Immersive virtual reality boosts the effectiveness of spinal cord stimulation for chronic pain – Newswise

December 26, 2020 medical

Newswise December 23, 2020 For patients receiving spinal cord stimulation (SCS) for chronic pain, integration with an immersive virtual reality (VR) system allowing patients to see as well as feel the effects of electrical stimulation on a virtual image of their own body can enhance the pain-relieving effectiveness of SCS, reports a study in PAIN, the official publication of the International Association for the Study of Pain (IASP). The journal is published in the Lippincott portfolio by Wolters Kluwer.

The integrated SCS-VR approach improves pain control over SCS alone, with fast-acting and long-lasting effects that may increase with repeated use, according to the new collaborative research by Olaf Blanke, MD, of Ecole polytechnique fdrale de Lausanne (EPFL), Geneva, Switzerland, Ali Rezai, MD, of West Virginia University Rockefeller Neuroscience Institute, and Vibhor Krishna MD, PhD, of the Ohio State University and their colleagues. To our knowledge this study shows, for the first time that it is possible to integrate immersive and multisensory VR with spinal neuromodulation and reduce chronic pain, the researchers write.

Integrated SCS-VR puts patients in the picture to help control chronic pain

Drs. Blanke, Rezai, Krishna and their team tested their integrated SCS-VR digiceutical method in 15 patients with chronic leg pain. All patients already had SCS implants for chronic leg pain, in most cases related to failed back surgery syndrome.

Spinal cord stimulation uses mild electrical impulses to interrupt pain signals before they reach the brain. While SCS is an effective and increasingly common treatment for chronic pain, it has limitations: stimulation reduces pain in only about half of patients and rarely eliminates pain completely.

Previous studies have shown that immersive and embodied VR integrating an image of the patients body or avatar into a 3D scene viewed in a VR headset may have pain-relieving properties. The new approach integrates SCS with VR for the first time, allowing patients to see and feel the effect of SCS on a real-time virtual image of their own body or avatar. The stimulated area of the patients virtual leg as shown in VR lit up when the electrical current was on.

For example, if the right thigh tingled during SCS, the same area of the patients virtual thigh was illuminated in VR. In the new study, pain scores with integrated SCS-VR were compared with VR alone, with SCS turned off; and with incongruent SCS-VR, with SCS turned on but a different area of the virtual scene illuminated.

The results showed lower pain ratings when integrated SCS-VR was used. Average pain score (on a continuous visual analog scale) decreased from 6.2 before treatment to 2.72 with congruent SCS-VR when the stimulated area of the leg lit up during SCS. Pain scores decreased by an average of 44 percent with congruent SCS-VR, compared to 23 percent with incongruent SCS-VR. Virtual reality alone had little or no effect on pain scores.

All but 1 of the 15 patients had reduced pain scores during SCS-VR. Importantly and in contrast to the control conditions, the effect lasted for at least ten minutes after SCS was turned off; repeated applications of SCS-VR had larger effects on pain scores. VR-SCS also induced changes in leg embodiment when viewing the VR scene, patients had the impression they were looking at their real legs, and that the illuminated area was actually causing the SCS-induced tingling sensation.

The immersive, personalized SCS-VR approach combines neuromodulation, VR, and the latest research from cognitive neuroscience of multisensory integration into a single therapeutic solution, the researchers write. Integrated VR is a completely noninvasive addition to SCS, with the potential to increase its pain-relieving effectiveness with no adverse effects.

Its not entirely clear how immersive VR increases the effect of SCS, but the new results show that its not just an effect of distraction. The matching visual and tactile signals may result in enhanced masking of pain inputs, Dr. Blanke, Rezai, Krishna and colleagues suggest. They conclude: [T]he strength of the effect, its selectivity, its ease of application, and consistent increase across sessions and long-term analgesia will facilitate the application of prolonged and more frequent therapy doses in future SCS-VR studies, likely further boosting the described effects.

Click here to read Enhancing analgesic spinal cord stimulation for chronic pain with personalized immersive virtual reality.

DOI: 10.1097/j.pain.0000000000002160

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About PAIN

PAIN is IASP's official journal. Published monthly, PAIN presents original research on the nature, mechanisms, and treatment of pain. Available to IASP members as a membership benefit, this peer-reviewed journal provides a forum for the dissemination of multidisciplinary research in the basic and clinical sciences. It is cited in Current Contents and Index Medicus.

About the International Association for the Study of Pain

IASP is the leading professional organization for science, practice, and education in the field of pain. Membership is open to all professionals involved in research, diagnosis, or treatment of pain. IASP has more than 7,000 members in 133 countries, 90 national chapters, and 20 special interest groups (SIGs). IASP brings together scientists, clinicians, health-care providers, and policymakers to stimulate and support the study of pain and translate that knowledge into improved pain relief worldwide.

Human Behavior

U.K. variant puts spotlight on immunocompromised patients’ role in the COVID-19 pandemic – Science Magazine

December 26, 2020 medical

Shoppers wear face masks on Regent Street in London on 19 December, the day the U.K. government imposed new restrictions to curb a rapidly spreading new SARS-CoV-2 variant.

By Kai KupferschmidtDec. 23, 2020 , 2:30 PM

Sciences COVID-19 reporting is supported by the Pulitzer Center and the Heising-Simons Foundation.

In June, Ravindra Gupta, a virologist at the University of Cambridge, heard about a cancer patient who had come into a local hospital the month before with COVID-19 and was still shedding virus. The patient was being treated for a lymphoma that had relapsed and had been given rituximab, a drug that depletes antibody-producing B cells. That made it hard for him to shake the infection with SARS-CoV-2.

Gupta, who studies how resistance to HIV drugs arises, became interested in the case and helped treat the patient, who died in August, 101 days after his COVID-19 diagnosis, despite being given the antiviral drug remdesivir and two rounds of plasma from recovered patients, which containedantibodies against the virus. When Gupta studied genome sequences from the coronavirus that infected the patient, he discovered that SARS-CoV-2 had acquired several mutations that might have allowed it to elude the antibodies.

