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Cortical Regions (cortical + regions)
Selected AbstractsAnomalous development of brain structure and function in spina bifida myelomeningoceleDEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 1 2010Jenifer Juranek Abstract Spina bifida myelomeningocele (SBM) is a specific type of neural tube defect whereby the open neural tube at the level of the spinal cord alters brain development during early stages of gestation. Some structural anomalies are virtually unique to individuals with SBM, including a complex pattern of cerebellar dysplasia known as the Chiari II malformation. Other structural anomalies are not necessarily unique to SBM, including altered development of the corpus callosum and posterior fossa. Within SBM, tremendous heterogeneity is reflected in the degree to which brain structures are atypical in qualitative appearance and quantitative measures of morphometry. Hallmark structural features of SBM include overall reductions in posterior fossa and cerebellum size and volume. Studies of the corpus callosum have shown complex patterns of agenesis or hypoplasia along its rostral-caudal axis, with rostrum and splenium regions particularly susceptible to agenesis. Studies of cortical regions have demonstrated complex patterns of thickening, thinning, and gyrification. Diffusion tensor imaging studies have reported compromised integrity of some specific white matter pathways. Given equally complex ocular motor, motor, and cognitive phenotypes consisting of relative strengths and weaknesses that seem to align with altered structural development, studies of SBM provide new insights to our current understanding of brain structure,function associations. © 2010 Wiley-Liss, Inc. Dev Disabil Res Rev 2010;16:23,30. [source] Differential effects of stress and amphetamine administration on Fos-like protein expression in corticotropin releasing factor-neurons of the rat brainDEVELOPMENTAL NEUROBIOLOGY, Issue 6 2007David Rotllant Abstract Corticotropin releasing factor (CRF) appears to be critical for the control of important aspects of the behavioral and physiological response to stressors and drugs of abuse. However, the extent to which the different brain CRF neuronal populations are similarly activated after stress and drug administration is not known. We then studied, using double immunohistochemistry for CRF and Fos protein, stress and amphetamine-induced activation of CRF neurons in cortex, central amygdala (CeA), medial parvocellular dorsal, and submagnocellular parvocellular regions of the paraventricular nucleus of the hypothalamus (PVNmpd and PVNsm, respectively) and Barrington nucleus (Bar). Neither exposure to a novel environment (hole-board, HB) nor immobilization (IMO) increased Fos-like immunoreactivity (FLI) in the CeA, but they did to the same extent in cortical regions. In other regions only IMO increased FLI. HB and IMO both failed to activate CRF+ neurons in cortical areas, but after IMO, some neurons expressing FLI in the PVNsm and most of them in the PVNmpd and Bar were CRF+. Amphetamine administration increased FLI in cortical areas and CeA (with some CRF+ neurons expressing FLI), whereas the number of CRF+ neurons increased only in the PVNsm, in contrast to the effects of IMO. The present results indicate that stress and amphetamine elicited a distinct pattern of brain Fos-like protein expression and differentially activated some of the brain CRF neuronal populations, despite similar levels of overall FLI in the case of IMO and amphetamine. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007. [source] Dense array EEG: Methodology and new hypothesis on epilepsy syndromesEPILEPSIA, Issue 2008Mark D. Holmes Summary Dense array EEG is a method of recording electroencephalography (EEG) with many more electrodes (up to 256) than is utilized with standard techniques that typically employ 19,21 scalp electrodes. The rationale for this approach is to enhance the spatial resolution of scalp EEG. In our research, dense array EEG is used in conjunction with a realistic model of head tissue conductivity and methods of electrographic source analysis to determine cerebral cortical localization of epileptiform discharges. In studies of patients with absence seizures, only localized cortical regions are involved during the attack. Typically, absences are accompanied by "wave,spike" complexes that show, both at the beginning and throughout the ictus, repetitive cycles of stereotyped, localized involvement of mainly mesial and orbital frontal cortex. Dense array EEG can also be used for long-term EEG video monitoring (LTM). We have used dense array EEG LTM to capture seizures in over 40 patients with medically refractory localization-related epilepsy, including both temporal and extra temporal cases, where standard LTM failed to reveal reliable ictal localization. One research goal is to test the validity of dense array LTM findings by comparison with invasive LTM and surgical outcome. Collection of a prospective series of surgical candidates who undergo both procedures is currently underway. Analysis of subjects with either generalized or localization-related seizures suggest that all seizures, including those traditionally classified as "generalized," propagate through discrete cortical networks. Furthermore, based on initial review of propagation patterns, we hypothesize that all epileptic seizures may be fundamentally corticothalamic or corticolimbic in nature. Dense array EEG may prove useful in noninvasive ictal localization, when standard methods fail. Future research will determine if the method will reduce the need for invasive EEG recordings, or assist in the appropriate placement of novel treatment devices. [source] Heat Shock Protein-27 Is Upregulated in the Temporal Cortex of Patients with EpilepsyEPILEPSIA, Issue 12 2004Hans-J Bidmon Summary:,Purpose: Heat shock protein-27 (HSP-27) belongs to the group of small heat shock proteins that become induced in response to various pathologic conditions. HSP-27 has been shown to protect cells and subcellular structures, particularly mitochondria, and serves as a carrier for estradiol. It is a reliable marker for tissues affected by oxidative stress. Oxidative stress and related cellular defence mechanisms are currently thought to play a major role during experimentally induced epileptic neuropathology. We addressed the question whether HSP-27 becomes induced in the neocortex resected from patients with pharmacoresistant epilepsy. Methods: Human epileptic temporal neocortex was obtained during neurosurgery, and control tissue was obtained at autopsy from subjects without known neurologic diseases. The tissues were either frozen for Western blot analysis or fixed in Zamboni's