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Abstract: Magnetic resonance imaging (MRI) is a vital tool for the study of brain structure and function. It is increasingly being used in individual differences research to examine brain-behaviour associations. Prior work has demonstrated low test-retest stability of functional MRI measures, highlighting the need to examine the longitudinal stability (test-retest reliability across long timespans) of MRI measures across brain regions and imaging metrics, particularly in adolescence. In this study, we examined the longitudinal stability of grey matter measures (cortical thickness, surface area, and volume) across brain regions, and testing sites in the Adolescent Brain Cognitive Development (ABCD) study release v4.0. Longitudinal stability ICC estimates ranged from 0 to .98, depending on the measure, parcellation, and brain region. We used Intra-Class Effect Decomposition (ICED) to estimate between-subjects variance and error variance, and assess the relative contribution of each across brain regions and testing sites on longitudinal stability. In further exploratory analyses we examined the influence of parcellation used (Desikan-Killiany-Tourville and Destrieux) on longitudinal stability. Our results highlight meaningful heterogeneity in longitudinal stability across brain regions, structural measures (cortical thickness in particular), parcellations, and ABCD testing sites. Differences in longitudinal stability across brain regions were largely driven by between-subjects variance, whereas differences in longitudinal stability across testing sites was largely driven by differences in error variance. We argue that investigations such as this are essential to capture patterns of longitudinal stability heterogeneity that would otherwise go undiagnosed. Such improved understanding allows the field to more accurately interpret results, compare effect sizes, and plan more powerful studies.

This metadata is mainly recorded and collected for a meta-analysis of brain imaging ALE on charitable giving

Note this registration has been withdrawn: Daily cycles in physiological processes and behavioral activity are a universal phenomenon of all living organisms (Bell-Pedersen et al., 2005). Among advanced organisms such as mammals, these cycles have given rise to the phenomenon of sleep behavior, a state of reduced consciousness and lowered responsiveness towards external stimuli. While asleep, animals are more vulnerable towards predator threat, emphasizing the critical role of sleep processes in providing sufficient benefits to offset such risks. In humans, there are evident interindividual differences in sleep and sleep-wake behavior, and these have been linked to a large variety of physical and mental health diseases, including cardiovascular disease, type-2 diabetes, and multiple psychiatric disorders (Wolk et al., 2005; Baglioni et al., 2016; Khandelwal et al., 2017). Although ample evidence suggests that sleep is modulated by a variety of interacting brain networks involving multiple neurotransmitter systems (Pace-Schott and Hobson, 2002; Brown et al., 2012), it still remains an impending question how interindividual differences in sleep and sleep-wake behavior manifest in the human brain. Over the past two decades, genome-wide association studies (GWAS) have emerged as an efficient method for discovering disease-associated genomic loci, and for studying the pleiotropic relationships between different complex traits (Visscher et al., 2017). For instance, previous genetic studies on sleep disturbance traits have demonstrated a genetic overlap with neuropsychiatric and metabolic traits (Lane et al., 2017), and a bidirectional causative relationship with psychiatric diseases (Sun et al., 2022). A commonly employed technique for calculating genetic correlations is LD score regression (Bulik-Sullivan et al., 2015a, 2015b). This computationally efficient approach utilizes GWAS summary statistics as input, eliminating the need for individual-level data access. LD score regression can be applied on GWAS summary statistics obtained from overlapping, partially overlapping, and non-overlapping samples. This enables to investigate the relationships between two traits that have originally been investigated in different samples. In our planned study, we seek to leverage the results from large GWAS to investigate the genetic overlap between sleep behavior (both objective and subjective) and brain imaging-derived phenotypes. There are several previous genetic studies on subjectively assessed sleep variables, including GWAS on insomnia, chronotype, sleep duration, daytime sleepiness, and daytime napping (Dashti et al., 2019; Jansen et al., 2019; Jones et al., 2019a; Wang et al., 2019; Dashti et al., 2021). Other GWAS have examined objective sleep behavior, including measures of sleep quality, efficiency, and timing derived from actigraphy (Jones et al., 2019b). Many of the derived GWAS summary statistics are publicly available at the sleep disorder knowledge portal (SDKP, http://www.sleepdisordergenetics.org). In addition, Smith et al. (2021) have published GWAS summary statistics on ~4.000 brain imaging-derived phenotypes (https://open.win.ox.ac.uk/ukbiobank/big40/). In our study, we will use these available GWAS summary statistics to compute genetic correlations between sleep behavior and brain imaging-derived phenotypes. With our analyses, we seek to provide novel insights into how interindividual differences in sleep behavior manifest in the brain.

Note this registration has been withdrawn: Daily cycles in physiological processes and behavioral activity are a universal phenomenon of all living organisms (Bell-Pedersen et al., 2005). Among advanced organisms such as mammals, these cycles have given rise to the phenomenon of sleep behavior, a state of reduced consciousness and lowered responsiveness towards external stimuli. While asleep, animals are more vulnerable towards predator threat, emphasizing the critical role of sleep processes in providing sufficient benefits to offset such risks. In humans, there are evident interindividual differences in sleep and sleep-wake behavior, and these have been linked to a large variety of physical and mental health diseases, including cardiovascular disease, type-2 diabetes, and multiple psychiatric disorders (Wolk et al., 2005; Baglioni et al., 2016; Khandelwal et al., 2017). Although ample evidence suggests that sleep is modulated by a variety of interacting brain networks involving multiple neurotransmitter systems (Pace-Schott and Hobson, 2002; Brown et al., 2012), it still remains an impending question how interindividual differences in sleep and sleep-wake behavior manifest in the human brain. Over the past two decades, genome-wide association studies (GWAS) have emerged as an efficient method for discovering disease-associated genomic loci, and for studying the pleiotropic relationships between different complex traits (Visscher et al., 2017). For instance, previous genetic studies on sleep disturbance traits have demonstrated a genetic overlap with neuropsychiatric and metabolic traits (Lane et al., 2017), and a bidirectional causative relationship with psychiatric diseases (Sun et al., 2022). A commonly employed technique for calculating genetic correlations is LD score regression (Bulik-Sullivan et al., 2015a, 2015b). This computationally efficient approach utilizes GWAS summary statistics as input, eliminating the need for individual-level data access. LD score regression can be applied on GWAS summary statistics obtained from overlapping, partially overlapping, and non-overlapping samples. This enables to investigate the relationships between two traits that have originally been investigated in different samples. In our planned study, we seek to leverage the results from large GWAS to investigate the genetic overlap between sleep behavior (both objective and subjective) and brain imaging-derived phenotypes. There are several previous genetic studies on subjectively assessed sleep variables, including GWAS on insomnia, chronotype, sleep duration, daytime sleepiness, and daytime napping (Dashti et al., 2019; Jansen et al., 2019; Jones et al., 2019a; Wang et al., 2019; Dashti et al., 2021). Other GWAS have examined objective sleep behavior, including measures of sleep quality, efficiency, and timing derived from actigraphy (Jones et al., 2019b). Many of the derived GWAS summary statistics are publicly available at the sleep disorder knowledge portal (SDKP, http://www.sleepdisordergenetics.org). In addition, Smith et al. (2021) have published GWAS summary statistics on ~4.000 brain imaging-derived phenotypes (https://open.win.ox.ac.uk/ukbiobank/big40/). In our study, we will use these available GWAS summary statistics to compute genetic correlations between sleep behavior and brain imaging-derived phenotypes. With our analyses, we seek to provide novel insights into how interindividual differences in sleep behavior manifest in the brain.

