Abstract TMP53: Preeclampsia Leads to Long Term Cerebral White Matter Damage and Cortical Atrophy: a Magnetic Resonance Imaging Study

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Timo Siepmann ◽  
Henry Boardman ◽  
Amy Bilderbeck ◽  
Ludovica Griffanti ◽  
Yvonne Kenworthy ◽  
...  

Introduction: Women with a history of preeclampsia have a two-fold higher risk of acute ischemic stroke even after controlling for classic cardiovascular risk factors. We determined whether specific patterns in cerebral damage are present after preeclampsia that may explain this risk. Methods: We performed brain magnetic resonance imaging in women between 5 and 15 years after either a preeclamptic or normotensive pregnancy. Analysis of white matter structure was undertaken using voxel-based segmentation of fluid attenuation inversion recovery sequences to assess white matter lesion volume and diffusion tensor imaging to measure microstructural integrity. Voxel-based analysis of grey matter volumes was performed in T1 weighted sequences with adjustment for skull size. Cardiovascular, obstetric profiles were assessed. Results: Thirty-four previously preeclamptic women (aged 42.8 ± 5.1 years, mean ± SD) and 49 controls were included. Previously preeclamptic women had reduced cortical grey matter volume (523.2 ± 30.1 vs 544.4 ± 44.7 ml, p<0.05) and, although both groups displayed frontal white matter damage, changes were more extensive in previously preeclamptic women. They displayed increased temporal lobe white matter disease (lesion volume: 23.2 ± 24.9 vs 10.9 ± 15.0 ml, p<0.05) and altered microstructural integrity (radial diffusivity 538 ± 19 vs. 526 ± 18*10 -6 mm 2 /sec, p<0.01), which also extended to occipital and parietal lobes. The degree of temporal lobe white matter change in previously preeclamptic women was independent of their current cardiovascular risk profile (p<0.05) and increased with time from index pregnancy (Figure). Conclusions: A history of preeclampsia is associated with temporal lobe white matter damage and cortical atrophy in young women, which is out of proportion to their classic cardiovascular risk profile and increases with time from pregnancy, consistent with ongoing susceptibility and cumulative brain damage.

Neurology ◽  
2017 ◽  
Vol 88 (13) ◽  
pp. 1256-1264 ◽  
Author(s):  
Timo Siepmann ◽  
Henry Boardman ◽  
Amy Bilderbeck ◽  
Ludovica Griffanti ◽  
Yvonne Kenworthy ◽  
...  

Objective:To determine whether changes in cerebral structure are present after preeclampsia that may explain increased cerebrovascular risk in these women.Methods:We conducted a case control study in women between 5 and 15 years after either a preeclamptic or normotensive pregnancy. Brain MRI was performed. Analysis of white matter structure was undertaken using voxel-based segmentation of fluid-attenuation inversion recovery sequences to assess white matter lesion volume and diffusion tensor imaging to measure microstructural integrity. Voxel-based analysis of gray matter volumes was performed with adjustment for skull size.Results:Thirty-four previously preeclamptic women (aged 42.8 ± 5.1 years) and 49 controls were included. Previously preeclamptic women had reduced cortical gray matter volume (523.2 ± 30.1 vs 544.4 ± 44.7 mL, p < 0.05) and, although both groups displayed white matter lesions, changes were more extensive in previously preeclamptic women. They displayed increased temporal lobe white matter disease (lesion volume: 23.2 ± 24.9 vs 10.9 ± 15.0 μL, p < 0.05) and altered microstructural integrity (radial diffusivity: 538 ± 19 vs 526 ± 18 × 10−6 mm2/s, p < 0.01), which also extended to occipital and parietal lobes. The degree of temporal lobe white matter change in previously preeclamptic women was independent of their current cardiovascular risk profile (p < 0.05) and increased with time from index pregnancy (p < 0.05).Conclusion:A history of preeclampsia is associated with temporal lobe white matter changes and reduced cortical volume in young women, which is out of proportion to their classic cardiovascular risk profile. The severity of changes is proportional to time since pregnancy, which would be consistent with continued accumulation of damage after pregnancy.


