MRI Susceptibility Changes Suggestive of Iron Deposition in the Thalamus after Ischemic Stroke

Etten, Ellis S. van; Dumas, Eve M.; Bogaard, Simon J.A. van den; Buchem, Mark A. van; Wermer, Marieke J.H.

doi:10.1159/000433560

Cited by 22 publications

(22 citation statements)

References 33 publications

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“…We speculate that, given a larger sample, TH may exhibit significantly increased susceptibility in PCAS patients than in healthy controls. Similar to our study, in a previous study that used signal intensity variation on T2 * -weighted images to reflect the changes of iron content, ischemic stroke patients, including those with infarcts in the distribution of PCA, showed increased iron accumulation in TH on the side ipsilateral to the infarct ( 43 ). Compared with healthy controls, both ACAS and PCAS patients exhibited significantly increased susceptibility in PU and GP.…”

Section: Discussionsupporting

confidence: 88%

Iron Deposition in Gray Matter Nuclei of Patients With Intracranial Artery Stenosis: A Quantitative Susceptibility Mapping Study

Mao¹,

Dou²,

Wang³

et al. 2022

Front. Neurol.

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Purpose: This study aimed to use quantitative susceptibility mapping (QSM) to systematically investigate the changes of iron content in gray matter (GM) nuclei in patients with long-term anterior circulation artery stenosis (ACAS) and posterior circulation artery stenosis (PCAS).Methods: Twenty-five ACAS patients, 25 PCAS patients, and 25 age- and sex-matched healthy controls underwent QSM examination. Patients were scored using the National Institutes of Health Stroke Scale (NIHSS) and modified Rankin Scale (mRS) to assess the degree of neural function deficiency. On QSM images, iron related susceptibility of GM nuclei, including bilateral caudate nucleus, putamen (PU), globus pallidus (GP), thalamus (TH), substantia nigra (SN), red nucleus, and dentate nucleus (DN), were assessed. Susceptibility was compared between bilateral GM nuclei in healthy controls, ACAS patients, and PCAS patients. Partial correlation analysis, with age as a covariate, was separately performed to assess the relationships of susceptibility with NIHSS and mRS scores.Results: There were no significant differences between the susceptibilities for left and right hemispheres in all seven GM nucleus subregions for healthy controls, ACAS patients, and PCAS patients. Compared with healthy controls, mean susceptibility of bilateral PU, GP, and SN in ACAS patients and of bilateral PU, GP, SN, and DN in PCAS patients were significantly increased (all P < 0.05). In addition, mean susceptibility of bilateral TH and SN in PCAS patients was significantly higher than in ACAS patients (both P < 0.05). With partial correlation analysis, mean susceptibility at bilateral PU of ACAS patients was significantly correlated with mRS score (r = 0.415, P < 0.05), and at bilateral PU in PCAS patients was correlated with NIHSS score (r = 0.424, P < 0.05).Conclusion: Our findings indicated that abnormal iron metabolism may present in different subregions of GM nuclei after long-term ACAS and PCAS. In addition, iron content of PU in patients with ACAS and PCAS was correlated with neurological deficit scores. Therefore, iron quantification measured by QSM susceptibility may provide a new insight to understand the pathological mechanism of ischemic stroke caused by ACAS and PCAS.

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Section: Discussionsupporting

confidence: 88%

Iron Deposition in Gray Matter Nuclei of Patients With Intracranial Artery Stenosis: A Quantitative Susceptibility Mapping Study

Mao¹,

Dou²,

Wang³

et al. 2022

Front. Neurol.

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“…Our results provide additional information concerning the temporality of remote neurodegeneration after infarct. Van Etten et al (2015) reported a lower average T2*-signal intensity in manually drawn region of interest within the entire thalamus at a single slice level as early as Day 1 after stroke onset. However, T2* signal intensity suffers from high intra-and inter-examination variability and we believe our quantitative R2* mapping method is more robust, particularly with the unbiased 3D atlas-driven regions of interest that we used here.…”

Section: Discussionmentioning

confidence: 93%

“…We first computed parameters of the R2* histogram [histogram parameters (HP): 5th percentile, median, 95th percentile and full-width at half-maximum] within the whole thalamus ipsilateral and contralateral to infarct. An asymmetry index of R2* (van Etten et al, 2015) for each parameter of the histogram was also calculated with:…”

Section: Co-registrationmentioning

confidence: 99%

Thalamic alterations remote to infarct appear as focal iron accumulation and impact clinical outcome

