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1
Thomas, Taya Louise. "Hypoperfusion of cerebral grey matter in dementia." Thesis, University of Bristol, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.702468.
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Reduced cerebral blood flow (CBF) has been reported in patients with Alzheimer's disease (AD), with increasing evidence to suggest that the hypoperfusion contributes to decline in cognitive function and possibly to progression of the neurodegeneration. Key proteins that are upregulated under conditions of cerebral hypoxia are the hypoxia inducible factor-ia (HIFia) and neuroglobin (NGB) which both induce the transcription of mUltiple genes, including some involved in the production of amyloid-β (Aβ) and the angiogenic growth factor, vascular endothelia growth factor (VEGF). This thesis describes a series of studies to investigate the molecular evidence of hypoxia in post-mortem brain tissue from patients with AD, vascular dementia (VaD), dementia with Lewy bodies (DLB; all cases with little or no cerebrovascular disease) and non-demented controls. qRT-PCR and ELISA were used to investigate the mRNA and protein expression of HIFla, NGB and VEGF. Hypoxia was also indirectly assessed by the measurement of myelinassociated glycoprotein (MAG), which is more sensitive to ischaemia than other myelin proteins, and comparing it to the relatively stable proteolipid protein-1 (PLP). The relationship to the severity of the two main structural abnormalities of the microvasculature, arteriolosclerotic small vessel disease (SVD) and cerebral amyloid angiopathy (CAA), both of which can cause cerebral ischaemia and cognitive impairment; the levels of total Aβ, Aβ1-40 and Aβ1.42 and severity of AD pathology as determined by Braak tangle stage; and the level and activity of angiotensin-converting enzyme (ACE), which catalyses the production of a powerful vasoconstrictor angiotensin II, and the level ofthe vasoconstrictor, endothelin-1 (ET-1) were also assessed. NGB protein level did not differ significantly in AD or VaD compared to controls but MAG protein level was reduced in both disease groups, consistent with what was previously demonstrated in the white matter, and was found to decrease with increasing severity of SVD. In contrast, VEGF protein was elevated in both disease groups but particularly AD; it correlated with the level of insoluble Aβ, Aβ1-42 and the Aβ1-42:Aβ1-40 ratio and to a lesser extent with the Braak tangle stage and ACE activity. There was no relationship between the level of ET-1 and VEGF. There was also only a weak relationship between VEGF or NGB and the severity of SVD or CAA. It seems likely that the increase in VEGF protein in AD is largely related to the accumulation of A~ rather than to SVD or to vasoconstriction mediated by ET-1 or angiotensin II. In DLB, NGB protein level was significantly increased in the cingulate cortex and MAG protein level reduced, although not significantly. There was no significant change in VEGF level. The mechanism of hypoperfusion seems likely to differ from that in AD. Together these findings suggest that the molecular assessment of hypoxia may provide a useful means to investigate different mechanisms of reduced CBF in various forms of dementia.
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Niepel, Graham. "Deep grey matter and fatigue in multiple sclerosis." Thesis, University of Nottingham, 2012. http://eprints.nottingham.ac.uk/14594/.
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Fatigue is a common and major symptom in multiple sclerosis (MS). A number of potential mechanisms exist as to the cause of MS-fatigue. These include that it is an immune-mediated symptom or that it is due to neuroendocrine or autonomic dysfunction. Studies have shown reduced activity in cortical and deep grey matter regions and disruption of cortico-subcortical circuits has been theorised. This may lead to difficulty in the planning or pre-movement stage of activity with compensatory overactivity contributing to fatigue. Finally, dysfunction of the hypocretin system, deficiency of which occurs in narcolepsy, has also been suggested. A number of deep grey matter structures, including the basal ganglia, thalamus and hypothalamus, are implicated in these mechanisms and the work presented in this thesis explores their role. Conventional magnetic resonance imaging (MRI) techniques whilst crucial in diagnosis and monitoring disease activity are generally felt to correlate poorly with disability and symptomatology. Quantitative MRI techniques have been shown to provide a more comprehensive evaluation of the extent of MS pathology and correlate better with clinical deficit. Tl relaxation time measurement is one such quantitative MRI technique and has been shown to demonstrate abnormalities in small structures such as the pyramidal tracts and correlate with disability. Firstly, we measured the T1 relaxation times of the thalamus and basal ganglia in a cohort of MS patients and assessed for any relationship with fatigue severity. Secondly, in view of its key role in the autonomic, neuroendocrine and hypocretin pathways, we performed the same measurement in the hypothalamus of a cohort of patients and again assessed for any relationship to fatigue. Subsequently, to further evaluate any possible contribution from the hypocretin system we measured cerebrospinal fluid (CSF) hypocretin-1 levels in patients with a number of neurological diseases including a cohort of MS patients and evaluated for any relationship with severity of self-reported fatigue and hypersomnolence. Studies in MS-fatigue, including those undertaken by our group, traditionally rely on self-reported measures of fatigue severity. These questionnaire-based measures are subject to a number of drawbacks including rater bias and lack of definition of fatigue. In the final study, we assessed the effectiveness of the wakefulness-promoting drug, modafinil, in MS patients with and without fatigue by assessing its effect on objective measures of alertness and vigilance, including neurophysiological and laboratory-based measures. In addition, in this study we evaluated any potential role of the autonomic system in MS-fatigue. We found significantly higher T1 relaxation times in a number of deep grey matter structures including the thalamus, putamen and latterly the hypothalamus in MS patients as compared to controls. The T1 relaxation time of the thalamus was higher in fatigued patients as compared to non-fatigued patients and it correlated with fatigue severity. We found lower CSF hypocretin-1 levels in patients with MS and inflammatory disorders as compared to non-inflammatory conditions and this was significant in the inflammatory cohort. However, we found no relationship with fatigue or hypersomnolence severity. We did, however, detect a significant difference on a sympathetic cardiovascular reflex test between fatigued and non-fatigued patients. Finally we noted a significant improvement with modafinil, as compared to placebo, in a number of objective measures of alertness in patients with MS-fatigue and notably this was not a class-effect. To this extent, the findings from this thesis provide evidence for the potential involvement of pathology in the thalamus in the mechanism of MS-fatigue, possibly through disruption of cortico-subcortical circuits. In addition, in a separate cohort of patients there was evidence of a relationship between autonomic disturbance and fatigue. We have however found no evidence of a relationship between the hypocretin system and fatigue in MS. Finally we have demonstrated supportive evidence for a role for modafinil in the treatment of fatigue, a symptom for which, despite its frequency and severity, there is often a paucity of treatment options available for MS specialists.
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Gilmore, Christopher Patrick. "Spinal cord grey matter pathology in multiple sclerosis." Thesis, University of Nottingham, 2008. http://eprints.nottingham.ac.uk/10496/.
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Background: Traditionally, Multiple Sclerosis (MS) has been considered to be a predominantly white matter (WM) disease. More recent studies have revealed considerable grey matter (GM) involvement in the brain. However there is a paucity of literature examining GM pathology in the spinal cord. Objectives and methods: We use human post-mortem material to explore various aspects of spinal cord GM pathology in MS including (i) the extent and pattern of spinal cord demyelination, (ii) the relative contributions of GM and WM volume loss to spinal cord atrophy, (iii) the extent of neuronal pathology within the spinal cord and (iv) the sensitivity of post-mortem MRI for detecting spinal cord GM plaques. Results: Within the spinal cord, GM demyelination is more extensive than WM demyelination with many lesions showing a novel morphological pattern whereby the plaque borders maintain a strict respect for the GM/WM boundary. Demyelination is more extensive in the spinal cord GM than in other brain regions examined. Post-mortem MR imaging at 4.7 Tesla is highly sensitive for detecting the spinal cord GM plaques. We demonstrate substantial neuronal loss in the spinal cord in MS, observing reductions in both interneuron and motoneuron numbers. This neuronal loss occurs predominantly within GM plaques. We also observe reductions in interneuron size, both within plaques and in the myelinated GM. Despite this, we find no evidence of spinal cord GM atrophy. Conclusions: This study represents the first detailed examination of spinal cord GM involvement in MS. We demonstrate substantial GM pathology in the spinal cord, further challenging the concept that MS is a predominantly WM disease. A greater understanding of this pathology may provide important insights into MS pathogenesis and mechanisms of disability in the disease.
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Mikhael, Shadia S. "Brain cortical variability, software, and clinical implications." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/33210.
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It is essential to characterize and quantify naturally occurring morphometric changes in the human brain when investigating the onset or progression of neurodegenerative disorders. The aim of this thesis is to characterize the properties and measure the performance of several popular automated magnetic resonance image analysis tools dedicated to brain morphometry. The thesis begins with an overview of morphometric analysis methods, followed by a literature review focusing on cortical parcellation protocols. Our work identified unanimous protocol weaknesses across all packages in particular issues when addressing cortical variability. The next chapters present a ground truth dataset and a dedicated software to analyse manually parcellated data. The dataset (https://datashare.is.ed.ac.uk/handle/10283/2936) includes 10 healthy middle-aged subjects, whose metrics we used as reference against automated tools. To develop the ground truth dataset, we also present a manual parcellation protocol (https://datashare.is.ed.ac.uk/handle/10283/3148) providing step-by-step instructions for outlining three cortical gyri known to vary with ageing and dementia: the superior frontal gyrus, the cingulate gyrus and the supramarginal gyrus. The software, Masks2Metrics (https://datashare.is.ed.ac.uk/handle/10283/3018), was built in Matlab to calculate cortical thickness, white matter surface area, and grey matter volume from 3D binary masks. Characterizing these metrics allowed further understanding of the assumptions made by software when creating and measuring anatomical parcels. Next, we present results from processing the raw T1-weighted volumes in the latest versions of several automated image analysis tools-FreeSurfer (versions 5.1 and 6.0), BrainGyrusMapping, and BrainSuite (version 13a)- against our ground truth. Tool repeatability for the same system was confirmed as multiple runs yielded identical results. Compared to our ground truth, the closest results were generated by BrainGyrusMapping for volume metrics and by FreeSurfer 6.0 for thickness and surface area metrics. In conclusion, our work sheds light on the significance of clearly detailed parcellation protocols and accurate morphometric tools due to the implications that they both will have. We therefore recommend extra caution when selecting image analysis tools for a study, and the use of independent publicly available ground truth datasets and metrics tools to assist with the selection process.
