a tool to help him savor every day, be a good father and husband, make amends, not deceive. © 1996-2013 The Washington Post
By Glen Tellis, Rickson C. Mesquita, and Arjun G. Yodh Terrence Murgallis, a 20 year-old undergraduate student in the Department of Speech-Language Pathology at Misericordia University has stuttered all his life and approached us recently about conducting brain research on stuttering. His timing was perfect because our research group, in collaboration with a team led by Dr. Arjun Yodh in the Department of Physics and Astronomy at the University of Pennsylvania, had recently deployed two novel optical methods to compare blood flow and hemoglobin concentration differences in the brains of those who stutter with those who are fluent. These noninvasive methods employ diffusing near-infrared light and have been dubbed near-infrared spectroscopy (NIRS) for concentration dynamics, and diffuse correlation spectroscopy (DCS) for flow dynamics. The near-infrared light readily penetrates through intact skull to probe cortical regions of the brain. The low power light has no known side-effects and has been successfully utilized for a variety of clinical studies in infants, children, and adults. DCS measures fluctuations of scattered light due to moving targets in the tissue (mostly red blood cells). The technique measures relative changes in cerebral blood flow. NIRS uses the relative transmission of different colors of light to detect hemoglobin concentration changes in the interrogated tissues. Though there are numerous diagnostic tools available to study brain activity, including positron emission tomography (PET), magnetic resonance imaging (MRI), and magnetoencephalography (MEG), these methods are often invasive and/or expensive to administer. In the particular case of electroencephalography (EEG), its low spatial resolution is a significant limitation for investigations of verbal fluency. © 2013 Scientific American
Link ID: 18426 - Posted: 07.30.2013
By Dina Fine Maron All eyes were on Perry Cohen when he froze at the microphone. His voice failed him. He couldn’t read his notes. Eventually, the once-powerful Parkinson’s disease speaker had to be helped off the stage halfway through his speech. That was in February 2012, but the memory of that day is emblazoned in his mind. “It was the adrenaline and the pressure of speaking — it drained all the dopamine out,” Cohen says, referring to the brain chemical that is found lacking in the neurodegenerative disorder. “That’s why my symptoms got worse.” When Cohen learned he had Parkinson’s disease 17 years ago his symptoms were subtle. In the past couple years, however, the deterioration of his nervous system has become increasingly obvious, ultimately threatening to silence one of the most prominent voices in the Parkinson’s patient community. Cohen is now first in line to try a novel treatment he hopes will halt or even reverse the symptoms of his Parkinson’s disease. Two months ago he became the inaugural patient to undergo a gene therapy treatment led by the National Institutes of Health. The trial attempts to devise an intervention for Parkinson’s disease at the root of the problem: protecting dopamine in the brain. Researchers in this trial are attempting to surgically deliver a gene into the body that will make a natural protein to protect dopaminergic neurons, the brain cells attacked by the disease. To date no Parkinson’s treatment is geared toward reversing the progression of Parkinson’s disease. © 2013 Scientific American
Recycling is not only good for the environment, it’s good for the brain. A study using rat cells indicates that quickly clearing out defective proteins in the brain may prevent loss of brain cells. Results of a study in Nature Chemical Biology suggest that the speed at which damaged proteins are cleared from neurons may affect cell survival and may explain why some cells are targeted for death in neurodegenerative disorders. The research was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. One of the mysteries surrounding neurodegenerative diseases is why some nerve cells are marked for destruction whereas their neighbors are spared. It is especially puzzling because the protein thought to be responsible for cell death is found throughout the brain in many of these diseases, yet only certain brain areas or cell types are affected. In Huntington’s disease and many other neurodegenerative disorders, proteins that are misfolded (have abnormal shapes), accumulate inside and around neurons and are thought to damage and kill nearby brain cells. Normally, cells sense the presence of malformed proteins and clear them away before they do any damage. This is regulated by a process called proteostasis, which the cell uses to control protein levels and quality. In the study, Andrey S. Tsvetkov and his colleagues showed that differences in the rate of proteostasis may be the clue to understanding why certain nerve cells die in Huntington’s, a genetic brain disorder that leads to uncontrolled movements and death.
