Category: Neurology

PFAS Influence the Development and Function of the Brain

Photo by Ryan Zazueta on Unsplash

Some per- and polyfluoroalkyl substances (PFAS) are poorly degradable and are also known as “forever chemicals”. They adversely affect health and can lead to liver damage, obesity, hormonal disorders, and cancer. A research team from the Helmholtz Centre for Environmental Research (UFZ) has investigated the effects of PFAS on the brain.

Using a combination of modern molecular biology methods and the zebrafish model, the researchers revealed the mechanism of action and identified the genes involved, which are also present in humans. The test procedure developed at the UFZ could be used for the risk assessment of other neurotoxic chemicals. The study was recently published in Environmental Health Perspectives

Because of their special properties – heat resistance, water and grease repellence, and high durability – PFAS are used in many everyday products (eg, cosmetics, outdoor clothing, and coated cookware). But it is precisely these properties that make them so problematic. “Because some PFAS are chemically stable, they accumulate in the environment and enter our bodies via air, drinking water, and food”, says UFZ toxicologist Prof Dr Tamara Tal. Even with careful consumption, it is nearly impossible to avoid this group of substances, which has been produced since the 1950s and now includes thousands of different compounds. “There is a great need for research, especially when it comes to developing fast, reliable, and cost-effective test systems for assessing the risks of PFAS exposure”, says Tal. So far, the environmental and health consequences have been difficult to assess.

In their current study, the researchers investigated how PFAS exposure affects brain development. To do this, they used the zebrafish model, which is frequently used in toxicology research. One advantage of this model is that around 70% of the genes found in zebrafish (Danio rerio) are also found in humans. The findings from the zebrafish model can therefore likely be transferred to humans. In their experiments, the researchers exposed zebrafish to two substances from the PFAS group (PFOS and PFHxS), which have a similar structure. The researchers then used molecular biological and bioinformatic methods to investigate which genes in the brains of the fish larvae exposed to PFAS were disrupted compared to the control fish, which were not exposed. “In the zebrafish exposed to PFAS, the peroxisome proliferator-activated receptor (ppar) gene group, which is also present in a slightly modified form in humans, was particularly active”, says Sebastian Gutsfeld, PhD student at the UFZ and first author of the study. “Toxicity studies have shown this to be the case as a result of exposure to PFAS – albeit in the liver. We have now also been able to demonstrate this for the brain”.

But what consequences does an altered activity of the ppar genes triggered by PFAS exposure have for brain development and behaviour of zebrafish larvae? The researchers investigated this in further studies using the zebrafish model. Using CRISPR/Cas9 ‘gene scissors’ the researchers were able to “selectively cut individual or several ppar genes and prevent them from functioning normally”, explains Gutsfeld. “We wanted to find out which ppar genes are directly linked to a change in larval behaviour triggered by PFAS exposure”. Proof of the underlying mechanism was directly provided. In contrast to genetically unaltered zebrafish, the knockdown fish in which the gene scissors were used should not show any behavioural changes after exposure to PFAS.

The two behavioural endpoints

In one series of experiments, the researchers continuously exposed zebrafish to PFOS or PFHxS during their early developmental phase between day one and day four and in another series of experiments only on day five. On the fifth day, the researchers then observed swimming behaviour. They used two different behavioural endpoints for this purpose. In one endpoint, swimming activity was measured during a prolonged dark phase. PFAS-exposed fish swam more than fish not exposed to PFAS, whether continuously exposed to PFAS during brain development or shortly before the behaviour test. Interestingly, hyperactivity was only present when the chemical was around. When the researchers removed PFOS or PFHxS, hyperactivity subsided. In the second endpoint, the startle response after a dark stimulus was measured. “In zebrafish exposed to PFOS for four days, we observed hyperactive swimming behaviour in response to the stimulus”, says Gutsfeld. In contrast, zebrafish only exposed to PFOS or PFHxS on the fifth day did not have a hyperactive startle response.

Based on these responses, the researchers conclude that PFOS exposure is associated with abnormal consequences – particularly during sensitive developmental phases of the brain. Using knockdown zebrafish, the researchers identified two genes from the ppar group that mediate the behaviour triggered by PFOS. 

“Because these genes are also present in humans, it is possible that PFAS also have corresponding effects in humans”, concludes Tal. The scientists working with Tal want to investigate the neuroactive effects of other PFAS in future research projects and expand the method so that it can ultimately be used to assess the risk of chemicals in the environment, including PFAS.

