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Cortical Gray Matter (cortical + gray_matter)

Distribution by Scientific Domains
Medical Sciences75%

Selected Abstracts

Neuroimaging of cortical development and brain connectivity in human newborns and animal models

JOURNAL OF ANATOMY, Issue 4 2010
Gregory A. Lodygensky
Abstract Significant human brain growth occurs during the third trimester, with a doubling of whole brain volume and a fourfold increase of cortical gray matter volume. This is also the time period during which cortical folding and gyrification take place. Conditions such as intrauterine growth restriction, prematurity and cerebral white matter injury have been shown to affect brain growth including specific structures such as the hippocampus, with subsequent potentially permanent functional consequences. The use of 3D magnetic resonance imaging (MRI) and dedicated postprocessing tools to measure brain tissue volumes (cerebral cortical gray matter, white matter), surface and sulcation index can elucidate phenotypes associated with early behavior development. The use of diffusion tensor imaging can further help in assessing microstructural changes within the cerebral white matter and the establishment of brain connectivity. Finally, the use of functional MRI and resting-state functional MRI connectivity allows exploration of the impact of adverse conditions on functional brain connectivity in vivo. Results from studies using these methods have for the first time illustrated the structural impact of antenatal conditions and neonatal intensive care on the functional brain deficits observed after premature birth. In order to study the pathophysiology of these adverse conditions, MRI has also been used in conjunction with histology in animal models of injury in the immature brain. Understanding the histological substrate of brain injury seen on MRI provides new insights into the immature brain, mechanisms of injury and their imaging phenotype. [source]

Frequent Hemorrhagic Lesions in Cerebral Toxoplasmosis in AIDS Patients

JOURNAL OF NEUROIMAGING, Issue 2 2009
Satyakam Bhagavati MD
ABSTRACT Cerebral toxoplasmosis is a frequent complication in immunosuppressed patients such as AIDS (acquired immunodeficiency syndrome). Frequently, lesions are located deep in the brain which are inaccessible for biopsy making rapid diagnosis dependent on accurate interpretation of neuroimaging findings. The commonest cranial CT findings reported in toxoplasmosis are ring enhancing hypodense lesions in basal ganglia or cortical gray matter. Hemorrhage has only rarely been described and is usually seen following antitoxoplasma treatment. We reviewed the records of 11 AIDS patients with cerebral toxoplasmosis and found multiple hemorrhagic cerebral, cerebellar, or brain stem lesions in 7 of 11 patients. Six patients had hemorrhage at the time of initial clinical presentation and one developed hemorrhage following 2 weeks of antitoxoplasma treatment. We conclude that hemorrhagic lesions are frequently found on cranial MRI scans in cerebral toxoplasmosis. AIDS patients presenting with hemorrhagic cerebral lesions should be considered for a trial of presumptive antitoxoplasma treatment. [source]

Conventional DTI vs. slow and fast diffusion tensors in cat visual cortex

MAGNETIC RESONANCE IN MEDICINE, Issue 5 2003
Itamar Ronen
Abstract Diffusion tensor imaging (DTI) uses water diffusion anisotropy in axonal fibers to provide a tool for analyzing and tracking those fibers in brain white matter. In the present work, multidirectional diffusion MRI data were collected from a cat brain and decomposed into slow and fast diffusion tensors and directly compared with conventional DTI data from the same imaging slice. The fractional anisotropy of the slow diffusing component (Dslow) was significantly higher than the anisotropy measured by conventional DTI while reflecting a similar directionality and appeared to account for most of the anisotropy observed in gray matter, where the fiber density is notoriously low. Preliminary results of fiber tracking based on the slow diffusion component are shown. Fibers generated based on the slow diffusion component appear to follow the vertical fibers in gray matter. DslowTI may provide a way for increasing the sensitivity to anisotropic structures in cortical gray matter. Magn Reson Med 49:785,790, 2003. © 2003 Wiley-Liss, Inc. [source]

Xenon enhances hypothermic neuroprotection in asphyxiated newborn pigs

ANNALS OF NEUROLOGY, Issue 3 2010
Elavazhagan Chakkarapani MBBS
Objective To investigate whether inhaling 50% xenon during hypothermia (HT) offers better neuroprotection than xenon or HT alone. Methods Ninety-eight newborn pigs underwent a 45-minute global hypoxic-ischemic insult severe enough to cause permanent brain injury, and 12 pigs underwent sham protocol. Pigs then received intravenous anesthesia and were randomized to 6 treatment groups: (1) normothermia (NT; rectal temperature 38.5°C, n = 18); (2) 18 hours 50% xenon with NT (n = 12); (3) 12 hours HT (rectal temperature 33.5°C, n = 18); (4) 24 hours HT (rectal temperature 33.5°C, n = 17); (5) 18 hours 50% xenon with 12 hours HT (n = 18); and (6) 18 hours 50% xenon with 24 hours HT (n = 17). Fifty percent xenon was administered via a closed circle with 30% oxygen and 20% nitrogen. After 10 hours rewarming, cooled pigs remained normothermic until terminal perfusion fixation at 72 hours. Global and regional brain neuropathology and clinical neurological scores were performed. Results Xenon (p = 0.011) and 12 or 24 hours HT (p = 0.003) treatments offered significant histological global, and regional neuroprotection. Combining xenon with HT yielded an additive neuroprotective effect, as there was no interaction effect (p = 0.54). Combining Xenon with 24 hours HT offered 75% global histological neuroprotection with similarly improved regional neuroprotection: thalamus (100%), brainstem (100%), white matter (86%), basal ganglia (76%), cortical gray matter (74%), cerebellum (73%), and hippocampus (72%). Neurology scores improved in the 24-hour HT and combined xenon HT groups at 72 hours. Interpretation Combining xenon with HT is a promising therapy for severely encephalopathic infants, doubling the neuroprotection offered by HT alone. ANN NEUROL 2010 [source]