fixative for the topographic detection of HSP-27 at the cellular level by means of immunohistochemistry. Results: HSP-27 was highly expressed in all epilepsy specimens and in the cortex of a patient who died in the final stage of multiple sclerosis (positive control), whereas only low amounts of HSP-27 were detectable in control brains. In epilepsy patients, HSP-27 was present in astrocytes and in the walls of blood vessels. The intracortical distribution patterns varied strongly among the epilepsy specimens. Conclusions: These results demonstrate that HSP-27 becomes induced in response to epileptic pathology. Although the functional aspects of HSP-27 induction during human epilepsy have yet to be elucidated, it can be concluded that HSP-27 is a marker for cortical regions in which a stress response has been caused by seizures. [source] Brain Blood-flow Alterations Induced by Therapeutic Vagus Nerve Stimulation in Partial Epilepsy: II.EPILEPSIA, Issue 9 2004Low Levels of Stimulation, Prolonged Effects at High Summary:,Purpose: To measure vagus nerve stimulation (VNS)-induced cerebral blood flow (CBF) effects after prolonged VNS and to compare these effects with immediate VNS effects on CBF. Methods: Ten consenting partial epilepsy patients had positron emission tomography (PET) with intravenous [15O]H2O. Each had three control scans without VNS and three scans during 30 s of VNS, within 20 h after VNS began (immediate-effect study), and repeated after 3 months of VNS (prolonged study). After intrasubject subtraction of control from stimulation scans, images were anatomically transformed for intersubject averaging and superimposed on magnetic resonance imaging (MRI) for anatomic localization. Changes on t-statistical maps were considered significant at p < 0.05 (corrected for multiple comparisons). Results: During prolonged studies, CBF changes were not observed in any regions that did not have CBF changes during immediate-effect studies. During both types of studies, VNS-induced CBF increases were similarly located in the bilateral thalami, hypothalami, inferior cerebellar hemispheres, and right postcentral gyrus. During immediate-effect studies, VNS decreased bilateral hippocampal, amygdalar, and cingulate CBF and increased bilateral insular CBF; no significant CBF changes were observed in these regions during prolonged studies. Mean seizure frequency decreased by 25% over a 3-month period between immediate and prolonged PET studies, compared with 3 months before VNS began. Conclusions: Seizure control improved during a period over which some immediate VNS-induced CBF changes declined (mainly over cortical regions), whereas other VNS-induced CBF changes persisted (mainly over subcortical regions). Altered synaptic activities at sites of persisting VNS-induced CBF changes may reflect antiseizure actions. [source] The correlation between cerebral glucose metabolism and benzodiazepine receptor density in the acute vegetative stateEUROPEAN JOURNAL OF NEUROLOGY, Issue 6 2002J. Rudolf This paper compares the results of parallel positron emission tomography (PET) studies of regional cerebral glucose metabolism with the radiotracer 18F-fluorodeoxyglucose (FDG) and benzodiazepine receptor (BZR) density by PET using the BZR ligand 11C-flumazenil (FMZ), a tracer of neuronal integrity, in nine patients with acute vegetative state (AVS, duration <1 month). Overall glucose utilization was significantly reduced in AVS in comparison with age-matched controls (global metabolic rate for glucose 26 ,mol/100 g/min in AVS vs. 31 ,mol/100 g/min in controls). FMZ-PET demonstrated a considerable reduction of BZR binding sites in all cortical regions that grossly corresponded to the extent of reduction of cerebral glucose metabolism assessed with FDG-PET, whilst the cerebellum was spared from neuronal loss. In controls, cortical relative flumazenil binding was not lower than five times the average white matter activity, whilst in AVS, nearly all values were below this threshold. There was no relevant overlap of the data of relative flumazenil binding between both groups. The comparison of FDG- and FMZ-PET findings in AVS demonstrates that alterations of cerebral glucose consumption do not represent mere functional inactivation, but irreversible structural brain damage. [source] Cortical efferents of the perirhinal, postrhinal, and entorhinal cortices of the ratHIPPOCAMPUS, Issue 12 2009Kara L. Agster Abstract We investigated the cortical efferents of the parahippocampal region by placing injections of the anterograde tracers, Phaseolus vulgaris -leuccoagglutinin, and biotinylated dextran amine, throughout the perirhinal (PER), postrhinal (POR), and entorhinal cortices of the rat brain. The resulting density of labeled fibers was evaluated in 25 subregions of the piriform, frontal, insular, temporal, cingulate, parietal, and occipital areas. The locations of labeled terminal fibers differed substantially depending on whether the location of the injection site was in PER area 35, PER area 36, POR, or the lateral or the medial entorhinal (LEA and MEA). The differences were greater for sensory regions. For example, the POR efferents preferentially target visual and spatial regions, whereas the PER efferents target all sensory modalities. The cortical efferents of each region largely reciprocate the cortical afferents, though the degree of reciprocity varied across originating and target regions. The laminar pattern of terminal fibers was consistent with the notion that the efferents are feedback projections. The density and amount of labeled fibers also differed substantially depending on the regional location of injection sites. PER area 36 and POR give rise to a greater number of heavy projections, followed by PER area 35. LEA also gives rise to widespread cortical efferents, arising mainly from a narrow band of cortex adjacent to the PER. In contrast, the remainder of the LEA and the MEA provides only weak efferents to cortical regions. Prior work has shown that nonspatial and spatial information is transmitted to the hippocampus via the PER-LEA and POR-MEA pathways, respectively. Our findings suggest that the return projections follow the same pathways, though perhaps with less segregration. © 2009 Wiley-Liss, Inc. [source] Functional connectivity with the hippocampus during successful memory formationHIPPOCAMPUS, Issue 8 2005Charan Ranganath Abstract Although it is well established that the hippocampus is critical for episodic memory, little is known about how the hippocampus interacts with cortical regions during successful memory formation. Here, we used event-related functional magnetic resonance imaging (fMRI) to identify areas that exhibited differential functional connectivity with the hippocampus during