Link ID: 18403 - Posted: 07.23.2013
By Melinda Wenner Moyer Many studies over the past decade have pointed to pesticides as a potential cause of Parkinson's disease, a neurodegenerative condition that impairs motor function and afflicts a million Americans. Yet scientists have not had a good idea of how these chemicals harm the brain. A recent study suggests a possible answer: pesticides may inhibit a biochemical pathway that normally protects dopaminergic neurons, the brain cells selectively attacked by the disease. Preliminary research also indicates that this pathway plays a role in Parkinson's even when pesticides are not involved, providing an exciting new target for drug development. Past studies have shown that a pesticide called benomyl, which lingers in the environment despite having been banned in the U.S. in 2001 because of health concerns, inhibits the chemical activity of aldehyde dehydrogenase (ALDH) in the liver. Researchers at the University of California, Los Angeles, U.C. Berkeley, the California Institute of Technology and the Greater Los Angeles Veterans Affairs Medical Center wondered whether the pesticide might also affect levels of ALDH in the brain. ALDH's job is to break down DOPAL, a naturally forming toxic chemical, rendering it harmless. To find out, the researchers exposed different types of human brain cells—and, later, whole zebra fish—to benomyl. They found that it “killed almost half of the dopamine neurons while leaving all other neurons tested intact,” according to lead author and U.C.L.A. neurologist Jeff Bronstein. When they zeroed in on the affected cells, they confirmed that the benomyl was indeed inhibiting the activity of ALDH, which in turn spurred the toxic accumulation of DOPAL. Interestingly, when the scientists lowered DOPAL levels using a different technique, benomyl did not harm the dopamine neurons, a finding that suggests that the pesticide kills these neurons specifically because it allows DOPAL to build up. © 2013 Scientific American,
Here’s yet another reason to get off the couch: new research findings suggest that regularly breaking a sweat may lower the risk of having a stroke. A stroke can occur when a blood vessel in the brain gets blocked. As a result, nearby brain cells will die after not getting enough oxygen and other nutrients. A number of risk factors for stroke have been identified, including smoking, high blood pressure, diabetes and being inactive. For this study, published in the journal Stroke, Michelle N. McDonnell, Ph.D., from the University of South Australia, Adelaide and her colleagues obtained data from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study. REGARDS is a large, long-term study funded by the NIH National Institute of Neurological Disorders and Stroke (NINDS) to look at the reasons behind the higher rates of stroke mortality among African-Americans and other residents living in the Southeastern United States. “Epidemiological studies such as REGARDS provide an important opportunity to explore race, genetics, environmental, and lifestyle choices as stroke risk factors,” said Claudia Moy, Ph.D., program director at NINDS. Over 30,000 participants supplied their medical history over the phone. The researchers also visited them to obtain health measures such as body mass index and blood pressure. At the beginning of the study, the researchers asked participants how many times per week they exercised vigorously enough to work up a sweat. The researchers contacted participants every six months to see if they had experienced a stroke or a mini-stroke known as a transient ischemic attack (TIA). To confirm their responses, the researchers reviewed participants’ medical records.
