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Background and Aim: Despite progress made over the last 30 years, stroke is still a leading cause of disability and mortality; likewise, its burden is expected to increase over the next decades, due to population growth and aging. The development of drugs with better safety-efficacy profiles as well as strategies able to improve ischemic stroke management from the pre-hospital setting is needed., Summary: The pathophysiology of ischemic stroke involves multiple pathways resulting in cerebral artery obstruction and brain tissue ischemia. To date, the only approved drug for acute ischemic stroke is intravenous thrombolytic alteplase. Intravenous thrombolysis (IVT) can be administered alone or in combination with endovascular treatment (EVT) with mechanical thrombectomy, in case of large vessel occlusion and generally within 6 h from symptoms onset. The risk of potential bleeding complications, especially symptomatic intracerebral hemorrhage, is one of the reasons for the reluctance to administer IVT. Tenecteplase is a promising alternative fibrinolytic agent, having a better safety profile than alteplase. Moreover, recent evidences have allowed an extension of the IVT ± EVT time window for patients with unknown onset time and for those with a known onset time thanks to the new "tissue-window" approach guided by advanced neuroimaging techniques, which also helps in collateral circulation estimation. Regarding primary-secondary prevention, researchers are focused on improving the efficacy of antithrombotic drugs with a "hemostasis-sparing" approach. Neuroprotective agents are also under development, particularly stem cells. The COVID-19 pandemic has critically stressed global healthcare systems, with collateral damage resulting in access delivery of only emergency care, such as ischemic stroke. Regarding telemedicine, it has had a minor role in acute stroke management, and with the onset of COVID-19, this role will most likely be adopted to increase access and delivery in stroke assessment, but also in the follow-up., (© 2022 S. Karger AG, Basel.)

Background: In this randomized trial, currently utilized standard treatments were compared with enoxaparin for the prevention of venous thromboembolism (VTE) in patients with intracerebral hemorrhage (ICH)., Methods: Enoxaparin (0.4 mg daily for 10 days) was started after 72 h from the onset of ICH. The primary outcome was symptomatic or asymptomatic deep venous thrombosis as assessed by ultrasound at the end of study treatment. The safety of enoxaparin was also assessed. We included the results of this study in a meta-analysis of all relevant studies comparing anticoagulants with standard treatments or placebo., Results: PREVENTIHS was prematurely stopped after the randomization of 73 patients, due to the low recruitment rate. The prevalence of any VTE at 10 days was 15.8% in the enoxaparin group and 20.0% in the control group (RR 0.79 [95% CI 0.29-2.12]); 2.6% of enoxaparin and 8.6% of standard therapy patients had severe bleedings (RR 0.31 [95% CI 0.03-2.82]). When these results were meta-analyzed with the results of the selected studies (4,609 patients; 194 from randomized trials), anticoagulants were associated with a nonsignificant reduction in any VTE (OR 0.81; 95% CI 0.43-1.51), in pulmonary embolism (OR 0.53; 95% CI, 0.17-1.60), and in mortality (OR 0.85; 95% CI 0.64-1.12) without increase in hematoma enlargement (OR 0.97; 95% CI, 0.31-3.04)., Conclusions: In patients with acute ICH, the use of anticoagulants to prevent VTE was safe but the overall level of evidence was low due to the low number of patients included in randomized clinical trials., (© 2020 S. Karger AG, Basel.)

Carotid stenosis is generally associated with high risks of stroke and vascular events. In asymptomatic and symptomatic patients, with or without revascularization, optimal managements of carotid artery stenosis require the use of medications or lifestyle modifications (stopping smoking and monitoring hypertension, hyperlipidemia, and diabetes) to control the processes associated with atheroma to reduce the risk of embolic events. Moreover, antiplatelet therapy should be considered. There is little evidence that antiplatelet therapy is beneficial in preventing stroke or the progression of stenosis in asymptomatic patients, whereas, evidence of a benefit from antiplatelet therapy for secondary prevention of recurrent stroke in symptomatic patients with carotid atherosclerosis is more robust. Also, in patients undergoing carotid endarterectomy, perioperative antithrombotic therapy should include aspirin, while the addition of clopidogrel should be decided case-by-case. Furthermore, perioperative antithrombotic therapy in patients undergoing carotid stenting should consist a combination of aspirin plus clopidogrel.

Fatigue is a disabling and persistent symptom affecting many stroke survivors and is a predictor for death after stroke onset. Post-stroke fatigue is a multidimensional motor-perceptive, emotional and cognitive experience that has become of interest for stroke researchers only in the recent past. More studies are still needed to understand the pathophysiology, clinical characteristics, associated factors and best treatment strategy. The aim of this narrative review was to provide a comprehensive knowledge, from current literature, regarding the epidemiology, clinical characteristics and treatment of fatigue in order to provide physicians with better tools for treating this debilitating symptom that worsens outcome., (© 2014 S. Karger AG, Basel.)

