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Introduction: Atrial fibrillation (AF) is a major risk factor for ischaemic stroke and transient ischaemic attack (TIA), and AF detection can be challenged by asymptomatic and paroxysmal presentation. Long-term ECG monitoring after ischaemic stroke or TIA is recommended by all major societies in cardiology and cerebrovascular medicine as a secondary prophylactic measure. However, data on stroke reduction are lacking, and the recommendations show significant diversity. Methods and analysis: AF SPICE is a multicentre, national, investigator-initiated, randomised, parallel-group, register-based trial comparing extended ECG monitoring versus standard ECG monitoring in patients admitted with ischaemic stroke or TIA, with a composite endpoint of stroke, all-cause-mortality and intracerebral bleeding. Patients aged ≥ 70 years without previous AF will be randomised 1:1 to control (standard ECG monitoring) or intervention (extended ECG monitoring). In the control arm, patients will undergo 48±24 hours (ie, a range of 24-72hours) of continuous ECG monitoring according to national recommendations. In the intervention arm, patients will undergo 14+14 days of continuous ECG monitoring 3months apart using an ECG patch device, which will provide an easy-accessed, well-tolerated 14-day continuous ECG recording. All ECG patch recordings will be read in a core facility. In cases of AF detection, oral anticoagulation will be recommended if not contraindicated. A pilot phase has been concluded in 2022, which will transcend into the main trial during 2023-2026, including approximately 30 stroke units. The sample size was calculated to be 3262 patients. The primary outcome will be collected from register data during a 36-month follow-up. Ethics and dissemination: Ethical approval has been provided by the Swedish Ethical Review Authority, reference 2021-02770. The trial will be conducted according to the ethical principles of the Declaration of Helsinki and national regulatory standards.

E-book: 978-3-318-05885-7

Basilaristrombos är ett akut och livshotande tillstånd. Intravenös trombolys är förstahandsbehandling, men ibland kan det vara en fördel att kombinera eller ersätta behandlingen med trombektomi. Lyckade behandlingsresultat med trombektomi finns beskrivna ända upp till 12–24 timmar efter insjuknandet. I fallbeskrivningarna diskuteras basilaristrombos hos två patienter som insjuknat med oklar medvetandesänkning. DT-angiografi gav diagnosen, och trombektomi kunde utföras 10 respektive 13 timmar efter insjuknandet. Långtidsresultatet var gott. Slutsatsen är att DT alltid ska kompletteras med DT-angiografi vid utredning av en akut medvetandepåverkad patient. Trombektomi bör övervägas om basilaristrombos påvisas., [Thrombectomy gave good results in basilar thrombosis. Prolonged time window for the intervention is proposed]. Basilar stroke is one of the most devastating acute cerebral vascular events. Intravascular thrombectomy may be performed beyond the 4.5 hours intravenous thrombolysis time window. However, the time window for thrombectomy in basilar stroke remains unclear. In our clinics, two cases of coma of unknown origin were diagnosed through CT angiography as distal basilar occlusion and treated with thromb­ectomy. Recanalization was achieved at 10 hours after stroke onset in case 1 and at 13 hours in case 2. The first patient regained consciousness shortly after operation and walked unlimited at 2 months after stroke. The second patient woke up slowly with cortical blindness, cerebellar ataxia, and unilateral weakness. At 10 months post stroke, he moved unlimited with mRS 2. Therefore, acute brain CT scan should always be accompanied with CT angiography in cases of coma of unknown origin for the differential diagnosis of basilar stroke where thrombectomy may be considered up to 13 hours after stroke onset.

Stroke ranks as the #1 cause of handicapping humans in adult life. Up to date, there is no medication available to cure the post stroke neurological deficits. Fortunately, stroke patients usually experience spontaneous neurologic improvements at various degrees, which start days after a stroke and last up to 18 months. The pathophysiological mechanisms responsible for the post stroke spontaneous recovery are scarcely understood. Endogenous neurogenesis is one of the plausible pathways. In response to an acute ischemic insult, endogenous cells inside the cerebral cortex have been found to be able to divide at as early as 24-48 hours after ischemia to generate daughter neurons in the penumbral cortex, which gives rise to a quick in situ cortical neurogenesis. Meanwhile, the proliferation of neural stem cells in the subventricular zone is augmented after stroke. These stem cells, in addition to following a rostral migrating stream to their routine destination olfactory bulbs, as they usually do under physiological circumstances, start to migrate towards the infarct region. One week after stroke, they arrive at the periinfarct cortex where they differentiate into neurons, which contributes to a late phase cortical neurogenesis. Whether or not newborn neurons may function in the post stroke adult brains is a crucial issue in neurogenesis research. For the newborn neurons to function, one of the fundamental prerequisites is that they must be capable of synthesizing neurotransmitters. To specifically address this question, the biosynthesis of the excitatory neurotransmitter acetylcholine (Ach) and the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) is examined in adult rat brains after a photothrombotic cortical "ring" stroke with spontaneous reperfusion. To label the newborn brain cells, the DNA duplication marker 5-bromodeoxyuridine (BrdU) is repeatedly injected so that it becomes incorporated into the nuclear DNA while brain cells proliferate. Single/double/t