Breakthrough PTSD treatment achieves 68% remission rate in clinical trial

 A new approach to treating post-traumatic stress disorder (PTSD) has received FDA clearance, offering a personalized alternative for people who have not found sufficient relief through existing treatments. Developed by California-based Wave Neuroscience in collaboration with researchers at the Texas A&M Health Institute of Biosciences and Technology, the technology uses brain activity measurements to guide targeted magnetic stimulation.

Early clinical trial findings have been encouraging. According to Wave Neuroscience, patients experienced a 52% reduction in PTSD symptoms, while 68% achieved remission. The full findings are still being prepared for public release, but researchers believe the technology could significantly expand treatment options for millions of people.

The need for more effective PTSD care is substantial. In the United States, approximately 17.5 veterans die by suicide each day, and about 7% of veterans receive a PTSD diagnosis annually.

PTSD can develop after traumatic experiences such as military combat, serious accidents, natural disasters, or violence. An estimated 6% of Americans will experience PTSD during their lifetime, with higher rates among women and veterans.

Why Current PTSD Treatments Are Not Enough

Since PTSD was formally recognized as a diagnosis in 1980, treatment has largely centered on psychotherapy and medications known as selective serotonin reuptake inhibitors (SSRIs), including sertraline and fluoxetine.

Although these approaches can help, many patients continue to experience symptoms despite receiving treatment.

A 2020 review of PTSD medications found that patients reported improvements ranging from 6.8 to 10.1 points on symptom assessments. However, remission rates reached only 10.9% at most.

Wave Neuroscience reported substantially stronger preliminary outcomes in its clinical trial. Erik Won, DO, the company's chief medical officer, described the results as a major advance over previously reported medication outcomes.

“In comparison to that study, our FDA trial reported a 52% reduction in symptoms, so more than a four-fold increase in efficacy,” Won said. “And more importantly, we saw 68% remission in our clinical trial. So, it’s really a quantum change, an inflection point in what we can offer to patients. From a clinical care perspective, that’s really meaningful.”

These findings are promising, although the results come from different studies and should not be interpreted as a direct comparison of treatment effectiveness.

How Personalized Brain Stimulation Works

The newly cleared system uses Magnetic e-Resonance Therapy (MeRT), a technology that combines measurements of brain activity with targeted magnetic stimulation

First, an electroencephalogram (EEG) records the brain's electrical signals. This information helps guide a personalized treatment plan using transcranial magnetic stimulation, or TMS.

During TMS, a coil positioned against the scalp delivers magnetic pulses that stimulate brain activity. The technique has already been used for other psychiatric conditions, including treatment-resistant depression.

What distinguishes MeRT is its use of an AI-assisted algorithm to customize stimulation protocols based on each patient's brain activity rather than relying on a standardized approach.

“Transcranial magnetic stimulation, or TMS, was previously FDA cleared for treatment-resistant depression,” Won said. “By adding an augmented AI derived multivariate algorithm, we were able to personalize protocols that received FDA clearance for post-traumatic stress disorder, which should open up market access to about 13 million people who may be struggling with PTSD.”

Dr. Kenneth S. Ramos, a physician-scientist at Texas A&M Health with extensive experience in precision medicine, helped guide the research.

His work focuses on adapting medical care to the characteristics of individual patients instead of assuming that everyone will respond to the same treatment.

“Most clinical interventions for the treatment of PTSD do not work very well,” Ramos said. “So, this is a huge area where identifying interventions that could hopefully add quality of life to the people impacted by this disorder would be tremendously impactful.”

Wave Neuroscience CEO Fred Walke said Ramos was a natural fit for the project because of his expertise in personalized medicine.

Targeting PTSD With Greater Precision

Conventional TMS generally follows treatment protocols that are less individualized. MeRT builds on the same underlying technology but adjusts treatment according to the patient's specific brain activity.