Link ID: 18393 - Posted: 07.20.2013
By GRETCHEN REYNOLDS Two newly published studies investigate the enticing possibility that we might one day be able to gain the benefits of exercise by downing a pill, rather than by actually sweating. But while some of the research holds out promise for an effective workout pill, there remains the question of whether such a move is wise. The more encouraging of the new studies, which appears this week in Nature Medicine, expands on a major study published last year in Nature. In that study, researchers at the Scripps Research Institute in Jupiter, Fla., reported that a compound they had created and injected into obese mice increased activation of a protein called REV-ERB, which is known to partially control animals’ circadian rhythms and internal biological clocks. The injected animals lost weight, even on a high-fat diet, and improved their cholesterol profiles. Unexpectedly, the treated mice also began using more oxygen throughout the day and expending about 5 percent more energy than untreated mice, even though they were not moving about more than the other animals. In fact, in most cases, they were more physically lazy and inactive than they had been before the injections. The drug, it seemed, was providing them with a workout, minus the effort. Intrigued, the Scripps scientists, in conjunction with researchers from the Pasteur Institute in France and other institutions, set out to see what their compound might be doing inside muscles to provide this ersatz exercise. They knew that their drug increased the potency of the REV-ERB protein, but no one yet knew what REV-ERB actually does in muscles. So they began by developing a strain of mice that could not express very much of the protein in their muscle cells. Copyright 2013 The New York Times Company
Link ID: 18384 - Posted: 07.18.2013
It only takes one bad apple to spoil the bunch, and the same may be true of certain proteins in the brain. Studies have suggested that just one rogue protein (in this case, a protein that is misfolded or shaped the wrong way) can act as a seed, leading to the misfolding of nearby proteins. According to an NIH-funded study, various forms of these seeds — originating from the same protein — may lead to different patterns of misfolding that result in neurological disorders with unique sets of symptoms. “This study has important implications for Parkinson’s disease and other neurodegenerative disorders,” said National Institute of Neurological Disorders and Stroke (NINDS) Director Story Landis, Ph.D. “We know that among patients with Parkinson’s disease, there are variations in the way that the disorder affects the brains. This exciting new research provides a potential explanation for why those differences occur.” An example of such a protein is alpha-synuclein, which can accumulate in brain cells, causing synucleinopathies, multiple system atrophy, Parkinson’s disease, Parkinson’s disease with dementia (PDD), and dementia with Lewy bodies (DLB). In addition, misfolded proteins other than alpha-synuclein sometimes aggregate, or accumulate, in the same brains. For example, tau protein collects into aggregates called tangles, which are the hallmark of Alzheimer’s disease and are often found in PDD and DLB brains. Findings from this study raise the possibility that different structural shapes, or strains, of alpha-synuclein may contribute to the co-occurrence of synuclein and tau accumulations in PDD or DLB.
Brendan Maher Hugh Rienhoff says that his nine-year-old daughter, Bea, is “a fire cracker”, “a tomboy” and “a very sassy, impudent girl”. But in a forthcoming research paper, he uses rather different terms, describing her hypertelorism (wide spacing between the eyes) and bifid uvula (a cleft in the tissue that hangs from the back of the palate). Both are probably features of a genetic syndrome that Rienhoff has obsessed over since soon after Bea’s birth in 2003. Unable to put on much muscle mass, Bea wears braces on her skinny legs to steady her on her curled feet. She is otherwise healthy, but Rienhoff has long worried that his daughter’s condition might come with serious heart problems. Rienhoff, a biotech entrepreneur in San Carlos, California, who had trained as a clinical geneticist in the 1980s, went from doctor to doctor looking for a diagnosis. He bought lab equipment so that he could study his daughter’s DNA himself — and in the process, he became a symbol for the do-it-yourself biology movement, and a trailblazer in using DNA technologies to diagnose a rare disease (see Nature 449, 773–776; 2007). “Talk about personal genomics,” says Gary Schroth, a research and development director at the genome-sequencing company Illumina in San Diego, California, who has helped Rienhoff in his search for clues. “It doesn’t get any more personal than trying to figure out what’s wrong with your