Posts tagged cortex
Articles and news from the latest research reports.
The gene mutation that causes Huntington’s disease appears in every cell in the body, yet kills only two types of brain cells. Why? UCLA scientists used a unique approach to switch the gene off in individual brain regions and zero in on those that play a role in causing the disease in mice.
Published in the April 28 online edition of Nature Medicine, the research sheds light on where Huntington’s starts in the brain. It also suggests new targets and routes for therapeutic drugs to slow the devastating disease, which strikes an estimated 35,000 Americans.
“From day one of conception, the mutant gene that causes Huntington’s appears everywhere in the body, including every cell in the brain,” explained X. William Yang, professor of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior at UCLA. “Before we can develop effective strategies to treat the disorder, we need to first identify where it starts and how it ravages the brain.”
Huntington’s disease is passed from parent to child through a mutation in a gene called huntingtin. Scientists blame a genetic “stutter” — a repetitive stretch of DNA at one end of the altered gene—for the cell death and brain atrophy that progressively deprives patients of their ability to move, speak, eat and think clearly. No cure exists, and people with aggressive cases may die in as little as 10 years.
Huntington’s disease targets cells in two brain regions for destruction: the cortex and the striatum. Far more neurons die in the striatum—a cerebral region named after its striped layers of gray and white matter. But it’s unclear whether cortical neurons play a role in the disease, including striatal neurons’ malfunction and death.
Yang’s team used a unique approach to uncover where the mutant gene wreaks the most damage in the brain.
In 2008, Yang collaborated with co-first author Michelle Gray, a former UCLA postdoctoral researcher now at the University of Alabama, to engineer a mouse model for Huntington’s disease. The scientists inserted the entire human huntintin gene, including the stutter, into the mouse genome. As the animals’ brains atrophied, the mice developed motor and psychiatric-like problems similar to the human patients.
In the current study, Yang and Nan Wang, co-first author and UCLA postdoctoral researcher, took the model one step further. They integrated a “genetic scissors” that snipped off the stutter and shut down the defective gene—first in the cortical neurons, then the striatal neurons and finally in both sets of cells. In each case, they measured how the mutant gene influenced disease development in the cells and affected the animals’ brain atrophy, motor and psychiatric-like symptoms.
“The genetic scissors gave us the power to study the role of any cell type in Huntington’s,” said Wang. “We were surprised to learn that cortical neurons play a key role in initiating aspects of the disease in the brain.”
The UCLA team discovered that reducing huntingtin in the cortex partially improved the animals’ symptoms. More importantly, shutting down mutant huntingtin in both the cortical and striatal neurons—while leaving it untouched in the rest of the brain— corrected every symptom they measured in the mice, including motor and psychiatric-like behavioral impairment and brain atrophy.
“We have evidence that the gene mutation highjacks communication between the cortical and striatal neurons,” explained Yang. “Reducing the defective gene in the cortex normalized this communication and helped lessen the disease’s impact on the striatum.”
“Our research helps to shed lights on an age-old question in the field,” he added. “Where does Huntington’s disease start? Equally important, our findings provide crucial insights on where to target therapies to reduce mutant gene levels in the brain—we should target both cortical and striatal neurons.”
Some of the current experimental therapies can be delivered only to limited brain areas, because their properties do not allow them to broadly spread in the brain.
The UCLA team’s next step will be to study how mutant huntingtin affects cortical and striatal neurons’ function and communication, and to identify therapeutic targets that may normalize cellular miscommunication to help slow progression of the disease.
Similar connectivity profiles in humans and monkeys used to generate a Theory of Mind
The ability to infer emotion or intention in others from their outward appearance and behavior, has been called a “Theory of Mind” (TOM). While cognitive scientists have debated whether animals other than humans possess a TOM, many animals (like monkeys) clearly react to facial expression or body movements. One area of the human brain that has received considerable attention in discussions of TOM, is the temporo-parietal junction (TPJ). If each half of the brain is viewed as a boxing glove, the TPA corresponds to the junction between the “thumb” and body of the glove. To explore whether the TPJ regions of humans and monkeys have similar “functional connectivity” profiles, a group of Oxford researchers turned to high resolution at-rest fMRI. The researchers generated correlation maps between each time series obtained for specific voxel regions of interest. Their results, just published in PNAS, show that the most similar TPJ connectivity profiles correspond to areas that process, among other things, faces and social stimuli within the temporal cortex.