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Waters, Alexander Juergen. "Control of spinal nociception by the midbrain periaqueductal grey matter." Thesis, University of Bristol, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310695.
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Crook, Jonathan James. "Functional connections between the periaqueductal grey matter and the cerebellum." Thesis, University of Bristol, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.633195.
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The periaqueductal grey matter (PAG) is a key structure in the expression of behavioural responses to pain and fear; however the motor pathways that mediate these crucial survival behaviours are poorly understood. Previous anatomical studies have suggested connections between the PAG and the cerebellum, a hindbrain motor structure which has recently also been implicated in emotional function and the expression of survival behaviours, such as freezing behaviour. This thesis provides evidence of a possible anatomical pathway between these two structures, and describes investigations into a possible function of this connection. In sodium pentobarbital anaesthetised rats, cerebellar cortical field potentia Is were recorded in response to electrical stimulation in the PAG. Stimulation at both "IPAG and dlPAG sites was found to evoke bilateral climbing fibre field potentia Is in lateral regions of cerebellar vermallobule VIII. Fos expression was significantly increased in the fastigial nucleus A module in animals that underwent stereotaxic procedures, compared to anaesthetic control animals. Animals that received noxious pinches of the snout also tended to display greater numbers of Fos labelled neurons in this region. Animals that underwent excitation of the vlPAG with dl-homocysteic acid (DLH) displayed significantly fewer Fos labelled neurons in the A module than saline injected animals. This may reflect a vlPAG mediated depression of the noxious input to the cerebellum originating from stereotaxic and surgical procedures employed during the experiment. The functional significance of the PAG-Iobule VIII connection was investigated by lesioning connections to/from lateral lobule VIII using CTb-saporin. On average, lesioned animals displayed significantly reduced freezing behaviour during presentation of an aversively conditioned auditory tone. The animals that displayed the greatest reduction in freezing also displayed significantly fewer Fos labelled neurons in the caudal vIPAG. This suggests that vermallobule VIII supports neuronal activation of the caudal vlPAG during exposure to conditioned fear stimuli.
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Ueno, Tsukasa. "Sex-specific regional grey matter volume correlates of daily activities." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263563.
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Paquola, Casey. "The enduring impact of childhood maltreatment on grey matter development." Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/18566.
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Childhood maltreatment doubles an individual’s risk of developing a psychiatric disorder, yet the neurobiological nature of the enduring impact of childhood maltreatment remains elusive. This thesis explores the long-term effect of childhood maltreatment on grey matter. The primary aims of this thesis are to discern the spatial extent, temporal profile and physiological breadth of the developmental impact of childhood maltreatment amongst young people with emerging mental disorder. Chapter II comprises of a meta-analysis of thirty-eight published articles and demonstrates that adults with a history of childhood maltreatment most commonly exhibit reduced grey matter in the hippocampus, amygdala and right dorsolateral prefrontal cortex, compared to non-maltreated adults. Chapters III-V contain three original studies, involving a cohort of 123 young people, aged 14-26, with emerging mental illness. Chapter III bridges a gap between cross-sectional child and adult studies by longitudinally mapping the developmental trajectory of the hippocampus and amygdala following childhood maltreatment. This study provided the first direct evidence that childhood maltreatment stunts hippocampal development into young adulthood. Chapter IV assesses the utility of the cumulative stress and mismatch hypotheses in understanding the contribution of childhood abuse and recent stress to the structure and function of the limbic system. Chapter V extends on recent advances in connectome research to examine the effect of childhood maltreatment on structural covariance networks. Investigation of the correspondence of structural covariance with structural connectivity and functional connectivity revealed that reduced grey matter across the network is likely related to deceased functional coactivation following childhood maltreatment. Chapter VI discusses the significance of these studies in understanding how maltreatment shapes brain development and increases the risk of psychiatric illness.
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Hansen, Brian, Leif Østergaard, and Peter Vestergaard-Poulsen. "A fractal based model of diffusion MRI in cortical grey matter." Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-190860.
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Hansen, Brian, Leif Østergaard, and Peter Vestergaard-Poulsen. "A fractal based model of diffusion MRI in cortical grey matter." Diffusion fundamentals 11 (2009) 73, S. 1-2, 2009. https://ul.qucosa.de/id/qucosa%3A14038.
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Browne, Eleanor. "Tertiary lymphoid organ neogenesis in grey matter pathology in multiple sclerosis." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/30813.
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Chronic meningeal inflammation is suggested to contribute to the progression of secondary progressive multiple sclerosis (SPMS) in part by driving cortical grey matter pathology. The presence of tertiary lymphoid organ-like (TLO) structures in a large proportion of SPMS cases is associated with faster clinical progression and more severe cortical pathology, suggesting that TLO neogenesis and chronic meningeal inflammation contribute to progression. Gene expression of the cytokine lymphotoxin-alpha (LTα), implicated in TLO formation and cytotoxicity, and the lymphoid chemokines CXCL13 and CCL21, was determined in post-mortem SPMS meninges by qPCR. LTα was increased in SPMS, while substantially increased CXCL13 expression was associated with the presence of TLOs in SPMS. As LTα induces CXCL13 during inflammation, we investigated the hypothesis that LTα drives TLO formation and exacerbates cortical pathology in SPMS, using an animal model of cortical demyelination driven by meningeal inflammation. Subclinical experimental autoimmune encephalomyelitis was induced in female dark agouti rats by immunisation with 5-10μg of recombinant mouse myelin oligodendrocyte glycoprotein (rmMOG) in incomplete Freund's adjuvant. Injection of LTα and the cytokine interferon-γ into the subarachnoid space 21 days post-immunisation induced substantial meningeal infiltration with B cell-rich areas, T cells, macrophages and channel formation reminiscent of early TLOs, accompanied by microglial activation, extensive demyelination, and remyelination within 21 days. To study chronic meningeal cytokine expression we injected a VSV-G pseudotyped lentiviral vector (LV) expressing green fluorescent protein (GFP) or human LTα (LVLTα) into the subarachnoid space. Meningeal GFP expression was induced up to 90 days post-injection. Human LTα expression was detected in rat brain and CSF, with widespread microglial activation and meningeal infiltrates of macrophages, B and T cells resembling TLOs, in naïve and rmMOG-immunised rats at 90 days post-LVLTα, while extensive demyelination was present only in rmMOG-immunised rats. This suggests that chronic meningeal LTα expression is sufficient for widespread microglial activation, but demyelination requires an anti-myelin response in this model. These findings support the hypothesis that chronic meningeal inflammation drives cortical pathology, and LTα/TLO neogenesis may represent a novel therapeutic target for SPMS.
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Sethi, V. "3T magnetic resonance imaging of cortical grey matter lesions in Multiple Sclerosis." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1458360/.
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Radiological and histopathological studies have established that in addition to the classical white matter (WM) demyelinating lesions, cortical grey matter (CGM) lesions are also a significant part of the pathology in multiple sclerosis (MS), and contribute to the clinical and cognitive deficits seen in MS patients. Double inversion recovery (DIR) has been identified as a good sequence for the radiological detection of cortical grey matter lesions. In this project I investigated the role of phase sensitive inversion recovery (PSIR), a T1-weighted MRI sequence, using a 3T MRI scanner, for the detection of CGM lesions in multiple sclerosis. Detection of CGM lesions on a standard DIR sequence (1x1x3mm resolution) was compared with a higher resolution PSIR sequence (0.5x0.5x2mm), to explore if it can help improve the study of CGM lesions. A representative cohort, including patients with relapsing remitting (RR), primary progressive (PP) and secondary progressive (SP)MS, was recruited in this project, together with controls in order to allow a comparison of findings with those of healthy subjects who do not have MS. I systematically investigated if the use of high resolution PSIR scans can improve CGM lesion detection and classification, when compared to DIR. Using the PSIR sequence, I studied the hypothesis that the distribution of lesions impacts the pattern of cognitive impairment seen in patients. CGM lesion volumes were estimated for frontal, temporal , parietal and occipital lobes and cognitive tests were conducted (Hayling, Stroop, immediate and 4 delayed story and figure recall, PASAT (Paced auditory serial addition test) and SDMT (Symbol digit modality test)). Differences between phenotypes and associations with cognitive measures were explored using a multiple regression model. A follow up study was undertaken to understand how CGM lesions evolve with time and in order to explore potential specificity of PSIRdetected CGM lesions, I compared the findings of CGM lesion detection in MS patients, with patients diagnosed with Fabry’s disease. Compared with DIR, high resolution PSIR was found to detect a significantly greater number of CGM lesions and also improved the classification of CGM lesions. A fronto-temporal dominance of CGM lesions was noted in my study. Different CGM and JC lesion subtypes were found to be associated with cognitive function; the relationship being influenced by the lobar location and the cognitive function being assessed. In the follow-up study I found that people with SPMS have a grater accrual of CGM lesions than RRMS and the process appeared to be independent of WM lesion accrual. CGM lesions were also seen in patients with Fabry’s disease though the frequency was less that in MS. The data presented in my study suggests that PSIR has the potential to improve the quantitative and qualitative study of CGM lesions. CGM lesions were noted across all disease phenotypes, though more common in progressive disease. The distribution, accrual and evolution of CGM lesions provides insights into the pathogenesis of MS and helps understand the contribution of CGM lesions to neurological and cognitive impairment. Detection of CGM lesions has a potential role to help with a diagnosis of MS when it suspected but not confirmed.
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Fox, Kieran Charles Ryan. "Enhanced introspective accuracy and brain grey matter concentration in long-term meditation practitioners." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/43051.
