Scientists discover biological mechanism of hearing loss caused by loud noise — and find a way to prevent it

Anyone who has ever been to a loud concert knows the feeling of ringing ears. Some people experience temporary or even permanent hearing loss or drastic changes in their perception of sound after the loud noises stop. Thanos Tzounopoulos, Ph.D., director of the Pittsburgh Hearing Research Center at the University of Pittsburgh School of Medicine has focused his scientific career on investigating how hearing works and developing ways to treat tinnitus and hearing loss.
In a paper published today in the Proceedings of the National Academy of Sciences, Tzounopoulos and his Pitt collaborators Amantha Thathiah, Ph.D., and Chris Cunningham, Ph.D., discovered a molecular mechanism of noise-induced hearing loss and showed that it could be mitigated with medication.  
The study showed that noise-induced hearing loss, which affects millions of Americans, stems from cellular damage in the inner ear that is associated with the excess of free-floating zinc – a mineral that is essential for proper cellular function and hearing. Experiments in mice showed drugs that work as molecular sponges trapping excess zinc can help restore lost hearing or, if administered before an expected loud sound exposure, can protect from hearing loss.
“Noise-induced hearing loss impairs millions of lives but, because the biology of hearing loss is not fully understood, preventing hearing loss has been an ongoing challenge,” said senior author Thanos Tzounopoulos, Ph.D., endowed professor and vice-chair of research of otolaryngology at Pitt.
While some experience noise-induced hearing loss as a result of an acute traumatic injury to the ear, others notice a sudden hearing impairment after being continuously exposed to loud noise, for example in a battlefield or at a construction site. Others notice their hearing deteriorating after attending a loud music show.
Researchers say such noise-induced hearing loss can be debilitating. Some people start hearing sounds that aren’t there, developing a condition called tinnitus, which severely affects a person’s quality of life.
Tzounopoulos’ research, which focuses on the biology of hearing, tinnitus and hearing loss, strived to determine the mechanistic underpinnings of the condition in the effort to lay the groundwork for the development of effective and minimally invasive treatments in the future.

By performing experiments in mice and on isolated cells of the inner ear, researchers found that hours after mice are exposed to loud noise, their inner ear zinc level spikes. Loud sound exposure causes a robust release of zinc into the extra and intracellular space which, ultimately, leads to cellular damage and disrupts normal cell to cell communication.
Thankfully, this discovery opens doors for a possible solution. Experiments showed mice who were treated with a slow-releasing compound that trapped excess free zinc were less prone to hearing loss and were protected from noise-induced damage.
Researchers are currently developing a treatment to be tested in preclinical safety studies with the goal of making it available as a simple, over-the-counter option to protect oneself from hearing loss.
Other authors of the study are first author Brandon Bizup, Ph.D., and co-author Sofie Brutsaert, both of Pitt.

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Salt substitutes help to maintain healthy blood pressure in older adults

The replacement of regular salt with a salt substitute can reduce incidence of hypertension, or high blood pressure, in older adults without increasing their risk of low blood pressure episodes, according to a recent study in the Journal of the American College of Cardiology. People who used a salt substitute had a 40% lower incidence and likelihood of experiencing hypertension compared to those who used regular salt.
According to the World Health Organization, hypertension is the leading risk factor for cardiovascular disease and mortality. It affects over 1.4 billion adults and results in 10.8 million deaths per year worldwide. One of the most effective ways to reduce hypertension risk is to reduce sodium intake. This study looks at salt substitutes as a better solution to control and maintain healthy blood pressure than reducing salt alone.
“Adults frequently fall into the trap of consuming excess salt through easily accessible and budget-friendly processed foods,” said Yangfeng Wu, MD, PhD, lead author of the study and Executive Director of Peking University Clinical Research Institute in Beijing, China. “It’s crucial to recognize the impact of our dietary choices on heart health and increase the public’s awareness of lower-sodium options.”
Researchers in this study evaluated the impact of sodium reduction strategies on blood pressure in elderly adults residing in care facilities in China. While previous studies prove that reducing salt intake can prevent or delay new-onset hypertension, long-term salt reduction and avoidance can be challenging.
The DECIDE-Salt study included 611 participants 55 years or older from 48 care facilities split into two groups: 24 facilities (313 participants) replacing usual salt with the salt substitute and 24 facilities (298 participants) continuing the use of usual salt. All participants had blood pressure

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Non-invasive techniques to detect skin cancer

