Using ergonomics to reduce pain from technology use

How to prevent autism burnout

The use of smartphones, tablets and laptops has become commonplace throughout the world and has been especially prevalent among college students. Recent studies have found that college students have higher levels of screen time, and they utilize multiple devices at higher rates compared to previous generations.

With the increased use of these devices, especially smartphones, students tend to use a less-traditional workplace such as a couch or chair with no desk, leading to an increase in musculoskeletal disorders in that age group. A team of Texas A&M researchers led by Mark E. Benden conducted a study looking at the technology students use, the postures they adapt when they use their devices, and the amount of pain the students were currently experiencing.

Benden and his co-authors found that smartphones have become the most common link to educational materials though they have the least favorable control and display scenario from an ergonomic perspective. Additionally, the team concluded that regardless of device, ergonomic interventions focused on improving posture and facilitating stress management may reduce the likelihood of pain.

The results of the team’s study were published recently in the open-access, peer reviewed journal BMC Public Health.

“When we started this study a few years ago it was because we had determined that college students were the heavy users of smartphones,” Benden said. “Now those same levels we were concerned about in college students are seen in 40-year-olds and college students have increased to new levels.”

Benden, professor and head of the Department of Environmental and Occupational Health (EOH) at the Texas A&M University School of Public Health and director of the Ergo Center, co-authored the study with EOH associate professors Adam Pickens, S. Camille Peres, and Matthew Lee Smith, Ranjana Mehta, associate professor in the Wm Michael Barnes ’64 Department of Industrial & Systems Engineering, Brett Harp, a recent EOH graduate, and Samuel Towne Jr., adjunct assistant professor at the School of Public Health.

The research team used a 35-minute online survey that asked participants about their technology use, posture when using the technology, current level of pain or discomfort, and their activity and stress levels.

Among the respondents, 64 percent indicated that their smartphone was the electronic device they used most frequently, followed by laptops, tablets and desktop computers. On average, the students used their smartphone 4.4 hours per day, and they indicated that when doing so, they were more likely to do so on the couch or at a chair with no desk.

“It is amazing to consider how quickly smartphones have become the dominant tech device in our daily lives with little research into how that level of use would impact our health,” Benden said.

The researchers found that posture components and stress more consistently contributed to the pain reported by the students, not the variables associated with the devices they were using.

Still, the researchers point out that in our ever-increasing technology-focused society, efforts are needed to ensure that pain is deferred or delayed until an individual’s later years to preserve the productivity of the workforce.

“Now that we are moving toward hybrid and/or remote workspaces for our jobs, college students are taking habits formed in dorm and apartment rooms during college into young adulthood as employees in home offices,” Benden said. “We need to get this right or it could have adverse impacts on an entire generation.”

New autism marker discovered in kids

Autism and siblings

 Why do so many children with autism often suffer from epilepsy? Northwestern Medicine scientists have discovered an important brain protein that quiets overactive brain cells and is at abnormally low levels in children with autism. 

This protein can be detected in the cerebrospinal fluid, making it a promising marker to diagnose autism and potentially treat the epilepsy that accompanies the disorder. 

Scientists knew when this gene is mutated, it causes autism combined with epilepsy. About 30% to 50% of children with autism also have epilepsy. Autism, which is 90% genetic, affects 1/58 children in the U.S. 

Appropriately nicknamed “catnap2,” the protein, CNTNAP2, is produced by the brain cells when they become overactive. Because the brains of children with autism and epilepsy don’t have enough of CNTNAP2, scientists found, their brains don’t calm down, which leads to seizures.

For the study, Penzes and colleagues analyzed the cerebrospinal fluid in individuals with autism and epilepsy, and in mouse models. Scientists have analyzed the cerebrospinal fluid from patients with Alzheimer’s disease and Parkinson’s disease to help diagnose disease and measure response to treatment, but this is the first study showing it is an important biomarker in autism.

The study will be published Dec. 17 in Neuron.

The new finding about CNTNAP2’s role in calming the brain in autism and epilepsy may lead to new treatments.

“We can replace CNTNAP2,” said lead study author Peter Penzes, the director of the Center for Autism and Neurodevelopment at Northwestern University Feinberg School of Medicine. “We can make it in a test tube and should be able inject it into children’s spinal fluid, which will go back into their brain.” 

Penzes’ lab is currently working on this technique in preclinical research. 

The level in the spinal cord is proxy for the level in the brain, said Penzes, also the Ruth and Evelyn Dunbar Professor of Psychiatry and Behavioral Sciences at Northwestern.