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The accuracy of subjective reports, especially those involving introspection of one’s own internal processes, remains unclear, and research has demonstrated large individual differences in introspective accuracy. It has been hypothesized that introspective accuracy may be heightened in persons who engage in meditation practices, due to the highly introspective nature of such practices. We undertook a preliminary exploration of this hypothesis, examining introspective accuracy in a cross-section of meditation practitioners (1 - 15,000 hrs experience). Expert meditators showed significantly better introspective accuracy than novices; overall meditation experience also significantly predicted individual introspective accuracy. We then undertook a neuroimaging study (with a partially overlapping sample of meditators) to investigate possible structural brain differences between long-term meditators with high introspective accuracy, and meditation-naïve control subjects. Using magnetic resonance imaging to acquire 3D anatomical brain images, we used voxel-based morphometry to assess grey matter concentration differences between groups, and also as a function of meditation experience. Between-groups results suggest significantly greater concentrations of grey matter in primary somatosensory cortex in long-term meditators vs. controls; among meditators, grey matter concentration was found to increase in several regions key to body-awareness with increasing experience in the body-scanning meditation practice.
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Harris, J. J. "Energy consumption and signalling in the white and grey matter of the CNS." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1399237/.
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Neural computation is energetically expensive, and the brain’s limited energy supply imposes constraints on its information processing capability. How the brain has evolved to perform computational tasks within these energetic constraints is largely unknown. The theoretical and experimental work in this thesis examines how the white and grey matter – which have different computational roles – balance the trade-off between energy consumption and signalling. In the white matter, I show that the maintenance of cellular resting potentials accounts for the largest portion of signalling-related energy use. Maintaining this cost in myelinating oligodendrocytes outweighs the energetic saving on action potentials that myelin provides, but allows for faster action potential propagation. This design places computational benefit above energetic economy. Nevertheless, I show that action potential propagation in the white matter need not rely on metabolic collaboration of axons with oligodendrocytes, and that myelin itself is unlikely to produce ATP as has been proposed. In the grey matter, where synapses account for the largest portion of signalling-related energy consumption, I used electrophysiology to investigate the relationship between information transmission and energy consumption at the retinogeniculate synapse. I found that the number of postsynaptic receptors is set, not to maximise information transmission across the synapse, but to maximise the ratio of information transmitted to energy used on reversing the postsynaptic ion influx. This design places energetic efficiency above computational advantage, as the synapse could theoretically transmit more information if the postsynaptic response were larger. The results of this work suggest that energy supply and demand have played critical roles in shaping the way that the brain has evolved to process information, both in the white and grey matter. We should keep these energetic factors in mind when considering the brain’s adaptation to any computational task. The thesis also contains a description of experiments investigating mitochondrial trafficking in oligodendrocytes, and searching for plasticity of conduction speed in the white matter. A review of how energy supply to the brain alters with age, and how this may affect the BOLD (blood oxygenation level dependent) signal, is included as an Appendix.
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Laubach, Markus [Verfasser]. "Associations between executive functioning and cortical grey matter volume in the elderly / Markus Laubach." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/1189138891/34.
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Newbold, Marcus Clifford Thomas John. "Mapping metabolite concentrations in grey and white matter using magnetic resonance spectroscopic imaging (MRSI)." Thesis, King's College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392143.
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Schalks, Renée. "Chronic meningeal inflammation as a cause of cortical grey matter pathology in multiple sclerosis." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/23217.
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Subpial demyelination in cerebral cortical grey matter is associated with clinical progression in multiple sclerosis and is suggested to result from diffusion of pro-inflammatory cytokines from areas of meningeal inflammation into the cortex. In order to test this hypothesis we have developed an animal model of subpial demyelination driven by meningeal inflammation, involving delivery of cytokines into the subarachnoid space (SAS). Dark Agouti rats were immunised with a subclinical dose (10μg) of recombinant mouse myelin oligodendrocyte glycoprotein followed 21-24 days later by injection of TNF (1.25-5μg) and IFN-γ (75-300ng) into the SAS of the sagittal sulcus. The presence of the cytokines in the SAS resulted in acute demyelination and inflammation followed by resolution of pathology. This supports the hypothesis that cytotoxic/pro-inflammatory molecules diffuse from areas of meningeal inflammation into the underlying cortex resulting in microglial activation and subpial demyelination. Increasing the doses of TNF and IFN-γ resulted in increased extent, but not duration, of pathology due to the acute presence of the cytokines. We conclude that a chronic inflammatory milieu in the CSF/meningeal compartment is required to achieve chronic microglial activation and subpial demyelination and neuronal loss. In order to achieve the chronic presence of the cytokines in the SAS a high titre VSV-G-pseudotyped lentiviral vector carrying the enhanced green fluorescent protein (eGFP) gene under control of the CMV promoter was tested. It induced extensive and long-term, up to 12 weeks, eGFP expression in the sagittal sulcus in the absence of long-term microglial activation in naïve animals. Expression was localised to astrocytes, leptomeningeal cells and a small number of pyramidal neurons. The vector did not induce non-specific demyelination and inflammation in animals immunised with a subclinical dose of rmMOG. In order to achieve more localised expression, the vector was injected with collagen hydrogel. The hydrogel delayed eGFP expression but increased its spread along the anteroposterior axis. The distribution and duration of expression appeared optimal for achieving the chronic presence of TNF and IFN-γ in the CSF/meningeal compartment required to develop this novel model, if expression at the injection site could be increased using the hydrogel, which requires optimisation. We propose that the chronic presence of the cytokines will result in chronic meningeal inflammation and cortical grey matter pathology, allowing evaluation of the role of cytotoxic/pro-inflammatory molecules. The identity of several of the cytotoxic/pro-inflammatory molecules suggested to diffuse from areas of meningeal inflammation were also identified in post-mortem MS meninges using PCR arrays. Expression of CXCL13, IL5RA, IFNG and CXCL9 were increased, and that of CXCL1 decreased, in MS patients, consistent with an inflammatory milieu in the CSF/meningeal compartment and suggesting that these molecules may represent novel therapeutic targets for modulating meningeal inflammation and cortical pathology.
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Vanzulli, Ilaria. "Metabotropic glutamate receptors in oligodendrocytes and astrocytes in white and grey matter brain regions." Thesis, University of Portsmouth, 2014. https://researchportal.port.ac.uk/portal/en/theses/metabotropic-glutamate-receptors-in-oligodendrocytes-and-astrocytes-in-white-and-grey-matter-brain-regions(c7ad700f-3a22-4e1f-b008-1588145ab108).html.
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Glial cells express a wide range of neurotransmitter receptors throughout the central nervous system (CNS). In this thesis, I have investigated glial neurotransmitter signaling mechanisms in CNS white matter, using the mouse optic nerve as a model white matter and with a particular focus on metabotropic glutamate receptors (mGluR). The transcriptomic profiling of postnatal, adult and ageing optic nerve identified a pre-eminence of glutamatergic neurotransmission in the optic nerve and highlighted a switch to GABAergic signaling in the ageing white matter, without a loss of glutamatergic neurotransmission. Immunostaining showed expression of group I and group II mGluR in optic nerve astrocytes and oligodendrocytes and their functionality was demonstrated by live cell calcium imaging. Activation of group I and group II mGluR is shown to protect both oligodendrocytes and astrocytes from hypoxia/ischaemia, using an oxygen and glucose deprivation (OGD) model in the isolated intact mouse optic nerve. A key finding is that mGluR were expressed by glia at all ages and were not developmentally downregulated, as had been suggested from previous in vitro studies. In addition, the genomic analysis indicated disruption of OPCs in ageing tissue, and significant age-related disruption of OPCs was confirmed in the triple transgenic mouse model of Alzheimer’s disease (3xTg AD). This study provides new insight into mGluR expression and function in white matter glia.
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Serber, Stacy Lee. "Cerebral blood flow, grey matter volumes, and autonomic nervous system function in heart failure." Diss., Restricted to subscribing institutions, 2007. http://proquest.umi.com/pqdweb?did=1383469311&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.
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Brubaker, Christopher John. "A Multimodal Magnetic Resonance Study of the Effects of Childhood Lead Exposure on Adult Brain Structure." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1248964743.
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Cuthill, Daniel. "Involvement of excitotoxicity or oxidative stress in the pathophysiology of white and grey matter injury." Thesis, University of Glasgow, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414444.
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Van, De Pavert S. H. P. "Grey matter pathology in multiple sclerosis : in vivo and post mortem magnetic resonance imaging studies." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1551600/.
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The extent and clinical relevance of grey matter (GM) pathology in multiple sclerosis (MS) is increasingly recognised. Previous work has shown that GM pathology is more closely associated with some aspects of clinical disability than white matter (WM) injury, which has been suggested to arise independently. Magnetic resonance imaging (MRI) allows the study of GM lesions, atrophy, and non-lesional injury with techniques including double inversion recovery (DIR), volumetric scans, and magnetisation transfer ratio (MTR), respectively. This thesis includes three independent in vivo and post mortem MRI studies specifically addressing (1) the clinical impact and spatial distribution of DIR-detected GM lesions and atrophy, (2) the longitudinal development of MTR changes in thalamo-cortical systems, and (3) the histopathological substrates underlying MTR in the MS brain. This work shows that (1) DIR-detected GM lesions are mainly found throughout the cerebellar and cerebral cortex, whereas particularly subcortical GM structures show atrophy. Both GM lesions and atrophy contribute to disability, suggesting that the substrates of disability in MS are both pathologically and spatially heterogeneous. (2) WM injury to thalamo-cortical systems is most likely to precede (both thalamic and cortical) GM damage. In addition, lower regional cortical MTR is found not to be consistently associated with lower cortical volume, suggesting that significant cortical microstructural damage can occur in the absence of atrophy. Furthermore, observed hemispheric asymmetries and WM tract inhomogeneities emphasise the need for more refined statistical models to detect disease-specific changes. (3) MTR is associated with histologically quantified myelin (and to a lesser extent neuronal content) in normal appearing grey matter and normal appearing white matter, but not in cortical lesions and chronic inactive WM lesions. Finally, the cytological make-up differs significantly between normal appearing and lesional WM and GM, and provides extra evidence for microglia-mediated mitochondria damage in normal appearing MS tissue.
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Clavenstam, Isabell. "The Effect of Methamphetamine Abuse on Brain Structure and Function." Thesis, University of Skövde, School of Humanities and Informatics, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-3106.