A study conducted by Aston University researchers has demonstrated that the appearance of ageing skin looks noticeably different compared to younger skin, when examined under polarised laser light.
The scientists believe that their new finding could pave the way for new, non-invasive light-based techniques to detect diseases, including cancer, in older individuals. This could significantly enhance early-stage treatment options for various skin conditions.
It has already been established that two classes of polarised, linearly and circularly, can detect changes in skin that aren’t visible to the human eye.
The new study indicates that the altered light scattering properties of ageing skin are largely due to changes in the skin’s texture, which are associated with the depletion of collagen fibres in the dermal layer.
The research was led by Igor Meglinski, professor in quantum biophotonics & biomedical engineering and conducted under his guidance with Dr Viktor Dremin from Aston University’s Institute of Photonic Technologies. The paper “Incremental residual polarization caused by aging in human skin” will be published in the May 2024 edition of the Journal of Biomedical Optics.
The researchers analysed images of the middle fingers of 32 volunteers aged 22 to 76 to study skin aging. They also used the Monte Carlo method, a mathematical technique, to represent the effects of light circulation within the human skin. This technique was developed by Professor Meglinski in 2001. Combined with the visual data from the images, this enabled the researchers to draw conclusions about the optical properties of ageing skin.
Professor Meglinski said: “Our research offers a comprehensive analysis of how aging affects human skin polarisation properties. This could be a stepping stone to developing non-invasive, light-based techniques for early detection of skin conditions, including cancer, in the elderly.”
The findings of the research could support the development of a method of skin analysis which doesn’t rely on the patient undergoing biopsies or surgery.
It could provide instant assessments of age-related skin changes that can be extended to monitor changes associated with the development of diabetes and other conditions.
The research was conducted alongside researchers at the University of Oulu in Finland and the University of Latvia.

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Strongest contender in decades in fight against breast cancer

For decades, hormonal treatment of breast cancer has been going in one direction — blocking estrogen. Now a global study involving researchers at the University of Adelaide has discovered there may be another, less toxic way to defeat the most common form of breast cancer.
The study found the drug enobosarm stimulates the androgen receptor (AR), making it effective against estrogen receptor-positive (ER+) breast cancer, which constitutes up to 80 per cent of all breast cancer cases.
“The effectiveness of enobosarm lies in its ability to activate the AR and trigger a natural defence mechanism in breast tissue, thereby slowing the growth of ER+ breast cancer, which relies on the hormone estrogen to grow and spread,” said senior co-author Professor Wayne Tilley, Director of the Dame Roma Mitchell Cancer Research Laboratories at the University of Adelaide.
“This clinical study is supported by our pre-clinical research, previously published in Nature Medicine, which established that the AR is a tumour suppressor in both normal breast tissue and ER+ breast cancer.”
Along with investigators from the University of Adelaide and Dana-Farber Cancer Institute (DFCI) in Boston, USA, the international study also included researchers from the University of Liverpool in the UK and other experts around the world.
The team assessed enobosarm’s efficacy and safety in 136 postmenopausal women with advanced or metastatic ER-positive, HER2-negative breast cancer. Enobosarm showed significant anti-tumour activity and was well-tolerated by patients, without adversely affecting their quality of life or causing masculinising symptoms.
This discovery represents the first advancement in hormonal treatment of ER+ breast cancer in decades and offers a promising new oral treatment strategy for the most prevalent form of breast cancer.

The new hormonal strategy, published in The Lancet Oncology, differs from the existing standard-of-care hormonal treatments, which have been around for decades and involve suppressing estrogen activity in the body or inhibiting the ER.
Although successful initially, treatments targeting ER can cause severe side effects and treatment-resistant progression of the disease is common.
“Our findings are very promising. They demonstrate that stimulating the androgen receptor pathway with enobosarm can be beneficial,” said senior co-author and study Principal Investigator Dr Beth Overmoyer from DFCI.
“This is the first time a non-estrogen receptor hormonal treatment approach has been shown to be clinically advantageous in ER+ breast cancer. The study supports further investigation of enobosarm in earlier stages of breast cancer as well as in combination with targeted therapies, such as ribociclib, a CDK 4/6 inhibitor.”
Around 57 Australians are diagnosed with breast cancer every day, with more than 2.3 million cases identified globally each year.
“The data strongly encourages more clinical trials for AR-stimulating drugs in treating AR-positive and ER-positive breast cancer. The fact that this drug is well-tolerated also opens possibilities for its use in breast cancer prevention,” said co-author Dr Stephen Birrell, a clinical affiliate of the University of Adelaide.

