Category: Neurology

Categories : NeurologyTags :

Chronic Sinusitis Linked to Neural Functions

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A small proof-of-concept study found that sinonasal inflammation was associated with neural changes that could precede cognitive symptoms in young people.

In comparison to healthy controls, people with chronic rhinosinusitis showed decreased functional connectivity within the frontoparietal network, a major cognition modulating hub, in resting-state functional MRI imaging. The frontoparietal network allows individuals to coordinate behaviour in a rapid, accurate, and flexible goal-driven manner.

These individuals also had greater connectivity of this region to the default mode network (areas that are activated during introspective and self-referential processing) and decreased connectivity to the salience network (areas involved in detection and response to stimuli) on brain imaging, reported Aria Jafari, MD, of University of Washington in Seattle, and colleagues.

Compared to controls, individuals with more severe rhinosinusitis inflammation tended to have greater differences in functional connectivity, Dr Jafari and colleagues stated. 

“Although definitive conclusions are not possible given the limitations inherent in the data set, including lack of rhinosinusitis-specific clinical information, our results present initial evidence for functional connectivity alterations as a potential basis for cognitive impairments seen in patients affected by chronic rhinosinusitis and may help direct future research,” Dr Jafari and colleagues said.

However, in this study, no cognitive deficits accompanied the functional connectivity changes. People with chronic rhinosinusitis and their matched controls shared similar cognitive status and similar sleep quality, with no between-group differences in olfaction, taste, and pain, either.

It was suggested by the researchers that, “given the brain’s ability to adapt and compensate, particularly in young and cognitively healthy individuals, our findings may represent early and subclinical functional brain alterations that may precede or be more sensitive than anticipated behavioral responses.”

“It is possible that a clinical chronic rhinosinusitis cohort with broader age distribution and more significant symptoms may have even greater changes in functional brain connectivity in the regions identified in this study,” they added.

“Overall, I do think that this study gives credence to the large body of evidence that patients with chronic rhinosinusitis, or in this case sinonasal inflammation, do have issues with cognition,” commented Nicholas Rowan, MD, of Johns Hopkins University School of Medicine in Baltimore, who was not part of the study.

Sinonasal inflammation and chronic rhinosinusitis have well established negative impacts on quality of life, according to Rowan. Previous research has found that medical or surgical intervention for chronic rhinosinusitis can alleviate cognitive dysfunction.

“Though unfortunately, the findings here are not actionable from a clinical standpoint, they do provide novel information for further prospective study of patients with chronic rhinosinusitis, as well as laboratory studies that are aimed to better understand the mechanism of why patients with CRS have such substantial quality of life implications,” according to Dr Rowan.

Although comorbid psychiatric disorders and sleep dysfunction are among the proposed mechanisms for cognitive dysfunction, the researchers said their data was supportive of a direct association of immune molecules with brain function.

Using data from The Human Connectome Project, the case-control study included 22 people with radiologic sinonasal inflammation who were matched 1:1 by age and sex to healthy controls. Sinonasal inflammation was classified as moderate in 13 people and severe in nine.

All were young adults age 22 to 35, and 68% were male.

Limitations included the retrospective nature of the study and the small sample size. Since cognitively normal participants identified radiographically from a large database, this limited the generalisability of the results, the authors added.

“Future prospective studies are warranted to determine the applicability of these findings to a clinical chronic rhinosinusitis population,” they said.

Source: MedPage Today

Journal information: Jafari A, et al “Association of sinonasal inflammation with functional brain connectivity” JAMA Otolaryngal Head Neck Surg 2021; DOI: 10.1001/jamaoto.2021.0204.

Categories : Injury & Trauma NeurologyTags :

Brain Glue Heals Neural Damage from Brain Injuries

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In a new study, researchers at the University of Georgia’s (UGA) Regenerative Biosciences Center have shown that the “brain glue” they developed protects against loss of brain tissue after a severe injury, and may also help in functional neural repair.

Significant traumatic brain injury (TBI) commonly results in extensive tissue loss and long-term disability, with no clinical treatments available to prevent this.

The new finding is the first to provide visual and functional evidence of the repair of brain neural circuits involved in reach-to-grasp movement in brain glue-implanted animals following severe TBI.

