293 research outputs found

    Adaptive Bayesian Iterative Transmission Reconstruction for Attenuation Correction in Myocardial Perfusion Imaging with SPECT/Slow-Rotation Low-Output CT Systems

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    Objectives. SPECT/slow-rotation low-output CT systems can produce streak artifacts in filtered backprojection (FBP) attenuation maps, impacting attenuation correction (AC) in myocardial perfusion imaging. This paper presents an adaptive Bayesian iterative transmission reconstruction (ABITR) algorithm for more accurate AC. Methods. In each iteration, ABITR calculated a three-dimensional prior containing the pixels with attenuation coefficients similar to water, then used it to encourage these pixels to the water value. ABITR was tested with a cardiac phantom and 4 normal patients acquired by a GE Millennium VG/Hawkeye system. Results. FBP AC and ABITR AC produced similar phantom results. For the patients, streak artifacts were observed in the FBP and ordered-subsets expectation-maximization (OSEM) maps but not in the ABITR maps, and ABITR AC produced more uniform images than FBP AC and OSEM AC. Conclusion. ABITR can improve the quality of the attenuation map, producing more uniform images for normal studies

    Two systems for empathy: a double dissociation between emotional and cognitive empathy in inferior frontal gyrus versus ventromedial prefrontal lesions

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    Recent evidence suggests that there are two possible systems for empathy: a basic emotional contagion system and a more advanced cognitive perspective-taking system. However, it is not clear whether these two systems are part of a single interacting empathy system or whether they are independent. Additionally, the neuroanatomical bases of these systems are largely unknown. In this study, we tested the hypothesis that emotional empathic abilities (involving the mirror neuron system) are distinct from those related to cognitive empathy and that the two depend on separate anatomical substrates. Subjects with lesions in the ventromedial prefrontal (VM) or inferior frontal gyrus (IFG) cortices and two control groups were assessed with measures of empathy that incorporate both cognitive and affective dimensions. The findings reveal a remarkable behavioural and anatomic double dissociation between deficits in cognitive empathy (VM) and emotional empathy (IFG). Furthermore, precise anatomical mapping of lesions revealed Brodmann area 44 to be critical for emotional empathy while areas 11 and 10 were found necessary for cognitive empathy. These findings are consistent with these cortices being different in terms of synaptic hierarchy and phylogenetic age. The pattern of empathy deficits among patients with VM and IFG lesions represents a first direct evidence of a double dissociation between emotional and cognitive empathy using the lesion method. Keywords: Emotional empathy; cognitive empathy; mirror neurons; inferior frontal gyrus; ventromedial prefrontal cortex Abbreviations: ANOVA = analysis of variance; BA = Brodmann area; EC = empathic concern scale; FS = fantasy scale; HC = healthy control; IFG = inferior frontal gyrus; IRI = Interpersonal Reactivity Index; MNS = mirror neuron system; PC = posterior lesion; PD = personal distress scale; PT = perspective-taking scale; ToM = Theory of Mind; VM = ventromedial prefrontal; WCST = Wisconsin Card Sorting Test

    Neuropsychiatric manifestation of confusional psychosis due to Cryptococcus neoformans var. grubii in an apparently immunocompetent host: a case report

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    Cognitive disorders like dementia, delirium, depression, anxiety, psychosis and mania are the commonest neuropsychiatric manifestations. We discuss here a case of an adult women presenting with neuropsychiatric manifestations of confusional psychosis owing to Cryptococcosis. The principal cause was consequently established by culturing Cryptococcus neoformans from the cerebrospinal fluid confirmed as C. neoformans var. grubii (Serotype A) by genotypic methods. Antifungal therapy with IV Amphotericin B lead to sustained improvement and recovery of the patient from behavioural disorders. The case discussed here invokes the need for the vigilance it demands in delineating organic brain syndromes for a favourable treatment outcome

    Temporal dysfunction in traumatic brain injury patients : primary or secondary impairment?

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    Adequate temporal abilities are required for most daily activities. Traumatic brain injury (TBI) patients often present with cognitive dysfunctions, but few studies have investigated temporal impairments associated with TBI. The aim of the present work is to review the existing literature on temporal abilities in TBI patients. Particular attention is given to the involvement of higher cognitive processes in temporal processing in order to determine if any temporal dysfunction observed in TBI patients is due to the disruption of an internal clock or to the dysfunction of general cognitive processes. The results showed that temporal dysfunctions in TBI patients are related to the deficits in cognitive functions involved in temporal processing rather than to a specific impairment of the internal clock. In fact, temporal dysfunctions are observed when the length of temporal intervals exceeds the working memory span or when the temporal tasks require high cognitive functions to be performed. The consistent higher temporal variability observed in TBI patients is a sign of impaired frontally mediated cognitive functions involved in time perception. -- Keywords : traumatic brain injury, time perception, time reproduction, time production, time discrimination, executive function

    Is sleep disruption a risk factor for Alzheimerā€™s disease?