When the brain first begins to develop in the womb, the cortex is basically a smooth sheet. The most noticeable topological feature in the cortex of all higher vertebrates, the lateral or Sylvian fissure, begins to take shape as an invagination in the side that proceeds from front to back. This fold, with the TPA at its apex, remains as the primary feature of the cortex even as it grows increasingly convoluted. It is little wonder that many of the most interesting mental phenomena, and malady, are often attributed to this region. Stimulation of this area has produced effects as widespread as out of body experiences, impostor syndromes, and even phantom body doubles with precise geometrically offsets to the primary body position.
It is a bit of a paradox perhaps, that many studies which look for uniform or predictable features in the brain have instead hit upon the very region where any such pigeonholing is most labile. In other words, when the brain folds, the TPA is precisely the region where the most scrunching happens, with the result the mature structure typically shows the most variance. In animals like cats and many monkeys, the cortical gyri and sulci, have virtually the same pattern in each individual. In humans however, attempts to assign names to specific folds of the TPA region is like playing a game of pin the tail on the donkey. For example, the Angular gyrus, Wernicke’s area, Supramarginal gyrus, and Inferior parietal area, can all be variously designated as part of the TPA.
Recent attempts to define a default mode network (DMN) using fMRI have included this same region. In theory, the DMN can be used to distinguish sleep from arousal. It was noted that neurons which project out of the cortex in this region have, in effect, more options open to them than those virtually anywhere else in the brain. For example, directly under the angular gyrus is the area known as the temporo-parietal fiber association area. It includes at least seven long range white matter superhighways. That is not to say TPA neurons have free reign to board any tract they choose, (especially those like the optic radiations whose foundations are strongly and quickly set by myelin), but certainly the wide variance in behavioral correlates of these cells has an anatomical basis.
The Oxford study used Macaques, a monkey which has been on a separate evolutionary path from humans for around 30 million years. They note that the superior temporal (STS) region of the Macaque contains face cells that have been found to be more responsive to social cues rather than to identity. The researchers included the STS in their MRI meta-analysis, and also incorporated information from the BrainMap database, a large repository of neuroimaging data. While it is encouraging to see big data being put to use, it is often difficult to follow exactly how the data is processed to yield the so-called “activation likelihood estimation maps for activity elicited by theory of mind paradigms and by face discrimination or processing.”
As various federal projects begin to assemble connectomes for the human brain, functional connectivity studies that use highly processed MRI data, will need to be made as simple and straightforward as possible if they are to be put to widespread use. MRI tractography is a related technology that can assign physical connectivity by performing a meta-analysis on diffusion tensor data. Using scans and connectomes to generate theories to explain some of the strange mental phenomena generated secondary to stroke or by various kinds of electromagnetic stimulation are the best approaches we have at the moment. New technologies generated by the BRAIN Initiative will hopefully allow a finer-grained exploration of theory of mind.
Mice Give New Clues to Origins of OCD
Columbia Psychiatry researchers have identified what they think may be a mechanism underlying the development of compulsive behaviors. The finding suggests possible approaches to treating or preventing certain characteristics of OCD.
OCD consists of obsessions, which are recurrent intrusive thoughts, and compulsions, which are repetitive behaviors that patients perform to reduce the severe anxiety associated with the obsessions. The disorder affects 2–3 percent of people worldwide and is an important cause of illness-related disability, according to the World Health Organization.
Using a new technology in a mouse model, the researchers found that repeated stimulation of specific circuits linking the brain’s cortex and striatum produces progressive repetitive behavior. By targeting this region, it may be possible to stop abnormal circuit changes before they become pathological behaviors in people at risk for obsessive-compulsive disorder (OCD). The study, which was led by Susanne Ahmari, MD, PhD, assistant professor of clinical psychiatry at Columbia Psychiatry and the New York State Psychiatric Institute, was published in the June 7 issue of Science.
While the obsessions and compulsions that are the hallmarks of OCD are thought to be centered in the cortex, which controls thoughts, and the striatum, which controls movements, little is known about how abnormalities in these brain regions lead to compulsive behaviors in patients.
To simulate the increased activity that takes place in the brains of OCD patients, Dr. Ahmari and her colleagues used a new technology called optogenetics, in which light-activated ion channels are expressed in subsets of neurons in mice, and neural circuits are then selectively activated using light delivered through fiberoptic probes.