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The great amount of METH abuse all over the world causes enormous social and criminal justice problems. In the human brain the abuse of METH causes implications on both structures and functions given rise to acute as well as long term symptoms. In this essay the effects of METH abuse is described in the manner of the drug mechanism such as the impact on neurotransmitters, structural deficits with decreased and increased volumes and the implication on attention, memory, decision making and emotions. Results from studies showing brain structural and cognitive impairments in METH abusers and in prenatal METH exposed children.
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Gardner, Christopher James. "Grey matter demyelination and neurodegeneration in multiple sclerosis : a new animal model for studying disease mechanisms." Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/9228.
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Multiple sclerosis is the commonest neurological disease affecting young adults. Whilst the initial relapsing-remitting disease phase is associated with inflammatory demyelination and is treatable with immunomodulatory drugs, the secondary progressive phase (SP-MS) is associated with ongoing axonal loss and cortical atrophy and is currently untreatable. Studies of SP-MS have revealed the presence of extensive subpial demyelinated lesions within the cerebral cortex. This pathology is associated with a high level of meningeal inflammation, a gradient of cell loss from the cortical surface and high levels of microglia activation. To test the hypothesis that pro-inflammatory cytokines diffusing from the cerebral meninges could be responsible, we have established an animal model mimicking cortical grey matter pathology. Female DA rats were immunised with 5μg recombinant myelin oligodendrocyte glycoprotein (rmMOG) in incomplete Freunds adjuvant (IFA). This dose was insufficient to initiate encephalomyelitis, but did initiate an anti-MOG humoral immune response in the periphery. Twenty days post-immunisation animals received an injection of tumour necrosis factor (TNF) and interferon gamma (IFNγ) into the subarachnoid space at the sagittal sulcus. Immunohistochemistry revealed areas of subpial demyelination extending through cortical layers I–III. Lesions were maximal after 7 days and had resolved by remyelination at 14 days. A gradient of microglia/macrophage activation was present from the cortical surface. The extent of demyelination correlated with activation of microglia in the cortex and macrophages within the meninges. Activated microglia were observed contacting myelin, oligodendrocytes and neurons. In the demyelinated cortex, expression of the TNF receptors TNFR1A and TNFR1B was upregulated on oligodendrocytes and perivascular macrophages respectively. CD8+ T cells were observed in the meninges, corpus callosum and scattered throughout the grey matter, whereas CD4+ T cells and CD79a+ B cells were restricted to the meninges. Oligodendrocyte numbers were reduced in the upper cortical layers prior to demyelination (days 1 and 3 post-injection), but were still present in demyelinated lesions at day 7. Numbers of neurons and astrocytes were not changed. Control animals immunised with IFA and injected with cytokines had increased presence of inflammatory cells within the meninges but no demyelination. Animals immunised with rmMOG and injected with PBS had no demyelination or immune response within the meninges or cortex. Thus, acute subpial demyelination was dependent on a pre-existing immune response against myelin protein, coupled with generalised pro-inflammatory signalling within the meninges. These findings support our hypothesis of a role for meningeal inflammation in the cortical pathology of MS and describe for the first time an animal model that can be used to study the molecular mechanisms involved. Future research will aim to maintain meningeal inflammation and produce a model of chronic demyelination.
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Hermann, Moritz [Verfasser], Alexander [Akademischer Betreuer] Flügel, Alexander [Gutachter] Flügel, and Holger [Gutachter] Reichardt. "Analysis of autoimmune lesions in grey matter / Moritz Hermann ; Gutachter: Alexander Flügel, Holger Reichardt ; Betreuer: Alexander Flügel." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2018. http://d-nb.info/1161183221/34.
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Johnson, Eileanoir. "Structural cortical grey matter changes during the transition from premanifest to manifest Huntington's disease : a methodological evaluation." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10048599/.
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Huntington’s disease (HD) is a genetic neurodegenerative disease characterised by motor, cognitive and psychiatric symptoms. Atrophy of subcortical brain structures has been well characterised and changes in the white matter are being mapped with increasing frequency, but structural changes in the cortex have been relatively overlooked in previous research. With recently trialled therapies specifically targeting the cortex, a better understanding of the pattern and progression of atrophy in this region should provide valuable measures for determining the impact of these novel treatments on the degenerative process. This thesis performs a methodological comparison aimed at optimising techniques to measure cortical characteristics in an HD cohort, and then applies the optimised techniques in a group of HD gene carriers undergoing conversion from pre-manifest HD to manifest HD quantifying cortical change during this critical period. Several tools for the quantification of cortical volume and cortical thickness are examined via detailed analyses using two datasets. This investigation results in a series of recommendations for the use of such tools, as well as the selection of the most appropriate measures for use in the second part of this thesis. In addition, since subcortical atrophy measures are widely used in HD research, the performance of one of the segmentation tools was evaluated by comparison with manual segmentations of the caudate and putamen. Finally, a novel multivariate analysis method is applied, based on the principles of DCM, to measure the rate, timing and acceleration of cortical GM change in a subgroup of 49 motor converters from the TRACK-HD cohort. This cortical atrophy is then related both to the biological underpinning of the disease in terms of CAG length and also the behavioural presentation of motor and cognitive symptoms. These findings present the first detailed characterisation of cortical grey matter change in HD, and have important implications for the understanding of HD progression.
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Bodini, B. "Exploring the relationship between white and grey matter damage in primary progressive multiple sclerosis with structural magnetic resonance imaging." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1419097/.
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In the first part of this thesis, an introduction of the main characteristics of the primary-progressive form of multiple sclerosis (PPMS) (Chapter I), and of the acquisition and post-processing of the conventional and quantitative magnetic resonance imaging techniques employed in the studies presented in this thesis (Chapter II), will be presented. In the second part of this thesis, several advanced imaging techniques will be employed to answer the following two key questions on PPMS: 1) Is there is a spatial and temporal link between the pathological processes occurring in the normal appearing white matter (WM) and in the grey matter (GM) of patients with PPMS?; 2) Which regions of WM and GM abnormalities significantly contribute to clinical progression and cognitive dysfunction over time in patients with PPMS? To answer the first question, I first used tract-based spatial statistics (TBSS) and voxel-based morphometry (VBM), to explore the spatial relationship between the damage occurring in the normal-appearing WM and GM in patients with early PPMS (Chapter III). Then, I moved onto exploring the temporal relationship linking the pathological changes affecting the two compartments, employing magnetization transfer imaging (MTI) and diffusion-based tractography (Chapter IV). To answer the second question, I first looked at the prognostic role of WM lesion location in a study conducted on a large population of patients with well- established PPMS who were followed-up for ten years in five different European centres (Chapter V). Then, using a novel approach which combines MTI and TBSS, I explored the regions of short-term accrual of microstructural damage in patients with early PPMS (Chapter VI). Finally, I moved onto examining the relative contribution of WM and GM damage to long-term motor and cognitive disability in PPMS (Chapter VII). In the final Chapter, I will summarise the results of the studies presented in this thesis, provide an answer to the two key questions on PPMS, and propose future directions for research.
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Tijms, Betty Marije. "Extracting morphological networks from individual grey matter MRI scans in healthy subjects and people at high risk for schizophrenia." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/9604.
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Recently graph theory has been successfully applied to magnetic resonance imaging data. However, it remains unclear as to what the nodes and edges in a network should represent. This problem is particularly difficult when extracting morphological networks (i.e., from grey matter segmentations). Existing morphological network studies have used anatomical regions as nodes that are connected by edges when these regions covary in thickness or volume across a sample of subjects. Covariance in cortical thickness or volume has been hypothesised to be caused by anatomical connectivity, experience driven plasticity and/or mutual trophic influences. A limitation of this approach is that it requires magnetic resonance imaging (MRI) scans to be warped into a standard template. These warping processes could filter out subtle structural differences that are of most interest in, for example, clinical studies. The focus of the work in this thesis was to address these limitations by contributing a new method to extract morphological networks from individual cortices. Briefly, this method divides the cortex into small regions of interest that keep the three-dimensional structure intact, and edges are placed between any two regions that have a statistically similar grey matter structure. The method was developed in a sample of 14 healthy individuals, who were scanned at two different time points. For the first time individual grey matter networks based on intracortical similarity were studied. The topological organisation of intracortical similarities was significantly different from random topology. Additionally, the graph theoretical properties were reproducible over time supporting the robustness of the method. All network properties closely resembled those reported in other imaging studies. The second study in this thesis focussed on the question whether extracting networks from individual scans would be more sensitive than traditional methods (that use warping procedures) to subtle grey matter differences in MRI data. In order to investigate this question, the method was applied to the first round of scans from the Edinburgh High Risk study of Schizophrenia (EHRS), before any of the subjects was diagnosed with (symptoms of) the disease. Where traditional methods failed to find differences at the whole brain level between the high risk group and healthy controls, the new method did find subtle disruptions of global network topology between the groups. Finally, the diagnostic value of the networks was studied with exploratory analyses that found that, in comparison to healthy controls, people at high risk of schizophrenia showed more intracortical similarities in the left angular gyrus. Furthermore within the high risk group an increase of intracortical similarities could predict disease outcome up to 74% accuracy. The main conclusion of this thesis was that the new method provides a robust and concise statistical description of the grey matter structure in individual cortices, that is of particular importance for the study of clinical populations when structural disruptions are subtle.
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Chaudun, Fabrice. "Involvement of dorsomedial prefrontal projections pathways to the basolateral amygdala and ventrolateral periaqueductal grey matter in conditioned fear expression." Thesis, Bordeaux, 2016. http://www.theses.fr/2016BORD0118/document.
