Category: Neurology

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Human Instruction with AI Guidance Gives the Best Results in Neurosurgical Training

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Study has implications beyond medical education, suggesting other fields could benefit from AI-enhanced training

Artificial intelligence (AI) is becoming a powerful new tool in training and education, including in the field of neurosurgery. Yet a new study suggests that AI tutoring provides better results when paired with human instruction.

Researchers at the Neurosurgical Simulation and Artificial Intelligence Learning Centre at The Neuro (Montreal Neurological Institute-Hospital) of McGill University are studying how AI and virtual reality (VR) can improve the training and performance of brain surgeons. They simulate brain surgeries using VR, monitor students’ performance using AI and provide continuous verbal feedback on how students can improve performance and prevent errors. Previous research has shown that an intelligent tutoring system powered by AI developed at the Centre outperformed expert human teachers, but these instructors were not provided with trainee AI performance data.

In their most recent study, published in JAMA Surgery, the researchers recruited 87 medical students from four Quebec medical schools and divided them into three groups: one trained with AI-only verbal feedback, one with expert instructor feedback, and one with expert feedback informed by real-time AI performance data. The team recorded the students’ performance, including how well and how quickly their surgical skills improved while undergoing the different types of training.

They found that students receiving AI-augmented, personalised feedback from a human instructor outperformed both other groups in surgical performance and skill transfer. This group also demonstrated significantly better risk management for bleeding and tissue injury – two critical measures of surgical expertise. The study suggests that while intelligent tutoring systems can provide standardised, data-driven assessments, the integration of human expertise enhances engagement and ensures that feedback is contextualised and adaptive.

“Our findings underscore the importance of human input in AI-driven surgical education,” said lead study author Bianca Giglio. “When expert instructors used AI performance data to deliver tailored, real-time feedback, trainees learned faster and transferred their skills more effectively.”

While this study was specific to neurosurgical training, its findings could carry over to other professions where students must acquire highly technical and complex skills in high-pressure environments.

“AI is not replacing educators – it’s empowering them,” added senior author Dr Rolando Del Maestro, a neurosurgeon and current Director of the Centre. “By merging AI’s analytical power with the critical guidance of experienced instructors, we are moving closer to creating the ‘Intelligent Operating Room’ of the future capable of assessing and training learners while minimising errors during human surgical procedures.”

Source: McGill University

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Mother’s Microbes Play Role in Neonatal Brain Development

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Photo by Christian Bowen on Unsplash

New research from Michigan State University finds that microbes play an important role in shaping early brain development, specifically in a key brain region that controls stress, social behaviour, and vital body functions.

The study, published in Hormones and Behavior, used a mouse model to highlight how natural microbial exposure not only impacts brain structure immediately after birth but may even begin influencing development while still in the womb. A mouse model was chosen because mice share significant biological and behavioural similarities with humans and there are no other alternatives to study the role of microbes on brain development.

This work is of significance because modern obstetric practices, like peripartum antibiotic use and Cesarean delivery, disrupt maternal microbes. In the United States alone, 40% of women receive antibiotics around childbirth and one-third of all births occur via Cesarean section.

“At birth, a newborn body is colonised by microbes as it travels through the birth canal. Birth also coincides with important developmental events that shape the brain. We wanted to further explore how the arrival of these microbes may affect brain development,” said Alexandra Castillo Ruiz, lead author of the study and assistant professor in the MSU Department of Psychology.

The research team focused on a brain region called the paraventricular nucleus of the hypothalamus (PVN), which plays a central role in regulating stress, blood pressure, water balance, and even social behaviour. Their previous work had shown that mice raised without microbes, or germ-free mice, had more dying neurons in the PVN during early development. The new study set out to determine whether this increased cell death translated to changes in neuron number in the long run, and if any effects could be caused by the arrival of microbes at birth or if they began in the womb via signals from maternal microbes.

To find out, the researchers used a cross-fostering approach. Germ-free newborn mice were placed with mothers that had microbes and compared them to control groups. When the brains of these mice were examined just three days after birth, results were striking: All mice gestated by germ-free mothers had fewer neurons in the PVN, regardless of whether they received microbes after birth. They also found that germ-free adult mice had fewer neurons in the PVN.

