Alterations of White Matter in Brain Tied to Cognitive Impairment

 How is your competent? doctor identifying your white matter damage and then fixing it? DOING NOTHING LIKE USUAL? So, you DON'T have a functioning stroke doctor, do you? RUN AWAY!

Alterations of White Matter in Brain Tied to Cognitive Impairment

Alterations of white matter in the brain occur to a larger extent among patients with major depressive disorder (MDD) compared with healthy individuals, according to study results published in Lancet Psychiatry.

Cognitive deficits occur frequently in MDD and are known to be associated with worse disease outcomes. Although white matter microstructure has been linked to depressive recurrence and cognitive performance, longitudinal studies are needed to determine the underlying mechanisms and related measures of disease course.

Researchers of an observational, prospective, case-control study aimed to determine the link between white matter integrity and cognitive performance in patients with MDD vs those without psychiatric disorders over a period of 2 years.

Participants aged between 18 and 65 years of Caucasian ancestry were identified for the current analysis, using the German Marburg-Münster Affective Disorders Cohort Study (MACS). Using neuropsychologic tests, the researchers assessed clinical data and cognitive performance, at baseline and 2 years of follow-up. Diffusion-weighted imaging was also performed, using magnetic resonance imaging (MRI) scans.

Our findings emphasise the crucial role of white matter microstructure and disease progression in depression-related cognitive dysfunction, making both priority targets for future treatment development.

Of 881 participants identified at baseline between 2014 and 2019, 418 (47%) had MDD (mean age, 36.8 years; women, 66%) and 463 were healthy individuals (mean age, 35.6 years; women, 64%). Follow-up was conducted at mean of 2.2 years, between 2016 and 2021.

In the depression-associated analysis, the researchers found that compared with healthy participants, patients with MDD, specifically acute depression, had worse scores on the neuropsychologic tests at all timepoints, indicating lower cognitive performance (P <.0001; sr²=0.056).

The researchers noted a significant association between diagnosis and time, with patients with MDD vs healthy control participants showing a greater decline in white matter integrity over time (P =.026; sr²=0.002). However, cognitive decline was associated with changes in white matter integrity over time across both groups (P <.0001; sr²=0.004). Cross-sectional analysis also showed that lower cognitive performance was linked to reduced white matter integrity at all timepoints.

In a mediation analysis, adverse disease course and changes in white matter integrity were found to be predictors of cognitive deficits (β=0.073; P =.0022 and β=0.071; P =.0040, respectively).

Limitations of the analysis included MDD symptoms being based on patient self-reports; potential confounding factors; and lack of fully accounting for clinical characteristics, such as medication use and comorbidities, which may have affected cognitive performance and white matter integrity.

“Our findings [emphasize] the crucial role of white matter microstructure and disease progression in depression-related cognitive dysfunction, making both priority targets for future treatment development,” the researchers concluded.

This study was funded by German Research Foundation (DFG). Multiple study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of the authors’ disclosures.

References:

Growth hormone promotes myelin repair after chronic hypoxia via triggering pericyte-dependent angiogenesis

 Ask you competent? doctor if you need myelin repair post stroke, and don't accept not knowing as an answer. YOUR FUCKING DOCTOR IS SUPPOSED TO BE COMPETENT! Only over a decade for your doctor to become competent in myelin!

In here is both myelin repair topics and whether stroke causes myelin damage.

• myelin (73 posts to April 2011)

Growth hormone promotes myelin repair after chronic hypoxia via triggering pericyte-dependent angiogenesis

• Shu-Yu Ren ¹⁰
• Yu Xia ¹⁰
• Bin Yu
• 
  
• Lan Xiao
• Zhang-Xue Hu
• Feng Mei ¹¹
• Show all authors
• Show footnotes

Published:April 22, 2024DOI:https://doi.org/10.1016/j.neuron.2024.03.026

Highlights

• •
  GH treatment promotes myelin repair and functional recovery after hypoxia
• •
  GHR is selectively expressed by a subpopulation of pericytes
• •
  GHR-positive pericyte-tip cells lead blood vessel bridging and branching
• •
  GHR-positive pericytes modulate angiogenesis and govern myelination indirectly

