This article provides a review of brain tissue alterations that may be detectable using diffusion magnetic resonance imaging MRI (dMRI) approaches and an overview and perspective on the modern dMRI toolkits for characterizing alterations that follow traumatic brain injury (TBI). Noninvasive imaging is a cornerstone of clinical treatment of TBI and has become increasingly used for preclinical and basic research studies. In particular, quantitative MRI methods have the potential to distinguish and evaluate the complex collection of neurobiological responses to TBI arising from pathology, neuroprotection, and recovery. dMRI provides unique information about the physical environment in tissue and can be used to probe physiological, architectural, and microstructural features. Although well-established approaches such as diffusion tensor imaging are known to be highly sensitive to changes in the tissue environment, more advanced dMRI techniques have been developed that may offer increased specificity or new information for describing abnormalities. These tools are promising, but incompletely understood in the context of TBI. Furthermore, model dependencies and relative limitations may impact the implementation of these approaches and the interpretation of abnormalities in their metrics. The objective of this paper is to present a basic review and comparison across dMRI methods as they pertain to the detection of the most commonly observed tissue and cellular alterations following TBI.
Despite the long history of traumatic brain injury (TBI) as a prevalent cause of death and disability in humans, defining the neurobiological underpinnings of damage and recovery following TBI remains a central challenge. The complex collection of physiological, cellular, and molecular changes that follow TBI can appear to be remarkably heterogeneous, but at the same time they are highly organized into coordinated responses such as neurodegeneration, inflammation, and regeneration. The corpus of histological studies spanning a variety of experimental animal models of TBI have provided crucial insights about the pathomechanisms and cellular alterations that accompany posttraumatic tissue change, but considerable work remains to determine the spatiotemporal evolution of abnormalities, interrelationships among different tissue responses, and their impact on health and behavioral outcomes. Noninvasive imaging in animal models has the potential to build on what is known from histology by providing longitudinal and whole-brain information, but for this approach to be successful it is essential to first improve the understanding of how imaging abnormalities correspond to tissue and cellular changes.
Diffusion magnetic resonance imaging (dMRI) methods are particularly promising for the development of imaging markers of TBI pathology because they are sensitive to microscale water displacement as a proxy for tissue environment geometry and provide a range of quantitative scalar metrics across the whole brain. Furthermore, dMRI may be combined with other conventional or advanced magnetic resonance imaging (MRI) methods such as arterial spin labeling, susceptibility-weighted imaging, or a variety of contrast agent MRI approaches to provide complementary and comprehensive outcome measures. Standard dMRI methods and especially diffusion tensor imaging (DTI) have already demonstrated sensitive detection of abnormalities in a number of experimental models of TBI. In the past decade, multiple advanced dMRI approaches have extended beyond the conventional models with the goals of improving the physical description of water diffusion (e.g., by modeling “non-Gaussian” diffusion) or parameterizing dMRI with respect to the expected biological environment (e.g., by modeling cellular compartments and/or fiber geometry). These new tools will be valuable if they are able to improve the sensitivity or specificity of dMRI following TBI; however, we lack a systematic understanding of how dMRI methods differ from one another for detecting and describing tissue alterations.
A number of excellent reviews exist to describe the current understanding of cellular mechanisms of TBI in general (Bramlett & Dietrich, 2015; Pekna & Pekny, 2012) and within particular areas of neurobiology including neurodegeneration (Johnson, Stewart, & Smith, 2013; Stoica & Faden, 2010), inflammation (Burda, Bernstein, & Sofroniew, 2016; Ziebell & Morganti-Kossmann, 2010), and myelin changes (Armstrong, Mierzwa, Marion, & Sullivan, 2016), among others. As well, several existing reviews have been published regarding MRI and DTI to study human TBI (Brody, Mac Donald, & Shimony, 2015; Duhaime et al., 2010; Hulkower, Poliak, Rosenbaum, Zimmerman, & Lipton, 2013), and recently a pertinent overview and summary of advanced dMRI tools and their relevance to clinical outcomes was published (Douglas et al., 2015). The focus of the present review is to combine what is known from work in experimental models of TBI about tissue and cellular alterations that may affect the physical tissue environment with a comparative description of the major methods for dMRI that may be differentially sensitive to TBI-related tissue change alongside several important caveats for their use and interpretation. The first section provides a categorical summary of cellular response to trauma, emphasizing alterations with microstructural, architectural, or neuroanatomical manifestations that may give rise to detectable dMRI abnormalities, including a review of the existing dMRI studies in experimental TBI models. The second section contains a comparative overview of presently available dMRI methods from standard approaches to advanced techniques. The objective of this article is to provide a reference for the current understanding of these topics as well as a perspective to help guide selection of dMRI tools based on particular aspects of TBI questions.