Now, his analysis, reported in a preprint on medRxiv earlier this month, has become a crucial puzzle piece for researchers trying to understand the importance of B.1.1.7, the new SARS-CoV-2 variant first found in the United Kingdom. That strain, which appears to spread faster than others, contains one of the mutations that Gupta found, and researchers believe B.1.1.7, too, may have originated in an immunocompromised patient who had a long-running infection. Its a perfectly logical and rational hypothesis, says infectious disease scientist Jeremy Farrar, director of the Wellcome Trust.

Scientists are still trying to figure out the effects of the mutations in B.1.1.7, whose emergence led the U.K. government to tighten coronavirus control measures and other countries in Europe to impose U.K. travel bans. But the new variant, along with research by Gupta and others, has also drawn attention to the potential role in COVID-19 of people with weakened immune systems. If they provide the virus with an opportunity to evolve lineages that spread faster, are more pathogenic, or elude vaccines, these chronic infections are not just dangerous for the patients, but might have the potential to alter the course of the pandemic.

Its still very unclear whether that is the case, but Farrar believes its important to ensure doctors take extra precautions when caring for such people: Until we know for sure, I think, treating those patients under pretty controlled conditions, as we would somebody who has drug resistant tuberculosis, actually makes sense.

Researchers concern mostly focuses on cancer patients being treated for chemotherapy and similar situations. We dont yet know about people who are immunocompromised because of HIV, for instance, Farrar says.

B.1.1.7 attracted scientists attention because it was linked to an outbreak in Englands Kent county that was growing faster than usual. Sequences showed that virus had accumulated a slew of mutations that together caused 17 amino acid changes in the virus proteins, eight of them in the crucial spike protein. Among them are at least three particularly concerning ones.

One is 69-70del, a deletion that Gupta also found in his Cambridge, U.K., patient whose virus seemed to evade the immune system. It leads to the loss of two amino acids in the spike protein. In lab experiments, Gupta found that lentivirus engineered to carry the SARS-CoV-2 spike protein with this deletion was twice as infectious.

The second is N501Y, a mutation that evolutionary biologist Jesse Bloom of the Fred Hutchinson Cancer Research Center has shown to increase how tightly the protein binds to the angiotensin-converting enzyme 2 (ACE2) receptor, its entry point into human cells. The mutation is also present in 501Y.V2, a variant discovered by researchers in South Africa who investigated rapidly growing outbreaks in three coastal provinces. We found that this lineage seems to be spreading much faster, says Tulio de Oliveira, a virologist at the University of KwaZulu-Natal whose work first alerted U.K. scientists to the importance of N501Y. Anytime you see the same mutation being independently selected multiple times, it increases the weight of evidence that that mutation is probably beneficial in some way for the virus, Bloom says.

The third worrisome change is P681H, which alters the site where the spike protein has to be cleaved to enter human cells. It is one of the sites on spike where SARS-CoV-2 differs from SARS-CoV-1, the virus that caused the worldwide outbreak of severe acute respiratory syndrome in 2003, and the change there may allow it to spread more easily. This one is probably as important as N501Y, says Christian Drosten, a virologist at Charit University Hospital in Berlin.

So far, SARS-CoV-2 typically acquires only one to two mutations per month. And B.1.1.7 is back to this pace now, suggesting it doesnt mutate faster normally than other lineages. Thats why scientists believe it may have gone through a lengthy bout of evolution in a chronically infected patient who then transmitted the virus late in their infection. We know this is rare but it can happen, says World Health Organization epidemiologist Maria Van Kerkhove. Stephen Goldstein, a virologist at the University of Utah, agrees. Its simply too many mutations to have accumulated under normal evolutionary circumstances. It suggests an extended period of within-host evolution, he says.

People with a weakened immune system may give the virus this opportunity, as Guptas data show. More evidence comes from a paper published in The New England Journal of Medicine on 3 December that described an immunocompromised patient in Boston infected with SARS-CoV-2 for 154 days before he died. Again, the researchers found several mutations, including N501Y. It suggests that you can get relatively large numbers of mutations happening over a relatively short period of time within an individual patient, says William Hanage of the Harvard T.H. Chan School of Public Health, one of the authors. (In patients who are infected for a few days and then clear the virus, there simply is not enough time for this, he says.) When such patients are given antibody treatments for COVID-19 late in their disease course, there may already be so many variants present that one of them is resistant, Goldstein says.

Its simply too many mutations to have accumulated under normal evolutionary circumstances. It suggests an extended period of within-host evolution.

The question is whether the mutations arising in such patients could also help the virus spread more rapidly. In research published a few years ago, Bloom showed some of the mutations that arose in influenza viruses in immunocompromised patients later spread globally. Its totally possible that whats happening in immunocompromised patients could foreshadow what happens in the future with the pandemic, Bloom says. But adaptations that help a virus outperform other viruses in a patient can also be very different from what a virus needs to better transmit from patient to patient, he says.

U.K. scientists and others were initially cautious about concluding that B.1.1.7s mutations made the virus better at spreading from person to person. But the new variant is rapidly replacing others, says Mge evik, an infectious disease specialist at the University of St.Andrews. We cant really rule out the possibility that seasonality and human behavior explain some of the increase, she says. But it certainly seems like there is something to do with this variant. Drosten says he was initially skeptical, but has become more convinced as well.

But exactly what impact each mutation has is much more difficult to assess than spotting them or showing theyre on the rise, says Seema Lakdawala, a biologist at the University of Pittsburgh. Animal experiments can help show an effect, but they have limitations. Hamsters already transmit SARS-CoV-2 virus rapidly, for instance, which could obscure any effect of the new variant. Ferrets transmit it less efficiently, so a difference may be more easily detectable, Lakdawala says. But does that really translate to humans? I doubt it. A definitive answer may be months off, she predicts.