Summary

White matter injury (WMI) causes oligodendrocyte precursor cell (OPC) differentiation arrest and functional deficits, with no effective therapies to date. Here, we report increased expression of growth hormone (GH) in the hypoxic neonatal mouse brain, a model of WMI. GH treatment during or post hypoxic exposure rescues hypoxia-induced hypomyelination and promotes functional recovery in adolescent mice. Single-cell sequencing reveals that Ghr mRNA expression is highly enriched in vascular cells. Cell-lineage labeling and tracing identify the GHR-expressing vascular cells as a subpopulation of pericytes. These cells display tip-cell-like morphology with kinetic polarized filopodia revealed by two-photon live imaging and seemingly direct blood vessel branching and bridging. Gain-of-function and loss-of-function experiments indicate that GHR signaling in pericytes is sufficient to modulate angiogenesis in neonatal brains, which enhances OPC differentiation and myelination indirectly. These findings demonstrate that targeting GHR and/or downstream effectors may represent a promising therapeutic strategy for WMI.

Graphical abstract

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Endovascular Brain-Computer Interfaces in Poststroke Paralysis

This assumes you actually have functioning motor neurons that are still generating signals but can't get thru(Meaning your white mater is damaged, the solution to white matter damage is axon pathfinding and dendritic branching). Since most of my motor cortex and pre-motor cortex is dead this would be useless for me. What is your solution for me?

• axon pathfinding (35 posts to March 2012)

• dendritic branching (38 posts to February 2012)

• neurite outgrowth (29 posts to January 2012)

Endovascular Brain-Computer Interfaces in Poststroke Paralysis

Jamie F.M. Brannigan,

Adam Fry,

Nicholas L. Opie,

Bruce C.V. Campbell,

Peter J. Mitchell and

Thomas J. Oxley

Originally published29 Nov 2023https://doi.org/10.1161/STROKEAHA.123.037719Stroke. 2023;0

Abstract

Stroke is a leading cause of paralysis, most frequently affecting the upper limbs and vocal folds. Despite recent advances in care, stroke recovery invariably reaches a plateau, after which there are permanent neurological impairments. Implantable brain-computer interface devices offer the potential to bypass permanent neurological lesions. They function by (1) recording neural activity, (2) decoding the neural signal occurring in response to volitional motor intentions, and (3) generating digital control signals that may be used to control external devices. While brain-computer interface technology has the potential to revolutionize neurological care, clinical translation has been limited. Endovascular arrays present a novel form of minimally invasive brain-computer interface devices that have been deployed in human subjects during early feasibility studies. This article provides an overview of endovascular brain-computer interface devices and critically evaluates the patient with stroke as an implant candidate. Future opportunities are mapped, along with the challenges arising when decoding neural activity following infarction. Limitations arise when considering intracerebral hemorrhage and motor cortex lesions; however, future directions are outlined that aim to address these challenges.

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White Matter Wonders: Re-imagining the Brain’s Silent Majority

 But isn't white matter scanning already available?

FDA grants 510(k) clearance for software to image the brain’s white matter August 2023 

Your doctor needs to know the EXACT OBJECTIVE DAMAGE  to your white matter. Then s/he can propose the correct rehab protocols that fix such damage. That would be the case if there was any competency at all in the stroke medical world.

It is your doctor's responsibility to objectively know the damage to both the gray matter and the white matter in your brain. Without that knowledge your doctor is totally guessing what needs to be done to get you recovered.   Which might explain those doctors who prescribe E.T.(Evaluate and Treat) to the therapists. They know nothing about stroke rehab so they are punting responsibility to the therapists. From this research it seems imperative your doctor knows EXACTLY how to initiate axon pathfinding, neurite outgrowth and dendritic branching through your damaged white matter.

• axon pathfinding (35 posts to March 2012)

• dendritic branching (38 posts to February 2012)

• neurite outgrowth (29 posts to January 2012)

And if your doctor knows nothing about semaphorins you don't have a stroke doctor. Run away.

Semaphorins and their Signaling Mechanisms January 2018

From there: 

Early studies revealed that semaphorins function as axon guidance molecules,(We need this to have our white matter do the connections needed.)

The latest here: 

White Matter Wonders: Re-imagining the Brain’s Silent Majority

Summary: Historically, scientific research has largely focused on the gray matter of the brain, leaving the equally important white matter understudied. However, a recent groundbreaking study has used fMRI to detect significant brain activity in white matter.

When subjects performed tasks, researchers observed increased BOLD signals throughout the white matter.