Continue —> Diffusion MRI and the detection of alterations following traumatic brain injury – Hutchinson – 2017 – Journal of Neuroscience Research – Wiley Online Library
Figure 2. Cross-model comparison of scalar maps in the injured brain. A range of tissue and injury-related contrasts may be visually observed in this collage of 16 representative metrics in the same slice from different dMRI models. This cross-model view of scalar maps demonstrates the potential for nonredundant information about regions of injury that may be gleaned from different models. DTI metrics of fractional anisotropy (FA), trace (TR), axial and radial diffusivity (Dax and Drad), directionally encoded color (DEC) map weighted by lattice index, DEC weighted by Westin linear anisotropy (WL) and DEC weighted by Westin planar anisotropy (WP), DKI metrics of mean kurtosis (MK), axial and radial kurtosis (AK and RK) and kurtosis FA (KFA), MAP-MRI metrics of return to the origin, axis, and plane probabilities (RTOP, RTAP, and RTPP), propagator anisotropy (PA) and non-Gaussianity (NG) and NODDI metrics of compartment volume fractions for isotropic free water (Viso), intracellular water (Vic) and intracellular restricted water (Vir), and orientation dispersion index (ODI). Insets of each map show tissue near the injury site where dMRI values are expected to be abnormal.
Ischemic damage to the brain triggers substantial reorganization of spared areas and pathways, which is associated with limited, spontaneous restoration of function. A better understanding of this plastic remodeling is crucial to develop more effective strategies for stroke rehabilitation. In this review article, we discuss advances in the comprehension of post-stroke network reorganization in patients and animal models. We first focus on rodent studies that have shed light on the mechanisms underlying neuronal remodeling in the perilesional area and contralesional hemisphere after motor cortex infarcts. Analysis of electrophysiological data has demonstrated brain-wide alterations in functional connectivity in both hemispheres, well beyond the infarcted area. We then illustrate the potential use of non-invasive brain stimulation (NIBS) techniques to boost recovery. We finally discuss rehabilitative protocols based on robotic devices as a tool to promote endogenous plasticity and functional restoration.
Following an ischemic insult within the motor cortex, one or more body parts contralateral to the infarct result impaired or paretic. The degree of the motor impairment depends on many factors, such as the extent of the infarct, the identity of the damaged region(s) and the effectiveness of the early medical care. Substantial functional recovery can occur in the first weeks after stroke, mainly due to spontaneous mechanisms (Kwakkel et al., 2004; Cramer, 2008; Darling et al., 2011; Ward, 2011; Grefkes and Fink, 2014). About 26% of stroke survivors are able to carry on everyday activities (Activity of Daily Living or ADLs, i.e., eating, drinking, walking, dressing, bathing, cooking, writing) without any help, but another 26% is forced to shelter in a nursing home (Carmichael, 2005). Impairments of upper and lower limbs are particularly disabling as they impact on the degree of independence in ADLs. Overall, a significant percentage of the patients exhibit persistent disability following ischemic attacks. Therefore, it is critical to increase our knowledge of post-stroke neuroplasticity for implementing novel rehabilitative strategies. In this review we summarize data about plastic reorganizations after injury, both in the ipsilesional and contralesional hemisphere. We also describe non-invasive brain stimulation (NIBS) techniques and robotic devices for stimulating functional recovery in humans and rodent stroke models.
Neuroplasticity After Stroke
The term brain plasticity defines all the modifications in the organization of neural components occurring in the central nervous system during the entire life span of an individual (Sale et al., 2009). Such changes are thought to be highly involved in mechanisms of aging, adaptation to environment and learning. Moreover, neuronal plastic phenomena are likely to be at the basis of adaptive modifications in response to anatomical or functional deficit or brain damage (Nudo, 2006). Ischemic damage causes a dramatic alteration of the entire complex neural network within the affected area. It has been amply demonstrated, by many studies, that the cerebral cortex exhibits spontaneous phenomena of brain plasticity in response to damage (Gerloff et al., 2006; Nudo, 2007). The destruction of neural networks indeed stimulates a reorganization of the connections and this rewiring is highly sensitive to the experience following the damage (Stroemer et al., 1993; Li and Carmichael, 2006). Such plastic phenomena involve particularly the perilesional tissue in the injured hemisphere, but also the contralateral hemisphere, subcortical and spinal regions.
