As a translational neuroscientist, this work immediately piqued my interest. It has direct implications for the research my lab does: We transplant young neurons into damaged brain areas in mice in an attempt to treat epileptic seizures and the damage they’ve caused. Like many labs, part of our work is based on a foundational belief that the hippocampus is a brain region where new neurons are born throughout life.
If the new study is right, and human brains for the most part don’t add new neurons after infancy, researchers like me need to reconsider the validity of the animal models we use to understand various brain conditions – in my case temporal lobe epilepsy. And I suspect other labs that focus on conditions including drug addiction, depression and post-traumatic stress disorder are thinking about what the UCSF study means for their investigations, too.
Neurogenesis – the production of new neurons – was previously thought to only occur during embryonic life, a time of extremely rapid brain growth and expansion, and the rodent findings were met with considerable skepticism. Then researchers discovered that new neurons are also born throughout life in the songbird brain, a species scientists use as a model for studying vocal learning. It started to look like neurogenesis plays a key role in learning and neuroplasticity – at least in some brain regions in a few animal species.
Even so, neuroscientists were skeptical that many nerve cells could be renewed in the adult brain; evidence was scant that dividing cells in mammalian brains produced new neurons, as opposed to other cell types. It wasn’t until researchers extracted neural stem cells from adult mouse brains and grew them in cell culture that scientists showed these precursor cells could divide and differentiate into new neurons. Now it is generally well accepted that neurogenesis takes place in two areas of the adult rodent brain: the olfactory bulbs, which process smell information, and the hippocampus, a region characterized by neuroplasticity that is required for forming new declarative memories.
Adult neural stem cells cluster together in what scientists call niches – hotbeds for cultivating the birth and growth of new neurons, recognizable by their distinctive architecture. Despite the mounting evidence for regional growth of new neurons, these studies underscored the point that the adult brain harbors only a few stem cell niches and their capacity to produce neurons is limited to just a few types of cells.
With this knowledge, and new tools for labeling proliferating cells and identifying maturing neurons, scientists began to look for postnatal neurogenesis in primate and human brains.
What’s happening in adult human brains?
Many neuroscientists believe that by understanding the process of adult neurogenesis we’ll gain insights into the causes of some human neurological disorders. Then the next logical step would be trying to develop new treatments harnessing neurogenesis for conditions such as Alzheimer’s disease or trauma-induced epilepsy. And stimulating resident stem cells in the brain to generate new neurons is an exciting prospect for treating neurodegenerative diseases.
However, obtaining rigorous proof for adult neurogenesis in the human and primate brain has been technically challenging – both due to the limited experimental approaches and the larger sizes of the brains, compared to reptiles, songbirds and rodents.
But even when scientists saw evidence for new neurons in the brain, they tended to be scarce. Some neurogenesis experts were skeptical that evidence based on incorporating BrdU into DNA was a reliable method for proving that new cells were actually being born through cell division, rather than just serving as a marker for other normal cell functions.
Further questions about how long human brains retain the capacity for neurogenesis arose in 2011, with a study that compared numbers of newborn neurons migrating in the olfactory bulbs of infants versus older individuals up to 84 years of age. Strikingly, in the first six months of life, the baby brains contained lots of chains of young neurons migrating into the frontal lobes, regions that guide executive function, long-range planning and social interactions. These areas of the human cortex are hugely increased in size and complexity compared to rodents and other species. But between 6 to 18 months of age, the migrating chains dwindled to a thin stream. Then, a very different pattern emerged: Where the migrating chains of neurons had been in the infant brain, a cell-free gap appeared, suggesting that neural stem cells become depleted during the first six months of life.
Now the largest and most comprehensive study conducted to date presents even stronger evidence that robust neurogenesis doesn’t continue throughout adulthood in the human hippocampus – or if it does persist, it is extremely rare. This work is controversial and not universally accepted. Critics have been quick to cast doubt on the results, but the finding isn’t totally out of the blue.
So where does this leave the field of neuroscience? If the UCSF scientists are correct, what does that mean for ongoing research in labs around the world?
Because lots of studies of neurological diseases are done in mice and rats, many scientists are invested in the possibility that adult neurogenesis persists in the human brain, just as it does in rodents. If it doesn’t, how valid is it to think that the mechanisms of learning and neuroplasticity in our model animals are comparable to those in the human brain? How relevant are our models of neurological disorders for understanding how changes in the hippocampus contribute to disorders such as the type of epilepsy I study?