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    Sleep disturbances are routinely encountered in Alzheimerā€™s disease (AD) and affect about 25ā€“40% of patients in the mild-to-moderate stages of the disease. In many, sleep pathology may represent a symptom of the underlying neurodegeneration. However, a history of sleep disruption occurring years prior to onset of cognitive symptoms could represent a potential risk factor for AD. The aim of the present narrative review was to evaluate current evidence linking sleep disturbances with AD development and to understand the mechanisms that may contribute to this. Although the mechanisms by which poor sleep may contribute to AD genesis is not fully understood, emerging evidence linking disturbances in the sleep wake cycle with AĪ² deposition is shedding light on the relationship between sleep pathology and the subsequent development of AD. AĪ² burden appears to be enhanced by sleep-wake cycle disruptions and is suspected as being an important mechanism by which sleep disruptions contribute in AD development. Other mechanisms triggered by sleep disruption may also be involved in AD development, such as brain hypoxia, oxidative stress, circadian activity rhythms disturbances, overexpression of orexins, and blood-brain barrier impairment. Further understanding of the link between sleep disturbances and future development of AD is still needed before sleep disturbances are clearly marked as a preventable risk factor for AD. In these circumstances, early lifestyle interventions to help increase the quantity and quality of sleep may have a favorable outcome on decreasing the incidence of AD and this needs to be investigated further

    A clinical evaluation of an ex vivo organ culture system to predict patient response to cancer therapy

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    IntroductionEx vivo organ cultures (EVOC) were recently optimized to sustain cancer tissue for 5ā€‰days with its complete microenvironment. We examined the ability of an EVOC platform to predict patient response to cancer therapy.MethodsA multicenter, prospective, single-arm observational trial. Samples were obtained from patients with newly diagnosed bladder cancer who underwent transurethral resection of bladder tumor and from core needle biopsies of patients with metastatic cancer. The tumors were cut into 250ā€‰Ī¼M slices and cultured within 24ā€‰h, then incubated for 96ā€‰h with vehicle or intended to treat drug. The cultures were then fixed and stained to analyze their morphology and cell viability. Each EVOC was given a score based on cell viability, level of damage, and Ki67 proliferation, and the scores were correlated with the patientsā€™ clinical response assessed by pathology or Response Evaluation Criteria in Solid Tumors (RECIST).ResultsThe cancer tissue and microenvironment, including endothelial and immune cells, were preserved at high viability with continued cell division for 5ā€‰days, demonstrating active cell signaling dynamics. A total of 34 cancer samples were tested by the platform and were correlated with clinical results. A higher EVOC score was correlated with better clinical response. The EVOC system showed a predictive specificity of 77.7% (7/9, 95% CI 0.4ā€“0.97) and a sensitivity of 96% (24/25, 95% CI 0.80ā€“0.99).ConclusionEVOC cultured for 5ā€‰days showed high sensitivity and specificity for predicting clinical response to therapy among patients with muscle-invasive bladder cancer and other solid tumors

    Lipid Classes and Fatty Acid Patterns are Altered in the Brain of Ī³-Synuclein Null Mutant Mice

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    The well-documented link between Ī±-synuclein and the pathology of common human neurodegenerative diseases has increased attention to the synuclein protein family. The involvement of Ī±-synuclein in lipid metabolism in both normal and diseased nervous system has been shown by many research groups. However, the possible involvement of Ī³-synuclein, a closely-related member of the synuclein family, in these processes has hardly been addressed. In this study, the effect of Ī³-synuclein deficiency on the lipid composition and fatty acid patterns of individual lipids from two brain regions has been studied using a mouse model. The level of phosphatidylserine (PtdSer) was increased in the midbrain whereas no changes in the relative proportions of membrane polar lipids were observed in the cortex of Ī³-synuclein-deficient compared to wild-type (WT) mice. In addition, higher levels of docosahexaenoic acid were found in PtdSer and phosphatidylethanolamine (PtdEtn) from the cerebral cortex of Ī³-synuclein null mutant mice. These findings show that Ī³-synuclein deficiency leads to alterations in the lipid profile in brain tissues and suggest that this protein, like Ī±-synuclein, might affect neuronal function via modulation of lipid metabolism

    Consensus classification of posterior cortical atrophy

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    INTRODUCTION: A classification framework for posterior cortical atrophy (PCA) is proposed to improve the uniformity of definition of the syndrome in a variety of research settings. METHODS: Consensus statements about PCA were developed through a detailed literature review, the formation of an international multidisciplinary working party which convened on four occasions, and a Web-based quantitative survey regarding symptom frequency and the conceptualization of PCA. RESULTS: A three-level classification framework for PCA is described comprising both syndrome- and disease-level descriptions. Classification level 1 (PCA) defines the core clinical, cognitive, and neuroimaging features and exclusion criteria of the clinico-radiological syndrome. Classification level 2 (PCA-pure, PCA-plus) establishes whether, in addition to the core PCA syndrome, the core features of any other neurodegenerative syndromes are present. Classification level 3 (PCA attributable to AD [PCA-AD], Lewy body disease [PCA-LBD], corticobasal degeneration [PCA-CBD], prion disease [PCA-prion]) provides a more formal determination of the underlying cause of the PCA syndrome, based on available pathophysiological biomarker evidence. The issue of additional syndrome-level descriptors is discussed in relation to the challenges of defining stages of syndrome severity and characterizing phenotypic heterogeneity within the PCA spectrum. DISCUSSION: There was strong agreement regarding the definition of the core clinico-radiological syndrome, meaning that the current consensus statement should be regarded as a refinement, development, and extension of previous single-center PCA criteria rather than any wholesale alteration or redescription of the syndrome. The framework and terminology may facilitate the interpretation of research data across studies, be applicable across a broad range of research scenarios (e.g., behavioral interventions, pharmacological trials), and provide a foundation for future collaborative work
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