Surrogate biomarkers of outcome for wake-up ischemic stroke.

BACKGROUND: Wake-up ischemic stroke (IS) has been usually excluded from acute stroke therapy options for being outside of the safe treatment window. We identified risk factors, and clinical or molecular biomarkers that could be therapeutic targets for wake-up stroke prevention, thus hopefully leading to a decrease in its mortality and disability in medium to long-term outcome. METHODS: 4251 ischemic stroke (IS) patients from a prospectively registered database were recruited; 3838 (90.3%) had known onset-symptom time, and 413 (9.7%) were wake-up strokes. The main endpoint was to analyze the association between different serum biomarkers with wake-up IS episodes and their progression. Leukocytes count, serum levels of C-reactive protein, fibrinogen, interleukin 6 (IL-6), and vitamin D were analyzed as inflammation biomarkers; N-terminal pro-B-type Natriuretic-Peptide and microalbuminuria, used as atrial/endothelial dysfunction biomarkers; finally, glutamate levels as excitotoxicity biomarker. In addition, demographic, clinical and neuroimaging variables associated with the time-evolution of wake-up IS patients and functional outcome at 3 months were evaluated. Good and poor functional outcome were defined as mRS ≤2 and mRS > 2 at 3 months, respectively. RESULTS: Wake-up IS showed a poorer outcome at 3-months than in patients with known on-set-symptom time (59.1% vs. 48.1%; p < 0.0001). Patients with wake-up IS had higher levels of inflammation biomarkers; IL-6 levels at admission (51.5 ± 15.1 vs. 27.8 ± 18.6 pg/ml; p < 0.0001), and low vitamin D levels at 24 h (5.6 ± 5.8 vs. 19.2 ± 9.4 ng/ml; p < 0.0001) are worthy of attention. In a logistic regression model adjusted for vitamin D, OR was 15.1; CI 95%: 8.6-26.3, p < 0.0001. However, we found no difference in vitamin D levels between patients with or without clinical-DWI mismatch (no: 18.95 ± 9.66; yes: 17.84 ± 11.77 ng/mL, p = 0.394). No difference in DWI volume at admission was found (49.3 ± 96.9 ml in wake-up IS patients vs. 51.7 ± 98.2 ml in awake IS patients; p = 0.895). CONCLUSIONS: Inflammatory biomarkers are the main factors that are strongly associated with wake-up IS episodes. Wake-up IS is associated with lower vitamin D levels. These data indicate that vitamin D deficiency could become a therapeutic target to reduce wake-up IS events.

Early Neurological Change After Ischemic Stroke Is Associated With 90-Day Outcome.

BACKGROUND AND PURPOSE: Large-scale observational studies of acute ischemic stroke (AIS) promise to reveal mechanisms underlying cerebral ischemia. However, meaningful quantitative phenotypes attainable in large patient populations are needed. We characterize a dynamic metric of AIS instability, defined by change in National Institutes of Health Stroke Scale score (NIHSS) from baseline to 24 hours baseline to 24 hours (NIHSSbaseline - NIHSS24hours = ΔNIHSS6-24h), to examine its relevance to AIS mechanisms and long-term outcomes. METHODS: Patients with NIHSS prospectively recorded within 6 hours after onset and then 24 hours later were enrolled in the GENISIS study (Genetics of Early Neurological Instability After Ischemic Stroke). Stepwise linear regression determined variables that independently influenced ΔNIHSS6-24h. In a subcohort of tPA (alteplase)-treated patients with large vessel occlusion, the influence of early sustained recanalization and hemorrhagic transformation on ΔNIHSS6-24h was examined. Finally, the association of ΔNIHSS6-24h with 90-day favorable outcomes (modified Rankin Scale score 0-2) was assessed. Independent analysis was performed using data from the 2 NINDS-tPA stroke trials (National Institute of Neurological Disorders and Stroke rt-PA). RESULTS: For 2555 patients with AIS, median baseline NIHSS was 9 (interquartile range, 4-16), and median ΔNIHSS6-24h was 2 (interquartile range, 0-5). In a multivariable model, baseline NIHSS, tPA-treatment, age, glucose, site, and systolic blood pressure independently predicted ΔNIHSS6-24h (R2=0.15). In the large vessel occlusion subcohort, early sustained recanalization and hemorrhagic transformation increased the explained variance (R2=0.27), but much of the variance remained unexplained. ΔNIHSS6-24h had a significant and independent association with 90-day favorable outcome. For the subjects in the 2 NINDS-tPA trials, ΔNIHSS3-24h was similarly associated with 90-day outcomes. CONCLUSIONS: The dynamic phenotype, ΔNIHSS6-24h, captures both explained and unexplained mechanisms involved in AIS and is significantly and independently associated with long-term outcomes. Thus, ΔNIHSS6-24h promises to be an easily obtainable and meaningful quantitative phenotype for large-scale genomic studies of AIS.