“Our study shows that microbes play an important role in sculpting a brain region that is paramount for body functions and social behaviour. In addition, our study indicates that microbial effects start in the womb via signaling from maternal microbes,” said Castillo-Ruiz.

Rather than shunning our microbes, we should recognise them as partners in early life development,” said Castillo-Ruiz. “They’re helping build our brains from the very beginning.”

Source: Michigan State University

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Test Detects Brain Cancers in Cerebrospinal Fluid with High Accuracy

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A novel, multi-analyte test developed by researchers at Johns Hopkins Medicine can accurately identify brain cancers using small samples of cerebrospinal fluid (CSF), offering a promising new tool to guide clinical decision-making.

The findings, supported by funding from the National Institutes of Health, were published in Cancer Discovery and demonstrate that combining multiple biological markers, including tumour-derived DNA and immune cell signatures, is more effective for diagnosing central nervous system cancers than using any one marker alone.

“This study highlights how much more information we can gain when we evaluate several analytes together,” says senior study author Chetan Bettegowda, MD, PhD, Professor and Director of the Department of Neurosurgery at the Johns Hopkins University School of Medicine. “The ability to detect cancers with high specificity and also gain insight into the immune environment of the brain could be an important advance in the care of patients with brain tumours.”

To evaluate the potential of a multi-analyte approach, investigators analysed 206 CSF samples, including samples from patients with high-grade gliomas, medulloblastomas, metastases and central nervous system lymphomas. Their test, called CSF-BAM (cerebrospinal fluid–B/T cell receptor, aneuploidy and mutation), measured chromosomal abnormalities, tumour-specific mutations, and T and B cell receptor sequences. In combination, these markers identified brain cancers with more than 80% sensitivity (ability to detect cancer) and 100% specificity (correctly identified those who were cancer-free) in the validation cohort. The 100% specificity means no false positives were recorded among individuals with noncancerous conditions.

The study also showed that the assay could distinguish between the immune cell populations present in cancer and noncancer cases, offering additional biological context that could be helpful in more-challenging clinical scenarios. Investigators say this ability to categorize T and B cell populations in the CSF provides insights into both disease presence and immune response.

“Many patients with brain lesions face invasive diagnostic procedures to confirm a cancer diagnosis,” says Christopher Douville, MD, assistant professor of oncology and a senior study author. “A tool like this could help us make better-informed decisions about who really needs a biopsy and who doesn’t.”

Researchers say the test could be particularly useful for cases in which conventional imaging or cytology is inconclusive, or in situations when obtaining tissue for diagnosis is risky or not possible. The multi-analyte approach, they say, enables clinicians to better detect cancer and better understand the disease status, supporting a more tailored approach to patient care.

Source: Johns Hopkins Medicine

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Groundbreaking Spinal Scaffold Allows Nerve Fibres to Regrow

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New research combines 3D printing, stem cell biology, and lab-grown tissues for possible treatments of spinal cord injuries. Photo provided by: McAlpine Research Group, University of Minnesota

For the first time, a research team at the University of Minnesota Twin Cities demonstrated a groundbreaking process that combines 3D printing, stem cell biology, and lab-grown tissues for spinal cord injury recovery. 

The study was recently published in Advanced Healthcare Materials. Currently, there is no way to completely reverse the damage and paralysis from the injury. A major challenge is the death of nerve cells and the inability of nerve fibres to regrow across the injury site. This new research tackles this problem head-on.

The method involves creating a unique 3D-printed framework for lab-grown organs, called an organoid scaffold, with microscopic channels. These channels are then populated with regionally specific spinal neural progenitor cells (sNPCs), which are cells derived from human adult stem cells that have the capacity to divide and differentiate into specific types of mature cells.

“We use the 3D printed channels of the scaffold to direct the growth of the stem cells, which ensures the new nerve fibres grow in the desired way,” said Guebum Han, a former University of Minnesota mechanical engineering postdoctoral researcher and first author on the paper who currently works at Intel Corporation. “This method creates a relay system that when placed in the spinal cord bypasses the damaged area.”

n their study, the researchers transplanted these scaffolds into rats with spinal cords that were completely severed. The cells successfully differentiated into neurons and extended their nerve fibres in both directions – rostral (toward the head) and caudal (toward the tail) – to form new connections with the host’s existing nerve circuits. 