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Genetic cause of low birth weight among children conceived after fertility treatment

VUB professor Claudia Spits, of the Reproduction and Genetics research group, has identified a genetic cause for the increased risk of low birth weight in babies born following assisted reproductive technologies such as IVF. “Previous studies have identified treatment-related causes for low birth weight, but this is the first time we have been able to identify an underlying genetic factor,” says Professor Spits. She organised a large-scale study with Brussels IVF (the centre for reproductive medicine at UZ Brussel), the centre for medical genetics (CMG) at UZ Brussel and Maastricht University Medical Centre (UMC).
Initially, she studied the DNA of babies born both from spontaneous pregnancies and after fertility treatment. She found that in both groups, a greater risk of low birth weight was associated with certain mutations in mitochondrial DNA, and that these mutations were slightly more common in children born after fertility treatment. Mitochondria are the “energy factories” in the cell that are inherited through the mother. If they do not function properly, as they develop, they can cause a variety of health problems such as cardiovascular disease and diabetes.
To determine whether these mutations are transmitted from mother to child, the researchers also studied the DNA of the mothers. Analysis showed that children born after fertility treatment have more new, non-transmitted mutations than babies conceived without assistance.
As a final step, the group studied oocytes obtained through hormonal stimulation and through natural cycle, to determine whether hormonal stimulation was harmful. The mitochondrial mutations did not necessarily appear to be caused by hormonal stimulation. “In particular, a combination of age-related factors in conjunction with hormonal stimulation can lead to a higher risk of abnormal oocytes,” says Spits.
“The risk of mutations in the oocyte’s mitochondrial DNA increases with age. During a normal cycle, mechanisms exist to remove mutated oocytes and select only healthy cells. However, with hormonal stimulation to boost oocyte production, this mechanism is switched off and mutated oocytes are released.”
Spits’ team will conduct further studies, but these insights can be immediately implemented in assisted reproductive technology (ART) treatments to limit the risk of oocytes with mutagenic mitochondria. “It appears that the larger the number of oocytes obtained after hormonal stimulation, the higher the chance of mutations. In the future, we can pay more attention to achieving a proper balance between an adequate oocyte yield and minimizing the risk of mutations.” Spits concludes.

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Artificial cartilage with the help of 3D printing

Is it possible to grow tissue in the laboratory, for example to replace injured cartilage? At TU Wien (Vienna), an important step has now been taken towards creating replacement tissue in the lab — using a technique that differs significantly from other methods used around the world.
A special high-resolution 3D printing process is used to create tiny, porous spheres made of biocompatible and degradable plastic, which are then colonized with cells. These spheroids can then be arranged in any geometry, and the cells of the different units combine seamlessly to form a uniform, living tissue. Cartilage tissue, with which the concept has now been demonstrated at TU Wien, was previously considered particularly challenging in this respect.
Tiny spherical cages as a scaffold for the cells
“Cultivating cartilage cells from stem cells is not the biggest challenge. The main problem is that you usually have little control over the shape of the resulting tissue,” says Oliver Kopinski-Grünwald from the Institute of Materials Science and Technology at TU Wien, one of the authors of the current study. “This is also due to the fact that such stem cell clumps change their shape over time and often shrink.”
To prevent this, the research team at TU Wien is working with a new approach: specially developed laser-based high-resolution 3D printing systems are used to create tiny cage-like structures that look like mini footballs and have a diameter of just a third of a millimeter. They serve as a support structure and form compact building blocks that can then be assembled into any shape.
Stem cells are first introduced into these football-shaped mini-cages, which quickly fill the tiny volume completely. “In this way, we can reliably produce tissue elements in which the cells are evenly distributed and the cell density is very high. This would not have been possible with previous approaches,” explains Prof. Aleksandr Ovsianikov, head of the 3D Printing and Biofabrication research group at TU Wien.
Growing together perfectly
The team used differentiated stem cells — i.e. stem cells that can no longer develop into any type of tissue, but are already predetermined to form a specific type of tissue, in this case cartilage tissue. Such cells are particularly interesting for medical applications, but the construction of larger tissue is challenging when it comes to cartilage cells. In cartilage tissue, the cells form a very pronounced extracellular matrix, a mesh-like structure between the cells that often prevents different cell spheroids from growing together in the desired way.