processing of novel objects that were subsequently remembered or forgotten on a postscan test. Functional connectivity with the hippocampus was enhanced during successful, as compared with unsuccessful, memory formation, in a distributed network of limbic cortical areas,including perirhinal, orbitofrontal, and retrosplenial/posterior cingulate cortex,that are anatomically connected with the hippocampal formation. Increased connectivity was also observed in lateral temporal, medial parietal, and medial occipital cortex. These findings demonstrate that successful memory formation is associated with transient increases in cortico-hippocampal interaction. © 2005 Wiley-Liss, Inc. [source] Comparing MEG and fMRI views to naming actions and objectsHUMAN BRAIN MAPPING, Issue 6 2009Mia Liljeström Abstract Most neuroimaging studies are performed using one imaging method only, either functional magnetic resonance imaging (fMRI), electroencephalography (EEG), or magnetoencephalography (MEG). Information on both location and timing has been sought by recording fMRI and EEG, simultaneously, or MEG and fMRI in separate sessions. Such approaches assume similar active areas whether detected via hemodynamic or electrophysiological signatures. Direct comparisons, after independent analysis of data from each imaging modality, have been conducted primarily on low-level sensory processing. Here, we report MEG (timing and location) and fMRI (location) results in 11 subjects when they named pictures that depicted an action or an object. The experimental design was exactly the same for the two imaging modalities. The MEG data were analyzed with two standard approaches: a set of equivalent current dipoles and a distributed minimum norm estimate. The fMRI blood-oxygen-level dependent (BOLD) data were subjected to the usual random-effect contrast analysis. At the group level, MEG and fMRI data showed fairly good convergence, with both overall activation patterns and task effects localizing to comparable cortical regions. There were some systematic discrepancies, however, and the correspondence was less compelling in the individual subjects. The present analysis should be helpful in reconciling results of fMRI and MEG studies on high-level cognitive functions. Hum Brain Mapp, 2009. © 2009 Wiley-Liss, Inc. [source] Differential parametric modulation of self-relatedness and emotions in different brain regionsHUMAN BRAIN MAPPING, Issue 2 2009Georg Northoff Abstract Our sense of self is strongly colored by emotions although at the same time we are well able to distinguish affect and self. Using functional magnetic resonance imaging, we here tested for the differential effects of self-relatedness and emotion dimensions (valence, intensity) on parametric modulation of neural activity during perception of emotional stimuli. We observed opposite parametric modulation of self-relatedness and emotion dimensions in the dorsomedial prefrontal cortex and the ventral striatum/nucleus accumbens, whereas neural activity in subcortical regions (tectum, right amygdala, hypothalamus) was modulated by self-relatedness and emotion dimensions in the same direction. In sum, our results demonstrate that self-relatedness is closely linked to emotion dimensions of valence and intensity in many lower subcortical brain regions involved in basic emotional systems and, at the same time, distinct from them in higher cortical regions that mediate cognitive processes necessary for becoming aware of one's self, for example self-consciousness. Hum Brain Mapp, 2009. © 2007 Wiley-Liss, Inc. [source] Aging and the interaction of sensory cortical function and structureHUMAN BRAIN MAPPING, Issue 1 2009Ann M. Peiffer Abstract Even the healthiest older adults experience changes in cognitive and sensory function. Studies show that older adults have reduced neural responses to sensory information. However, it is well known that sensory systems do not act in isolation but function cooperatively to either enhance or suppress neural responses to individual environmental stimuli. Very little research has been dedicated to understanding how aging affects the interactions between sensory systems, especially cross-modal deactivations or the ability of one sensory system (e.g., audition) to suppress the neural responses in another sensory system cortex (e.g., vision). Such cross-modal interactions have been implicated in attentional shifts between sensory modalities and could account for increased distractibility in older adults. To assess age-related changes in cross-modal deactivations, functional MRI studies were performed in 61 adults between 18 and 80 years old during simple auditory and visual discrimination tasks. Results within visual cortex confirmed previous findings of decreased responses to visual stimuli for older adults. Age-related changes in the visual cortical response to auditory stimuli were, however, much more complex and suggested an alteration with age in the functional interactions between the senses. Ventral visual cortical regions exhibited cross-modal deactivations in younger but not older adults, whereas more dorsal aspects of visual cortex were suppressed in older but not younger adults. These differences in deactivation also remained after adjusting for age-related reductions in brain volume of sensory cortex. Thus, functional differences in cortical activity between older and younger adults cannot solely be accounted for by differences in gray matter volume. Hum Brain Mapp 2009. © 2007 Wiley-Liss, Inc. [source] Selective visuo-haptic processing of shape and textureHUMAN BRAIN MAPPING, Issue 10 2008Randall Stilla Abstract Previous functional neuroimaging studies have described shape-selectivity for haptic stimuli in many cerebral cortical regions, of which some are also visually shape-selective. However, the literature is equivocal on the existence of haptic or visuo-haptic texture-selectivity. We report here on a human functional magnetic resonance imaging (fMRI) study in which shape and texture perception were contrasted using haptic stimuli presented to the right hand, and visual stimuli presented centrally. Bilateral selectivity for shape, with overlap between modalities, was found in a dorsal set of parietal areas: the postcentral sulcus and anterior, posterior and ventral parts of the intraparietal sulcus (IPS); as well as ventrally in the lateral occipital complex. The magnitude of visually- and haptically-evoked activity was significantly correlated across subjects in the left posterior IPS and right lateral occipital complex, suggesting that these areas specifically house representations of object shape. Haptic shape-selectivity was also found in the left postcentral gyrus, the left lingual gyrus, and a number of frontal cortical