This discovery challenges conventional beliefs about the brain’s activity and emphasizes the potential importance of white matter in understanding various brain disorders.

Key Facts:

1. The Vanderbilt team, led by John Gore, Ph.D., utilized fMRI to identify BOLD signals, indicative of brain activity, in the white matter—previously a little-researched area.
2. When subjects performed tasks during the study, there was a noticeable increase in BOLD signals in the white matter across the entire brain.
3. Despite the current lack of full understanding about these white matter signals, they’re believed to hold valuable insights, especially since many brain disorders, including epilepsy and multiple sclerosis, disrupt the brain’s “connectivity.”

Source: Vanderbilt University

The human brain is made up of two kinds of matter: the nerve cell bodies (gray matter), which process sensation, control voluntary movement, and enable speech, learning and cognition, and the axons (white matter), which connect cells to each other and project to the rest of the body.

Historically, scientists have concentrated on the gray matter of the cortex, figuring that’s where the action is, while ignoring white matter, even though it makes up half the brain. Researchers at Vanderbilt University are out to change that.

For several years, John Gore, Ph.D., director of the Vanderbilt University Institute of Imaging Science, and his colleagues have used functional magnetic resonance imaging (fMRI) to detect blood oxygenation-level dependent (BOLD) signals, a key marker of brain activity, in white matter.

In their latest paper, published Oct. 12 in the Proceedings of the National Academy of Sciences, the researchers report that when people who are having their brains scanned by fMRI perform a task, like wiggling their fingers, BOLD signals increase in white matter throughout the brain.

“We don’t know what this means,” said the paper’s first author, Kurt Schilling, Ph.D., research assistant professor of Radiology and Radiological Sciences at VUMC. “We just know that something is happening. There truly is a powerful signal in the white matter.”

It is important to pursue this because disorders as diverse as epilepsy and multiple sclerosis disrupt the “connectivity” of the brain, Schilling said. This suggests that something is going on in white matter.

To find out, the researchers will continue to study changes in white matter signals they’ve previously detected in schizophrenia, Alzheimer’s disease and other brain disorders. Through animal studies and tissue analysis, they also hope to determine the biological basis for these changes.

In gray matter, BOLD signals reflect a rise in blood flow (and oxygen) in response to increased nerve cell activity.

Perhaps the axons, or the glial cells that maintain the protective myelin sheath around them, also use more oxygen when the brain is “working.” Or perhaps these signals are somehow related to what’s going on in the gray matter.

But even if nothing biological is going on in white matter, “there’s still something happening here,” Schilling said. “The signal is changing. It’s changing differently in different white matter pathways and it’s in all white matter pathways, which is a unique finding.”

One reason that white matter signals have been understudied is that they have lower energy than gray matter signals, and thus are more difficult to distinguish from the brain’s background “noise.”

The VUMC researchers boosted the signal-to-noise ratio by having the person whose brain was being scanned repeat a visual, verbal or motor task many times to establish a trend and by averaging the signal over many different white matter fiber pathways.

“For 25 or 30 years, we’ve neglected the other half of the brain,” Schilling said. Some researchers not only have ignored white matter signals but have removed them from their reports of brain function.

The Vanderbilt findings suggest that many fMRI studies thus “may not only underestimate the true extent of brain activation, but also … may miss crucial information from the MRI signal,” the researchers concluded.

About this neuroscience research news

Author: Bill Snyder
Source: Vanderbilt University
Contact: Bill Snyder – Vanderbilt University
Image: The image is credited to Neuroscience News

Original Research: Closed access.
“Whole-brain, gray, and white matter time-locked functional signal changes with simple tasks and model-free analysis” by Kurt G. Schilling et al. PNAS

FDA grants 510(k) clearance for software to image the brain’s white matter

 This would be great for getting an objective damage diagnosis on white matter damage from your stroke, because right now your doctor has no clue what white matter damage there is and what protocols are needed for dendritic branching and axon pathfinding to fix white matter damage.  This would allow factual proof that the protocols used fix white matter damage.

• dendritic branching (38 posts to February 2012)

• dendritic spine formation (6 posts to February 2017)

• axon pathfinding (36 posts to March 2012)

• axon regeneration (13 posts to June 2016)

FDA grants 510(k) clearance for software to image the brain’s white matter

The FDA has granted 510(k) clearance to a Canadian neuroimaging company for its quantitative imaging software, which assists neurologists and radiologists dealing with brain white matter issues for adjunctive care.

