scholarly journals Influences of lobar gray matter and white matter lesion load on cognition and mood

2010 ◽  
Vol 181 (2) ◽  
pp. 90-96 ◽  
Author(s):  
Susanne G. Mueller ◽  
Wendy J. Mack ◽  
Dan Mungas ◽  
Joel H. Kramer ◽  
Valerie Cardenas-Nicolson ◽  
...  
Keyword(s):  
White Matter ◽  
Gray Matter ◽  
White Matter Lesion ◽  
Lesion Load

Fatigue in multiple sclerosis is associated with the disruption of frontal and parietal pathways

2009 ◽  
Vol 15 (3) ◽  
pp. 337-344 ◽  
Author(s):  
J Sepulcre ◽  
JC Masdeu ◽  
J Goñi ◽  
G Arrondo ◽  
N Vélez de Mendizábal ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
White Matter ◽  
Gray Matter ◽  
Parietal Lobe ◽  
White Matter Lesion ◽  
Lesion Load ◽  
Attentional Processes ◽  
Fatigue Score ◽  
Gray Matter Atrophy ◽  
The Right

Background Fatigue is one of the most frequent and disturbing symptoms in multiple sclerosis (MS), directly affecting the patient’s quality of life. However, many questions remain unclear regarding the anatomic brain correlate of MS-related fatigue. Objective To assess the relationship between fatigue and white matter lesion location and gray matter atrophy. Methods In this study, 60 patients with MS were evaluated with the Modified Fatigue Impact Scale and magnetic resonance imaging. Location of white matter lesion was analyzed using a voxel-by-voxel lesion probability mapping approach and gray matter atrophy degree and location using an optimized voxel-based morphometry method. Results We found a correlation between lesion load and fatigue score (T2 lesion load: r = 0.415, P = 0.001; T1 lesion load r = 0.328, P = 0.011). Moreover, fatigue correlated with lesions in the right parietotemporal (periatrial area, juxtaventricular white matter deep in the parietal lobe and callosal forceps) and left frontal (middle-anterior corpus callosum, anterior cingulum and centrum semiovale of the superior and middle frontal gyri) white matter regions ( P < 0.001 in all cases). Finally, fatigue score significantly correlated with gray matter atrophy in frontal regions, specifically, the left superior frontal gyrus and bilateral middle frontal gyri ( P < 0.001 in all cases). Conclusion Our results suggest that the symptom of fatigue is associated with a disruption of brain networks involved in cognitive/attentional processes.

Microstructural fronto-striatal and temporo-insular alterations are associated with fatigue in patients with multiple sclerosis independent of white matter lesion load and depression

2019 ◽  
Vol 26 (13) ◽  
pp. 1708-1718 ◽  
Author(s):  
Miklos Palotai ◽  
Michele Cavallari ◽  
Ismail Koubiyr ◽  
Alfredo Morales Pinzon ◽  
Aria Nazeri ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
White Matter ◽  
Physical Disability ◽  
Disease Duration ◽  
White Matter Lesion ◽  
Brain Magnetic Resonance Imaging ◽  
Brain Regions ◽  
Specific Substrate ◽  
Patient Stratification ◽  
Lesion Load

Background: Fatigue in multiple sclerosis (MS) has been inconsistently associated with disruption of specific brain circuitries. Temporal fluctuations of fatigue have not been considered. Objective: The aim of this study was to investigate the association of fatigue with brain diffusion abnormalities, using robust criteria for patient stratification based on longitudinal patterns of fatigue. Methods: Patient stratification: (1) sustained fatigue (SF, n = 26): latest two Modified Fatigue Impact Scale (MFIS) ⩾ 38; (2) reversible fatigue (RF, n = 25): latest MFIS < 38 and minimum one previous MFIS ⩾ 38; and (3) never fatigued (NF, n = 42): MFIS always < 38 (five assessments minimum). 3T brain magnetic resonance imaging (MRI) was used to perform voxel-wise comparison of fractional anisotropy (FA) between the groups controlling for age, sex, disease duration, physical disability, white matter lesion load (T2LV), and depression. Results: SF and, to a lesser extent, RF patients showed lower FA in multiple brain regions compared to NF patients, independent of age, sex, disease duration, and physical disability. In cingulo-postcommissural-striato-thalamic regions, the differences in FA between SF and NF (but not between RF and NF or SF) patients were independent of T2LV, and in ventromedial prefronto-precommissuro-striatal and temporo-insular areas, independent of T2LV and depression. Conclusion: Damage to ventromedial prefronto-precommissuro-striatal and temporo-insular pathways appears to be a specific substrate of SF in MS.

White Matter Lesion Load Increases the Risk of Low CSF Aβ42 in Apolipoprotein E-ɛ4 Carriers Attending a Memory Clinic

2011 ◽  
Vol 21 (2) ◽  
pp. e78-e82 ◽  
Author(s):  
Vidar Stenset ◽  
Dag Hofoss ◽  
Lisbeth Johnsen ◽  
Audun Elnaes Berstad ◽  
Anne Negaard ◽  
...  
Keyword(s):  
White Matter ◽  
Apolipoprotein E ◽  
White Matter Lesion ◽  
Memory Clinic ◽  
Lesion Load

Brain atrophy evolution and lesion load accrual in multiple sclerosis: a 2-year follow-up study

2008 ◽  
Vol 15 (2) ◽  
pp. 204-211 ◽  
Author(s):  
G Tedeschi ◽  
D Dinacci ◽  
M Comerci ◽  
L Lavorgna ◽  
G Savettieri ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
White Matter ◽  
Disease Progression ◽  
Gray Matter ◽  
Brain Atrophy ◽  
Disease Duration ◽  
Lesion Load ◽  
Whole Brain ◽  
Gray Matter Atrophy