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A l’heure actuelle, une des principales questions des neurosciences comportementales est de comprendre les bases neurales des apprentissages et de comprendre comment des modifications au sein de circuits neuronaux spécifiques contrôlent les changements comportementaux liés à une expérience particulière. De nombreuses études ont récemment mis en évidence le rôle important des circuits neuronaux dans les phénomènes d’apprentissages associatifs, et notamment dans la régulation des comportements de peur. Cependant, leurs caractéristiques anatomiques et fonctionnelles restent encore largement inconnues. L’une des principales fonctions des circuits neuronaux est leur capacité à adapter le comportement en fonction de la nature des informations internes ou environnementales disponibles. Malgré de nombreux progrès réalisés sur la compréhension des substrats et mécanismes neuronaux sous tendant le conditionnement de peur au sein de structures telles que l'amygdale (AMG), le cortex préfrontal dorso-médian (dmPFC) et la substance grise periaqueducale (PAG), les mécanismes neuronaux gouvernant les interactions inter-structure ainsi que le contrôle local de ces différents circuits neuronaux restent encore largement inconnus. Dans ce contexte, ce travail de thèse a eupour objectifs principaux, d’évaluer la contribution des voies de projections dmPFC-BLA et dmPFC-vlPAG dans la régulation des comportements de peur, et, d’identifier les mécanismes neuronaux sous-jacent contrôlant l'expression de la peur. Afin de répondre à ces questions, nous avons utilisé conjointement des enregistrements électrophysiologiques unitaires et de potentiels de champs couplés à des approches optogénétiques au cours de l’expression de la peur conditionnée. Nous avons pu mettre en évidence un nouveau mécanisme neuronal basé sur une oscillation cérébrale à 4 Hz entre le dmPFC et le BLA impliqué dans la synchronisation neuronale des neurones de ces deux structures nécessaire à l’expression de la peur. Nous avons aussi démontré que le dmPFC via ses projections sur le vlPAG contrôle directement l’expression de la peur. Ensemble, nos données contribuent à une meilleure compréhension des circuits neuronaux ainsi que des mécanismes du comportement de peur qui dans le futur pourront aider à une amélioration thérapeutique des troubles anxieuxA central endeavour of modern neuroscience is to understand the neural basis of learningand how the selection of dedicated circuits modulates experience-dependent changes inbehaviour. Decades of research allowed a global understanding of the computations occurring inhard-wired networks during associative learning, in particular fear behaviour. However, brainfunctions are not only derived from hard-wired circuits, but also depend on modulation of circuitfunction. It is therefore realistic to consider that brain areas contain multiple potential circuitswhich selection is based on environmental context and internal state. Whereas the role of entirebrain areas such as the amygdala (AMG), the dorsal medial prefrontal cortex (dmPFC) or theperiaqueductal grey matter (PAG) in fear behaviour is reasonably well understood at themolecular and synaptic levels, there is a big gap in our knowledge of how fear behaviour iscontrolled at the level of defined circuits within these brain areas. More particularly, whereas thedmPFC densely project to both the basolateral amygdala (BLA) and PAG, the contributions ofthese two projections pathway during fear behaviour are largely unknown. Beside theinvolvement of these neuronal pathways in the transmission of fear related-information, theneuronal mechanisms involved in the encoding of fear behaviour within these pathways are alsovirtually unknown. In this context, the present thesis work had two main objectives. First,evaluate the contribution of the dmPFC-BLA and dmPFC-vlPAG pathways in the regulation offear behaviour, and second, identify the neuronal mechanisms controlling fear expression in thesecircuits. To achieve these goals, we used a combination of single unit and local field potentialrecordings coupled to optogenetic approaches in behaving animals submitted to a discriminativefear conditioning paradigm. Our results first, identified a novel neuronal mechanism of fear expression based on the development of 4 H oscillations within dmPFC-BLA circuits thatdetermine the dynamics of freezing behaviour and allows the long-range synchronization offiring activities to drive fear behaviour. Secondly, our results identified the precise circuitry at thelevel of the dmPFC and vlPAG that causally regulate fear behaviour. Together these data provideimportant insights into the neuronal circuits and mechanisms of fear behaviour. Ultimately thesefindings will eventually lead to a refinement of actual therapeutic strategies for pathological conditions such as anxiety disorders
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Derakhshan, Mishkin. "Using magnetic resonance imaging for the in vivo detection and characterization of cerebral grey matter pathology in patients with multiple sclerosis." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116946.
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Magnetic resonance imaging has become an invaluable tool in clinical neurology because of its ability to provide excellent contrast between different soft tissues of the brain, including pathologically altered tissues. Image processing methods can be used to further the detection and quantification of such tissues, as has been the case for the well-studied white matter (WM) lesions in the brains of patients with multiple sclerosis (MS). Considered an immune-mediated disease of the central nervous system, MS has long been believed to be a disease of the WM, though recent studies have shifted the focus to the pathologically altered grey matter (GM) tissue, which is difficult to visualize in vivo. As the appreciation grows for cortical GM pathology in patients with MS, so does the need for imaging methods that capture said pathology and for understanding the relationship of those methods to the clinical outcome of the patient. Hence, the main objective of this thesis was to evaluate and develop image processing methods for the in vivo quantification of GM pathology in patients with MS. We reveal the strengths and weaknesses of the currently available techniques for measuring GM pathology, highlighting the need for separate cortical and deep GM methodologies. We also, introduced a novel surface-based technique involving magnetization transfer ratio (MTR) images for imaging putative areas of subpial demyelination, the most common form of cortical lesion seen on postmortem analysis that has yet to be captured via in vivo imaging techniques. Finally, we showed that, of the imaging metrics available for measuring cortical pathology, widespread cortical damage detected with surface-based measures of MTR have the strongest relationship to cognitive performance in cognitively impaired patients with MS. Importantly, all cross-sectional studies were performed using images typically obtained in the clinical setting and at the accessible field strengths of 1.5 T and 3 T, giving the work instant clinical feasibility and relevance.L'imagerie par résonance magnétique est un outil précieux en neurologie grâce à sa capacité à fournir un excellent contraste entre différents tissus du cerveau, y compris les tissus altérés pathologiquement. Les méthodes de traitement d'image peuvent être utilisées pour favoriser la détection et la quantification de ces tissus, comme dans le cas des lésions de la substance blanche (SB) du cerveau des patients atteints de sclérose en plaques (SEP). Considérée comme une maladie auto-immune du système nerveux central, la SEP a longtemps été étudiée comme une maladie de la substance blanche. Des études récentes ont déplacé l'attention vers les pathologies de matière grise (SG) du tissu qui sont difficiles à visualiser in vivo. L'appréciation se développe pour la pathologie de la SG corticale chez les patients atteints de SEP, tout comme le besoin de méthodes d'imagerie qui capturent ladite pathologie et la compréhension de la relation de ces méthodes à l'évolution clinique du patient. Par conséquent, l’objectif principal de cette thèse est l'évaluation et le développement de méthodes de traitement d'image pour la quantification in vivo de la pathologie de SG chez les patients avec la SEP. Nous révélons les forces et les faiblesses des techniques disponibles pour mesurer la pathologie de SG, soulignant la nécessité de séparer les méthodes pour le SG corticale et profonde. Ensuite, on présente une nouvelle technique de surface impliquant des images de rapport de transfert de magnétisation (MTR) pour étudier les zones possibles de démyélinisation sous-pie-mère, la forme la plus commune de lésion corticale observée en analyse post-mortem qui n'ait pas encore été vue par l'intermédiaire d'imagerie in vivo. Enfin, nous montrons que, parmis les indicateurs disponibles pour mesurer pathologie corticale en imagerie, les lésions corticales détectées à l'aire de mesures de MTR sur des surfaces ont la corrélation la plus forte avec la performance cognitive chez des patients atteints de SEP avec des facultés cognitives affaiblies. Fait important, toutes les études transversales ont été réalisées à partir d'images obtenues typiquement en milieu clinique et à des niveaux de champs de 1,5 T et 3 T, conférant à cet ouvrage faisabilité et pertinence clinique.
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BALLESTEROS, CAROLINA IRURITA. "ROLE OF DORSAL AND VENTRAL HIPPOCAMPUS ON CONDITIONED AND UNCONDITIONED FEAR ELICITED BY DORSAL PERIAQUEDUCTAL GREY MATTER ELECTRICAL STIMULATION IN RATS." PONTIFÍCIA UNIVERSIDADE CATÓLICA DO RIO DE JANEIRO, 2012. http://www.maxwell.vrac.puc-rio.br/Busca_etds.php?strSecao=resultado&nrSeq=19918@1.
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PONTIFÍCIA UNIVERSIDADE CATÓLICA DO RIO DE JANEIROEste estudo investiga o papel do hipocampo no comportamento de defesa condicionado e incondicionado examinando o efeito de lesões eletrolíticas pré-treino no hipocampo dorsal e ventral de ratos expostos a dois tipos de estímulos aversivos: estimulação elétrica da matéria cinzenta periaquedutal dorsal e choque nas patas. A lesão na parte dorsal e ventral diminuiu significativamente o comportamento defensivo condicionado. No comportamento defensivo incondicionado, a lesão ventral alterou significativamente o congelamento pré-fuga e a fuga. Os resultados sugerem um papel específico da parte dorsal e ventral do hipocampo na modulação de defesa através da utilização do modelo animal de ataque de pânico e TAG.
This study investigates the role of the hippocampus in both unconditioned and conditioned defense behavior by examining the effects of pre-training electrolytic lesions to the dorsal and ventral hippocampus in male rats exposed to two types of threat stimuli: electrical stimulation of the DPAG and footshock. Our results indicate that ventral and dorsal lesions significantly attenuated conditioned defensive behavior. During unconditioned trials, ventral hippocampal lesion altered threshold needed for escape and pre-escape freezing. These results suggest a specific role of the ventral and dorsal hippocampus in modulating GAD and panic-attack like behaviors in certain animal model of defense.
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Nicolas, Renaud, Florent Aubry, Jérémie Pariente, Xavier Franceries, Nicolas Chauveau, Laure Saint-Aubert, François Chollet, Stephane Breil, and Pierre Celsis. "Water diffusion in q-space imaging as a probe of cell local viscosity and anomalous diffusion in grey and white matter." Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-186332.