According to a press release from Imeka, the Advanced Neuro Diagnostic Imaging (ANDI) software extracts white matter bundles that connect specific regions of the brain and analyzes their microstructure. The artificial intelligence-assisted device processes diffusion-weighted images via modeling, tractography and fiber bundling to map microstructural properties of the white matter.

Imeka received 510(k) clearance from the FDA for its brain white matter imaging software. Image: Adobe Stock

ANDI then generates a Digital Imaging Communications in Medicine (DICOM) report, which focuses on the bundles with the greatest deviation from the normative range, and offers a detailed analysis of all bundles’ microstructural and macrostructural values, the company said.

“We are pleased to announce FDA 510(k) clearance of ANDI, our quantitative imaging software, and make the technology available to health care providers across the U.S.,” Imeka CEO Jean-René Bélanger said in the release. “This also comes at a very crucial time with the announcement of the addition of two new CPT III codes by the AMA for quantitative brain MRI assessment, which we expect our clients to be able to get reimbursement from, starting in January 2024."

Secondary White Matter Injury and Therapeutic Targets After Subarachnoid Hemorrhage

 You'll have to ask your doctor for the 100% recovery protocols for this.

Secondary White Matter Injury and Therapeutic Targets After Subarachnoid Hemorrhage

Xufang Ru^1,2†, Ling Gao^3†, Jiru Zhou⁴, Qiang Li^1,2, Shilun Zuo⁵, Yujie Chen^1,2*, Zhi Liu^1,2* and Hua Feng^1,2

• ¹State Key Laboratory of Trauma, Burn and Combined Injury, Department of Neurosurgery, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China
• ²Chongqing Key Laboratory of Precision Neuromedicine and Neuroregenaration, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China
• ³Department of General Practice, Audio-Visual Education Center, Third Military Medical University (Army Medical University), Chongqing, China
• ⁴Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
• ⁵Department of Neurology, Xinqiao Hospital, Third Military Medical University (Army Medical University), Chongqing, China

Aneurysmal subarachnoid hemorrhage (SAH) is one of the special stroke subtypes with high mortality and mobility. Although the mortality of SAH has decreased by 50% over the past two decades due to advances in neurosurgery and management of neurocritical care, more than 70% of survivors suffer from varying degrees of neurological deficits and cognitive impairments, leaving a heavy burden on individuals, families, and the society. Recent studies have shown that white matter is vulnerable to SAH, and white matter injuries may be one of the causes of long-term neurological deficits caused by SAH. Attention has recently focused on the pivotal role of white matter injury in the pathophysiological processes after SAH, mainly related to mechanical damage caused by increased intracerebral pressure and the metabolic damage induced by blood degradation and hypoxia. In the present review, we sought to summarize the pathophysiology processes and mechanisms of white matter injury after SAH, with a view to providing new strategies for the prevention and treatment of long-term cognitive dysfunction after SAH.

Introduction

Aneurysmal subarachnoid hemorrhage (SAH) is one of the special stroke subtypes with high mortality and mobility. Neurosurgical clipping or endovascular coiling is highly recommended for the early repair of ruptured aneurysms (1), focusing the medical management of SAH patients on early brain injury and delayed cerebral ischemia (2). However, more than 70% of survivors suffer from varying degrees of neurological deficits and cognitive impairments, leaving a heavy burden on individuals, families, and the society (3). Compared with cohorts with unruptured intracranial aneurysm, patients with aneurysmal SAH have higher mean diffusivity in white matter, leading to cognitive impartment 3 months after SAH onset (4). Apparently, the mammillothalamic tract is more vulnerable than the corticospinal tract in SAH patients with a good Glasgow Outcome Scale at 3 months after ictus (5), which demonstrates a correlation between early brain injury and long-term cognitive dysfunction after SAH.

White matter contains most of the volume of human brain and is made up of neural axons and myelin sheath. As early as 1989, the autopsy of six SAH cases had reported the remarkable hyperemia and edema in the deep frontal white matter, with microscopic axonal degeneration (6). Despite that enormous progresses have been made in the pathophysiology of early brain injury after SAH, the mechanisms of white matter injury are still a blur (7). Unlike intracerebral hemorrhage and traumatic brain injury, most SAH patients, especially those without obvious hematoma volume, do not usually fracture the nervous tract due to primary mechanical stress but suffer with remarkable secondary brain injury and neurological deficits. Mechanical pressure due to increased intracerebral pressure, glial response, and ischemia is considered as the pivotal mechanism of white matter injury after SAH but lacks high-quality clinical and basic research evidence (7).