own kid.” Now nearly a decade into his quest, Rienhoff has arrived at an answer. Through the partial-genome sequencing of his entire family, he and a group of collaborators have found a mutation in the gene that encodes transforming growth factor-β3 (TGF-β3). Genes in the TGF-β pathway control embryogenesis, cell differentiation and cell death, and mutations in several related genes have been associated with Marfan syndrome and Loeys–Dietz syndrome, both of which have symptomatic overlap with Bea’s condition. The mutation, which has not been connected to any disease before, seems to be responsible for Bea’s clinical features, according to a paper to be published in the American Journal of Medical Genetics. © 2013 Nature Publishing Group,
Sid Perkins Sporting feats such as baseball's 100-mile-per-hour fastball are made possible by a suite of anatomical features that appeared in our hominin ancestors about 2 million years ago, a video study of college athletes suggests. And this ability to throw projectiles may have been crucial for human hunting, which in turn may have had a vital role in our evolution. “Throwing projectiles probably enabled our ancestors to effectively and safely kill big game,” says Neil Roach, a biological anthropologist at George Washington University in Washington DC, who led the work. Eating more calorie-rich meat and fat would have helped early hominins' brains and bodies to grow, enabling our ancestors to expand into new regions of the world, he suggests. The study is published today in Nature1. Although some primates occasionally throw objects, and with a fair degree of accuracy, only humans can routinely hurl projectiles with both speed and accuracy, says Roach. Adult male chimpanzees can throw objects at speeds of around 30 kilometres per hour, but even a 12-year-old human can pitch a baseball three times faster than that, he notes. In fact, the quickest motion that the human body produces — rotation of the humerus, the long bone in the upper arm, at a rate that is briefly equivalent to 25 full rotations in a single second — occurs while a person is throwing a projectile. © 2013 Nature Publishing Group,
By Meghan Rosen Paralyzed rats can now decide for themselves when it’s time to take a leak. Animals in a new study regained bladder control thanks to a new treatment that coaxes severed nerves to grow. Instead of dribbling out urine, the rodents squeezed out shots of pee almost as well as healthy rats do, researchers report June 25 in the Journal of Neuroscience. The study is the first to regenerate nerves that restore bladder function in animals with severely injured spinal cords. “This is a very big deal,” says neurologist John McDonald of the Kennedy Krieger Institute in Baltimore, Md. If the treatment works in people with spinal cord injuries, he says, “it would change their lives.” Unlike paralyzed rats, severely paralyzed humans can’t leak urine to relieve a full bladder. Unless injured people are fitted with a catheter, urine backs up into the kidneys. “These people get kidney failure all the time,” says study leader Jerry Silver, a neuroscientist at Case Western Reserve University in Cleveland. “It’s a terrible problem. If they didn’t have the catheter, they would die.” Some of the worst spinal cord injuries sever the bundle of nerve cells that reach from a mammal’s brain down through the vertebrae. The neurons can’t just grow back. Instead, the cells’ stumps get stuck in a gummy thicket of scar tissue that forms around the wound. © Society for Science & the Public 2000 - 2013
by Mara Hvistendahl and Martin Enserink A mysterious group of viruses known for their circular genome has been detected in patients with severe disease on two continents. In papers published independently this week, researchers report the discovery of agents called cycloviruses in Vietnam and in Malawi. The studies suggest that the viruses—one of which also widely circulates in animals in Vietnam—could be involved in brain inflammation and paraplegia, but further studies are needed to confirm a causative link. The discovery in Vietnam grew out of a frustrating lack of information about the causes of some central nervous system (CNS) infections such as encephalitis and meningitis, which can be fatal or leave lasting damage. "There are a lot of severe cases in the hospitals here, and very often we can't come to a diagnosis," says H. Rogier van Doorn, a clinical virologist with the Oxford University Clinical Research Unit in the Hospital for Tropical Diseases, Ho Chi Minh City. Extensive diagnostic tests turn up pathogens in only about half of patients with such infections, he says. Van Doorn and colleagues in Vietnam and at the University of Amsterdam's Academic Medical Center hoped that they might uncover new pathogens using a powerful new technique called next-generation sequencing. The group sequenced all the genetic material in cerebrospinal fluid (CSF) samples taken from more than 100 patients with undiagnosed CNS infections. One sample batch returned a promising lead: a viral sequence belonging to the Circoviridae family. © 2010 American Association for the Advancement of Science
