Chronic kidney disease (CKD) is associated to a higher stroke risk. Anemia is a common consequence of CKD, and is also a possible risk factor for cerebrovascular diseases. The purpose of this study ...was to examine if anemia and CKD are independent risk factors for mortality after stroke.
This historic cohort study was based on a stroke registry and included patients treated for a first clinical stroke in the stroke unit of one academic hospital over a three-year period. Mortality predictors comprised demographic characteristics, CKD, glomerular filtration rate (GFR), anemia and other stroke risk factors. GFR was estimated by means of the simplified Modification of Diet in Renal Disease formula. Renal function was assessed according to the Kidney Disease Outcomes Quality Initiative (K/DOQI)-CKD classification in five groups. A value of hemoglobin < 120 g/L in women and < 130 g/L in men on admission defined anemia. Kaplan-Meier survival curves and Cox models were used to describe and analyze one-year survival.
Among 890 adult stroke patients, the mean (Standard Deviation) calculated GFR was 64.3 (17.8) ml/min/1.73 m2 and 17% had anemia. Eighty-two (10%) patients died during the first year after discharge. Among those, 50 (61%) had K/DOQI CKD stages 3 to 5 and 32 (39%) stages 1 or 2 (p < 0.001). Anemia was associated with an increased risk of death one year after discharge (p < 0.001). After adjustment for other factors, a higher hemoglobin level was independently associated with decreased mortality one year after discharge hazard ratio (95% CI) 0.98 (0.97-1.00).
Both CKD and anemia are frequent among stroke patients and are potential risk factors for decreased one-year survival. The inclusion of patients with a first-ever clinical stroke only and the determination of anemia based on one single measure, on admission, constitute limitations to the external validity. We should investigate if an early detection and management of both CKD and anemia could improve survival in stroke patients.
•Selective attention guides behavior by prioritizing relevant sensory information.•Thalamo-cortical loops may play a strategic role in shaping priority maps.•Prioritization may be achieved via a ...pulvinar-mediated generation of α-oscillations.•Alpha oscillations may orchestrate the synchrony of cortico-cortical interaction.•Which may ultimately bias sensory representations.
Selective attention is a fundamental cognitive function that guides behavior by selecting and prioritizing salient or relevant sensory information of our environment. Despite early evidence and theoretical proposal pointing to an implication of thalamic control in attention, most studies in the past two decades focused on cortical substrates, largely ignoring the contribution of subcortical regions as well as cortico-subcortical interactions. Here, we suggest a key role of the pulvinar in the selection of salient and relevant information via its involvement in priority maps. Prioritization may be achieved through a pulvinar-mediated generation of alpha oscillations, which may then modulate neuronal gain in thalamo-cortical circuits. Such mechanism might orchestrate the synchrony of cortico-cortical interaction, by rendering neural communication more effective, precise and selective. We propose that this theoretical framework will support a timely shift from the prevailing cortico-centric view of cognition to a more integrative perspective of thalamic contributions to attention and executive control processes.
In acute ischemic stroke, intravenous thrombolysis (IVT) and acute endovascular therapy (EVT) have been shown to reduce long-term disability in randomized trials. International guidelines are ...partially not up to date and may not address situations for which there is limited scientific evidence. The goals of the present guidelines are to summarize the current scientific data for acute revascularization treatments to make sure that all Swiss Centers apply a similar, evidence, or consensus-based treatment standard. A multidisciplinary working group of the Swiss Stroke Society (SSS) searched and reviewed the literature on new randomized controlled trials (RCTs), large case series, meta-analyses, and other guidelines since the previous recommendations in 2009 to elaborate the consensus guidelines. The new RCTs have confirmed the effectiveness of IVT in various populations up to 4.5 h and proven the benefit of acute EVT up to approximately 8 h. For patients with unknown onset (including wake-up stroke), IVT and EVT can be effective up to 24 h after last proof of good health if patients are selected with advanced neuroimaging. Multiple case series and meta-analyses allow narrowing down the indications and relative and absolute contraindications to optimize the benefit–risk ratio of acute revascularization.