sites. Haptic texture-selectivity was found in ventral somatosensory areas: the parietal operculum and posterior insula bilaterally, as well as in the right medial occipital cortex, overlapping with a medial occipital cortical region, which was texture-selective for visual stimuli. The present report corroborates and elaborates previous suggestions of specialized visuo-haptic processing of texture and shape. Hum Brain Mapp 2008. © 2007 Wiley-Liss, Inc. [source] Voxel-based analysis of MRI detects abnormal visual cortex in children and adults with amblyopiaHUMAN BRAIN MAPPING, Issue 2 2005Janine D. Mendola Abstract Amblyopia, sometimes called "lazy eye," is a relatively common developmental visual disorder well characterized behaviorally; however, the neural substrates associated with amblyopia in humans remain unclear. We hypothesized that abnormalities in the cerebral cortex of subjects with amblyopia exist, possibly as a result of experience-dependent neuronal plasticity. Anatomic magnetic resonance imaging (MRI) and psychophysical vision testing was carried out on 74 subjects divided into two age ranges, 7,12 years and 18,35 years, and three diagnoses, strabismic amblyopia, anisometropic amblyopia, and normal vision. We report a behavioral impairment in contrast sensitivity for subjects with amblyopia, consistent with previous reports. When the high-resolution MRI brain images were analyzed quantitatively with optimized voxel-based morphometry, results indicated that adults and children with amblyopia have decreased gray matter volume in visual cortical regions, including the calcarine sulcus, known to contain primary visual cortex. This finding was confirmed with a separate region-of-interest analysis. For the children with amblyopia, additional gray matter reductions in parietal-occipital areas and ventral temporal cortex were detected, consistent with recent reports that amblyopia can result in spatial location and object processing deficits. These data are the first to provide possible neuroanatomic bases for the loss of binocularity and visual sensitivity in children and adults with amblyopia. Hum Brain Mapp 25:222,236, 2005. © 2005 Wiley-Liss, Inc. [source] Isotropic resolution diffusion tensor imaging with whole brain acquisition in a clinically acceptable timeHUMAN BRAIN MAPPING, Issue 4 2002Derek Kenton Jones Abstract Our objective was to develop a diffusion tensor MR imaging pulse sequence that allows whole brain coverage with isotropic resolution within a clinically acceptable time. A single-shot, cardiac-gated MR pulse sequence, optimized for measuring the diffusion tensor in human brain, was developed to provide whole-brain coverage with isotropic (2.5 × 2.5 × 2.5 mm) spatial resolution, within a total imaging time of approximately 15 min. The diffusion tensor was computed for each voxel in the whole volume and the data processed for visualization in three orthogonal planes. Anisotropy data were further visualized using a maximum-intensity projection algorithm. Finally, reconstruction of fiber-tract trajectories i.e., ,tractography' was performed. Images obtained with this pulse sequence provide clear delineation of individual white matter tracts, from the most superior cortical regions down to the cerebellum and brain stem. Because the data are acquired with isotropic resolution, they can be reformatted in any plane and the sequence can therefore be used, in general, for macroscopic neurological or psychiatric neuroimaging investigations. The 3D visualization afforded by maximum intensity projection imaging and tractography provided easy visualization of individual white matter fasciculi, which may be important sites of neuropathological degeneration or abnormal brain development. This study has shown that it is possible to obtain robust, high quality diffusion tensor MR data at 1.5 Tesla with isotropic resolution (2.5 × 2.5 × 2.5 mm) from the whole brain within a sufficiently short imaging time that it may be incorporated into clinical imaging protocols. Hum. Brain Mapping 15:216,230, 2002. © 2002 Wiley-Liss, Inc. [source] The functional neuroanatomy of geriatric depressionINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 8 2009Gwenn S. Smith Abstract Objective Positron Emission Tomography (PET) studies of cerebral glucose metabolism have demonstrated sensitivity in evaluating the functional neuroanatomy of treatment response variability in depression, as well as in the early detection of functional changes associated with incipient cognitive decline. The evaluation of cerebral glucose metabolism in late life depression may have implications for understanding treatment response variability, as well as evaluating the neurobiological basis of depression in late life as a risk factor for dementia. Methods Sixteen patients with geriatric depression and 13 comparison subjects underwent resting PET studies of cerebral glucose metabolism, as well as magnetic resonance (MR) imaging scans to evaluate brain structure. Results Cerebral glucose metabolism was elevated in geriatric depressed patients relative to comparison subjects in anterior (right and left superior frontal gyrus) and posterior (precuneus, inferior parietal lobule) cortical regions. Cerebral atrophy (increased cerebrospinal fluid [CSF] and decreased grey and white matter volumes) were observed in some of these regions, as well. Regional cerebral metabolism was positively correlated with severity of depression and anxiety symptoms. Conclusions In contrast to decreased metabolism observed in normal aging and neurodegenerative conditions such as Alzheimer's disease, cortical glucose metabolism was increased in geriatric depressed patients relative to demographically matched controls, particularly in brain regions in which cerebral atrophy was observed, which may represent a compensatory response. Copyright © 2009 John Wiley & Sons, Ltd. [source] Predictive value of renal histological changes for postoperative renal function improvement in children with congenital ureteropelvic junction stenosisINTERNATIONAL JOURNAL OF UROLOGY, Issue 6 2002Ahmet Erbagci Abstract Background: The aim of this study was to evaluate the relationship between renal function, as measured by diuretic radionuclide renography, and the outcome of pyeloplasty. A study was designed to evaluate renal parenchymal biopsy specimens derived from children undergoing corrective surgery for ureteropelvic junction (UPJ) stenosis, and compare these to preoperative and postoperative renal function status. Methods: Thirty-five children with congenital unilateral UPJ stenosis were evaluated. In addition to all conventional diagnostic procedures for UPJ stenosis, differential renal functional (DRF) activity was assessed in each of these children by obtaining 99mTc