Source: Helmholtz Centre for Environmental Research – UFZ

Cannabis Use in Adolescence has Visible Effects on Brain Structure

Photo by Anna Shvets

Cannabis use may lead to thinning of the cerebral cortex in adolescents according to a recent study.  The study demonstrates that THC – or tetrahydrocannabinol, an active substance in cannabis – causes shrinkage of the dendritic arborisation, neurons’ “network of antennae” whose role is critical for communication between neurons. This results in the atrophy of certain regions of the cerebral cortex – bad news at an age when the brain is maturing.  

The study, led by Graciela Pineyro and Tomas Paus, involved researchers at CHU Sainte-Justine and professors at the Université de Montréal Faculty of Medicine, was published in The Journal of Neuroscience.

“If we take the analogy of the brain as a computer, the neurons would be the central processor, receiving all information via the synapses through the dendritic network,” explains Tomas Paus, who is also a professor of psychiatry and neuroscience at Université de Montréal. “So a decrease in the data input to the central processor by dendrites makes it harder for the brain to learn new things, interact with people, cope with new situations, etc. In other words, it makes the brain more vulnerable to everything that can happen in a young person’s life.”

A multi-level approach to better understand the effect on humans

This project is notable for the complementary, multi-level nature of the methods used. “By analysing magnetic resonance imaging (MRI) scans of the brains of a cohort of teenagers, we had already shown that young people who used cannabis before the age of 16 had a thinner cerebral cortex,” explains Tomas Paus. “However, this research method doesn’t allow us to draw any conclusions about causality, or to really understand THC’s effect on the brain cells.”  

Given the limitations of MRI, the introduction of the mouse model by Graciela Pineyro’s team was key. “The model made it possible to demonstrate that THC modifies the expression of certain genes affecting the structure and function of synapses and dendrites,” explains Graciela Pineyro, who is also a professor in the Department of Pharmacology and Physiology at Université de Montréal. “The result is atrophy of the dendritic arborescence that could contribute to the thinning observed in certain regions of the cortex.”  

Interestingly, these genes were also found in humans, particularly in the thinner cortical regions of the cohort adolescents who experimented with cannabis. By combining their distinct research methods, the two teams were thus able to determine with a high degree of certainty that the genes targeted by THC in the mouse model were also associated to the cortical thinning observed in adolescents. 

With cannabis use on the rise among North American youth, and commercial cannabis products containing increasing concentrations of THC, it’s imperative that we improve our understanding of how this substance affects brain maturation and cognition. This successful collaborative study, involving cutting-edge techniques in cellular and molecular biology, imaging and bioinformatics analysis, is a step in the right direction for the development of effective public health measures.

Source: University of Montreal

Can Space Radiation Affect Astronauts’ Long-term Cognition?

Photo: Pixabay CC0

During missions into outer space, galactic cosmic radiation (GCR) will penetrate current spacecraft shielding and thus pose a significant risk to human health. Previous studies have shown that GCR can cause short-term cognitive deficits in male rodents. Now a study published in the Journal of Neurochemistry reveals that GCR exposure can also cause long-lasting learning deficits in female rodents.

The impact of GCR on cognition was lessened when mice were fed an antioxidant and anti-inflammatory compound called CDDO-EA.

Beyond its immediate implications for space exploration, the findings contribute to a broader understanding of radiation’s long-term impact on cognitive health.

“Our study lays the groundwork for future causal delineation of how the brain responds to complex GCR exposure and how these brain adaptations result in altered behaviours,” said co-corresponding author Sanghee Yun, PhD, of the Children’s Hospital of Philadelphia Research Institute and the University of Pennsylvania Perelman School of Medicine.

Source: Wiley

Insights into How the Brain Regenerates Lost Myelin

Myelin sheath damage. Credit: Scientific Animations CC4.0

The neurons of the brain are protected by an insulating layer called myelin. In certain diseases like multiple sclerosis, the protective myelin layer around neurons is damaged and lost, leading to death of neurons and disability. New research published in The FEBS Journal reveals the importance of a protein called C1QL1 for promoting the replacement of the specialised cells that produce myelin. The findings could have important implications for the ongoing effort to develop new and improved therapies for the treatment of demyelinating diseases.

In experiments conducted in mice, deleting the gene that codes for C1QL1 caused a delay in the rate at which oligodendrocytes (the cells that make myelin) mature, leading to reduced myelination of neurons.