When brain cells are too active because of overstimulation, they produce more CNTNAP2, which floats away and binds to other brain cells to quiet them down. The protein also leaks into the cerebrospinal fluid, where scientists were able to measure it. Thus, it gave them a clue for how much is produced in the brain.

The level in the spinal cord is proxy for the level in the brain, said Penzes, also the Ruth and Evelyn Dunbar Professor of Psychiatry and Behavioral Sciences at Northwestern.

Functioning Labels Harm Autistic People


On December 6th, a group of autism researchers commissioned by The Lancet released a report on the future of autism services and research. This report primarily deals with the need for better services and research for autistic people, including the need for individualized services, and research that prioritizes quality of life. Unfortunately, media coverage of this report has focused on a brief recommendation to create an administrative classification called “profound autism.” Articles about the report have focused on this recommendation, and some have used it to argue that “profound autism” should be a separate autism diagnosis, in spite of the fact that the report specifically says it is not being proposed as a diagnostic term. Autistic people are failed by this coverage. It is a shame that a report focused on the need to improve and research services and support for autistic people is being overshadowed by a sidebar recommendation to apply functioning labels to autistic people with the highest support needs — a recommendation which will fail to improve services or quality of life for these individuals. 

Self-advocates with intellectual disabilities and AAC users have long spoken out against the harm caused by functioning labels like “severe autism” or “low-functioning” autism, as have parents of autistic people with the most significant support needs. “Profound autism” is just an attempt to rebrand the same harmful notion. The reality is that autistic people, just like people with Down Syndrome or Cerebral Palsy, have a wide range of abilities and support needs, for lots of different reasons. The Lancet Commission conflates needing 24/7 support with having a measured IQ of 50 or below or being nonspeaking, but this is a harmful oversimplification — for example, there are many autistic people who speak or who have higher IQs but who require around-the-clock services, and there are autistic AAC users who live independently. We also know that IQ tests are notoriously unreliable for autistic people, particularly nonspeaking autistics. Nor is it clear why the presence of co-occurring disabilities like intellectual disability or speech apraxia should result in a different label, when co-occurring disabilities are common in autistic people and already accounted for by the DSM.

Autistic people need and deserve better services, especially those of us with the highest needs — but the “profound autism” label doesn’t help. “Profound autism” doesn’t give us any actionable information about why a person needs support or what support they need. It doesn’t tell us if a person has speech apraxia or complex medical needs, or if the person needs access to AAC or specific mental health supports. It also doesn’t reflect what we know about people with significant developmental disabilities generally, which is that high expectations and inclusive services benefit everyone and we can’t predict what someone can achieve with the right support. 

Instead of rehashing old, harmful arguments about functioning labels, we should focus on improving the services available to all autistic people — which is what the majority of the Lancet Commission report is actually about. Many autistic people with a wide range of needs go without any services, and even those of us with services too often lack the kind of robust, high-quality, individualized, and respectful supports that would truly enable us to live our best lives. To begin to address this, researchers and policymakers must focus on services that can improve quality of life. When a report directing researchers to do just that is derailed to promote functioning labels, this harms autistic people. We need media outlets — and autism organizations — to focus on recommendations that will truly make a difference in the lives of autistic people. Our community’s unmet needs are critical, and must not be pushed under the rug in favor of resurrecting harmful functioning labels once more. ASAN will continue to advocate for research and services that meet the needs, and promote the dignity, of all autistic people.

Research shows combining two drugs used to treat fibromyalgia improves patient outcomes

Man with fibromyalgia
Man with fibromyalgia


Queen’s University researcher Ian Gilron has uncovered a more effective way of treating fibromyalgia, a medical condition characterized by chronic widespread pain typically accompanied by fatigue, as well as sleep, mood and memory problems.

The results of the trial suggest that combining pregabalin, an anti-seizure drug, with duloxetine, an antidepressant, can safely improve outcomes in fibromyalgia, including not only pain relief, but also physical function and overall quality of life. Until now, these drugs have been proven, individually, to treat fibromyalgia pain.

“Previous evidence supports added benefits with some drug combinations in fibromyalgia,” says, Dr. Gilron (Anesthesiology, Biomedical Sciences). “We are very excited to present the first evidence demonstrating superiority of a duloxetine-pregabalin combination over either drug alone.”