One hypothesis that scientists are discussing is that the virus has increased how strongly it binds to the ACE2 receptor on human cells, and that this allows it to better infect children than before, expanding its playing field. But the evidence for that is very thin so far, evik says. Even if children turn out to make up a higher proportion of people infected with the new variant, that could be because the variant spread at a time when there was a lockdown but schools were open. Another hypothesis is that P681H helps the virus better infect cells higher up in the respiratory tract, from where it can spread more easily than from deep in the lungs, Drosten says.

One important question is whether the South African or U.K. lineage might lead to more severe disease or even evade vaccine-induced immunity. So far there is little reason to think so. Although some mutations have been shown to let the virus evade monoclonal antibodies, vaccines and natural infections both appear to lead to a broad immune response that targets many parts of the virus, says Shane Crotty of the La Jolla Institute for Immunology. It would be a real challenge for a virus to escape from that. The measles and polio viruses have never learned to escape the vaccines targeting them, he notes: Those are historical examples suggesting not to freak out.

At a press conference yesterday, BioNTech CEO Uur ahin pointed out that the U.K. variant differed in only nine out of more than 1270 amino acids of the spike protein encoded by the messenger RNA in the very effective COVID-19 vaccine his company developed together with Pfizer. Scientifically it is highly likely that the immune response by this vaccine also can deal with the new virus, he said. Experiments are underway that should confirm that in the first week of 2021, ahin added.

Sbastien Calvignac-Spencer, an evolutionary virologist at the Robert Koch Institute, says this marks the first time countries have taken such drastic actions as the U.K. lockdown and the travel bans based on genomic surveillance in combination with epidemiological data. Its pretty unprecedented at this scale, he says. But the question of how to react to disconcerting mutations in pathogens will crop up more often as genomic surveillance expands, he predicts. People are happy they prepared for a category 4 hurricane even if predictions turn out to be wrong and the storm is less severe, Calvignac-Spencer says. This is a bit the same, except that we have much less experience with genomic surveillance than we have with the weather forecast.

Although the rise of B.1.1.7 in the United Kingdom is troubling, Farrar says he is equally concerned about the other variant spreading quickly in South Africa and that has now been detected in two travelers in the United Kingdom as well. It includes two further mutations in the part of the spike protein that binds to its receptor on human cells, K417N and E484K. These could impact the binding of the virus to human cells and also its recognition by the immune system, Farrar says. These South African mutations I think are more worrying than the constellation of the British variant. South African hospitals are already struggling, he adds. Weve always asked, Why has sub-Saharan Africa escaped the pandemic to date? Answers have focused on the relative youth of the population and the climate. Maybe if you just increase transmission a bit, that is enough to get over these factors, Farrar says.

To Van Kerkhove, the arrival of B.1.1.7 shows how important it is to follow viral evolution closely. The United Kingdom has one of the most elaborate monitoring systems in the world, she says. My worry is: How much of this is happening globally, where we dont have sequencing capacity? Other countries should beef up their efforts, she says. And all countries should do what they can to minimize transmission of SARS-CoV-2 in the months ahead, Van Kerkhove says. The more of this virus circulates, the more opportunity it will have to change, she says. Were playing a very dangerous game here.

Human Behavior

The coronavirus is mutating. What does that mean for us? – Minneapolis Star Tribune

December 26, 2020 medical

Just as vaccines begin to offer hope for a path out of the pandemic, officials in Britain on Saturday sounded an urgent alarm about what they called a highly contagious new variant of the coronavirus circulating in England.

Citing the rapid spread of the virus through London and surrounding areas, Prime Minister Boris Johnson imposed the country's most stringent lockdown since March.

"When the virus changes its method of attack, we must change our method of defense," he said.

In South Africa, a similar version of the virus has emerged, shares one of the mutations seen in the British variant, according to scientists who detected it. That virus has been found in up to 90% of the samples whose genetic sequences have been analyzed in South Africa since mid-November.

Scientists are worried about these variants but not surprised by them. Researchers have recorded thousands of tiny modifications in the genetic material of the coronavirus as it has hopscotched across the world.

Some variants become more common in a population simply by luck, not because the changes somehow supercharge the virus. But as it becomes more difficult for the pathogen to survive because of vaccinations and growing immunity in human populations researchers also expect the virus to gain useful mutations enabling it to spread more easily or to escape detection by the immune system.

"It's a real warning that we need to pay closer attention," said Jesse Bloom, an evolutionary biologist at the Fred Hutchinson Cancer Research Center in Seattle. "Certainly, these mutations are going to spread, and definitely, the scientific community, we need to monitor these mutations, and we need to characterize which ones have effects."

The British variant has about 20 mutations, including several that affect how the virus locks onto human cells and infects them. These mutations may allow the variant to replicate and transmit more efficiently, said Muge Cevik, an infectious disease expert at the University of St. Andrews in Scotland and a scientific adviser to the British government.

But the estimate of greater transmissibility British officials said the variant was as much as 70% more transmissible is based on modeling and has not been confirmed in lab experiments, Cevik added.

"Overall, I think we need to have a little bit more experimental data," she said. "We can't entirely rule out the fact that some of this transmissibility data might be related to human behavior."

In South Africa, too, scientists were quick to note that human behavior was driving the epidemic, not necessarily new mutations whose effect on transmissibility had yet to be quantified.

The British announcement also prompted concern that the virus might evolve to become resistant to the vaccines just now rolling out. The worries are focused on a pair of alterations in the viral genetic code that may make it less vulnerable to certain antibodies.

But several experts urged caution, saying it would take years not months for the virus to evolve enough to render the current vaccines impotent.

"No one should worry that there is going to be a single catastrophic mutation that suddenly renders all immunity and antibodies useless," Bloom said. "It is going to be a process that occurs over the time scale of multiple years and requires the accumulation of multiple viral mutations. It's not going to be like an on-off switch."

Like all viruses, the coronavirus is a shape-shifter. Some genetic changes are inconsequential, but some may give it an edge.

