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concussion (腦震盪) |
concussion
腦震盪
concussion (腦震盪)
腦震盪 (concussion)
【名詞】
concussion
腦震盪
discussion
討論
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腦震盪症候群(Post-concussion
syndrome, PCS)為腦震盪(輕度的創傷性腦損傷,
MTBI)後所產生的一系列症狀，它可能持續幾週、幾個月或有時一年以上。
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Stanford senior a pioneer in
traumatic brain injury research
Source (資訊來源):
Info cited on 2017-03-12-WD7 (資訊引用於 中華民國106年3月12日) by 湯偉晉
(WeiJin Tang)
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Stanford Report, December 11, 2013
Stanford senior a pioneer in
traumatic brain injury research
Stanford biology student Theo Roth spent the past few
summers developing an experiment for observing the brain's cellular response to
a concussion. The never-before-seen action could one day lead to therapies that
mitigate brain damage following mild traumatic brain injuries.
BY BJORN CAREY
L.A. Cicero
Theo Roth
Senior Theo Roth's MRI research images of a brain after a
mild traumatic brain injury demonstrate damage to the meninges, or the
protective layer surrounding the brain.
The lifelong fallout of a concussive brain injury is
well-documented. A blow to the head – whether it comes from an NFL tackle, a
battlefield explosion or a fall off a ladder – can cause brain damage
responsible for a debilitating degree of memory loss, mood swings, seizures and
more.
And though the blunt instrument that inflicts such damage is
typically known, the cellular mechanisms that inflict such trouble have so far
remained a mystery.
Now, a biology student at Stanford and researchers at the
National Institutes of Health have devised a method for observing the immediate
effects of a mild traumatic brain injury (TBI) in real time in mice. The work
has revealed how individual cells respond to the injury and has helped the
researchers suggest a possible therapeutic approach for limiting brain damage
in humans.
The results were published online in Nature on Dec. 8.
The bulk of direct research concerning the physiological
effects of TBIs is conducted post mortem. Scientists dissect a deceased
patient's tissue to learn the full extent of the injury and what types of brain
cells were damaged or killed.
But very little is known about what happens at the cellular
level in the first hours after an injury, which has hindered the development of
therapies that could prevent such damage from occurring in the first place.
For the past several years, Theo Roth, a senior majoring in
biology at Stanford, has spent his summers and other academic breaks working in
Dorian McGavern's lab at the National Institute of Neurological Disorders and
Stroke (NINDS), part of the National Institutes of Health. In that time, Roth
and other members of McGavern's research group designed a model in which they
could inflict a specific injury to a mouse's brain and use an intracranial
microscope to image individual cells, starting at five minutes after the
injury.
"We can actually see how all the cell populations there
react dynamically," said Roth, the first author on the research paper.
"Then, knowing what the cells do – how they change function and morphology
– we could piece together what their roles are and how they interact, and then
what types of interventions might be relevant."
Evidence in humans
The brain's first line of defense is called the meninges, a
thin layer of tissue that wraps the brain and creates a nearly impermeable
barrier to harmful molecules. At the direct site of the injury, however, Roth
found that the meninges can become damaged, tearing blood vessels and causing
hemorrhaging. As cells in the meninges and other nearby tissues die, their
toxic innards – in particular, molecules called reactive oxygen species (ROS) –
can leak through the meninges onto healthy brain cells.
The brain tries to plug the holes in the meninges, Roth
said, by quickly mobilizing special cells called microglia toward the site of
the injury, a reaction that had never been seen in living brains before this
study. The patch isn't perfect, however, and some ROS and other potentially
toxic molecules still leak through to the brain cells. Within nine to 12 hours
after the initial injury, brain cells begin to die.
These observations were very similar to analysis of human
MRI scans conducted by study co-author Lawrence Latour, a scientist from NINDS
and the Center for Neuroscience and Regenerative Medicine.
Latour examined 142 patients who had recently suffered a
concussion but whose initial MRI scans had not revealed any physical damage to
the brain tissue. Many of these patients were sent home from the hospital with
the negative scans, but had since suffered headaches, memory loss or other
hallmark symptoms of a mild brain injury.
Latour injected the patients with a dye and conducted a
follow-up MRI scan; in 49 percent of these patients, Latour and his colleagues
saw the dye leaking through the meninges. This, the study authors said,
indicates that a similar process involving the meninges, microglia and
oxidative agents can play a role in causing neurologic damage in humans.
This realization could lead to devising emergency therapies.
A roadmap for treatment
The researchers began searching for ways to prevent the
damage caused when ROS pass through the meninges. They zeroed in on a natural
antioxidant molecule found in human cells called glutathione that can chemically neutralize ROS
molecules.
By applying glutathione directly on the mouse's skull moments after the
injury, the scientists were able to reduce cell death by 67 percent. Even
applying glutathione
three hours after the injury had a positive effect, reducing cell death by 51
percent.
"This idea that we have a time window within which to
work, potentially up to three hours, is exciting and may be clinically
important," said McGavern, the senior author of the study.
Furthermore, because applying glutathione directly to the skull minimized the
damage, drug delivery via a subcutaneous patch might work as well as more
invasive procedures.
There are several steps before the technique could be
attempted in humans. The long-term effects in mice need to be measured and it
must be determined whether effective amounts of glutathione or other therapeutic drugs can pass
through the human skull.
"The acute phase of a traumatic brain injury is thought
to be untreatable," Roth said. "But this is a promising start."
Roth isn't sure of his role in the next steps of this
research; he is currently applying to dual MD-PhD programs with a goal of
eventually working in academic medicine, most likely therapeutic research.
"It was an incredible experience for me," Roth
said. "I was able to work in a lab –with advanced equipment and techniques
– that was willing to have an undergraduate come in and do advanced independent
work."
MEDIA CONTACT
Bjorn Carey, Stanford News Service: (650) 725-1944,
bccarey@stanford.edu
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