Background To investigate in a large cohort of patients with multiple sclerosis (MS), lesion load and atrophy evolution, and the relationship between clinical and magnetic resonance imaging (MRI) correlates of disease progression. Methods Two hundred and sixty-seven patients with MS were studied at baseline and two years later using the same MRI protocol. Abnormal white matter fraction, normal appearing white matter fraction, global white matter fraction, gray matter fraction and whole brain fraction, T2-hyperintense, and T1-hypointense lesions were measured at both time points. Results The majority of patients were clinically stable, whereas MRI-derived brain tissue fractions were significantly different after 2 years. The correlation between MRI data at baseline and their variation during the follow-up showed that lower basal gray matter atrophy was significantly related with higher progression of gray matter atrophy during follow-up. The correlation between MRI parameters and disease duration showed that gray matter atrophy rate decreased with increasing disease duration, whereas the rate of white matter atrophy had a constant pattern. Lower basal gray matter atrophy was associated with increased probability of developing gray matter atrophy at follow-up, whereas gray matter atrophy progression over 2 years and new T2 lesion load were risk factors for whole brain atrophy progression. Conclusions In MS, brain atrophy occurs even after a relatively short period of time and in patients with limited progression of disability. Short-term brain atrophy progression rates differ across tissue compartments, as gray matter atrophy results more pronounced than white matter atrophy and appears to be a early phenomenon in the MS-related disease progression.

scholarly journals Cognitive correlates of white matter lesion load and brain atrophy

Neurology ◽  
2015 ◽  
Vol 85 (5) ◽  
pp. 441-449 ◽  
Author(s):  
Chuanhui Dong ◽  
Nooshin Nabizadeh ◽  
Michelle Caunca ◽  
Ying Kuen Cheung ◽  
Tatjana Rundek ◽  
...  
Keyword(s):  
White Matter ◽  
Brain Atrophy ◽  
White Matter Lesion ◽  
Lesion Load ◽  
Cognitive Correlates

scholarly journals Higher white matter hyperintensity lesion load is associated with reduced long-range functional connectivity

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Fanny Quandt ◽  
Felix Fischer ◽  
Julian Schröder ◽  
Marlene Heinze ◽  
Iris Lettow ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
White Matter ◽  
Functional Connectivity ◽  
White Matter Hyperintensities ◽  
Small Vessel Disease ◽  
White Matter Lesion ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
Lesion Load ◽  
Vessel Disease

Abstract Cerebral small vessel disease is a common disease in the older population and is recognized as a major risk factor for cognitive decline and stroke. Small vessel disease is considered a global brain disease impacting the integrity of neuronal networks resulting in disturbances of structural and functional connectivity. A core feature of cerebral small vessel disease commonly present on neuroimaging is white matter hyperintensities. We studied high-resolution resting-state EEG, leveraging source reconstruction methods, in 35 participants with varying degree of white matter hyperintensities without clinically evident cognitive impairment in an observational study. In patients with increasing white matter lesion load, global theta power was increased independently of age. Whole-brain functional connectivity revealed a disrupted network confined to the alpha band in participants with higher white matter hyperintensities lesion load. The decrease of functional connectivity was evident in long-range connections, mostly originating or terminating in the frontal lobe. Cognitive testing revealed no global cognitive impairment; however, some participants revealed deficits of executive functions that were related to larger white matter hyperintensities lesion load. In summary, participants without clinical signs of mild cognitive impairment or dementia showed oscillatory changes that were significantly related to white matter lesion load. Hence, oscillatory neuronal network changes due to white matter lesions might act as biomarker prior to clinically relevant behavioural impairment.

Gray matter atrophy cannot be fully explained by white matter damage in patients with MS

2020 ◽  
Vol 27 (1) ◽  
pp. 39-51 ◽  
Author(s):  
Jian Zhang ◽  
Antonio Giorgio ◽  
Claudia Vinciguerra ◽  
Maria Laura Stromillo ◽  
Marco Battaglini ◽  
...  
Keyword(s):  
White Matter ◽  
Gray Matter ◽  
Similar Data ◽  
White Matter Damage ◽  
Lesion Load ◽  
Posterior Cortex ◽  
Data Set ◽  
Close Link ◽  
Random Patterns ◽  
Normal Controls

Background: Source-based morphometry (SBM) was recently used for non-random “patterns” of gray matter (GM) atrophy or white matter (WM) microstructural damage. Objective: To assess whether and to what extent such patterns may be inter-related in MS. Methods: SBM was applied to images of GM concentration and fractional anisotropy (FA) in MS patients ( n = 41, median EDSS = 1) and normal controls (NC, n = 28). The same procedure was repeated on an independent and similar data set (39 MS patients and 13 NC). Results: We found in MS patterns of GM atrophy and reduced FA ( p < 0.05, corrected). Deep GM atrophy was mostly (70%) explained by lesion load in projection tracts and lower FA in posterior corona radiata and thalamic radiation. By contrast, sensorimotor and posterior cortex atrophy was less (50%) dependent from WM damage. All patterns correlated with EDSS ( r from −0.33 to −0.56, p < 0.03) while the only cognition-related correlation was between posterior GM atrophy pattern and processing speed ( r = 0.45, p = 0.014). Reliability analysis showed similar results. Conclusion: In relatively early MS, we found a close link between deep GM atrophy pattern and WM damage while sensorimotor and posterior cortex patterns were partially independent from WM damage and perhaps related to primary mechanisms. Patterns were clinically relevant.

Sign in / Sign up

Export Citation Format

Share Document