Scientists fear the latter possibility especially. The vaccination of millions of people may exert enormous pressure on the virus to become resistant to the immune response, setting back the global fight by years.

Already, there are small changes in the virus that have arisen independently multiple times across the world, suggesting the mutations are helpful to the pathogen. The mutation affecting antibody susceptibility technically called the 69-70 deletion, meaning there are missing letters in the genetic code has been seen at least three times: in Danish minks, in people in Britain and in an immune-suppressed patient who became much less sensitive to convalescent plasma.

"This thing's transmitting. It's acquiring. It's adapting all the time," said Dr. Ravindra Gupta, a virologist at the University of Cambridge who last week detailed the deletion's recurrent emergence and spread. "But people don't want to hear what we say, which is, this virus will mutate."

The new genetic deletion changes the spike protein on the surface of the coronavirus, which it needs to infect human cells. Variants of the virus with this deletion arose independently in Thailand and Germany in early 2020 and became prevalent in Denmark and England in August.

Scientists initially thought the new coronavirus was stable and unlikely to escape vaccine-induced immune response, said Dr. Deepti Gurdasani, a clinical public health researcher at Queen Mary University of London.

"But it's become very clear over the last several months that mutations can occur," she said. "As selection pressure increases with mass vaccination, I think these mutants will become more common."

Several recent papers have shown that the coronavirus can evolve to avoid recognition by a single monoclonal antibody, a mixture of two antibodies or even convalescent serum given to a specific individual.

Fortunately, the body's entire immune system is a much more formidable adversary.

The Pfizer-BioNTech and Moderna vaccines induce an immune response only to the spike protein carried by the coronavirus on its surface. But each infected person produces a large, unique and complex repertoire of antibodies to this protein.

"The fact is that you have a thousand big guns pointed at the virus," said Kartik Chandran, a virus expert at the Albert Einstein College of Medicine in New York. "No matter how the virus twists and weaves, it's not that easy to find a genetic solution that can really combat all these different antibody specificities, not to mention the other arms of the immune response."

In short: It will be very hard for the coronavirus to escape the body's defenses, despite the many variations it may adopt.

Escape from immunity requires that a virus accumulate a series of mutations, each allowing the pathogen to erode the effectiveness of the body's defenses. Some viruses, like influenza, amass those changes relatively quickly. But others, like the measles virus, collect hardly any of the alterations.

Even the influenza virus needs five to seven years to collect enough mutations to escape immune recognition entirely, Bloom noted. His lab Friday published a new report showing that common cold coronaviruses also evolve to escape immune detection but over many years.

The scale of the infections in this pandemic may be quickly generating diversity in the new coronavirus. Still, a vast majority of people worldwide have yet to be infected, and that has made scientists hopeful.

"It would be a little surprising to me if we were seeing active selection for immune escape," said Emma Hodcroft, a molecular public health researcher at the University of Bern in Switzerland.

"In a population that's still mostly naive, the virus just doesn't need to do that yet," she said. "But it's something we want to watch out for in the long term, especially as we start getting more people vaccinated."

Immunizing about 60% of a population within about a year and keeping the number of cases down while that happens will help minimize the chances of the virus mutating significantly, Hodcroft said.

Still, scientists will need to closely track the evolving virus to spot mutations that may give it an edge over vaccines.

Scientists routinely monitor mutations in flu viruses in order to update vaccines and should do the same for the coronavirus, said Trevor Bedford, an evolutionary biologist at the Fred Hutchinson Cancer Research Center in Seattle.

"You can imagine a process like exists for the flu vaccine, where you're swapping in these variants, and everyone's getting their yearly COVID shot," he said. "I think that's what generally will be necessary."

The good news is that the technology used in the Pfizer-BioNTech and Moderna vaccines is much easier to adjust and update than conventional vaccines. The new vaccines also generate a massive immune response, so the coronavirus may need many mutations over years before the vaccines must be tweaked, Bedford said.

In the meantime, he and other experts said, the Centers for Disease Control and Prevention and other government agencies should set up a national system to link viral sequence databases with on-the-ground data like whether an infection occurred despite vaccination.

"These are useful pokes for scientists and governments to get systems in place now, before we might need them, especially as we start vaccinating people," Hodcroft said. "But the public should not necessarily be panicking."

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The coronavirus is mutating. What does that mean for us? - Minneapolis Star Tribune

Human Behavior

What You Need to Know About the New Variant of COVID-19 – HealthDay News

December 26, 2020 medical

TUESDAY, Dec. 22, 2020 (HealthDay News) -- For Americans who are worried about the new coronavirus variant that is circulating in Britain, experts in the United States urge everyone to stay calm.

So far, the new variant only seems to spread more easily, with no evidence of higher virulence (ability to cause harm), researchers at Northwestern Medicine in Chicago explained.

"There's no reason to get scared or panic, we just need to closely monitor this variant," said Dr. Ramon Lorenzo-Redondo, a scientist who studies COVID-19. Still, he predicted that it won't be long before the variant is detected in the United States.

Three Northwestern experts -- Lorenzo-Redondo, a research assistant professor in infectious diseases; Dr. Michael Ison, a professor of infectious diseases; and Dr. Marc Sala, an assistant professor of pulmonary and critical care -- answer some key questions people might have about the new variant.

How soon before this variant makes it to the U.S.?

"The variant might already be present here and observed soon," Lorenzo-Redondo said. "That's due to the number of patients that have been infected by this variant, the increase observed in November and the high connectivity between the U.S. and the U.K. It has already been detected in other countries."

Sala noted that "the time frame of the variant's [spread] depends entirely on human behavior, including government-imposed travel restrictions."

What is known about the variant's contagiousness and virulence?

"Right now, we know this variant has increased rapidly in the U.K. and accounts for a high proportion of new cases there," Lorenzo-Redondo said. This suggests a higher transmission rate, but this and other viral properties need to be confirmed in the lab. Meanwhile, the first analyses don't suggest increased virulence, only increased transmission, he added.