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Extraction of accurate quantitative parameters to characterize
water diffusion in complex porous media like brain tissue in neuroimaging is a challenging inverse problem, that depends on medium\'s structural and geometrical factors [1,3]. If the role of membranes is generally invoked, probe collisions with the insoluble cytoskeleton network and water hydrodynamic interactions with dissolved macromolecules and cytoskeleton occur as well [2]. The latter two interactions have been shown to determine the phenomenological “anomalous diffusion” of probes in the cytoplasm [4,5,6,7,8]. Additionally, the diffusion of small solutes in cytoplasm could be slowed by the local micro-viscosity of the aqueous phase, a phenomenon generally not taken into account in simulations. We suggest that the Grey and White Matter contrast in Diffusion Decay Imaging (DDI) could be caused by differences in cytoskeleton structures, composed respectively of actin and tubulin that could act by the elimination of one possible water diffusion pathlength by the volume occupied by the network phase. This could explain why anomalous DDI signal has been shown to be independent of membrane integrity [9]. Cytoplasm is able to rapidly shift from a sol (aqueous solutions embedded with insolubles particles) to a gel state (a colloidal solutions with a structured semi-solid and an aqueous fluid phase) or to a viscous solution when the insoluble particles become soluble. Does water have the ability of being a sensor of its local “self-viscosity” ? What is the length of the water diffusion\'s path compared to cells size ? Compared to this path length, how many cellular structures should be probed by water\'s translational diffusion ? We try to respond to these questions by investigating Diffusion Decay Imaging models and their effects on the hypothese-free q-space diffusion propagator shape [3], containing all informations concerning viscosity-slowed gaussian diffusion, structural informations [3] and restricted diffusion [1].
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Nicolas, Renaud, Florent Aubry, Jérémie Pariente, Xavier Franceries, Nicolas Chauveau, Laure Saint-Aubert, François Chollet, Stephane Breil, and Pierre Celsis. "Water diffusion in q-space imaging as a probe of cell local viscosity and anomalous diffusion in grey and white matter." Diffusion fundamentals 14 (2010) 3, S. 1-4, 2010. https://ul.qucosa.de/id/qucosa%3A12798.
Full textAbstract:
Extraction of accurate quantitative parameters to characterize
water diffusion in complex porous media like brain tissue in neuroimaging is a challenging inverse problem, that depends on medium\''s structural and geometrical factors [1,3]. If the role of membranes is generally invoked, probe collisions with the insoluble cytoskeleton network and water hydrodynamic interactions with dissolved macromolecules and cytoskeleton occur as well [2]. The latter two interactions have been shown to determine the phenomenological “anomalous diffusion” of probes in the cytoplasm [4,5,6,7,8]. Additionally, the diffusion of small solutes in cytoplasm could be slowed by the local micro-viscosity of the aqueous phase, a phenomenon generally not taken into account in simulations. We suggest that the Grey and White Matter contrast in Diffusion Decay Imaging (DDI) could be caused by differences in cytoskeleton structures, composed respectively of actin and tubulin that could act by the elimination of one possible water diffusion pathlength by the volume occupied by the network phase. This could explain why anomalous DDI signal has been shown to be independent of membrane integrity [9]. Cytoplasm is able to rapidly shift from a sol (aqueous solutions embedded with insolubles particles) to a gel state (a colloidal solutions with a structured semi-solid and an aqueous fluid phase) or to a viscous solution when the insoluble particles become soluble. Does water have the ability of being a sensor of its local “self-viscosity” ? What is the length of the water diffusion\''s path compared to cells size ? Compared to this path length, how many cellular structures should be probed by water\''s translational diffusion ? We try to respond to these questions by investigating Diffusion Decay Imaging models and their effects on the hypothese-free q-space diffusion propagator shape [3], containing all informations concerning viscosity-slowed gaussian diffusion, structural informations [3] and restricted diffusion [1].
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Griffiths, Jennifer Louise. "An investigation into the effects of the oestrous cycle on GABA_A-receptor subunit expression in the periaqueductal grey matter of the rat." Thesis, University of Birmingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.423371.
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Freing, Alina [Verfasser], Michael [Akademischer Betreuer] [Gutachter] Knauth, and Martin [Gutachter] Weber. "Grey Matter Perfusion in Clinically Isolated Syndrome and Relapsing-Remitting Multiple Sclerosis / Alina Freing ; Gutachter: Michael Knauth, Martin Weber ; Betreuer: Michael Knauth." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2017. http://d-nb.info/1142001377/34.
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McNulty, Victoria. "Estimation of grey and white matter and whole cerebral hemisphere volume by using the cavalieri slices method in combination with 3D MR imaging." Thesis, University of Liverpool, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368670.
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Baasch, Roland. "FMRI guided DTI at the grey-white matter interface : with application to a connectivity analysis of the default mode network in Urbach-Wiethe disease." Master's thesis, University of Cape Town, 2011. http://hdl.handle.net/11427/12246.
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Includes abstract.Includes bibliographical references.
The cerebral cortex is composed of a thin layer of Grey Matter (GM), functionally subdivided into discrete regions which are connected in a large scale network via White Matter (WM) tracts. With fMRI (Functional Magnetic Resonance Imaging) it is possible to identify cortical regions involved in specific tasks, and with DTI (Diffusion Tensor Imaging) the structural connections between these areas can be mapped. The aim of this thesis is to to identify and track only those WM tracts entering and leaving a GM Region Of Interest (ROI) defined by fMRI.
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Whitford, Thomas James. "A longitudinal study of brain structure in the early stages of schizophrenia." Thesis, The University of Sydney, 2007. http://hdl.handle.net/2123/1895.
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Schizophrenia is a severe mental illness that affects approximately 1% of the population worldwide, and which typically has a devastating effect on the lives of its sufferers. The characteristic symptoms of the disease include hallucinations, delusions, disorganized thought and reduced emotional expression. While many of the early theories of schizophrenia focused on its psychosocial foundations, more recent theories have focused on the neurobiological underpinnings of the disease. This thesis has four primary aims: 1) to use magnetic resonance imaging (MRI) to identify the structural brain abnormalities present in patients suffering from their first episode of schizophrenia (FES), 2) to elucidate whether these abnormalities were static or progressive over the first 2-3 years of patients’ illness, 3) to identify the relationship between these neuroanatomical abnormalities and patients’ clinical profile, and 4) to identify the normative relationship between longitudinal changes in neuroanatomy and electrophysiology in healthy participants, and to compare this to the relationship observed between these two indices in patients with FES. The aim of Chapter 2 was to use MRI to identify the neuroanatomical changes that occur over adolescence in healthy participants, and to identify the normative relationship between the neuroanatomical changes and electrophysiological changes associated with healthy periadolescent brain maturation. MRI and electroencephalographic (EEG) scans were acquired from 138 healthy participants between the ages of 10 and 30 years. The MRI scans were segmented into grey matter (GM) and white matter (WM) images, before being parcellated into the frontal, temporal, parietal and occipital lobes. Absolute EEG power was calculated for the slow-wave, alpha and beta frequency bands, for the corresponding cortical regions. The age-related changes in regional tissue volumes and regional EEG power were inferred with a regression model. The results indicated that the healthy participants experienced accelerated GM loss, EEG power loss and WM gain in the frontal and parietal lobes between the ages of 10 and 20 years, which decelerated between the ages of 20 and 30 years. A linear relationship was also observed between the maturational changes in regional GM volumes and EEG power in the frontal and parietal lobes. These results indicate that the periadolescent period is a time of great structural and electrophysiological change in the healthy human brain. The aim of Chapter 3 was to identify the GM abnormalities present in patients with FES, both at the time of their first presentation to mental health services (baseline), and over the first 2-3 years of their illness (follow-up). MRI scans were acquired from 41 patients with FES at baseline, and 47 matched healthy control subjects. Of these participants, 25 FES patients and 26 controls returned 2-3 years later for a follow-up scan. The analysis technique of voxel-based morphometry (VBM) was used in conjunction with the Statistical Parametric Mapping (SPM) software package in order to identify the regions of GM difference between the groups at baseline. The related analysis technique of tensor-based morphometry (TBM) was used to identify subjects’ longitudinal GM change over the follow-up interval. Relative to the healthy controls, the FES patients were observed to exhibit widespread GM reductions in the frontal, parietal and temporal cortices and cerebellum at baseline, as well as more circumscribed regions of GM increase, particularly in the occipital lobe. Furthermore, the FES patients lost considerably more GM over the follow-up interval than the controls, particularly in the parietal and temporal cortices. These results indicate that patients with FES exhibit significant structural brain abnormalities very early in the course of their illness, and that these abnormalities progress over the first few years of their illness. Chapter 4 employed the same methodology to investigate the white matter abnormalities exhibited by the FES subjects relative to the controls, both at baseline and over the follow-up interval. Compared to controls, the FES patients exhibited volumetric WM deficits in the frontal and temporal lobes at baseline, as well as volumetric increases at the fronto-parietal junction bilaterally. Furthermore, the FES patients lost considerably more WM over the follow-up interval than did the controls in the middle and inferior temporal cortex bilaterally. While there is substantial evidence indicating that abnormalities in the maturational processes of myelination play a significant role in the development of WM abnormalities in FES, the observed longitudinal reductions in WM were consistent with the death of a select population of temporal lobe neurons over the follow-up interval. The aim of Chapter 5 was to investigate the clinical correlates of the GM abnormalities exhibited by the FES patients at baseline. The volumes of four distinct cerebral regions where 31 patients with FES exhibited reduced GM volumes relative to 30 matched controls were calculated and correlated with patients’ scores on three primary symptom dimensions: Disorganization, Reality Distortion and Psychomotor Poverty. The results indicated that the greater the degree of atrophy exhibited by the FES patients in three of these four ‘regions-of-reduction’, the less severe their degree of Reality Distortion. These results suggest that an excessive amount of GM atrophy may in fact preclude the formation of hallucinations or highly systematized delusions in patients with FES. The aim of Chapter 6 was to identify the relationship between the longitudinal changes in brain structure and brain electrophysiology exhibited by 19 FES patients over the first 2-3 years of their illness, and to compare it to the normative relationship between the two indices reported in Chapter 2. The methodology employed for the parcellation of the MRI and EEG data was identical to Chapter 2. The results indicated that, in contrast to the healthy controls, the longitudinal reduction in GM volume exhibited by the FES patients was not associated with a corresponding reduction in EEG power in any brain lobe. In contrast, EEG power was observed to be maintained or even to increase over the follow-up interval in these patients. These results were consistent with the FES patients experiencing an abnormal elevation of neural synchrony. Such an abnormality in neural synchrony could potentially form the basis of the dysfunctional neural connectivity that has been widely proposed to underlie the functional deficits present in patients with schizophrenia. The primary aim of Chapter 7 was to assimilate the findings from the preceding empirical chapters with the theoretical framework provided in the literature, into an integrated and testable model of schizophrenia. The model emphasized dysfunctions in brain maturation, specifically in the normative processes of synaptic ‘pruning’ and axonal myelination, as playing a key role in the development of disintegrated neural activity and the subsequent onset of schizophrenic symptoms. The model concluded with the novel proposal that disintegrated neural activity arises from abnormal elevations in the synchrony of synaptic activity in patients with first-episode schizophrenia.