Time Trends in Intracerebral Hemorrhage Associated with Oral Anticoagulation and Its Risks Factors in Spain from 2008 to 2015.

BACKGROUND: Intracerebral hemorrhage (ICH) is 7- to 10-fold higher in anticoagulated patients. Given the more extended use of oral anticoagulants, an increase in the prevalence of ICH associated with oral anticoagulation (ICH-OAC) could be expected. However, there is no previous study that assesses the time trends of ICH-OAC in Spain. METHODS: We conducted a combined data analysis after creating a joint database of the 3 most important epidemiological studies on ICH-OAC of our country: the EPICES study (2008-2009), the TAC Registry (TR) study (2012-2013) and the TAC Registry 2 (TR2) study (2015). We finally included 65, 235, and 366 patients from the EPICES, TR, and TR2 studies, respectively. RESULTS: We have observed a 3.73-fold increase in the crude annual incidence of ICH-OAC throughout the period of study, with proportion of ICH-OAC out of total ICH increasing from 8.4% in 2008 to 18.2% in 2015. Age, dyslipidemia, and prior antiplatelet treatment increased during the study, but we found no statistically significant differences in other risk factors for ICH-OAC. CONCLUSIONS: The incidence of ICH-OAC is increasing in our country. It might at least be partly explained by aging of the population, with mean age at presentation being higher in the last years.

Regulatory T cells participate in the recovery of ischemic stroke patients.

BACKGROUND: Recent preclinical studies have shown that regulatory T cells (Treg) play a key role in the immune response after ischemic stroke (IS). However, the role of Treg in human acute IS has been poorly investigated. Our aim was to study the relationship between circulating Treg and outcome in human IS patients. METHODS: A total of 204 IS patients and 22 control subjects were recruited. The main study variable was good functional outcome at 3 months (modified Rankin scale ≤2) considering infarct volume, Early Neurological Deterioration (END) and risk of infections as secondary variables. The percentage of circulating Treg was measured at admission, 48, 72 h and at day 7 after stroke onset. RESULTS: Circulating Treg levels were higher in IS patients compared to control subjects. Treg at 48 h were independently associated with good functional outcome (OR, 3.5; CI: 1.9-7.8) after adjusting by confounding factors. Patients with lower Treg at 48 h showed higher frequency of END and risk of infections. In addition, a negative correlation was found between circulating Treg at 48 h (r = - 0.414) and 72 h (r = - 0.418) and infarct volume. CONCLUSIONS: These findings suggest that Treg may participate in the recovery of IS patients. Therefore, Treg may be considered a potential therapeutic target in acute ischemic stroke.

Trends in stroke outcomes in the last ten years in a European tertiary hospital.

BACKGROUND: Studying the impact of demographic changes and progress in the management of stroke patients is necessary in order to organize care structures for the coming years. Consequently, we analyzed the prognostic trends of patients admitted to the Stroke Unit of a tertiary hospital in the last ten years. METHODS: The University Clinical Hospital of Santiago de Compostela is the referral hospital for stroke in a catchment area that accounts for 16.5% of the population of Galicia. Data from patients admitted to the Stroke Unit were registered prospectively. A multinomial logistic regression was performed to determine the influence of new trends in demographic factors and in the management of patients with acute stroke. For the expected trend of progression, a 2008-2011 and 2012-2017 time series model was made by selecting the most appropriate model. RESULTS: In the last 10 years, the age of stroke onset has only increased in women (from 74.4 ± 2.2 years in 2008 to 78.8 ± 2.1 years in 2017; p = 0.037), and the same happens with the severity of neurological symptoms (ischemic stroke (IS), p < 0.0001; from 14 [10, 19] in 2008 to 19 [15, 26] in 2017), with a higher percentage of cardioembolic strokes (40.7% vs. 32.2% of cardioembolic strokes in women vs. men, p < 0.0001). In a multiple linear regression model, hospital improvement was mainly associated with the use of reperfusion treatment (B 53.11, CI 95% 49.87, 56.36, p < 0.0001). A differentiated multinomial logistic regression analysis conducted for the whole sample with ischemic strokes in the two time periods (2008-2011 and 2012-2017) showed no differences in the influence of factors associated with higher morbidity and mortality. The modeling of time series showed a distinct falling trend in mortality, with a slight increase in good outcome as well as morbidity in both ischemic and hemorrhagic stroke. CONCLUSIONS: Our results showed that mortality decreased in the entire sample; however, although outcome at discharge improved in ischemic stroke, severe disability also increased in these patients. Importantly, this tendency towards increased morbidity seems to be confirmed for the coming years.