For the most part, Sala agreed. "Epidemiologic and modeling data suggests it is more transmissible and indeed appears to be outcompeting the other COVID-19 variants," he said. "It does not seem to cause more severe illness. However, this is all very preliminary and lacks experimental confirmation."

Can a variant limit the effectiveness of the vaccine? "These mutations do not seem to impact vaccine efficacy, but they need to be fully characterized," Lorenzo-Redondo said. "Theoretically, new mutations can impact vaccine efficacy as in other viruses, but the low mutation rate of this virus compared to others like flu or HIV-1 makes this more difficult," he explained.

"However, it is possible that if the vaccine starts to be deployed and is effective, we could observe changes in the virus to adapt and escape from the immune response promoted by the vaccine," he cautioned. "But again, the low mutation rate makes the adaptation of this virus to a vaccine less likely."

How common are variants of viruses and do they generally impact effectiveness of vaccines or treatments?

"Sometimes variants can have great impacts on vaccines or treatments. That's why it is so important to keep monitoring the variants circulating, to detect any possible mutation that could make vaccination or treatment less effective," Lorenzo-Redondo explained. But, "this virus seems to be adapting to spread as much as possible and, so far, all mutations seem to be increasing transmission, not virulence. That's probably because there is no evolutionary advantage for this virus to increase virulence."

What is a variant?

Ison explained that "variants occur when there is a change in the genetic material of the virus that results in a change in proteins the virus makes. In this case, there were a few changes related to the spike protein. These have changed the spike, but [the] changes are not predicted to change the efficacy of the vaccine."

Still, studies are ongoing to understand the impact of the variant, Ison noted.

How does the discovery of the variant impact our social distancing behaviors?

"This variant spreads the same way as the previous ones," Lorenzo-Redondo said. "Therefore, the safe behavior measures must remain the same. This variant shows we can't relax our social precautions." He added that with such high numbers of infections around the world, spikes in the virus will keep happening.

Ison stressed that people should still focus on not traveling, wearing a mask, maintaining social distance and hand hygiene.

According to Lorenzo-Redondo, "Because the virus keeps changing continuously, the greater the number of infected people, the more chances the virus gets to get better at infecting us."

More information

Visit the U.S. Centers for Disease Control and Prevention for more on the coronavirus pandemic.

SOURCE: Northwestern Medicine, news release, Dec. 22, 2020

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What You Need to Know About the New Variant of COVID-19 - HealthDay News

Human Behavior

Study: Women Who Begin Annual Mammograms At Age 40 Are Healthier Than Other Women in Their 40s – Pharmacy Times

December 26, 2020 medical

Study: Women Who Begin Annual Mammograms At Age 40 Are Healthier Than Other Women in Their 40s

The value of mammograms at age 40 has been debated, with just about 35% of women beginning at that age. According to MIT, mammograms for women in their 40s catch relatively few cases of breast cancer, often generate positive results, and produce some cases of unnecessary treatment. Because of these concerns, the US Preventive Services Task Force recommended in 2009 that women start regular mammogram screening at age 50 years, not 40.

The study authors noted, however, that simply changing age recommendations is not an optimal way to make breast cancer screening policies without other interventions. Given that women who opt in to testing in their 40s are relatively healthier, changing the age guidelines has a relatively limited impact. On the other hand, if mammogram screenings reached more women from ages 40 to 49, the authors said those tests would likely detect more cases per screening than they currently do.

Debates over when to recommend screening are missing a key point, said economist and co-author Amy Finkelstein, PhD, in a prepared statement. There are arguments about what the costs and benefits are of screening women at a certain age, but these tend to overlook the fact that those who follow the recommendations differ from the rest of the population. This makes the problem more complicated. You cant just forget human behavior and human selection when designing recommended health care policies.

The authors said targeting screening to high-risk groups who are less compliant with recommendations could be more effective than general age-based recommendations. Health insurance data show than about 90% of mammograms for middle-aged women are negative, 9.7% are false positives, and just 0.7% are authentically positive, and previous studies have found limited benefits for women ages 40 to 49.

To further investigate the problem, the investigators used a clinical model of breast cancer disease progression in the absence of treatment, which had been developed by medical researchers. They used multiple sources of data to approximate the overall incidence of breast cancer in the entire population, including individuals who are not screened.

In total, they found that 10% of women who start having mammograms before age 40 have a relatively high positive test rate of 0.84%, potentially because they experience symptoms leading to the mammogram. In contrast, just 0.56% of the women who started getting mammograms at age 40 test positive, and the number of late-stage cases among them decreases by 6 percentage points compared to people who get screened before age 40.

The team also considered women who do not get mammograms even when they are recommended above age 40. Compared to this group, compliers are also more likely to get other forms of preventive care, including flu shots and cervical cancer screenings, and have fewer emergency room visits for any reason. Although they said it is more difficult to assess the incidence of breast cancer among noncompliers, the clinicians model suggests that the risk among these unscreened women is likely higher than it is among compliers.

Based on these findings, the study authors said screenings should be targeted to higher-risk groups, potentially based on factors such as the age of mothers at first birth or genetic markers. However, they still noted that age-based guidance can hold value, and other methods require further research.

When you make age-based recommendations, it looks like the people who are most likely to follow them are the ones for whom its least beneficialwhich doesnt mean its not beneficial, but those are not the people you most want to target, Finkelstein concluded.

REFERENCECan mammogram screening be more effective? [news release]. MIT; December 17, 2020. Accessed December 18, 2020.https://news.mit.edu/2020/mammogram-age-guidance-1217

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Study: Women Who Begin Annual Mammograms At Age 40 Are Healthier Than Other Women in Their 40s - Pharmacy Times

Human Behavior

Coronavirus: Heres how our brains track where we and others go – Hindustan Times

December 26, 2020 medical

As COVID cases rise, physically distancing yourself from other people has never been more important. Now a new University of California, Los Angeles (UCLA) study reveals how your brain navigates places and monitors someone else in the same location. Published December 23 in Nature, the findings suggest that our brains generate a common code to mark where other people are in relation to ourselves.