Fibromyalgia was initially thought to be a musculoskeletal disorder. Research now suggests it’s a disorder of the central nervous system – the brain and spinal cord. Researchers believe that fibromyalgia amplifies painful sensations by affecting the level and activity of brain chemicals responsible for processing pain signals.

“The condition affects about 1.5 to 5 per cent of Canadians – more than twice as many women as men. It can have a devastating on the lives of patients and their families,” explains Dr. Gilron. “Current treatments for fibromyalgia are either ineffective or intolerable for many patients.”

This study is the latest in a series of clinical trials – funded by the Canadian Institutes of Health Research (CIHR) – that Dr. Gilron and his colleagues have conducted on combination therapies for chronic pain conditions. By identifying and studying promising drug combinations, their research is showing how physicians can make the best use of current treatments available to patients.

“The value of such combination approaches is they typically involve drugs that have been extensively studied and are well known to health-care providers,” says Dr. Gilron.

Hydroxychloroquine Not Linked to Longer Heart Rhythm Intervals in Rheumatoid Arthritis or Lupus Patients

Heart attack

 

New research presented at ACR Convergence, the American College of Rheumatology’s annual meeting, discovers that use of hydroxychloroquine, a generic drug, does not cause any significant differences in QTc length or prolonged QTc, key measures of heart rate, in people with rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE) (abstract #0431).

Rheumatoid arthritis is the most common type of autoimmune arthritis. It is caused when the immune system (the body’s defense system) is not working properly. RA causes pain and swelling in the wrist and small joints of the hand and feet. SLE is a chronic disease that causes systemic inflammation which affects multiple organs.

Hydroxychloroquine is a cornerstone treatment for SLE, and patients with RA may also take the drug either alone or in combination with other treatments. However, there are concerns about its possible heart-related side effects: the prolongation of QTc, or the time span the heart takes to contract and relax, and the development of arrhythmia (irregular heartbeats). This new study assessed QTc lengths in patients with RA and SLE and its association with hydroxychloroquine use.

Hydroxychloroquine remains the foundation of disease-modifying antirheumatic drug therapy in rheumatic disease patients. Given recent concerns surrounding hydroxychloroquine’s use in COVID-19 patients and subsequent arrhythmic events, we wanted to examine the associations between its use and the QTc length on electrocardiograms in a large, asymptomatic cohort of RA and SLE patients,” says study co-author Elizabeth Park, MD, Rheumatology Fellow at Columbia University Irving Medical Center.

The study analyzed data on 681 RA and SLE patients without clinical cardiovascular disease, including two prospective RA cohorts of 307 patients and a retrospective SLE cohort of 374patients, that included electrocardiogram (EKG) results. The researchers explored the association between QTc length and hydroxychloroquine use by these patients, and they adjusted the data for disease-specific characteristics and cardiovascular disease (CVD) risk factors. Of the whole study group (RA and SLE), 54% used hydroxychloroquine and 44% had QTc lengths of more than 440 milliseconds. They found that the adjusted QTc length among hydroxychloroquine users was comparable to those who did not use the drug.

Their results also showed that hydroxychloroquine use did not significantly predict prolonged QTc for either the whole cohort or the RA and SLE patient cohorts. However, nine out of 11 of the SLE patients who did have a prolonged QTc were taking hydroxychloroquine. Yet these observations were too small to detect statistically significant differences between the hydroxychloroquine groups.

Prolonged QTc, or more than 500 milliseconds, was not associated with arrhythmias or deaths among these patients. The study also did not find any significant interactions between hydroxychloroquine and other QTc-prolonging medications in the patients. Hydroxychloroquine use combined with other QTc-prolonging medications resulted in a comparable QTc interval to hydroxychloroquine alone. In the SLE group, hydroxychloroquine combined with anti-psychotic drugs did result in longer QTc compared to using hydroxychloroquine alone, however.

“Overall, the use of hydroxychloroquine did not predict QTc length, even while adjusting for critical confounding factors, namely the use of other QTc-prolonging medications,” says Dr. Park. “Our findings reinforce the fact that hydroxychloroquine remains a safe, effective long-term disease-modifying drug for our rheumatic disease patients. It’s important to remember that COVID-19 patients who received hydroxychloroquine were likely critically ill. Therefore, the effect of COVID-19 itself on the heart and subsequent arrhythmia must be considered. They also likely concurrently received azithromycin, another QTc-prolonging medication. Our next steps are to stratify data by length and cumulative dose of hydroxychloroquine therapy and analyze the associations with QTc length.”