The new nerve cells integrated seamlessly into the host spinal cord tissue over time, leading to significant functional recovery in the rats.

“Regenerative medicine has brought about a new era in spinal cord injury research,” said Ann Parr, professor of neurosurgery at the University of Minnesota. “Our laboratory is excited to explore the future potential of our ‘mini spinal cords’ for clinical translation.”

While the research is in its beginning stages, it offers a new avenue of hope for those with spinal cord injuries. The team hopes to scale up production and continue developing this combination of technologies for future clinical applications.

Source: University of Minnesota

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New Research Shows that Macrophages Help Prevent the Development of Neuropathy

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Source: Pixabay CC0

An increase in high-fat, high-fructose foods in people’s diets has contributed to a dramatic increase in type 2 diabetes. This, in turn, has led to an increase in peripheral neuropathy. About half of people with type 2 diabetes are affected, and of these, about half experience severe neuropathic pain.

The damage begins as axons from sensory neurons begin to retract and disappear from the tissues they innervate. New research from the lab of Clifford Woolf, MB, BCh, PhD, director of the F.M. Kirby Neurobiology Center at Boston Children’s Hospital, reveals that months before the damage occurs, immune cells flood into peripheral nerves in an apparent attempt to protect them. This surprising insight, published in Nature, could lead to strategies to prevent peripheral neuropathy or at least minimize and slow the onset of the damage.

Immune cells prevent nerve damage

A team led by Sara Hakim, PhD, a graduate student in the lab, created a mouse model of diabetes induced by a high-fat, high-fructose diet. The model showed that these mice developed all the major features of diabetes within eight to 12 weeks of starting the diet. At about six months, axons in the skin began to degenerate, indicating the presence of neuropathy.

“Diabetic neuropathy takes years, or even decades to develop in humans,” says Hakim, who is now at Vertex. “By using a mouse model in which symptoms slowly develop over months, we were able to catch the progression of the disease over time, and observe those early protective responses when the body is still trying to fight the disease.”

The researchers suspected that peripheral neuropathy is caused by the immune system, so used single-cell sequencing to detect changes in immune cells near sensory neuron axons in peripheral nerves.

One type of immune cell residing in nerves, a pro-inflammatory macrophage, began producing chemokines. These signaling molecules recruited a second population of circulating macrophages, which began infiltrating the nerve 12 weeks after the mice began the diet – as sensory symptoms were starting to appear but before nerve degeneration was seen.

Previously, macrophages were thought to have a pathogenic role in diabetes and were mainly reacting to axon loss. But Hakim, Woolf, and colleagues observed just the opposite.

“To our great surprise, when we blocked infiltration of macrophages into the nerve, neuropathy started getting worse, not better,” says Woolf. “The macrophages were protective. They slowed down the onset of neuropathy and reduced its impact.”

Potential strategies for peripheral neuropathy

The Woolf Lab is now exploring how the infiltrating macrophages protect against peripheral neuropathy. The next step would be to find a way to induce and sustain this protection and identify biomarkers that would flag those people with diabetes who are at risk.

One potential protective strategy might involve accelerating the recruitment of macrophages into nerves; another might involve mimicking their protective function by harnessing compounds they secrete, such as galectin 3.

“Since we could profile the cells and identify what genes they are expressing, we found a number of signalling molecules known to be protective,” says Woolf. “We can now go through that list and check to see which are most active.”

The latest work reinforces the idea that pain isn’t just a disease of neurons, but results from interactions between the nervous system and the immune system. In a study last year, the Woolf Lab discovered thousands of molecular interactions between pain-sensing neurons and different types of immune cells.

Now, the plot is thickening with this example of immune cells acting to prevent painful nerve damage. “We’ve now revealed a novel, slower protective effect of the immune system,” Woolf says.