diethylenetriaminepentaacetic acid renogram curves. All children underwent dismembered pyeloplasty, and follow-up renogram evaluation was conducted 6 and 12 months after surgical repair. Biopsy specimens from renal cortical regions obtained during the surgical correction of UPJ stenosis were evaluated, and changes in renal histology were graded from I to V according to their severity. Spearman's correlation test was used to compare the histological evaluation results and the basal, 6- and 12-month follow-up DRF findings. A Wilcoxon paired test was used to evaluate statistical differences between values. Results: The findings showed a positive correlation between the severity of histological changes and DRF activity. All kidneys (22) with a DRF activity value of < 40% preoperatively demonstrated at least grade III changes when biopsy specimens were examined. Of children with a DRF activity value > 40% (13), only three showed severe histological changes. Histological grades were correlated between basal (r = ,0.4; P = 0.019), 6-month (r = 0.54; P = 0.002) and 12-month (r = 0.54; P = 0.02) findings. In the Wilcoxon paired test, there was a statistically significant difference between basal and 6-month values (P < 0.05), and also between basal and 12-month values (P < 0.01). There was no statistically significant difference between 6- and 12-month values (P > 0.20). Conclusion: Comparative evaluation of postoperative renal function with DRF activity and renal parenchymal histological alterations revealed a close correlation in terms of renal function improvement potential following reconstructive surgery in children with UPJ stenosis. [source] Porosity of human mandibular condylar boneJOURNAL OF ANATOMY, Issue 3 2007G. A. P. Renders Abstract Quantification of porosity and degree of mineralization of bone facilitates a better understanding of the possible effects of adaptive bone remodelling and the possible consequences for its mechanical properties. The present study set out first to give a three-dimensional description of the cortical canalicular network in the human mandibular condyle, in order to obtain more information about the principal directions of stresses and strains during loading. Our second aim was to determine whether the amount of remodelling was larger in the trabecular bone than in cortical bone of the condyle and to establish whether the variation in the amount of remodelling was related to the surface area of the cortical canals and trabeculae. We hypothesized that there were differences in porosity and orientation of cortical canals between various cortical regions. In addition, as greater cortical and trabecular porosities are likely to coincide with a greater surface area of cortical canals and trabeculae available for osteoblastic and osteoclastic activity, we hypothesized that this surface area would be inversely proportional to the degree of mineralization of cortical and trabecular bone, respectively. Micro-computed tomography was used to quantify porosity and mineralization in cortical and trabecular bone of ten human mandibular condyles. The cortical canals in the subchondral cortex of the condyle were orientated in the mediolateral direction, and in the anterior and posterior cortex in the superoinferior direction. Cortical porosity (average 3.5%) did not differ significantly between the cortical regions. It correlated significantly with the diameter and number of cortical canals, but not with cortical degree of mineralization. In trabecular bone (average porosity 79.3%) there was a significant negative correlation between surface area of the trabeculae and degree of mineralization; such a correlation was not found between the surface area of the cortical canals and the degree of mineralization of cortical bone. No relationship between trabecular and cortical porosity, nor between trabecular degree of mineralization and cortical degree of mineralization was found, suggesting that adaptive remodelling is independent and different between trabecular and cortical bone. We conclude (1) that the principal directions of stresses and strains are presumably directed mediolaterally in the subchondral cortex and superoinferiorly in the anterior and posterior cortex, (2) that the amount of remodelling is larger in the trabecular than in the cortical bone of the mandibular condyle; in trabecular bone variation in the amount of remodelling is related to the available surface area of the trabeculae. [source] Genetically Based Influences on the Site-Specific Regulation of Trabecular and Cortical Bone Morphology,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 4 2004Stefan Judex Abstract The degree of site-specificity by which genes influence bone quantity and architecture was investigated in the femur of three strains of mice. Morphological indices were highly dependent on both genetic makeup as well as anatomical location showing that the assessment of bone structure from a single site cannot be extrapolated to other sites even within a single bone. Introduction: The identification of genes responsible for establishing peak BMD will yield critical information on the regulation of bone quantity and quality. Whereas such knowledge may eventually uncover novel molecular drug targets or enable the identification of individuals at risk of osteoporosis, the site-specificity by which putative genotypes cause low or high bone mass (and effective bone morphology) is essentially unknown. Materials and Methods: ,CT was used to determine morphological and microarchitectural features of the femora harvested from three genetically distinct strains of 4-month-old female mice, each with distinct skeletal mass (low: C57BL/6J [B6], medium: BALB/cByJ [BALB], high: C3H/HeJ [C3H]). Two trabecular regions (distal epiphysis and metaphysis) were considered in addition to four cortical regions within the metaphysis and diaphysis. Results and Conclusions: Comparing morphological properties of the different trabecular and cortical femoral regions between the three strains of mice, it was apparent that high or low values of specific parameters of bone morphology could not be consistently attributed to the same genetic strain. Trabecular metaphyseal bone volume, for instance, was 385% larger in C3H mice than in B6 mice, yet the two strains displayed similar bone volume fractions in the epiphysis. Similarly, BALB mice had 48% more trabecular bone than C3H mice in the epiphysis, but there were no strain-specific differences in cortical bone area at the diaphysis. These data suggest that the genetic control of bone mass and morphology, even within a given bone, is highly site-specific and that a comprehensive search for genes that are indicative of bone quantity and quality may also have to occur on a