Multi-parametric structural magnetic resonance imaging in relation to cognitive dysfunction in long-standing multiple sclerosis

2015 ◽  
Vol 22 (5) ◽  
pp. 608-619 ◽  
Author(s):  
Marita Daams ◽  
Martijn D Steenwijk ◽  
Menno M Schoonheim ◽  
Mike P Wattjes ◽  
Lisanne J Balk ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
White Matter ◽  
Cognitive Dysfunction ◽  
Cognitive Deficits ◽  
Grey Matter ◽  
White Matter Damage ◽  
Diffuse White Matter ◽  
Brain White Matter ◽  
Deep Grey Matter ◽  
Imaging Markers

Background: Cognitive deficits are common in multiple sclerosis. Most previous studies investigating the imaging substrate of cognitive deficits in multiple sclerosis included patients with relatively short disease durations and were limited to one modality/brain region. Objective: To identify the strongest neuroimaging predictors for cognitive dysfunction in a large cohort of patients with long-standing multiple sclerosis. Methods: Extensive neuropsychological testing and multimodal 3.0T MRI was performed in 202 patients with multiple sclerosis and 52 controls. Cognitive scores were compared between groups using Z-scores. Whole-brain, white matter, grey matter, deep grey matter and lesion volumes; cortical thickness, (juxta)cortical and cerebellar lesions; and extent and severity of diffuse white matter damage were measured. Stepwise linear regression was used to identify the strongest predictors for cognitive dysfunction. Results: All cognitive domains were affected in patients. Patients showed extensive atrophy, focal pathology and damage in up to 75% of the investigated white matter. Associations between imaging markers and average cognition were two times stronger in cognitively impaired patients than in cognitively preserved patients. The final model for average cognition consisted of deep grey matter DGMV volume and fractional anisotropy severity (adjusted R²=0.490; p<0.001). Conclusion: From all imaging markers, deep grey matter atrophy and diffuse white matter damage emerged as the strongest predictors for cognitive dysfunction in long-standing multiple sclerosis.

Fingolimod treatment reverses signs of diffuse white matter damage in multiple sclerosis: A pilot study

2021 ◽  
Vol 48 ◽  
pp. 102690
Author(s):  
Maija Saraste ◽  
Svetlana Bezukladova ◽  
Marcus Sucksdorff ◽  
Virva Saunavaara ◽  
Eero Rissanen ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
White Matter ◽  
Pilot Study ◽  
White Matter Damage ◽  
Diffuse White Matter

Dementia in multiple sclerosis: report of a case with cortical grey matter involvement and frontal-type-like clinical features

2011 ◽  
Vol 26 (S2) ◽  
pp. 485-485
Author(s):  
R. Correia ◽  
D. Dias ◽  
A.J. Bastos-Leite ◽  
E. Rio ◽  
R. Curral
Keyword(s):  
Multiple Sclerosis ◽  
Case Report ◽  
White Matter ◽  
Frontal Lobe ◽  
Cognitive Dysfunction ◽  
Clinical Features ◽  
Grey Matter ◽  
Psychiatric Symptoms ◽  
Eating Behaviour ◽  
Cortical Grey Matter

Background/introductionAlthough multiple sclerosis (MS), a demyelinating disease of unknown aetiology, is primarily a white matter disease, it may also involve the grey matter, a feature not often demonstrated in vivo by means of magnetic resonance imaging (MRI). The involvement of cortical grey matter in MS may account for cognitive dysfunction and behavioural abnormalities.ObjectiveThe purpose of this report is to present the case of a patient with MS and clinical features mimicking dementia of the frontal type due to clear-cut cortical grey matter involvement in the left frontal lobe.Case reportA 55-year-old woman with relapsing remitting MS developed a clinical picture characterized by frontal deficits (e.g. attention, verbal fluency, and speed processing), disinhibition, loss of insight, perseveration, abnormal eating behaviour, agitation, insomnia, and depersonalization phenomena. Neuropsychological evaluation also revealed abnormal performance on the Trail Making and the Stroop tests. Besides typical demyelinating lesions and “black holes”, MRI showed a striking pattern of left frontal opercular involvement including cortical thinning, focal knife-edge appearance of the gyri, and marked gliosis in the adjacent white matter.DiscussionCognitive deficits in MS are typically subcortical, due to the expected predominance of white matter lesions. Nonetheless, the involvement of grey matter structures may contribute to a different pattern of cognitive dysfunction. For example, hippocampal involvement has been linked to memory impairment. This particular case report additionally illustrates how cortical grey matter involvement in the frontal lobe may lead (not unexpectedly) to a clinical condition mostly characterised by frontal deficits and psychiatric symptoms.

scholarly journals Automated quantification of deep grey matter structures and white matter lesions using magnetic resonance imaging in relapsing remission multiple sclerosis