Prevention of stroke and transient ischemic attack includes both conventional approaches to vascular risk factor management (blood pressure lowering, cholesterol reduction with statins, smoking cessation and antiplatelet therapy) and more specific interventions, such as carotid revascularization or anticoagulation for atrial fibrillation. The objective of this review is to discuss effective interventions for optimal primary and secondary stroke prevention., ((c) 2010 S. Karger AG, Basel.)

Stroke was never identified as a significant, autonomous field of activity of the emerging school of neurology at La Salpêtrière, which developed after the appointment of Jean-Martin Charcot (1825-1893) during the last days of 1861. However, stroke was already present in Charcot's first paper (1851), which dealt with a case of multiple organ cardiac embolism, including middle cerebral artery infarction, at a time when the studies of Rudolf Virchow on thromboembolism were unknown in France. A few years later, Charcot made a still up-to-date description of vascular intermittent claudication, which had only been reported in the horse. In the 1860s, Charcot and his pupils presented several major works dealing with cerebrovascular disease, including famous studies on miliary aneurysms in cerebral hemorrhage. This work was done with Charles Bouchard, at the time Charcot's 'interne', but who would become one of his 'political' opponents 2 decades later, when in 1892, as president of the 'agrégation' jury, he rejected the professorship application of 4 protégés of Charcot, including Joseph Babinski and Georges Gilles de la Tourette. Further work on cerebrovascular disease by Charcot included histological studies of brain 'softening', paraneoplastic cerebral arterial occlusion and consequences of stroke (e.g. arthropathies, vegetative changes, contractures and abnormal movements). Brain localization, one of Charcot's major neurological topics, was also largely based on stroke case studies. Charcot's work on stroke remains poorly recognized, but it demonstrates his unique skills in stimulating scientific work in younger colleagues, many of whom subsequently became major figures of neurology and psychiatry., (2010 S. Karger AG, Basel.)

Ischemic penumbra was first defined by Astrup in 1981 as perfused brain tissue at a level within the thresholds of functional impairment and morphological integrity, which has the capacity to recover if perfusion is improved. It exists, even for a short period of time in the center of ischemia, from which irreversible necrosis propagates to the neighboring tissues over time. Penumbra has become the focus of intense imaging research to differentiate it from infarction. Accurate detection of this 'tissue at risk' could be used to identify patients who would benefit most from acute treatment. Currently, recombinant tissue plasminogen activator (rtPA) is the only approved drug that has shown significant benefits in acute stroke patients when administered intravenously less than 4.5 h after stroke. However, its use is limited. Discrimination between infarct core and the surrounding potentially salvageable tissue is useful to better identify patients suitable for treatment. This can be achieved by positron emission tomography, single-photon-emission computed tomography, computed tomography perfusion scan and perfusion-weighted and diffusion-weighted magnetic resonance imaging. Identification of the penumbra might enable selective rtPA use in patients with large penumbras and small infarct cores, even beyond the 4.5-hour time window, where the penumbra may persist for more than 12 h. The purpose of this review was to describe neuroimaging modalities capable of identifying penumbra tissue so as to provide surrogate markers for new trials in acute ischemic stroke patients.

The safety of spinal manipulation is an issue that demands regular and rigorous assessment, as manipulation of the upper spine has been associated with serious adverse events such as cerebrovascular accidents due to cervical artery dissection. A correlation between stroke and cervical manipulation has been reported with increasing frequency, and each new report seems to reignite debate between neurologists and manual therapists. Specific risk factors for cerebrovascular complications related to spinal manipulation have not been identified yet; for this reason, any patient may be at risk, particularly those below 45 years of age. Patients undergoing spinal manipulative therapy need to consent to the possible risk of stroke or vascular injury from the procedure., (2008 S. Karger AG, Basel.)

