Ticagrelor versus clopidogrel in dual antiplatelet therapy after minor stroke or transient ischemic attack: an updated network meta-analysis.

BACKGROUND: Dual antiplatelet therapy (DAPT) with clopidogrel plus aspirin is a well-established practice after a minor stroke or transient ischemic attack (TIA). However, ticagrelor plus aspirin may be an alternative. AIMS: We systematically searched PubMed, Embase, and Cochrane Central from inception to January 2024. We included randomized controlled trials (RCTs) enrolling adults with acute minor stroke or TIA within 72 hours of the onset of the symptoms. RESULTS: A total of 8 RCTs were included in our meta-analysis. Ticagrelor plus aspirin (RR, 0.70; 95% CrI 0.52, 0.91) and clopidogrel plus aspirin (RR, 0.79; 95% CrI 0.64, 0.98) were superior to aspirin in preventing stroke recurrence in overall analysis. Excluding studies with dual antiplatelet up to 90 days, ticagrelor plus aspirin was the only strategy that maintained superiority compared with aspirin regarding stroke recurrence (RR, 0.70; 95% CrI 0.51, 0.95) and ischemic stroke (RR, 0.68; 95% CrI 0.47, 0.94). There was no significant difference between treatment groups regarding hemorrhagic stroke, functional disability, and mortality. CONCLUSIONS: DAPTs were superior to aspirin in preventing recurrence or ischemic stroke. Although no significant difference was observed between DAPTs, ticagrelor plus aspirin may be related to worse major bleeding results, including intracranial bleeding. Ticagrelor plus aspirin is a considerable option for patients after a minor stroke or TIA.

Coumestrol pre-treatment improves spatial learning and memory deficits following transient cerebral ischemia recruiting hippocampal GluR2 AMPA receptors.

Transient global ischemia is a leading cause of learning and memory dysfunction and induces a pattern of delayed neuronal death in the CA1 subfield of the hippocampus by down-regulating GluR2 mRNA AMPA receptors in this cerebral area. This study sought to investigate the neuroprotective effect of coumestrol against spatial memory impairment induced by global ischemia that leads to neural death by reducing the GluR2 receptors content in the hippocampal CA1 area. Our studies demonstrated that coumestrol administration prevented spatial memory deficits in mice. These findings suggest a cognitive enhancement role of coumestrol against cognitive impairment in ischemic events.

Risk of Early Bleeding with Dual Antiplatelet Therapy in Acute Stroke and Transient Ischemic Attack Regardless of NIHSS Admission.

BACKGROUND: Dual antiplatelet therapy (DAT) is a therapeutic option for patients with minor ischemic stroke (IS) or transient ischemic attack (TIA). No study has evaluated the incidence of early bleeding in patients with moderate to major ischemic stroke. The current study aimed to analyze both the frequency of early bleeding and hospital morbidity related to DAT for either acute IS or TIA regardless of admission National Institute of Health Stroke Scale (NIHSS) score. METHODS: This was a retrospective analysis based on data collected from a prospective data bank of a single center. We included patients who underwent DAT in the first 24 hours of symptom onset with a loading dose (aspirin 300 mg + clopidogrel 300 mg) on the first day, followed by a maintenance dose (aspirin 100 mg + clopidogrel 75 mg). We analyzed intracranial and/or extracranial hemorrhage that had occurred during the hospital admission, symptomatic bleeding, modified Rankin Scale (mRS) score at discharge, and death rates as outcomes. RESULTS: Of the 119 patients analyzed, 94 (79 %) had IS and 25 (21 %) had TIA. Hemorrhage occurred in 11 (9.2 %) and four (3.4 %) patients with TIA or NIHSS ≤ 3, respectively, although none were symptomatic. Patients with bleeding as a complication had higher admission NIHSS [4 (3-7) vs. 2 (1-4), p = 0.044] and had higher mRS at discharge (mRS 2 [1-5] vs. mRS 1 [0-2], p = 0.008). These findings did not indicate increased mortality, as one (9 %) patient died from bleeding and two (1.8 %) patients died without bleeding (p = 0.254). CONCLUSION: DAT seems to be a safe therapy in patients regardless of admission NIHSS if started within the first 24 h after symptom onset because only 1.6 % of patients had symptomatic bleeding.

[Dual antiplatelet therapy for secondary stroke prevention in patients with acute ischemic stroke. CIERTO group recommendation]. / Doble terapia antiagregante en pacientes con accidente cerebrovascular isquémico agudo. Recomendación del grupo CIERTO.