Ramos emphasized that even small biological differences between people can have major implications for medical care. Humans are approximately 99.9% genetically alike, yet the remaining 0.1% contributes to differences that can influence how individuals respond to treatment.

Source: ScienceDaily

Scientists discover why chronic back pain feels so personal

 For people living with chronic back pain, even a simple movement can trigger a sudden surge of pain. Now, scientists have discovered that these painful episodes activate a surprising part of the brain, one closely connected to our sense of identity and how we think about ourselves.

Researchers at UC San Diego School of Medicine found that movement-triggered pain in people with chronic low back pain (cLBP) activates a brain network that normally becomes less active during ordinary pain. The discovery suggests that persistent back pain may become deeply intertwined with a person's sense of self, potentially helping explain why conventional pain treatments often provide limited relief.

According to the World Health Organization, low back pain is the leading cause of disability worldwide. When pain persists for more than 12 weeks, it is considered chronic. For many patients, everyday movements can provoke sudden flare-ups that make an already difficult condition even harder to manage.

Although the brain plays a central role in how pain is experienced, researchers have struggled to identify the precise brain circuits responsible for pain triggered by movement.

Chronic Back Pain Activates the Brain's Sense of Self

The new study, published on October 5, 2026, in the British Journal of Anaesthesia, identified an unexpected response involving the brain's Default Mode Network (DMN).

Sometimes called the "self network," the DMN consists of interconnected regions in the frontal, parietal, and temporal lobes. These areas are especially active when our attention turns inward, such as when we reflect on personal experiences, think about our identity, or consider our thoughts and emotions. In contrast, the network generally becomes less active when we direct our attention toward something happening around us.

The researchers discovered that sudden back pain caused by movement switched this network on rather than off. This unusual response suggests that chronic pain involves more than the processing of physical sensations. It may also engage the brain systems that shape how people experience themselves.

The findings could help researchers understand why treatments that focus primarily on suppressing pain symptoms do not always work well for chronic low back pain. They also raise the possibility that targeting the DMN could offer a different approach to treatment.

Brain Scans Reveal a Surprising Difference Between Chronic and Acute Pain

To investigate what happens in the brain during a pain flare, the researchers recruited 114 patients with chronic low back pain.

Each participant completed a "leg raise test," a standard clinical procedure used to provoke back pain. During the test, researchers monitored changes in brain blood flow using a specialized functional MRI method called arterial spin labeling. This technique allows scientists to track patterns of brain activity by measuring blood flow without relying on an injected contrast agent.

The team also examined how participants responded to a separate painful stimulus. They applied a harmless but uncomfortable heat sensation to the calf, similar to the brief pain someone might experience when accidentally touching a hot stove.

Comparing these two situations revealed a striking difference.

When movement triggered a flare of chronic back pain, the DMN became more active. However, when participants experienced the painful heat stimulus, the same network became less active, following the brain's typical response to acute pain.

The researchers also identified several other important patterns:

• Patients with more severe chronic back pain showed stronger connections between the DMN and the primary somatosensory cortex, a brain region responsible for processing physical sensations, including signals from the back.
• Greater pain intensity during the leg raise test was associated with increased activity in brain regions involved in sensation and movement.
• Increases in heart rate during the test reliably reflected the intensity of the pain flare.

Together, these findings provide new evidence that chronic pain flares involve brain processes associated with personal identity, not just the physical experience of pain.

Why the Brain Reacts Differently to Chronic Pain

During ordinary acute pain, the brain generally reduces activity in the DMN so it can concentrate on the immediate source of danger. This response helps shift attention away from internal thoughts and toward an external threat.

But the UC San Diego researchers found that movement triggered chronic back pain produced the opposite effect.

"In every pain study, when you're experiencing pain, the DMN deactivates," said corresponding author Fadel Zeidan, PhD, professor in the Department of Anesthesiology, endowed professor at the Sanford Institute for Empathy and Compassion, and director of the Pain Health and Mindfulness Laboratory at UC San Diego School of Medicine. "What we show for the first time ever is that when you have a pain flare, it turns on instead. You start to identify the experience with who you are."