Using ultrasound as a detection device in the body, including the brain, has been extensively investigated. Unfortunately, previous ultrasound-based methods on the brain have suffered from the severe distortion caused by the skull bone. The authors have recently developed a technique that allows ultrasound to propagate through the skull with significantly reduced distortion using a shear mode technique. The current project will develop a device for noninvasive identification of the presence of foreign bodies inside the skull, and the localization of such objects. The device will be lightweight, portable, durable, battery-operated, easy to use, and appropriate for effective and practical battlefield use in forward areas. The device will operate in two modes. In the first mode, it will function as a hand-held device powered by AA batteries. In this mode it will provide a simple yes/no indication of the presence of foreign bodies as a function of location in the brain. In the second mode, the same device will also be capable of interfacing with a laptop computer via a USB interface. In this mode, imaging and analysis software will form an image of regions in the brain that can be interpreted by a medic or relayed to a remote medical professional for evaluation.

This is the third annual report for the award made on September 15, 2008. Since the last report the above study has recruited 72 patients. Thirty six of these patients completed their one month scan, 25 completed their 6 month scan an d2 completed their 18 month scan. Since the last annual report, the IRB protocol went through additional modifications, mainly to streamline the process of recruitment of moderate and severe patients into the study. Currently we have screened over 300 patients that have been admitted to the Shock Trauma Center. At this point the recruitment process is smooth although there are some challenges in the recruitment of the severe patients within the first 10 days of injury. Several presentations were made at international meetings mainly on the resting state data which clearly show a decrease in the default mode network among the mildly injured patients that seem to take as long as 6 months to recover to the control levels. A manuscript of retrospective analysis of severely injured TBI patients to determine whether DTI parameters would be predictive of their outcomes has now led to a full manuscript which is being submitted to the Journal of Neurotrauma injured patients.

The purpose of this research program is to develop an imaging-based protocol to improve diagnosis and outcome prediction of mild traumatic brain injury (mTBI). Our major findings over the last year include: First, we have demonstrated that these new advanced MRI methods nicely complement conventional imaging methods in their ability to detect mTBI in the acute setting. Second, susceptibility weighted imaging and mapping (SWIM) are able to delineate venous structures and microbleeds making it possible to quantify and monitor evolution of pathological changes. Third, we have continued to use DTI data to look for local variations in ADC and FA values to assess tissue damage. And fourth, we have begun to accelerate the data collect process in patients with added support in both Radiology and Emergency medicine for both volunteers and mTBI patients. The significance of this work to date is that we are now able to find evidence of damage in mTBI where that has heretofore been difficult with conventional MRI. Keywords: Mild traumatic brain injury, susceptibility weighted imaging and mapping, temporal nature of TBI recovery, medullary vein damage.

The purpose of this research program is to develop an imaging-based protocol to improve diagnosis and outcome prediction of mild traumatic brain injury (mTBI). Our major findings over the last year include: First, we have demonstrated that these new advanced MRI methods nicely complement conventional imaging methods in their ability to detect mTBI in the acute setting. Second, susceptibility weighted imaging and mapping (SWIM) are able to delineate venous structures and microbleeds making it possible to quantify and monitor evolution of pathological changes. Third, we have continued to use DTI data to look for local variations in ADC and FA values to assess tissue damage. And fourth, we have begun to accelerate the data collect process in patients with added support in both Radiology and Emergency medicine for both volunteers and mTBI patients. The significance of this work to date is that we are now able to find evidence of damage in mTBI where that has heretofore been difficult with conventional MRI. Keywords: Mild traumatic brain injury, susceptibility weighted imaging and mapping, temporal nature of TBI recovery, medullary vein damage.

This article is from International Medical Case Reports Journal , volume 7 . Abstract A 60-year-old man presented with headache, dizziness, and disorientation one day after consumption of isopropanol along with ethanol. Computed tomography (CT) of the brain performed immediately was unremarkable. The patient collapsed within the hospital 30 minutes after the CT scan was done, and remained comatose until death, showing no improvement with symptomatic treatment. Magnetic resonance imaging of the brain and spine done 6 days after admission revealed bilaterally symmetrical hyperintensities involving the cerebral and cerebellar cortex and white matter, basal ganglia, thalami, and brainstem on T2-weighted, fluid attenuated inversion recovery and diffusion weighted images; similar hyperintensities were seen involving the swollen and edematous cervical spinal cord and cerebellar tonsillar herniation compressing the proximal cervical cord. Petechial hemorrhages were also noted within the brainstem. These features are compatible with toxic injury to the brain and cervical spinal cord. To our knowledge, the magnetic resonance imaging features of brain and spinal cord injury and cerebellar tonsillar herniation, secondary to isopropanol intoxication have not been reported in the published literature before.

This article is from Journal of Emergencies, Trauma, and Shock , volume 7 . Abstract Background:: Venous thromboembolic prophylaxis (VTEp) is often delayed following traumatic brain injury (TBI), yet animal data suggest that it may reduce cerebral inflammation and improve cognitive recovery. We hypothesized that earlier VTEp initiation in severe TBI patients would result in more rapid neurologic recovery and reduced progression of brain injury on radiologic imaging. Study Design:: Medical charts of severe TBI patients admitted to a level 1 trauma center in 2009-2010 were queried for admission Glasgow Coma Scale (GCS), head Abbreviated Injury Scale, Injury Severity Score (ISS), osmotherapy use, emergency neurosurgery, and delay to VTEp initiation. Progression (+1 = better, 0 = no change, −1 = worse) of brain injury on head CTs and neurologic exam (by bedside MD, nurse) was collected from patient charts. Head CT scan Marshall scores were calculated from the initial head CT results. Results:: A total of 22, 34, and 19 patients received VTEp at early ( 5 days) time intervals, respectively. Clinical and radiologic brain injury characteristics on admission were similar among the three groups (P > 0.05), but ISS was greatest in the early group (P < 0.05). Initial head CT Marshall scores were similar in early and late groups. The slowest progression of brain injury on repeated head CT scans was in the early VTEp group up to 10 days after admission. Conclusion:: Early initiation of prophylactic heparin in severe TBI is not associated with deterioration neurologic exam and may result in less progression of injury on brain imaging. Possible neuroprotective effects of heparin in humans need further investigation.

This article is from Journal of Emergencies, Trauma, and Shock , volume 7 . Abstract Background:: Venous thromboembolic prophylaxis (VTEp) is often delayed following traumatic brain injury (TBI), yet animal data suggest that it may reduce cerebral inflammation and improve cognitive recovery. We hypothesized that earlier VTEp initiation in severe TBI patients would result in more rapid neurologic recovery and reduced progression of brain injury on radiologic imaging. Study Design:: Medical charts of severe TBI patients admitted to a level 1 trauma center in 2009-2010 were queried for admission Glasgow Coma Scale (GCS), head Abbreviated Injury Scale, Injury Severity Score (ISS), osmotherapy use, emergency neurosurgery, and delay to VTEp initiation. Progression (+1 = better, 0 = no change, −1 = worse) of brain injury on head CTs and neurologic exam (by bedside MD, nurse) was collected from patient charts. Head CT scan Marshall scores were calculated from the initial head CT results. Results:: A total of 22, 34, and 19 patients received VTEp at early ( 5 days) time intervals, respectively. Clinical and radiologic brain injury characteristics on admission were similar among the three groups (P > 0.05), but ISS was greatest in the early group (P < 0.05). Initial head CT Marshall scores were similar in early and late groups. The slowest progression of brain injury on repeated head CT scans was in the early VTEp group up to 10 days after admission. Conclusion:: Early initiation of prophylactic heparin in severe TBI is not associated with deterioration neurologic exam and may result in less progression of injury on brain imaging. Possible neuroprotective effects of heparin in humans need further investigation.