We studied how our brain reacts when we navigate a physical space -- first alone and then with others, said senior author Nanthia Suthana, the Ruth and Raymond Stotter Chair in Neurosurgery and an assistant professor of neurosurgery and psychiatry at the David Geffen School of Medicine at UCLA and Jane and Terry Semel Institute for Neuroscience and Human Behavior.

Our results imply that our brains create a universal signature to put ourselves in someone elses shoes, added Suthana, whose laboratory studies how the brain forms and recalls memories.

Suthana and her colleagues observed epilepsy patients whose brains had been surgically implanted earlier with electrodes to control their seizures. The electrodes resided in the medial temporal lobe, the brain centre linked to memory and suspected to regulate navigation, much like a GPS device.

Earlier studies have shown that low-frequency brain waves by neurons in the medial temporal lobe help rodents keep track of where they are as they navigate a new place, said first author Matthias Stangl, a postdoctoral scholar in Suthanas lab. We wanted to investigate this idea in people -- and test whether they could also monitor others near them -- but were hampered by existing technology.

Using a $3.3 million award from the National Institutes of Healths BRAIN Initiative, Suthanas lab invented a special backpack containing the computer that wirelessly connects to brain electrodes. This enabled her to study research subjects as they moved freely instead of lying still in a brain scanner or hooked up to a recording device.

In this experiment, each patient wore the backpack and was instructed to explore an empty room, find a hidden spot and remember it for future searches. While they walked, the backpack recorded their brain waves, eye movements and paths through the room in real-time.

As the participants searched the room, their brain waves flowed in a distinctive pattern, suggesting that each persons brain had mapped out the walls and other boundaries. Interestingly, the patients brain waves also flowed in a similar manner when they sat in a corner of the room and watched someone else approach the location of the hidden spot.

The finding implies that our brains produce the same pattern to track where we and other people are in a shared environment.

Why is this important?

Everyday activities require us to constantly navigate around other people in the same place, said Suthana, who is also an assistant professor of psychology at UCLAs College of Letters and Science and of bioengineering at the Henry Samueli School of Engineering. Consider choosing the shortest airport security line, searching for a space in a crowded parking lot or avoiding bumping into someone on the dance floor.

In a secondary finding, the UCLA team discovered that what we pay attention to may influence how our brains map out a location. For example, the patients brain waves flowed stronger when they searched for the hidden spot -- or witnessed another person approaches the location -- than when they simply explored the room.

Our results support the idea that, under certain mental states, this pattern of brain waves may help us recognize boundaries, said Stangl. In this case, it was when people were focused on a goal and hunting for something.

Future studies will explore how peoples brain patterns react in more complex social situations, including outside the laboratory. The UCLA team has made the backpack available to other researchers to accelerate discoveries about the brain and brain disorders.

Coauthors included Uros Topalovic, Cory Inman, Sonja Hiller, Diane Villaroman, Zahra Aghajan, Dawn Eliashiv and Itzhak Fried, all from UCLA; Leonardo Christov-Moore from USC; Nicholas Hasulak from NeuroPace Inc; Vikram Rao from UCSF and Casey Halpern from the Stanford University School of Medicine.

The study was supported with funding from the NIHs Brain Initiative, McKnight Foundation and Keck Foundation.

(This story has been published from a wire agency feed without modifications to the text. Only the headline has been changed. )

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Human Behavior

Jensen: Shocked, shocked to find hypocrisy in humans – Chattanooga Times Free Press

December 26, 2020 medical

No precise estimate is available, but after watching an excess of cable television programming lately, I would say at least 40% of current news shows are composed of what I call "Hypocrisy Watch." Someone somewhere has failed to live up to their moral code and an intrepid reporter is there to say, "Gotcha."

One day it's the governor of California sitting maskless at a fancy restaurant with people from multiple households close together, when he's told his constituents to do none of those things. Then it's the mayor of Austin, Texas, posting a warning on Facebook against travel as he was vacationing in Cabo San Lucas, Mexico. D.C. Mayor Muriel Bowser traveled to Delaware to attend a Joe Biden rally, and Maryland dining even got some free publicity when a photo of Philadelphia Mayor Jim Kenney eating at the Chesapeake Inn Restaurant was posted on social media in late August.

As journalism, this is cheap stuff. It used to be your transgression had to be pretty serious to warrant big headlines and excited, on-the-street TV stand-ups. The local minister getting caught in an affair? An oncologist sneaking a cigarette down the hall? A Weight Watchers counselor with love handles? No, no, no. Breathless coverage was reserved for famous people who truly abused their position, like televangelist Kenneth Copeland, who begs for money for his ministry but gave his wife a $200,000 Lamborghini SUV and owns three private jets.

But the COVID-19 pandemic appears to have changed all that. A lot of folks deeply resent stay-at-home orders, lockdowns, restrictions, suggestions, whatever you want to call them, and they are looking for villains. Find anyone preaching restrictions but not following them? Well, for many, that's a deal-breaker. Why should I have to take coronavirus precautions when fill in name here doesn't do that?

I'm not here to defend any of this behavior. But I also have to be honest and recognize that I'm human. I have tried to do the right thing during the pandemic. I don't do in-person restaurant dining. I wear a mask where it's appropriate. But am I perfect? Should I have visited a Delaware beach in October with my spouse? Do I replace my mask frequently enough? Should I have invited the neighbors to sit on my front porch? Is that enough?

I've been pondering this since the weekend, when word came out that Dr. Deborah Birx, coordinator of the White House coronavirus response, was revealed to have visited a Delaware beach resort, too. Only she did it the day after Thanksgiving with three generations from two households, and it seems to be something of a pattern. As The Associated Press reported, she also regularly visits her home in Potomac, where her parents and daughter live. This is not ax murdering, but it doesn't exactly square with best COVID-19 practices either. And so, she's getting blasted on social media.

