Effect of intrinsic and extrinsic factors on global and regional cortical thickness.

Global and regional cortical thicknesses based on T1-weighted magnetic resonance images acquired at 1.5 T and 3 T were measured on a relatively large cohort of 295 subjects using FreeSurfer software. Multivariate regression analysis was performed using Pillai's trace test to determine significant differences in cortical thicknesses measured at these two field strengths. Our results indicate that global cortical thickness is not affected by the field strength or gender. In contrast, the regional cortical thickness was observed to be field dependent. Specifically, the cortical thickness in regions such as parahippocampal, superior temporal, precentral and posterior cingulate is thicker at 3 T than at 1.5 T. In contrast regions such as cuneus and pericalcarine showed higher cortical thickness at 1.5 T than at 3 T. These differences appear to be age-dependent. The differences in regional cortical thickness between field strengths were similar in both genders. Further, male vs. female differences in regional cortical thickness were observed only at 1.5 T and not at 3 T. Our results indicate that magnetic field strength has a significant effect on the estimation of regional, but not global, cortical thickness. In addition, the pulse sequence, scanner type, and spatial resolution do not appear to have significant effect on the measured cortical thickness

Unadjusted means and mean differences (95% confidence interval) of regional cortical thickness by field strength (1.5 T vs. 3 T) for right and left hemispheres in 295 controls using multivariate regression model.

<p>The regions with the significant field strength effect (p<0.05) on cortical thickness are denoted with “*”.</p><p>Note: overall field strength effect on regional cortical thickness is significant with p-value <0.0001 using Pillai's Trace test. ⁺STS  =  superior temporal sulcus.</p

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<p>Note: overall field strength effect on regional cortical thickness is significant with p-value <0.0001 using Pillai's Trace test; Factors ajusted for include: age, gender, resolution, scanner type, sequence, and interactions of field*age, and field*gender. <b>⁺</b>STS  =  superior temporal sulcus.</p

Histogram distribution for the samples – (a) Female, (b) Male, (c) 1.5 T and (d) 3 T.

<p>Histogram distribution for the samples – (a) Female, (b) Male, (c) 1.5 T and (d) 3 T.</p

Regional cortical thickness of the 34 segmented regions plotted for the three age groups.

<p>Regional cortical thickness of the 34 segmented regions plotted for the three age groups.</p

Expanded neurochemical profile in the early stage of Huntington disease using proton magnetic resonance spectroscopy

International audienceThe striatum is a well-known region affected in Huntington disease (HD). However, other regions, including the visual cortex, are implicated. We have identified previously an abnormal energy response in the visual cortex of patients at an early stage of HD using 31P magnetic resonance spectroscopy (31P MRS). We therefore sought to further characterize these metabolic alterations with 1H MRS using a well-validated semi-localized by adiabatic selective refocusing (semi-LASER) sequence that allows the measurement of an expanded number of neurometabolites. Ten early affected patients [Unified Huntington Disease Rating Scale (UHDRS), total motor score = 13.6 ± 10.8] and 10 healthy volunteers of similar age and body mass index (BMI) were recruited for the study. We performed 1H MRS in the striatum – the region that is primarily affected in HD – and the visual cortex. The protocol allowed a reliable quantification of 10 metabolites in the visual cortex and eight in the striatum, compared with three to five metabolites in previous 1H MRS studies performed in HD. We identified higher total creatine (p < 0.05) in the visual cortex and lower glutamate (p < 0.001) and total creatine (p < 0.05) in the striatum of patients with HD compared with controls. Less abundant neurometabolites [glutamine, γ-aminobutyric acid (GABA), glutathione, aspartate] showed similar concentrations in both groups. The protocol allowed the measurement of several additional metabolites compared with standard vendor protocols. Our study points to early changes in metabolites involved in energy metabolism in the visual cortex and striatum of patients with HD. Decreased striatal glutamate could reflect early neuronal dysfunction or impaired glutamatergic neurotransmission

Demographic information for the sample of 295 controls split into both genders and field strengths.

<p>Demographic information for the sample of 295 controls split into both genders and field strengths.</p

Sample distribution based on image resolution, pulse sequence and scanner manufacturer type.

<p>*Statistical analysis based on scanner type excluded 2 datasets from the sample population.</p

Lateral and medial views of inflated right hemisphere at 1.5 T and 3 T for male vs. female differences in cortical thickness.

<p>The labeled regions are: (A) and (B) precentral, (C) transverse temporal, (D) isthmus cingulate, (E) lingual and (F) cuneus</p

Imaging central nervous system myelin by positron emission tomography in multiple sclerosis using [methyl-¹¹C]-2-(4'-methylaminophenyl)- 6-hydroxybenzothiazole.

International audienceOBJECTIVE: Imaging of myelin tracts in vivo would greatly improve the monitoring of demyelinating diseases such as multiple sclerosis (MS). To date, no imaging technique specifically targets demyelination and remyelination. Recently, amyloid markers related to Congo red have been shown to bind to central nervous system (CNS) myelin. Here we questioned whether the thioflavine-T derivative 2-(4'-methylaminophenyl)-6-hydroxybenzothiazole (PIB), which also binds to amyloid plaques, could serve as a myelin marker. METHODS: PIB fixation to myelin was studied by fluorescence in the normal and dysmyelinating mouse brain, as well as in the postmortem brain of MS patients. Positron emission tomography (PET) experiments were conducted using [¹¹C]PIB in baboons and in a proof of concept clinical study in 2 MS patients. RESULTS: Applied directly on tissue sections or after intraperitoneal injection, PIB stained CNS myelin, and the decrease in the level of fixation paralleled the amount of myelin loss in a dysmyelinating mutant. In normally myelinated areas of postmortem MS brain, demyelinated and remyelinated lesions were clearly distinguishable by the differential intensity of labeling observed with PIB. PET using intravenously injected radiolabeled [¹¹C]PIB imaged CNS myelin in baboons and humans. In MS patients, the dynamic analysis of PET acquisitions allowed quantitative assessment of demyelination. INTERPRETATION: PIB could be used as an imaging marker to quantify myelin loss and repair in demyelinating diseases