This article is from Journal of Emergencies, Trauma, and Shock , volume 7 . Abstract Background:: Venous thromboembolic prophylaxis (VTEp) is often delayed following traumatic brain injury (TBI), yet animal data suggest that it may reduce cerebral inflammation and improve cognitive recovery. We hypothesized that earlier VTEp initiation in severe TBI patients would result in more rapid neurologic recovery and reduced progression of brain injury on radiologic imaging. Study Design:: Medical charts of severe TBI patients admitted to a level 1 trauma center in 2009-2010 were queried for admission Glasgow Coma Scale (GCS), head Abbreviated Injury Scale, Injury Severity Score (ISS), osmotherapy use, emergency neurosurgery, and delay to VTEp initiation. Progression (+1 = better, 0 = no change, −1 = worse) of brain injury on head CTs and neurologic exam (by bedside MD, nurse) was collected from patient charts. Head CT scan Marshall scores were calculated from the initial head CT results. Results:: A total of 22, 34, and 19 patients received VTEp at early ( 5 days) time intervals, respectively. Clinical and radiologic brain injury characteristics on admission were similar among the three groups (P > 0.05), but ISS was greatest in the early group (P < 0.05). Initial head CT Marshall scores were similar in early and late groups. The slowest progression of brain injury on repeated head CT scans was in the early VTEp group up to 10 days after admission. Conclusion:: Early initiation of prophylactic heparin in severe TBI is not associated with deterioration neurologic exam and may result in less progression of injury on brain imaging. Possible neuroprotective effects of heparin in humans need further investigation.

Stereotactic needle biopsy (SNB) is performed to collect tissue samples from deep-seated lesions. Recently, intraoperative 5-aminolevulinic acid (5-ALA) fluorescence has also been applied to confirm the adequacy of bioptic specimens. Objective of the present review is to clarify if this technique may render intra-operative pathological examination not necessary

This article is from International Journal of Molecular Sciences , volume 15 . Abstract Nuclear medicine techniques (single photon emission computerized tomography, SPECT, and positron emission tomography, PET) represent molecular imaging tools, able to provide in vivo biomarkers of different diseases. To investigate brain tumours and metastases many different radiopharmaceuticals imaged by SPECT and PET can be used. In this review the main and most promising radiopharmaceuticals available to detect brain metastases are reported. Furthermore the diagnostic contribution of the combination of SPECT and PET data with radiological findings (magnetic resonance imaging, MRI) is discussed.

This article is from Frontiers in Physiology , volume 4 . Abstract Imaging the brain during complex and intensive movements is challenging due to the susceptibility of brain-imaging methods for motion and myogenic artifacts. A few studies measured brain activity during either single-joint or low-intensity exercises; however, the cortical activation state during larger movements with increases up to maximal intensity has barely been investigated so far. Eleven right-handed volunteers (22–45 years in age) performed isometric leg extensions with their right leg at 20, 40, 60, 80, and 100% of their maximal voluntary contraction. Contractions were hold for 20 s respectively. Electroencephalographic (EEG) and electromyographic (EMG) activity was recorded. Standardized low-resolution brain electromagnetic tomography (sLORETA) was used to localize the cortical current density within the premotor (PMC), primary motor (M1), primary somatosensory (S1) and somatosensory association cortex (SAC). ANOVA was used for repeated measures for comparison of intensities and between the left and right hemispheres. The quality of the EEG signal was satisfying up to 80% intensity. At 100% half of the participants were not able to keep their neck and face muscles relaxed, leading to myogenic artifacts. Higher contralateral vs. ipsilateral hemispheric activity was found for the S1, SAC and, PMC. M1 possessed higher ipsilateral activity. The highest activity was localized in the M1, followed by S1, PMC, and SAC. EMG activity and cortical current density within the M1 increased with exercise intensity. EEG recordings during bigger movements up to submaximal intensity (80%) are possible, but maximal intensities are still hard to investigate when subjects contracted their neck and face muscles at the same time. Isometric contractions mainly involve the M1, whereas the S1, PMC, and SAC seem not to be involved in the force output. Limitations and recommendations for future studies are discussed.

This article is from Molecular Psychiatry , volume 18 . Abstract In response to queries about whether brain imaging technology has reached the point where it is useful for making a clinical diagnosis and for helping to guide treatment selection, the American Psychiatric Association (APA) has recently written a position paper on the Clinical Application of Brain Imaging in Psychiatry. The following perspective piece is based on our contribution to this APA position paper, which specifically emphasized the application of neuroimaging in mood disorders. We present an introductory overview of the challenges faced by researchers in developing valid and reliable biomarkers for psychiatric disorders, followed by a synopsis of the extant neuroimaging findings in mood disorders, and an evidence-based review of the current research on brain imaging biomarkers in adult mood disorders. Although there are a number of promising results, by the standards proposed below, we argue that there are currently no brain imaging biomarkers that are clinically useful for establishing diagnosis or predicting treatment outcome in mood disorders.

This article is from Frontiers in Human Neuroscience , volume 8 . Abstract Despite recent advancements in MR imaging, non-invasive mapping of myelin in the brain still remains an open issue. Here we attempted to provide a potential solution. Specifically, we developed a processing workflow based on T1-w and T2-w MR data to generate an optimized myelin enhanced contrast image. The workflow allows whole brain mapping using the T1-w/T2-w technique, which was originally introduced as a non-invasive method for assessing cortical myelin content. The hallmark of our approach is a retrospective calibration algorithm, applied to bias-corrected T1-w and T2-w images, that relies on image intensities outside the brain. This permits standardizing the intensity histogram of the ratio image, thereby allowing for across-subject statistical analyses. Quantitative comparisons of image histograms within and across different datasets confirmed the effectiveness of our normalization procedure. Not only did the calibrated T1-w/T2-w images exhibit a comparable intensity range, but also the shape of the intensity histograms was largely corresponding. We also assessed the reliability and specificity of the ratio image compared to other MR-based techniques, such as magnetization transfer ratio (MTR), fractional anisotropy (FA), and fluid-attenuated inversion recovery (FLAIR). With respect to these other techniques, T1-w/T2-w had consistently high values, as well as low inter-subject variability, in brain structures where myelin is most abundant. Overall, our results suggested that the T1-w/T2-w technique may be a valid tool supporting the non-invasive mapping of myelin in the brain. Therefore, it might find important applications in the study of brain development, aging and disease.