In my lab, we transplant embryonic mouse or human neurons into the adult hippocampus in mice, after damage caused by epileptic seizures. We aim to repair this damage and suppress seizures by seeding the mouse hippocampus with neural stem cells that will mature and form new connections. In temporal lobe epilepsy, studies in adult rodents suggest that naturally occurring hippocampal neurogenesis is problematic. It seems that the newborn hippocampal neurons become highly excitable and contribute to seizures. We’re trying to inhibit these newborn hyperexcitable neurons with the transplants. But if humans don’t generate new hippocampal neurons, then maybe we’re developing a treatment in mice for a problem that has a different mechanism in people.
Perhaps our species has evolved separate mechanisms for neuroplasticity, distinct from those used by species such as rats and mice. One possibility is that there are other sites in the human brain where neurogenesis occurs – its a big structure and more exploration will be necessary. If it turns out to be true that the human brain has a diminished capacity for neurogenesis after birth, the finding will have important implications for how neuroscientists like me think about tackling brain disorders.
Perhaps most importantly, this work underscores how crucial it is to learn how to increase the longevity of the neurons we do have, born early in life, and how we might replace or repair neurons that become damaged.
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.”
Objectives: Mirror therapy is a unique treatment with a touch of modality that is purported to improve the motor function of the affected limb in individuals with hemiplegia. Previous studies have focused on the neuro-physiological factors underlying the mechanism of the clinical effect of this technique. The present study aims to understand the mechanism using the rehabilitation method and neuro-occupation model as well as analyze the effects of mirror therapy on the upper limb function of subjects with spastic hemiplegic cerebral palsy. Methods: Single subject design known as withdrawal design was used by a convenience sample of four subjects. The study involved three observational phases known as baseline, treatment, and withdrawal phases that took place during a 10 week period. The study contained a home-based mirror therapy protocol whereby the participants were instructed to do some exercises on a daily basis. The improvement of the hand function of the hemiplegic side was examined by Box and Block test along with two more activities including Threading Beads and Stacking Rings. Results: The ability to perform the Box and Block test, Threading Beads, and Stacking Rings tended to remain steady in the baseline phase, whereas there was a noticeable improvement during the treatment phase and a decline in the withdrawal phase. Discussion: From the perspective of visual feedback neuro-occupation model, it could be hypothesized that alterations to the sensory system caused by the mirror reflection of non affected hand may have led to the destabilization of the sensory cortices that changed the participants’ intention, meaning, and perception, thereby improving the subject’s motor control.
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Elsevier Health Sciences, Oct 30, 2017 – 576 pages
Boost your skills in planning and managing physical rehabilitation! Neuroscience: Fundamentals for Rehabilitation,5th Edition provides a practical guide to the nervous system and how it affects the practice of physical and occupational therapy. Case studies and first-person stories from people with neurologic disorders make it easier to apply your knowledge to the clinical setting. New to this edition are new chapters on neuroanatomy imaging and neurologic examination techniques. Written by noted PT educator Laurie Lundy-Ekman, this book uses evidence-based research to help you understand neurologic disorders and treat clients who have physical limitations due to nervous system damage or disease.
Logical, systems approach to neuroscience makes it easier to master complex information and provides a framework for conducting a neurologic examination and evaluation.
A clinical perspective of neuroscience is provided through case studies, personal stories written by patients, and summaries of key features of neurologic disorders and the body systems they affect.
Five sections — Overview of Neurology, Neuroscience at the Cellular Level, Development of the Nervous System, Vertical Systems, and Regions — first show how neural cells operate, and then allow you to apply your knowledge of neuroscience.
Emphasis on topics critical to physical rehabilitation includes coverage of abnormal muscle tone, chronic pain, control of movement, and differential diagnosis of dizziness.
Hundreds of color-coded illustrations show body structures and functions across systems.
Clinical Notes case studies demonstrate how neuroscience knowledge may be applied to clinical situations.
Pathology boxes provide a quick summary of the features of neurologic disorders commonly encountered in rehabilitation practice.
New! Neuroimaging and Neuroanatomy Atlaschapter includesMRI and CT images.
NEW!Neurologic Disorders and the Neurologic Examinationchapter provides detailed descriptions and photographs of techniques.