Source: ScienceDaily

Magic mushrooms rewire the brain in a way scientists didn't expect

 A new study from the University of California, Santa Cruz, has revealed how psilocybin, the psychedelic substance found in "magic mushrooms," changes the brain by reorganizing connections between nerve cells. The findings could eventually help scientists develop treatments for mental health conditions that capture some of psilocybin's potential benefits without producing hallucinations.

The research, published October 15 in Nature Neuroscience, found that psilocybin rapidly encourages brain cells to form new connections and helps those connections mature. At the same time, it promotes the removal of certain older connections, suggesting that its effects involve more than simply increasing communication between neurons.

Experiments in mice also revealed something especially intriguing. The researchers were able to separate the cellular changes responsible for this rewiring from a behavioral response commonly associated with psychedelic effects. This suggests that some of psilocybin's effects on brain structure may be achievable without the hallucinations typically associated with the drug.

The discovery could provide a foundation for developing medications that enhance the brain's ability to adapt and reorganize itself, a property known as neuroplasticity. Such treatments might eventually offer new approaches for depression, post-traumatic stress disorder (PTSD), and other psychiatric conditions.

The team also identified a particular group of neurons in the cerebral cortex that plays an essential role in psilocybin's effects on brain connections. Importantly, the researchers discovered that the drug does not affect every brain in the same way. Its influence depends partly on whether the brain has previously experienced chronic stress.

"I consider this work a major advance, particularly in our understanding of how psilocybin reshapes neural circuits and its potential implications for treating mental disorders," said senior author Yi Zuo, professor of molecular, cell, and developmental biology at UC Santa Cruz.

Why Scientists Are Taking a New Look at Psychedelics

Scientific interest in psychedelic drugs has changed dramatically over the past century. During the middle of the 20th century, substances such as psilocybin and LSD attracted attention from Western researchers because of their powerful effects on perception, consciousness, and mood.

Early studies suggested these compounds might have applications in psychiatric treatment. However, scientific investigations slowed substantially after the United States passed the Controlled Substances Act in 1970, which imposed strict restrictions on these substances.

In recent years, researchers have renewed their interest in psychedelics, particularly their ability to produce rapid and potentially lasting changes in brain function.

Scientists sometimes describe these compounds as "psychoplastogens" because they can stimulate neuroplasticity after a single dose. Neuroplasticity refers to the brain's capacity to change its structure and activity by forming, strengthening, reorganizing, or removing connections between neurons.

This property is particularly interesting for mental health treatment because conditions such as depression can involve disruptions in the circuits responsible for regulating mood, emotions, and behavior.

The U.S. Food and Drug Administration (FDA) has previously recognized the therapeutic potential of psychedelic research by granting Breakthrough Therapy designations to substances including psilocybin and MDMA. These designations are intended to accelerate the development and review of promising treatments for serious medical conditions.

In September 2026, the FDA took another step toward evaluating psychedelic treatments by organizing a public hearing titled "Considerations for Potential Future Therapeutic Use of Psychedelic Drugs."

Experts discussed how healthcare professionals administering psychedelic treatments should be qualified, how potential risks could be managed through Risk Evaluation and Mitigation Strategy (REMS) programs, and how future clinical trials should be designed.

As regulators examine ways psychedelic treatments might eventually become part of mainstream healthcare, researchers are increasingly focused on understanding exactly what these substances do to the brain. Identifying the cellular mechanisms behind their effects could help scientists develop treatments that are both effective and safer to administer.

Watching Psilocybin Rewire the Brain

To investigate how psilocybin changes brain structure, the UC Santa Cruz team used an advanced imaging method called two-photon microscopy.

This technology allows scientists to observe extremely small structures inside living tissue with remarkable detail. Using it, the researchers followed individual connections on neurons in living mice over several weeks, allowing them to see how those structures changed after psilocybin treatment.

