Posts Tagged brain

[WEB PAGE] Excitatory magnetic brain stimulation reduces emotional arousal to fearful faces, study shows

February 6, 2018

A new study in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging looks at the modulation of emotion in the brain

A new study published in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging reports that processing of negative emotion can be strengthened or weakened by tuning the excitability of the right frontal part of the brain.

Using magnetic stimulation outside the brain, a technique called repetitive transcranial magnetic stimulation (rTMS), researchers at University of Münster, Germany, show that, despite the use of inhibitory stimulation currently used to treat depression, excitatory stimulation better reduced a person’s response to fearful images.

The findings provide the first support for an idea that clinicians use to guide treatment in depression, but has never been verified in a lab. “This study confirms that modulating the frontal region of the brain, in the right hemisphere, directly effects the regulation of processing of emotional information in the brain in a ‘top-down’ manner,” said Cameron Carter, M.D., Editor of Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, referring to the function of this region as a control center for the emotion-generating structures of the brain. “These results highlight and expand the scope of the potential therapeutic applications of rTMS,” said Dr. Carter.

In depression, processing of emotion is disrupted in the frontal region of both the left and right brain hemispheres (known as the dorsolateral prefrontal cortices, dlPFC). The disruptions are thought to be at the root of increased negative emotion and diminished positive emotion in the disorder. Reducing excitability of the right dlPFC using inhibitory magnetic stimulation has been shown to have antidepressant effects, even though it’s based on an idea-that this might reduce processing of negative emotion in depression-that has yet to be fully tested in humans.

Co-first authors Swantje Notzon, M.D., and Christian Steinberg, Ph.D, and colleagues divided 41 healthy participants into two groups to compare the effects of a single-session of excitatory or inhibitory magnetic stimulation of the right dlPFC. They performed rTMS while the participants viewed images of fearful faces to evoke negative emotion, or neutral faces for a comparison.

Excitatory and inhibitory rTMS had opposite effects-excitatory reduced visual sensory processing of fearful faces, whereas inhibitory increased visual sensory processing. Similarly, excitatory rTMS reduced participants’ reaction times to respond to fearful faces and reduced feelings of emotional arousal to fearful faces, which were both increased by inhibitory rTMS.

Although the study was limited to healthy participants, senior author Markus Junghöfer, Ph.D., notes that “…these results should encourage more research on the mechanisms of excitatory and inhibitory magnetic stimulation of the right dlPFC in the treatment of depression.”

 

via Excitatory magnetic brain stimulation reduces emotional arousal to fearful faces, study shows

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[ARTICLE] Robotic Arm with Brain – Computer Interfacing – Full Text PDF

Abstract

Brain Computer Interfaces (BCI), is a modern technology which is currently revolutionizing the field of signal processing. BCI helped in the evolution of a new world where man and computer had never been so close. Advancements in cognitive neuro-sciences facilitated us with better brain imaging techniques and thus interfaces between machines and the human brain became a reality. Electroencephalography (EEG), which is the measurement and recording of electric signals using sensors arrayed across the scalp can be used for applications like prosthetic devices, applications in warfare, gaming, virtual reality and robotics upon signal conditioning and processing.

This paper is entirely based on Brain-Computer Interface with an objective of actuating a robotic arm with the help of device commands derived from EEG signals. This system unlike any other existing technology is purely non-invasive in nature, cost effective and is one of its kinds that can serve various requirements such as prosthesis. This paper suggests a low cost system implementation that can even serve as a reliable substitute for the existing technologies of prosthesis like BIONICS. […]

via Robotic Arm with Brain – Computer Interfacing – ScienceDirect

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[WEB SITE] Monthly cycles of brain activity linked to seizures in patients with epilepsy

January 8, 2018
UC San Francisco neurologists have discovered monthly cycles of brain activity linked to seizures in patients with epilepsy. The finding, published online January 8 in Nature Communications, suggests it may soon be possible for clinicians to identify when patients are at highest risk for seizures, allowing patients to plan around these brief but potentially dangerous events.

“One of the most disabling aspects of having epilepsy is the seeming randomness of seizures,” said study senior author Vikram Rao, MD, PhD, an assistant professor of neurology at UCSF and member of the UCSF Weill Institute for Neurosciences. “If your neurologist can’t tell you if your next seizure is a minute from now or a year from now, you live your life in a state of constant uncertainty, like walking on eggshells. The exciting thing here is that we may soon be able to empower patients by letting them know when they are at high risk and when they can worry less.”

