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Background: Most approaches to transient ischaemic attack (TIA) triage use clinical scores and vascular imaging; however, some biomarkers have been suggested to improve the prognosis of TIA patients., Methods: Serum levels of copeptin, adiponectin, neopterin, neuron-specific enolase, high-sensitivity C-reactive protein, IL-6, N-terminal pro-B-type natriuretic peptide, S100β, tumour necrosis factor-alpha and IL-1α as well as clinical characteristics were assessed on consecutive TIA patients during the first 24 h of the onset of symptoms., Results: Among 237 consecutive TIA patients, 12 patients (5%) had a stroke within 7 days and 15 (6%) within 90 days. Among all candidate biomarkers analysed, only copeptin was significantly increased in patients with stroke recurrence (SR) within 7 days (P = 0.026) but not within 90 days. A cut-off point of 13.8 pmol/l was established with a great predictive negative value (97.4%). Large artery atherosclerosis (LAA) [hazard ratio (HR) 12.7, 95% CI 3.2-50.1, P < 0.001] and copeptin levels ≥13.8 pmol/l (HR 3.9, 95% CI 1.01-14.4, P = 0.039) were independent predictors of SR at the 7-day follow-up. LAA was the only predictor of 90-day SR (HR 7.4, 95% CI 2.5-21.6, P < 0.001). ABCD3I was associated with 7- and 90-day SRs (P = 0.025 and P = 0.034, respectively). The association between copeptin levels and LAA had a diagnostic accuracy of 90.3%., Conclusions: Serum copeptin could be an important prognostic biomarker to guide management decisions among TIA patients. Therefore, TIA patients with copeptin levels below 13.8 pmol/l and without LAA have an insignificant risk of 7-day SR and could be managed on an outpatient basis., (© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background and Purpose: The etiological classification of patients with transient ischaemic attack (TIA) is a difficult endeavor and the use of serum biomarkers could improve the diagnostic accuracy. The aim of this study was to correlate atrial fibrillation, the main cardioembolic etiology (CE), with different serum biomarkers measured in consecutive TIA patients., Methods: The concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha, neuron-specific enolase, high-sensitivity C-reactive protein, IL-1-α and the N-terminal pro-B type natriuretic peptide (NT-proBNP) were quantified in the serum of 140 patients with TIA and 44 non-stroke subjects. Measurements were performed at different times throughout evolution: within 24 h of symptoms onset and at days 7 and 90., Results: With the exception of IL-6, all biomarkers were higher in TIA patients than in controls. NT-proBNP was significantly related to the presence or new diagnosis of AF at all time points analyzed. Furthermore, the baseline NT-proBNP level was significantly higher than values at the 7-day and 90-day follow-up. For this reason, different cut-off values were obtained at different times: 313 pg/ml at baseline [odds ratio (OR) = 18.99, P < 0.001], 181 pg/ml at 7 days (OR = 11.4, P = 0.001) and 174 pg/ml (OR = 8.46, P < 0.001) at 90 days., Conclusion: High levels of NT-proBNP determined during the first 3 months after a TIA were associated with AF. Consequently, this biomarker may be useful to reclassify undetermined TIA patients as having disease of CE., (© 2013 The Author(s) European Journal of Neurology © 2013 EFNS.)

Patients and Methods: The carotid intima media thickness (IMT) is a new prognostic marker of vascular events. We studied its usefulness in the diagnosis workup of 211 consecutive transient ischemic attack (TIA) patients from the REGITELL registration. GIM was measured according to Mannheim criteria. It was established its relationship to the main prognostic variables described in TIA: ABCD2 scale, symptomatology and etiologic subtypes according to TOAST classification., Results: Men value of carotid IMT was 0.91 ± 0.20 mm. After Bonferroni adjustment, IMT was associated with age of 60 years or older (0.95 ± 0.19 mm; p < 0.001), male sex (0.95 ± 0.20 mm; p = 0.003), ABCD2 scale (p < 0.001), association of risk factors are greater than or equal to 2 (0.94 ± 0.20 mm; p < 0.001), carotid plaque presence (0.98 ± 0.19 mm; p < 0.001), intracranial stenosis (1.09 ± 0.18 mm; p = 0.001), presence of ischemic chronic lesions on head CT (p <0.001) and etiology (p < 0.001). The patients presented with isolated sensory symptoms had significantly lower IMT (0.77 ± 0.18 mm; p = 0.002). Belonging to the third tertile of IMT was only an independent predictor of large-artery atherosclerosis (OR = 3,06; CI 95% = 1.31-7.13; p = 0.01)., Conclusion: Based on our results, IMT determination seems to not improve the diagnostic accuracy of other ultrasonographic characteristics like the presence of plaques or the degree of stenosis.