“Our work provides a holistic view of what’s going on in the recovery of the damaged region while the animal is accomplishing a specific reach-and-grasp task,” said lead investigator Lohitash Karumbaiah, an associate professor in the University of Georgia’s College of Agricultural and Environmental Sciences.

The brain glue developed by Prof Karumbaiah was designed to mimic the meshwork of sugars supporting brain cells. The hydrogel contains key structures that bind to two protective protein factors that can enhance the survival and regrowth of brain cells after severe TBI: basic fibroblast growth factor and brain-derived neurotrophic factor.

In previous research, Prof Karumbaiah and his team demonstrated that the brain glue conferred significant protection to brain tissue from severe TBI damage. In order to tap the neuroprotective capability of the original, they changed the delivery surface of protective factors to help accelerate the regeneration and functional activity of brain cells.

“Animal subjects that were implanted with the brain glue actually showed repair of severely damaged tissue of the brain,” said Karumbaiah. “The animals also elicited a quicker recovery time compared to subjects without these materials.”

The team used a tissue-cleaning method to make the brain less opaque, allowing them to 3-D image the cells’ response in the reach-to-grasp circuit, which is similar in rats and humans.

“Because of the tissue-clearing method, we were able to obtain a deeper view of the complex circuitry and recovery supported by brain glue,” said Prof Karumbaiah. “Using these methods along with conventional electrophysiological recordings, we were able to validate that brain glue supported the regeneration of functional neurons in the lesion cavity.”

“Doing the behavioral studies, the animal work and the molecular work sometimes takes a village,” said Karumbaiah. “This research involved a whole cross-section of RBC undergraduate and graduate students, as well as faculty members from both UGA and Duke University.”

Source: Medical Xpress

Journal information: Charles-Francois V. Latchoumane et al. Engineered glycomaterial implants orchestrate large-scale functional repair of brain tissue chronically after severe traumatic brain injury, Science Advances (2021). DOI: 10.1126/sciadv.abe0207

Categories : NeurologyTags :

Study Reveals More Secrets of Leptin’s Role in Appetite Control

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A new study describes how leptin, an appetite-suppressing hormone released from adipose tissue, is involved in appetite suppression through the dopamine pathway.  

Since the discovery of leptin in the 1990s, many questions still remain over how it suppresses appetite. Now, a new study in mice describes novel neurocircuitry between midbrain structures that control feeding behaviours under the modulatory control of leptin.

Leptin links the body and the brain, providing information about its metabolic state and influencing energy balance. Animals deficient for leptin rapidly become obese without its regulatory control of feeding behaviour, showing just how important it is.

“This process is shaped by communication between bodily fat storages (via a hormone called leptin) and the brain’s dopamine reward system. This leptin-dopamine axis is critically important for body weight control, but its modes of action were not well understood,” said Roger Adan, PhD, Department of Translational Neuroscience, University Medical Centre Utrecht.

Not only does leptin suppress eating through signals to brain regions controlling eating behaviours, but it also lowers food’s reward value in the brain’s dopamine (DA) reward system. That food-reward pathway was known to involve dopaminergic neurons of the ventral tegmental area (VTA) signaling to the nucleus accumbens (NAc). However, these DA neurons do not have receptors for leptin.

The researchers mapped the new microcircuitry with a combination of technologies, including optogenetics, chemogenetics and electrophysiology.

“Although leptin receptors are present on [some] dopamine neurons that signal food reward, we discovered that leptin receptors are also present on inhibitory neurons that more strongly regulate the activity of dopamine neurons. Some of these inhibitory neurons suppressed food seeking when [animals were] hungry, whereas others [did so] only when [animals were] in a sated state,” said Professor Adan, also of the Department of Translational Neuroscience, University Medical Center Utrecht and University Utrecht.

John Krystal, MD, Editor of Biological Psychiatry, said of the study, “It turns out that leptin plays key modulatory roles in an elegant circuit that unites midbrain and limbic reward circuitry. By inhibiting hypothalamic neurons and ultimately suppressing the activity of dopamine neurons in the midbrain that signal reward and promote feeding, leptin reduces food intake in animals under conditions when caloric intake has exceeded energy use.”