Epilepsy is a chronic disease characterized by recurrent seizures — brief storms of electrical activity in the brain that can cause convulsions, hallucinations, or loss of consciousness. Epilepsy researchers around the world have been working for decades to identify patterns of electrical activity in the brain that signal an oncoming seizure, but with limited success. In part, Rao says, this is because technology has limited the field to recording brain activity for days to weeks at most, and in artificial inpatient settings.

At UCSF Rao has pioneered the use of an implanted brain stimulation device that can quickly halt seizures by precisely stimulating a patient’s brain as a seizure begins. This device, called the NeuroPace RNS® System, has also made it possible for Rao’s team to record seizure-related brain activity for many months or even years in patients as they go about their normal lives. Using this data, the researchers have begun to show that seizures are less random than they appear. They have identified patterns of electrical discharges in the brain that they term “brain irritability” that are associated with higher likelihood of having a seizure.

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The new study, based on recordings from the brains of 37 patients fitted with NeuroPace implants, confirmed previous clinical and research observations of daily cycles in patients’ seizure risk, explaining why many patients tend to experience seizures at the same time of day. But the study also revealed that brain irritability rises and falls in much longer cycles lasting weeks or even months, and that seizures are more likely to occur during the rising phase of these longer cycles, just before the peak. The lengths of these long cycles differ from person to person but are highly stable over many years in individual patients, the researchers found.

The researchers show in the paper that when the highest-risk parts of a patient’s daily and long-term cycles of brain irritability overlap, seizures are nearly seven times more likely to occur than when the two cycles are mismatched.

Rao’s team is now using this data to develop a new approach to forecasting patients’ seizure risk, which could allow patients to avoid potentially dangerous activities such as swimming or driving when their seizure risk is highest, and to potentially take steps (such as additional medication doses) to reduce their seizure risk, similar to how people with asthma know to take extra care to bring their inhalers when pollen levels are high.

“I like to compare it to a weather forecast,” Rao said. “In the past, the field has focused on predicting the exact moment a seizure will occur, which is like predicting when lightning will strike. That’s pretty hard. It may be more useful to be able tell people there is a 5 percent chance of a thunderstorm this week, but a 90 percent chance next week. That kind of information lets you prepare.”

Source:
https://www.ucsf.edu/

via Monthly cycles of brain activity linked to seizures in patients with epilepsy

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[ARTICLE] The Functional Recovery and the Associated Cortical Reorganization Following Constraint-Induced Movement Therapies (CIMTs) in Stroke. – Full Text PDF

Abstract

Constraint-Induced Movement Therapies (CIMTs) including the original Constraint- Induced Movement Therapy (CIMT) and the Modified Constraint-Induced Movement Therapy (mCIMT) gained considerable popularity as a treatment approach for upper extremity rehabilitation among patients with mild-to-moderate stroke.

However, a major barrier in rehabilitation generally and in CIMTs specifically; is the limited objectivity of some commonly used outcome measures and lack sensitivity to define “True” recovery vs. compensation. Thereby, they may not sufficiently detect of long term consequences and the associated neurological recovery. An essential approach to overcome such barrier is to better understand functional motor recovery, associated neural changes and how they may relate to recovery of the pre-morbid movement pattern.

Such Understanding for these relationships would add more in-depth insights on the
functional relevance of plastic brain changes in stroke following CIMTs to optimize the field of neuro-rehabilitation. This review synthesizes findings from studies to on the use of the CIMTs including CIMT and mCIMT as efficient practice in the management of upper limb dysfunction following a stroke. The analysis will include (1) the functional recovery and (2) the cortical reorganization following the use of mCIMT and CIMT on patients in the chronic stage following stroke.

Introduction

Stroke is considered the fifth leading cause of death in the United
States [1]. To date, stroke affects at least 6.4 million persons in the United
States [2]. Projections show that by 2030, an additional 3.4 million
people above 18 years will have had a stroke which is approximately a
20.5% increase in prevalence from 2012 statistics [1]. Stroke is a leading
cause of serious long-term disability in the United States [1].