“What we found was really surprising,” said Dr. Ahmari. “That activation of cortico-striatal circuits did not lead directly to repetitive behaviors in the mice. But if we repeatedly stimulated for multiple days in a row for only five minutes a day, we saw a progressive development of repetitive behaviors—in this case, repetitive grooming behavior—that persisted up to two weeks after the stimulation was stopped.”
She added, “And not only that, when we treated the mice with fluoxetine, one of the most common medications used for OCD, their behavior went back to normal.” The current study, as well as others currently being performed by Dr. Ahmari and her team, may ultimately provide clues for new treatment targets in terms of both novel drug development and direct stimulation techniques, including deep brain stimulation (DBS).
Research Shows How Ritalin Affects Brains of Kids With ADHD
Ritalin activates specific areas of the brain in children with attention-deficit/hyperactivity disorder (ADHD), mimicking the brain activity of children without the condition, a new review says.
"This suggests that Ritalin does bring the brain [of a child with ADHD] back to the brain the typically developing kid has," said study author Constance Moore, associate director of the translational center for comparative neuroimaging at the University of Massachusetts Medical School.
Analyzing data from earlier studies that looked at how children’s brains were affected by doing certain tasks that are sometimes challenging for kids with ADHD, the researchers found that Ritalin (methylphenidate) was having a visible impact on three areas of the brain known to be associated with ADHD: the cortex, the cerebellum and the basal ganglia.
The study could be helpful in diagnosing and treating children with ADHD, Moore said. “It may be helpful to know that in certain children, Ritalin is having a physiological effect in the areas of the brain involved with attention and impulse control,” she said.
The research was published recently in the Harvard Review of Psychiatry.
Nine studies analyzed by the researchers used functional MRI to evaluate brain changes after children had taken a single dose of Ritalin. The children were involved in different types of tasks that tested their ability to focus and inhibit an impulse to act.
For example, to observe the brain’s reaction during a test of what is called “inhibitory control,” a child was told that every time he saw a zero show up on a screen, he should push the button on the right; every time he saw an X appear, he should push the left button. The children would then be asked to flip their responses, pushing the left button when they saw a zero.
"That’s hard to do," Moore said, "because you’ve developed the habit [of pushing the other button], so you have to suppress your impulse. If you do 20 zeros and keep pressing and then you see an X, most kids with ADHD will hit the wrong button."
In three out of five of the inhibitory control studies, Ritalin at least partially normalized brain activation in ADHD children.
To note how the brain reacted to a selective attention test, Moore said, children would first be asked, for example, what word they were seeing. The word would be “red,” and the color of the type also would be red. Then they would be shown the word “red,” but the color of the type would be green. In several studies, Ritalin affected activation in the frontal lobes during such inhibitory control tasks.
Most of the studies included in the review were performed in the United States or the United Kingdom. The majority of participants were adolescent boys, and all studies compared their results to healthy children of the same approximate age.
Because none of the studies looked at the correlation between ADHD symptoms and whether the child was taking Ritalin, there is no way to link the changes in brain activation with clinical improvement, Moore said. “It’s possible that kids who are not responsive to Ritalin may have brain changes too,” she said.
ADHD affects between 3 percent and 7 percent of school-aged children in the United States, according to the American Psychiatric Association. Boys are more likely to have ADHD than girls.
One expert was not surprised by the results.
"The review article shows there is a consensus of well-designed imaging studies showing that [Ritalin] has an impact on the frontal cortex of the brain, where we have long believed these patients have issues," said Dr. Andrew Adesman, chief of developmental and behavioral pediatrics at the Steven & Alexandra Cohen Children’s Medical Center of New York, in New Hyde Park. Adesman wondered if Ritalin may play a role in helping the brain mature.
"Their data provides partial support for that," he said. "But if anything, the medicine seems to help the brain look more normal and doesn’t seem to do anything bad to it."
(Source: consumer.healthday.com)
Neon exposes hidden ALS cells
A small group of elusive neurons in the brain’s cortex play a big role in ALS (amyotrophic lateral sclerosis), a swift and fatal neurodegenerative disease that paralyzes its victims. But the neurons have always been difficult to study because there are so few of them and they look so similar to other neurons in the cortex.