Background and Objectives: A new radiological-clinical score (ABCDI) has been recently described to predict the risk of stroke recurrence after a transient ischemic attack (TIA). We validated this score in a cohort of patients with TIA (REGITELL)., Patients and Methods: We studied 310 consecutive patients with TIA. Clinical scales (ABCD and ABCD2) and radiological-clinical scales (ABCDI and ABCD2I) were quantified. Radiological clinical scales were calculated by adding one point for the presence of ischemic brain injury in CT scan to its eponymous clinical score. We established its relationship with the risk of recurrence at 7 and 90 days, and the presence of an atheromatous etiology (AE)., Results: During the first week of follow-up, 18 (5.8%) patients suffered a recurrence, whereas 24 (7.7%) had a recurrence at 90 days. The multivariate study (Cox regression) identified the recurrence of episodes (hazard ratio [HR] 2.92, 95% CI 1.11 to 7.64, p=0.029) and AE (HR 3.13 95% CI: 1.17 to 8.36, p=0.023) as independent predictors of new stroke at 7 days and only AE for stroke at three months (RR 3.33, 95% CI: 1,42-7,77, p=0.006). The predictors (logistic regression) of AE were recurrence of episodes (odds ratio [OR] 3.12, 95% CI 1.58-6.14, p=0.001) and presence of ischemic lesions on CT scan (OR 2.69, 1.38-5.28, p=0.004)., Conclusions: The ABCDI and ABCD2I scales are not useful in our population. The risk of recurrence after a TIA cannot only be established by clinical scores or CT scan findings., (Copyright © 2009 Elsevier España, S.L. All rights reserved.)

Introduction: Cerebrovascular disease can cause different memory disorders depending on the area of the brain involved. More specifically, ischemic lesions in the frontal region can be associated to short-term verbal memory disorders., Patients and Methods: Two groups of subjects were studied, 10 of whom were patients who presented a frontal cerebral infarction and 10 healthy controls. They were administered a memory task involving word recognition. While they were performing the task the electrical activity of their brains was recorded in order to examine event-related potentials (ERP)., Results: The patients' performance of the task was poorer than that of the healthy control subjects. Likewise, while the latter displayed a predominantly frontal distribution of ERPs, in the patients the frontal activity diminished and was seen to be chiefly temporoparietooccipital., Conclusions: These findings allow important conclusions to be drawn about the characteristics of the memory disorder presented by these patients.

Introduction and Development: Over the last two decades antiphospholipid syndrome (APS) has started to be recognized from the association of apparently anionic phospholipid-specific antibodies with thrombosis, thrombocytopenia and recurrent foetal losses. This syndrome affects patients with systemic lupus erythematosus and is considered to be an important cause of thromboembolic disease. Antiphospholipid antibodies are serum immunoglobulins that react with negatively charged phospholipids, albeit directly or by means of a cofactor, affect the coagulation system, and promote thrombosis. Recent research has been directed towards gaining an understanding of the mechanisms by which these antibodies are able to play a direct role in the pathophysiology of thrombosis, and the extent to which certain risk factors, such as smoking, high blood pressure, lipid disorders and so on, exert an influence over the expression of phospholipids in the cerebral endothelium., Conclusion: These antibodies have no single mechanism of action; different authors have described different pathological mechanisms, which help us to understand the heterogeneous clinical manifestations of APS.

Aims: In this study we describe the main findings from research into the autoreactive process triggered by activated T lymphocytes, which are generated in the peripheral compartment and then migrate towards the central nervous system (CNS) in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) its animal model., Method: The different strategies that have been developed to date for the immunological treatment of MS have been designed to intervene in the pathogenic process of the disease by blocking the activation of T cells and B cells with specific antigens, interfering with immunological effector mechanisms and inhibiting the migration of lymphocytes towards the CNS. The cause of the inflammatory response in MS has still not been defined, but the findings from EAE studies and in patients with MS suggest that the disease has an autoimmune aetiology involving autoreactive T cells which are specific for antigens in the myelin membrane. To activate these cells at least two cues are needed during antigen recognition and later the T CD4+ lymphocytes are differentiated in two subpopulations, Th1 and Th2, which differ in the pattern of secretion of cytosines depending on the stage of the disease process. The progressions of EAE and MS give rise to changes in the primary and secondary self reactive responses of the T cells during the progression of the disease., Conclusion: The pathological immune mechanisms mediated by activated myelin specific T lymphocytes play a key role in the progression and recuperation, as well as the mediation, of tissue damage during the course of MS and EAE.

Introduction and Method: The study of antiphospholipid antibodies has aroused a great deal of interest among researchers, as some of them are related to neurological diseases and in particular with cerebral ischemia. Cases of strokes in which the aetiology is unknown have been reported in young patients. Until now anticardiolipin antibodies and lupus anticoagulant have received the most attention in studies, but recently descriptions have been published of anticardiolipin antibodies with other particularities that can act as more specific immunity markers for strokes of undetermined origin in young adults. Recent research has been directed towards gaining an understanding of the mechanisms that allow these antibodies to play a direct role in the physiopathology of thrombosis and how certain risk factors smoking, high blood pressure, lipid disorders can exert an influence on the expression of phospholipids in the cerebral endothelium. Several authors have described different pathological mechanisms that help to understand the heterogeneous clinical manifestations of antiphospholipid syndrome., Conclusion: There is a need to study the different possible antigens of the antiphospholipid antibodies, as well as their specificities and pathological mechanisms, in greater depth in order to obtain a phospholipid immunity marker that is useful in the diagnosis of young stroke patients who are positive for these antibodies.