One of the main pillars of acute ischemic stroke management is antiplatelet therapy. Different treatment schemes have been compared, suggesting that the combination of multiple antiplatelet drugs is associated with a reduced risk of stroke recurrence. However, it has also been associated with an increased risk of bleeding complications which, in the long term, surpass the mentioned benefits. However, considering that most stroke recurrences occur i n the short term, a time limited double antiplatelet scheme could result in significant benefits to patients with acute ischemic stroke. On this basis, we conducted a rapid systematic review of the literature in order to evaluate the effects of a short-term double antiplatelet therapy both on stroke recurrence and complications. All trials comparing double versus single antiplatelet therapy in patients with acute ischemic stroke were included. Results showed that double therapy reduces recurrence risk but probably marginally increases major bleeding complications. We suggest double antiplatelet therapy for the initial management of patients with minor (Score NIH < or equal to 3 or transient isquemic attack -TIA) acute ischemic stroke.

El inicio precoz del tratamiento con antiagregantes plaquetarios es considerado el estándar de cuidado para pacientes con accidente cerebrovascular isquémico agudo. Distintos esquemas de antiagregación se han comparado con resultados que sugieren que la combinación de múltiples antiagregantes se asocian a menor riesgo de recurrencia de accidente cerebrovascular (ACV) pero a expensas de un aumento en el riesgo de sangrado, lo que a largo plazo termina opacando dichos beneficos. Sin embargo, considerando que el riesgo de recurrencia de ACV es mayor en el periodo inmediato al evento, la indicación de doble tratamiento antiagregante por tiempos limitados podría asociarse a beneficios relevantes. Con este concepto, se realizó una revisión sistemática rápida con el objetivo de evaluar el efecto del tratamiento con doble antiagregación por un periodo corto intentando maximizar el beneficio y reducir al mínimo el riesgo de sangrado. Se incluyeron todos los estudios primarios identificados en los que se comparó un esquema de doble antiagregación, iniciado en el periodo agudo del evento índice (ACV o accidente isquémico transitorio - AIT), contra un esquema de simple antiagregación. El cuerpo de la evidencia mostró que la intervención (doble antiagregación) reduce el riesgo de recurrencia de ACV y probablemente se asocie a un aumento marginal en el riesgo de sangrado mayor. Sugerimos indicar doble esquema antiplaquetario para el tratamiento inicial de pacientes con ACV isquémico menor (Score NIH < o igual a 3 o AIT).

Doble terapia antiagregante en pacientes con accidente cerebrovascular isquémico agudo: Recomendación del grupo CIERTO / Dual antiplatelet therapy for secondary stroke prevention in patients with acute ischemic stroke. CIERTO group recommendation

El inicio precoz del tratamiento con antiagregantes plaquetarios es considerado el estándar de cuidado para pacientes con accidente cerebrovascular isquémico agudo. Distintos esquemas de antiagregación se han comparado con resultados que sugieren que la combinación de múltiples antiagregantes se asocian a menor riesgo de recurrencia de accidente cerebrovascular (ACV) pero a expensas de un aumento en el riesgo de sangrado, lo que a largo plazo termina opacando dichos beneficos. Sin embargo, considerando que el riesgo de recurrencia de ACV es mayor en el periodo inmediato al evento, la indicación de doble tratamiento antiagregante por tiempos limitados podría asociarse a beneficios relevantes. Con este concepto, se realizó una revisión sistemática rápida con el objetivo de evaluar el efecto del tratamiento con doble antiagregación por un periodo corto intentando maximizar el beneficio y reducir al mínimo el riesgo de sangrado. Se incluyeron todos los estudios primarios identificados en los que se comparó un esquema de doble antiagregación, iniciado en el periodo agudo del evento índice (ACV o accidente isquémico transitorio - AIT), contra un esquema de simple antiagregación. El cuerpo de la evidencia mostró que la intervención (doble antiagregación) reduce el riesgo de recurrencia de ACV y probablemente se asocie a un aumento marginal en el riesgo de sangrado mayor. Sugerimos indicar doble esquema antiplaquetario para el tratamiento inicial de pacientes con ACV isquémico menor (Score NIH < o igual a 3 o AIT).

One of the main pillars of acute ischemic stroke management is antiplatelet therapy. Different treatment schemes have been compared, suggesting that the combination of multiple antiplatelet drugs is associated with a reduced risk of stroke recurrence. However, it has also been associated with an increased risk of bleeding complications which, in the long term, surpass the mentioned benefits. However, considering that most stroke recurrences occur i n the short term, a time limited double antiplatelet scheme could result in significant benefits to patients with acute ischemic stroke. On this basis, we conducted a rapid systematic review of the literature in order to evaluate the effects of a short-term double antiplatelet therapy both on stroke recurrence and complications. All trials comparing double versus single antiplatelet therapy in patients with acute ischemic stroke were included. Results showed that double therapy reduces recurrence risk but probably marginally increases major bleeding complications. We suggest double antiplatelet therapy for the initial management of patients with minor (Score NIH < or equal to 3 or transient isquemic attack -TIA) acute ischemic stroke.