Source: ScienceDaily

Scientists find surprisingly little evidence that medical cannabis helps you sleep

 A major new scientific review is raising questions about whether medical cannabis actually helps people with insomnia. Despite growing interest in cannabis as a sleep treatment, researchers found that the available evidence is too weak to reliably determine whether it improves sleep quality, sleep duration, or how well people function during the day.

Insomnia affects millions of people and can make it difficult to fall asleep, remain asleep throughout the night, or wake up feeling rested. Beyond the frustration of sleepless nights, the condition can seriously disrupt daily life and increase the likelihood of developing anxiety or depression.A major new scientific review is raising questions about whether medical cannabis actually helps people with insomnia. Despite growing interest in cannabis as a sleep treatment, researchers found that the available evidence is too weak to reliably determine whether it improves sleep quality, sleep duration, or how well people function during the day.

Insomnia affects millions of people and can make it difficult to fall asleep, remain asleep throughout the night, or wake up feeling rested. Beyond the frustration of sleepless nights, the condition can seriously disrupt daily life and increase the likelihood of developing anxiety or depression.

Treatments for insomnia include cognitive behavioral therapy, which helps people change thoughts and habits that interfere with sleep, as well as medications such as antidepressants and antipsychotics. However, these approaches do not work equally well for everyone, fueling interest in alternative options.

Medical cannabis has attracted particular attention because of its potential to improve sleep. Unlike recreational cannabis, regulated medical products typically contain carefully measured amounts of THC and CBD, two compounds found in cannabis, and are administered as tablets, sprays, or oils. Despite its growing popularity, scientists have continued to debate whether cannabis offers meaningful benefits for people with insomnia.

Major Review Finds Little Evidence of Sleep Benefits

To investigate, researchers from The Cochrane Associate Centre at the Universidad Hospital Italiano de Buenos Aires and the University of Manitoba examined nine clinical studies involving 537 adults between the ages of 18 and 76 who were receiving treatment for insomnia.

Most of the studies involved people with primary insomnia, meaning their sleep problems were not attributed to another medical condition. Eight trials compared regulated medical cannabis with a placebo, an inactive treatment used to measure whether a therapy produces genuine benefits. The remaining trial compared cannabis with amitriptyline, an antidepressant that is sometimes used to treat sleep problems.

Across the placebo comparisons, medical cannabis produced little or no clinically meaningful improvement in sleep quality, satisfaction with sleep, total hours slept, or daytime functioning.

The researchers also identified potential drawbacks. Participants who received medical cannabis were substantially more likely to experience mild side effects, including dizziness and dry mouth, than those given a placebo. However, this finding came from a relatively small number of studies, limiting confidence in the result.

There was some indication that medical cannabis might improve overall quality of life. Yet the evidence supporting this possibility was highly uncertain. When the findings were combined, the results were consistent with outcomes ranging from a slight decline in quality of life to a substantial improvement.

"The main message is that the research currently available is not sufficient to reliably answer whether medical cannabis helps people with insomnia," says Dr. Lucia Varela, lead author of the study from the University of Manitoba, Canada. "This does not mean that medical cannabis is ineffective. It means that, based on the evidence we have, we cannot draw reliable conclusions about its effectiveness for insomnia in the general population."

Why Scientists Remain Uncertain About Cannabis and Insomnia

One of the biggest problems was the quality of the research itself. The reviewers rated their confidence in the available evidence as low or very low, citing small study populations, conflicting findings, and potential bias in how the trials were conducted.

Another challenge was the lack of consistency between studies. Researchers tested different medical cannabis products, making it difficult to directly compare their results or determine whether particular formulations might work better than others.

The studies were also relatively short. The longest followed participants for just 12 weeks, leaving major unanswered questions about whether medical cannabis could provide lasting sleep benefits or produce additional effects with prolonged use.

More Research Is Needed Before Cannabis Can Be Recommended

The researchers also cautioned that the study participants did not adequately represent the broader population of people living with insomnia.

