Inferior Parietal White Matter Research Articles

Diffusivity Changes in Posterior Cortical Atrophy and Logopenic Progressive Aphasia: A Longitudinal Diffusion Tensor Imaging Study.

Posterior cortical atrophy (PCA) and logopenic progressive aphasia (LPA) are associated with characteristic patterns of structural network degeneration. Little is known about longitudinal patterns of white matter tract degeneration in these phenotypes. To assess longitudinal patterns of white matter degeneration and identify phenotype specific cross-sectional and longitudinal diffusion tensor imaging (DTI) biomarkers in PCA and LPA. Twenty-five PCA, 22 LPA and 25 cognitively unimpaired (CU) individuals were recruited and underwent structural MRI that included a DTI sequence with a follow-up one year later. Cross-sectional and longitudinal mixed effects models were fit to assess the effects of diagnosis on baseline and annualized change in regional DTI metrics. Discriminatory power was investigated using the area under the receiver operating characteristic curves (AUROC). PCA and LPA showed overlapping white matter degeneration profiles predominantly in the left occipital and temporal lobes, the posterior thalamic radiation and sagittal stratum at baseline, as well as the parietal lobe longitudinally. PCA showed degeneration in the occipital and parietal white matter, cross-sectionally and longitudinally, compared to CU, while LPA showed greater degeneration in the temporal and inferior parietal white matter and the inferior fronto-occipital fasciculus cross-sectionally, and in parietal white matter longitudinally compared to CU. Cross-sectionally, integrity of the inferior occipital white matter was best able to differentiate PCA from LPA, with an AUROC of 0.82. These findings contribute to our understanding of white matter degeneration and support usage of DTI as a useful additional diagnostic biomarker for PCA and LPA.

Relationship between visuoperceptual functions and parietal structural abnormalities in temporal lobe epilepsy.

Progressive gray matter volume reductions beyond the epileptogenic area has been described in temporal lobe epilepsy. There is less evidence regarding correlations between gray and white matter volume changepres and multi-domain cognitive performance in this setting. We aimed to investigate correlations between volume changes in parietal structures and visuospatial performance in temporal lobe epilepsy patients. we performed a cross-sectional study comparing global and regional brain volume data from 34 temporal lobe epilepsy patients and 30 healthy controls. 3D T1-weighted sequences were obtained on a 3.0 T magnet, and data were analyzed using age and sex-adjusted linear regression models. Global and regional brain volumes and cortical thickness in patients were correlated with standardized visual memory, visuoperceptual, visuospatial, and visuoconstructive parameters obtained in a per-protocol neuropsychological assessment. temporal lobe epilepsy patients had smaller volume fractions of the deep gray matter structures, putamen and nucleus accumbens, and larger cerebrospinal fluid volume fraction than controls. Correlations were found between: 1) visual memory and precuneus and inferior parietal cortical thickness; 2) visuoperceptual performance and precuneus and supramarginal white matter volumes; 3) visuospatial skills and precuneus, postcentral, and inferior and superior parietal white matter volumes; 4) visuoconstructive performance and inferior parietal white matter volume. Brain volume loss is widespread in temporal lobe epilepsy. Volumetric reductions in parietal lobe structures were associated with visuoperceptual cognitive performance.

Atrophic brain signatures of mild forms of neurocognitive impairment in virally suppressed HIV infection.

There is a lack of evidence for the neurobiological underpinning of asymptomatic neurocognitive impairment (ANI) and mild neurocognitive disorders (MNDs) in virally suppressed HIV-positive persons. We hypothesized that such mild impairment would be associated with focal brain atrophy. A cross-sectional observational study. Eighty-five virally suppressed HIV-positive and 44 geographically, demographically and lifestyle comparable HIV-negative men underwent anatomical MRI, neuropsychological evaluation and HIV laboratory tests. Volumes of interest (VOI) from magnetic resonance (MR) images were extracted using FreeSurfer to yield grey and white matter volumes in regions associated with HIV-related brain injury. HIV-associated neurocognitive disorder (HAND) [ANI = 38%, MND = 13%, HIV-associated dementia (HAD) = 3% vs. neuropsychologically-normal] was classified using Global Deficit Score (GDS ≥0.5) and functional decline. Effects of HIV status on VOI were assessed with multivariate analyses controlling for family-wise error. HAND categories and HIV biomarker effects on VOI were assessed with multiple regression. Relative to the HIV-negative group, the HIV-positive group demonstrated subcortical grey (d = 0.50-0.60) and white matter (d = 0.43-0.69) atrophy, with relative cortical sparing (d = 0.23). ANI showed reduced medial-orbitofrontal white matter compared with NP-normal cases (P = 0.04). MND showed enlarged lateral ventricles (P = 0.02) and reduced caudal-middle-frontal white matter (P = 0.04), caudal-anterior-cingulate white matter (P = 0.006) and inferior-parietal white matter (P = 0.04) compared with neuropsychologically normal. Across the HIV-positive group, lower CD4+/CD8 ratio was the strongest predictor of atrophy in subcortical regions. Across HAND categories, HIV disease duration uniquely predicted greater medial-orbitofrontal white matter atrophy only in ANI (P = 0.002). ANI shows specific frontal white matter atrophy to which HIV disease duration is a unique contributor. MND is characterized by more widespread subcortical atrophy.