Pharmacological preclinical comparison of tenecteplase and alteplase for the treatment of acute stroke.

Alteplase (rtPA) remains the standard thrombolytic drug for acute ischemic stroke. However, new rtPA-derived molecules, such as tenecteplase (TNK), with prolonged half-lives following a single bolus administration, have been developed. Although TNK is currently under clinical evaluation, the limited preclinical data highlight the need for additional studies to elucidate its benefits. The toxicities of rtPA and TNK were evaluated in endothelial cells, astrocytes, and neuronal cells. In addition, their in vivo efficacy was independently assessed at two research centers using an ischemic thromboembolic mouse model. Both therapies were tested via early (20 and 30 min) and late administration (4 and 4.5 h) after stroke. rtPA, but not TNK, caused cell death only in neuronal cultures. Mice were less sensitive to thrombolytic therapies than humans, requiring doses 10-fold higher than the established clinical dose. A single bolus dose of 2.5 mg/kg TNK led to an infarct reduction similar to perfusion with 10 mg/kg of rtPA. Early administration of TNK decreased the hemorrhagic transformations compared to that by the early administration of rtPA; however, this result was not obtained following late administration. These two independent preclinical studies support the use of TNK as a promising reperfusion alternative to rtPA.

Effect of early vs. delayed extubation on functional outcome among patients with acute ischemic stroke treated with endovascular thrombectomy under general anesthesia: the prospective, randomized controlled EDESTROKE trial study protocol.

BACKGROUND: Recent meta-analyses and randomized studies have shown that among patients with acute ischemic stroke undergoing endovascular thrombectomy, general anesthesia with mechanical ventilation is associated with better functional status compared to local anesthesia and sedation, and they recommend its use. But once the procedure is completed, when is the optimal moment for extubation? Currently, there are no guidelines recommending the optimal moment for extubation. Prolonged mechanical ventilation time could potentially be linked to increased complications such as pneumonia or disturbances in cerebral blood flow due to the vasodilatation produced by most anesthetic drugs. However, premature extubation in a patient who has suffered a stroke could led to complications such as agitation, disorientation, abolished reflexes, sudden fluctuations in blood pressure, alterations in cerebral blood flow, respiratory distress, bronchial aspiration, and the need for reintubation. We therefore designed a randomized study hypothesizing that early compared with delayed extubation is associated with a better functional outcome 3 months after endovascular thrombectomy treatment under general anesthesia for acute ischemic stroke. METHODS: This investigator-initiated, single-center, prospective, parallel, evaluated blinded, superiority, randomized controlled trial will include 178 patients with a proximal occlusion of the anterior circulation treated with successful endovascular thrombectomy (TICI 2b-3) under general anesthesia. Patients will be randomly allocated to receive early (< 6 h) or delayed (6-12 h) extubation after the procedure. The primary outcome measure is functional independence (mRS of 0-2) at 90 days, measured with the modified Rankin Score (mRS), ranging from 0 (no symptoms) to 6 (death). DISCUSSION: This will be the first trial to compare the effect of mechanical ventilation duration (early vs delayed extubation) after satisfactory endovascular thrombectomy for acute ischemic stroke under general anesthesia. TRIAL REGISTRATION: The study protocol was approved April 11, 2023, by the by the Santiago-Lugo Research Ethics Committee (CEI-SL), number 2023/127, and was registered into the clinicaltrials.gov clinical trials registry with No. NCT05847309. Informed consent is required. Participant recruitment begins on April 18, 2023. The results will be submitted for publication in a peer-reviewed journal and presented at one or more scientific conferences.