Women accounted for nearly three-quarters (72.66% of participants), and the research was heavily weighted toward younger adults. As a result, it remains unclear whether the findings would apply equally to men, older individuals, or people whose insomnia occurs alongside other medical conditions.

Taken together, these limitations mean that the existing research cannot establish whether medical cannabis is an effective insomnia treatment. The authors emphasize that larger, more rigorous clinical trials are needed before it can be confidently recommended for improving sleep."The main message is that the research currently available is not sufficient to reliably answer whether medical cannabis helps people with insomnia," says Dr. Lucia Varela, lead author of the study from the University of Manitoba, Canada. "This does not mean that medical cannabis is ineffective. It means that, based on the evidence we have, we cannot draw reliable conclusions about its effectiveness for insomnia in the general population."

Why Scientists Remain Uncertain About Cannabis and Insomnia

One of the biggest problems was the quality of the research itself. The reviewers rated their confidence in the available evidence as low or very low, citing small study populations, conflicting findings, and potential bias in how the trials were conducted.

Another challenge was the lack of consistency between studies. Researchers tested different medical cannabis products, making it difficult to directly compare their results or determine whether particular formulations might work better than others.

The studies were also relatively short. The longest followed participants for just 12 weeks, leaving major unanswered questions about whether medical cannabis could provide lasting sleep benefits or produce additional effects with prolonged use.

More Research Is Needed Before Cannabis Can Be Recommended

The researchers also cautioned that the study participants did not adequately represent the broader population of people living with insomnia.

Women accounted for nearly three-quarters (72.66% of participants), and the research was heavily weighted toward younger adults. As a result, it remains unclear whether the findings would apply equally to men, older individuals, or people whose insomnia occurs alongside other medical conditions.

Taken together, these limitations mean that the existing research cannot establish whether medical cannabis is an effective insomnia treatment. The authors emphasize that larger, more rigorous clinical trials are needed before it can be confidently recommended for improving sleep.

Source: ScienceDaily

Six popular sugar substitutes linked to faster brain aging

 Sugar substitutes are often promoted as a healthier way to enjoy sweet foods and drinks without consuming as much sugar. However, new research suggests that some of these widely used sweeteners may have an unexpected downside for long-term brain health.

A study published in Neurology, the medical journal of the American Academy of Neurology, found that people who consumed the most low- and no-calorie sweeteners experienced significantly faster declines in memory and thinking skills than those who consumed the least. The association was particularly pronounced among people with diabetes.

Researchers examined seven sweeteners commonly used in foods and beverages: aspartame, saccharin, acesulfame-K, erythritol, xylitol, sorbitol and tagatose. These ingredients frequently appear in ultra-processed products, including diet sodas, flavored waters, energy drinks, yogurt and low-calorie desserts. Some are also sold separately for sweetening foods and beverages.

"Low- and no-calorie sweeteners are often seen as a healthy alternative to sugar; however, our findings suggest certain sweeteners may have negative effects on brain health over time," said study author Claudia Kimie Suemoto, MD, PhD, of the University of São Paulo in Brazil.

Importantly, the findings show an association rather than a proven cause-and-effect relationship. Researchers cannot conclude from this study that consuming these sweeteners directly damages the brain or causes memory loss.

Study Tracks Nearly 13,000 Adults for Eight Years

To investigate whether sugar substitutes might be connected to cognitive health, researchers analyzed data from 12,772 adults across Brazil. Participants were 52 years old on average when the study began and were followed for approximately eight years.

At the beginning of the study, participants completed detailed dietary questionnaires describing the foods and drinks they had consumed during the previous year. Researchers used these responses to estimate each person's daily intake of the seven sweeteners.

Participants were then separated into three groups according to how much of the sweeteners they consumed. Those in the lowest consumption group averaged 20 milligrams per day (mg/day), while those in the highest group averaged 191 mg/day. For comparison, 191 milligrams of aspartame is roughly the amount found in one can of diet soda.