Arm paresis is one of the most common impairments after stroke
[3,4]. After six months, about two-thirds of patients continue to suffer
from arm sensorimotor impairment that impacts the individual’s
activities of daily living [5]. Motor deficits consist of weakness of
specific muscles [6], abnormal muscle tone [7-9], abnormal postural
adjustments [10], abnormal movement synergies [11], lack of mobility
between structures at the shoulder girdle [10] and incorrect timing
of components within a movement pattern [12]. As a result of such
impairment, patients may progressively avoid using the affected arm in
favor of the unaffected arm for successful ADL, resulting in a learned
non-use phenomenon [13].[…]

Full Text PDF

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[WEB SITE] Findings reveal how seizures can have lasting detrimental effects on memory

October 16, 2017

Although it’s been clear that seizures are linked to memory loss and other cognitive deficits in patients with Alzheimer’s disease, how this happens has been puzzling. In a study published in the journal Nature Medicine, a team of researchers reveals a mechanism that can explain how even relatively infrequent seizures can lead to long-lasting cognitive deficits in animal models. A better understanding of this new mechanism may lead to future strategies to reduce cognitive deficits in Alzheimer’s disease and other conditions associated with seizures, such as epilepsy.

“It’s been hard to reconcile how infrequent seizures can lead to persistent changes in memory in patients with Alzheimer’s disease,” said corresponding author Dr. Jeannie Chin, assistant professor of neuroscience at Baylor College of Medicine. “To solve this puzzle, we worked with a mouse model of Alzheimer’s disease focusing on the genetic changes that seizures might trigger in the memory center of the brain, the hippocampus, that could lead to loss of memory or other cognitive deficits.”

The researchers measured the levels of a number of proteins involved in memory and learning and found that levels of the protein deltaFosB strikingly increase in the hippocampus of Alzheimer’s disease mice that had seizures. DeltaFosB already is well known for its association with other neurological conditions linked to persistent brain activity of specific brain regions, such as addiction. In this study, the researchers found that after a seizure, the deltaFosB protein remains in the hippocampus for an unusually long time; its half-life – the time it takes for the amount of protein to decrease by half – is eight days. Most proteins have a half-life that is between hours and a day or two.

“Interestingly, because deltaFosB is a transcription factor, meaning that its job is to regulate the expression of other proteins, these findings led us to predict that the increased deltaFosB levels might be responsible for suppressing the production of proteins that are necessary for learning and memory,” Chin said. “In fact, we found that when the levels of deltaFosB increase, those of other proteins, such as calbindin, decrease. Calbindin also has been known for a long time to be involved in Alzheimer’s disease and epilepsy, but its mechanism of regulation was not known. We then hypothesized that deltaFosB might be regulating the production of calbindin.”

Further investigations supported the researchers’ hypothesis. The scientists showed that deltaFosB can bind to the gene calbindin suppressing the expression of the protein. When they either prevented deltaFosB activity or experimentally increased calbindin expression in the mice, calbindin levels were restored and the mice improved their memory. And when researchers experimentally increased deltaFosB levels in normal mice, calbindin expression was suppressed and the animals’ memory deteriorated, demonstrating that deltaFosB and calbindin are key regulators of memory.

Connecting pieces of the puzzle

“Our findings have helped us answer the question of how even infrequent seizures can have such lasting detrimental effects on memory,” Chin said. “We found that seizures can increase the levels of deltaFosB in the hippocampus, which results in a decrease in the levels of calbindin, a regulator of memory processes. DeltaFosB has a relatively long half-life, therefore even when seizures are infrequent, deltaFosB remains in the hippocampus for weeks acting like a brake, reducing the production of calbindin and other proteins, and disrupting the consequent brain activity involved in memory. The regulation of gene expression far outlasts the actual seizure event that triggered it.”

The scientists found the same changes in deltaFosB and calbindin levels in the hippocampus of Alzheimer’s disease patients and in the temporal lobe of epilepsy patients. However, they underscore that it is too soon to know whether regulating deltaFosB or calbindin could improve or prevent memory problems or other cognitive deficits in people with Alzheimer’s disease. However, “now that we know that the levels of deltaFosB and calbindin are effective markers of brain activity in the hippocampus and memory function, we propose that these markers could potentially help assess clinical therapies for Alzheimer’s and other diseases with seizures,” Chin said.