NEW! Diagnostic Clinical Reasoning boxes help you develop the ability to recognize patterns of signs and symptoms associated with specific diagnoses.
NEW! Updated content reflects the most current research findings.
NEW! Reader-friendly approach converts long, technical chapters into smaller, more accessible chapters.
NEW! Reorganized chapters progress from the cellular view to the systems view to the regional view.
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.
For Noah Falstein, the future of virtual reality depends not only on understanding the technology and the market, but understanding the fundamental underpinnings of the human brain.
“It’s like you’re going through a mountain pass,” he said at VRDC Fall 2017 in San Francisco today, speaking to an audience made up of game developers as well as people in other industries. Right now, VR is still new territory, and on the other side of that mountain pass, a fertile valley might open up, or maybe not. “Along the way, it’s easy to get stuck,” he said.
But Falstein, who is a true believer in the future of VR, AR, and MR, says that neuroscience is the compass to point this new technology in the correct direction.
A history of conveying images
Falstein is a true veteran of game development, working at companies including Williams Electronics and LucasArts, and most recently was chief game designer at Google. He now runs his own design consultancy company, The Inspiracy.
Falstein briefly went over humankind’s quest to share images, using the example of a 20,000-year-old cave painting. “Our ancestors have been struggling with this for a long time,” he said—the desire to convey something one might personally see to other people. From cave paintings to camcorders, to smartphones with advanced cameras, to VR today, humans have been trying all kinds of ways to convey images that inform or evoke emotions in other people.
Falstein’s approach to understanding the uses and applications of immersive computing lies in trying to understand how the brain itself works and how it has evolved.
“One of the first things that comes up in VR is the potential of motion sickness,” Falstein said. “I think we’re always going to have some people at the end of that spectrum who just have trouble in VR when they move too swiftly,” he said, but there are some ways to minimize motion sickness.
Falstein explained how motion sickness is evolutionary—when a person is poisoned, it disrupts the inner ear, creating a disconnect between actual movement and the movement one feels in their head. This leads to nausea, which is a great way to throw up and purge a poison mushroom or food that has turned.
He acknowledged that there’s always a person in the studio who’s the most susceptible to motion sickness who is used as the motion sickness guinea pig. “I frankly don’t think we’ll have a better [motion sickness testing] system than that for some time to come,” he said.
He stated some well-known (among VR game devs) facts about preventing VR motion sickness: you need a fast frame rate (90+ is best); devs must minimize lag when the head moves (20ms or less); they should get all visual cues right; minimize acceleration; and come up with creative anti-sickness solutions based on how our visual field and vestibular system interact.
He also explained how blurring or eliminating peripheral vision during acceleration can help fight motion sickness. Some games and Google Earth in VR use this method, and as eye tracking systems become more advanced, users will have more comfortable VR experiences, he said.
“It turns out that VR is really good at scaring people,” he said. Movie directors figured this out fairly early in film, and VR developers have found this out too.
“Why is horror in VR so strong?” Falstein explained how the human brain—particularly the amygdala—does the quick, raw processing of fear, anger, and aggression (fight of flight), and also arousal and intimacy.
“In video games, we’re really good at the fight or flight stuff, but the intimacy and empathy stuff, we’re still working on that,” he said.
But with VR, as it “tricks” more of your senses, there’s opportunity for more intimacy and it also appeals stronger to empathy, he said.
Falstein also talked about the possibilities in storytelling when it comes to movies shown in VR, such as short stories in VR (like Google’s Spotlight Stories series), 180-degree movie viewing, or shared or single-viewer experiences. “There’s going to be strong ‘replay’ value for things they missed [on first view],” Falstein said. There are also opportunities for monetization through ads and product placement.
Falstein briefly pointed out how games as medicine is a new market with massive opportunity, and VR can be part of this in treating issues like phobias, PTSD, acute pain, and strokes, as well as training doctors and caregivers.
“It’s really exciting stuff,” he said, “and the future is in your hands.”