very site-specific basis. [source] Activation of MKK6, an upstream activator of p38, in Alzheimer's diseaseJOURNAL OF NEUROCHEMISTRY, Issue 2 2001Xiongwei Zhu Mitogen-activated protein kinase (MAPK) p38 has been implicated in the pathogenesis of Alzheimer's disease, but the upstream cascade leading to p38 activation has not been elucidated in the disease. In the present study, we focused on mitogen-activated protein kinase kinase 6 (MKK6), one of the upstream activators of p38 MAPK. We found that MKK6 was not only increased but also specifically associated with granular structures in the susceptible neurons in the hippocampus and cortex of Alzheimer's disease patients, but was only weakly diffuse in the cytoplasm in neurons in control cases. Immunoblot analysis demonstrated a significant increase of MKK6 level in Alzheimer's disease compared with age-matched controls. In this regard, in hippocampal and cortical regions of individuals with Alzheimer's disease, the activated phospho-MKK6 was localized exclusively in association with pathological alterations including neurofibrillary tangles, senile plaques, neuropil threads and granular structures, overlapping with activated p38 MAPK suggesting both a functional and mechanic link. By immunoblot analysis, phospho-MKK6 is also significantly increased in AD compared with control cases. Together, these findings lend further credence to the notion that the p38 MAPK pathway is dysregulated in Alzheimer's disease and also indicates an active role for this pathway in disease pathogenesis. [source] Voxel-Based Morphometry and Voxel-Based Relaxometry in Parkinsonian Variant of Multiple System AtrophyJOURNAL OF NEUROIMAGING, Issue 3 2010Loukia C. Tzarouchi MD ABSTRACT BACKGROUND AND PURPOSE Multiple system atrophy (MSA) is a progressive neurodegenerative disorder divided into a parkinsonian (MSA-P) and a cerebellar variant. The purpose of this study was to assess regional brain atrophy and iron content using Voxel-based morphometry (VBM) and Voxel-based relaxometry (VBR) respectively, in MSA-P. METHODS Using biological parametric mapping the effect of brain atrophy was evaluated in T2 relaxation time (T2) measurements by applying analysis of covariance (ANCOVA) and correlation analysis to the VBM and VBR data. Eleven patients with MSA-P (aged 61.9 ± 11.7 years, disease duration 5.42 ± 2.5 years) and 11 controls were studied. RESULTS In comparison to the controls the patients showed decreased gray matter in the putamen, the caudate nuclei, the thalami, the anterior cerebellar lobes, and the cerebral cortex, and white matter atrophy in the pons, midbrain, and peduncles. VBR analysis showed prolonged T2 in various cortical regions. On ANCOVA, when controlling for gray and white matter volume, these regions of prolonged T2 were shrunk. Negative correlation was demonstrated between T2 and gray and white matter volume. CONCLUSIONS Diffuse brain atrophy, mainly in the motor circuitry is observed in MSA-P. Normalization for atrophy should always be performed in T2 measurements. [source] Whole-brain functional magnetic resonance imaging mapping of acute nociceptive responses induced by formalin in rats using atlas registration-based event-related analysisJOURNAL OF NEUROSCIENCE RESEARCH, Issue 8 2008Yen-Yu I. Shih Abstract Nociceptive neuronal activation in subcortical regions has not been well investigated in functional magnetic resonance imaging (fMRI) studies. The present report aimed to use the blood oxygenation level-dependent (BOLD) fMRI technique to map nociceptive responses in both subcortical and cortical regions by employing a refined data processing method, the atlas registration-based event-related (ARBER) analysis technique. During fMRI acquisition, 5% formalin (50 ,l) was injected into the left hindpaw to induce nociception. ARBER was then used to normalize the data among rats, and images were analyzed using automatic selection of the atlas-based region of interest. It was found that formalin-induced nociceptive processing increased BOLD signals in both cortical and subcortical regions. The cortical activation was distributed over the cingulate, motor, somatosensory, insular, and visual cortices, and the subcortical activation involved the caudate putamen, hippocampus, periaqueductal gray, superior colliculus, thalamus, and hypothalamus. With the aid of ARBER, the present study revealed a detailed activation pattern that possibly indicated the recruitment of various parts of the nociceptive system. The results also demonstrated the utilization of ARBER in establishing an fMRI-based whole-brain nociceptive map. The formalin induced nociceptive images may serve as a template of central nociceptive responses, which can facilitate the future use of fMRI in evaluation of new drugs and preclinical therapies for pain. © 2008 Wiley-Liss, Inc. [source] Prenatal Alcohol Exposure Affects Frontal,Striatal BOLD Response During Inhibitory ControlALCOHOLISM, Issue 8 2007Susanna L. Fryer Background: Prenatal alcohol exposure can lead to widespread cognitive impairment and behavioral dysregulation, including deficits in attention and response inhibition. This study characterized the neural substrates underlying the disinhibited behavioral profile of individuals with fetal alcohol spectrum disorders (FASD). Methods: Children and adolescents (ages 8,18) with (n=13) and without (n=9) histories of heavy prenatal alcohol exposure underwent functional magnetic resonance imaging while performing a response inhibition (go/no-go) task. Results: Despite similar task performance (mean response latency, performance accuracy, and signal detection), blood oxygen level-dependent (BOLD) response patterns differed by group. Region-of-interest analyses revealed that during portions of the behavioral task that required response inhibition, alcohol-exposed participants showed greater BOLD response across prefrontal cortical regions (including the left medial and right middle frontal gyri), while they showed less right caudate nucleus activation, compared with control participants. Conclusions: These data provide an account of response inhibition-related brain functioning in youth with FASD. Furthermore, results suggest that the frontal,striatal circuitry thought to mediate inhibitory control is sensitive to alcohol teratogenesis. [source] Cortical locations of maximal spindle activity: magnetoencephalography (MEG) studyJOURNAL OF SLEEP RESEARCH, Issue 2 2009VALENTINA GUMENYUK Summary The aim of this study was to determine the main cortical regions related to maximal spindle activity of sleep stage 2 in healthy individual subjects during a brief morning nap using magnetoencephalography (MEG). Eight volunteers (mean age: 26.1 ± 8.7, six women) all right handed, free of any medical psychiatric