Professor Adan concluded that, “Targeting these neurons may provide a new avenue for the treatment of anorexia nervosa and to support dieting in people with obesity.”

Source: News-Medical.Net

Journal information: Omrani, A., et al. (2021) Identification of novel neurocircuitry through which leptin targets multiple inputs to the dopamine system to reduce food reward seeking. Biological Psychiatry. doi.org/10.1016/j.biopsych.2021.02.017.

Categories : NeurologyTags :

Shared Neural System May Be Used for Different Memory Stores

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The brain may have a shared neural system that is involved in the retrieval of facts and personal memories used in everyday life, new research has found.

Factual memory had long been categorised into two stores; factual memory and memory of personal experiences. These two repositories in concert enable people to make sense of the world around them. Individuals with retrograde amnesia can fail to remember personal experiences, but still recall factual knowledge. These two stores have been shown by decades of clinical and experimental research to be stored across two separate regions of the brain.

But the new study suggests that a shared set of brain regions play an important role in controlling the successful retrieval of weak memories.

When participants were asked to retrieve fact memories and personal memories, researchers used functional MRI imaging to study how these regions changed in activity levels.

Lead researcher Dr Deniz Vatansever, formerly of the University of York and now working for the Institute of Science and Technology for Brain-inspired Intelligence, Fudan University said: “The new research suggests that despite their functional differences, successfully retrieving weak information from these two memory systems might be dependent upon a shared brain mechanism.

“Our memories allow us to make sense and flexibly interact with the world around us. Although in most cases, our strongly encoded memories might be sufficient for the task at hand, remembering to pack a beach towel for an upcoming seaside holiday, this strong memory may be irrelevant in other instances, such as when packing for a business trip. As such, we need to tightly control the retrieval of relevant memories to solve different tasks under different circumstances. Our results indicate that this control process might be shared across both factual and personal memory types.”

The researchers said their findings may be applicable to memory disorders, including dementia, where patients’ quality of life is affected by being unable to remember important information. The findings could also be relevant in the development of a new generation of AI, which use long-term memory in solving computational problems. 

“In order to generate appropriate thoughts and behaviors, we have to draw on our memory stores in a highly flexible way,” said senior author Elizabeth Jefferies, and professor, Department of Psychology, University of York. “This new study highlights control processes within the brain that allow us to focus on unusual aspects of the meanings of words and to retrieve weakly encoded personal experiences. This control over memory allows us to be creative and to adapt as our goals or circumstances change.”

Source: News-Medical.Net

Journal information: Vatansever, D., et al. (2021) Varying demands for cognitive control reveals shared neural processes supporting semantic and episodic memory retrieval. Nature Communications. doi.org/10.1038/s41467-021-22443-2.

Categories : NeurologyTags :

Sugar-sweetened Drinks During Adolescence Impacts Cognition in Adulthood

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New research has shown that, in rats, daily consumption of sugar-sweetened drinks during adolescence impairs performance on a learning and memory task during adulthood. 

The researchers also demonstrated that changes in the bacteria in the gut may be the key to the sugar-induced memory impairment. Evidence in support of this comes from the observation of similar memory deficits even when the bacteria, called Parabacteroides, were experimentally enriched in the guts of animals that had never consumed sugar.

“Early life sugar increased Parabacteroides levels, and the higher the levels of Parabacteroides, the worse the animals did in the task,” said first author Emily Noble, assistant professor, College of Family and Consumer Sciences, University of Georgia. “We found that the bacteria alone was sufficient to impair memory in the same way as sugar, but it also impaired other types of memory functions as well.”

Data from the Centers for Disease Control and Prevention show American children between the ages 9-18 exceed the recommendation of limiting added sugars to less than 10 percent of calories per day, with the bulk of the calories coming from sugar-sweetened beverages.

Since the hippocampus is still developing into late adolescence and plays a role in a variety of cognitive functions, researchers sought to understand more about its susceptibility to a high-sugar diet via gut microbiota.

Juvenile rats were given their normal chow and an 11% sugar solution, comparable to commercially available sugar-sweetened beverages. Researchers then had the rats perform a hippocampus-dependent memory task designed to measure episodic contextual memory, or remembering the context where they had seen a familiar object before.