Our experience of the body is not direct; rather, it is mediated by perceptual information, influenced by internal information, and recalibrated through stored implicit and explicit body representation (body memory). This paper presents an overview of the current investigations related to body memory by bringing together recent studies from neuropsychology, neuroscience, and evolutionary and cognitive psychology. To do so, in the paper, we explore the origin of representations of human body to elucidate their developmental process and, in particular, their relationship with more explicit concepts of self. First, it is suggested that our bodily experience is constructed from early development through the continuous integration of sensory and cultural data from six different representations of the body, i.e., the Sentient Body (Minimal Selfhood), the Spatial Body (Self Location), the Active Body (Agency), the Personal Body (Whole Body Ownership – Me); the Objectified Body (Objectified Self – Mine), and the Social Body (Body Satisfaction – Ideal Me). Then, it is suggested that these six representations can be combined in a coherent supramodal representation, i.e. the “body matrix”, through a predictive, multisensory processing activated by central, top–down, attentional processes. From an evolutionary perspective, the main goal of the body matrix is to allow the self to protect and extend its boundaries at both the homeostatic and psychological levels. From one perspective, the self extends its boundaries (peripersonal space) through the enactment and recognition of motor schemas. From another perspective, the body matrix, by defining the boundaries of the body, also defines where the self is present, i.e., in the body that is processed by the body matrix as the most likely to be its one and in the space surrounding it. In the paper we also introduced and discusses the concept of “embodied medicine”: the use of advanced technology for altering the body matrix with the goal of improving our health and well-being.
The body is an object of perception, just like any other object in the world. Yet, at the same time, the body is different (Aspell, Lenggenhager, & Blanke, 2012). From one perspective, it provides the background conditions that enable perception and action (cognitive approach); from another perspective, it is associated closely with our sense of self and its intentionality (volitional approach).
However, to study the experience of the body is not an easy task. As noted by Olaf Blanke (2012), the body is the most multi-sensory “object” in the world; it requires the processing and integration of different bodily signals in the premotor, temporoparietal, posterior parietal, and extrastriate cortices. In addition, our experience of the body is not direct (Figure 1), but it is (Blanke, Slater, & Serino, 2015; Pazzaglia & Zantedeschi, 2016; Riva, […]
Objective: This presentation will review the basic neuroscience research origins and the effects of Constraint-Induced Movement therapy (CIMT) on CNS structural neuroplasticity.
Background: Experimental hemiparesis in primates overcame chronic limb nonuse by applying specific behavioral neuroscience principles. This research led to formulating a model for the origination of sustained motor disability after neurological injury and its improvement by a novel therapeutic program. The therapy became adapted to treating children and adults and termed CIMT. Over the past 25 years multiple worldwide Randomized Controlled Trials of CIMT enrolled nearly 2000 patients with diverse neurological disorders (stroke, cerebral palsy [CP], multiple sclerosis [MS]), which indicated superiority of the approach against control therapies, with large treatment Effect Sizes and sustained retention of improved spontaneous real-world use of the hemiparetic limb. Ongoing research will describe basic and clinical neuroimaging methods to explore the basis for the clinical efficacy of CIMT.
Design/Methods: (1) Basic neuroscience models of experimental limb nonuse in rodents that had undergone adapted CIMT, which were followed by histological studies. (2) Voxel-based morphometry (VBM) of grey matter and Tract-based spatial statistics (TBSS) of white matter on structural brain MRI, which evaluated neuroplastic changes after upper extremity CIMT.
Results: (1) CIMT in rodents resulted in increased CNS axonal growth, synaptogenesis, and neurogenesis compared to control interventions, parallel with improved paretic limb use. (2) VBM demonstrated profuse cortical and subcortical grey matter increase following CIMT for stroke, CP, and MS. TBSS indicated significantly improved white matter integrity in MS. Neither structural brain changes nor comparable improved paretic limb use followed control interventions.
Conclusions: CIMT is increasing worldwide practice to improve reduced real-world limb use in chronic hemiparesis in diverse neurological diseases and ages of patients. Structural CNS changes following CIMT may support improved and extended functional use of the paretic limb.
Patients with epilepsy face many challenges, but perhaps the most difficult of all is the unpredictability of seizure occurrence. One of the most commonly reported triggers for seizures is stress.
A recent review article in the European journal Seizure, by researchers at University of Cincinnati Epilepsy Center at the UC Gardner Neuroscience Institute, looks at the stress-seizure relationship and how adopting stress reduction techniques may provide benefit as a low risk form of treatment.
The relationship between stress and seizures has been well documented over the last 50 years. It has been noted that stress can not only increase seizure susceptibility and in rare cases a form of reflex epilepsy, but also increase the risk of the development of epilepsy, especially when stressors are severe, prolonged, or experienced early in life.