Acute stroke treatment has advanced substantially over the last years. Important milestones constitute intravenous thrombolysis, endovascular therapy (EVT), and treatment of stroke patients in ...dedicated units (stroke units). At present in Switzerland there are 13 certified stroke units and 10 certified EVT-capable stroke centers. Emerging challenges for the prehospital pathways are that (i) acute stroke treatment remains very time sensitive, (ii) the time window for acute stroke treatment has opened up to 24 h in selected cases, and (iii) EVT is only available in stroke centers. The goal of the current guideline is to standardize the prehospital phase of patients with acute stroke for them to receive the optimal treatment without unnecessary delays. Different prehospital models exist. For patients with large vessel occlusion (LVO), the Drip and Ship model is the most commonly used in Switzerland. This model is challenged by the Mothership model where stroke patients with suspected LVO are directly transferred to the stroke center. This latter model is only effective if there is an accurate triage by paramedics, hence the patient may benefit from the right treatment in the right place, without loss of time. Although the Cincinnati Prehospital Stroke Scale is a well-established scale to detect acute stroke in the prehospital setting, it neglects nonmotor symptoms like visual impairment or severe vertigo. Therefore we suggest “acute occurrence of a focal neurological deficit” as the trigger to enter the acute stroke pathway. For the triage whether a patient has a LVO (yes/no), there are a number of scores published. Accuracy of these scores is borderline. Nevertheless, applying the Rapid Arterial Occlusion Evaluation score or a comparable score to recognize patients with LVO may help to speed up and triage prehospital pathways. Ultimately, the decision of which model to use in which stroke network will depend on local (e.g. geographical) characteristics.
Le syndrome de vasoconstriction réversible est une cause fréquente de céphalées en coup de tonnerre aigues et récurrentes. Souvent « réversible », l’issue de cette maladie peut être fatale (<1 %).
...Nous présentons le cas d’une femme de 55 ans qui développe un syndrome de vasoconstriction réversible (SVCR) d’évolution dramatique et fatale en trois semaines. Les facteurs déclenchants identifiés sont une utilisation d’un vasoconstricteur intranasal (tuaminoheptane) dans un contexte d’ancienne toxicomanie à l’héroïne sous buprénorphine et de consommation active de cannabis. Des surveillances rapprochées cliniques, bioparamétriques, écho-Dopplers carotidovertébraux et transcraniens, angiographies cérébrales ont été instaurées précocement pour mettre en correspondance les aggravations cliniques et le vasospasme artériel. Selon les recommandations d’expert, la première ligne de traitement utilisée est la nimodipine (orale ou intra-veineuse) bien qu’aucun protocole ne soit véritablement établi. Ce traitement est vasodilatateur à faible dose mais peut devenir délétère à plus forte dose par réduction de la perfusion cérébrale (hypotension artérielle globale). En guise de seconde ligne de traitement, la thérapie triple H a été initiée avec de hautes doses de noradrénaline, ciblant une perfusion cérébrale optimale, l’effet vasoconstricteur de la noradrénaline étant plutôt épargneur des vaisseaux intracérébraux. Enfin, nous avons tenté des interventions intra-artérielles (nimodipine, ballonnet, bloc stéllaire) sans efficacité pérenne.
Le débit sanguin et l’index de Lindegaard de l’artère cérébrale moyenne à l’écho-Doppler augmentent quelques heures avant les aggravations cliniques, outil possible pour prédire les périodes d’évolution du SVCR et anticiper la réaction en cascade de perte d’autorégulation vasculaire intracérébrale. Un traitement optimal introduit au bon moment pourrait contre-carrer le mécanisme physiopathologique, par exemple nimodipine en titration.
Les challenges diagnostiques et thérapeutiques restent entiers pour tout SVCR sévère. Une étude approfondie de formes « non réversibles » pourrait permettre d’en améliorer la compréhension, la surveillance et la thérapie.
EEG and serum neuron-specific enolase (NSE) are used for outcome prognostication in patients with postanoxic coma; however, it is unclear if EEG abnormalities reflect transient neuronal dysfunction ...or neuronal death. To assess this question, EEG abnormalities were correlated with NSE. Moreover, NSE cutoff values and hypothermic EEG features related with poor outcome were explored.
In a prospective cohort of 61 adults treated with therapeutic hypothermia (TH) after cardiac arrest (CA), multichannel EEG recorded during TH was assessed for background reactivity and continuity, presence of epileptiform transients, and correlated with serum NSE collected at 24-48 hours after CA. Demographic, clinical, and functional outcome data (at 3 months) were collected and integrated in the analyses.