After mice were fed a drug that destroys myelin, recovery of oligodendrocytes and myelination were delayed in mice lacking the C1QL1 protein. Causing mice to express more C1QL1, however, led to increased numbers of oligodendrocytes and more myelination upon drug withdrawal, suggesting that C1QL1 helps to restore the damaged myelin layer.  Thus, investigational therapies that boost C1QL1 may hold promise against demyelinating diseases.

“Our basic research on C1QL1 is nascent, but there is potential that it is relevant for a novel treatment for multiple sclerosis,” said corresponding author David C. Martinelli, PhD, of the University of Connecticut Health Center. “New drug treatment options for patients with multiple sclerosis could have a large impact on their quality of life.”

Source: Wiley

Scientists Definitively Reveal the Brain’s Elusive Glymphatic System

Erin Yamamoto, MD, and Juan Piantino, MD, are among the co-authors of a new study from Oregon Health & Science University that used imaging of neurosurgery patients to definitively reveal the existence of waste-clearance pathways in the human brain known as the glymphatic system. (OHSU/Christine Torres Hicks)

Scientists have long theorised about a network of pathways in the brain that are believed to clear metabolic proteins that would otherwise build up and potentially lead to Alzheimer’s and other forms of dementia. But they had never definitively revealed this network in people – until now.

A new study involving five patients undergoing brain surgery at Oregon Health & Science University provides imaging of this network of perivascular spaces (fluid-filled structures along arteries and veins) within the brain for the first time.

“Nobody has shown it before now,” said senior author Juan Piantino, MD, associate professor of pediatrics (neurology) in the OHSU School of Medicine and a faculty member of the Neuroscience Section of the Papé Family Pediatric Research Institute at OHSU. “I was always skeptical about it myself, and there are still a lot of skeptics out there who still don’t believe it. That’s what makes this finding so remarkable.”

The findings appear in the Proceedings of the National Academy of Sciences.

The study combined the injection of an inert contrasting agent with a special type of magnetic resonance imaging to discern cerebrospinal fluid flowing along distinct pathways in the brain 12, 24 and 48 hours following surgery. In definitively revealing the presence of an efficient waste-clearance system within the human brain, the new study supports the promotion of lifestyle measures and medications already being developed to maintain and enhance it.

“This shows that cerebrospinal fluid doesn’t just get into the brain randomly, as if you put a sponge in a bucket of water,” Piantino said. “It goes through these channels.”

More than a decade ago, scientists at the University of Rochester first proposed the existence of a network of waste-clearance pathways in the brain akin to the body’s lymphatic system, part of the immune system. Those researchers confirmed it with real-time imaging of the brains of living mice. Due to its dependence on glial cells in the brain, they coined the term “glymphatic system” to describe it.

However, scientists had yet to confirm the existence of the glymphatic system through imaging in people.

Pathways revealed in patients

The new study examined five OHSU patients who underwent neurosurgery to remove tumours in their brains between 2020 and 2023. In each case, the patients consented to having a gadolinium-based inert contrasting agent injected through a lumbar drain used as part of the normal surgical procedure for tumour removal. The tracer would be carried with cerebrospinal fluid into the brain.

Afterward, each patient underwent magnetic resonance imaging, or an MRI, at different time points to trace the spread of cerebrospinal fluid.

Rather than diffusing uniformly through brain tissue, the images revealed fluid moving along pathways — through perivascular spaces in clearly defined channels. Researchers documented the finding with a specific kind of MRI known as fluid attenuated inversion recovery, or FLAIR. This type of imaging is sometimes used following the removal of tumors in the brain. As it turns out, it also revealed the gadolinium tracer in the brain, whereas the standard MRI sequences did not.

“That was the key,” Piantino said.

“You can actually see dark perivascular spaces in the brain turn bright,” said co-lead author Erin Yamamoto, MD, a resident in neurological surgery in the OHSU School of Medicine. “It was quite similar to the imaging the Rochester group showed in mice.”

Clearing waste from the brain

Scientists believe this network of pathways effectively flushes the brain of metabolic wastes generated by its energy-intensive work. Wastes include proteins such as amyloid and tau, which have been shown to form clumps and tangles in brain images of patients with Alzheimer’s disease.

Emerging research suggests medications that may be useful, but much of the focus around the glymphatic system has revolved around lifestyle-based measures to improve the quality of sleep, such as maintaining a regular sleep schedule, establishing a relaxing routine, and avoiding screens in the bedroom before bed. Especially at night during deep sleep, researchers believe a well-functioning glymphatic system efficiently carries waste proteins toward veins exiting the brain.