This article is from Frontiers in Human Neuroscience , volume 8 . Abstract Early bilingual exposure, especially exposure to two languages in different modalities such as speech and sign, can profoundly affect an individual's language, culture, and cognition. Here we explore the hypothesis that bimodal dual language exposure can also affect the brain's organization for language. These changes occur across brain regions universally important for language and parietal regions especially critical for sign language (Newman et al., 2002). We investigated three groups of participants (N = 29) that completed a word repetition task in American Sign Language (ASL) during fNIRS brain imaging. Those groups were (1) hearing ASL-English bimodal bilinguals (n = 5), (2) deaf ASL signers (n = 7), and (3) English monolinguals naïve to sign language (n = 17). The key finding of the present study is that bimodal bilinguals showed reduced activation in left parietal regions relative to deaf ASL signers when asked to use only ASL. In contrast, this group of bimodal signers showed greater activation in left temporo-parietal regions relative to English monolinguals when asked to switch between their two languages (Kovelman et al., 2009). Converging evidence now suggest that bimodal bilingual experience changes the brain bases of language, including the left temporo-parietal regions known to be critical for sign language processing (Emmorey et al., 2007). The results provide insight into the resilience and constraints of neural plasticity for language and bilingualism.

This article is from Frontiers in Neurology , volume 5 . Abstract Ischemia is a common and deleterious secondary injury following traumatic brain injury (TBI). A great challenge for the treatment of TBI patients in the neurointensive care unit (NICU) is to detect early signs of ischemia in order to prevent further advancement and deterioration of the brain tissue. Today, several imaging techniques are available to monitor cerebral blood flow (CBF) in the injured brain such as positron emission tomography (PET), single-photon emission computed tomography, xenon computed tomography (Xenon-CT), perfusion-weighted magnetic resonance imaging (MRI), and CT perfusion scan. An ideal imaging technique would enable continuous non-invasive measurement of blood flow and metabolism across the whole brain. Unfortunately, no current imaging method meets all these criteria. These techniques offer snapshots of the CBF. MRI may also provide some information about the metabolic state of the brain. PET provides images with high resolution and quantitative measurements of CBF and metabolism; however, it is a complex and costly method limited to few TBI centers. All of these methods except mobile Xenon-CT require transfer of TBI patients to the radiological department. Mobile Xenon-CT emerges as a feasible technique to monitor CBF in the NICU, with lower risk of adverse effects. Promising results have been demonstrated with Xenon-CT in predicting outcome in TBI patients. This review covers available imaging methods used to monitor CBF in patients with severe TBI.

This is talk 22 of 31 at the Conference on Brain Network Dynamics held at the University of California at Berkeley on January 26-27, 2007. Speaker is Barry Horwitz, Brain Imaging and Modeling Section Voice, Speech and Language Branch, NIDCD Bethesda, MD 20892. http://neuroscience.nih.gov/Lab.asp?Org_ID=223 . Full title: Combined Use of Brain Network Modeling and Functional Brain Imaging: Integrating Neuroscientific Data Across Different Spatiotemporal Scales. Abstract: Formidable conceptual problems exist in interpreting human functional neuroimaging data in terms of the underlying neural activity. To overcome these difficulties, we have developed two neurobiologically realistic brain network models (one for vision, one for audition) of the object recognition pathway in human neocortex in which data at different spatiotemporal levels can be simulated and cross-validated by multiple disciplines, including PET and fMRI. Our models, based on neurophysiological and neuroanatomical data from primate and human studies, enable us to simultaneously simulate cellular electrophysiological and PET/fMRI activities in multiple, interconnected brain regions (including primary and secondary sensory cortex, anterior temporal cortex, and prefrontal cortex). This type of network modeling provides a mechanism by which assumptions about the neural bases for high-level cognitive, sensorimotor and emotional processes can have their physiological consequences tested.

This is talk 22 of 31 at the Conference on Brain Network Dynamics held at the University of California at Berkeley on January 26-27, 2007. Speaker is Barry Horwitz, Brain Imaging and Modeling Section Voice, Speech and Language Branch, NIDCD Bethesda, MD 20892. http://neuroscience.nih.gov/Lab.asp?Org_ID=223 . Full title: Combined Use of Brain Network Modeling and Functional Brain Imaging: Integrating Neuroscientific Data Across Different Spatiotemporal Scales. Abstract: Formidable conceptual problems exist in interpreting human functional neuroimaging data in terms of the underlying neural activity. To overcome these difficulties, we have developed two neurobiologically realistic brain network models (one for vision, one for audition) of the object recognition pathway in human neocortex in which data at different spatiotemporal levels can be simulated and cross-validated by multiple disciplines, including PET and fMRI. Our models, based on neurophysiological and neuroanatomical data from primate and human studies, enable us to simultaneously simulate cellular electrophysiological and PET/fMRI activities in multiple, interconnected brain regions (including primary and secondary sensory cortex, anterior temporal cortex, and prefrontal cortex). This type of network modeling provides a mechanism by which assumptions about the neural bases for high-level cognitive, sensorimotor and emotional processes can have their physiological consequences tested.

Lithium magnetic resonance imaging (⁷Li-MRI) is a pioneering technique that directly determines the distribution of lithium in the brain. This is an observational study of euthymic patients with bipolar disorder taking lithium as a long-term treatment, either once (n=30) or twice-daily (n=30). ⁷Li-MRI will be performed three times within a 10-hour period, with repeated serum lithium level sampling, tremor analysis and ataxia rating.

This article is from ASN NEURO , volume 4 . Abstract Metabolic signals are used for imaging and spectroscopic studies of brain function and disease and to elucidate the cellular basis of neuroenergetics. The major fuel for activated neurons and the models for neuron–astrocyte interactions have been controversial because discordant results are obtained in different experimental systems, some of which do not correspond to adult brain. In rats, the infrastructure to support the high energetic demands of adult brain is acquired during postnatal development and matures after weaning. The brain's capacity to supply and metabolize glucose and oxygen exceeds demand over a wide range of rates, and the hyperaemic response to functional activation is rapid. Oxidative metabolism provides most ATP, but glycolysis is frequently preferentially up-regulated during activation. Underestimation of glucose utilization rates with labelled glucose arises from increased lactate production, lactate diffusion via transporters and astrocytic gap junctions, and lactate release to blood and perivascular drainage. Increased pentose shunt pathway flux also causes label loss from C1 of glucose. Glucose analogues are used to assay cellular activities, but interpretation of results is uncertain due to insufficient characterization of transport and phosphorylation kinetics. Brain activation in subjects with low blood-lactate levels causes a brain-to-blood lactate gradient, with rapid lactate release. In contrast, lactate flooding of brain during physical activity or infusion provides an opportunistic, supplemental fuel. Available evidence indicates that lactate shuttling coupled to its local oxidation during activation is a small fraction of glucose oxidation. Developmental, experimental, and physiological context is critical for interpretation of metabolic studies in terms of theoretical models.