Of the seven sweeteners examined, sorbitol had the highest average intake, at 64 mg/day. Sorbitol belongs to a category of sweeteners called sugar alcohols, which provide sweetness and are commonly used as sugar substitutes.

Throughout the study, participants completed cognitive assessments at three points: the beginning, middle, and end. These tests measured several abilities essential for everyday mental functioning, including memory, language, and the speed at which the brain processes information.

Researchers evaluated verbal fluency, or the ability to quickly retrieve and produce words, along with working memory, which allows people to temporarily hold and use information. They also tested word recall and processing speed to determine how these abilities changed over time.

High Sweetener Consumption Linked to 62% Faster Cognitive Decline

The results revealed a striking difference between people who consumed the most sweeteners and those who consumed the least.

After accounting for factors that could influence cognitive health, including age, sex, high blood pressure, and cardiovascular disease, researchers found that participants in the highest consumption group experienced a 62% faster decline in overall thinking and memory abilities compared with those in the lowest group.

That difference was equivalent to approximately 1.6 additional years of cognitive aging over the study period.

Even moderate consumption was associated with measurable differences. Participants in the middle group experienced a 35% faster decline than those consuming the least, equivalent to roughly 1.3 additional years of cognitive aging.

These estimates describe changes in cognitive test performance rather than a direct measurement of biological brain aging. They also do not mean that everyone who consumes artificial sweeteners will experience memory problems.

Stronger Links Found in Adults Under 60 and People With Diabetes

When researchers examined different age groups, they discovered that the association was not consistent across all participants.

Among adults younger than 60, higher sweetener consumption was linked to faster declines in verbal fluency and overall cognitive performance. However, researchers did not find a similar association among participants older than 60.

The relationship was also stronger in people with diabetes than in those without the condition. This finding is especially relevant because people with diabetes frequently turn to sugar substitutes to help manage their sugar intake.

Examining the sweeteners individually revealed another important distinction. Six of the seven substances were associated with faster declines in overall cognitive performance, particularly memory.

Those six were aspartame, saccharin, acesulfame-K, erythritol, sorbitol and xylitol.

Tagatose was the exception. Researchers found no association between its consumption and cognitive decline in this study. However, that finding does not establish that tagatose protects the brain or is necessarily safer than other sweeteners.

Should People Rethink Artificial Sweeteners?

The findings raise important questions about whether replacing sugar with low-calorie alternatives always delivers the health benefits consumers expect, particularly when it comes to the brain.

"While we found links to cognitive decline for middle-aged people both with and without diabetes, people with diabetes are more likely to use artificial sweeteners as sugar substitutes," Suemoto said. "More research is needed to confirm our findings and to investigate if other refined sugar alternatives, such as applesauce, honey, maple syrup or coconut sugar, may be effective alternatives."

Researchers also acknowledged several limitations. The analysis did not cover every artificial sweetener available on the market, so the findings cannot necessarily be applied to all sugar substitutes.

In addition, dietary information came from participants' own recollections of what they had eaten and drunk. Because people may forget foods, underestimate portions, or inaccurately report their habits, these estimates may not perfectly reflect actual sweetener consumption.

The observational design also means that other factors could help explain the relationship between sweetener intake and cognitive decline, despite researchers' efforts to account for several important health differences.

Further studies will be needed to determine whether the sweeteners themselves contribute to changes in brain function, why certain groups appear more strongly affected, and whether different sugar alternatives produce different long-term outcomes.

Source: ScienceDaily

A single brain signal may explain schizophrenia's most puzzling symptoms

 Scientists have identified a brain signal that may help explain why schizophrenia produces such a wide variety of symptoms, including difficulties with perception, movement, and speech. The discovery suggests that problems that appear unrelated could actually stem from a shared disruption in how the brain processes information.