Is Dr. Birx the greatest public health practitioner on the planet? This I don't know. I have heard quite a few doctors say she should have been much more outspoken months ago when President Donald Trump was making some misleading and harmful statements about the coronavirus and its prospects for disappearing. Still, I just can't get that worked up by the thought she counseled one set of behaviors for all Americans and then chose a slightly different one for herself. She made some wrong choices. It's what we humans do at times. It doesn't mean the rest of us should give up on doing our best to slow the spread of a virus that has taken hundreds of thousands of lives in this country. What I'd prefer to see is a little less holier-than-thou pontification unless, of course, it extends to billionaire media barons like Rupert Murdoch getting a COVID-19 shot while misinformation about the vaccine is spread on his TV network. That I would probably enjoy.

The Baltimore Sun

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Jensen: Shocked, shocked to find hypocrisy in humans - Chattanooga Times Free Press

Human Behavior

Did the pandemic stave off climate change? Here’s what the science says – Salon

December 26, 2020 medical

Shortly after the COVID-19 pandemic caused international lockdowns, amemesurfaced: the words "nature is healing" overlain on a scene of environmental recovery, perhaps a shot of crystal-clear skies over an oft-polluted city. Whether made seriously or in jest, the underlying idea was thatas humans were forced to stay indoors and reduce resource consumption, the planet wouldrecovereven as humanity reeled from a deadly disease. True stories like wild goats reclaiming a city in Wales andfake ones about dolphins swimming in the canals of Venice circulated the internet.

Behind the joke was a real, serious proposition:the notion that humanity, by being forced to reduce ourgreenhouse gas emissions,may have inadvertently been savingourselvesfrom the impending climate change apocalypse. But was there any truth to this idea?

Certainly, there were hints: aforementioned instances ofwildlife returning to urban areas,and a drop in oil pricesthat signified a reduction in demand. But on a macroscopicscale, quantifying the way human behavior may have affected carbon emissions in 2020 is much harder.Indeed, Salon reached out to a pair of climate change experts who had somewhat different conclusions.

"The estimates vary among the different groups doing these sorts of calculations, but the consensus seems to be about a 7% decrease [in greenhouse gas emissions] relative to 2019 levels," Dr. Michael E. Mann, a distinguished professor of atmospheric science at Penn State University, wrote to Salon. Although the holiday season traditionally exacerbates greenhouse gas emissions as people consume more and travel more between Thanksgiving and the start of the new year Mann was optimistic that this year would not see as much of an increase as usual.

"The average for the year is pretty much baked in at this point," Mann explained, adding that air travel is a "very small contributor," accounting for only 3 percent oftotal carbon emissions. Mann concluded that, "regardless" of holiday travel,"the decrease in carbon emissions for 2020 will be the largest on record," as high as6 to 7 percent.

Kevin Trenberth, a distinguished scholar at the National Center for Atmospheric Research, was more pessimistic.

"There has been a lot of rhetoric based on the Global Carbon Project suggesting a substantial decrease in emissions with the pandemic," Trenberth emailed Salon, referring to a recentstudywhich found that global carbon dioxide emissions from both fossil fuels and industry are expected to decline by roughly 7% in 2020. "This was a 'bottom up'estimate based on estimates of emissions from various places. It gives the wrong result."

Trenberth argued, if scientists use a 'top down'approach based on the actual amounts of carbon dioxide in the atmosphere, they reach a different conclusion. Citing the data from theNational Oceanic and Atmospheric Administration's (NOAA) facility at Mauna Loa, he claimed "that has shown no slow down at all. The rates of increase on average over the previous 5 years was 2.8 ppm per year and exactly the same rate applies to the last 12 months." The NOAA announced earlier this month that there is more than a 50% chance that 2020 will be the hottest year on record.

"The reason relates to the sources," Trenberth argued. "The [Global Carbon Project] is correct that fossil fuel emissions are down, but they have evidently been entirely compensated for by emissions from other sources: in particular wildfires. These are especially the bushfires in Australia a year or so ago, the wildfires in places like the Pantanal and Brazil, and especially the record wildfires in California, Oregon, Colorado, and so forth."

Mann pointed out an unsettling fact: in the long run, climate change will kill far more than COVID-19. And it cannot be vaccinated against and stopped as easily.

"Ultimately climate inaction will be even more deadly, costing millions of lives," Mann told Salon. "If there is a silver lining, it is that the failure of the current administration to respond meaningfully to the pandemic lays bare the deadliness of ideologically-motivated science denial. This applies to the even greater crisis of human-caused climate change and the need to treat it as the emergency it is."

Recent studies reaffirmMann's observations. Scientists at McGill University recently revealed that a more sophisticated that the threshold for dangerous global warming is likely to occur between 2027 and 2042, while a recent paperby top glaciologists and sea level experts that sea level rises due to climate change are likely to surpass the high end of previous expert projections. The World Health Organization estimates that 250,000 people will perish each year between 2030 and 2050 due to climate changerelated factors.

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Did the pandemic stave off climate change? Here's what the science says - Salon

Human Behavior

New COVID-19 strain may be easier to transmit to others – KIIITV.com

December 26, 2020 medical

Health officials are hoping it sounds worse than it is.

CORPUS CHRISTI, Texas During this time of year when were used to hearing phrases like peace on earth and holiday cheer, the term mutating virus seems appropriately out of place.

Health officials are hoping it sounds worse than it is.

When a new strain of COVID-19 was detected in England, other countries began to announce new travel restrictions to the U-K. Meanwhile, British Prime Minister Boris Johnson put in place plans for a Christmas lockdown

The idea of a new COVID-19 variant is inherently scary for many people, but health experts tell us that a mutation is a natural occurrence. That includes Dr Jaime Fergie, an Infectious Disease Specialist with Driscoll Children's Hospital, who tells 3News, Since the beginning of this pandemic, we have seen mutations in the virus, so this is not really totally new. There are a large number of mutations that have occurred.