“We found that rats that consumed sugar in early life had an impaired capacity to discriminate that an object was novel to a specific context, a task the rats that were not given sugar were able to do,” Prof Noble said.

A second memory task measured basic recognition memory, a hippocampal-independent memory function that involves the animals’ ability to recognise something they had seen previously. Sugar had no effect on the animals’ recognition memory.

“Early life sugar consumption seems to selectively impair their hippocampal learning and memory,” Prof Noble said.

Further analysis revealed that high sugar consumption led to elevated levels of Parabacteroides in the gut microbiome, the more than 100 trillion microorganisms in the gastrointestinal tract that play a role in human health and disease.

To determine the mechanism by which bacteria impacted memory and learning, researchers experimentally increased levels of Parabacteroides in the microbiome of rats that had never consumed sugar. Those animals showed impairments in both hippocampal dependent and hippocampal-independent memory tasks.

“(The bacteria) induced some cognitive deficits on its own,” Prof Noble said.

Future research is needed to better identify these gut-brain signaling specific pathways.

“The question now is how do these populations of bacteria in the gut alter the development of the brain?” Prof Noble said. “Identifying how the bacteria in the gut are impacting brain development will tell us about what sort of internal environment the brain needs in order to grow in a healthy way.”

Source: News-Medical.Net

Journal information: Noble, E. E., et al. (2021) Gut microbial taxa elevated by dietary sugar disrupt memory function. Translational Psychiatry. doi.org/10.1038/s41398-021-01309-7.

Categories : Diseases, Syndromes and Conditions NeurologyTags :

Mystery Brain Disease Baffles Canadian Doctors

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Doctors in Canada are struggling to explain a spate of cases involving memory loss, hallucinations and muscle atrophy.

For more than a year public health officials in New Brunswick province have been tracking a “cluster” of 43 cases of suspected neurological disease with no known cause.

A leaked memo from the province’s public health agency asking physicians to be on the lookout for symptoms similar to Creutzfeldt-Jakob disease (CJD), a rare, fatal and largely sporadic disease caused by prion proteins. Symptoms such as memory loss, vision problems and abnormal jerking movements were similar enough to trigger an alert with Canada’s CJD surveillance network. However, it was confirmed that this disease was not CJD.

“We don’t have evidence to suggest it’s a prion disease,” said Dr Alier Marrero, the neurologist leading New Brunswick’s investigation.
Patients initially reported unexplained pains, spasms and behavioural changes, easily misdiagnosed as anxiety or depression.

However, over 18 to 36 months they began to develop cognitive decline, muscle wasting, drooling and teeth chattering. Some also began experiencing frightening hallucinations, including the sensation of crawling insects on their skin.  

Each time a possible case arises, a battery of tests is administered to determine if they match the cluster. Cases have risen from only one in 2015 to 24 in 2020, and so far five people are believed to have died from the illness.

“We have not seen over the last 20-plus years a cluster of diagnosis-resistant neurological disease like this one,” said Michael Coulthart, head of Canada’s CJD surveillance network.

The majority of cases are linked a sparsely populated region of the province, with the overall number of cases in the cluster remaining low. However, New Brunswick has a population of fewer than 800 000 people.

Dr Marrero and his team have consulted experts in neurology, environmental health, field epidemiology, zoonotics and toxicology to better understand the possible cause of the mysterious illness.

A growing team of researchers are trying to pin down a common cause or perhaps environmental effect.

“We don’t know what is causing it,” said Dr Marrero. “At this time we only have more patients appearing to have this syndrome.”

Valerie Sim, a researcher of neurodegenerative diseases at the University of Alberta cautioned against jumping to conclusions. “I don’t really know if we even have a defined syndrome. There just isn’t enough information yet,” she said.

She observed that key markers for degenerative neurological illnesses had not been identified, with the cluster’s wide range of symptoms being “atypical” for most brain diseases. Conversely, the scope of symptoms could be explained by certain cancers, dementia or even misdiagnoses.

Frustratingly, when the ailment is unclear a number of tools can be deployed, “and then the patient somehow recovers. You come away never knowing what they actually had,” said Sim.

“We see odd neurological syndromes from time to time. Sometimes we figure them out. Sometimes we don’t.”