Source: Boston Children’s Hospital

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Researchers Find TBI Link to Development of Malignant Brain Tumours

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Coup and contrecoup brain injury. Credit: Scientific Animations CC4.0

New research led by investigators at Mass General Brigham suggests a link between a history of traumatic brain injury (TBI) and risk of developing a malignant brain tumour. By evaluating data from 2000–2024 of more than 75 000 people with a history of mild, moderate or severe TBI, the team found the risk of developing a malignant brain tumour was significantly higher compared to people without a history of TBI. The results were published in JAMA Network Open.

“I see these results as alarming,” said co-senior author and corresponding author Saef Izzy, MD, FNCS, FAAN, a neurologist and head of the Immunology of CNS Injury Program at Brigham and Women’s Hospital, a founding member of the Mass General Brigham healthcare system. “Our work over the past five years has shown that TBI is a chronic condition with lasting effects. Now, evidence of a potential increased risk of malignant brain tumours adds urgency to shift the focus from short-term recovery to lifelong vigilance.

“Alongside our earlier findings linking TBI and cardiovascular disease, this underscores the importance of long-term monitoring for anyone with a history of TBI.”

The team divided the severity of TBI between mild, moderate and severe, with participants suffering from incidents ranging from car accidents to falls. In the two categories of moderate and severe, 0.6% of people (87 out of 14 944) developed brain tumours within 3-to-5 years after the TBI, which was a higher percentage than controls. Mild cases of TBI, such as those caused by concussions, were not associated with an increased risk of tumour. The aim of the study was not to establish a cause-and-effect link between moderate-to-severe TBI and malignant tumours, but rather to explore whether an association exists. Determining causality and understanding the underlying mechanisms will require a dedicated translational study in the future.

A previous study showed veterans of the Iraq and Afghanistan wars who suffered TBI experienced an increased risk of brain tumours, but previous studies on civilian populations showed conflicting results. The collaborative team of researchers used an international disease classifying system known as ICD codes to exclude anyone in the study with a history of brain tumour, benign tumours, and risk factors such as radiation exposure.

Previous neurotrauma studies from Mass General Brigham have looked at patients with a history of TBI and found an association with the emergence of anxiety, depression, and other psychiatric, neurological, and cardiovascular diseases, but the current study focuses on malignant tumour development.

Future imaging studies could draw a connection between the location of the TBI and where tumours developed in the brains of participants. The team would like to further study patients with repeated injuries, such as falls. 

“While there is an increased risk of tumour from TBI, the overall risk remains low. Still, brain tumour is a devastating disease and often gets detected in later stages,” said lead author Sandro Marini, MD, a neurologist at Mass General Brigham. “Now, we’ve opened the door to monitor TBI patients more closely.”

Source: Mass General Brigham

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The Neurons Responsible for Day-to-day Blood Glucose Regulation

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Photo by Anna Shvets

The brain controls the release of glucose in a wide range of stressful circumstances, including fasting and low blood sugar levels.

However, less attention has been paid to its role in day-to-day situations.

In a study published in Molecular Metabolism, University of Michigan researchers have shown that a specific population of neurons in the hypothalamus help the brain maintain blood glucose levels under routine circumstances.

Over the past five decades, researchers have shown that dysfunction of the nervous system can lead to fluctuations in blood glucose levels, especially in patients with diabetes.

Some of these neurons are in the ventromedial nucleus of the hypothalamus, a region of the brain that controls hunger, fear, temperature regulation and sexual activity.

“Most studies have shown that this region is involved in raising blood sugar during emergencies,” said Alison Affinati, MD, PhD, assistant professor of internal medicine and member of Caswell Diabetes Institute.

“We wanted to understand whether it is also important in controlling blood sugar during day-to-day activities because that’s when diabetes develops.”

The group focused on VMHCckbr neurons, which contain a protein called the cholecystokinin b receptor.

They used mouse models in which these neurons were inactivated.

By monitoring the blood glucose levels, the researchers found that VMHCckbr neurons play an important role in maintaining glucose during normal activities, including the early part of the fasting period between the last meal of the day and waking up in the morning.

“In the first four hours after you go to bed, these neurons ensure that you have enough glucose so that you don’t become hypoglycaemic overnight,” Affinati said.

