Using MRI and diffusion tensor imaging, Frøkjær et al. assessed brain microstructure in 26 patients with both longstanding diabetes and gastrointestinal symptoms and contrasted these data with information from 23 control subjects.
Our primary hypotheses focused on evaluating brain microstructure in the midbrain ventral tegmental area/substantia nigra (VTA/SN), the medial forebrain bundle (MFB), and the amygdalofugal pathway (AFP).
Based on imaging findings in the MDD literature, we further hypothesized that MDD subjects would exhibit abnormal brain microstructure in white matter adjacent to orbitofrontal cortex (FOC), anterior cingulate cortex (ACC), paracingulate cortex (PAC), subgenual prefrontal cortex (SGC), and dorsolateral prefrontal cortex (DLPFC).
We predicted MDD subjects would exhibit abnormal brain microstructure in (1) the medial forebrain bundle (MFB) and contiguous lateral nucleus of the hypothalamus (LNH), along with (2) regions feeding the MFB/LNH, including the ventral tegmental area/substantia nigra (VTA/SN), and (3) the amygdalofugal pathway.
Using magnetic resonance diffusion tensor imaging, we characterized brain microstructure in areas involved in visceral sensory processing and correlated these findings to clinical parameters.
This study assessed the relationship between stereoscopic vision, visual perception, and brain microstructure in a cohort of VLBW children at the age of 4 years.
Orientation preference in this profile originates from the directional nature of brain microstructure, arising in particular in the white matter.
The qMT data demonstrated that inflammation induced a rapid change in brain microstructure, reflected in increased magnetization exchange from free (water) to macromolecular-bound protons, within a discrete region of insular cortex implicated in representing internal physiologic states including inflammation.
Because regional alterations in brain microstructure were detected in the present alcoholic sample in most regions known to support verbal episodic memory (medial temporal lobe), these findings add further evidence for genuine episodic memory deficits in alcoholism [2].
Our analysis has revealed for the first time evidence of defined modifications in the brain microstructure and neuroconnectivity, in co-occurrence with synaptic efficacy alterations, in a murine model of chronic T. gondii infection.