Source: Findings reveal how seizures can have lasting detrimental effects on memory

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[BLOG POST] Strength training improves the nervous system’s ability to drive muscles

Imagine that the New Year has just begun. You’ve made a resolution to improve your physical fitness. In particular, you want to improve your muscle strength. You’ve heard that people with stronger muscles live longer and have less difficulty standing, walking, and using the toilet when they get older (Rantanen et al. 1999; Ruiz et al. 2008). So, you join a fitness centre and hire a personal trainer. The trainer assesses your maximal strength, and then guides you through a 4-week program that involves lifting weights which are about 80% of your maximum.

Sure enough, after the program, you become stronger (probably around 20% stronger) (Carroll et al. 2011). You think this is great – and it is! You are so excited, you decide to stand in front of your mirror, flex your biceps, and take a selfie (your plan is to post the picture to Facebook to show your friends how much bigger your muscles got). However, after examining the picture, you realise your muscles did not get bigger. Or perhaps they did get a little bigger, but not enough to explain your substantial improvement in strength. You are somewhat disappointed in this, but then you remember your goal was to get stronger, not necessarily bigger, so you post the picture, anyway.

Magnetic stimulation of the brain can be used to test how well a person can voluntarily drive their muscles.

Interestingly, the observations you made are completely consistent with the scientific literature. Within the first weeks of strength training, muscle strength can improve without a change in the size or architecture of the muscle (e.g., Blazevich et al. 2007). Consequently, researchers have speculated that initial improvements in muscle strength from strength training are due primarily to changes in the central nervous system. One hypothesis has been that strength training helps the nervous system learn how to better “drive” or communicate with muscles. This ability is termed voluntary activation, and it can be tested by stimulating the motor area of an individual’s brain while they perform a maximal contraction (Todd et al. 2003). If the stimulation produces extra muscle force, it means that the individual’s nervous system was not maximally activating their muscles. Currently, there is no consensus as to whether voluntary activation can actually be improved by strength training.

Therefore, we conducted a randomised, controlled trial in which one group of participants completed four weeks of strength training, while a control group did not complete the training (Nuzzo et al. in press). For the group who performed the training, each exercise session consisted of four sets of strong contractions of the elbow flexor muscles (i.e., the muscles that bend the elbow, such as the biceps). Before and after the four week intervention, both groups were tested for muscle strength, voluntary activation, and several other measures. The participants were healthy, university-aged, and they had limited or no experience with strength training.

WHAT DID WE FIND?

Prior to the intervention, the strength training and control groups had similar levels of muscle strength and activation of the elbow flexor muscles. After the intervention, the group who performed the strength training improved their strength by 13%. They also improved their voluntary activation from 88.7% to 93.4%. The control group did not improve muscle strength or voluntary activation.

SIGNIFICANCE AND IMPLICATIONS

The results from our study show that four weeks of strength training improves the brain’s ability to “drive” the elbow flexor muscles to produce their maximal force. This helps to explain how muscles can become stronger, without a change in muscle size or architecture. Moreover, the results suggest that clinicians should consider strength training as a treatment for patients with motor impairments (e.g., stroke), as these individuals are likely to have poor voluntary activation (Bowden et al. 2014).

PUBLICATION

Nuzzo JL, Barry BK, Jones MD, Gandevia SC, Taylor JL. Effects of four weeks of strength training on the corticomotoneuronal pathway. Med Sci Sports Exerc,  doi: 10.1249/MSS.0000000000001367.

KEY REFERENCES

Blazevich AJ, Gill ND, Deans N, Zhou S. Lack of human muscle architectural adaptation after short-term strength training. Muscle Nerve 35: 78-86.

Bowden JL, Taylor JL, McNulty PA. Voluntary activation is reduced in both the more- and less-affected upper limbs after unilateral stroke.Front Neurol 5: 239, 2014.

Carroll TJ, Selvanayagam VS, Riek S, Semmler RG. Neural adaptations to strength training: moving beyond transcranial magnetic stimulation and reflex studies. Acta Physiol 202: 119-140, 2011.

Rantanen T, Guralnik JM, Foley D, Masaki K, Leveille S, Curb JD, White L. Midline hand grip strength as a predictor of old age disability.JAMA 281: 558-560, 1999.