Schizophrenia is a complex psychiatric disorder that can affect how people experience the world, interact with their surroundings, and communicate with others. These symptoms are typically studied as separate features of the condition, but new research suggests they may have more in common than previously recognized.

The study, published in Science Advances, was conducted by scientists from McGill University, the McConnell Brain Imaging Centre, the University of Montreal, the Research Centre of the University of Montreal Health Centre, and the Douglas Research Centre. Their findings point to a common brain mechanism that may help explain several distinct symptoms of schizophrenia.

A Weakened Brain Signal Links Multiple Schizophrenia Symptoms

To investigate this connection, researchers examined beta-band brain activity in 25 people diagnosed with schizophrenia and 25 healthy participants. Beta-band activity refers to rhythmic patterns of electrical activity in the brain that are involved in coordinating information processing, perception, and movement.

Participants completed tasks designed to test how accurately they could judge the timing of visual and auditory information. The researchers also analyzed their speech to look for signs of disorganized thinking and communication.

The results revealed a striking pattern. People with schizophrenia showed weaker and slower beta-band activity than those in the control group. More importantly, the participants with the most pronounced abnormalities in this brain signal also tended to have greater difficulty processing the timing of sights and sounds, more disorganized speech, and more severe clinical symptoms.

These three features of schizophrenia are usually investigated independently. Finding that they were all associated with changes in the same brain signal suggests that a shared underlying process may contribute to the disorder's diverse effects.

A New Window Into How the Brain Processes Reality

"This gives us early but compelling evidence that measuring the brain's operations, especially how it builds and revises its own model of the world, may help us appreciate that there is a common thread behind the confusing array of symptoms we see in disorders like schizophrenia," said Dr. Lena Palaniyappan, senior author of the study, Professor of Psychiatry at McGill and director of the Centre of Excellence in Youth Mental Health at the Douglas Hospital.

The brain constantly uses incoming sensory information to develop and update its understanding of the surrounding environment. This process helps people interpret what they see and hear, anticipate events, and coordinate their actions. The new findings suggest that disruptions in this process could help explain why schizophrenia affects several different aspects of behavior and perception.

The researchers used high-resolution magnetoencephalography, or MEG, to measure brain activity. This imaging technique detects the tiny magnetic fields generated by electrical activity in the brain, allowing scientists to track changes in neural signals with exceptional precision. The scans were performed at the McConnell Brain Imaging Centre at the Montreal Neurological Institute-Hospital (The Neuro).

"What struck us was that the same weakened brain signal kept showing up wherever we looked, whether patients were processing a sound, a sight or completing a movement," said Hsi (Tiana) Wei, lead author of the study and postdoctoral scholar in McGill's Department of Psychiatry and the Douglas Research Centre. "Seeing the same pattern across these different domains suggested there may be a common underlying process linking the symptoms."

Could the Discovery Help Detect Psychosis Earlier?

Beyond providing new insight into schizophrenia, the findings could eventually help researchers identify young people who are at greater risk of developing psychosis. Psychosis involves a disruption in how someone perceives or interprets reality and can include experiences such as hallucinations or delusions.

Early identification is particularly important because the first signs of schizophrenia often appear during adolescence but may go unrecognized for an extended period.

"The very first sign of schizophrenia begins in our adolescence, but this often gets missed for a long time. If this finding is confirmed in larger samples, we may have a potentially useful method to identify who, among youth seeking help for mental health, needs extra support to prevent psychosis," Palaniyappan said.

However, the researchers emphasized that the results are preliminary. The study included only 50 participants, and additional research involving larger, independent groups will be necessary to determine how reliably the brain signal is associated with speech disturbances and overall symptom severity.

"This is a first, modest-size study, and the associations with speech and clinical severity will need to be tested in larger independent samples before we can be confident in them," Wei said.

If future studies confirm the findings, measuring beta-band activity could potentially become a useful tool for identifying people who need earlier support. Wei also suggested that the brain signal may deserve investigation as a possible target for future schizophrenia treatments.