'Costa da Morte' ataxia is spinocerebellar ataxia 36: clinical and genetic characterization.

Spinocerebellar ataxia 36 has been recently described in Japanese families as a new type of spinocerebellar ataxia with motor neuron signs. It is caused by a GGCCTG repeat expansion in intron 1 of NOP56. Family interview and document research allowed us to reconstruct two extensive, multigenerational kindreds stemming from the same village (Costa da Morte in Galicia, Spain), in the 17th century. We found the presence of the spinocerebellar ataxia 36 mutation co-segregating with disease in these families in whom we had previously identified an ~0.8 Mb linkage region to chromosome 20 p. Subsequent screening revealed the NOP56 expansion in eight additional Galician ataxia kindreds. While normal alleles contain 5-14 hexanucleotide repeats, expanded alleles range from ~650 to 2500 repeats, within a shared haplotype. Further expansion of repeat size was frequent, especially upon paternal transmission, while instances of allele contraction were observed in maternal transmissions. We found a total of 63 individuals carrying the mutation, 44 of whom were confirmed to be clinically affected; over 400 people are at risk. We describe here the detailed clinical picture, consisting of a late-onset, slowly progressive cerebellar syndrome with variable eye movement abnormalities and sensorineural hearing loss. There were signs of denervation in the tongue, as well as mild pyramidal signs, but otherwise no signs of classical amyotrophic lateral sclerosis. Magnetic resonance imaging findings were consistent with the clinical course, showing atrophy of the cerebellar vermis in initial stages, later evolving to a pattern of olivo-ponto-cerebellar atrophy. We estimated the origin of the founder mutation in Galicia to have occurred ~1275 years ago. Out of 160 Galician families with spinocerebellar ataxia, 10 (6.3%) were found to have spinocerebellar ataxia 36, while 15 (9.4%) showed other of the routinely tested dominant spinocerebellar ataxia types. Spinocerebellar ataxia 36 is thus, so far, the most frequent dominant spinocerebellar ataxia in this region, which may have implications for American countries associated with traditional Spanish emigration.

Results of a focused cardiac ultrasound program conducted by neurologists within a stroke care network with cardiac imaging units.

INTRODUCTION AND OBJECTIVES: Recently, neurologists have begun to perform focused cardiac ultrasound for the detection of a cardiac source of embolism in stroke patients, requiring them to undergo a prior accredited training process. We designed a prospective study to analyze the incidence of heart disease detected by a focused cardiac ultrasound program within a stroke care network with cardiac imaging units and to identify the outcomes of detected structural heart disease at 1 year of follow-up. METHODS: We included patients admitted to a university hospital for ischemic stroke or a transient ischemic attack between 2017 and 2021 who were evaluated by focused cardiac ultrasound. We studied the presence of structural heart disease and cardioembolic sources. We analyzed cardiovascular events (CVE) during the first year of follow-up. RESULTS: Focused cardiac ultrasound was performed in 706 patients. Structural heart disease was detected in 52.1% and a cardioembolic source in 31.9%. Adverse CVE occurred in 5.49% of the patients in the first year of follow-up. The presence of de novo structural heart disease was independently associated with a higher probability of adverse CVE (HR, 1.72; 95%CI, 1.01- 2.91; P=.046). CONCLUSIONS: Focused cardiac ultrasound within a stroke care network with cardiac imaging units is an accessible technique with high diagnostic yield. Its use allows clinical and therapeutic actions in the prevention of stroke recurrences and other CVEs in this group of patients.

Familial hemiplegic migraine with prolonged global aura: follow-up findings of subtraction ictal SPECT co-registered to MRI (SISCOM).

All authors contributed equally to this work. Susana Arias-Rivas wrote the main paper. Manuel Rodriguez-Yáñez investigated the supplementary data. Julia Cortés and Pablo Aguiar performed the nuclear image studies and analysed and described the neuroimaging results. María Pardo, Rogelio Leira and Jose Castillo jointly conceived the study, followed the patient and prepared the manuscript. Miguel Blanco discussed the results. All authors discussed the results and implications and commented on the manuscript at all stages.

Amitriptyline for post-COVID headache: effectiveness, tolerability, and response predictors.