Ruiz JR, Sui X, Lobelo F, Morrow Jr. JR, Jackson AW, Sjöström M, Blair SN. Association between muscular strength and mortality in men: prospective cohort study. BMJ 337: a439, 2008.

Todd G, Taylor JL, Gandevia SC. Measurement of voluntary activation of fresh and fatigued human muscles using transcranial magnetic stimulation. J Physiol 555: 661-671, 2003.

AUTHOR BIO

Jim Nuzzo is a Postdoctoral Fellow at Neuroscience Research Australia (NeuRA). His research investigates how strength training alters the neural connections between the brain and muscles. Click here to read Jim’s other blogs.

Source: Strength training improves the nervous system’s ability to drive muscles – Motor Impairment

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[Editorial] Motor Priming for Motor Recovery: Neural Mechanisms and Clinical Perspectives – Neurology

Editorial on the Research Topic

Motor Priming for Motor Recovery: Neural Mechanisms and Clinical Perspectives

The Oxford dictionary defines the term priming as “a substance that prepares something for use or action.” In this special issue, we define motor priming as a technique, experience, or activity targeting the motor cortex resulting in subsequent changes in motor behavior. Inadequate functional recovery after neural damage is a persisting burden for many, and this insufficiency highlights the need for new neurorehabilitation paradigms that facilitate the capacity of the brain to learn and recover. The concept of motor priming has gained importance in the last decade. Numerous motor priming paradigms have emerged to demonstrate success to improve functional recovery after injury. Some of the successful priming paradigms that have shown to alter motor behavior and are easily implementable in clinical practice include non-invasive brain stimulation, movement priming, motor imagery, and sensory priming. The full clinical impact of these priming paradigms has not yet been realized due to limited evidence regarding neural mechanisms, safety and effectiveness, dosage, individualization of parameters, identification of the appropriate therapies that need to be provided in combination with the priming technique, and the vital time window to maximize the effectiveness of priming. In this special issue, four manuscripts address critical questions that will enhance our understanding of motor priming paradigms and attempt to bridge the gap between neurophysiology and clinical implementation.

In their study, “Non-Invasive Brain Stimulation to Enhance Upper Limb Motor Practice Poststroke: A Model for Selection of Cortical Site,” Harris-Love and Harrington elegantly address the extremely important issue of individualizing brain stimulation for upper limb stroke recovery. Many brain stimulation techniques show high interindividual variability and low reliability as the “one-size-for-all” does not fit the vast heterogeneity in recovery observed in stroke survivors. In this article, the authors propose a novel framework that personalizes the application of non-invasive brain stimulation based on understanding of the structural anatomy, neural connectivity, and task attributes. They further provide experimental support for this idea with data from severely impaired stroke survivors that validate the proposed framework.

The issue of heterogeneity poststroke is also addressed by Lefebvre and Liew in “Anatomical Parameters of tDCS to modulate the motor system after stroke: A review.” These authors discuss the variability in research using tDCS for the poststroke population. According to the authors, the most likely sources of variability include the heterogeneity of poststroke populations and the experimental paradigms. Individually based variability of results could be related to various factors including: (1) molecular factors such as baseline measures of GABA, levels of dopamine receptor activity, and propensity of brain-derived neurotropic factor expression; (2) time poststroke, (3) lesion location; (4) type of stroke; and (5) level of poststroke motor impairment. Variability related to experimental paradigms include the timing of the stimulation (pre- or post-training), the experimental task, and whether the protocol emphasizes motor performance (a temporary change in motor ability) or motor learning based (more permanent change in motor ability). Finally, the numerous possibilities of electrode placement, neural targets, and the different setups (monocephalic versus bi-hemispheric) add further complexity. For future work with the poststroke population, the authors suggest that tDCS experimental paradigms explore individualized neural targets determined by neuronavigation.

In another exciting study in this issue, Estes et al. tackle the timely topic of spinal reflex excitability modulated by motor priming in individuals with spinal cord injury. The authors choose to test four non-pharmacological interventions: stretching, continuous passive motion, transcranial direct current stimulation, and transcutaneous spinal cord stimulation to reduce spasticity. Three out of four techniques were associated with reduction in spasticity immediately after treatment, to an extent comparable to pharmacological approaches. These priming approaches provide a low-cost and low-risk alternative to anti-spasticity medications.