“People thought these perivascular spaces were important, but it had never been proved,” Piantino said. “Now it has.”

The authors credited the late Justin Cetas, MD, PhD, who initiated the study as an OHSU neurosurgeon before leaving the university to become chair of neurological surgery at his alma mater, the University of Arizona Health Sciences Center in Tucson. He died in a motorcycle accident in 2022.

Source: Oregon Health & Science University

Risk Factor for Autism Linked to Y Chromosome

Chromosomes. Credit: NIH

Increased risk for autism appears to be linked to the Y chromosome, a Geisinger study found, offering a new explanation for the greater prevalence of autism in males. The results were published in Nature Communications.

Autism spectrum disorder (ASD) is nearly four times more prevalent among males than females, but the reason for this disparity is not well understood. One common hypothesis involves the difference in sex chromosomes between males (XY) and females (XX).

“A leading theory in the field is that protective factors of the X chromosome lower autism risk in females,” said Matthew Oetjens, PhD, assistant professor at Geisinger’s Autism & Developmental Medicine Institute.

The Geisinger research team, led by Dr Oetjens and Alexander Berry, PhD, staff scientist, sought to determine the effects of the X and Y chromosomes on autism risk by examining ASD diagnoses in people with an abnormal number of X or Y chromosomes, a genetic condition known as sex chromosome aneuploidy.

The team analysed genetic and ASD diagnosis data on 177 416 patients enrolled in the Simons Foundation Powering Autism Research (SPARK) study and Geisinger’s MyCode Community Health Initiative.

They found that individuals with an additional X chromosome had no change in ASD risk, but that those with an additional Y chromosome were twice as likely to have an ASD diagnosis.

This suggests a risk factor associated with the Y chromosome instead of a protective factor associated with the X chromosome.

“While these may seem like two sides of the same coin, our results encourage us to look for autism risk factors on the Y chromosome instead of limiting our search to protective factors on the X chromosome,” Dr. Berry said.

“However, further research is needed to identify the specific risk factor associated with the Y chromosome.”

This analysis also confirms prior work by showing that the loss of an X or Y chromosome, known as Turner syndrome, is associated with a large increase in ASD risk. Further research is needed to determine whether the ASD risk factors associated with sex chromosome aneuploidy explains the sex difference in ASD prevalence.

Source: Geisinger Health System via Science Daily

Research Reveals a New Target to Treat Anxiety

A healthy neuron. Credit: NIH

Scientists at Université de Montréal and its affiliated Montreal Clinical Research Institute (IRCM) have uncovered unique roles for a protein complex in the structural organisation and function of brain cell connectivity, as well as in specific cognitive behaviours.

The work by a team led by Hideto Takahashi, director of the IRCM’s synapse development and plasticity research unit, in collaboration with Steven Connor’s team at York University and Masanori Tachikawa’s team at Japan’s Tokushima University is published in The EMBO Journal.

Although defects in synapse organisation are linked to many neuropsychiatric conditions, the mechanisms responsible for this organisation are poorly understood. The new study’s findings could provide valuable therapeutic insights, the researchers believe.

Two goals are important to bear in mind with this research, said Takahashi, an associate research medical professor in molecular biology and neuroscience at UdeM.

“One is to uncover novel molecular mechanisms for brain cell communication,” he said. “The other is to develop a new unique animal model of anxiety disorders displaying panic disorder- and agoraphobia-like behaviours, which helps us develop new therapeutic strategies.”

Understanding the mechanisms

Synapses are essential for neuronal signal transmission and brain functions. Defects in excitatory synapses, which activate signal transmission to target neurons, and those in synaptic molecules predispose to many mental illnesses.

Takahashi’s team has previously discovered a new protein complex within the synaptic junction, called TrkC-PTPσ, which is only found in excitatory synapses. The genes coding for TrkC (NTRK3) and PTPσ (PTPRS) are associated with anxiety disorders and autism, respectively. However, the mechanisms by which this complex regulates synapse development and contributes to cognitive functions are unknown.

The work carried out in the new study by first author Husam Khaled, a doctoral student in Takahashi’s laboratory, showed that the TrkC-PTPσ complex regulates the structural and functional maturation of excitatory synapses by regulating the phosphorylation, a biochemical protein modification, of many synaptic proteins, while disruption of this complex causes specific behavioural defects in mice.