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Mina Rizkallah ◽  
Mohamed Hefida ◽  
Mohamed Khalil ◽  
Rasha Mahmoud Dawoud
Keyword(s):  
Multiple Sclerosis ◽  
Statistical Analysis ◽  
White Matter ◽  
Grey Matter ◽  
Brain Volume ◽  
Correlation Coefficients ◽  
White Matter Lesions ◽  
The Other ◽  
Automated Segmentation ◽  
Deep Grey Matter

Abstract Background Brain volume loss (BVL) is widespread in MS and occurs throughout the disease course at a rate considerably greater than in the general population. In MS, brain volume correlates with and predicts future disability, making BVL a relevant measure of diffuse CNS damage leading to clinical disease progression, as well as serving as a useful outcome in evaluating MS therapies. The aim of our study was to evaluate the role of automated segmentation and quantification of deep grey matter structures and white matter lesions in Relapsing Remitting Multiple Sclerosis patients using MR images and to correlate the volumetric results with different degrees of disability based on expanded disability status scale (EDSS) scores. Results All the patients in our study showed relative atrophy of the thalamus and the putamen bilaterally when compared with the normal control group. Statistical analysis was significant for the thalamus and the putamen atrophy (P value < 0.05). On the other hand, statistical analysis was not significant for the caudate and the hippocampus (P value > 0.05); there was a significant positive correlation between the white matter lesions volume and EDSS scores (correlation coefficient of 0.7505). On the other hand, there was a significant negative correlation between the thalamus and putamen volumes, and EDSS scores (correlation coefficients < − 0.9), while the volumes of the caudate and the hippocampus had a very weak and non-significant correlation with the EDSS scores (correlation coefficients > − 0.35). Conclusions The automated segmentation and quantification tools have a great role in the assessment of brain structural changes in RRMS patients, and that it became essential to integrate these tools in the daily medical practice for the great value they add to the current evaluation measures.

Correlation Analysis Between Local Cerebral Blood Flow and Severity of Vascular Cognitive Dysfunction

2021 ◽  
Vol 11 (7) ◽  
pp. 1798-1806
Author(s):  
Jinling Wang ◽  
Xin Xu ◽  
Wanhui Dong
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
White Matter ◽  
Cognitive Dysfunction ◽  
Control Group ◽  
Disease Group ◽  
White Matter Damage ◽  
Brain White Matter ◽  
Flow Perfusion ◽  
Cerebrovascular Stenosis

Research methods: This paper analyses the correlation between cerebral blood flow perfusion caused by cerebral vascular stenosis and the reduction of patients with cognitive dysfunction and white matter damage. A total of 118 patients with reduced cerebral blood flow perfusion due to cerebrovascular stenosis were selected to be included in the disease group, and 118 patients with no cerebrovascular stenosis and no neurological disease were included in the control group. The cerebral blood flow perfusion index and cognitive function index were compared between the two groups of patients. The correlation between each index and the degree of brain white matter damage was analysed. Results: The scores of brain white matter damage in patients with disease group were higher than those in control group, and cCBV, cCBF, TTP, MTT, MoCA, MMSE, ADL, and WMS were lower than those in control group, and the difference was statistically significant (P < 0.05). cCBV, cCBF, TTP, MTT, and white matter damage scores were highly correlated with MoCA, MMSE, ADL, and WMS (P < 0.05). There is a clear correlation between cerebral vascular perfusion, cognitive dysfunction, and white matter damage in patients with cerebrovascular stenosis. The more severe the perfusion of cerebral blood flow, the more severe the cognitive dysfunction and the white matter damage.

scholarly journals Contrasting the brain imaging features of MOG-Antibody disease, with AQP4-Antibody NMOSD and Multiple Sclerosis

2020 ◽  
Author(s):  
Silvia Messina ◽  
Romina Mariano ◽  
Adriana Roca-Fernandez ◽  
Ana Cavey ◽  
Maciej Jurynczyk ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Visual Acuity ◽  
White Matter ◽  
Grey Matter ◽  
Optic Chiasm ◽  
Lesion Volume ◽  
Imaging Features ◽  
Conventional Imaging ◽  
Cortical Lesions ◽  
Deep Grey Matter