Background: Dysphagia is common after stroke. We aimed to study the prognosis of dysphagia (assessed clinically) over the first 3 months after acute stroke and to determine whether specific neurovascular-anatomical sites were associated with swallowing dysfunction., Methods: We prospectively examined consecutive patients with acute first-ever stroke. The assessment of dysphagia was made using standardized clinical methods. The arterial territories involved were determined on CT/MRI. All patients were followed up for 3 months., Results: 34.7% of 406 patients had dysphagia. Dysphagia was more frequent in patients with hemorrhagic stroke (31/63 vs. 110/343; p = 0.01). In patients with ischemic stroke, the involvement of the arterial territory of the total middle cerebral artery was more frequently associated with dysphagia (28.2 vs. 2.2%; p < 0.0001). Multivariate analysis revealed that stroke mortality and disability were independently associated with dysphagia (p < 0.0001)., Conclusions: The frequency of dysphagia was relatively high. Regarding anatomical-clinical correlation, the most important factor was the size rather than the location of the lesion. Dysphagia assessed clinically was a significant variable predicting death and disability at 90 days., (Copyright 2004 S. Karger AG, Basel)

Background: Several studies have attempted to identify criteria for predicting functional prognosis after stroke, but often with contradictory results. The purpose of this study was to predict the functional outcome at discharge of first-time stroke patients included consecutively in the Lausanne Stroke Registry., Methods: We studied 3,628 sequential patients with first-ever stroke who were admitted consecutively to the Centre Hospitalier Universitaire Vaudois. Functional status was evaluated using the Rankin disability scale at discharge. We studied the prognostic value of historical, clinical and instrumental variables related to functional outcome at discharge. The factors studied were age, sex, risk factors, ECG results, occurrence of transient ischemic attacks (TIAs), extension of cerebral infarction, presumed cause of stroke, clinical findings and demographic characteristics. Univariate analysis was performed on each variable by comparing the number of functionally independent with that of dependent patients at the moment of discharge. The significant variables of the univariate analysis were subjected to multivariate analysis with a backward logistic regression procedure to find those with an independent effect on the outcome., Results: A total of 3,156 patients, excluding 117 patients with ischemic stroke who died during hospitalization and 355 with brain hemorrhage, were included; 2,867 patients belonged to the nil, mild or moderate disability groups (modified Rankin score 1-4; functionally at least partially independent patients), while 291 patients belonged to the severe disability group (modified Rankin score 5; functionally dependent patients). The mean duration of stay in hospital of the severe disability group was 31.2 days (SD = 16.2). Multivariate analysis showed that impaired consciousness on admission, limb weakness, progressive worsening, infarct in the superficial and deep territory of the middle cerebral artery, ischemic heart disease and cardiac arrhythmia were predictors of severe disability at discharge. Age was not an independent predictor of poor outcome. Hypercholesterolemia was significantly related to a better outcome., Conclusions: Some prognostic indicators associated with functional outcome at discharge are available during the first few hours after onset of stroke. This is important for the management of the individual stroke patient and for organizing suitable rehabilitation planning., (Copyright 2000 S. Karger AG, Basel)

We studied 25 patients with an acute thalamic stroke (infarct or hemorrhage) on CT or MRI scan and sensory dysfunction, among the 3,628 patients with first-time stroke included in the Lausanne Stroke Registry. Twelve patients had a right-sided infarct, 11 a left-sided infarct, and 2 a left-sided thalamic hemorrhage. Sensory symptoms or signs were the only clinical abnormality. The presumed causes of stroke were small artery disease in 21 patients including both cases of hemorrhage, emboligenic heart disease in 2, while the etiology of ischemic stroke was undetermined in 2 patients. Nine patients had a loss of all modalities of sensation with faciobrachiocrural distribution, 5 patients suffered dissociated sensory loss with faciobrachiocrural distribution and 11 patients showed a dissociated involvement of sensation with a partial distribution pattern. The inferolateral region (thalamogeniculate arteries) was involved in all patients. Six patients complained of pain and/or dysesthesias during the stroke; 5 of them had involvement of the nucleus ventrocaudalis (in 3 with damage to the nucleus ventro-oralis intermedius, and in one to the pulvinar) and 1 patient had involvement of the nucleus ventro-oralis intermedius. Eighteen patients complained of paresthesias in the contralateral part of the body; 16 of them had involvement of the nucleus ventrocaudalis (in 4 with damage to the nucleus ventro-oralis intermedius, in 1 with damage to the nucleus ventro-oralis intermedius, and nucleus ventro-oralis externus, and in one with damage to the nucleus parvocellularis and pulvinar). Four patients developed delayed pain and/or dysesthesias; all of them had involvement of the nucleus ventrocaudalis (in 1 with damage to the nucleus parvocellularis and pulvinar). Time lag from stroke onset to developing pain ranged from 2 to 15 days (mean 10.5 days). One patient with dissociated involvement of sensation with a partial distribution pattern had paresthesias and dissociated hemisensory loss involving position sense without pain and temperature sensations. This patient had involvement of the posterolateral part of the nucleus ventrocaudalis. In conclusion, sensory dysfunction and delayed pain are more often found in thalamic lesions that involve the nucleus ventrocaudalis, and nucleus ventro-oralis intermedius. Restricted sensory abnormalities correlate with very small lesions located in critical areas within these nuclei.