or sleep disorders were studied. Whole-head 148-channel MEG and a conventional polysomnography montage (EEG; C3, C4, O1 and O2 scalp electrodes and EOG, EMG and ECG electrodes) were used for data collection. Sleep MEG/EEG spindles were visually identified during 15 min of stage 2 sleep for each participant. The distribution of brain activity corresponding to each spindle was calculated using a combination of independent component analysis and a current source density technique superimposed upon individual MRIs. The absolute maximum of spindle activation was localized to frontal, temporal and parietal lobes. However, the most common cortical regions for maximal source spindle activity were precentral and/or postcentral areas across all individuals. The present study suggests that maximal spindle activity localized to these two regions may represent a single event for two types of spindle frequency: slow (at 12 Hz) and fast (at 14 Hz) within global thalamocortical coherence. [source] Neuroimaging of Language: Why Hasn't a Clearer Picture Emerged?LINGUISTICS & LANGUAGE COMPASS (ELECTRONIC), Issue 4 2009Evelina Fedorenko Two broad questions have driven dozens of studies on the neural basis of language published in the last several decades: (i) Are distinct cortical regions engaged in different aspects of language? (ii) Are regions engaged in language processing specific to the domain of language? Neuroimaging has not yet provided clear answers to either question. In this paper, we discuss one factor that is a likely contributor to the unclear state of affairs in the neurocognition of language, and that, in our opinion, has not received sufficient attention in the recent literature. In particular, fMRI studies of language have relied, almost exclusively, on group analyses, in which data from multiple individuals are co-registered to and analyzed in a common space. We argue that this approach can obscure functional specificity because of the anatomical variability across individual brains, and we advocate the use of an alternative approach , the functional localization approach , that circumvents this problem. [source] Neuroanatomical substrate of visuospatial and visuoperceptual impairment in Parkinson's disease,MOVEMENT DISORDERS, Issue 8 2009Joana B. Pereira MSc Abstract To determine magnetic resonance imaging patterns of gray matter (GM) atrophy underlying visuospatial and visuoperceptual impairment in Parkinson's disease (PD), we applied voxel-based morphometry to 36 nondemented PD patients and correlated their whole brain GM density with performance on three visuospatial and visuoperceptual tests. In addition, group comparisons between patients and 20 healthy controls were also performed. Correlations between visuospatial performance and GM density were found in the superior parietal lobules and the superior occipital gyrus of PD patients. Poor performance on visuoperceptual tests was also found to be significantly associated with GM decreases in the fusiform, the parahippocampus, and the middle occipital gyrus. Finally, group comparisons between controls and patients showed widespread GM cortical reductions in PD, involving posterior temporal and parietal regions. Taken together, these findings suggest that visuospatial and visuoperceptual dysfunctions reflect structural GM changes in temporo-parietal cortical regions of PD patients. © 2009 Movement Disorder Society [source] Excessive dopamine neuron loss in progressive supranuclear palsyMOVEMENT DISORDERS, Issue 4 2008Karen E. Murphy BSc(Hons) Abstract Progressive supranuclear palsy (PSP) and Parkinson's disease (PD) differ in their response to dopaminergic replacement therapies, despite having a similar degree of neuronal degeneration in the dopaminergic substantia nigra. We observed more widespread dopamine neuron loss in the extranigral A10 midbrain cell groups in PSP compared with PD. These cell groups innervate subcortical and cortical regions and may be required for adequate response to levodopa therapy. © 2007 Movement Disorder Society [source] Unresolved issues relating to the Shaking Palsy on the celebration of James Parkinson's 250th birthdayMOVEMENT DISORDERS, Issue S17 2007Andrew J. Lees MD Abstract James Parkinson's Essay on the Shaking Palsy published in 1817 provided the first clear clinical description for the disorder now known throughout the world by his name. His primary reason for publishing his monograph shortly before his retirement from medical practice was to draw the medical profession's attention to a malady, which had not yet been defined as a nosological entity. He also hoped that the eminent anatomists of the day would be stimulated to elucidate the pathological lesion responsible for the clinical picture and that this in turn might lead to a rational cure. The concept of Parkinson's disease remains clinically based and successive generations of neurologists have refined and embellished Parkinson's seminal descriptions. Narrative accounts by affected individuals have also helped physicians understand what it is like to live with Parkinson's disease. For many years, the pathological hallmarks of Parkinson's disease were disputed and there were few clinico-pathological reports with adequate clinical description. However, most neurologists now link severe loss of nigral cells in the ventrolateral tier of the pars compacta of the substantia nigra with bradykinesia and the presence of Lewy bodies in a number of discrete brain stem and cortical regions with Parkinson's disease. There are many unanswered clinical questions relating to Parkinson's disease including the striking heterogeneity and frequent limb asymmetry. It also remains somewhat uncertain whether Parkinson's disease is ever truly unilateral by the time of clinical presentation and whether the hand rather than the foot is the most common site of onset. Hyposmia and visual hallucinations are helpful pointers in distinguishing Parkinson's disease from atypical Parkinsonism and should be specifically enquired about in the history. Simple reliable cultural-specific smell identification batteries are an urgent need and target of clinical research. It remains to be determined whether Alzheimer type dementia as opposed to a dysexecutive syndrome should be considered a part of Parkinson's disease and further detailed clinico-pathological correlative studies are needed. It is also unclear whether autosomal dominant monogenetic Parkinsonism due to synuclein or LRRK-2 mutations will prove to be identical clinically with Parkinson's disease and for the present it is wiser to regard Parkinson's disease as a sporadic disorder. Parkinson was an active political reformer and if alive today would certainly be campaigning to translate more effectively the rich seam