Source: The Guardian

Categories : NeurologyTags :

New Test Picks up Concussion Biomarkers in Saliva

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A new test has been found to effectively pick up concussion biomarkers in the saliva of rugby players.

This paves the way for a non-invasive, easy-to-use pitch-side test to rapidly detect concussions for early treatment. Concussion is a serious problem in contact sports, with players such as college American Football athletes consistently underestimating its risk. Missing a concussion can have a range of consequences, from delayed recovery to more serious (albeit rare) injuries such as traumatic brain swelling.

Detecting concussions requires an assessment by a clinician of the signs and symptoms of the injury. However, recent advances in DNA sequencing technology have made it possible to use small non-coding RNAs (sncRNAs) as biomarkers in rapid tests. sncRNAs regulate the expression of different cellular proteins associated with various diseases, such as cancer and Alzheimer’s disease.

t is thought that since saliva can receive cellular signals directly from the cranial nerves in the mouth and throat, biomarkers from a brain injury would quickly show up.

A panel of 14 sncRNAs differentiated concussed players from those where traumatic brain injury had been suspected but ruled out, and from the comparison group, both straight after the game and 36–48 hours later.

Over two seasons, samples were collected before the rugby season began from 1028 players from the two elite professional tiers, and during standardised ‘gold standard’ head injury assessments at three time points—during the game, afterwards, and 36–48 hours later from 156 of these players .

The researchers also took saliva samples from a comparison group of 102 uninjured players, as well as 66 with muscle or joint injuries, and so had not had head injury assessments.

However, the researchers stressed that the observational study nature and design of this study cannot show that the biomarker test is any better than a gold standard clinical test for concussion.

“In community sport, [sncRNAs] may provide a non-invasive diagnostic test that is comparable in accuracy to the level of assessment available in a professional sport setting,” while the test could be added to current head injury evaluation protocols at the elite level,” they add.

And as the biology of concussion is still not fully understood, sncRNAs might help to shed light on the response to injury as this evolves over time, they suggest.

“The detection of signatures of concussion at early time points in saliva (a non-invasively sampled biofluid) presents both at the pitch side, and in primary care and emergency medicine departments, an opportunity to develop a new and objective diagnostic tool for this common clinical presentation,” they conclude.

As an addendum to their findings, they added: “A patented salivary concussion test is in the process of being commercialized as an over-the-counter test for elite male athletes.

“Meanwhile our research team aims to collect further samples from players in two elite men’s rugby competitions to provide additional data to expand the test and develop its use. This will guide the prognosis and safe return to play after concussion and further establish how the test will work alongside the head injury assessment process.”

The researchers plan to add more participants to the SCRUM study, such as female athletes and community players.
Source: Medical Xpress

Journal information: Valentina Di Pietro et al. Unique diagnostic signatures of concussion in the saliva of male athletes: the Study of Concussion in Rugby Union through MicroRNAs (SCRUM), British Journal of Sports Medicine (2021). DOI: 10.1136/bjsports-2020-103274

Categories : NeurologyTags :

‘Zombie’ Genes Lurch into Activity After Brain Death

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Researchers have found that genes in cells in recently harvested brain tissue remained active for up to 24 hours – and some ‘zombie’ genes even increased their expression.

Using recently harvested brain tissue as a surrogate for actual death, the researchers investigated the activity of genes.

Dr Jeffrey Loeb, the John S Garvin Professor and head of neurology and rehabilitation at the UIC College of Medicine and corresponding author on the paper, noticed along with his team that the pattern of gene expression in fresh human brain tissue differed from published reports of postmortem brain gene expression from people without neurological disorders or from people with a wide variety of neurological disorders, ranging from autism to Alzheimer’s.

“We decided to run a simulated death experiment by looking at the expression of all human genes, at time points from zero to 24 hours, from a large block of recently collected brain tissues, which were allowed to sit at room temperature to replicate the postmortem interval,” Dr Loeb said.

They found that some ‘zombie’ genes were more expressed after the simulated death. These were specific to glial cells, which have an inflammatory role. The researchers observed that these cells continued to grow long arm-like appendages for many hours after death.

“That glial cells enlarge after death isn’t too surprising given that they are inflammatory and their job is to clean things up after brain injuries like oxygen deprivation or stroke,” said Dr Loeb.