There is an increasing awareness that adjuvant chemotherapy administration for breast cancer and other malignancies can cause cognitive impairment or chemobrain in a significant proportion of patients . Little is known regarding its cause or even its duration and/or permanence. Rodent models are available for studying toxicity from doxorubicin and other chemotherapeutic agents and behavioral impairment has been demonstrated using them. The overall goal of this project is to investigate this impairment at a mechanistic level by determining the effects of doxorubicin, one of the agents commonly used for the adjuvant chemotherapy of breast cancer, on brain function using functional magnetic resonance imaging (fMRI) and behavioral techniques in a rat model. Female rats are treated with doxorubicin weekly, for six weeks. One week later, they are behaviorally tested and imaged using fMRI. Measures will also be made in rats, one and three months after doxorubicin treatment. To date, we have observed that treatment with doxorubicin alters brain activation in response to both visual and somatosensory stimulation with the effects greatest in the visual system. In addition, doxorubicin significantly decreases functional connectivity in the rat visual system. This supports our hypothesis that treatment with doxorubicin will cause changes in neuronal functional activity that can be detected and quantified using fMRI methods. Furthermore, it is consistent with impaired visual cognitive processing reported after chemotherapy.

There is an increasing awareness that adjuvant chemotherapy administration for breast cancer and other malignancies can cause cognitive impairment or chemobrain in a significant proportion of patients . Little is known regarding its cause or even its duration and/or permanence. Rodent models are available for studying toxicity from doxorubicin and other chemotherapeutic agents and behavioral impairment has been demonstrated using them. The overall goal of this project is to investigate this impairment at a mechanistic level by determining the effects of doxorubicin, one of the agents commonly used for the adjuvant chemotherapy of breast cancer, on brain function using functional magnetic resonance imaging (fMRI) and behavioral techniques in a rat model. Female rats are treated with doxorubicin weekly, for six weeks. One week later, they are behaviorally tested and imaged using fMRI. Measures will also be made in rats, one and three months after doxorubicin treatment. To date, we have observed that treatment with doxorubicin alters brain activation in response to both visual and somatosensory stimulation with the effects greatest in the visual system. In addition, doxorubicin significantly decreases functional connectivity in the rat visual system. This supports our hypothesis that treatment with doxorubicin will cause changes in neuronal functional activity that can be detected and quantified using fMRI methods. Furthermore, it is consistent with impaired visual cognitive processing reported after chemotherapy.

The purpose of this research is oriented towards understanding the reading, language, and articulation deficits associated with Neurofibromatosis Type 1 (NF-1) and relating these deficits to the underlying pathophysiology of NF-1 as revealed by Magnetic Resonance Spectroscopy Imaging (MRSI) . A second goal is to determine how differences in activation, as measured by functional Magnetic Resonance Imaging (fMRI), are linked to the cognitive/academic impairments associated with NF-l. A third goal is to further understand how T-2 weighted hyperintensities on Magnetic Resonance Imaging (MRI) scans are related to cognitive/academic impairments associated with NF-l. Each aim addresses the research in terms of pathophysiology and how cognitive/academic functioning of children with NF-1 compares to control groups when examined in both genetic (i.e., sibling) as well as general population (both reading disabled and non-reading disabled) contexts. We hypothesize that abnormalities of NAA, Choline, or their ratios, will exist in the thalamus and will correlate with language, reading, and articulation deficits in NF-1, defined by lowering of the cognitive scores of each child with NF-1 relative to his/her unaffected sibling. For the second goal, we hypothesize that children with NF-1 will activate their brains similarly to reading disabled children during fMRI tasks. For the third goal, we hypothesize that reading, language, and articulation deficits will correlate with the number of brain locations with T2-weighted hyperintensities. Thus, neuroimaging permits the pursuit of furthering our understanding of how the NF-1 gene affects the brain in terms of basic neurobiologic factors (ultrastructural, physiological, and localization) as well as their impacts on cognition (reading, language, and articulation) in NF-1.

The purpose of this research is oriented towards understanding the reading, language, and articulation deficits associated with Neurofibromatosis Type 1 (NF-1) and relating these deficits to the underlying pathophysiology of NF-1 as revealed by Magnetic Resonance Spectroscopy Imaging (MRSI) . A second goal is to determine how differences in activation, as measured by functional Magnetic Resonance Imaging (fMRI), are linked to the cognitive/academic impairments associated with NF-l. A third goal is to further understand how T-2 weighted hyperintensities on Magnetic Resonance Imaging (MRI) scans are related to cognitive/academic impairments associated with NF-l. Each aim addresses the research in terms of pathophysiology and how cognitive/academic functioning of children with NF-1 compares to control groups when examined in both genetic (i.e., sibling) as well as general population (both reading disabled and non-reading disabled) contexts. We hypothesize that abnormalities of NAA, Choline, or their ratios, will exist in the thalamus and will correlate with language, reading, and articulation deficits in NF-1, defined by lowering of the cognitive scores of each child with NF-1 relative to his/her unaffected sibling. For the second goal, we hypothesize that children with NF-1 will activate their brains similarly to reading disabled children during fMRI tasks. For the third goal, we hypothesize that reading, language, and articulation deficits will correlate with the number of brain locations with T2-weighted hyperintensities. Thus, neuroimaging permits the pursuit of furthering our understanding of how the NF-1 gene affects the brain in terms of basic neurobiologic factors (ultrastructural, physiological, and localization) as well as their impacts on cognition (reading, language, and articulation) in NF-1.

This article is from Scientific Reports , volume 4 . Abstract Mild blast-induced traumatic brain injury (mbTBI) poses special diagnostic challenges due to its overlapping symptomatology with other neuropsychiatric conditions and the lack of objective outcome measures. Diffusion tensor imaging (DTI) can potentially provide clinically relevant information toward a differential diagnosis. In this study, we aimed to determine if single and repeated (5 total; administered on consecutive days) mild blast overpressure exposure results in detectable structural changes in the brain, especially in the hippocampus. Fixed rat brains were analyzed by ex vivo DTI at 2 h and 42 days after blast (or sham) exposure(s). An anatomy-based region of interest analysis revealed significant interactions in axial and radial diffusivity in a number of subcortical structures at 2 h only. Differences between single- and multiple-injured rats were largely in the thalamus but not the hippocampus. Our findings demonstrate the value and the limitations of DTI in providing a better understanding of mbTBI pathobiology.

This article is from Scientific Reports , volume 4 . Abstract Mild blast-induced traumatic brain injury (mbTBI) poses special diagnostic challenges due to its overlapping symptomatology with other neuropsychiatric conditions and the lack of objective outcome measures. Diffusion tensor imaging (DTI) can potentially provide clinically relevant information toward a differential diagnosis. In this study, we aimed to determine if single and repeated (5 total; administered on consecutive days) mild blast overpressure exposure results in detectable structural changes in the brain, especially in the hippocampus. Fixed rat brains were analyzed by ex vivo DTI at 2 h and 42 days after blast (or sham) exposure(s). An anatomy-based region of interest analysis revealed significant interactions in axial and radial diffusivity in a number of subcortical structures at 2 h only. Differences between single- and multiple-injured rats were largely in the thalamus but not the hippocampus. Our findings demonstrate the value and the limitations of DTI in providing a better understanding of mbTBI pathobiology.