To do so, the neurons direct the body to burn fat through a process called lipolysis.

The fats are broken down to produce glycerol, which is used to make sugar.

When the group activated the VMHCckbr neurons in mice, the animals had increased glycerol levels in their bodies.

These findings could explain what happens in patients with prediabetes, since they show an increase in lipolysis during the night.

The researchers believe that in these patients, the VMHCckbr neurons could be overactive, contributing to higher blood sugar.

These nerve cells, however, only controlled lipolysis, which raises the possibility that other cells might be controlling glucose levels through different mechanisms.

“Our studies show that the control of glucose is not an on-or-off switch as previously thought,” Affinati said.

“Different populations of neurons work together, and everything gets turned on in an emergency. However, under routine conditions, it allows for subtle changes.”

The team is working to understand how all the neurons in the ventromedial nucleus co-ordinate their functions to regulate sugar levels during different conditions, including fasting, feeding and stress.

They are also interested in understanding how the brain and nervous system together affect the body’s control of sugar, especially in the liver and pancreas.

Source: University of Michigan

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New Study Upends Decades-old Assumptions About Brain Plasticity

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A new study from Pitt researchers challenges a decades-old assumption in neuroscience by showing that the brain uses distinct transmission sites – not a shared site – to achieve different types of plasticity. The findings, published in Science Advances, offer a deeper understanding of how the brain balances stability with flexibility, a process essential for learning, memory and mental health.

Neurons communicate through a process called synaptic transmission, where one neuron releases chemical messengers called neurotransmitters from a presynaptic terminal. These molecules travel across a microscopic gap called a synaptic cleft and bind to receptors on a neighbouring postsynaptic neuron, triggering a response.

Traditionally, scientists believed spontaneous transmissions (signals that occur randomly) and evoked transmissions (signals triggered by sensory input or experience) originated from one type of canonical synaptic site and relied on shared molecular machinery. Using a mouse model, the research team, led by Oliver Schlüter, associate professor of neuroscience, discovered that the brain instead uses separate synaptic transmission sites to carry out regulation of these two types of activity, each with its own developmental timeline and regulatory rules.

“We focused on the primary visual cortex, where cortical visual processing begins,” said Yue Yang, a research associate in the Department of Neuroscience and first author of the study. “We expected spontaneous and evoked transmissions to follow a similar developmental trajectory, but instead, we found that they diverged after eye opening.”

As the brain began receiving visual input, evoked transmissions continued to strengthen. In contrast, spontaneous transmissions plateaued, suggesting that the brain applies different forms of control to the two signaling modes.

To understand why, the researchers applied a chemical that activates otherwise silent receptors on the postsynaptic side. This caused spontaneous activity to increase, while evoked signals remained unchanged – strong evidence that the two types of transmission operate through functionally distinct synaptic sites.

This division likely enables the brain to maintain consistent background activity through spontaneous signaling while refining behaviourally relevant pathways through evoked activity. This dual system supports both homeostasis and Hebbian plasticity, the experience-dependent process that strengthens neural connections during learning.

“Our findings reveal a key organizational strategy in the brain,” said Yang. “By separating these two signaling modes, the brain can remain stable while still being flexible enough to adapt and learn.”

The implications could be broad. Abnormalities in synaptic signaling have been linked to conditions like autism, Alzheimer’s disease and substance use disorders. A better understanding of how these systems operate in the healthy brain may help researchers identify how they become disrupted in disease.

“Learning how the brain normally separates and regulates different types of signals brings us closer to understanding what might be going wrong in neurological and psychiatric conditions,” Yang said.

Source: University of Pittsburgh

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Discovery Offers Hope for Breathing Recovery After Spinal Cord Injuries

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Innovative research paves way for more effective treatment for ALS and other neurodegenerative diseases

View of the spinal cord. Credit: Scientific Animations CC4.0

Respiratory complications are the most common cause of illness and death for the 300 000 Americans living with spinal cord injury, according to the Christopher & Dana Reeve Foundation.  

But the results of a new study, led by researchers at Case Western Reserve University’s School of Medicine, show promise that a group of nerve cells in the brain and spinal cord, called interneurons, can boost breathing when the body faces certain physiological challenges, such as exercise and environmental conditions associated with altitude.