BACKGROUND: Headache is one of the most frequently reported symptoms in post-COVID patients. The clinical phenotype of COVID-19 headache combines phenotypic features of both tension-type headache (TTH) and migraine. We aimed to assess the effectiveness, side effects and predictors of amitriptyline (AMT) response in a real-world study setting. METHODS: We performed an observational multicentric study with a retrospective cohort. All consecutive patients with confirmed COVID-19 infection who received AMT for post-COVID headache from March 2020 to May 2021 were included. Response was evaluated by the reduction in the number of headache days per month (HDM) between weeks 8 and 12, compared with the baseline. We explored which variables were associated with a higher probability of response to AMT. RESULTS: Forty-eight patients were eligible for the study, 40/48 (83.3%) females, aged 46.85 (SD: 13.59) years. Patients had history of migraine 15/48 (31.3%) or TTH 5/48 (10.4%). The mean reduction of HDM was 9.6 (SD: 10.9; 95% CI 6.5, 12.7) days. Only 2/48 (5%) of patients discontinued AMT due to poor tolerability. History of TTH (10.9, 95% CI 1.3, 20.6) and nausea (- 8.5, 95% CI - 14.6, - 2.5) were associated with AMT response. CONCLUSIONS: This study provides real-world evidence of the potential benefit of AMT in patients with post-COVID-19 headache, especially in patients with history of TTH and without concomitant nausea.

Carotid web: the challenging diagnosis of an under-recognized entity.

BACKGROUND: Determining the cause of acute ischemic stroke is crucial for patient management, particularly for preventing future stroke. In recent years, carotid web (CW), a non-atherosclerotic disorder of the carotid wall, has been found to be an underestimated source of cerebral emboli. OBJECTIVE: The present study aimed to analyze the clinical, radiological, and pathological findings, along with the treatments performed in patients with CW and ipsilateral ischemic events. METHODS: Patients with anterior circulation ischemic stroke or transient ischemic attack and ipsilateral CW were prospectively included from January 2019 to December 2021. RESULTS: Nine patients were enrolled. The median age was 55 (43-62) years, with a female-to-male ratio of 3.5:1. Of the total, seven patients (78%) consulted for recurrent ipsilateral ischemic events. Despite medical treatment, 44% of the patients experienced new episodes. Computed tomographic angiography was suggestive of CW in all cases in which it was performed. The interval between the first ischemic event and diagnosis of CW was of 13 (6-68) months. After ruling out any other possible etiology, every patient underwent carotid revascularization, one underwent stenting and eight underwent carotidectomy. No severe or long-term complications were noted. Histological studies confirmed the diagnosis of CW. There were no recurrences after carotid revascularization during a follow-up of 24 (13-35) months. CONCLUSION: Knowledge of CW and differentiating it from atheroma plaques is essential, as medical management seems to be insufficient in many cases. Revascularization, which has been shown to be safe and effective, might be the best treatment modality.

Unilateral calf atrophy secondary to a de novo mutation of the caveolin-3 gene.

A 23-year-old man was evaluated for atrophy of the left calf. He had a myopathic pattern on electromyography. Light microscopy showed dystrophic changes and reduced immunostaining for dysferlin and caveolin-3. The subsarcolemmal space was enlarged, and abnormal vesicles were visible with electron microscopy. A genetic study showed a heterozygous A45T mutation at exon 2 of the caveolin-3 gene. Such a mutation has been reported previously with limb-girdle muscular dystrophy type 1C and rippling muscle disease phenotypes.

Results of a Single Center's Stenting Procedure for the Treatment of Carotid Stenosis.

BACKGROUND: Stenting may be a safer alternative to endarterectomy for treating carotid artery stenosis (CAS), but its long-term efficacy is uncertain. There is a lack of long-term and noncontrolled clinical trial data that reflects "real-world" CAS. This study aimed to analyze the long-term efficacy and safety of our center's CAS procedure. METHODS: We retrospectively analyzed our database of patients who underwent CAS. Patient demographic data, previous risk factors, diagnostic and procedural information, and clinical and image follow-up data were collected from up to 1 year after treatment. RESULTS: Overall, 187 patients were analyzed. Our patient population largely comprised higher-risk patients compared with the patient populations of randomized controlled trials. We had more symptomatic (n = 145, 77.5%) than asymptomatic patients (n = 42, 22.5%), and 49% of patients had >90% stenosis. By the 30-day follow-up, there were 10 major adverse events (5.3%) observed in 8 patients (4.2%), including 7 strokes (3 ischemic and 4 hemorrhagic) and 3 deaths. By the 1-year follow-up, 6 strokes and 5 deaths occurred in 9 patients (4.8%), and color Doppler control showed that 87.6% of patients had stenosis-free stents. CONCLUSIONS: Despite our high-risk population group, there were high rates of successful stent placement, low complication rates, good clinical outcomes, and low rates of stenting restenosis.