In the present review, we sought to summarize the pathophysiology processes and mechanisms of white matter injury after SAH, with a view to providing new strategies for the prevention and treatment of long-term cognitive dysfunction after SAH.

More at link.

 

Study shows reduction in brain injury after stroke patients were treated with their own stem cells

Why bone marrow?  Urine would be much faster and definitely more interesting.

Turning urine into brain cells could help fight Alzheimer’s, Parkinson’s

December 2012

The most important thing from this seems to be the ability to know what damage was objectively determined in your white matter. That knowledge could then be used to determine objectively what interventions of axon pathfinding and dendritic branching work. Thus being able to create protocols. This is so fucking obvious that stroke leaders should add it to the stroke strategy and thus create research to solve the pathfinding and branching needs.

Study shows reduction in brain injury after stroke patients were treated with their own stem cells

March 12, 2021 / Yimy Villa

Illustration showing the mechanism of an ischemic stroke. In an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction of that area of the brain. Here, a blood clot is the reason for restricted blood flow.

Stroke is the third leading cause of death and serious long-term disability and affects nearly 800,000 Americans a year, with someone in the U.S. suffering a stroke every 40 seconds. Roughly 87% of all strokes are ischemic strokes, meaning that a clot blocks blood flow to the brain. Unfortunately 90% of those who suffer an ischemic stroke also end up suffering from weakness or paralysis to one side of the body.

A study conducted by Muhammad Haque, Ph.D. and Sean Savitz, M.D. at The University of Texas Health Science Center at Houston (UTHealth) found that treating patients with stem cells from their own bone marrow could lead to a reduction in brain injury after a stroke caused by a blood clot.

For this study, there were 37 patients from ages 18 to 80. While all received the standard stroke treatment and rehabilitation follow-up, 17 patients whose strokes were the most severe received a bone marrow stem cell therapy. To measure any improvement, the UTHealth team used 3D brain imaging of the patients obtained from MRI scans. They used these images to compare changes in white matter of those treated with their own bone marrow stem cells to those who were not treated.

White matter is a specific type of tissue in the brain that is critical for motor function because it is responsible for carrying movement-related information to the spinal cord.

Three months after the stroke, the MRI scans of each patient showed the expected decrease after a stroke. However, scans taken 12 months after the stroke occurred showed an improvement on average in the 17 patients who received bone marrow cell therapy.

In a press release from UTHealth, Dr. Haque elaborates on what these results could mean for developing treamtents for stroke patients.

“We envision that future clinical trials might be directed toward identifying white matter protection or repair as an important mechanistic target of efficacy studies and potency assays for bone marrow cell therapies.”

The full results to this study were published in STEM CELLS Translational Medicine.

 

Icometrix announces ischaemic stroke solution

I wondered if it does white matter damage from the stroke. It does find white matter hyperintensities from this research.  

How does icobrain enhance your radiological reporting for MS?

 

Because if white matter damage is found then that requires different protocols to solve. And your doctor has none.  

The latest here:

Icometrix announces ischaemic stroke solution

In a press release, icometrix announced the addition of icobrain cva, a stroke solution, to the icobrain portfolio. According to the company, this announcement follows clearance from the US Food and Drug Administration (FDA) and CE-marking of its image processing software for the analysis and communication of the tissue perfusion state on computer tomography (CT) perfusion scans in patients with ischaemic stroke. 

According to icometrix, the icobrain cva is a fully-automated software solution for the quantitative assessment of tissue perfusion on CT. The company claims that icobrain cva reports the volume of the core and perfusion lesion by quantifying reduced cerebral blood flow, volume, and transit time. Additionally, icometrix states the report includes information on the correctness of the selected arterial input function and the quality of the output.  

The press release details that icobrain cva provides physicians with fast, fully automated, and state-of-the-art insights to support treatment decisions in acute ischaemic stroke. It is further stated that the automated assessment of tissue parameters in an acute clinical setting by icobrain cva will allow more patients to get the right treatment and can improve patient outcomes and care while increasing efficiency. 