In-hospital mortality was 41%, and 82% of survivors had good neurologic outcome at 3 months. Serum NSE and EEG findings were strongly correlated (Spearman rho = 0.45; p < 0.001). Median NSE peak values were higher in patients with unreactive EEG background (p < 0.001) and discontinuous patterns (p = 0.001). While all subjects with nonreactive EEG died, 5 survivors (3 with good outcome) had NSE levels >33 μg/L.
The correlation between EEG during TH and serum NSE levels supports the hypothesis that early EEG alterations reflect permanent neuronal damage. Furthermore, this study confirms that absent EEG background reactivity and presence of epileptiform transients are robust predictors of poor outcome after CA, and that survival with good neurologic recovery is possible despite serum NSE levels> 33 μg/L. This underscores the importance of multimodal assessments in this setting.
Data on behavioral changes after thalamic lesion are sparse and largely based on isolated reports of patients with thalamic strokes. However, recent findings suggest that behavioral patterns can be ...delineated on the basis of the four main arterial thalamic territories. The anterior pattern consists mainly of perseverations and superimposition of unrelated information, apathy, and amnesia. After paramedian infarct, the most frequent features are disinhibition syndromes, with personality changes, loss of self-activation, amnesia, and, in the case of extensive lesions, thalamic "dementia"; this pattern may often be difficult to distinguish from primary psychiatric disorders, especially when neurologic dysfunction is lacking. After inferolateral lesion, executive dysfunction may develop but is often overlooked, although it may occasionally lead to severe long-term disability. After posterior lesion, whereas cognitive dysfunction with neglect and aphasia are well known, no specific behavioral syndrome has been reported. In the future, perfusion CT, functional MRI, and tractography using diffusion imaging in stroke patients may provide a better understanding of the role of the corticothalamic relationship in behavioral changes associated with thalamic stroke.
Does the brain become more resilient after a first stroke to reduce the consequences of a new lesion? Although recurrent strokes are a major clinical issue, whether and how the brain prepares for a ...second attack is unknown. This is due to the difficulties to obtain an appropriate dataset of stroke patients with comparable lesions, imaged at the same interval after onset. Furthermore, timing of the recurrent event remains unpredictable.
Here, we used a novel clinical lesion simulation approach to test the hypothesis that resilience in brain networks increases during stroke recovery. Sixteen highly selected patients with a lesion restricted to the primary motor cortex were recruited. At 3 time points of the index event (10 days, 3 weeks, 3 months), we mimicked recurrent infarcts by deletion of nodes in brain networks (resting-state functional magnetic resonance imaging). Graph measures were applied to determine resilience (global efficiency after attack) and wiring cost (mean degree) of the network.
At 10 days and 3 weeks after stroke, resilience was similar in patients and controls. However, at 3 months, although motor function had fully recovered, resilience to clinically representative simulated lesions was higher compared to controls (cortical lesion
=0.012; subcortical:
=0.009; cortico-subcortical:
=0.009). Similar results were found after random (
=0.012) and targeted (
=0.015) attacks.
Our results suggest that, in this highly selected cohort of patients with lesions restricted to the primary motor cortex, brain networks reconfigure to increase resilience to future insults. Lesion simulation is an innovative approach, which may have major implications for stroke therapy. Individualized neuromodulation strategies could be developed to foster resilient network reconfigurations after a first stroke to limit the consequences of future attacks.
After stroke restricted to the primary motor cortex (M1), it is uncertain whether network reorganization associated with recovery involves the periinfarct or more remote regions. We studied 16 ...patients with focal M1 stroke and hand paresis. Motor function and resting-state MRI functional connectivity (FC) were assessed at three time points: acute (<10 days), early subacute (3 weeks), and late subacute (3 months). FC correlates of recovery were investigated at three spatial scales, (i) ipsilesional non-infarcted M1, (ii) core motor network (M1, premotor cortex (PMC), supplementary motor area (SMA), and primary somatosensory cortex), and (iii) extended motor network including all regions structurally connected to the upper limb representation of M1. Hand dexterity was impaired only in the acute phase (P = 0.036). At a small spatial scale, clinical recovery was more frequently associated with connections involving ipsilesional non-infarcted M1 (Odds Ratio = 6.29; P = 0.036). At a larger scale, recovery correlated with increased FC strength in the core network compared to the extended motor network (rho = 0.71;P = 0.006). These results suggest that FC changes associated with motor improvement involve the perilesional M1 and do not extend beyond the core motor network. Core motor regions, and more specifically ipsilesional non-infarcted M1, could hence become primary targets for restorative therapies.
PDF