In a new preclinical study, a Northwestern Medicine® scientist has isolated the motor neurons in the brain that die in ALS and, for the first time, dressed them in a green fluorescent jacket. Now they’re impossible to miss and easy to study.
The cells slide on neon jackets when they are born and continue to wear them as they age and become sick. As a result, scientists will now be able to track what goes wrong in these cells to cause their deaths and be able to search for effective treatments.
"We have developed the tool to investigate what makes these cells become vulnerable and sick," said Hande Ozdinler, senior author of the study and assistant professor of neurology at Northwestern University Feinberg School of Medicine. "This was not possible before."
Ozdinler and colleagues also identified the motor neurons that don’t die, enabling scientists to study what protects them.
The study will be published in the Journal of Neuroscience on May 1.
ALS, also known as Lou Gehrig’s disease, causes the death of muscle-controlling nerve cells in the brain and spinal cord (motor neurons). It results in rapidly progressing paralysis and death usually within three to five years of the onset of symptoms.
There are about 75,000 upper motor neurons affected in ALS out of some 2 billion cells in the brain. Previously, the only way to study the upper motor neurons was to extract them through surgery, a difficult process that was beyond the scope of most scientists and still didn’t allow examination of the ailing neurons at various stages of the disease.
"You couldn’t study them at the cellular level, so the research field ignored them," Ozdinler said. She is one of the few scientists in the country who studies cortical motor neurons. Most of ALS research has focused on the death of motor neurons in the spinal cord.
Key puzzle piece: Why ALS moves so swiftly
But the brain’s motor neurons are a key piece of the ALS puzzle. Their disintegration explains why the disease advances more swiftly than other neurodegenerative diseases. It had previously been thought that the spinal motor neurons died first and their demise led to the secondary death of the brain’s motor neurons. But Ozdinler’s recent research showed that the motor neurons in the brain and spinal cord die simultaneously.
"The whole system collapses at once," Ozdinler said. "It’s degeneration from both ends which is why the disease moves so swiftly."
Every voluntary movement is initiated and modulated by upper motor neurons — answering a cell phone, typing an email, walking to the store. The upper motor neurons tell the spinal motor neurons what to do. In ALS, both the directing neurons and the neurons that create the movement disintegrate at the same time.
Finding the light that never goes out
Ozdinler spent the last four years figuring out how to permanently sheath cortical motor neurons in fluorescence.
Although scientists can flag spinal cord motor neurons in fluorescence, it wears off as the neuron ages because the process uses an embryonic gene. Ozdinler wanted a longer lasting effect so scientists could study the neuron as it ages and develops ALS. She sorted through 6,000 upper motor neuron genes that are vulnerable to ALS before she found one — UCHL1 — that is expressed through adulthood.
She used that gene — which had been cloned with the fluorescence molecule — and created a mouse model whose upper motor neurons shimmer in green. Then she mated that mouse with an ALS transgenic mouse model. The result is a mouse with fluorescent diseased motor neurons in the brain.
"Now we have a model of one motor neuron population that dies and one that is resistant," Ozdinler said. "That’s the perfect experiment. You can ask what does this neuron have that makes it resistant and what does the other one have that makes it vulnerable? That’s what we will find out."
Marina Yasvoina, a graduate student, and Baris Genc, a postdoctoral fellow, both in Ozdinler’s lab, are the lead authors of the paper. Ozdinler collaborated with Gordon Shepherd, associate professor of physiology, and C.J. Heckman, professor in physiology, both at Feinberg.
"This work was possible thanks to the collaborative nature of Northwestern," Ozdinler said.
(Source: eurekalert.org)
MRI shows brain abnormalities in migraine patients
A new study suggests that migraines are related to brain abnormalities present at birth and others that develop over time. The research is published online in the journal Radiology.
Migraines are intense, throbbing headaches, sometimes accompanied by nausea, vomiting and sensitivity to light. Some patients experience auras, a change in visual or sensory function that precedes or occurs during the migraine. More than 300 million people suffer from migraines worldwide, according to the World Health Organization.
Previous research on migraine patients has shown atrophy of cortical regions in the brain related to pain processing, possibly due to chronic stimulation of those areas. Cortical refers to the cortex, or outer layer of the brain.
Much of that research has relied on voxel-based morphometry, which provides estimates of the brain’s cortical volume. In the new study, Italian researchers used a different approach: a surface-based MRI method to measure cortical thickness.