Dr Loeb is director of the UI NeuroRepository, which preserves human brain tissues from patients with neurological disorders who gave their consent to use their tissue after death, or during surgery to treat disorders such as epilepsy, where some brain tissue is removed to treat the condition in lesionectomy. This procedure involves removing structural brain lesions — typically malformations of cortical development, low-grade neoplasms, or vascular malformations. Some of the tissue harvested through these various means can be used for research, as in this study.

About 80% of genes, many of which are involved in cellular ‘housekeeping’ activities, kept functioning up to 24 hours after death. Another group of genes involved in cognition and seizure control faded within a few hours of death. These are important to the study of schizophrenia and Alzheimer’s disease, according to Dr Loeb.

The ‘zombie’ genes ramped up activity as the others were winding down, with these changes peaking at 12 hours.

“Our findings don’t mean that we should throw away human tissue research programs, it just means that researchers need to take into account these genetic and cellular changes, and reduce the post-mortem interval as much as possible to reduce the magnitude of these changes,” Dr Loeb said. “The good news from our findings is that we now know which genes and cell types are stable, which degrade, and which increase over time so that results from postmortem brain studies can be better understood.”

Source: Medical Xpress

Journal information: Fabien Dachet et al. Selective time-dependent changes in activity and cell-specific gene expression in human postmortem brain, Scientific Reports (2021). DOI: 10.1038/s41598-021-85801-6

Categories : Neurology PaediatricsTags :

Boy’s Brain Rewires After Stroke as a Newborn

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Photo by cottonbro from Pexels

Researchers have reported the case of a boy whose brain was able to rewire after a severe stroke that damaged much of his brain.

In the seventh grade, 13-year old Daniel Carr amazed his baseball coach with his ability to throw with his left hand, saying that it was the fastest he’d ever seen. However, he was unable to properly catch with his right hand.

Hearing this from the coach, Kellie Carr, Daniel’s mother, realised that his son had a number of quirks, such as favouring his left side when he was an infant, and his left-handedness emerged well before the normal age of two or three. However, she was unable to get any explanation for this until she met Nico Dosenbach, MD, PhD, who informed her that her son had had a stroke when he was a newborn.

MRI scans revealed large, bilateral voids in Daniel’s brain, but incredibly, he had no cognitive, behavioural or motor problems other than a lack of strength and dexterity in his right arm.
“The extent of Daniel’s injuries may be on the edge of what’s compatible with life,” Dosenbach said.

Dainel’s remarkable recovery can be explained by his young age at the time the stroke.

“The brain can compensate more quickly and completely for strokes sustained in early childhood,” he said. “By contrast, large strokes in adults often cause death or severe functional impairment with little chance of recovery. However, the mechanics behind this are only beginning to be understood.”

More MRI scans were done on Daniel’s brain to determine its structure and pathology. Dosenbach and Laumann conducted high-resolution functional MRI scans to understand how Daniel’s brain had reorganised itself.
With his mother’s consent, Daniel was further tested over a period of six years, including batteries of neurological tests, and more scans done. Timothy Laumann, MD, PhD, now a fourth-year psychiatry resident at Barnes-Jewish Hospital, had the expertise to analyse the data.

Looking at his medical records, the physician-scientists noted that he had an infection as a newborn, and was hospitalised with an IV drip. However, none of the physicians had suspected a stroke, which happens to one in every 4000 newborns. Daniel was sent home after a week, the doctors having suspected a viral infection.

“The risk of having a pediatric stroke greatly increases with a medical problem, especially an infection during the newborn period,” Dosenbach said. “However, usually there are more obvious signs that a stroke occurred. I can understand how no one suspected it.”

The researchers compared the images of Daniel’s brain to others of young adults, as well as Dosenbach’s own brain, which he had imaged and studied extensively.

“Part of Daniel’s brain structure is gone,” Laumann explained, referring to their analysis of the MRI data. “He’s missing almost a quarter of his cortex.”

The dead tissue was replaced by pockets of cerebrospinal fluid, which acts as a shock absorber, as well as delivering nutrients and removing waste. The surviving neurons formed interconnected islands that restored cognitive and motor functions, and neighbourhoods of healthy tissue were again reconnected.

