cortical stroke
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2021 ◽  
Vol 12 ◽  
Author(s):  
Naveed Akhtar ◽  
Salman Al-Jerdi ◽  
Saadat Kamran ◽  
Rajvir Singh ◽  
Blessy Babu ◽  
...  

Background and Purpose: Nocturnal non-dipping blood pressure and heart rate are associated with an increased risk of cardiovascular disease. The effects of such variance on cerebrovascular disease have not been well studied.Methods: The 24-h ambulatory blood pressure (ABPM) and heart rate were monitored with B-pro in patients with acute stroke within the initial week of hospital admission. The risk factor profiles, clinical presentation, imaging, and short-term prognosis were compared in nocturnal dippers and non-dippers (more than 10% nocturnal decrease) of blood pressure and heart rate.Results: We enrolled 234 patients in whom ABPM and MRI data were available. Heart rate data were available in 180 patients. Lacunar sub-cortical stroke was the most common acute lesion (58.9%), while hypertension (74%) and diabetes (41.5%) were the most common associated risk factors. ABPM revealed non-dipping in 69% of patients. On univariate analysis, Small Vessel Disease (SVD) was significantly more frequent in non-dippers vs. dippers (BP: 56.8 vs. 40.3% p = 0.02; heart rate: 57.9 vs. 40.7% p = 0.03). Silent strokes were also more frequent in non-dippers vs. dippers (BP: 40.7 vs. 26.4% p = 0.35; heart rate: 44.6 vs. 25.4% p = 0.01). Multivariate analysis revealed SVD to be significantly related to age, hypertension, blood pressure non-dipping, and severity of symptoms at index event.Conclusions: The presence of nocturnal non-dipping of blood pressure and heart rate are associated with an increased risk of silent stroke and SVD. Increased use of ABPM may allow for improved diagnosis of non-dippers.


2021 ◽  
Author(s):  
Yunqing Song ◽  
Masaya Hirashima ◽  
Tomohiko Takei

Muscle synergies have been proposed as functional modules to simplify the complexity of body motor control; however, their neural implementation is still unclear. Converging evidence suggests that output projections of the spinal premotor interneurons (PreM-INs) underlie the formation of muscle synergies, but they exhibit a substantial variation across neurons and exclude standard models assuming a small number of unitary "modules" in the spinal cord. Here we compared neural network models for muscle synergies to seek a biologically plausible model that reconciles previous clinical and electrophysiological findings. We examined three neural network models: one with random connections (non-synergy model), one with a small number of spinal synergies (simple synergy model), and one with a large number of spinal neurons representing muscle synergies with a certain variation (population synergy model). We found that the simple and population synergy models emulate the robustness of muscle synergies against cortical stroke observed in human stroke patients. Furthermore, the size of the spinal variation of the population synergy matched well with the variation in spinal PreM-INs recorded in monkeys. These results suggest that a spinal population with moderate variation is a biologically plausible model for the neural implementation of muscle synergies.


2021 ◽  
Vol 15 ◽  
Author(s):  
Joris van der Cruijsen ◽  
Maria Carla Piastra ◽  
Ruud W. Selles ◽  
Thom F. Oostendorp

The inconsistent response to transcranial electric stimulation in the stroke population is attributed to, among other factors, unknown effects of stroke lesion conductivity on stimulation strength at the targeted brain areas. Volume conduction models are promising tools to determine optimal stimulation settings. However, stroke lesion conductivity is often not considered in these models as a source of inter-subject variability. The goal of this study is to propose a method that combines MRI, EEG, and transcranial stimulation to estimate the conductivity of cortical stroke lesions experimentally. In this simulation study, lesion conductivity was estimated from scalp potentials during transcranial electric stimulation in 12 chronic stroke patients. To do so, first, we determined the stimulation configuration where scalp potentials are maximally affected by the lesion. Then, we calculated scalp potentials in a model with a fixed lesion conductivity and a model with a randomly assigned conductivity. To estimate the lesion conductivity, we minimized the error between the two models by varying the conductivity in the second model. Finally, to reflect realistic experimental conditions, we test the effect rotation of measurement electrode orientation and the effect of the number of electrodes used. We found that the algorithm converged to the correct lesion conductivity value when noise on the electrode positions was absent for all lesions. Conductivity estimation error was below 5% with realistic electrode coregistration errors of 0.1° for lesions larger than 50 ml. Higher lesion conductivities and lesion volumes were associated with smaller estimation errors. In conclusion, this method can experimentally estimate stroke lesion conductivity, improving the accuracy of volume conductor models of stroke patients and potentially leading to more effective transcranial electric stimulation configurations for this population.


2021 ◽  
Vol 429 ◽  
pp. 119615
Author(s):  
Y Chan ◽  
Y Wong ◽  
N Khalid ◽  
A Flores-Martin ◽  
L Frank ◽  
...  
Keyword(s):  

2021 ◽  
pp. 154596832110413
Author(s):  
Michel R. T. Sinke ◽  
Geralda A. F. van Tilborg ◽  
Anu E. Meerwaldt ◽  
Caroline L. van Heijningen ◽  
Annette van der Toorn ◽  
...  