"For the first time, we assessed cortical thickness and surface area abnormalities in patients with migraine, which are two components of cortical volume that provide different and complementary pieces of information," said Massimo Filippi, M.D., director of the Neuroimaging Research Unit at the University Ospedale San Raffaele and professor of neurology at the University Vita-Salute’s San Raffaele Scientific Institute in Milan. "Indeed, cortical surface area increases dramatically during late fetal development as a consequence of cortical folding, while cortical thickness changes dynamically throughout the entire life span as a consequence of development and disease."
Dr. Filippi and colleagues used magnetic resonance imaging (MRI) to acquire T2-weighted and 3-D T1-weighted brain images from 63 migraine patients and 18 healthy controls. Using special software and statistical analysis, they estimated cortical thickness and surface area and correlated it with the patients’ clinical and radiologic characteristics.
Compared to controls, migraine patients showed reduced cortical thickness and surface area in regions related to pain processing. There was only minimal anatomical overlap of cortical thickness and cortical surface area abnormalities, with cortical surface area abnormalities being more pronounced and distributed than cortical thickness abnormalities. The presence of aura and white matter hyperintensities—areas of high intensity on MRI that appear to be more common in people with migraine—was related to the regional distribution of cortical thickness and surface area abnormalities, but not to disease duration and attack frequency.
"The most important finding of our study was that cortical abnormalities that occur in patients with migraine are a result of the balance between an intrinsic predisposition, as suggested by cortical surface area modification, and disease-related processes, as indicated by cortical thickness abnormalities," Dr. Filippi said. "Accurate measurements of cortical abnormalities could help characterize migraine patients better and improve understanding of the pathophysiological processes underlying the condition."
Additional research is needed to fully understand the meaning of cortical abnormalities in the pain processing areas of migraine patients, according to Dr. Filippi.
"Whether the abnormalities are a consequence of the repetition of migraine attacks or represent an anatomical signature that predisposes to the development of the disease is still debated," he said. "In my opinion, they might contribute to make migraine patients more susceptible to pain and to an abnormal processing of painful conditions and stimuli."
The researchers are conducting a longitudinal study of the patient group to see if their cortical abnormalities are stable or tend to worsen over the course of the disease. They are also studying the effects of treatments on the observed modifications of cortical folding and looking at pediatric patients with migraine to assess whether the abnormalities represent a biomarker of the disease.
(Source: eurekalert.org)
Brain-to-brain interface allows transmission of tactile and motor information between rats
Researchers have electronically linked the brains of pairs of rats for the first time, enabling them to communicate directly to solve simple behavioral puzzles. A further test of this work successfully linked the brains of two animals thousands of miles apart—one in Durham, N.C., and one in Natal, Brazil.
The results of these projects suggest the future potential for linking multiple brains to form what the research team is calling an “organic computer,” which could allow sharing of motor and sensory information among groups of animals. The study was published Feb. 28, 2013, in the journal Scientific Reports.
"Our previous studies with brain-machine interfaces had convinced us that the rat brain was much more plastic than we had previously thought," said Miguel Nicolelis, M.D., PhD, lead author of the publication and professor of neurobiology at Duke University School of Medicine. "In those experiments, the rat brain was able to adapt easily to accept input from devices outside the body and even learn how to process invisible infrared light generated by an artificial sensor. So, the question we asked was, ‘if the brain could assimilate signals from artificial sensors, could it also assimilate information input from sensors from a different body?’"
To test this hypothesis, the researchers first trained pairs of rats to solve a simple problem: to press the correct lever when an indicator light above the lever switched on, which rewarded the rats with a sip of water. They next connected the two animals’ brains via arrays of microelectrodes inserted into the area of the cortex that processes motor information.
Subcortical Damage Is ‘Primary Cause’ of Neurological Deficits after ‘Awake Craniotomy’
Injury to the subcortical structures of the inner brain is a major contributor to worsening neurological abnormalities after “awake craniotomy” for brain tumors, reports a study in the February issue of Neurosurgery, official journal of the Congress of Neurological Surgeons. The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.
During a procedure intended to protect critical functional areas in the outer brain (cortex), damage to subcortical areas—which may be detectable on MRI scans—is a major risk factor for persistent neurological deficits. “Our ability to identify and preserve cortical areas of function can still result in significant neurological decline postoperatively as a result of subcortical injury,” write Dr. Victoria T. Trinh and colleagues of The University of Texas MD Anderson Cancer Center, Houston.