Kuchcinski

Munsch

Lopes

et al. 2017

Brain

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See Duering and Schmidt (doi:10.1093/awx135) for a scientific commentary on this article.Thalamic alterations have been observed in infarcts initially sparing the thalamus but interrupting thalamo-cortical or cortico-thalamic projections. We aimed at extending this knowledge by demonstrating with in vivo imaging sensitive to iron accumulation, one marker of neurodegeneration, that (i) secondary thalamic alterations are focally located in specific thalamic nuclei depending on the initial infarct location; and (ii) such secondary alterations can contribute independently to the long-term outcome. To tackle this issue, 172 patients with an infarct initially sparing the thalamus were prospectively evaluated clinically and with magnetic resonance imaging to quantify iron through R2* map at 24-72 h and at 1-year follow-up. An asymmetry index was used to compare R2* within the thalamus ipsilateral versus contralateral to infarct and we focused on the 95th percentile of R2* as a metric of high iron content. Spatial distribution within the thalamus was analysed on an average R2* map from the entire cohort. The asymmetry index of the 95th percentile within individual nuclei (medio-dorsal, pulvinar, lateral group) were compared according to the initial infarct location in simple and multiple regression analyses and using voxel-based lesion-symptom mapping. Associations between the asymmetry index of the 95th percentile and functional, cognitive and emotional outcome were calculated in multiple regression models. We showed that R2* was not modified at 24-72 h but showed heterogeneous increase at 1 year mainly within the medio-dorsal and pulvinar nuclei. The asymmetry index of the 95th percentile within the medio-dorsal nucleus was significantly associated with infarcts involving anterior areas (frontal P = 0.05, temporal P = 0.02, lenticular P = 0.01) while the asymmetry index of the 95th percentile within the pulvinar nucleus was significantly associated with infarcts involving posterior areas (parietal P = 0.046, temporal P < 0.001) independently of age, gender and infarct volume, which was confirmed by voxel-based lesion-symptom mapping. The asymmetry index of the 95th percentile within the entire thalamus at 1 year was independently associated with poor functional outcome (P = 0.04), poor cognitive outcome (P = 0.03), post-stroke anxiety (P = 0.04) and post-stroke depression (P = 0.02). We have therefore identified that iron accumulates within the thalamus ipsilateral to infarct after a delay with a focal distribution that is strongly linked to the initial infarct location (in relation with the pattern of connectivity between thalamic nuclei and cortical areas or deep nuclei), which independently contributes to functional, cognitive and emotional outcome.

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“…The MRI changes correspond with histological validation of reactive microglia/infiltrating macrophages and chronic accumulation of iron (8), indicating MRI as a potential tool to detect longitudinal changes in the secondary thalamic injury. Similarly, van Etten et al report hypointense signals in ipsilesional thalamus on T2 * -weighted MRI of unilateral ischemic stroke patients, suggesting accumulation of toxic iron in secondary thalamic injury (38). In patients with focal cortical infarction, a delayed shrinkage in the thalamus is detected by MRI scanned at late phase (31.6 ± 16.6 months after the initial stroke) (39).…”

Section: Methods and Strategies To Identify Secondary Thalamic Injurymentioning

confidence: 94%

Inflammatory Responses in the Secondary Thalamic Injury After Cortical Ischemic Stroke

et al. 2020

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Stroke is one of the major causes of chronic disability worldwide and increasing efforts have focused on studying brain repair and recovery after stroke. Following stroke, the primary injury site can disrupt functional connections in nearby and remotely connected brain regions, resulting in the development of secondary injuries that may impede long-term functional recovery. In particular, secondary degenerative injury occurs in the connected ipsilesional thalamus following a cortical stroke. Although secondary thalamic injury was first described decades ago, the underlying mechanisms still remain unclear. We performed a systematic literature review using the NCBI PubMed database for studies that focused on the secondary thalamic degeneration after cortical ischemic stroke. In this review, we discussed emerging studies that characterized the pathological changes in the secondary degenerative thalamus after stroke; these included excitotoxicity, apoptosis, amyloid beta protein accumulation, blood-brain-barrier breakdown, and inflammatory responses. In particular, we highlighted key findings of the dynamic inflammatory responses in the secondary thalamic injury and discussed the involvement of several cell types in this process. We also discussed studies that investigated the effects of blocking secondary thalamic injury on inflammatory responses and stroke outcome. Targeting secondary injuries after stroke may alleviate network-wide deficits, and ultimately promote stroke recovery.

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MRI Susceptibility Changes Suggestive of Iron Deposition in the Thalamus after Ischemic Stroke

Cited by 22 publications

References 33 publications

Iron Deposition in Gray Matter Nuclei of Patients With Intracranial Artery Stenosis: A Quantitative Susceptibility Mapping Study

Iron Deposition in Gray Matter Nuclei of Patients With Intracranial Artery Stenosis: A Quantitative Susceptibility Mapping Study

Thalamic alterations remote to infarct appear as focal iron accumulation and impact clinical outcome

Inflammatory Responses in the Secondary Thalamic Injury After Cortical Ischemic Stroke

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