Continue —> Frontiers | Neuroplastic Changes Following Brain Ischemia and their Contribution to Stroke Recovery: Novel Approaches in Neurorehabilitation | Frontiers in Cellular Neuroscience
Figure 3. Example of a novel robotic system that integrates functional grasping, active reaching arm training and bimanual tasks. An example of a novel robotic system that integrates functional grasping, active reaching arm training and bimanual tasks, consisting of: (i) Virtual Reality: software applications composed of rehabilitative and evaluation tasks; (ii) TrackHold: robotic device to support the weight of the user’s limb during tasks execution; (iii) Robotic Hand Exos: active hand exoskeleton to assist grasping tasks; and (iv) Handgrip sensors to support the bilateral grasping training and evaluation (modified from Sgherri et al., 2017).
The nervous system works like a great orchestra. Specially the music of Mozart with its´ “Mozart´s effect” is appropriate to use in neurosurgery. The paper investigates the relationship between music and neurosurgery, Mozart´s music in neurosurgical practice.
Material and Methods
We used digital catalogues like “pubmed” as well as the libraries of universities. Key words were “Wolfgang Amadeus Mozart”, “neurosurgery and music”.
At the first half of 20 century, neurosurgical approach of some musicians have resulted with fatal outcome such as Maurice Ravel, Josef Hassid,George Gershwin. The cause of this is probably that neurosurgery has not been developed yet in the first half of the 20th century. In last three decades, the neurosurgical operations of musician show that musicians has rich associations between auditory, somatic, and sensorial systems.
It is clear that we have much to learn from studies about music and brain function that derive from our surgical experiences with patients. The neuronal plasticity of musician‘s brain may be different than non-musicians´. Musicians with enhanced motor skills have greater capacity for plasticity because of enriched interhemispheric connections. Listening music, and of Mozart´s effect in neurosurgical practice, intensive care, or rehabilitation was documented in much studies. As authors, we mean something different: Its effectiveness shouldbe studied. We can concluded that, in current neurosurgical practice that Mozart has an effect. More research and clinical studies are needed.
Source: Neurosurgery and Music; The effect of Wolfgang Amadeus Mozart
FEBRUARY 3, 2017
Summary: Researchers report adult neurogenesis not only helps increase the number of cells in a neural network, it also promotes plasticity in the existing network. Additionally, they have identified the role the Bax gene plays in synaptic pruning.
Source: University of Alabama at Birmingham.
One goal in neurobiology is to understand how the flow of electrical signals through brain circuits gives rise to perception, action, thought, learning and memories.
Linda Overstreet-Wadiche, Ph.D., and Jacques Wadiche, Ph.D., both associate professors in the University of Alabama at Birmingham Department of Neurobiology, have published their latest contribution in this effort, focused on a part of the brain that helps form memories — the dentate gyrus of the hippocampus.
The dentate gyrus is one of just two areas in the brain where new neurons are continuously formed in adults. When a new granule cell neuron is made in the dentate gyrus, it needs to get ‘wired in,’ by forming synapses, or connections, in order to contribute to circuit function. Dentate granule cells are part of a circuit that receive electrical signals from the entorhinal cortex, a cortical brain region that processes sensory and spatial input from other areas of the brain. By combining this sensory and spatial information, the dentate gyrus can generate a unique memory of an experience.
Overstreet-Wadiche and UAB colleagues posed a basic question: Since the number of neurons in the dentate gyrus increases by neurogenesis while the number of neurons in the cortex remains the same, does the brain create additional synapses from the cortical neurons to the new granule cells, or do some cortical neurons transfer their connections from mature granule cells to the new granule cells?
Their answer, garnered through a series of electrophysiology, dendritic spine density and immunohistochemistry experiments with mice that were genetically altered to produce either more new neurons or kill off newborn neurons, supports the second model — some of the cortical neurons transfer their connections from mature granule cells to the new granule cells.