Risk Factors for Neurological Deficits after Awake Craniotomy
The researchers analyzed factors associated with worsening neurological function after awake craniotomy for brain tumor surgery. In awake craniotomy, the patient is sedated but conscious so as to be able to communicate with the surgeon during the operation.
The patient is asked to perform visual and verbal tasks while specific areas of the cortex are stimulated, generating a functional map of the brain surface. This helps the surgeon navigate safely to the tumor without damaging the “eloquent cortex”—critical areas of the brain involved in language or movement.
The study included 241 patients who underwent awake craniotomy with functional brain mapping from 2005 through 2010. Of these, 40 patients developed new neurological abnormalities. Dr. Trinh and colleagues examined potential predictive factors—including changes on a type of MRI scan called diffusion-weighted imaging (DWI).
Of the 40 cases with new neurological deficits, 36 developed while the surgeon was operating in the subcortical areas of the brain. These are the inner structures of the brain, located beneath the outer, folded brain cortex. Just one abnormality developed while the surgeon was operating in the cortex only.
MRI Changes May Reflect Subcortical Damage
Neurological abnormalities developing while the surgeon was operating in the subcortex were likely to remain after surgery, and to persist at three months’ follow-up evaluation. Dr. Trinh and coauthors write, “Patients with intraoperative deficits during subcortical dissection were over six times more likely to have persistently worsened neurological function at three-month follow-up.”
In these patients, MRI scans showing more severe changes in the DWI pattern in the subcortex also predicted lasting neurological abnormalities. Of patients who had neurological deficits immediately after surgery and significant DWI changes, 69 percent had persistent deficits three months after surgery.
Patients who had “positive” cortical mapping—that is, in whom eloquent cortex was located during functional mapping—were somewhat more likely to have neurological abnormalities immediately after surgery. However, the risk of lasting abnormalities was not significantly higher compared to patients with negative cortical mapping.
Awake craniotomy with brain stimulation produces a “real-time functional map” of the brain surface that is invaluable to the neurosurgeon in deciding how best to approach the tumor. The new results suggest that, even when the eloquent cortex is not located on cortical mapping, subcortical areas near the tumor can still be injured during surgery. “Subcortical injury is the primary cause of neurological deficits following awake craniotomy procedures,” Dr. Trinh and colleagues write.
The researchers add, “Preserving subcortical areas during tumor resections may reduce the severity of both immediate and late neurological sequelae.” Based on their findings, they believe subcortical mapping techniques may play an important role in avoiding complications after awake craniotomy.
(Source: lww.com)
BrainBow is a technique where cells are made to express several fluorescent proteins, in essentially random amounts. The randomness derives from feedback loops in gene expression. Mixing of fluorescence wavelengths yields a remarkable colour contrast on the single-neuron level.
The method was originally developed by Jeff W. Lichtman and Joshua R. Sanes at the Department of Neurobiology, Harvard Medical School.
Read more about BrainBow on Wikipedia or an introduction at the Harvard Gazette.
Botox may help stroke patients
Injecting botox into the arm muscles of stroke survivors, with severe spasticity, changes electrical activity in the brain and may assist with longer-term recovery, according to new research.
Researchers at NeuRA (Neuroscience Research Australia) monitored nerve activity in the arms and brains of stroke survivors before and after botulinum toxin (botox) injections in rigid and stiff muscles in the arm.
They found that botox indeed improved arm muscles, but also altered brain activity in the cortex – the brain region responsible for movement, memory, learning and thinking.
“Botulinum toxin is used to treat a range of muscular and neurological conditions and our data shows that this treatment results in electrical and functional changes within the brain itself”, says Dr William Huynh, lead author of the study and a research neurologist at NeuRA.
“This effect of botox on the brain may arise because the toxin travels to the central nervous system directly, or because muscles treated with botox are sending different signals back to the brain”.
“Either way, we found that botox treatment in affected muscles not only improves muscle disorders in stroke patients, but also normalises electrical activity in the brain, particularly in the half of the brain not damaged by stroke”.
“Restoring normal activity in the unaffected side of the brain is particularly important because we suspect that abnormal information sent from affected muscles to the brain may be disrupting patients’ long-term recovery”, Dr Huynh concluded.
This paper is published in the journal Muscle and Nerve.