If the 3D-printed porous spheres are colonized with cells in the desired way, the spheres can be arranged in any desired shape. The crucial question is now: do the cells of different spheroids also combine to form a uniform, homogeneous tissue?
“This is exactly what we have now been able to show for the first time,” says Kopinski-Grünwald. “Under the microscope, you can see very clearly: neighboring spheroids grow together, the cells migrate from one spheroid to the other and vice versa, they connect seamlessly and result in a closed structure without any cavities — in contrast to other methods that have been used so far, in which visible interfaces remain between neighboring cell clumps.”
The tiny 3D-printed scaffolds give the overall structure mechanical stability while the tissue continues to mature. Over a period of a few months, the plastic structures degrade, they simply disappear, leaving behind the finished tissue in the desired shape.
First step towards medical application
In principle, the new approach is not limited to cartilage tissue, it could also be used to tailor different kinds of larger tissues such as bone tissue. However, there are still a few tasks to be solved along the way — after all, unlike in cartilage tissue, blood vessels would also have to be incorporated for these tissues above a certain size.
“An initial goal would be to produce small, tailor-made pieces of cartilage tissue that can be inserted into existing cartilage material after an injury,” says Oliver Kopinski-Grünwald. “In any case, we have now been able to show that our method for producing cartilage tissue using spherical micro-scaffolds works in principle and has decisive advantages over other technologies.”

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Sister cells uncover pre-existing resistant states in cancer

In many cancers, such as ovarian cancer, each round of chemotherapy kills the majority of cancer cells, while a small population of them survives through treatment. These cells are typically more resistant for the next cycle of therapy and can thus regrow to a deadly, treatment resistant tumour.
In a recent study published in Nature Communications, researchers at the University of Helsinki wanted to know how this small population of surviving cells differs from the other more sensitive cells already before the treatment. To enable this cellular time travel, they developed ReSisTrace, a methodology that takes advantage of the similarity of sister cells to trace back pre-existing treatment resistance in cancer.
Labeling cancer cells with genetic barcodes
“In ReSisTrace, we label cancer cells uniquely with genetic barcodes and allow them to divide once, so that we get two identical sister cells that share the same barcode. We then analyse single-cell gene expression from half of the cells before the treatment, while treating the other half with chemotherapy, or other anti-cancer treatment. From the surviving cells we can identify the barcodes of resistant cells. Using their sister cells analysed before the treatment, we can discover how the cells that will survive through treatment differ from the pre-sensitive cells, thus revealing the pre-existing resistant states,” says Jun Dai, PhD student in Anna Vähärautio’s group, who developed the methodology to trace sister cells.
The method was applied to reveal resistant cell states against chemotherapy, targeted therapy or innate immunity in high-grade serous ovarian cancer. “We found that genes associated with proteostasis and mRNA surveillance are important to explain pre-existing treatment resistance. Interestingly, we found that DNA repair deficiency that is very common in ovarian cancer, sensitised these cells to not only chemotherapy and PARP inhibitors but also to NK killing,” says Shuyu Zheng, a PhD student from Jing Tang’s group, who spearheaded the computational analysis.
Associate Professor Jing Tang’s laboratory then leveraged the revealed gene expression changes to predict small molecules that could shift the cells from a resistant state to a sensitive state. “We developed a computational method to correlate the resistant states with the gene expression changes induced by a drug. Ideally, if a drug can reverse the resistant cells’ gene expression profiles, then it can be considered as a potential hit to overcome the resistance,” says Associate Professor Jing Tang, and a team leader in Systems Oncology Research program, University of Helsinki.
Researchers found that most of the predicted small molecules indeed changed the gene expression patterns of cancer cells towards sensitive states. Most importantly, after adding these drugs, cancer cells were significantly more sensitive to carboplatin, PARP inhibitor or NK killing, illustrating that the pre-resistance states identified by ReSisTrace were functionally relevant and targetable. “Our novel experimental-computational approach really leverages the power of single-cell omics and pharmacological data integration,” Associate Professor Jing Tang summarises.
Widely applicable method to identify and target pre-existing resistant cell states across cancer types
“The method we developed reveals the features of cells that will — in the future — become resistant to anti-cancer treatments by coupling cell state and fate in sister cell resolution. It is widely applicable to identify and target pre-existing resistant cell states across cancer types, as well as against different treatment modalities, including immunotherapies. Our approach paves the way for development of sequential cancer therapies that can block resistance before it even emerges,” concludes Anna Vähärautio, K. Albin Johansson Cancer Research Fellow, Foundation for the Finnish Cancer Institute and a team leader in Systems Oncology Research program, University of Helsinki.