Building blocks of the brain

Neurons are the building blocks of the brain and the nervous system that are responsible for sending and receiving signals that control the brain and body functions. Neighbouring neurons communicate through synapses, which act like bridges that allow the passage of signals between them.

This process is essential for proper brain functions such as learning, memory and cognition. Defects in synapses or their components can disrupt communication between neurons, and lead to various brain disorders.

By generating mice with specific genetic mutations that disrupt the TrkC-PTPσ complex, Takahashi’s team uncovered the unique functions of this complex. They demonstrated that this complex regulates the phosphorylation of many proteins involved in synapse structure and organisation.

High-resolution imaging of the mutant mice brains revealed abnormal synapse organisation, and further study of their signaling properties showed an increase in inactive synapses with defects in signal transmission. Observing the behaviour of the mutant mice, the scientists saw that they exhibited elevated levels of anxiety, especially enhanced avoidance in unfamiliar conditions, and impaired social behaviours.

Source: University of Montreal

Tiny Magnetic Discs Offer Remote Brain Stimulation without Genetic Modifications

The magnetic core of the nanodisc is magnetostrictive, which means it changes shape when magnetised. The rainbow nanodisc on the right is changing shape, allowing for the pink brain neuron to be stimulated. Image: Courtesy of the researchers

Novel magnetic nanodiscs could provide a much less invasive way of stimulating parts of the brain, paving the way for stimulation therapies without implants or genetic modification, MIT researchers report in Nature Nanotechnology.

The scientists envision that the tiny discs – about 250nm across – would be injected directly into the chosen brain location. From there, they could be activated at any time simply by applying an external magnetic field. The new particles could quickly find applications in biomedical research, and eventually, after sufficient testing, might be applied to clinical uses.

The research is described in the paper by Polina Anikeeva, a professor in MIT’s departments of Materials Science and Engineering and Brain and Cognitive Sciences, graduate student Ye Ji Kim, and 17 others at MIT and in Germany.

Deep brain stimulation (DBS) uses electrodes implanted in the target brain regions to treat symptoms of neurological and psychiatric conditions such as Parkinson’s disease and obsessive-compulsive disorder. Despite its efficacy, the surgical difficulty and clinical complications associated with DBS limit the number of cases where such an invasive procedure is warranted. The new nanodiscs could provide a much more benign way of achieving the same results.

Over the past decade other implant-free methods of producing brain stimulation have been developed, but were limited by spatial resolution or access. Other magnetic approaches studied needed genetic modifications to work, ruling it out for humans.

Since all nerve cells are sensitive to electrical signals, Kim, a graduate student in Anikeeva’s group, hypothesised that a magnetoelectric nanomaterial that can efficiently convert magnetisation into electrical potential could offer a path toward remote magnetic brain stimulation.

To this end, the researchers created nanodiscs with a magnetic core and piezolectric shell. When the core was squeezed by a magnetic field, strain in the shell produces a varying electrical polarisation. This enables the particles to deliver electrical pulses to neurons. The disc shape enhances the magnetostriction effect more than 1000-fold compared to spherical particles used previously.

After testing the nanodiscs with neurons in vitro, the researchers then injected small droplets of nanodisc-bearing solution into specific regions of the brains of mice. With an electromagnet, they turned on and off the stimulation in that region. That electrical stimulation “had an impact on neuron activity and on behaviour,” Kim says.

The team found that the magnetoelectric nanodiscs could stimulate a deep brain region, the ventral tegmental area, that is associated with feelings of reward.

The team also stimulated another brain area, the subthalamic nucleus, associated with motor control. “This is the region where electrodes typically get implanted to manage Parkinson’s disease,” Kim explains. The researchers were able to successfully demonstrate the modulation of motor control through the particles. Specifically, by injecting nanodiscs only in one hemisphere, the researchers could induce rotations in healthy mice by applying magnetic field.

The nanodiscs could trigger the neuronal activity comparable with conventional implanted electrodes delivering mild electrical stimulation. The authors achieved subsecond temporal precision for neural stimulation with their method yet observed significantly reduced foreign body responses as compared to the electrodes, potentially allowing for even safer deep brain stimulation.

The multilayered chemical composition and physical shape and size of the new multilayered nanodiscs is what made precise stimulation possible.

While the researchers successfully increased the magnetostrictive effect, the second part of the process, converting the magnetic effect into an electrical output, still needs more work, Anikeeva says. While the magnetic response was a thousand times greater, the conversion to an electric impulse was only four times greater than with conventional spherical particles.