Neuromyelitis optica associated with aquaporin-4-antibodies (NMOSD-AQP4) and myelin oligodentrocyte-glycoprotein antibody-associated disorder (MOGAD) have been recently recognised as different from multiple sclerosis. Although conventional MRI may help distinguish multiple sclerosis from antibody-mediated diseases, the use of quantitative and non-conventional imaging may give more pathological information and explain the clinical differences. We compared, using non-conventional imaging, brain MRI findings in 75 subjects in remission with NMOSD-AQP4, MOGAD, multiple sclerosis or healthy controls (HC). Volumetrics, white matter and cortical lesions, and tissue integrity measures using diffusion imaging, were analysed in the four groups along with their association with disability (expanded disability status scale [EDSS] and visual acuity). The volumetric analysis showed that, deep grey matter volumes were significantly lower in multiple sclerosis (p=0.0001) and MOGAD (p=0.02), compared to HC. Relapsing MOGAD had lower white matter, pallidus and hippocampus volumes than in monophasic (p<0.05). Optic chiasm volume was reduced only in NMOSD-AQP4 who had at least one episode of optic neuritis (ON) (NMOSD-AQP4-ON vs NMOSD-AQP4 p<0.001, HC p<0.001, MOGAD-ON p=0.04, multiple sclerosis-ON p=0.02) likely reflecting the recognised posterior location of NMOSD-AQP4-ON and its severity. Lesion volume was greatest in multiple sclerosis followed by MOGAD and in these two diseases, the lesion volume correlated with disease duration (multiple sclerosis R=0.46, p=0.05, MOGAD R=0.81, p<0.001), cortical thickness (multiple sclerosis R=-0.64, p=0.0042, MOGAD=-0.71, p=0.005) and deep grey matter volumes (multiple sclerosis R=-0.65, p=0.0034, MOGAD R=-0.93, p<0.001). Lesional-fractional anisotropy (FA) was reduced and mean diffusivity increased in all patients, but overall, FA was only reduced in the non-lesional tissue in multiple sclerosis (p=0.01), although focal reductions were noted in NMOSD-AQP4, reflecting mainly optic nerve and corticospinal tract pathways. Cortical/juxtacortical lesions were seen in a minority of MOGAD, while cortical/juxtacortical and purely cortical lesions were identified in the majority of multiple sclerosis and in none of the NMOSD-AQP4. Non-lesional FA in NMOSD-AQP4, lower white-matter volume and female sex in multiple sclerosis, and lower brainstem volume in MOGAD were the best predictors of EDSS disability (accounting for 46%, 49% and 19% respectively). Worse visual acuity associated with lower optic chiasm volume in NMOSD-AQP4 and lower thalamus volume in MOGAD (accounting for 58% and 35% respectively). Although MOGAD patients had good outcomes, deep grey matter atrophy was present. In contrast, NMOSD-AQP4 patients showed a relative sparing of deep grey matter volumes, despite greater residual disability as compared with MOGAD patients. NMOSD-AQP4 but not MOGAD patients showed reduced FA in non-lesional tissue.

scholarly journals Diffuse White Matter Damage Is Absent in Neuromyelitis Optica

2009 ◽  
Vol 31 (1) ◽  
pp. 76-79 ◽  
Author(s):  
F. Aboul-Enein ◽  
M. Krššák ◽  
R. Höftberger ◽  
D. Prayer ◽  
W. Kristoferitsch
Keyword(s):  
White Matter ◽  
Neuromyelitis Optica ◽  
White Matter Damage ◽  
Diffuse White Matter

scholarly journals A higher proportion of ermin-immunopositive oligodendrocytes in areas of remyelination

PLoS ONE ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. e0256155
Author(s):  
Intakhar Ahmad ◽  
Stig Wergeland ◽  
Eystein Oveland ◽  
Lars Bø
Keyword(s):  
Multiple Sclerosis ◽  
White Matter ◽  
Corpus Callosum ◽  
Mouse Model ◽  
Grey Matter ◽  
Early Stage ◽  
Relative Proportion ◽  
Normal Appearing White Matter ◽  
The Brain

Incomplete remyelination is frequent in multiple sclerosis (MS)-lesions, but there is no established marker for recent remyelination. We investigated the role of the oligodendrocyte/myelin protein ermin in de- and remyelination in the cuprizone (CPZ) mouse model, and in MS. The density of ermin+ oligodendrocytes in the brain was significantly decreased after one week of CPZ exposure (p < 0.02). The relative proportion of ermin+ cells compared to cells positive for the late-stage oligodendrocyte marker Nogo-A increased at the onset of remyelination in the corpus callosum (p < 0.02). The density of ermin-positive cells increased in the corpus callosum during the CPZ-phase of extensive remyelination (p < 0.0001). In MS, the density of ermin+ cells was higher in remyelinated lesion areas compared to non-remyelinated areas both in white- (p < 0.0001) and grey matter (p < 0.0001) and compared to normal-appearing white matter (p < 0.001). Ermin immunopositive cells in MS-lesions were not immunopositive for the early-stage oligodendrocyte markers O4 and O1, but a subpopulation was immunopositive for Nogo-A. The data suggest a relatively higher proportion of ermin immunopositivity in oligodendrocytes compared to Nogo-A indicates recent or ongoing remyelination.

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