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A standard blood test can predict a heart attack

Using the results of a standard blood test and an online tool, you can find out if you are at increased risk of having a heart attack within six months. The tool has been developed by a research group at Uppsala University in the hope of increasing patients’ motivation to change their lifestyle.
Heart attacks are the most common cause of death in the world and are increasing globally. Many high-risk people are not identified or do not take their preventive treatment. Now researchers led by Professor Johan Sundström at Uppsala University have found that heart attacks can be predicted with a standard blood test. The problem, according to the researchers, is that risk factors have previously been verified in studies involving five to ten years of follow-up, where only factors that are stable over time can be identified.
“However, we know that the time just before a heart attack is very dynamic. For example, the risk of a heart attack doubles during the month after a divorce, and the risk of a fatal heart event is five times as high during the week after a cancer diagnosis,” says Sundström, who is a cardiologist and professor of epidemiology at Uppsala University.
Together with other European researchers, he has proceeded from the hypothesis that several important biological processes are active during the months before a heart attack and that these could be detected using a simple blood test.
“We wanted to develop methods that would enable the health services to identify people who will soon suffer their first heart attack,” Sundström says.
The research group had access to blood samples from 169,053 individuals without prior cardiovascular disease in six European cohorts. Within six months, 420 of these people suffered their first heart attack. Their blood was then compared with blood from 1,598 healthy members of the cohorts.
“We identified around 90 molecules that were linked to a risk of a first heart attack. However, the samples that are already taken in healthcare now are enough to predict the risk. We hope that this will increase people’s motivation to take their preventive medicine or stop smoking, for example,” says Sundström.

The researchers have also developed a simple online tool in which anyone can find out their risk of having a heart attack within six months.
“This was one of the aims of the entire study, since we know that people feel relatively low motivation to follow preventive treatments. If you find out that you happen to have an increased risk of suffering a heart attack soon, perhaps you will feel more motivated to prevent it,” Sundström says.
The researchers will now study the 90 or so new molecules to understand them better and see whether there are any possibilities of treatment.
“We hope to be able to carry out a new study here in Uppsala to see whether the online tool provides the kind of motivation we intend,” Sundström concludes.
One of the six cohorts is from the Uppsala-based population study EpiHealth.

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Protein modifications key influencers in neurodegenerative diseases

Neurodegenerative diseases, such as Alzheimer’s and Parkinson’s, present a significant health challenge, affecting over 50 million people globally. One common feature of these diseases is the accumulation of misfolded protein aggregates in the brain, known as amyloid fibrils, which disrupt normal cell function and eventually lead to cell death​​.
In a new study, scientists led by Hilal Lashuel at EPFL and Matthew R. Pratt at USC have made a significant advancement in understanding how post-translational modifications (PTMs) — changes that happen to proteins after they are synthesized in the cell — can influence the formation and pathogenicity of these amyloid fibrils.
The researchers studied the protein alpha-synuclein, which is linked to the formation of amyloid fibrils in Parkinson’s disease. The researchers looked at a specific modification that the protein undergoes, technically known as “O-linked β-N-acetylglucosamine” or O-GlcNAc for short.
O-GlcNAc is a kind of modification that adds a single sugar molecule, to specific serine or threonine residues in the protein, thereby altering its function and properties. It has been linked to several biological processes, including protein aggregation and neurodegeneration​​. This modification, particularly on alpha-synuclein, has been shown to slow down amyloid aggregation and potentially protect neurons​​.
Previous studies by Pratt’s and Lashuel’s groups, suggested that increasing the O-GlcNAc modification could have therapeutic potential in early stages of neurodegenerative disease, altering the properties of protein aggregates to prevent their seeding and spread in the brain, potentially slowing disease progression.
Building on this, the team employed innovative chemical methods to produce modified alpha-synuclein fibrils, working with the group of Virginia Lee at the University of Pennsylvania. They also used cell and animal models to study how O-GlcNAc affects the pathogenic properties of alpha-synuclein, and worked with the group of Lorena Saelices at UT Southwestern Medical Center to observe the modified fibrils with cryo-electron microscopy.
The study showed that the increased modification produces fibrils with distinct structural and biochemical features. These fibrils result in a strain of amyloid fibril with a dramatically reduced ability to seed aggregation in neurons and animalmodels of Parkinson’s disease. Interestingly, this strain of fibrils can seed aggregation in vitro, but not in neurons or live mice.
“Our findings show that this environment in the cell plays an important role in determining the pathogenicity of this protein,” says Anne-Laure Mahul-Mellier, one of the study’s co-first authors.
The study suggests that modifications like O-GlcNAc could play a role in modulating the pathogenicity of alpha-synuclein, which opens up new avenues for research and potential treatments. For instance, targeting the O-GlcNAc modification process could lead to therapies that alter the progression of Parkinson’s by influencing the ability of pathogenic alpha-synuclein species to spread to different brain regions.
In a related Research Briefing by Nature, the authors write: “[O]ur work on the O- GlcNac modification of [alpha-synuclein] sheds new light on the molecular determinants of the pathobiology of amyloid fibrils and provides new therapeutic targets for preventing amyloid growth and spreading at both early and late stages of disease development and progression.”