Keyword: Movement Disorders
Link ID: 18311 - Posted: 06.25.2013
The paralyzing syndrome Guillain-Barré syndrome isn't linked to receiving common vaccines, according to a U.S. study. Concerns about the association of Guillain-Barré syndrome with vaccines have "flourished" since there was a hint of an increased risk after the 1976 swine flu vaccine campaign. It hasn’t been clearly linked since then. The syndrome is an acute inflammatory disease that results in destruction of a nerve’s myelin sheath and some nerves, which in severe cases can progress to complete paralysis and even death. Researchers from the U.S. Centers for Disease Control and Prevention and Kaiser Permanente Vaccine Study Center in Oakland, Calif. looked back at cases of GBS over 13 years in the state that were confirmed by a neurologist who reviewed the medical records. In the 13-year study period 415 patients were confirmed with GBS only 25 had received a vaccine within six weeks before onset of the disease. "In summary, this study did not find any association between influenza vaccine or any other vaccine and development of GBS within six weeks following vaccination," Dr. Roger Baxter, co-director of the Kaiser Permanente Vaccine Study Center and his co-authors concluded in Monday's online issue of Clinical Infectious Diseases. © CBC 2013
By Amy Mathews Amos, My symptoms started in January 2008, with deep pain in my bladder and the sense that I had to urinate constantly. I was given a diagnosis of interstitial cystitis, a chronic bladder condition with no known cure. But in the following months, pain spread to my thighs, knees, hips, buttocks, abdomen and back. By the time my condition was properly diagnosed three years later, I had seen two urogynecologists, three orthopedists, six physical therapists, two manual therapists, a rheumatologist, a neurologist, a chiropractor and a homeopath. What was wrong? Something completely unexpected, given my symptoms: myofascial pain syndrome, a condition caused by muscle fibers that contract but don’t release. That constant contraction creates knots of taut muscle, or trigger points, that send pain throughout the body, even to parts that are perfectly healthy. Most doctors have never heard of myofascial pain syndrome and few know how to treat it. In my case, trigger points in my pelvic floor — the bowl of muscle on the bottom of the pelvis — referred pain to my bladder. Points along my thighs pulled on my knee joints, creating sharp pain when I walked. Points in my hips, buttocks and abdomen threw my pelvis and lower spine out of alignment, pushing even more pain up my back. The pain was so severe at times that I could sit for only brief periods. “Why didn’t anybody know this?” I asked my doctor, Timothy Taylor, soon after he correctly diagnosed the reason for my pain. “Because doctors don’t specialize in muscles,” he said. “It’s the forgotten organ.” © 1996-2013 The Washington Post
By E. Paul Zehr As an infant, the Man Of Steel escaped Krypton’s red sun in a rocket lovingly prepared for him by his parents. Kal-L (but more commonly known as Kal-El) arrived under our yellow sun in Smallville to eventually become Clark Kent. Since his debut in Action Comics #1 in June of 1938, Superman has accumulated a pretty long list of “super abilities”. For me, though, I really like the list of his abilities that come from the 1940s radio serials. This was back when Superman was described as “faster than a speeding bullet, more powerful than a locomotive, and able to leap tall buildings in a single bound”. These descriptions all have to do with super-strength when you get right down to it. And with this summer’s “Man of Steel” Superman re-boot, super-strength is the focus of this post. I have to admit I’ve always found the explanation for Superman’s powers to be, well, a bit dubious. He has his powers because of our yellow sun. That is, because he was from a red sun planet (Krypton) somehow the yellow sun of Earth unleashes some inner super power mechanism that gives Superman all his…super-ness. Of course it’s a bit pure escapist fun. But what if there actually was something to that, though? I don’t mean something to the “yellow sun / red sun” stuff. You can just check in with our “friendly neighborhood physics” professor Jim Kakalios and his bok “Physics of Superheroes” for the real deal on that one. I mean rather the unleashing of some inner mechanism bit. What if something inside the human body could be unleashed—like removing the shackles from Hercules—and allow for dramatically increased strength? © 2013 Scientific American