In another clinical study in individuals with spinal cord injury, Gomes-Osman et al. examined effects of two different approaches to priming. Participants were randomized to either peripheral nerve stimulation (PNS) plus functional task practice, PNS alone, or conventional exercise therapy. The findings were unexpected. There was no change in somatosensory function or power grip strength in any of the groups. Interestingly, all of the interventions produced changes in precision grip of the weaker hand following training. However, only PNS plus functional task practice improved precision grip in both hands. The authors found that baseline corticospinal excitability were significantly correlated to changes in precision grip strength of the weaker hand. The lack of change in grip strength in any of the groups was surprising. Previous evidence suggests, however, that the corticomotor system is more strongly activated during precision grip as compared to power grip, and the authors suggest that interventions targeting the corticomotor system (i.e., various priming methods) may more strongly effect precision grip.

Overall, this special issue brings together an array of original research articles and reviews that further enhance our understanding of motor priming for motor recovery with an emphasis on neural mechanisms and clinical implementation. We hope that the studies presented encourage future studies on motor priming paradigms to optimize the potential for functional recovery in the neurologically disadvantaged population, and further our understanding of neuroplasticity after injury.

Author Contributions

SM and MS have made a substantial, direct, and intellectual contribution to the work and approved it for publication.

Conflict of Interest Statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Funding

SM is supported by funding from the National Institutes of Health (R01HD075777).

Source: Frontiers | Editorial: Motor Priming for Motor Recovery: Neural Mechanisms and Clinical Perspectives | Neurology

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[BLOG POST] Vagus Nerve Stimulation…Is it for YOU?

Epilepsy Talk

Having a Vagus Nerve Stimulator implanted can be a tough decision.  Is it right for you? Will it work? What are the side effects and consequences?

I did some research and got the low-down on what it is, how it works and some interesting statistics.  (If you are already acquainted with the VNS and are on the fence, you might want to just skip down to risks and benefits sections.)

How it works

Vagus Nerve Stimulation (VNS) has been used to treat more than 30,000 epilepsy patients worldwide. It’s designed to prevent or interrupt seizures or electrical disturbances in the brain for people with hard to control seizures. Used in conjunction with anti-seizure medications, the VNS uses electrical pulses that are delivered to the vagus nerve in the neck and travel up into the brain.

The good news is that the vagus nerve has very few pain fibers, so it’s…

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[WEB SITE] Research provides insights for why some epilepsy patients continue to experience postoperative seizures

New research from the University of Liverpool, published in the journal Brain, has highlighted the potential reasons why many patients with severe epilepsy still continue to experience seizures even after surgery.

Epilepsy continues to be a serious health problem and is the most common serious neurological disorder. Medically intractable temporal lobe epilepsy (TLE) remains the most frequent neurosurgically treated epilepsy disorder.

Many people with this condition will undergo a temporal lobe resection which is a surgery performed on the brain to control seizures. In this procedure, brain tissue in the temporal lobe is resected, or cut away, to remove the seizure focus.

Unfortunately, approximately one in every two patients with TLE will not be rendered completely seizure free after temporal lobe surgery, and the reasons underlying persistent postoperative seizures have not been resolved.

Reliable biomarkers

Understanding the reasons why so many patients continue to experience postoperative seizures, and identifying reliable biomarkers to predict who will continue to experience seizures, are crucial clinical and scientific research endeavours.

Researchers from the University’s Institute of Translational Medicine, led by Neuroimaging Lead Dr Simon Keller and collaborating with Medical University Bonn (Germany), Medical University of South Carolina (USA) and King’s College London, performed a comprehensive diffusion tensor imaging (DTI) study in patients with TLE who were scanned preoperatively, postoperatively and assessed for postoperative seizure outcome.

Diffusion tensor imaging (DTI) is a MRI-based neuroimaging technique that provides insights into brain network connectivity.

The results of these scans allowed the researchers to examine regional tissue characteristics along the length of temporal lobe white matter tract bundles. White matter is mainly composed of axons of nerve cells, which form connections between various grey matter areas of the brain, and carry nerve impulses between neurons allowing communication between different brain regions.

Through their analysis the researchers could determine how abnormal the white matter tracts were before surgery and how the extent of resection had affected each tract from the postoperative MRI scans.

