Hippocampal Complex Atrophy in Poststroke and Mild Cognitive Impairment

Selnes, Per; Grambaitė, Ramunė; Rincón, M.; Bjørnerud, Atle; Gjerstad, Leif; Hessen, Erik; Auning, Eirik; Johansen, Krisztina K.; Almdahl, Ina Selseth; Due‐Tønnessen, Paulina; Vegge, Kjetil; Bjelke, Börje; Fladby, Tormod

doi:10.1038/jcbfm.2015.110

Cited by 18 publications

(18 citation statements)

References 39 publications

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“…Our data suggest that neuronal loss in the ipsilesional amygdala and hippocampus precedes that in the thalamus. Hippocampal volume loss has been recognized as a hallmark of cognitive impairment in Alzheimer's disease, and was recently suggested to play a role in stroke as well ( 21 , 26 ). Post-stroke hippocampal atrophy is thought to be a predictor for post-stroke cognitive impairment ( 35 ).…”

Section: Discussionmentioning

confidence: 99%

Ongoing Secondary Degeneration of the Limbic System in Patients With Ischemic Stroke: A Longitudinal MRI Study

et al. 2019

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Purpose: Ongoing post-stroke structural degeneration and neuronal loss preceding neuropsychological symptoms such as cognitive decline and depression are poorly understood. Various substructures of the limbic system have been linked to cognitive impairment. In this longitudinal study, we investigated the post-stroke macro- and micro-structural integrity of the limbic system using structural and diffusion tensor magnetic resonance imaging.Materials and Methods: Nineteen ischemic stroke patients (11 men, 8 women, average age 53.4 ± 12.3, range 18–75 years), with lesions remote from the limbic system, were serially imaged three times over 1 year. Structural and diffusion-tensor images (DTI) were obtained on a 3.0 T MRI system. The cortical thickness, subcortical volume, mean diffusivity (MD), and fractional anisotropy (FA) were measured in eight different regions of the limbic system. The National Institutes of Health Stroke Scale (NIHSS) was used for clinical assessment. A mixed model for multiple factors was used for statistical analysis, and p-values <0.05 was considered significant.Results: All patients demonstrated improved NIHSS values over time. The ipsilesional subcortical volumes of the thalamus, hippocampus, and amygdala significantly decreased (p < 0.05) and MD significantly increased (p < 0.05). The ipsilesional cortical thickness of the entorhinal and perirhinal cortices was significantly smaller than the contralesional hemisphere at 12 months (p < 0.05). The cortical thickness of the cingulate gyrus at 12 months was significantly decreased at the caudal and isthmus regions as compared to the 1 month assessment (p < 0.05). The cingulum fibers had elevated MD at the ipsilesional caudal-anterior and posterior regions compared to the corresponding contralesional regions.Conclusion: Despite the decreasing NIHSS scores, we found ongoing unilateral neuronal loss/secondary degeneration in the limbic system, irrespective of the lesion location. These results suggest a possible anatomical basis for post stroke psychiatric complications.

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Section: Discussionmentioning

confidence: 99%

Ongoing Secondary Degeneration of the Limbic System in Patients With Ischemic Stroke: A Longitudinal MRI Study

et al. 2019

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“…Presence of both CVD and AD pathology is shown to have additive effects in terms of cognitive symptoms in AD, 42 and we recently demonstrated correlations between WMH load and neuropsychological tests of episodic memory, which typically are impaired in early AD. 43 WMHs are often considered markers of small vessel CVD and thought to originate from ischemia due to hypoperfusion. 44 In this case, WMHs may function to lower the threshold for symptomatic presentation in AD or to contribute to the clinical manifestations.…”

Section: Discussionmentioning

confidence: 99%

White matter hyperintensity microstructure in amyloid dysmetabolism

Kalheim

Bjørnerud

Fladby

et al. 2016

J Cereb Blood Flow Metab

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Accumulating evidence suggests associations between cerebrovascular disease (CVD) and Alzheimer's disease (AD). White matter hyperintensities of presumed vascular origin (WMHs) are increased in subjects with mild cognitive impairment (MCI) and AD, but the exact pathomechanistic link is unknown. The current study investigated effects of amyloid dysmetabolism on the microstructure of WMHs in subjects with MCI or subjective cognitive decline (N ¼ 51), dichotomized according to pathological or normal levels of amyloid-b peptide (Ab 42 ) in cerebrospinal fluid (CSF). Thirtyone subjects with low CSF Ab 42 (Abþ) and 20 subjects with normal CSF Ab 42 (AbÀ) were assessed with magnetic resonance diffusion tensor imaging (DTI), and fractional anisotropy (FA), radial diffusivity (DR), axial diffusivity (DA), and mean diffusivity (MD) were determined. There were no significant differences in WMH volume or distribution between the groups, and neither age nor WMH volume had significant impact on the DTI indices. Nevertheless, there were significantly higher DA, DR, and MD in WMHs in Abþ relative to AbÀ; however, no differences in FA were found. The present results suggest that amyloid accumulation is associated with impaired structural integrity (e.g. relating to more extensive demyelination and loss of axons) in WMHs putatively adding to effects of ischemia.

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“…Stroke leads to cognitive impairment partly due to the disruption of hippocampal function. Recent studies provided evidence that stroke causes hippocampal structural changes and dysregulation of hippocampal networks, leading to memory decline in humans [ 1 , 2 , 3 , 4 , 5 ]. Interestingly, cerebral ischemia has been shown to stimulate the proliferation of endogenous neural progenitor cells in animal models [ 6 ] and stroke patients [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

Growth Hormone Treatment Promotes Remote Hippocampal Plasticity after Experimental Cortical Stroke

Sanchez-Bezanilla

Åberg

Crock

et al. 2020

IJMS

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Cognitive impairment is common after stroke, and disturbances in hippocampal function are often involved, even in remote non-hippocampal injuries. In terms of hippocampal function, growth hormone (GH) is known to affects plasticity and cognition. We aimed to investigate whether GH treatment after an experimental cortical stroke could enhance remote hippocampal plasticity and the hippocampal-dependent visual discrimination task. C57BL6 male mice were subjected to cortical photothrombotic stroke. Stroke mice were then treated with either saline or GH at 48 h after occlusion for 28 days. We assessed learning and memory using mouse touchscreen platform for the visual discrimination task. We also evaluated markers of neural progenitor cells, synaptic plasticity and cerebrovascular remodelling in the hippocampal formation. GH treatment significantly improved the performance on visual discrimination task after stroke. We observed a concomitant increased number of bromodeoxyuridine-positive cells in the dentate gyrus of the hippocampus. We also detected increased protein levels and density of doublecortin, a neuronal precursor cells marker, as well as glutamate receptor 1 (GLuR1), a synaptic marker. These findings provide further neurobiological evidence for how GH treatment could be used to promote hippocampal plasticity in a remote region from the initial cortical injury, and thus enhance cognitive recovery after stroke.

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Hippocampal Complex Atrophy in Poststroke and Mild Cognitive Impairment

Cited by 18 publications

References 39 publications

Ongoing Secondary Degeneration of the Limbic System in Patients With Ischemic Stroke: A Longitudinal MRI Study

Ongoing Secondary Degeneration of the Limbic System in Patients With Ischemic Stroke: A Longitudinal MRI Study

White matter hyperintensity microstructure in amyloid dysmetabolism

Growth Hormone Treatment Promotes Remote Hippocampal Plasticity after Experimental Cortical Stroke

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