“Studies to date have looked at the relationship from many angles,” says Michael Privitera, MD, director of the UC Epilepsy Center and professor in the Department of Neurology and Rehabilitation Medicine at the UC College of Medicine. “The earliest studies from the 1980s were primarily diaries of patients who described experiencing more seizures on ‘high-stress days’ than on ‘low-stress days.'”
Privitera and Heather McKee, MD, an assistant professor in the Department of Neurology and Rehabilitation Medicine, looked at 21 studies from the 1980s to present–from patients who kept diaries of stress levels and correlation of seizure frequency, to tracking seizures after major life events, to fMRI studies that looked at responses to stressful verbal/auditory stimuli.
“Most all [of these studies] show increases in seizure frequency after high-stress events. Studies have also followed populations who have collectively experienced stressful events, such as the effects of war, trauma or natural disaster, or the death of a loved one,” says Privitera. All of which found increased seizure risk during such a time of stress.
For example, a 2002 study evaluated the occurrence of epileptic seizures during the war in Croatia in the early 1990s. Children from war-affected areas had epileptic seizures more often than children not affected by the war. Additionally, the 10-year follow up showed that patients who had their first epileptic seizure during a time of stress were more likely to have controlled epilepsy or even be off medication years later.
“Stress is a subjective and highly individualized state of mental or emotional strain. Although it’s quite clear that stress is an important and common seizure precipitant, it remains difficult to obtain objective conclusions about a direct causal factor for individual epilepsy patients,” says McKee.
Another aspect of the stress-seizure relationship is the finding by UC researchers that there were higher anxiety levels in patients with epilepsy who report stress as a seizure precipitant. The researchers suggest patients who believe stress is a seizure trigger may want to talk with their health care provider about screening for anxiety.
“Any patient reporting stress as a seizure trigger should be screened for a treatable mood disorder, especially considering that mood disorders are so common within this population,” adds McKee.
The researchers report that while some small prospective trials using general stress reduction methods have shown promise in improving outcomes in people with epilepsy, large-scale, randomized, controlled trials are needed to convince both patients and providers that stress reduction methods should be standard adjunctive treatments for people with epilepsy.
“What I think some of these studies point to is that efforts toward stress reduction techniques, though somewhat inconsistent, have shown promise in reducing seizure frequency. We need future research to establish evidence-based treatments and clarify biological mechanisms of the stress-seizure relationship,” says Privitera.
Overall, he says, recommending stress reduction methods to patients with epilepsy “could improve overall quality of life and reduce seizure frequency at little to no risk.”
Some low risk stress reduction techniques may include controlled deep breathing, relaxation or mindfulness therapy, as well as exercise, or establishing routines.
Winner of the Brainlab Community Neurosurgery Award, Sandro Krieg, MD, presented his research, Plasticity of Motor Representations in Patients with Brain Lesions: a Navigated TMS Study, during the 2017 American Association of Neurological Surgeons (AANS) Annual Scientific Meeting.
This study investigated the spatial distributions of motor representations in terms of tumor-induced brain plasticity by analyzing navigated transcranial magnetic stimulation (nTMS) motor maps derived from 100 patients with motor eloquently located brain tumors in or adjacent to the precentral gyrus (PrG).
The research evoked 8,774 motor potentials (MEPs) that were elicited in six muscles of the upper and lower extremity by stimulating four gyri in patients with five possible tumor locations. Regarding the MEP frequency of each muscle-gyrus subdivision per patient, the expected frequency was 3.53 (8,774 divided by 100 patients, further divided by six muscles and four gyri). Accordingly, the patient ratio for each subdivision was calculated by defining the per-patient minimum data points as three.
The tumor-location specific patient ratios were higher for frontal tumors in both gyri than for other tumor locations. This suggests that the finger representation reorganization in these frontal gyri, which corresponds to location of dorsal premotor areas, might be due to within-premotor reorganization rather than relocation of motor function from PrG into premotor areas one might expect from the Rolandic tumors. The research indicates that reorganization of the finger motor representations might be limited along the middle-to-dorsal dimension of the dorsal premotor areas (posterior MFG and SFG) and might not cross rostrally from the primary motor cortex (PrG) to the dorsal premotor cortex.