This article is from BMC Psychiatry , volume 12 . Abstract Background: Studies of individuals who do not meet criteria for major depressive disorder (MDD) but with subclinical levels of depressive symptoms may aid in the identification of neurofunctional abnormalities that possibly precede and predict the development of MDD. The purpose of this study was to evaluate relations between subclinical levels of depressive symptoms and neural activation patterns during tasks previously shown to differentiate individuals with and without MDD. Methods: Functional magnetic resonance imaging (fMRI) was used to assess neural activations during active emotion regulation, a resting state scan, and reward processing. Participants were twelve females with a range of depressive symptoms who did not meet criteria for MDD. Results: Increased depressive symptom severity predicted (1) decreased left midfrontal gyrus activation during reappraisal of sad stimuli; (2) increased right midfrontal gyrus activation during distraction from sad stimuli; (3) increased functional connectivity between a precuneus seed region and left orbitofrontal cortex during a resting state scan; and (4) increased paracingulate activation during non-win outcomes during a reward-processing task. Conclusions: These pilot data shed light on relations between subclinical levels of depressive symptoms in the absence of a formal MDD diagnosis and neural activation patterns. Future studies will be needed to test the utility of these activation patterns for predicting MDD onset in at-risk samples.

This article is from BMC Psychiatry , volume 12 . Abstract Background: Studies of individuals who do not meet criteria for major depressive disorder (MDD) but with subclinical levels of depressive symptoms may aid in the identification of neurofunctional abnormalities that possibly precede and predict the development of MDD. The purpose of this study was to evaluate relations between subclinical levels of depressive symptoms and neural activation patterns during tasks previously shown to differentiate individuals with and without MDD. Methods: Functional magnetic resonance imaging (fMRI) was used to assess neural activations during active emotion regulation, a resting state scan, and reward processing. Participants were twelve females with a range of depressive symptoms who did not meet criteria for MDD. Results: Increased depressive symptom severity predicted (1) decreased left midfrontal gyrus activation during reappraisal of sad stimuli; (2) increased right midfrontal gyrus activation during distraction from sad stimuli; (3) increased functional connectivity between a precuneus seed region and left orbitofrontal cortex during a resting state scan; and (4) increased paracingulate activation during non-win outcomes during a reward-processing task. Conclusions: These pilot data shed light on relations between subclinical levels of depressive symptoms in the absence of a formal MDD diagnosis and neural activation patterns. Future studies will be needed to test the utility of these activation patterns for predicting MDD onset in at-risk samples.

Treating breast cancer that has metastasized to the central nervous system remains a formidable challenge due to, 1) its high malignancy, 2) the difficulty in differentiating between tumor and healthy brain tissue, 3) the sensitivity of normal brain tissue to the toxicities of current therapies, 4) intrinsic cellular resistance of BMBC cells to chemotherapeutic drugs, and 5) the blood-brain barrier s (BBB) ability to prevent the passage of extrinsic substances such as drugs and contrast agents. Our aim is to develop magnetic contrast agents and targeted siRNA therapies capable of overcoming the blood brain barrier and to aid in both the diagnosis and treatment brain metastatic breast cancer. Magnetic nanoparticles with high susceptibility have been developed. These nanoparticles have been characterized to be monodispersed are working to engineer a nanovector that will aid in addressing the major challenges associated with the diagnosis and treatment of BMBC. The major components of the nanovector include a Fe3O4 superparamagnetic nanoparticle (NP) core and a shell comprised of a copolymer of polyethylene glycol (PEG)-grafted chitosan (C)-polyethyleneimine (P), or CP. The tumor targeting peptide, chlorotoxin (CTX), and siRNA (designed to knockdown the pro metastasis gene MENA) also are conjugated to the NP polymer overcoat.

Brain injury is a leading cause of death and disability in children. Recent advances in pediatric magnetic resonance imaging (MRI) techniques are revolutionizing our understanding of brain injury, its potential for recovery, and demonstrating enormous potential for advancing the field of neuroprotection. We have created a highly structured, collaborative, and multidisciplinary training program in BRAIN (Brain Research Advanced Imaging with NMR) to advance research skills of investigators from all branches of the US military focusing on pediatric brain injury. Our goal is to train, with the highest rigor, military trainees in conducting clinical research using advanced brain imaging technologies to study the causes and consequences of pediatric brain injury. Over the past year, we successfully implemented the on-site BRAIN training curriculum and we recruited and trained one civilian fellow. We developed an online learning management system, by creating and implementing methods for converting the existing in-classroom educational BRAIN seminars into self-directed online learning modules and courseware. Specifically, we developed a web-based portal site located at www.MilitaryMedED.com that users can search, upload, and house online training and education-related information. Our goal is to deploy this on-line BRAIN courseware to major DoD military bases to allow for a more broad-based teaching framework in which we anticipate far-reaching benefits.

We are developing robust low-magnetic-field implementations of MRI (LFI) focused on brain imaging with two complimentary test scanner systems: electromagnet and permanent magnet based. We are also developing injury-sensitive MRI based on the detection of free radicals associated with injury using the Overhauser effect and subsequently imaging that modified nuclear polarization using low-field MRI (OMRI). Much of the hardware development of the human head LFI test bed systems and the OMRI system is now complete. We now focused on imaging sequence development and optimization, image reconstruction, and the implementation of parallel imaging acceleration. We have successfully demonstrated high-speed free-radical OMRI, and investigated the sensitivity of spectroscopy- and image-based measurements to free radical concentrations as a path toward in vivo applications. Application of the suite of techniques and technologies from our work could advise future development of a deployable device with a high diagnostic impact, transforming diagnosis and monitoring of secondary injury prevalent in TBI.

This section has not changed since the previous report. The proposed research has the goal of understanding the brain system properties that underlie individual differences in cognitive performance and using this understanding to enhance performance of individuals and organizations. The proposed research will apply new leverage to this familiar problem using innovations in brain science from the past ten years that permit detailed noninvasive measurement of brain function, brain anatomy, and now the effect of magnetic brain stimulation, as they relate to cognitive performance. For example, the essence of fluid intelligence is the ability to adapt to a new task or problem. This ability cannot be characterized in simple behavioral terms such as speed of processing. In the new brain systems view, fluid intelligence consists of the ability to dynamically configure a new network (team) of brain areas that can effectively collaborate to perform a new task. The individual differences in fluid intelligence, according to this view, are underpinned by differences in this dynamic 'network configuration** ability, which we call adaptability. This new approach, when used in the context of a suitable integrating theoretical framework, has the potential of determining the brain bases of individual differences in cognition.

This article is from Neural Regeneration Research , volume 9 . Abstract None

This article is from Frontiers in Human Neuroscience , volume 8 . Abstract A new paradigm for human brain imaging, mobile brain/body imaging (MoBI), involves synchronous collection of human brain activity (via electroencephalography, EEG) and behavior (via body motion capture, eye tracking, etc.), plus environmental events (scene and event recording) to study joint brain/body dynamics supporting natural human cognition supporting performance of naturally motivated human actions and interactions in 3-D environments (Makeig et al., 2009). Processing complex, concurrent, multi-modal, multi-rate data streams requires a signal-processing environment quite different from one designed to process single-modality time series data. Here we describe MoBILAB (more details available at sccn.ucsd.edu/wiki/MoBILAB), an open source, cross platform toolbox running on MATLAB (The Mathworks, Inc.) that supports analysis and visualization of any mixture of synchronously recorded brain, behavioral, and environmental time series plus time-marked event stream data. MoBILAB can serve as a pre-processing environment for adding behavioral and other event markers to EEG data for further processing, and/or as a development platform for expanded analysis of simultaneously recorded data streams.