This opens the door to look at how this redistribution of synapses between the old and new neurons helps the dentate gyrus function. And it opens up tantalizing questions. Does this redistribution disrupt existing memories? How does this redistribution relate to the beneficial effects of exercise, which is a natural way to increase neurogenesis?
“Over the last 10 years there has been evidence supporting a redistribution of synapses between old and new neurons, possibly by a competitive process that the new cells tend to ‘win,’” Overstreet-Wadiche said. “Our findings are important because they directly demonstrate that, in order for new cells to win connections, the old cells lose connections. So, the process of adult neurogenesis not only adds new cells to the network, it promotes plasticity of the existing network.”
The study opens the door to look at how this redistribution of synapses between the old and new neurons helps the dentate gyrus function. NeuroscienceNews.com image is for illustrative purposes only.
“It will be interesting to explore how neurogenesis-induced plasticity contributes to the function of this brain region,” she continued. “Neurogenesis is typically associated with improved acquisition of new information, but some studies have also suggested that neurogenesis promotes ‘forgetting’ of existing memories.”
The researchers also unexpectedly found that the Bax gene, known for its role in apoptosis, appears to also play a role in synaptic pruning in the dentate gyrus.
“There is mounting evidence that the cellular machinery that controls cell death also controls the strength and number of synaptic connections,” Overstreet-Wadiche said. “The appropriate balance of synapses strengthening and weakening, collectively termed synaptic plasticity, is critical for appropriate brain function. Hence, understanding how synaptic pruning occurs may shed light on neurodevelopmental disorders and on neurodegenerative diseases in which a synaptic pruning gone awry may contribute to pathological synapse loss.”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
All of the work was performed in the Department of Neurobiology at UAB. In addition to Overstreet-Wadiche and Wadiche, co-authors of the paper, “Adult born neurons modify excitatory synaptic transmission to existing neurons,” published in eLife, are Elena W. Adlaf, Ryan J. Vaden, Anastasia J. Niver, Allison F. Manuel, Vincent C. Onyilo, Matheus T. Araujo, Cristina V. Dieni, Hai T. Vo and Gwendalyn D. King.
Much of the data came from the doctoral thesis research of Adlaf, a former UAB Neuroscience graduate student who is now a postdoctoral fellow at Duke University.
Funding: Funding for this research came from Civitan International Emerging Scholars awards, and National Institutes of Health awards or grants NS098553, NS064025, NS065920 and NS047466.
Source: Jeff Hansen – University of Alabama at Birmingham
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Adult-born neurons modify excitatory synaptic transmission to existing neurons” by Elena W Adlaf, Ryan J Vaden, Anastasia J Niver, Allison F Manuel, Vincent C Onyilo, Matheus T Araujo, Cristina V Dieni, Hai T Vo, Gwendalyn D King, Jacques I Wadiche, and Linda Overstreet-Wadiche in eLife. Published online January 30 2017 doi:10.7554/eLife.19886
Did You Know How Loud Balloons Can Be?
Adult-born neurons are continually produced in the dentate gyrus but it is unclear whether synaptic integration of new neurons affects the pre-existing circuit. Here we investigated how manipulating neurogenesis in adult mice alters excitatory synaptic transmission to mature dentate neurons. Enhancing neurogenesis by conditional deletion of the pro-apoptotic gene Bax in stem cells reduced excitatory postsynaptic currents (EPSCs) and spine density in mature neurons, whereas genetic ablation of neurogenesis increased EPSCs in mature neurons. Unexpectedly, we found that Bax deletion in developing and mature dentate neurons increased EPSCs and prevented neurogenesis-induced synaptic suppression. Together these results show that neurogenesis modifies synaptic transmission to mature neurons in a manner consistent with a redistribution of pre-existing synapses to newly integrating neurons and that a non-apoptotic function of the Bax signaling pathway contributes to ongoing synaptic refinement within the dentate circuit.
“Adult-born neurons modify excitatory synaptic transmission to existing neurons” by Elena W Adlaf, Ryan J Vaden, Anastasia J Niver, Allison F Manuel, Vincent C Onyilo, Matheus T Araujo, Cristina V Dieni, Hai T Vo, Gwendalyn D King, Jacques I Wadiche, and Linda Overstreet-Wadiche in eLife. Published online January 30 2017 doi:10.7554/eLife.19886
Source: Brain Plasticity: How Adult Born Neurons Get Wired – Neuroscience News