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Whitford, Thomas James. "A longitudinal study of brain structure in the early stages of schizophrenia." University of Sydney, 2007. http://hdl.handle.net/2123/1895.
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Doctor of Philosophy (PhD)Schizophrenia is a severe mental illness that affects approximately 1% of the population worldwide, and which typically has a devastating effect on the lives of its sufferers. The characteristic symptoms of the disease include hallucinations, delusions, disorganized thought and reduced emotional expression. While many of the early theories of schizophrenia focused on its psychosocial foundations, more recent theories have focused on the neurobiological underpinnings of the disease. This thesis has four primary aims: 1) to use magnetic resonance imaging (MRI) to identify the structural brain abnormalities present in patients suffering from their first episode of schizophrenia (FES), 2) to elucidate whether these abnormalities were static or progressive over the first 2-3 years of patients’ illness, 3) to identify the relationship between these neuroanatomical abnormalities and patients’ clinical profile, and 4) to identify the normative relationship between longitudinal changes in neuroanatomy and electrophysiology in healthy participants, and to compare this to the relationship observed between these two indices in patients with FES. The aim of Chapter 2 was to use MRI to identify the neuroanatomical changes that occur over adolescence in healthy participants, and to identify the normative relationship between the neuroanatomical changes and electrophysiological changes associated with healthy periadolescent brain maturation. MRI and electroencephalographic (EEG) scans were acquired from 138 healthy participants between the ages of 10 and 30 years. The MRI scans were segmented into grey matter (GM) and white matter (WM) images, before being parcellated into the frontal, temporal, parietal and occipital lobes. Absolute EEG power was calculated for the slow-wave, alpha and beta frequency bands, for the corresponding cortical regions. The age-related changes in regional tissue volumes and regional EEG power were inferred with a regression model. The results indicated that the healthy participants experienced accelerated GM loss, EEG power loss and WM gain in the frontal and parietal lobes between the ages of 10 and 20 years, which decelerated between the ages of 20 and 30 years. A linear relationship was also observed between the maturational changes in regional GM volumes and EEG power in the frontal and parietal lobes. These results indicate that the periadolescent period is a time of great structural and electrophysiological change in the healthy human brain. The aim of Chapter 3 was to identify the GM abnormalities present in patients with FES, both at the time of their first presentation to mental health services (baseline), and over the first 2-3 years of their illness (follow-up). MRI scans were acquired from 41 patients with FES at baseline, and 47 matched healthy control subjects. Of these participants, 25 FES patients and 26 controls returned 2-3 years later for a follow-up scan. The analysis technique of voxel-based morphometry (VBM) was used in conjunction with the Statistical Parametric Mapping (SPM) software package in order to identify the regions of GM difference between the groups at baseline. The related analysis technique of tensor-based morphometry (TBM) was used to identify subjects’ longitudinal GM change over the follow-up interval. Relative to the healthy controls, the FES patients were observed to exhibit widespread GM reductions in the frontal, parietal and temporal cortices and cerebellum at baseline, as well as more circumscribed regions of GM increase, particularly in the occipital lobe. Furthermore, the FES patients lost considerably more GM over the follow-up interval than the controls, particularly in the parietal and temporal cortices. These results indicate that patients with FES exhibit significant structural brain abnormalities very early in the course of their illness, and that these abnormalities progress over the first few years of their illness. Chapter 4 employed the same methodology to investigate the white matter abnormalities exhibited by the FES subjects relative to the controls, both at baseline and over the follow-up interval. Compared to controls, the FES patients exhibited volumetric WM deficits in the frontal and temporal lobes at baseline, as well as volumetric increases at the fronto-parietal junction bilaterally. Furthermore, the FES patients lost considerably more WM over the follow-up interval than did the controls in the middle and inferior temporal cortex bilaterally. While there is substantial evidence indicating that abnormalities in the maturational processes of myelination play a significant role in the development of WM abnormalities in FES, the observed longitudinal reductions in WM were consistent with the death of a select population of temporal lobe neurons over the follow-up interval. The aim of Chapter 5 was to investigate the clinical correlates of the GM abnormalities exhibited by the FES patients at baseline. The volumes of four distinct cerebral regions where 31 patients with FES exhibited reduced GM volumes relative to 30 matched controls were calculated and correlated with patients’ scores on three primary symptom dimensions: Disorganization, Reality Distortion and Psychomotor Poverty. The results indicated that the greater the degree of atrophy exhibited by the FES patients in three of these four ‘regions-of-reduction’, the less severe their degree of Reality Distortion. These results suggest that an excessive amount of GM atrophy may in fact preclude the formation of hallucinations or highly systematized delusions in patients with FES. The aim of Chapter 6 was to identify the relationship between the longitudinal changes in brain structure and brain electrophysiology exhibited by 19 FES patients over the first 2-3 years of their illness, and to compare it to the normative relationship between the two indices reported in Chapter 2. The methodology employed for the parcellation of the MRI and EEG data was identical to Chapter 2. The results indicated that, in contrast to the healthy controls, the longitudinal reduction in GM volume exhibited by the FES patients was not associated with a corresponding reduction in EEG power in any brain lobe. In contrast, EEG power was observed to be maintained or even to increase over the follow-up interval in these patients. These results were consistent with the FES patients experiencing an abnormal elevation of neural synchrony. Such an abnormality in neural synchrony could potentially form the basis of the dysfunctional neural connectivity that has been widely proposed to underlie the functional deficits present in patients with schizophrenia. The primary aim of Chapter 7 was to assimilate the findings from the preceding empirical chapters with the theoretical framework provided in the literature, into an integrated and testable model of schizophrenia. The model emphasized dysfunctions in brain maturation, specifically in the normative processes of synaptic ‘pruning’ and axonal myelination, as playing a key role in the development of disintegrated neural activity and the subsequent onset of schizophrenic symptoms. The model concluded with the novel proposal that disintegrated neural activity arises from abnormal elevations in the synchrony of synaptic activity in patients with first-episode schizophrenia.
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Nájera, Chávez Brenda Carolina [Verfasser]. "Sex related differences in clinical disability, MRI lesion load and atrophy of subcortical deep grey matter in patients with multiple sclerosis / Brenda Carolina Nájera Chávez." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2021. http://d-nb.info/1228859264/34.
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Batail, Jean-Marie. "Aspects cliniques et neurofonctionnels impliqués dans le cours évolutif de la dépression : l’expérience d’une cohorte en soins courants." Thesis, Rennes 1, 2018. http://www.theses.fr/2018REN1B055/document.
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Le but de ce travail est d’étudier deux dimensions sémiologiques, identifiées dans la littérature comme associées au trouble dépressif résistant, l’anxiété et l’apathie. Ces marqueurs cliniques et leurs corrélats radiologiques seront ensuite testés dans une analyse longitudinale du pronostic à 6 mois d’une cohorte de patients souffrant de dépression. Les données originales de ce travail sont issues de la cohorte LONGIDEP. Cette étude prospective, naturalistique, a été menée chez des patients souffrant d’un épisode dépressif majeur qui bénéficiaient, dans le cadre des soins courants, d’une évaluation clinique, neuropsychologique et d’une imagerie cérébrale à l’inclusion. Une nouvelle évaluation a été proposée à 6 mois de l’inclusion. Cette étude nous a permis de montrer que 1) l’apathie dans la dépression est associée à un profil clinique et physiopathologique spécifique, 2) l’analyse catégorielle et sémiologique de l’anxiété dans une population de sujet déprimés résistants n’étaient pas concordantes. Les déprimés résistants présentaient une hyperperfusion amygdale centro-médiane, 3) l’anxiété trait, un pattern cognitif associé à la mémoire visuo-spatiale étaient prédictifs d’une évolution péjorative de la dépression. Des anomalies structurales de régions impliquées dans la régulation émotionnelle et plus précisément l’adaptation au danger/peur, étaient associées à une évolution péjorative de la dépression. Des deux dimensions sémiologiques étudiées, l’anxiété apparaît être impliquées dans le pronostic de la dépression. L’étude des liens entre l’anxiété et les troubles de la motivation est une perspective de recherche pour la dépression résistanteThe aim of this work is to study anxiety and apathy in treatment resistant depression. These clinical factors and its imaging correlates will be tested in prediction of outcome in a 6-months follow-up. Original data were retrieved in LONGIDEP cohort. This is a prospective study conducted in routine care. Patients suffering from a mood depressive episode benefited from a clinical, neuropsychological and brain imaging. They were assessed once again at 6 months. Our study has shown that 1) apathy in depression is associated with specific clinical and pathophysiological patterns, 2) categorical and dimensional approach of anxiety in treatment resistant depression are not convergent. This latter population exhibited higher brain perfusion of centro-medial amygdala, 3) trait anxiety, cognitive patterns of visuospatial memory were predictive of pejorative outcome. Structural abnormalities in key regions involved in emotion regulation were associated with pejorative outcome of depression. Only anxiety was involved in outcome of depression. The link between anxiety and motivation should be studied in further works
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Pánková, Olga. "Výpočet pokročilých difusních parametrů šedé hmoty mozku z DKI MRI obrazů." Master's thesis, Vysoké učení technické v Brně. Fakulta elektrotechniky a komunikačních technologií, 2019. http://www.nusl.cz/ntk/nusl-401029.