2012 ◽  
Vol 8 (4S_Part_5) ◽  
pp. P176-P177
Author(s):  
Shiva Keihaninejad ◽  
Hui Zhang ◽  
Tim Shakespeare ◽  
Natalie Ryan ◽  
Ian Malone ◽  
...  

Author(s):  
Guilherme Artoni ◽  
Fernando Cendes ◽  
José C. V. Moreira ◽  
Marina K. M. Alvim ◽  
Lucas S. Silva ◽  
...  

Our research uses magnetic resonance imaging and statistical tools to compare patients with TEMPORAL LOBE EPILEPSY WITH AND WITHOUT hippocampal atrophy, SEARCHING FOR DIFFERENCES RELATED TO GREY AND WHITE MATTER ATROPHY.


2012 ◽  
Vol 8 (4S_Part_2) ◽  
pp. P52-P53
Author(s):  
Shiva Keihaninejad ◽  
Hui Zhang ◽  
Tim Shakespeare ◽  
Natalie Ryan ◽  
Ian Malone ◽  
...  

2020 ◽  
Author(s):  
Michele Veldsman ◽  
Emilio Werden ◽  
Natalia Egorova ◽  
Mohamed Salah Khlif ◽  
Amy Brodtmann

ABSTRACTObjectiveExecutive dysfunction affects 40% of stroke patients and is associated with poor quality of life. Stroke severity and lesion volume rarely predict whether a patient will have executive dysfunction. Stroke typically occurs on a background of cerebrovascular burden, which impacts cognition and brain network structural integrity. We investigated whether measures of white matter microstructural integrity and cerebrovascular risk factors better explain executive dysfunction than markers of stroke severity.MethodsWe used structural equation modelling to examine multivariate relationships between cerebrovascular risk, white matter microstructural integrity (fractional anisotropy and mean diffusivity), stroke characteristics and executive dysfunction in 126 stroke patients (mean age 68.4 years), three months post-stroke, and compared to 40 age- and sex-matched control participants. Executive function was measured using the Trail Making Tests, Clock Drawing task and Rey Complex Figure copy task. Microstructural integrity was estimated using a standard pipeline to process diffusion weighted images.ResultsExecutive function was below what would be expected for age and education level in stroke patients (t-test compared to controls t(79)=5.75, p<0.001). A multivariate structural equation model illustrated the complex relationship between executive function, white matter integrity, stroke characteristics and cerebrovascular risk. Pearson’s correlations confirmed a stronger relationship between executive dysfunction and white matter integrity, than executive dysfunction and stroke severity. Mediation analysis showed the relationship between executive function and white matter integrity is mediated by cerebrovascular burden.InterpretationWhite matter microstructural degeneration of the superior longitudinal fasciculus in the executive control network better explains executive dysfunction than markers of stroke severity.


Sexual Health ◽  
2018 ◽  
Vol 15 (4) ◽  
pp. 358 ◽  
Author(s):  
Harmanpreet Tiwana ◽  
Aiesha Ahmed

Background Common causes of temporal lobe hyper intensities are central nervous system infections like herpes simplex encephalitis, Lyme disease, limbic encephalitis and vascular pathology like Cerebral Autosomal Dominant Arteriopathy with Subcortical infarcts and Leukoencephalopathy. Methods: Personal assessment, laboratory data analysis and neuroimaging for the patient who was admitted to a central Pennsylvania tertiary care referral centre were conducted. Results: A 52-year-old male presented with a 1-year history of diffuse dysesthesia in upper and lower extremities with associated intermittent headaches and neck stiffness. Evaluation with lumbar puncture revealed increased nucleated cells (50 ul) with lymphocytic predominance (96%) and an elevated protein level of 109 mg/dl. Magnetic resonance imaging (MRI) of the brain showed T2/FLAIR hyper intensity in bilateral subcortical temporal white matter, left-greater-than-right and associated volume loss in cerebral parenchyma. Additional abnormal work up included reactive serum reactive plasma regain and Treponema pallidum antibody particle agglutination. Diagnosis of neurosyphilis was made and the patient was treated with intramuscular (IM) penicillin for 3 weeks. At the time of discharge, his headache and neck stiffness resolved and dysesthesias were decreased in intensity. Conclusions: The diagnosis of neurosyphilis is intricate, and no reference standard exists. Neuroimaging findings of neurosyphilis commonly are cerebral infarctions, leptomeningeal enhancement or non-specific white matter lesions. Less common features on fluid-attenuated inversion recovery (FLAIR) sequences are cortical atrophy and mesial temporal parenchymal signal changes. It is prudent to keep neurosyphilis in differential of mesial temporal lobe white matter changes, as early diagnosis and treatment results in better prognosis.


Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Leka Sivakumar ◽  
Thomas Jeerakathil ◽  
Negar Asdaghi ◽  
Richard Camicioli ◽  
Christian Beaulieu ◽  
...  

Background: Cognitive changes have been described in subacute TIA/minor stroke (TIA/MIS), but the temporal profile is unknown. We tested the hypothesis that TIA/MIS patients experience transient cognitive impairment, and that this can be predicted by Diffusion-Weighted Imaging (DWI) lesion volume. Methods: Acute TIA/MIS stroke (NIH stroke scale score ≤3) patients with no history of cognitive impairment were prospectively recruited within 72 h of onset. Patients underwent Montreal Cognitive Assessment (MoCA), Mini-Mental Status Examination (MMSE) and MRI, including DWI and Fluid-Attenuated Inverse Recovery (FLAIR) sequences, at baseline, days 7 and 30. DWI lesion and FLAIR chronic white matter hyperintensity (WMH) volumes were measured planimetrically. Results: Fifty patients (mean age 68 ±15.1 years) were imaged at a median (IQR) of 26.5 (28.5) h after onset. Cognitive impairment (scores ≤26) was detected more frequently with MoCA (31/50, 62%) than MMSE (13/50, 26%, p=0.009). Acute ischemic lesions (DWI) were present in 33 (66%) patients. Mean DWI volume at baseline was 4.5 ± 11.1ml. Patients with DWI lesions (22/33, 67%) had similar impairment rates as those without (9/17, 53%; p=0.34). Linear regression indicated no relationship between acute DWI lesion volume (log transformed) and baseline MoCA scores (β=0.028, 95% CI [-2.09, 2.44]). Impaired patients had larger WMH volumes (13.6 ± 21.9 ml) than unaffected patients (2.6 ± 3.2 ml, p=0.01). Log transformed WMH volumes were inversely predictive of baseline MoCA scores (β=-0.54, 95% CI [-7.84, -2.28]). Median MoCA scores improved over time (27(5) at day 7 and 28(5) at day 30). Patients with baseline impairment and an increase of ≥2 points on MoCA by day 30 were defined as reverters (N=20). DWI lesion frequency was similar in reverters and those with persisting impairment (75% vs 64%, p= 0.50), as was DWI (6.9 ±14.3 ml vs 1.2 ±1.9 ml; p= 0.113) and WMH lesion volume (17.0 ± 26.2 ml vs 8.1 ± 8.1 ml; p= 0.18). Conclusions: Most TIA/MIS patients have evidence of temporary acute cognitive impairment when assessed with MoCA. Deficits are correlated with chronic WMH, suggesting an unmasking of subclinical cognitive impairment. Temporary cognitive deficits should be considered in the management of TIA/MIS patients.


2017 ◽  
Vol 24 (5) ◽  
pp. 675-678 ◽  
Author(s):  
James F Sumowski ◽  
Victoria M Leavitt ◽  
Maria A Rocca ◽  
Matilde Inglese ◽  
Gianna Riccitelli ◽  
...  

Background/Objective: Memory deficits due to multiple sclerosis (MS) have been variably linked to lower subcortical grey matter (SCGM) and mesial temporal lobe (MTL) volumes. We investigated which is the better predictor and whether this changes across disease stages. Methods/Results: Memory was assessed in 315 patients. Magnetic resonance imaging (MRI) measured volumes of total brain, grey matter, white matter, MTL (hippocampus, amygdala) and SCGM (thalamus, caudate). MTL predicted memory in the total sample and in patients with earlier (<10 years) or later (⩾10 years) relapsing disease. SCGM (specifically thalamus) predicted memory in progressive patients. Conclusions: Neuroanatomical correlates of memory deficits differ across disease stages.


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