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Ischemic strokes are caused by a reduction in cerebral blood flow and both the ischemic period and subsequent reperfusion induce brain injury, with different tissue damage depending on the severity of the ischemic insult, its duration, and the particular areas of the brain affected. In those areas vulnerable to cerebral ischemia, the inhibition of protein translation is an essential process of the cellular response leading to delayed neuronal death. In particular, translation initiation is rate-limiting for protein synthesis and the eukaryotic initiation factor (eIF) 4F complex is indispensable for cap-dependent protein translation. In the eIF4F complex, eIF4G is a scaffolding protein that provides docking sites for the assembly of eIF4A and eIF4E, binding to the cap structure of the mRNA and stabilizing all proteins of the complex. The eIF4F complex constituents, eIF4A, eIF4E, and eIF4G, participate in translation regulation by their phosphorylation at specific sites under cellular stress conditions, modulating the activity of the cap-binding complex and protein translation. This work investigates the phosphorylation of eIF4G1 involved in the eIF4E/eIF4G1 association complex, and their regulation in ischemia-reperfusion (IR) as a stress-inducing condition. IR was induced in an animal model of transient cerebral ischemia and the results were studied in the resistant cortical region and in the vulnerable hippocampal CA1 region. The presented data demonstrate the phosphorylation of eIF4G1 at Ser1147, Ser1185, and Ser1231 in both brain regions and in control and ischemic conditions, being the phosphorylation of eIF4G1 at Ser1147 the only one found in the eIF4E/eIF4G association complex from the cap-containing matrix (m7GTP-Sepharose). In addition, our work reveals the specific modulation of the phosphorylation of eIF4G1 at Ser1147 in the vulnerable region, with increased levels and colocalization with eIF4E in response to IR. These findings contribute to elucidate the molecular mechanism of protein translation regulation that underlies in the balance of cell survival/death during pathophysiological stress, such as cerebral ischemia.

Transient ischemic attacks (TIAs) before an acute ischemic stroke (AIS) could induce ischemic tolerance (IT) phenomena. with an endogenous neuroprotective role (Ischemic preconditioning. IPC). A consecutive prospective cohort of patients with AIS were recruited from 8 different hospitals. Participants were classified by those with non-previous recent TIA vs. previous TIA (within seven days. TIA ≤7d). A total of 541 AIS patients were recruited. 40 (7.4%). of them had previous TIA ≤7d. In line with IPC. patients with TIA ≤7d showed: 1) a significantly less severe stroke at admission by NIHSS score. 2) a better outcome at 7–90 days follow-up and reduced infarct volumes. 3) a specific upregulated metabolomics/lipidomic profile composed of diverse lipid categories. Effectively. IPC activates an additional adaptive response on increasing circulation levels of structural and bioactive lipids to facilitate functional recovery after AIS which may support biochemical machinery for neuronal survival. Furthermore. previous TIA before AIS seems to facilitate the production of anti-inflammatory mediators that contribute to a better immune response. Thus. the IT phenomena contributes to a better adaptation of further ischemia. Our study provides first-time evidence of a metabolomics/lipidomic signature related to the development of stroke tolerance in AIS patients induced by recent TIA.

This case highlights the case of a woman in her 50´s and the association of Frank's sign with vascular disease. Earlobe crease or Frank's sign is a diagonal crease in the earlobe that extends diagonally from the tragus to the edge of the auricle with an angle of approximately 45°. Its presence increases with advancing age and is thought to be predictive of vascular disease. The recognition of this sign is considered a key factor in the identification of patients with high vascular risk and endothelial dysfunction. The association with a reperfusion syndrome, like our patient, is not known.