This article is from Neurobiology of Aging , volume 35 . Abstract A pressing need exists to disentangle age-related changes from pathologic neurodegeneration. This study aims to characterize the spatial pattern and age-related differences of biologically relevant measures in vivo over the course of normal aging. Quantitative multiparameter maps that provide neuroimaging biomarkers for myelination and iron levels, parameters sensitive to aging, were acquired from 138 healthy volunteers (age range: 19–75 years). Whole-brain voxel-wise analysis revealed a global pattern of age-related degeneration. Significant demyelination occurred principally in the white matter. The observed age-related differences in myelination were anatomically specific. In line with invasive histologic reports, higher age-related differences were seen in the genu of the corpus callosum than the splenium. Iron levels were significantly increased in the basal ganglia, red nucleus, and extensive cortical regions but decreased along the superior occipitofrontal fascicle and optic radiation. This whole-brain pattern of age-associated microstructural differences in the asymptomatic population provides insight into the neurobiology of aging. The results help build a quantitative baseline from which to examine and draw a dividing line between healthy aging and pathologic neurodegeneration.

This article is from NeuroImage : Clinical , volume 1 . Abstract Diabetes mellitus affects the brain. Both type 1 and type 2 diabetic patients are associated with white matter (WM) damage observable to diffusion tensor imaging (DTI). The underlying histopathological mechanisms, however, are poorly understood. The objectives of this study are 1) to determine whether streptozotocin (STZ)-induced type 1 diabetes is associated with WM damage observable to DTI; and 2) to understand the pathophysiological aspects underlying STZ-induced brain injuries. Male Sprague–Dawley rats received a single intraperitoneal injection of STZ (62 mg/kg). DTI was used to assess brain abnormalities at 4 weeks after induction, combined with histological assessments and ultrastructural analysis. Compared to controls, the STZ-induced rats showed significantly reduced fractional anisotropy (FA) in the motor/somatosensory cortex and striatum. Histologically, the cortex and striatum of the diabetic animals are characterized by demyelination and axonal degradation. In conclusion, STZ-induced diabetes is associated with striatal/cortical injuries observable to DTI. The DTI abnormalities are likely manifestations of demyelination and axonal degradation in the affected brain regions, and can potentially be used as surrogates for evaluating diabetic brain injuries.

This article is from Diabetes Care , volume 36 . Abstract OBJECTIVE: In patients with long-standing diabetes mellitus (DM), there is increasing evidence for abnormal processing of gastrointestinal sensations in the central nervous system. Using magnetic resonance diffusion tensor imaging, we characterized brain microstructure in areas involved in visceral sensory processing and correlated these findings to clinical parameters. RESEARCH DESIGN AND METHODS: Twenty-six patients with DM and gastrointestinal symptoms and 23 healthy control subjects were studied in a 3T scanner. The apparent diffusion coefficient (i.e., diffusivity of water) and fractional anisotropy (FA) (i.e., organization of fibers) were assessed in the “sensory matrix” (cingulate cortex, insula, prefrontal and secondary sensory cortex, amygdala, and corona radiata) and in corpus callosum. RESULTS: Patients had decreased FA values compared with control subjects in 1) all areas (P = 0.025); 2) anterior (P < 0.001), mid- (P = 0.001), and posterior (P < 0.001) cingulate cortex; 3) prefrontal cortex gray matter (P < 0.001); 4) corona radiata (P < 0.001); 5) secondary sensory cortex (P = 0.008); and 6) anterior white matter (P = 0.045), anterior gray matter (P = 0.002), and posterior gray matter (P = 0.002) insula. No difference was found in corpus callosum (P > 0.05). The microstructural changes in some areas correlated with clinical parameters such as bloating (anterior insula), mental well-being (anterior insula, prefrontal cortex, and mid-cingulated and corona radiata), autonomic function based on electrocardiographic results (posterior insula and anterior cingulate), and presence of gastroparesis (anterior insula). CONCLUSIONS: The findings of this explorative study indicate that microstructural changes of brain areas involved in visceral sensory processing are associated with autonomic dysfunction and therefore may be involved in the pathogenesis of gastrointestinal symptoms in DM patients.

Brain tumor is an uncontrolled growth of abnormal cell in the brain. Early diagnosis of brain tumor has a crucial step in this type of cancer, which is fatal. Magnetic resonance imaging (MRI) is one of the examination tools to examine brain anatomy in clinical practice. The high resolution and clear separation of the tissue enable medical experts to identify brain tumor. The earlier of brain tumor is detected, the wider of treatment options. However, manually analysed of brain anatomy on MRI images are time-consuming. Computer-aided diagnosis with automated way is helpful solution to help management with unreliable degrees of automation to trace various tissue boundaries. This study proposes convolutional neural network (CNN) with its excellences to automated features extraction in convolution layer. The popular architectures of CNN, i.e., visual geometry group16 (VGG16), residual network-50 (resNet-50), inceptionV3, mobileNet, and efficientNetB7 in medical image processing are compared to brain tumor classification task. As the results, VGG16 outperformed other architectures of CNN in this study. VGG16 yields 100% accuracy, precision, sensitivity, specificity, and F1-score for testing set data. The results show the excellent performance in classifying brain tumor and no tumor from MRI images that demonstrate the efficiency of system suggested.

Recent evidence indicates that neural adaptations related to changes in task performance occur in not only gray matter brain regions but also the white matter fiber tracts that connect the gray matter regions with one another. Here, we propose a framework for linking individual differences in global properties of the brain's anatomical connectivity, or connectome, to individual differences in task performance. We argue that this analysis framework may be optimally used on groups of patients with particular cognitive impairments to increase the dynamic range of task performance and optimize our sensitivity to detect structure-function relationships. In particular, patients suffering from mild traumatic brain injury may be an ideal group based on evidence suggesting an underlying cause of diffuse axonal injury that is widespread throughout the brain yet not detectable on structural magnetic resonance imaging (MRI) or computer tomography (CT) brain scans. The data discussed here lays the foundation for research on individual differences in structure-function relationships by comparing two diffusion-weighted imaging techniques that can be used to examine white matter structure in vivo in order to determine if one technique provides more reliable estimates of structural variability between individuals. While both methods show reproducibility of a particular individual's brain structure, Diffusion Tensor Imaging appears better able to reliably capture the variability between subjects. We conclude with a description of a physics-based modeling approach using diffusion-weighted imaging data that facilitates several avenues of Army-relevant research.

Traumatic axonal injury is a progressive process evoked by shear forces on the brain, gradually evolving from focal axonal alteration and cumulating in neural disconnection. Clinical classifiers and conventional neuroimaging are limited in traumatic axonal injury detection, outcome prediction, and treatment guidance. Diffusion weighted imaging is an advanced magnetic resonance imaging (MRI) technique that is sensitive to the movement of water molecules, providing additional information on the micro-structural arrangement of tissue. Quantitative analysis of diffusion metrics can aid in the localization of axonal injury and/or de(dys)myelination caused by trauma. Diffusion MRI tractography is an ex-tension of diffusion weighted imaging, and can provide additional information about white matter pathways and the integrity of brain neural networks. Both techniques are able to detect the early micro-structural changes caused by Traumatic Brain Injury (TBI), and can be used to increase understanding of the mechanisms of brain plasticity in recovery after brain injury and possibly optimize treatment planning of patients with Traumatic Brain Injury. This review focuses on the theoretical basis and applied advanced techniques of diffusion weighted imaging, their limitations and applications, and future directions in the application to TBI.