Diffusion Imaging Biomarkers of Regional White Matter Injury Correlate With Change in Executive Function and Processing Speed After Brain Radiation Therapy

To analyze region specific biomarkers of white matter (WM) integrity using diffusion imaging and test associations with executive functioning and processing speed in a prospective clinical trial. We hypothesized that regional changes in diffusion biomarkers of WM damage would correlate with changes in executive function and processing speed at 6-months post-radiotherapy (RT). We prospectively evaluated 25 primary brain tumor patients undergoing fractionated brain RT. Study patients underwent high-resolution volumetric MRI, diffusion weighted imaging (b-values 0, 500, 1500 s/mm2fit to single tensor), and neurocognitive assessment of executive functioning (Delis-Kaplan Executive Function System [D-KEFS] letter fluency and category switching total and Wisconsin Card Sorting Test [WCST] perseverative errors) and processing speed (D-KEFS Trail Making [TM] number and letter sequencing) prior to and 6 months after RT. Freesurfer software was run at each time point to segment regions of interest (ROIs) associated with these cognitive domains: left dorsolateral and bihemispheric anterior cingulate WM for executive functioning; bihemispheric inferior parietal and total right hemispheric WM for processing speed. Tumor, edema, and segmentation errors were censored. Change in diffusion biomarkers of mean diffusivity (MD) and fractional anisotropy (FA) were calculated for each ROI. Reliable change indices were calculated for change in cognition from pre-RT to 6 months post-RT. Pearson correlation coefficients were used to test associations between clinical variables and change in diffusion parameters and cognitive scores. Statistical significance was set to α = 0.05 with two-tailed tests. Executive function (D-KEFS category switching total, mean change -0.56, P = 0.017; WCST mean change -0.51, P = 0.006) and processing speed (TM number sequencing, mean change -0.40, P = 0.045) significantly declined post-RT. Change in executive function was positively correlated with age and years of education (r = 0.54, P = 0.012; r = 0.53, P = 0.013, respectively), while processing speed was negatively correlated with age (r = -0.51, P = 0.014). FA increased in total right hemispheric WM (mean change 0.0074±0.029) and all ROIs associated with executive function and processing speed. MD decreased in executive function ROIs, but remained relatively unchanged in ROIs associated with processing speed. While WM diffusion parameters were not associated with executive function decline, MD of both left and right inferior parietal WM and right total hemispheric WM were positively correlated with processing speed (TM letter sequencing, r = 0.60, P = 0.015; r = 0.57, P = 0.016; r = 0.51, P = 0.037, respectively). Diffusion changes in bihemispheric inferior parietal and total right hemispheric WM were significantly associated with changes in processing speed in brain tumor patients after RT.

Glutamatergic changes in the cerebral white matter associated with schizophrenic exacerbation

Glutamatergic dysfunction in the brain has been implicated in the pathophysiology of schizophrenia. This study was aimed to examine several brain chemical mediators, including Glx (glutamate + glutamine), using (1)H magnetic resonance spectroscopy (MRS) in medicated patients with schizophrenia, with and without psychotic exacerbation. (1)H MRS was acquired in 24 patients with schizophrenia, with psychotic exacerbation; 22 patients without exacerbation; and 27 age- and sex-matched healthy volunteers. The levels of metabolites were measured in the left frontal and inferior parietal white matter and compared across the three groups. The Glx level was significantly elevated in the left inferior parietal white matter in the patients with psychotic exacerbation in comparison with that in the healthy volunteers and the patients without exacerbation (P < 0.05). We also detected that there was a significant correlation between Positive and Negative Syndrome Scale-positive scale and Glx level in the left parietal white matter (r = 0.51, P < 0.001). Higher than normal Glx levels indicate glutamatergic overactivity in the left inferior parietal white matter with schizophrenic exacerbation, a finding that is in accordance with the glutamatergic hypothesis in schizophrenia. The Glx level measured by (1)H MRS could be a biomarker for exacerbation in schizophrenia.

White matter integrity and reaction time intraindividual variability in healthy aging and early-stage Alzheimer disease

Aging and early-stage Alzheimer disease (AD) have been shown to be associated with increased RT intraindividual variability (IIV, as reflected by the coefficient of variation) and an exaggeration of the slow tail of the reaction time (RT) distribution in attentional control tasks, based on ex-Gaussian analyses. The current study examined associations between white matter volume, IIV, and ex-Gaussian RT distribution parameters in cognitively normal aging and early-stage AD. Three RT attention tasks (Stroop, Simon, and a consonant-vowel odd-even switching task) in conjunction with MRI-based measures of cerebral and regional white matter volume were obtained in 133 cognitively normal and 33 early-stage AD individuals. Larger volumes were associated with less IIV and less slowing in the tail of the RT distribution, and larger cerebral and inferior parietal white matter volumes were associated with faster modal reaction time. Collectively, these results support a role of white matter integrity in IIV and distributional skewing, and are consistent with the hypothesis that IIV and RT distributional skewing are sensitive to breakdowns in executive control processes in normal and pathological aging.