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Thesis named Calculation of advanced diffusion parameters in brain grey matter from DKI MRI images deals with processing of diffusion-weighted images from DKI. The thesis contains review of literature on principle of diffusion, influence of diffusion on MRI, calculation of DTI and DKI parameters and clinical application of diffusion-weighted maps with focus on grey matter. The thesis focuses on software tools for processing and pre-processing DTI and DKI. The practical part consisted of two sections. Two different softwares were used to calculate maps of diffusion parameters. Diffusion parameters from anatomical structure sunstantia nigra were compared between group of healthy controls and patients with Parkinson’s disease. This comparison did not show any statisticaly significant difference. In the second step, a script for creating diffusion maps in software Diffusinal Kurtosis Estimator was made.
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Junior, Ailton Spiacci. "Envolvimento de diferentes sub-regiões do núcleo dorsal da rafe de ratos na mediação de respostas defensivas associadas à ansiedade e ao medo." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/17/17133/tde-14082013-181401/.
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O núcleo dorsal da rafe (NDR) é a principal fonte de projeções serotonérgicas que inervam o sistema límbico. Estudos mostram que o NDR é uma estrutura complexa, formada por distintas sub-regiões topograficamente organizadas e que apresentam diferentes propriedades neuroquímicas e funcionais. Tem sido proposto que duas vias serotonérgicas oriundas do NDR, o trato prosencefálico e o trato periventricular, modulam diferentemente a expressão de comportamentos defensivos associados aos transtornos de ansiedade generalizada e de pânico. O presente trabalho investigou se as respostas defensivas de esquiva e de fuga evocadas no modelo do labirinto em T elevado (LTE), relacionadas à ansiedade generalizada e ao pânico, respectivamente, recrutam diferentes sub-regiões do NDR. Na primeira etapa do trabalho, usando a técnica de imunoistoquímica para detecção da proteína Fos e da enzima triptofano hidroxilase, avaliamos a expressão da proteína Fos por neurônios serotonérgicos e não-serotonérgicos em diferentes sub-regiões do NDR, bem como em estruturas mesencefálicas vizinhas ao NDR, ou seja, o núcleo mediano da rafe (NMR) e substância cinzenta periaquedutal (SCP) de ratos em decorrência da expressão dos comportamento de esquiva inibitória ou fuga no LTE. Nossos resultados mostraram que os comportamentos de fuga e de esquiva evocados no LTE recrutam distintas populações neuronais do NDR, do NMR, bem como da SCP. Enquanto neurônios serotonérgicos localizados no nível médio e caudal do NDR, mais precisamente, nas sub-regiões dorsal (DRD), caudal (DRC) e interfascicular (DRI), bem como do NMR, estão envolvidos com a aquisição do comportamento de esquiva inibitória, neurônios não serotonérgicos das asas laterais do NDR/SCP ventrolateral, bem como das colunas, dorsomedial e dorsolateral da SCP participam da expressão da fuga. Na segunda parte deste trabalho, avaliamos os efeitos da administração do agonista de receptores AMPA/cainato, ácido caínico, no DRD, DRC e asas laterais do NDR sobre os comportamentos defensivos avaliados no LTE. Os resultados mostraram que a injeção de ácido caínico, tanto no DRD, quanto no DRC, facilita a aquisição da esquiva inibitória e também prejudica a expressão do comportamento de fuga. Já, a estimulação das asas laterais do NDR com ácido caínico induz a expressão do comportamento de fuga, sem alterar o comportamento de esquiva. Efeito oposto sobre o comportamento de fuga foi observado com a administração nesta região de cloreto de cobalto, um inibidor da transmissão sináptica. Nossos resultados mostraram ainda que a administração de ácido caínico nas asas laterais aumenta a distância percorrida pelos animais em uma arena circular, resultado indicativo da evocação da resposta de fuga. Por fim, avaliamos a o envolvimento da neurotransmissão mediada por receptores GABAA e por receptores CRF1 nas asas laterais do NDR, na expressão do comportamento de fuga expressa no LTE. Os resultados mostram que o bloqueio dos receptores GABAA nas asas laterais facilitou a expressão da fuga. Por outro lado a administração de antalarmina, antagonista de receptores CRF1 não alterou a expressão da resposta de fuga, porém prejudicou a aquisição da esquiva inibitória. Em conjunto, os resultados da primeira etapa indicam o envolvimento de diferentes sub-populações neuronais do NDR na expressão dos comportamentos de esquiva e fuga avaliados no LTE. Nossos resultados também apontam o envolvimento de neurônios serotonérgicos do NMR na expressão da esquiva inibitória, bem como a participação da SCP na resposta de fuga. Os resultados da segunda etapa indicam que neurônios serotonérgicos localizados no DRD e DRC possam dar origem aos tratos prosencefálico e periventricular abordados pela teoria de Deakin & Graeff (1991). Embora as asas laterais do NDR estejam marcantemente envolvidas na expressão/regulação da resposta de fuga, populações neuronais específicas dessa região também estão envolvidas na modulação do comportamento de esquiva inibitória.The dorsal raphe nucleus (DRN) is the main source of serotonergic projections that innervate the limbic system. A wealth of evidence indicates that the DRN is a complex structure composed by topographically organized sub-regions with distinct functional and neurochemical properties. It have been proposed that two serotonergic pathways originating in the DRN, the forebrain and periventricular tracts, distinctly modulate defensive behaviors associated with generalized anxiety disorder and panic disorder. The present study addressed the hypothesis that the two defensive responses evoked by the elevated T maze (ETM), i.e. escape and inhibitory avoidance which have been related to generalized anxiety and panic disorders, respectively, would recruit different subregions of the DRN. In the first part of this work, the number of doubly-immunostained cells for Fos protein and tryptophan hydroxylase, a marker of serotonergic neurons, was assessed within the rat DRN, median raphe nucleus (MRN) and PAG following inhibitory avoidance and escape performance in the ETM. Our results showed that these two defensive responses recruited distinct neuronal populations within the DRN, MRN and PAG. While serotonergic neurons located at the middle and caudal level of the DRN, specifically within the sub-regions dorsal (DRD), caudal (DRC) and interfascicular (DRI), and the MRN are implicated in the acquistion of inhibitory avoidance, nonserotonergic neurons in lateral wings (lwDR) of the DRN /ventrolateralPAG and the dorsal columns of PAG are implicated in the escape expression. In the second part of this study, we evaluated the effects caused by the administration of AMPA/kainate receptor agonist, kainic acid, into the DRD, DRC and lwDR of rats tested in the ETM. The results showed that injection of kainic acid into DRD and DRC facilitated inhibitory avoidance acquisition and impaired escape expression. On the other hand, stimulation of the lwDR by kainic acid facilitated escape expression, without interfering with inhibitory avoidance acquisition. Opposite effect on escape behavior was observed in this region followed injection of cobalt chloride, a synaptic transmission inhibitor. Our results also showed that administration of higher doses of kainic acid into the lwDR promptly evoked a vigorous escape reaction in animals tested in a circular arena. Finally, we evaluated the involvement of GABAA and CRF1 receptor-mediated neurotransmission in the lwDR in the regulation of the escape behavior measured by the ETM. Our results showed that the GABAA receptor antagonist bicuculine injected into the lwDR favored escape expression, without affecting inhibitory avoidance acquisition. On the other hand, local microinjection of the CRF1 receptor antagonist antalarmin impaired the acquisition of inhibitory avoidance, without changing escape expression. Together, our immunohistochemical results indicate the involvement of distinct DRN neuronal subpopulations in the regulation of escape and inhibitory avoidance responses. Our results also suggested that, while serotonergic neurons within the DRD, DRC, DRI and MRN are involved in inhibitory avoidance acquisition, non-serotonergic neurons of the vlPAG, dlPAG and dmPAG are involved in escape expression. The behavioral results with kainic acid indicated that the DRC and DRD may be the origin of the forebrain and periventricular tracts addressed by Deakin & Graeffs theory (1991). Although the lwDR are markedly implicated in escape regulation, specific neuronal populations within this region may also modulate inhibitory avoidance behavior.
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Giles, Sarah Elizabeth Tally. "Gray Matters: Aging in the Age of #grannyhair." Thesis, Virginia Tech, 2017. http://hdl.handle.net/10919/77878.
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Drawing on previous literature in cultural gerontology, ageism and age relations, and cultural appropriation this study analyzes the recent grannyhair trend on instagram. Recently, younger women have been coloring their hair combinations of white, silver, and gray and posting images of their style on instagram with the #grannyhair designation. In this study we use an intersectional approach to age and gender relations to explore this phenomenon. Previous studies show that women's behaviors and presentations of aging are policed by cultural standards of age-appropriate appearance and performance, particularly in regards to their hair. Qualitative content analysis of #grannyhair images are examined to assess the extent of age-based stereotypes and policing of age-appropriate behavior and appearance. This study found that instagram users engaged in this trend did not challenge age relations. Rather, boundaries of age-appropriate behaviors enacted in the #grannyhair trend are largely set by younger users. The ways in which young users utilize ageist stereotypes as a way to emphasize the contrast between their stylistic choices and their status as young attractive women framed the #grannyhair trend as one of appropriation. That is, young women adopted gray, white, and silver hair as a cultural symbol and changed its original meaning as a marker of old age. Conversations among both young and old instagram users echoing previous literature that details the contentious relationships old women have with their aging bodies, and hair specifically.Master of Science
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Yokoyama, Naoto. "Additive Effect of Cigarette Smoking on Gray Matter Abnormalities in Schizophrenia." Kyoto University, 2018. http://hdl.handle.net/2433/231006.
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Fukutomi, Hikaru. "Neurite imaging reveals microstructural variations in human cerebral cortical gray matter." Kyoto University, 2020. http://hdl.handle.net/2433/253174.
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Kato, Tadatsugu. "Neurocognitive impairment and gray matter volume reduction in HIV-infected patients." Kyoto University, 2020. http://hdl.handle.net/2433/258976.
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Nakamura, Kunio. "MRI Analysis to Detect Gray Matter Tissue Loss in Multiple Sclerosis." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1309874290.
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Uwatoko, Teruhisa. "Insular Gray Matter Volume and Objective Quality of Life in Schizophrenia." Kyoto University, 2019. http://hdl.handle.net/2433/242345.
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Fujiwara, Hironobu. "Anterior cingulate pathology and social cognition in schizophrenia: a study of gray matter, white matter and sulcal morphometry." Kyoto University, 2009. http://hdl.handle.net/2433/124279.
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