“With the launch of icobrain cva we address a persisting need in the treatment of acute ischaemic stroke. By democratising advanced CT perfusion analysis for healthcare systems worldwide, we take the next step in our mission to become a holistic brain solution provider,” says Wim Van Hecke, CEO at icometrix, Antwerp, Belgium. 

“The main challenge of current stroke solutions is correctly identifying the entry point of the injected contrast in the brain. icobrain cva introduces new, patented, deep learning technology into this identification process to achieve a more robust assessment of the infarcted area,” states Dirk Smeets, CTO at icometrix, Leuven, Belgium.

 

White Matter Damage Persists Over Time in Vets with TBI

 WHOM do we ask this same question for stroke? I'm quite sure I have lots of white matter damage than no one can tell exists or what the protocols are to fix it. I would need EXACT PROTOCOLS for axon pathfinding and dendritic branching to get around or thru the dead white matter.

White Matter Damage Persists Over Time in Vets with TBI

Neuroimaging results could offer prognostic markers of recovery or deterioration

by Ed Susman, Contributing Writer, MedPage Today December 2, 2020

Military veterans with moderate-to-severe traumatic brain injuries (TBI) had more changes to the brain's white matter than uninjured peers, which did not show signs of recovery over time, a researcher reported.

In an ongoing study that used a novel neuroimaging technique, vets with moderate-to-severe TBIs had lower fractional anisotropy (FA) scores at baseline versus non-TBI controls, with lower scores observed in 52 regions (72%) of the former patients' brains versus 17 regions (24%) in the latter group, according to Ping-Hong Yeh, PhD, of the Walter Reed National Military Medical Center in Bethesda, Maryland.

Also, for the FA trajectory over the 15 years of follow-up, non-TBI controls had significant FA increases (higher slope) between baseline and timepoint 2 (TP2) than those in the moderate-to-severe TBI group over 13 regions (18%), Yeh reported at the Radiological Society of North America virtual meeting.

"Traumatic brain injury patients have varying trajectories of white matter microstructural changes, which could be used as potential markers of recovery or deterioration," Yeh said, also noting in a statement that "Questions remain regarding the long-term impact of blast exposures. This study, with up to 15 years' follow-up, assesses the long-term effects of combat blast exposures."

However, Yeh cautioned that "We don't have the results regarding the correlates between neuroimaging findings and neuropsychological functions/symptoms yet. "Those will be our next study."

He added that "Currently there are no reliable biomarkers to predict the long-term outcome of combat-related brain injury. The findings of this research provide support for the potential prognostic utility of quantitative neuroimaging approach, and highlight the role that these imaging changes could play in potential stratification for clinical trial intervention."

Yeh and colleagues enrolled 285 military vets with TBIs (majority male; age 36.55) and 14 non-injured controls. For the MR neuroimaging, "An automated white matter tract segmentation method using a novel convolutional neural network based approach was applied to directly segment tracts," the authors explained.

They reported that most of the tracts were in the regions where the TBI group had lower FA than non-TBI controls at baseline. Also, the moderate-to-severe TBI group did not show significant changes of FA trajectory before TP2, and none of the participants had significant changes in FA trajectory after TP2.

Vincent Mathews, MD, of the Medical College of Wisconsin in Milwaukee, told MedPage Today, that "This study did not look at the effect of treatment on the observed magnetic resonance findings."

"However, one could potentially use this technique to evaluate if clinical improvement following therapy is related to improvement in these microstructural changes," said Mathews, who was not involved in the study.

"This is a continuing study and we will incorporate other modalities, such as functional MRI and neuropsychological testing, to better understand and validate whether this approach would be sensitive to identifying a therapeutic response, as well as the implication of these findings as they pertain to aging and the potential link to downstream dementia," Yeh said.

Yeh and colleagues conducted a related study in 2015 that demonstrated white matter T2 hyperintensities on MRI in a significant percentage of active duty military personnel with mild TBIs. At the time of publication in Radiology, co-author Gerard Riedy, MD, PhD, also at Walter Reed, stated, "This paper is just the tip of the iceberg. We have several more papers coming up that build on these findings and look at brain function, brain wiring, connectivity and perfusion, or brain blood flow."

Disclosures

Yeh and Mathews disclosed no relevant relationships with industry.

Primary Source

Radiological Society of North America

Source Reference: Yeh P-H, et al "Longitudinal Changes of White Matter Microstructure Following Traumatic Brain Injury in U.S. Military Service Members" RSNA 2020.