Surgery outcomes

The researchers identified preoperative abnormalities of two temporal lobe white matter tracts that are not included in standardised temporal lobe surgery in patients who had postoperative seizures but not in patients with no seizures after surgery.

The two tracts were in the ‘fornix’ area on the same side as surgery, and in the white matter of the ‘parahippocampal’ region on the opposite side of the brain.

The tissue characteristics of these white matter tracts enabled researchers to correctly identify those likely to have further seizures in 84% of cases (sensitivity) and those unlikely to have further seizures in 89% of cases (specificity). This is significantly greater than current estimates.

The researchers also found that a particular temporal lobe white matter tract called the ‘uncinate fasciculus’ was abnormal – and potentially involved in the generation of seizures – in patients with excellent and suboptimal postoperative outcomes.

However, it was found that significantly more of this tract was surgically resected/removed in the patients with an excellent outcome.

New insights

Dr Simon Keller, said: “There is scarce information on the prediction of postoperative seizure outcome using preoperative imaging technology, and this study is the first to rigorously investigate the tissue characteristics of temporal lobe white matter tracts with respect to future seizure classifications.

“Although there is some way to go before this kind of data can influence routine clinical practice, these results may have the potential to be developed into imaging prognostic markers of postoperative outcome and provide new insights for why some patients with temporal lobe epilepsy continue to experience postoperative seizures.”

Source: Research provides insights for why some epilepsy patients continue to experience postoperative seizures

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[WEB SITE] Brain surgery helps remove scar tissue causing seizures in epilepsy patients

By the time epilepsy patient Erika Fleck came to Loyola Medicine for a second opinion, she was having three or four seizures a week and hadn’t been able to drive her two young children for five years.

“It was no way to live,” she said.

Loyola epileptologist Jorge Asconapé, MD, recommended surgery to remove scar tissue in her brain that was triggering the seizures. Neurosurgeon Douglas Anderson, MD, performed the surgery, called an amygdalohippocampectomy. Ms. Fleck hasn’t had a single seizure in the more than three years since her surgery.

“I’ve got my life back,” she said. “I left my seizures at Loyola.”

Surgery can be an option for a minority of patients who do not respond to medications or other treatments and have epileptic scar tissue that can be removed safely. In 60 to 70 percent of surgery patients, seizures are completely eliminated, and the success rate likely will improve as imaging and surgical techniques improve, Dr. Anderson said.

Traditionally, patients would have to try several medications with poor results for years or decades before being considered for surgery, according to the Epilepsy Foundation. “More recently, surgery is being considered sooner,” the foundation said. “Studies have shown that the earlier surgery is performed, the better the outcome.” (Ms. Fleck is a service coordinator for the Epilepsy Foundation North/Central Illinois Iowa and Nebraska.)

Dr. Asconapé said Ms. Fleck was a perfect candidate for surgery because the scar tissue causing her seizures was located in an area of the brain that could be removed without damaging critical structures.

Ms. Fleck experienced complex partial seizures, characterized by a deep stare, unresponsiveness and loss of control for a minute or two. An MRI found the cause: A small area of scar tissue in a structure of the brain called the hippocampus. The subtle lesion had been overlooked at another center.

Epilepsy surgery takes about three hours, and patients typically are in the hospital for two or three days. Like all surgery, epilepsy surgery entails risks, including infection, hemorrhage, injury to other parts of the brain and slight personality changes. But such complications are rare, and they pose less risk to patients than the risk of being injured during seizures, Dr. Asconapé said.

Loyola has been designated a Level Four Epilepsy Center by the National Association of Epilepsy Centers. Level Four is the highest level of specialized epilepsy care available. Level Four centers have the professional expertise and facilities to provide the highest level of medical and surgical evaluation and treatment for patients with complex epilepsy.

Loyola’s comprehensive, multidisciplinary Epilepsy Center offers a comprehensive multidisciplinary approach to epilepsy and seizure disorders for adults and children as young as two years old. Pediatric and adult epileptologist consultation and state-of-the-art neuroimaging and electrodiagnostic technology are used to identify and assess complex seizure disorders by short- and long-term monitoring.

Source: Loyola University Health System

Source: Brain surgery helps remove scar tissue causing seizures in epilepsy patients

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