The researchers believe their discovery could lead to therapeutic treatments for patients with spinal cord injuries who struggle to breathe on their own. Their findings were recently published in the journal Cell Reports.

“While we know the brainstem sets the rhythm for breathing,” said Polyxeni Philippidou, an associate professor in the Department of Neurosciences at Case Western Reserve University School of Medicine and lead researcher, “the exact pathways that increase respiratory motor neuron output, have been unclear – until now.”

The research team included collaborators from the University of St. Andrews in the United Kingdom, the University of Calgary in Canada and the Biomedical Research Foundation Academy of Athens in Greece.

The study

By identifying a subset of interneurons as a new and potentially easy-to-reach point for treatment in spinal cord injuries and breathing-related diseases, the researchers believe doctors may be able to develop therapies to help improve breathing in people with such conditions.

The study showed that blocking signals from these spinal cord cells made it harder for the body to breathe properly when there was too much CO2 in the blood, a condition known as hypercapnia.

“These spinal cord cells are important for helping the body adjust its breathing in response to changes like high CO2 levels,” Philippidou said.

In this study, the team used genetically modified mouse models to explore the pathways involved in breathing. The researchers mapped neuron connections, measured neuron electrical activity, observed the models’ behaviour and used microscopy to visualise neuron structure and function – all focused on spinal cord nerve cells involved in breathing.

“We were able to define the genetic identity, activity patterns and role of a specialized subset of spinal cord neurons involved in controlling breathing,” Philippidou said.

The team is now testing whether targeting these neurons in neurodegenerative diseases like amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, and Alzheimer’s disease can help restore breathing.

Source: Case Western Reserve University

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Brain Study Shows TV and Gaming Boosts Young Adults’ Focus, Social Media Hinders It

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A world-first Swinburne-led study into young adults’ brain activity has found that TV and gaming are associated with increased focus, while social media is associated with decreased focus. 

In this study, published in Nature, 18-25 year olds exposed to phone screens for only three minutes experienced changes in mood, energy, tension, focus and happiness, explains one of the lead researchers Swinburne’s Dr Alexandra Gaillard. 

“Our study was the first to record brain activity during different forms of screen use on young adults using functional near-infrared spectroscopy (fNIRS). We found that different forms of screen use, including social media, are associated with distinct patterns in activity and mood states.” 

“Almost everyone owns a smart phone which they use for at least three hours a day for entertainment. Mood disorders are increasing in prevalence worldwide and we shouldn’t rule out the possibility that phones are a contributor.” 

The study found that oxygenated haemoglobin (HbO) levels increased more following social media use and gaming compared to TV viewing, while deoxygenated haemoglobin (HbR) levels increased more following gaming. 

“These findings suggest that interactive types of entertainment really do get the brain more engaged,” says Dr Gaillard.  

“Interestingly, though, when it came to social media, people reported feeling less focused—and those who felt less focused also showed lower levels of brain activity. On the flip side, gaming actually helped boost focus and showed a rise in deoxygenated haemoglobin, which means the brain was actively using more of the oxygen it was getting. In other words, gaming seemed to get the brain working harder in a good way.” 

With six months to go until Australia’s impending teen social media ban, there are still no clear pathways for age-checking tools and the positive impacts of the policy on different types of technology and platforms.  

Dr Gaillard says that while this study looked at young adults, these findings suggest a similar outcome to teenagers which should be considered by experts when implementing the ban. 

“If this is the effect on a fully developed brain, we urgently need to consider the impacts on teenagers and children who are increasingly using these technologies.” 

The Swinburne research team is calling for further research to understand the complex and nuanced relationship between screen activities and how they engage they brain. 

“Excessive screen time can negatively impact cognitive abilities, attention and executive functioning, but we also know how invaluable they can be in forming connections and a sense of belonging as well as improving educational outcomes.” 

“This isn’t a call for blanket reductions; screens certainly serve a purpose for unwinding and leisure. We ask that young people are conscious of how their activity impacts them and that they make choices that are right for them.” 

Source: Swinburne University