This one, though, may be worth watching for another reason. According to Fergie, This one is concerning a little bit because it appears, although it is early, that this virus is easier to transmit.

Although mutations do not tend to make the virus more harmful, the changes may make it more infectious, affecting how easily it is spread from person to person.

Of course, the first question most of us have is, 'What about the vaccine? If the virus changes, does the vaccine need to change, and should I just wait for a new one?'

Doctors say that getting the vaccine is still going to be your best bet.

So far, the initial impression, the initial studies we have is that the vaccines are going to work for these variants, says Dr. Fergie.

Keep in mind that although it may already be here, this particular strain of the virus has yet to be detected in the U.S.

Ultimately, health officials agree, getting a handle on the virus still comes down to human behavior. Thats why as we move through these early months of vaccine doses being administered, everyone should continue to wash their hands, watch their distance, and wear a mask.

For the latest updates on coronavirus in the Coastal Bend, click here.

An Educational Alternative to the Medical Model of Mental Health – James Moore

December 26, 2020 medical

The Journal of Humanistic Psychology, which has published high-profile challenges to psychiatric diagnosis, recently republished seminal articles for its 60th-anniversary. The issue aimed to spark renewed scholarship that challenges the current paradigm in psychiatry and clinical psychology as well as research on alternatives to the current paradigm.

The issue features, The Solving Problems in Everyday Living Model: Toward a Demedicalized, Education-Based Approach to Mental Health, by Tomi Gomory and colleagues from Florida State University. The Solving Problems in Everyday Living (SPIEL) approach is an educational model of care that would serve as an alternative to the contemporary medical model of mental health treatment. The model was a response to the criticisms of the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V) that occurred around 2013, highlighting the limitations of psychotherapy and the coercive nature of psychiatry. The authors explain:

We aim to offer practitioners an alternative, noncoercive, nonpatronizing, non-pathologizing, and humanistic approach for conceptualizing distress and distressing behavior, constructing the helping encounter, engaging with clients, and addressing clients problems-in-living.

The DSM has changed over time. More recent iterations have focused on descriptive diagnoses conceptualized as mental disorders. These disorders are most often understood to be medical conditions that could be identified by observable behaviors or reported experiences.

The authors explain that although diagnoses do not appear helpful in the process of change, they became a necessary procedure for helping professionals to receive compensation from the government or insurance companies. This current medical framework has often focused on finding the cause of abnormal behavior in the brain or neurological mechanisms. Gomorys and colleagues alternative to the medical model stems from the lack of empirical support for this psychiatric framework, as scientific practice demands that after data falsify a proposed hypothesis through multiple independent tests, newly proposed alternate theories, not yet falsified, should be tested. Their SPIEL model serves as an alternative model not yet falsified.

From their perspective, the behavior is not caused by biological factors but rather by a complexity of factors, including a persons history, their experiences in their environment, and the learned behaviors, thoughts, and language developed through the process of socialization.

The SPIEL model works as a model for reeducation. Instead of illnesses, this model understands a persons troubles to be problems in living that can be addressed by learning new ways of surviving in the world. The authors describe the role of practitioners who use SPIEL:

The job of the professional, drawing on his or her experiences with lifes travails, understanding of human behavior and development, expertise at interpersonal communication and in the use of rhetoric, is to identify and make explicit the problematic, habituated behavioral patterns, interpersonal style, and strategies of the learner for the learners consideration.

The learning experience ends when the learners problems have been resolved or when they no longer find the engagement helpful. SPIEL is considered primarily a learning or educational experience whereby the learner gains new understanding about themselves, others, and their emotional, behavioral, and interpersonal difficulties. Although this is a large part of some psychotherapeutic approaches, the very use of the term psychotherapy places this form of engagement within the medical field.

The proponents of SPIEL were mainly influenced by the commonalities in thought between Karl Popper and Paulo Freire. Paulo Freire was a Brazilian educator and activist who worked alongside disempowered communities. His critical pedagogy invites people to reflect on themselves and their position within our environment and context. By doing so, learners can then act upon their context differently in order to change their current conditions. Putting ones new knowledge and hypotheses to the test, the learner engages in praxis, taking a primary role in their own liberation and the process of personal and environmental change.

SPIEL, like Freire, also understands the teacher as a person who facilitates a process rather than an expert that assumes a position of power within the process of self-understanding. Instead, the processes are humanized as the learner takes an active role in learning about themselves and the world and finding emancipatory actions and ways of living authentically.

SPIEL was also influenced by Karl Popper, a 20th-centuryphilosopher of science. More specifically, this model takes from his notion of critical feedback, where a person challenges their prejudices, assumptions, and habits to identify possible problematic beliefs and behaviors. This allows the person to change and grow, developing new ways of understanding themselves, others, and the world, opening up the potential for creative ways of being.

Adding another layer, situational analysis invites the scrutiny of others so that the person can further learn about their context where problems occur and reflect on how they have tried to solve these problems. With this new layer of information, the person or group can either use previously successful attempts at solving the problem or create new solutions to unsolved issues.

These concepts are not unlike those utilized in psychosocial interventions such as cognitive-behavioral therapy, interpersonal therapy, and narrative therapy. The authors add that, in fact, feedback is a key component of successful psychotherapy. Yet, to engage in SPIEL more specifically, the following elements are necessary:

The SPIEL model proposes a change in the language around helping professions (such as problems of living, rather than mental illness, or learner rather than the patient) and advocates for empowering and person-centered practices. The presence of these elements within the encounter will facilitate a process of self-understanding that is ultimately noncoercive, and that can lead to the betterment of the persons suffering by finding solutions to their problems.

****

Gomory, T., Dunleavy, D. J., & Lieber, A. S. (2017).The Solving Problems in Everyday Living Model: Toward a Demedicalized, Education-Based Approach to Mental Health. Journal of Humanistic Psychology, 002216781772243. doi:10.1177/0022167817722430 (Link)

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An Educational Alternative to the Medical Model of Mental Health - James Moore