of neuroscientific research of the last decade into therapeutic benefits for the rising number of people who are developing the shaking palsy as a result of increasing longevity in the developed world. © 2007 Movement Disorder Society [source] Increased tau burden in the cortices of progressive supranuclear palsy presenting with corticobasal syndromeMOVEMENT DISORDERS, Issue 8 2005Yoshio Tsuboi MD Abstract The objective of this study is to better define the pathological characteristics of pathologically proven progressive supranuclear palsy (PSP) presenting with the corticobasal syndrome (CBS). PSP is characterized by early falls, vertical supranuclear ophthalmoplegia, and axial rigidity, whereas asymmetric limb features, including rigidity, bradykinesia, apraxia, alien limb phenomena, and cortical sensory loss are characteristic of CBS. We investigated clinicopathological characteristics of 5 cases of PSP that presented with CBS (CBS-PSP). Comprehensive pathological analysis was undertaken to determine the presence of concomitant pathological processes as well as quantitative tau burden in cortical regions of CBS-PSP, compared with 8 typical PSP cases (Typ-PSP). The clinical features in the CBS-PSP cases included asymmetrical features, apraxia, alien limb phenomena, and progressive aphasia. All cases had Parkinsonism, and vertical supranuclear ophthalmoplegia was noted in all but 1 case of CBS-PSP. Secondary neuropathological diagnoses included argyrophilic grain disease (AGD) in 1 of the 8 cases of Typ-PSP, whereas Alzheimer's disease (AD), Lewy body disease, AGD, and vascular disease was found in 3 cases of CBS-PSP. Image analysis of cortical tau burden performed in 8 Typ-PSP and 3 CBS-PSP cases revealed a significant increased tau burden in mid-frontal and inferior-parietal cortices in the CBS-PSP cases. This study demonstrates that when PSP presents as CBS, it is most likely due to either a concurrent cortical pathology from a secondary process such as AD or from the primary pathology of PSP extending into cortical areas that are primarily and commonly affected in CBD. © 2005 Movement Disorder Society [source] On the nature and evolution of the neural bases of human languageAMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY, Issue S35 2002Philip Lieberman Abstract The traditional theory equating the brain bases of language with Broca's and Wernicke's neocortical areas is wrong. Neural circuits linking activity in anatomically segregated populations of neurons in subcortical structures and the neocortex throughout the human brain regulate complex behaviors such as walking, talking, and comprehending the meaning of sentences. When we hear or read a word, neural structures involved in the perception or real-world associations of the word are activated as well as posterior cortical regions adjacent to Wernicke's area. Many areas of the neocortex and subcortical structures support the cortical-striatal-cortical circuits that confer complex syntactic ability, speech production, and a large vocabulary. However, many of these structures also form part of the neural circuits regulating other aspects of behavior. For example, the basal ganglia, which regulate motor control, are also crucial elements in the circuits that confer human linguistic ability andreasoning. The cerebellum, traditionally associated with motor control, is active in motor learning. The basal ganglia are also key elements in reward-based learning. Data from studies of Broca's aphasia, Parkinson's disease, hypoxia, focal brain damage, and a genetically transmitted brain anomaly (the putative "language gene," family KE), and from comparative studies of the brains and behavior of other species, demonstrate that the basal ganglia sequence the discrete elements that constitute a complete motor act, syntactic process, or thought process. Imaging studies of intact human subjects and electrophysiologic and tracer studies of the brains and behavior of other species confirm these findings. As Dobzansky put it, "Nothing in biology makes sense except in the light of evolution" (cited in Mayr, 1982). That applies with as much force to the human brain and the neural bases of language as it does to the human foot or jaw. The converse follows: the mark of evolution on the brains of human beings and other species provides insight into the evolution of the brain bases of human language. The neural substrate that regulated motor control in the common ancestor of apes and humans most likely was modified to enhance cognitive and linguistic ability. Speech communication played a central role in this process. However, the process that ultimately resulted in the human brain may have started when our earliest hominid ancestors began to walk. Yrbk Phys Anthropol 45:36,62, 2002. © 2002 Wiley-Liss, Inc. [source] Brain,computer interfacing based on cognitive controlANNALS OF NEUROLOGY, Issue 6 2010Mariska J. Vansteensel PhD Objective Brain,computer interfaces (BCIs) translate deliberate intentions and associated changes in brain activity into action, thereby offering patients with severe paralysis an alternative means of communication with and control over their environment. Such systems are not available yet, partly due to the high performance standard that is required. A major challenge in the development of implantable BCIs is to identify cortical regions and related functions that an individual can reliably and consciously manipulate. Research predominantly focuses on the sensorimotor cortex, which can be activated by imagining motor actions. However, because this region may not provide an optimal solution to all patients, other neuronal networks need to be examined. Therefore, we investigated whether the cognitive control network can be used for BCI purposes. We also determined the feasibility of using functional magnetic resonance imaging (fMRI) for noninvasive localization of the cognitive control network. Methods Three patients with intractable epilepsy, who were temporarily implanted with subdural grid electrodes for diagnostic purposes, attempted to gain BCI control using the electrocorticographic (ECoG) signal of the left dorsolateral prefrontal cortex (DLPFC). Results All subjects quickly gained accurate BCI control by modulation of gamma-power of the left DLPFC. Prelocalization of the relevant region was performed with fMRI and was confirmed using the ECoG signals obtained during mental calculation localizer tasks. Interpretation The results indicate that the cognitive control network is a suitable source of signals for BCI applications. They also demonstrate the feasibility of translating understanding about cognitive networks derived from functional neuroimaging into clinical applications. ANN NEUROL 2010 [source] | ||||||||||||||||