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Postmortem Studies (postmortem + studies)
Selected AbstractsAsynchrony of the early maturation of white matter bundles in healthy infants: Quantitative landmarks revealed noninvasively by diffusion tensor imagingHUMAN BRAIN MAPPING, Issue 1 2008Jessica Dubois Abstract Normal cognitive development in infants follows a well-known temporal sequence, which is assumed to be correlated with the structural maturation of underlying functional networks. Postmortem studies and, more recently, structural MR imaging studies have described qualitatively the heterogeneous spatiotemporal progression of white matter myelination. However, in vivo quantification of the maturation phases of fiber bundles is still lacking. We used noninvasive diffusion tensor MR imaging and tractography in twenty-three 1,4-month-old healthy infants to quantify the early maturation of the main cerebral fascicles. A specific maturation model, based on the respective roles of different maturational processes on the diffusion phenomena, was designed to highlight asynchronous maturation across bundles by evaluating the time-course of mean diffusivity and anisotropy changes over the considered developmental period. Using an original approach, a progression of maturation in four relative stages was determined in each tract by estimating the maturation state and speed, from the diffusion indices over the infants group compared with an adults group on one hand, and in each tract compared with the average over bundles on the other hand. Results were coherent with, and extended previous findings in 8 of 11 bundles, showing the anterior limb of the internal capsule and cingulum as the most immature, followed by the optic radiations, arcuate and inferior longitudinal fascicles, then the spinothalamic tract and fornix, and finally the corticospinal tract as the most mature bundle. Thus, this approach provides new quantitative landmarks for further noninvasive research on brain-behavior relationships during normal and abnormal development. Hum Brain Mapp, 2008. © 2007 Wiley-Liss, Inc. [source] The pathogenesis of cell death in Parkinson's disease , 2007MOVEMENT DISORDERS, Issue S17 2007C. Warren Olanow MD Abstract A number of factors have been implicated in the pathogenesis of cell death in Parkinson's disease (PD). These include oxidative stress, mitochondrial dysfunction, inflammation, excitotoxicity, and apoptosis. While the precise pathogenic mechanism leading to neurodegeneration in PD is not known, there is considerable evidence suggesting that cell death occurs by way of a signal-mediated apoptotic process. PD is also characterized by intracellular proteinaceous inclusions or Lewy bodies. Proteolytic stress arises as a consequence of the excessive production of misfolded proteins, which exceed the capacity of the ubiquitin-proteasome system to degrade them. Recent genetic and laboratory studies support the possible relevance of proteolytic stress to both familial and sporadic forms of PD. Postmortem studies have shown that in the SNc of sporadic PD patients there are reduced levels of the alpha subunit of the 20S proteasome and reduced proteolytic enzyme activities. A determination as to the precise cause of cell death in PD, and the identification of specific targets for the development of drugs that might modify disease progression is one of the most critical goals in PD research. It is anticipated that over the next few years there will be a flurry of scientific activity examining the mechanism of cell death and putative neuroprotective interventions. © 2007 Movement Disorder Society [source] Cerebellar metabolic symmetry in essential tremor studied with 1H magnetic resonance spectroscopic imaging: Implications for disease pathologyMOVEMENT DISORDERS, Issue 6 2004Elan D. Louis MD Abstract The pathological basis for essential tremor (ET) is not known; however, metabolic changes in the cerebellum can be observed in positron emission tomography (PET) and 1H magnetic resonance spectroscopic imaging (MRSI) studies. Tremor is relatively symmetric in ET, suggesting that underlying metabolic changes could be also symmetric. The degree of metabolic asymmetry in the cerebellum, however, has not yet been studied in ET, and knowledge about distribution and laterality of metabolic changes might shed some light on basic disease mechanisms. We measured brain metabolism (N -acetylaspartate[NAA]/creatine [tCR]) to obtain an asymmetry index for cerebellar cortical metabolism ET patients compared with that in controls. This index, a percentage, was calculated as |(value right , value left)|/(value right + value left) × 100. Multislice 1H MRSI data were acquired for 20 patients and 11 controls. In ET patients, mean right and left cerebellar cortical NAA/tCR values were 1.61 ± 0.42 and 1.55 ± 0.38, respectively, compared with 1.81 ± 0.62 and 1.87 ± 0.49 in controls. The difference between right and left cerebellar cortical NAA/tCR was also calculated for each subject. In ET patients, the mean right-left difference was 0.14 ± 0.11, compared with 0.32 ± 0.27 in controls (P = 0.016). The mean cerebellar cortical asymmetry index was low in ET (8.8 ± 6.1%), one-half of that in controls (17.0 ± 13.7%, P = 0.027). These data suggest that pathological lesions in ET patients, which remain elusive, might be distributed similarly in each cerebellar cortex. Postmortem studies are needed to confirm these preliminary imaging results. © 2004 Movement Disorder Society [source] Schizophrenia; from structure to function with special focus on the mediodorsal thalamic prefrontal loopACTA PSYCHIATRICA SCANDINAVICA, Issue 5 2009B. Pakkenberg Objective:, To describe structural and biochemical evidence from postmortem brains that implicates the reciprocal connections between the mediodorsal thalamic nucleus and the prefrontal cortex in cognitive symptoms of schizophrenia. Method:, The estimation of the regional volumes and cell numbers was obtained using stereological methods. The biochemical analyses of molecular expression in postmortem brain involve quantitative measurement of transcripts and proteins by in-situ (RNA) or Western blot/autoradiography in brains from patients with schizophrenia and comparison subjects. Results:, Stereological studies in postmortem brain from patients with schizophrenia have reported divergent and often opposing findings in the total number of neurons and volume of the mediodorsal (MD) thalamic