This article is from Neural Regeneration Research , volume 8 . Abstract The rapidly increasing prevalence of cognitive impairment and Alzheimer's disease has the potential to create a major worldwide healthcare crisis. Structural MRI studies in patients with Alzheimer's disease and mild cognitive impairment are currently attracting considerable interest. It is extremely important to study early structural and metabolic changes, such as those in the hippocampus, entorhinal cortex, and gray matter structures in the medial temporal lobe, to allow the early detection of mild cognitive impairment and Alzheimer's disease. The microstructural integrity of white matter can be studied with diffusion tensor imaging. Increased mean diffusivity and decreased fractional anisotropy are found in subjects with white matter damage. Functional imaging studies with positron emission tomography tracer compounds enable detection of amyloid plaques in the living brain in patients with Alzheimer's disease. In this review, we will focus on key findings from brain imaging studies in mild cognitive impairment and Alzheimer's disease, including structural brain changes studied with MRI and white matter changes seen with diffusion tensor imaging, and other specific imaging methodologies will also be discussed.

This article is from Frontiers in Oncology , volume 3 . Abstract Treatment of glioblastoma multiforme (GBM) and brain metastasis remains a challenge because of the poor survival and the potential for brain damage following radiation. Despite concurrent chemotherapy and radiation dose escalation, local recurrence remains the predominant pattern of failure in GBM most likely secondary to repopulation of cancer stem cells. Even though radiotherapy is highly effective for local control of radio-resistant tumors such as melanoma and renal cell cancer, systemic disease progression is the cause of death in most patients with brain metastasis. Preservation of quality of life (QOL) of cancer survivors is the main issue for patients with brain metastasis. Image-guided radiotherapy (IGRT) by virtue of precise radiation dose delivery may reduce treatment time of patients with GBM without excessive toxicity and potentially improve neurocognitive function with preservation of local control in patients with brain metastasis. Future prospective trials for primary brain tumors or brain metastasis should include IGRT to assess its efficacy to improve patient QOL.

This article is from Frontiers in Oncology , volume 3 . Abstract Treatment of glioblastoma multiforme (GBM) and brain metastasis remains a challenge because of the poor survival and the potential for brain damage following radiation. Despite concurrent chemotherapy and radiation dose escalation, local recurrence remains the predominant pattern of failure in GBM most likely secondary to repopulation of cancer stem cells. Even though radiotherapy is highly effective for local control of radio-resistant tumors such as melanoma and renal cell cancer, systemic disease progression is the cause of death in most patients with brain metastasis. Preservation of quality of life (QOL) of cancer survivors is the main issue for patients with brain metastasis. Image-guided radiotherapy (IGRT) by virtue of precise radiation dose delivery may reduce treatment time of patients with GBM without excessive toxicity and potentially improve neurocognitive function with preservation of local control in patients with brain metastasis. Future prospective trials for primary brain tumors or brain metastasis should include IGRT to assess its efficacy to improve patient QOL.

A method has been developed to determine the distribution of average spontaneous neuronal activity across the cerebral cortex from measurements of the field pattern across the human scalp. Computations of the mean short-term power, as well as the covariance between pairs of sensors, provide sufficient information to obtain a best estimate for the distribution of mean short-term image current power, as well as the covariance of image current between different locations on cerebral cortex. This method has applications for determining the spatial locations of alpha power suppression as regions of cortex participate in sensory or cognitive functions.... Magnetic source imaging, MSI, Alpha rhythm, Magnetic inverse problem, Spontaneous brain activity.

Brain metastasis represents a poor prognosis and is frequently the cause of death in breast cancer patients. Tumor microcirculation and oxygenation play important roles in malignant progression and metastasis, as well as response to various therapies. Understanding of hypoxia development and its relationship with blood brain barrier (BBB) during intracranial tumor growth will be crucial for clinical management of breast cancer brain metastasis. We have developed a MRI approach based on an interleaved T2*- and T1-weighted MRI sequence, which will provide information of both tumor vascular and tissue oxygenation. Moreover, by introducing hypoxia reporter gene (HRE-luciferase) into breast tumor lines, we will be able to use bioluminescence imaging to monitor hypoxia initiation and development of intracranial tumors. We will also correlate BBB function based on dynamic contrast enhanced (DCE) MRI with tumor hypoxia. We believe that integration of MRI and BLI will provide temporal and spatial information of tumor hypoxia evolution. Tumor hypoxia leads to resistance to anticancer therapies, in particular radiation, which is perhaps the most important treatment modality in our current armamentarium for brain metastasis. A combination of radiation with hypoxia modifier, 2-methoxyestradiol, on brain metastases will be evaluated by in vivo imaging.

The objective of this study is to develop a better biomarker for multiple sclerosis (MS) by combining genotype and imaging data. In this study, patients with MS undergo neurological evaluation to confirm diagnosis and determine disability level. They have blood drawn for genotyping, and undergo magnetic resonance imaging sensitive to both focal and diffuse effects in gray and white matter, including cortical thickness and subcortical volume measures, lesion volumetry, and voxel-based morphometry and diffusion imaging. We are continuing to progress with screening, enrollment, and testing of participants. We have encountered no adverse events. We continued to use our established procedures for acquiring, logging and backing up all data, and completing ongoing QA of the data. The genotyping will occur in batches; the blood samples are securely stored in our Molecular Diagnostics Laboratory until then. We are having biweekly to weekly research meetings, and additional meetings as needed, and I am monitoring the financial and administrative issues together with our Grants Manager. We are preparing a two conference submissions based on early results from this study, one on neurotrophic factor genotype as a predictor of hippocampal atrophy on MRI in MS, and one on a semi-automated program we have developed for MS lesion segmentation on fluid-attenuated inversion recovery images. These will be submitted to the International Neuropsychological Society for presentation at their Annual Meeting in February 2011.

The purpose of this research is oriented towards understanding the reading, language, and articulation deficits associated with Neurofibromatosis Type 1 (NF-l) and relating these deficits to the underlying pathophysiology of NF-l as revealed by Magnetic Resonance Spectroscopy Imaging (MRSI). A second goal is to determine how differences in activation, as measured by functional Magnetic Resonance Imaging (fMRI), are linked to the cognitive/academic impairments associated with NF-l. A third goal is to further understand how T-2 weighted hyperintensities on Magnetic Resonance Imaging (MRI) scans are related to cognitive/academic impairments associated with NF-l. Each aim addresses the research in terms of pathophysiology and how cognitive/academic functioning of children with NF-l compares to control groups when examined in both genetic (i.e., sibling) as well as general population (both reading disabled and non-reading disabled) contexts. We hypothesize that abnormalities of NAA, Choline, or their ratios, will exist in the thalamus and will correlate with language, reading, and articulation deficits in NF-l, defined by lowering of the cognitive scores of each child with NF-l relative to his/her unaffected sibling. For the second goal, we hypothesize that children with NF-l will activate their brains similarly to reading disabled children during fMRI tasks. For the third goal, we hypothesize that reading, language, and articulation deficits will correlate with the number of brain locations with T2-weighted hyperintensities. Thus, neuroimaging permits the pursuit of furthering our understanding of how the NF-l gene affects the brain in terms of basic neurobiologic factors (ultrastructural, physiological, and localization) as well as their impacts on cognition (reading, language, and articulation) in NF-l.