NT-pro-BNP: A novel predictor of stroke risk after transient ischemic attack.

BACKGROUND: Elevated levels of B-type natriuretic peptide (BNP) and NT-pro-BNP can predict an increased risk of cardiovascular events and ischemic stroke. The limited reliability to predict the risk of stroke after a transient ischemic attack (TIA) justifies the objective of our study to determine the role of NT-pro-BNP in patients with TIAs. METHODS: From our prospective stroke registry, we performed a retrospective study in all patients with the diagnosis of TIA admitted to the Stroke Unit of our Hospital between January 2008 and March 2018. NT-pro-BNP was determined in the first hours after TIA. The endpoint was the development of stroke during the follow-up. RESULTS: 381 patients were included. Mean time of follow-up was 36.8 (±16.4) months. 224 patients were hospitalized due to a stroke during the follow-up, and 157 were not. NT-pro-BNP serum levels were higher in patients who suffered a stroke compared to those who did not (p ≪ 0.001). We also found greater levels of this marker the earlier the stroke happened (p = 0.024). A cut-off point of 800 pg/mL of NT-pro-BNP predicted a stroke with a sensitivity of 64% and a specificity of 79% (p ≪ 0.001), and was independently associated with higher risk of stroke after a TIA (OR: 6.65, p ≪ 0.001). This association persisted for different etiopathogenic TIA groups (cardioembolic: OR 26.12, p ≪ 0.001; undetermined: OR 4.87, p = 0.006; atherothrombotic: OR 1.67, p = 0.044). CONCLUSIONS: The early determination of NT-pro-BNP is a simple and very useful alternative to predict the prognosis after TIA regardless of the etiopathogenesis of the TIA.

Oral Anticoagulation and Risk of Symptomatic Hemorrhagic Transformation in Stroke Patients Treated With Mechanical Thrombectomy: Data From the Nordictus Registry.

Introduction: We aimed to evaluate if prior oral anticoagulation (OAC) and its type determines a greater risk of symptomatic hemorrhagic transformation in patients with acute ischemic stroke (AIS) subjected to mechanical thrombectomy. Materials and Methods: Consecutive patients with AIS included in the prospective reperfusion registry NORDICTUS, a network of tertiary stroke centers in Northern Spain, from January 2017 to December 2019 were included. Prior use of oral anticoagulants, baseline variables, and international normalized ratio (INR) on admission were recorded. Symptomatic intracranial hemorrhage (sICH) was the primary outcome measure. Secondary outcome was the relation between INR and sICH, and we evaluated mortality and functional outcome at 3 months by modified Rankin scale. We compared patients with and without previous OAC and also considered the type of oral anticoagulants. Results: About 1.455 AIS patients were included, of whom 274 (19%) were on OAC, 193 (70%) on vitamin K antagonists (VKA), and 81 (30%) on direct oral anticoagulants (DOACs). Anticoagulated patients were older and had more comorbidities. Eighty-one (5.6%) developed sICH, which was more frequent in the VKA group, but not in DOAC group. OAC with VKA emerged as a predictor of sICH in a multivariate regression model (OR, 1.89 [95% CI, 1.01-3.51], p = 0.04) and was not related to INR level on admission. Prior VKA use was not associated with worse outcome in the multivariate regression model nor with mortality at 3 months. Conclusions: OAC with VKA, but not with DOACs, was an independent predictor of sICH after mechanical thrombectomy. This excess risk was associated neither with INR value by the time thrombectomy was performed, nor with a worse functional outcome or mortality at 3 months.

Obesity Paradox in Ischemic Stroke: Clinical and Molecular Insights.