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Adolescents with concussion may benefit from more activity earlier

Researchers at Nationwide Children’s Hospital have found that when it comes to concussion recovery, activity type matters. In a study published today in British Journal of Sports Medicine, researchers found that limiting screen time and returning to school early following a concussion may speed up recovery.
“Increased time spent in the classroom, participating in some after-school activities or working a job was associated in our study with faster symptom resolution, especially for participants with lower post-acute symptom scores,” said lead author Jingzhen Ginger Yang, PhD, MPH, principal investigator in the Center for Injury Research and Policy of the Abigail Wexner Research Institute at Nationwide Children’s. “However, when activities involved significant screen time — like surfing the internet or playing video/computer games — during the first week post-injury, symptoms resolved more slowly.”
While some research on pediatric concussion has suggested an earlier introduction of physical activity promotes recovery, little is known about the intensity and duration of cognitive activity post-concussion and its potential influence on concussion recovery outcomes.
This new study, conducted by experts in Nationwide Children’s Center for Injury Research and Policy, division of Sports Medicine, Center for Biobehavioral Health, and division of Emergency Medicine evaluated the intensity and duration of daily cognitive activity reported by adolescents (age 11-17 years) following concussion and examined the connections between these activities and symptom duration. Participants reported increases in low-intensity cognitive activities — such as listening to music, reading, watching television, and making or receiving phone calls — and total minutes of overall cognitive activities as their symptoms resolved.
Previous clinical guidelines for youth with concussions have recommended complete physical and mental rest until symptoms resolve to avoid re-injury and reduce the demands on injured tissue. However, recent clinical and experimental data have demonstrated that prolonged physical rest does little to improve functional outcomes, and the resulting isolation and withdrawal can have unintended physical, social and educational consequences.
“Children and teens should be encouraged to get back to their routines and take part in activities like clubs, jobs and homework after experiencing concussion, but keep in mind that for some patients, prolonged screen time in non-school activities such as gaming or internet scrolling can affect recovery if it is worsening their symptoms,” said co-author Thomas Pommering, DO, division chief and director of concussion clinics of Nationwide Children’s division of Sports Medicine. “We recommend concussion patients pick their screen activity wisely, focusing on school demands first.”
According to the study, the average time children returned to school after a concussion was almost one week. Symptoms resolved more slowly when returning to school was delayed. Additionally, participating in club activities was associated with faster symptom resolution.

“Having a better understanding of the appropriate ‘dosing’ and timing of introducing cognitive activity is critically needed for our patients,” explains co-author James MacDonald, MD, MPH, sports medicine physician at Nationwide Children’s. “Increased engagement in the classroom during the first week post-concussion, especially for youth with lower post-concussion symptom scores, can mean symptoms resolve faster and teens get back to normal life.”
The relationship between level of cognitive activity and symptom resolution may be bidirectional, with improving post-concussion symptoms prompting higher levels of cognitive activity and vice versa. Thus, controlling for current symptom levels when assessing associations between cognitive activity and symptom resolution, as this study did, is crucial.
This study has several important clinical implications: Adolescents with concussion, especially those with relatively less severe post-acute symptoms, may benefit from moderate- to high-intensity cognitive activity as early as the first week post-injury. Limiting (but not prohibiting) moderate-intensity activities involving significant screen time (e.g., surfing the internet or video/computer gaming) during the first-week post-injury may help speed recovery. Early introduction of returning to school following concussion is an important consideration that may hasten timelines for recovery.Families should collaborate with their child’s care team to develop a plan based on injury severity and recovery milestones.

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