“This massive enhancement of a thousand times didn’t completely translate into the magnetoelectric enhancement,” says Kim. “That’s where a lot of the future work will be focused, on making sure that the thousand times amplification in magnetostriction can be converted into a thousand times amplification in the magnetoelectric coupling.”

Further work is need before studies involving humans can begin, Kim says.

Source: MIT

Evidence Builds for Near Infrared Treatment of TBI

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

Birmingham scientists have shown light therapy delivered transcranially can aid tissue repair after mild traumatic brain injury (mTBI). Their research, published in Bioengineering & Translational Medicine, indicates that this novel method could result in a new treatment option in an area of medicine that currently has few, if any, treatment options.

Traumatic brain injury (mTBI) results when the initial trauma of head injury is magnified by a complex set of inflammatory changes that occur in the brain. These secondary processes, which take place from minutes to hours after head injury, can dramatically worsen outcomes for patients.

The method invented by scientists at the University of Birmingham, UK and patented by University of Birmingham Enterprise aims to protect against this secondary damage, and stimulate faster, and better recovery for patients.

We want to develop this method into a medical device that can be used to enhance recovery for patients with traumatic brain or spinal cord injury, with the aim of improving outcomes for patients.

Professor Zubair Ahmed, College of Medicine & Health

In the study, the Birmingham team, comprising researchers Professor Zubair Ahmed, Professor Will Palin, Dr Mohammed Hadis and surgeons Mr Andrew Stevens and Mr David Davies, examined the effect of two wavelengths of near infrared light (660nm and 810nm) on recovery following injury.

The study in preclinical models used daily two-minute bursts of infrared light, delivered by a laser, for three days post-injury.

The findings showed significant reductions in the activation of astrocytes and microglial cells, which are heavily implicated in the inflammatory processes in the brain that follow head trauma, and significant reductions in biochemical markers of apoptosis (cell death).

At four weeks, there were significant improvements in performance in functional tests involving balance and cognitive function. The red light therapy also accelerated recovery compared to controls, with superior outcomes for light with a wavelength of 810nm.

The study builds on research published earlier this year which showed near infrared light delivered directly to the site of spinal cord injury both improves survival of nerve cells and stimulates new nerve cell growth.

Professor Ahmed, who led the study, said: “We want to develop this method into a medical device that can be used to enhance recovery for patients with traumatic brain or spinal cord injury, with the aim of improving outcomes for patients.”

The researchers are seeking commercial partners to co-develop the device and take it to market.

Source: University of Birmingham

This Glowing Approach could Aid Carpal Tunnel-related Surgery

Fluorescein angiography capable of assessing neural blood flow in chronic nerve compression neuropathy

Fluorescein-enhanced contrast imaging shows a rabbit’s normal sciatic nerve, left, and a damaged one. Credit: Osaka Metropolitan University

In the modern office, it’s a daily struggle against the onset of carpal tunnel syndrome. The worst case could mean needing surgery to alleviate compression of the nerves or to repair damaged nerves. Helping surgeons visually check the areas where neural blood flow has decreased due to chronic nerve compression can lead to improvements in diagnostic accuracy, severity assessments, and outcome predictions.

With this in mind, an Osaka Metropolitan University-led research team involving Graduate School of Medicine student Kosuke Saito and Associate Professor Mitsuhiro Okada investigated the use of fluorescein angiography, a method employed in neurosurgery and ophthalmology to highlight blood vessels, to visualise neural blood flow in chronic nerve compression neuropathies like carpal tunnel syndrome. The findings were published in Neurology International.

The team found that fluorescein angiography could detect a decrease in neural blood flow in rats and rabbits with chronic nerve compression neuropathy. The results also correlated with electrodiagnostic findings.

Then fluorescein angiography was used for human patients undergoing open carpal tunnel release surgery, and the data also correlated strongly with electrodiagnostic testing. The findings indicate that fluorescein angiography might possess high diagnostic capabilities to assess neural blood flow during surgery.

“In surgery for severe chronic nerve compression neuropathy, the surgeon’s experience plays a big role in judging whether the surgical range is appropriate or whether additional treatment is necessary,” graduate student Saito noted. “This research has shown that fluorescein angiography can visualise impaired areas and assess the impairment severity, so we believe that it has the potential to contribute to improving accuracy for related surgeries.”

Source: Osaka Metropolitan University