Source: ScienceDaily

Scientists discover why chronic back pain feels so personal

 For people living with chronic back pain, even a simple movement can trigger a sudden surge of pain. Now, scientists have discovered that these painful episodes activate a surprising part of the brain, one closely connected to our sense of identity and how we think about ourselves.

Researchers at UC San Diego School of Medicine found that movement-triggered pain in people with chronic low back pain (cLBP) activates a brain network that normally becomes less active during ordinary pain. The discovery suggests that persistent back pain may become deeply intertwined with a person's sense of self, potentially helping explain why conventional pain treatments often provide limited relief.

According to the World Health Organization, low back pain is the leading cause of disability worldwide. When pain persists for more than 12 weeks, it is considered chronic. For many patients, everyday movements can provoke sudden flare-ups that make an already difficult condition even harder to manage.

Although the brain plays a central role in how pain is experienced, researchers have struggled to identify the precise brain circuits responsible for pain triggered by movement.

Chronic Back Pain Activates the Brain's Sense of Self

The new study, published on October 5, 2026, in the British Journal of Anaesthesia, identified an unexpected response involving the brain's Default Mode Network (DMN).

Sometimes called the "self network," the DMN consists of interconnected regions in the frontal, parietal, and temporal lobes. These areas are especially active when our attention turns inward, such as when we reflect on personal experiences, think about our identity, or consider our thoughts and emotions. In contrast, the network generally becomes less active when we direct our attention toward something happening around us.

The researchers discovered that sudden back pain caused by movement switched this network on rather than off. This unusual response suggests that chronic pain involves more than the processing of physical sensations. It may also engage the brain systems that shape how people experience themselves.

The findings could help researchers understand why treatments that focus primarily on suppressing pain symptoms do not always work well for chronic low back pain. They also raise the possibility that targeting the DMN could offer a different approach to treatment.

Brain Scans Reveal a Surprising Difference Between Chronic and Acute Pain

To investigate what happens in the brain during a pain flare, the researchers recruited 114 patients with chronic low back pain.

Each participant completed a "leg raise test," a standard clinical procedure used to provoke back pain. During the test, researchers monitored changes in brain blood flow using a specialized functional MRI method called arterial spin labeling. This technique allows scientists to track patterns of brain activity by measuring blood flow without relying on an injected contrast agent.

The team also examined how participants responded to a separate painful stimulus. They applied a harmless but uncomfortable heat sensation to the calf, similar to the brief pain someone might experience when accidentally touching a hot stove.

Comparing these two situations revealed a striking difference.

When movement triggered a flare of chronic back pain, the DMN became more active. However, when participants experienced the painful heat stimulus, the same network became less active, following the brain's typical response to acute pain.

The researchers also identified several other important patterns:

• Patients with more severe chronic back pain showed stronger connections between the DMN and the primary somatosensory cortex, a brain region responsible for processing physical sensations, including signals from the back.
• Greater pain intensity during the leg raise test was associated with increased activity in brain regions involved in sensation and movement.
• Increases in heart rate during the test reliably reflected the intensity of the pain flare.

Together, these findings provide new evidence that chronic pain flares involve brain processes associated with personal identity, not just the physical experience of pain.

Why the Brain Reacts Differently to Chronic Pain

During ordinary acute pain, the brain generally reduces activity in the DMN so it can concentrate on the immediate source of danger. This response helps shift attention away from internal thoughts and toward an external threat.

But the UC San Diego researchers found that movement triggered chronic back pain produced the opposite effect.

"In every pain study, when you're experiencing pain, the DMN deactivates," said corresponding author Fadel Zeidan, PhD, professor in the Department of Anesthesiology, endowed professor at the Sanford Institute for Empathy and Compassion, and director of the Pain Health and Mindfulness Laboratory at UC San Diego School of Medicine. "What we show for the first time ever is that when you have a pain flare, it turns on instead. You start to identify the experience with who you are."

Source: ScienceDaily