nucleus, and to a lesser degree in its reciprocally associated areas of the prefrontal cortex. Similarly, quantitative molecular postmortem studies have found large inter-subject and between-study variance at both the transcript and protein levels for receptors and their interacting molecules of several neurotransmitter systems in these interconnected anatomical regions. Combined, large variation in stereological and molecular studies indicates a complex and heterogeneous involvement of the MD thalamic-prefrontal loop in schizophrenia. Conclusion:, Based on a considerable heterogeneity in patients suffering from schizophrenia, large variation in postmortem studies, including stereological and molecular postmortem studies of the MD thalamus and frontal cortex, might be expected and may in fact partly help to explain the variable endophenotypic traits associated with this severe psychiatric illness. [source] GluR5,6,7 subunit immunoreactivity on apical pyramidal cell dendrites in hippocampus of schizophrenics and manic depressivesHIPPOCAMPUS, Issue 5 2001Francine M. Benes Abstract Recent postmortem studies have suggested that changes in the regulation of kainate-sensitive glutamate receptors (kainate receptors) in the hippocampus may play a role in schizophrenia. To explore this possibility further, the distribution of immunoreactivity (IR) for the GluR5,6,7 subunits of the KR was assessed in a cohort consisting of 15 normal controls, 15 schizophrenics, and 9 manic depressives matched for age and postmortem interval (PMI). Cross sections of hippocampus showed abundant GluR5,6,7 -IR on apical dendrites of pyramidal neurons in the stratum radiatum and stratum moleculare. In normal controls, both the numerical and length density of IR dendrites were much higher in sector CA2 than in sectors CA3 or CA1. When data for the individual groups were separately examined, the schizophrenics showed a 30,35% reduction in the density of GluR5,6,7 -IR dendrites found in both stratum radiatum and stratum moleculare of sectors CA3 and CA2, as well as proximal and middle portions of CA1. In CA2, the magnitude of this decrease in schizophrenia was 2.5 times larger than that seen in any of the other sectors. For the manic depressive group, no significant differences were observed in any sectors or laminae examined. The potential confounding effects of either age, PMI, or neuroleptic exposure do not explain the reduced density of IR dendrites detected in the schizophrenic group. Taken together, the preferential reduction of GluR5,6,7 -IR observed on apical dendrites of pyramidal neurons is consistent with a functional downregulation of the kainate receptor in the hippocampus of schizophrenic brain. Hippocampus 2001;11:482,491. © 2001 Wiley-Liss, Inc. [source] Essential tremor , Neurodegenerative or nondegenerative disease towards a working definition of ET,MOVEMENT DISORDERS, Issue 14 2009Günther Deuschl MD Abstract Essential tremor (ET) is a syndrome of tremor in posture and movement, but recent studies have revealed additional cerebellar motor disturbances, cognitive disturbances, personality changes, hearing loss, and olfactory deficits. Even dementia and shortened life expectancy were found in one cohort. Recent postmortem studies have found limited Lewy body pathology in some patients and Purkinje cell loss with torpedoes and Bergmann gliosis in others. These findings have led to the hypothesis that ET is a syndrome produced by at least two neurodegenerative diseases with more widespread clinical consequences than previously appreciated. We review the evidence for and against this hypothesis and conclude that studies purporting to support this hypothesis have failed to control for age-associated comorbidities, depression, medications, and other confounding factors. We propose the alternative hypothesis that abnormal neuronal oscillation is the fundamental abnormality in ET, and the well-documented cerebellar signs and symptoms, the controversial non-motor signs, and even the cerebellar pathology of ET could be caused by this oscillation. A major problem for many studies is the lack of a diagnostic gold standard. Lacking such a standard, we propose a subclassification of ET into three categories: hereditary ET, sporadic ET, and senile ET, which we believe will help researchers resolve many of the controversies in this field. © 2009 Movement Disorder Society [source] Consideration of the Impact of Reperfusion Therapy on the Quantitative Relationship between the Selvester QRS Score and Infarct Size by Cardiac MRIANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2010Stephanie A. M. Knippenberg M.D. Background: It has previously been shown that there is a good agreement between the Selvester QRS score and myocardial infarct (MI) size determined by postmortem histopathology in patients with nonreperfused MI. Currently, however, most patients with acute coronary thrombosis receive reperfusion therapy. Therefore, the aim of this study was to test the hypothesis that early reperfusion alters the quantitative relationship between Selvester QRS score and MI size. Methods: Twenty-seven patients with acute first-time reperfused MI were studied. Infarct size was determined by delayed contrast-enhanced magnetic resonance imaging (DE-MRI) and estimated with the 50-criteria/31-point Selvester QRS scoring system 1 week after admission. The findings in the present study were compared with previous postmortem studies exploring the quantitative relationship between Selvester QRS score and MI size in nonreperfused patients. Results: The quantitative relationship between QRS score and MI size by DE-MRI in the present study of early reperfused MI was significantly different from previous postmortem histopathology studies of nonreperfused MI (P < 0.0001). In the present study, each QRS point represented approximately 2% of the left ventricle, compared to approximately 3% in previous postmortem histopathology studies of nonreperfused MI. When only considering small to moderate MI sizes, there was no significant difference in the quantitative relationship between QRS score and infarct size (P > 0.05). Conclusions: There is a different quantitative relationship between QRS score and MI size in early reperfused MI compared to nonreperfused MI, partly explained by differences in MI size. Thus, the Selvester QRS scoring system may not be linearly related to MI size. Ann Noninvasive Electrocardiol 2010;15(3):238,244 [source] | |||||||||||||