It has recently emerged the concept of "obesity paradox," a term used to describe the unexpected improved prognosis and lower mortality rates found in several diseases in patients with higher body weight. Concerning stroke, few clinical studies have assessed this obesity paradox showing contradictory results. Therefore, our aim was to compare clinical evolution and inflammatory balance of obese and non-obese patients after ischemic stroke. We designed a prospective case-control study in patients with acute ischemic stroke categorized into obese (body mass index, BMI ≥ 30 kg/m2) and non-obese (BMI < 30 kg/m2). We compared clinical, anthropometric, radiological, and laboratory variables. The main outcome variable was the functional outcome at 3 months. We included 98 patients (48 non-obese and 50 obese). No differences in functional outcome at 3 months were found (p = 0.882) although a tendency of a greater recovery on neurological impairments was seen in obese subjects. Importantly, obese patients (p = 0.007) and patients who experienced poor outcome (p = 0.006) exhibited a higher reduction in body weight at 3 months after stroke. Moreover, pro-inflammatory IL-6 levels (p = 0.002) were higher in the obese group. However, IL-6 levels decreased over the first week in obese while increased in non-obese. On the contrary, levels of the anti-inflammatory IL-10 rose over the first week in obese patients, whereas remained stable in non-obese. In summary, despite exhibiting several factors associated with poor outcome, obese patients do not evolve worse than non-obese after ischemic stroke. Obesity may counterbalance the inflammatory reaction through an anti-inflammatory stream enhanced in the first moments of stroke.

Lesion location and other predictive factors of dysphagia and its complications in acute stroke.

BACKGROUND AND AIMS: Early detection of dysphagia is crucial in stroke patients as a result of increased morbidity and mortality due to malnutrition and respiratory tract infections. The aim of this study was to identify possible predictors of the onset of dysphagia following stroke in order to be able to act precociously. METHODS: Observational, prospective study in which a Volume-Viscosity Swallow Test (V-VST) was carried out in the first 72 h following admission to assess dysphagia in acute stroke patients with a previous result of <3 in the Eating Assessment Tool-10. Lesions were analysed by computed tomography and/or magnetic resonance, using the ABC/2 formula to calculate their volume. Likewise, 3-month follow-up was carried out for the evaluation of the occurrence of respiratory tract infections and deaths. RESULTS: Out of 106 patients admitted for acute stroke, 60 (56.60%) presented dysphagia (44.40% showing alterations in the effectiveness of swallowing and 33.30% in its safety). The factors that were related to dysphagia were: older age (76.40 ± 11.50 vs 66.37 ± 13.85 years, p = 0.0001), stroke severity as measured on the National Institute of Health Stroke Scale (6.81 ± 5.83 vs 3.38 ± 3.46, p = 0.001) and greater volume of the lesion (23.47 ± 47.15 vs 7.50 ± 14.53 ml, p = 0.042). The variables that were influenced by a greater lesion size were the presence of cough, oxygen desaturation and impaired labial seal. Dysphagia was not affected by the lateralization of the lesion or by the type of stroke (ischaemic/haemorrhagic). Despite the fact that 68.80% of the patients with a temporoparietal lesion presented dysphagia, no significant differences were observed regarding the location of the lesion in the regions studied. 27.3% of the patients with frontal lesions presented respiratory infections after discharge (p = 0.018), a condition which was also observed in 20.0% of patients with dysphagia (p = 0.044). Mortality during the 3-month follow-up period was 20.0% for patients with a positive V-VST (p = 0.005), due to respiratory infection in 66.6% of the cases (p = 0.0001). CONCLUSIONS: Post-stroke dysphagia was associated with the occurrence of respiratory tract infection and mortality. Our study also provides more information about how certain demographic and clinical factors, as well as neuroimaging patterns, influence dysphagia. This fact may help to identify at an early stage those patients with a greater risk of developing swallowing alterations.

The autoscopic phenomena in neurological clinic: a study of two cases.

Autoscopic phenomena are part of the reduplicative misidentification syndromes. These disorders may be a manifestation of both neurological and psychiatric conditions and consist of a double perception of the own body. These phenomena have been attributed to a dysfunction of the nondominant gyrus angularis. Two cases with this symptom are described. Case 1: A female with previous history of multiple sclerosis presented with episodes in which she saw herself in her extrapersonal space. Holter EEG was normal. An MRI scan showed multiple T2 hyperintensities. She was treated with carbamazepine and the symptom subsided. Case 2: A man presented with visual loss in the left field and episodic visualization of his own image. Examination confirmed left homonymous hemianopia. Serum glucose was 417 mg/dL. MRI was normal. Glycemia correction made the autoscopia disappear. In case 1, ephaptic transmission is proposed as the pathogenic mechanism and in the case 2, transient glucose toxicity is likely to explain the autoscopic phenomena.