NeuroImage. Clinical
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NeuroImage. Clinical · Jan 2014
Comparative StudyMeasurement of brain perfusion in newborns: pulsed arterial spin labeling (PASL) versus pseudo-continuous arterial spin labeling (pCASL).
Arterial spin labeling (ASL) perfusion-weighted imaging (PWI) by magnetic resonance imaging (MRI) has been shown to be useful for identifying asphyxiated newborns at risk of developing brain injury, whether or not therapeutic hypothermia was administered. However, this technique has been only rarely used in newborns until now, because of the challenges to obtain sufficient signal-to-noise ratio (SNR) and spatial resolution in newborns. ⋯ This study demonstrates that both ASL methods are feasible to assess brain perfusion in healthy and sick newborns. However, pCASL might be a better choice over PASL in newborns, as pCASL perfusion maps had a superior image quality that allowed a more detailed identification of the different brain structures.
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NeuroImage. Clinical · Jan 2014
Accurate GM atrophy quantification in MS using lesion-filling with co-registered 2D lesion masks.
In multiple sclerosis (MS), brain atrophy quantification is affected by white matter lesions. LEAP and FSL-lesion_filling, replace lesion voxels with white matter intensities; however, they require precise lesion identification on 3DT1-images. ⋯ These results demonstrate that for global GM volumetry, precise lesion masks on 3DT1 images can be replaced by co-registered 2DT2 lesion masks. This makes lesion-filling a feasible method for GM atrophy measurements in MS.
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NeuroImage. Clinical · Jan 2014
Anatomical and diffusion MRI of deep gray matter in pediatric spina bifida.
Individuals with spina bifida myelomeningocele (SBM) exhibit brain abnormalities in cortical thickness, white matter integrity, and cerebellar structure. Little is known about deep gray matter macro- and microstructure in this population. The current study utilized volumetric and diffusion-weighted MRI techniques to examine gray matter volume and microstructure in several subcortical structures: basal ganglia nuclei, thalamus, hippocampus, and amygdala. ⋯ These results provide further support that SBM differentially disrupts brain regions whereby some structures are volumetrically normal whereas others are reduced or enlarged. In the hippocampus, volumetric reduction coupled with increased MD may imply reduced cellular density and aberrant organization. Alternatively, the enlarged volume and significantly reduced MD in the putamen suggest increased density.
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NeuroImage. Clinical · Jan 2014
Voxel-based gray and white matter morphometry correlates of hallucinations in schizophrenia: The superior temporal gyrus does not stand alone.
Auditory verbal hallucinations (AVH) in schizophrenia (SZ) have been proposed to result from abnormal local, interregional and interhemispheric integration of brain signals in regions involved in language production and perception. This abnormal functional integration may find its base in morphological abnormalities. Structurally, AVHs have been frequently linked to abnormal morphology of the superior temporal gyrus (STG), but only a few studies investigated the relation of hallucination presence with both whole-brain gray matter (GM) and white matter (WM) morphometry. ⋯ Results suggest that STG GM abnormalities underlie the general susceptibility to experience psychotic symptoms and that additional abnormalities in a network of medial temporal, ventrolateral, putaminal, and parietal regions related to verbal memory and speech production may specifically increase the likelihood of experiencing AVH. Future studies should clarify the meaning of morphometry abnormalities for functional interregional communication.
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NeuroImage. Clinical · Jan 2014
Deficits in episodic memory retrieval reveal impaired default mode network connectivity in amnestic mild cognitive impairment.
Amnestic mild cognitive impairment (aMCI) is believed to represent a transitional stage between normal healthy ageing and the development of dementia. In particular, aMCI patients have been shown to have higher annual transition rates to Alzheimer's Disease (AD) than individuals without cognitive impairment. Despite intensifying interest investigating the neuroanatomical basis of this transition, there remain a number of questions regarding the pathophysiological process underlying aMCI itself. ⋯ The two groups showed no statistical difference in their DMN intra-connectivity. However when connectivity was analysed according to performance on measures of episodic memory retrieval, the two groups were separable, with aMCI patients demonstrating impaired functional connectivity between the hippocampal formation and the posterior cingulate cortex. We provide evidence that this lack of connectivity is driven by impaired communication from the posterior cingulate hub and does not simply represent hippocampal atrophy, suggesting that posterior cingulate degeneration is the driving force behind impaired DMN connectivity in aMCI.