Background. Recovery of motor function after stroke appears to be related to the integrity of axonal connections in the corticospinal tract (CST) and corpus callosum, which may both be affected after cortical stroke. Objective. In the present study, we aimed to elucidate the relationship of changes in measures of the CST and transcallosal tract integrity, with the interhemispheric functional connectivity and sensorimotor performance after experimental cortical stroke. Methods. We conducted in vivo diffusion magnetic resonance imaging (MRI), resting-state functional MRI, and behavior testing in twenty-five male Sprague Dawley rats recovering from unilateral photothrombotic stroke in the sensorimotor cortex. Twenty-three healthy rats served as controls. Results. A reduction in the number of reconstructed fibers, a lower fractional anisotropy, and higher radial diffusivity in the ipsilesional but intact CST, reflected remote white matter degeneration. In contrast, transcallosal tract integrity remained preserved. Functional connectivity between the ipsi- and contralesional forelimb regions of the primary somatosensory cortex significantly reduced at week 8 post-stroke. Comparably, usage of the stroke-affected forelimb was normal at week 28, following significant initial impairment between day 1 and week 8 post-stroke. Conclusions. Our study shows that post-stroke motor recovery is possible despite degeneration in the CST and may be supported by intact neuronal communication between hemispheres.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Gab Seok Kim ◽  
Jessica M. Stephenson ◽  
Abdullah Al Mamun ◽  
Ting Wu ◽  
Monica G. Goss ◽  
...  

AbstractSecondary injury following cortical stroke includes delayed gliosis and eventual neuronal loss in the thalamus. However, the effects of aging and the potential to ameliorate this gliosis with NMDA receptor (NMDAR) antagonism are not established. We used the permanent distal middle cerebral artery stroke model (pdMCAO) to examine secondary thalamic injury in young and aged mice. At 3 days post-stroke (PSD3), slight microgliosis (IBA-1) and astrogliosis (GFAP) was evident in thalamus, but no infarct. Gliosis increased dramatically through PSD14, at which point degenerating neurons were detected. Flow cytometry demonstrated a significant increase in CD11b+/CD45int microglia (MG) in the ipsilateral thalamus at PSD14. CCR2-RFP reporter mouse further demonstrated that influx of peripheral monocytes contributed to the MG/Mϕ population. Aged mice demonstrated reduced microgliosis and astrogliosis compared with young mice. Interestingly, astrogliosis demonstrated glial scar-like characteristics at two years post-stroke, but not by 6 weeks. Lastly, treatment with memantine (NMDAR antagonist) at 4 and 24 h after stroke significantly reduced gliosis at PSD14. These findings expand our understanding of gliosis in the thalamus following cortical stroke and demonstrate age-dependency of this secondary injury. Additionally, these findings indicate that delayed treatment with memantine (an FDA approved drug) provides significant reduction in thalamic gliosis.


Author(s):  
Yuk Man Chan ◽  
Yean Wong ◽  
Noorulain Khalid ◽  
Stephen Wastling ◽  
Andreas Flores‐Martin ◽  
...  
Keyword(s):  

2021 ◽  
Vol 15 ◽  
Author(s):  
Rehnuma Islam ◽  
Stasja Drecun ◽  
Balazs V. Varga ◽  
Ilan Vonderwalde ◽  
Ricky Siu ◽  
...  

Stroke is a leading cause of death and long-term disability worldwide. Current therapeutic options are limited in terms of their time for implementation and efficacy in promoting recovery. Cell transplantation has been shown to have promise in several animal models however significant challenges remain, including the optimal source of cells to promote neural repair. Here, we report on the use of a population of human ESC derived, cortically specified, neuroepithelial precursor cells (cNEPs) that are neurally restricted in their lineage potential. CNEPs have the potential to give rise to mature neural cell types following transplantation, including neurons, astrocytes and oligodendrocytes. With a view towards translation, we sought to determine whether this human cell source was effective in promoting improved functional outcomes following stroke. Undifferentiated cNEPs were transplanted in a pre-clinical endothelin-1 (ET-1) model of ischemic motor cortical stroke in immunocompromised SCID-beige mice and cellular and functional outcomes were assessed. We demonstrate that cNEP transplantation in the acute phase (4 days post-stroke) improves motor function as early as 20 days post-stroke, compared to stroke-injured, non-transplanted mice. At the time of recovery, a small fraction (<6%) of the transplanted cNEPs are observed within the stroke injury site. The surviving cells expressed the immature neuronal marker, doublecortin, with no differentiation into mature neural phenotypes. At longer survival times (40 days), the majority of recovered, transplanted mice had a complete absence of surviving cNEPS. Hence, human cNEPs grafted at early times post-stroke support the observed functional recovery following ET-1 stroke but their persistence is not required, thereby supporting a by-stander effect rather than cell replacement.


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