Remote thalamic microstructural abnormalities related to cognitive function in ischemic stroke patients.

Fernández‐Andújar, Marina; Doornink, Fleur; Dacosta-Aguayo, Rosalía; Soriano-Raya, Juan José; Miralbell, Júlia; Bargalló, Núria; López‐Cancio, Elena; Ossa, Natàlia Pérez de la; Gomis, Meritxell; Millán, Mònica; Barrios, Maite; Cáceres, Cynthia; Pera, Guillem; Forés, Rosa; Clemente, Imma C.; Dávalos, Antoni; Mataró, María

doi:10.1037/neu0000087

Cited by 31 publications

(25 citation statements)

References 82 publications

(118 reference statements)

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“…Santos and colleagues also demonstrate that secondary degeneration of thalamic nuclei via diaschisis can be associated with verticality misperception after stroke (44). In another study that evaluates patients at 3 months after stroke, the thalamic microstructural abnormalities detected by DTI imaging correlate with lower verbal fluency performance, suggesting the secondary abnormalities in thalamus are related to cognitive dysfunction (45). A prospective cohort study by Kuchcinski and colleagues demonstrate that the secondary thalamic alteration after focal cortical injury independently contributes to poor functional, cognitive and emotional outcome (46).…”

Section: Secondary Thalamic Injury Is Associated With Functional Behamentioning

confidence: 97%

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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Section: Secondary Thalamic Injury Is Associated With Functional Behamentioning

confidence: 97%

Inflammatory Responses in the Secondary Thalamic Injury After Cortical Ischemic Stroke

et al. 2020

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“…This phenomenon is characterized by a gradual and progressive neuroinflammatory response, which is inexorably coupled with cell death (Dihné et al, 2002;Iizuka et al, 1990;Pappata et al, 2000). With few exceptions, secondary neurodegeneration is associated with impaired functional recovery (Binkofski et al, 1996;Fernández-Andújar et al, 2014;Seitz et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

“…Clinical studies have identified that the thalamus is particularly sensitive to neurodegeneration post-stroke, with thalamic disturbances emerging within weeks of infarction and persisting in some cases for up to two years (Fernández-Andújar et al, 2014;Gerhard et al, 2005;Herve et al, 2005;Kataoka et al, 1989). Neuroimaging studies have revealed that there is a significant increase in mean http://dx.doi.org/10.1016/j.bbi.2015.02.014 0889-1591/Ó 2015 Elsevier Inc. All rights reserved.…”

Section: Introductionmentioning

confidence: 99%

“…diffusivity (an indicator of microstructural tissue changes) within the thalamus 6 months after middle cerebral artery occlusion (MCAO) . It has also been noted that numerous patients post-stroke present with a reduced mean fractional anisotropy within the thalamus, and that this alteration is associated with impaired cognitive function (Fernández-Andújar et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

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Chronic stress exacerbates neuronal loss associated with secondary neurodegeneration and suppresses microglial-like cells following focal motor cortex ischemia in the mouse

Jones

Zouikr

Patience

et al. 2015

Brain, Behavior, and Immunity

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“…SND involves the progressive death of neurons that were connected to the site of infarction but not initially damaged by the stroke. SND unfolds over a longer time scale than the infarction process and has recently been implicated as a potential modulator to a number of late phase functional recovery disturbances (Chen, Garcia, Huang, & Constantini, ; Dang et al, ; Fernandez‐Andujar et al, ).…”

Section: Introductionmentioning

confidence: 99%

Impaired microglia process dynamics post‐stroke are specific to sites of secondary neurodegeneration

Kluge

Kracht

Abdolhoseini

et al. 2017

Glia

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Stroke induces tissue death both at the site of infarction and at secondary sites connected to the primary infarction. This latter process has been referred to as secondary neurodegeneration (SND). Using predominantly fixed tissue analyses, microglia have been implicated in regulating the initial response at both damage sites post-stroke. In this study, we used acute slice based multiphoton imaging, to investigate microglia dynamic process movement in mice 14 days after a photothrombotic stroke. We evaluated the baseline motility and process responses to locally induced laser damage in both the peri-infarct (PI) territory and the ipsilateral thalamus, a major site of post-stroke SND. Our findings show that microglia process extension toward laser damage within the thalamus is lost, yet remains robustly intact within the PI territory. However, microglia at both sites displayed an activated morphology and elevated levels of commonly used activation markers (CD68, CD11b), indicating that the standardly used fixed tissue metrics of microglial "activity" are not necessarily predictive of microglia function. Analysis of the purinergic P Y receptor, a key regulator of microglia process extension, revealed an increased somal localization on nonresponsive microglia in the thalamus. To our knowledge, this is the first study to identify a non-responsive microglia phenotype specific to areas of SND post-stroke, which cannot be identified by the classical assessment of microglia activation but rather the localization of P Y to the soma.

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Remote thalamic microstructural abnormalities related to cognitive function in ischemic stroke patients.

Abstract: Our findings support the hypothesis that ischemic stroke lesions are associated with remote thalamic diffusion abnormalities, and that these abnormalities can contribute to cognitive dysfunction 3 months after a cerebrovascular event.

Cited by 31 publications

References 82 publications

Inflammatory Responses in the Secondary Thalamic Injury After Cortical Ischemic Stroke

Inflammatory Responses in the Secondary Thalamic Injury After Cortical Ischemic Stroke

Chronic stress exacerbates neuronal loss associated with secondary neurodegeneration and suppresses microglial-like cells following focal motor cortex ischemia in the mouse

Impaired microglia process dynamics post‐stroke are specific to sites of secondary neurodegeneration

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