“Our findings illustrate the brain’s tenacity at reorganizing and recovering functions damaged by a massive stroke affecting both sides of his brain,” Dosenbach said. “Future studies of functional remapping relative to tissue loss may provide additional insights. Our results raise the possibility that variability in outcomes may depend on specific features unique to an individual’s brain.”

Despite the extensive damage, Daniel completed tertiary education and now works as a diesel mechanic.

“His stroke still shocks me,” Kellie Carr said. “How could I have not known? But looking back, maybe it was better that way. I might have babied Daniel and been afraid to let him be a regular kid. Maybe the best thing for him was living normally.”

Daniel agreed: “I think about my right hand daily because I have to constantly think five steps ahead to figure out how to compensate for not being able to use it properly, like I did with the baseball glove. But the last thing I want is for people to act like something is wrong with me. I’m fine.”

Source: Medical Xpress

Journal information: Timothy O Laumann et al. Brain network reorganisation in an adolescent after bilateral perinatal strokes, The Lancet Neurology (2021). DOI: 10.1016/S1474-4422(21)00062-4

Categories : Neurology PaediatricsTags :

Early Interventions May Improve Infant Brain Health

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Image by Raman Oza from Pixabay

At the Cognitive Neuroscience Society’s (CNS) annual meeting, researchers from the University of Minnesota presented their work on early interventions to ameliorate negative effects on infant brain health.

Their two interventions consist of using engineered gut microbes for antibiotic-exposed infants and the other is a choline supplement to treat infants exposed to alcohol in the womb.

Dr Gale’s new research shows that infants with different compositions of gut bacteria process auditory and visual stimuli differently during memory tasks. “These results raise the possibility that gut bacteria are involved in the development of brain function,” she said.

The study compared the brain activity of infants who received antibiotics within their first month of life to those who did not. Using EEG, the researchers recorded a type of electrical activity called event related potentials (ERPs) in the infants’ brains in response to either their mother’s voice or a stranger’s voice – a “recognition memory” that can be assessed in preverbal infants before any behavioral changes are apparent. This has been shown to be an effective assessment of many aspects of cognitive development.

“Recognition memory is one of the earliest types of explicit memory to develop and is known to be dependent on medial temporal lobe structures, including the hippocampus, the brain region affected by microbiome perturbation in animal models,” explained Dr Cheryl Gale, of the University of Minnesota.

The ERP measurements of infants exposed to antibiotics showed an abnormal response to their mother’s voices compared to those unexposed.
While antibiotics were associated with impact on brain function, a causal relationship could not be established. “We don’t yet know if there is a definitive cause and effect relationship between microbes and brain function in human infants, but future research will hopefully be able to shed light on this,” Gale says.

The work raises the prospect of creating engineered microbes as an early life intervention. “Infancy is a critical time window for brain development, when therapeutic interventions can have effects for the life-course,” Gale said.

The other study was on foetal alcohol exposure, which is still a widespread problem, involved in some 8 in 1000 births worldwide, resulting in serious cognitive consequences. Dr Jeff Wozniak became aware of a lack of neural imaging studies in this very high-need population.

“So I became interested in using some of the tools that we had available here at the University of Minnesota to do high-quality imaging of brain structure and function in this understudied population to learn something about how the brain is altered by prenatal alcohol exposure at the earliest stages of development,” he said.

Together with colleagues, they identified a number of pathways by which alcohol impacts the foetus, such as interfering with the myelination of nerves. The researchers came up with a treatment: choline, an essential nutrient. This has been used in a number of double-blind, placebo-controlled clinical trials in 2-5 year olds with foetal alcohol exposure.
Children receiving choline early in life showed higher non-verbal intelligence, higher visual-spatial skill, higher working memory ability, better verbal memory, and fewer behavioral symptoms of attention deficit hyperactivity disorder (ADHD) than those in the placebo group.

“The further back you go and do your intervention, the more leverage you have to alter the developmental trajectory of that particular child,” Dr Wozniak said. “So that was the exciting thing about bringing those children back and looking at their development and seeing much larger choline versus placebo effects in cognitive functions like working memory and even behavioural differences in terms of ADHD.”

Source: News-Medical.Net