Approximately 40% of patients with cryptogenic stroke have a Permeable Foramen Oval, which is present in 20-25% of the healthy population. Controversy and doubt whether this structure should be closed when paradoxical embolism is suspected has been proposed to reduce the risk of recurrence. Some publications (trials CLOSURE I, RESPECT 2013 or PC TRIAL) discouraged it, based on the results obtained. New evidence published at the end of 2017 (CLOSE, REDUCE and RESPECT 2017 trials) changes the way of evidence to reopen the debate and delimit which patients the procedure should be considered since there is sufficient evidence to reduce the risk of recurrence in some selected patients

Objective: To determine whether the left atrial size can predict the development of atrial fibrillation (AF) in patients with embolic stroke of undetermined source (ESUS). Methods: Patients with ischemic stroke were included prospectively (January 2015-July 2015) when ESUS was suspected. Clinical and cardiac imaging data were recorded. Patients with cardiac failure were excluded. Results: a total of 55 patients were included. Medium age was 71 years. The proportion of patients who developed AF during the follow-up (1 year) was 23, 63%. 10 % of patients did not have any vascular risk factor. Basal ECG was normal in 98% of cases. The left atrial size volume was 36, 08 ml in patients who developed AF and 27, 14 ml in patients who did not. Conclusions: In patients with ESUS, left atrial size dimensions do not predict the occurrence of AF.

We present the experience for thrombolytic treatment using recombinant tisular plasminogen activator (rt-PA) at a university hospital. We analyze the influence of individual and collective acquired experience and of the activation of an out-of-hospital stroke code (OSC) on the delays to onset of treatment, number of patients treated and outcome.Prospective register of patients with ischemic stroke treated with rt-PA within the period 1/2004- 12/2006. Comparison of results between patients treated during the three years of study and based on the individual experience of the neurologist who applies the treatment and on the patients treated with or without activation of OSC.A total of 87 patients were treated (mean age: 66.6 +/- 13.7). Door-to-needle time was 79 +/- 21 min in 2004, 64 +/-22 in 2005 and 63 +/- 26 in 2006 (p=0.003). Experienced neurologists started thrombolysis sooner (door-to-needle time: 62 +/- 22 min vs 75 +/- 27, p=0.03). Activation of the ESC reduced door-to-needle time (53 +/ 17 min vs 65 +/- 21; p=0.032) and door-to-computed tomography scan time (21 +/- 10 min vs 29 +/-24; p=0.016). There were no differences in outcome in the different groups.Individual and collective acquired experience and the activation of an OSC can lower in-hospital delays. This contributes to increasing the number of patients eligible for thrombolysis. Thrombolytic therapy is safe and effective even when it is applied by inexperienced neurologists if strict guidelines are followed.

To analyse the incidence, risk factors, aetiology, treatment and clinical evolution of young patients with stroke.Retrospective registry of patients aged 55 years or younger hospitalised in a stroke unit during 2014. We recorded the incidence rate for all strokes and analysed demographic data, risk factors, degree of stress, stroke type and aetiology, reperfusion treatments and clinical evolution.The study included 110 patients, the majority of whom were men (60.9%, 1.6:1 ratio). The incidence rate was 13.3% (110 of 830 strokes). Most of the patients had cardiovascular risk factors. Smoking was the most common risk factor (56.4%), followed by arterial hypertension (50%), dyslipidaemia (42.7%), obesity (33%), diabetes (18.2%) and emboligenic heart disease (12.7%). Some 64.3% of the heart disease cases and 51.1% of the dyslipidaemia cases were discovered during hospitalisation. Some 57.2% of the patients experienced psychosocial stress in the stage prior to the stroke. Some 83.6% of the stroke cases were ischaemic, 12.7% were haemorrhagic and 3.6% were venous sinus thrombosis. Of the ischaemic stroke cases, 30.4% were cryptogenic, 23.9% were lacunar, 16.3% were from uncommon causes, 15.2% were atherothrombotic and 14.1% were cardioembolic. Some 78.6% of the cerebral haemorrhage cases were hypertensive. Some 23.3% of the ischaemic stroke cases underwent reperfusion treatments in the acute phase, achieving levels of functional independence at 3 months of 62.5%.The majority of stroke events in patients 55 years of age or younger appear to be related to a high prevalence of classical cardiovascular risk factors and possibly to psychosocial stress.