White Matter Abnormalities in Patients With Obsessive-Compulsive Disorder and Their First-Degree Relatives

Obsessive-compulsive disorder (OCD) is a common, heritable neuropsychiatric disorder, hypothetically underpinned by dysconnectivity of large-scale brain systems. The extent of white matter abnormalities in OCD is unknown, and the genetic basis of this disorder is poorly understood. The authors used diffusion tensor imaging, a magnetic resonance imaging technique, for examining white matter abnormalities in brain structure through quantification of water diffusion, to confirm whether white matter abnormalities exist in OCD. They also explored whether such abnormalities occur in healthy first-degree relatives of patients, indicating they may be endophenotypes representing increased genetic risk for OCD. The authors used diffusion tensor imaging to measure fractional anisotropy of white matter in 30 patients with OCD, 30 unaffected first-degree relatives, and 30 matched healthy comparison subjects. Regions of significantly abnormal fractional anisotropy in patients in relation to healthy comparison subjects were identified by permutation tests. The authors assessed whether these abnormalities were also evident in the first-degree relatives. A secondary region-of-interest analysis was undertaken to assess the extent of replication between our data and previous relevant literature. Patients with OCD demonstrated significantly reduced fractional anisotropy in a large region of right inferior parietal white matter and significantly increased fractional anisotropy in a right medial frontal region. Relatives also exhibited significant abnormalities of fractional anisotropy in these regions. These findings indicate that OCD is associated with white matter abnormalities in parietal and frontal regions. Similar abnormalities in unaffected first-degree relatives suggest these may be white matter endophenotypes for OCD.

Perfusion MRI detects rCBF abnormalities in early stages of HIV-cognitive motor complex.

To evaluate patients with early HIV-cognitive motor complex (HIV-CMC) for possible regional cerebral blood flow (rCBF) abnormalities on perfusion MRI (pMRI). Nuclear medicine techniques have demonstrated global and focal cerebral perfusion abnormalities in patients with HIV dementia. Ultrafast pMRI enables the measurement of rCBF throughout the brain without the need to apply radioactive tracers or ionizing radiation. pMRI was used to measure the rCBF in 19 patients with early stages of HIV-CMC and 15 healthy seronegative control subjects. The rCBF maps were registered to high-resolution anatomic MRI scans and transformed into Talairach space. Statistical analysis of the rCBF maps was performed with SPM96. Compared with the control subjects, the patients with HIV had statistically significantly decreased rCBF bilaterally in the inferior lateral frontal cortices (right: -15%, p < 0.002; left: -12%, p < 0.005) and in the inferior medial parietal brain region (-15%, p < 0.0009). In contrast, rCBF was increased bilaterally in the posterior inferior parietal white matter (right: +19%, p < 0.0001; left: + 17%, p < 0.001). Furthermore, rCBF abnormalities correlated significantly with clinical disease severity as measured by CD4 count, plasma viral load, Karnofsky score, and HIV dementia scale. Our results are consistent with previous findings from PET and SPECT studies. Furthermore, pMRI can detect rCBF abnormalities that correlate with disease severity in HIV-CMC. Because pMRI is more cost-effective, faster, and safer than nuclear medicine techniques for monitoring rCBF changes, pMRI may be more feasible for monitoring the effects of therapy for HIV-CMC.

High-resolution fluorodeoxyglucose positron emission tomography shows both global and regional cerebral hypometabolism in multiple sclerosis.

The authors study brain regional glucose metabolism prospectively in multiple sclerosis (MS) using high-resolution 2-[18-F]fluoro-2-deoxy-D-glucose positron emission tomography (FDG PET) in 25 MS patients of the Dent Neurologic Institute compared with 6 healthy subjects. Glucose metabolism is measured in 20 regions of interest using a line-profile technique. Compared with control subjects, a 9% reduction in total brain glucose metabolism is noted in MS patients (p < 0.05). Hypometabolism is widespread, including the cerebral cortex, subcortical nuclei, supratentorial white matter, and infratentorial structures. This reduction represents absolute regional decreases ranging from 3% to 18%. The most dramatic absolute reductions occur in the superior mesial frontal cortex, superior dorsolateral frontal cortex, mesial occipital cortex, lateral occipital cortex, deep inferior parietal white matter, and pons. The regional hypometabolism in the superior mesial frontal cortex and superior dorsolateral frontal cortex is statistically significant (p < 0.05), whereas the changes in the mesial occipital cortex (p = 0.07) and the lateral occipital cortex (p = 0.09) approach significance. The authors' findings suggest that widespread cerebral dysfunction occurs in MS, and that diaschisis or neuronal system disconnection resulting from white matter disease plays a major role. Cortical gray matter hypometabolism may also reflect direct MS involvement. The quantitative cerebral abnormalities detected by FDG PET may serve as a marker of disease activity in understanding the pathophysiological expression and therapeutic response of MS.