Optimal Duration of Aspirin Plus Clopidogrel After Ischemic Stroke or Transient Ischemic Attack.

Background and Purpose- The role of aspirin plus clopidogrel (A+C) therapy compared with aspirin monotherapy in patients presenting with acute ischemic stroke (IS) or transient ischemic attack remains uncertain. We conducted this study to determine the optimal period of efficacy and safety of A+C compared with aspirin monotherapy. Methods- Ten randomized controlled trials (15 434 patients) were selected using MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials (CENTRAL) (inception June 2018) comparing A+C with aspirin monotherapy in patients with transient ischemic attack or IS. The primary efficacy outcome was recurrent IS, and the primary safety outcome was major bleeding. The secondary outcomes were major adverse cardiovascular events (composite of stroke, myocardial infarction, and cardiovascular mortality) and all-cause mortality. We stratified analysis based on the short- (≤1 month), intermediate- (≤3 month), and long-term (>3 month) A+C therapy. Effects were estimated as relative risk (RR) with 95% CI. Results- A+C significantly reduced the risk of recurrent IS at short-term (RR, 0.53; 95% CI, 0.37-0.78) and intermediate-term (RR, 0.72; 95% CI, 0.58-0.90) durations. Similarly, major adverse cardiovascular event was significantly reduced by short-term (RR, 0.68; 95% CI, 0.60-0.78) and intermediate-term (RR, 0.76; 95% CI, 0.61-0.94) A+C therapy. However, long-term A+C did not yield beneficial effect in terms of recurrent IS (RR, 0.81; 95% CI, 0.63-1.04) and major adverse cardiovascular events (RR, 0.87; 95% CI, 0.71-1.07). Intermediate-term (RR, 2.58; 95% CI, 1.19-5.60) and long-term (RR, 1.87; 95% CI, 1.36-2.56) A+C regimens significantly increased the risk of major bleeding as opposed to short-term A+C (RR, 1.82; 95% CI, 0.91-3.62). Excessive all-cause mortality was limited to long-term A+C (RR, 1.45; 95% CI, 1.10-1.93). Conclusions- Short-term A+C is more effective and equally safe in comparison to aspirin alone in patients with acute IS or transient ischemic attack.

Postischemic fish oil treatment confers task-dependent memory recovery.

A series of our previous studies demonstrated that fish oil (FO), equivalent to 300mg/kg docosahexahenoic acid (DHA), facilitates memory recovery after transient, global cerebral ischemia (TGCI) in the aversive radial maze (AvRM). The present study sought to address two main issues: (i) whether the memory-protective effect of FO that has been observed in the AvRM can be replicated in the passive avoidance test (PAT) and object location test (OLT) and (ii) whether FO at doses that are lower than those used previously can also prevent TGCI-induced memory loss. In Experiment 1, naive rats were trained in the PAT, subjected to TGCI (4-vessel occlusion model), and tested for retrograde memory performance 8 and 15days after ischemia. Fish oil (300mg/kg/day DHA) was given orally for 8days. The first dose was delivered 4h postischemia. In Experiment 2, the rats were subjected to TGCI, treated with the same FO regimen, and then trained and tested in the OLT. In Experiment 3, the rats were trained in the AvRM, subjected to TGCI, administered FO (100, 200, and 300mg/kg DHA), and tested for memory performance up to 3weeks after TGCI. At the end of the behavioral tests, the brains were examined for neurodegeneration and neuroblast proliferation. All of the behavioral tests (PAT, OLT, and AvRM) were sensitive to ischemia, but only the AvRM was able to detect the memory-protective effect of FO. Ischemia-induced neurodegeneration and neuroblast proliferation were unaffected by FO treatment. These results suggest that (i) the beneficial effect of FO on memory recovery after TGCI is task-dependent, (ii) doses of FO<300mg/kg DHA can protect memory function in the radial maze, and (iii) cognitive recovery occurs in the absence of neuronal rescue and/or hippocampal neurogenesis.

Postischemic fish oil treatment restores long-term retrograde memory and dendritic density: An analysis of the time window of efficacy.

We reported that fish oil (FO) prevented the loss of spatial memory caused by transient, global cerebral ischemia (TGCI), provided the treatment covered the first days prior to and after ischemia. Continuing these studies, trained rats were subjected to TGCI, and FO was administered for 10days, with a time window of efficacy (TWE) of 4, 8 or 12h post-ischemia. Retrograde memory was assessed up to 43days after TGCI. In another experiment, ischemic rats received FO with a 4- or 12-h TWE, and dendritic density was assessed in the hippocampus and cerebral cortex. The brain lipid profile was evaluated in sham-operated and ischemic rats that were treated with FO or vehicle with a 4-h TWE. Ischemia-induced retrograde amnesia was prevented by FO administration that was initiated with either a 4- or 8-h TWE. Fish oil was ineffective after a 12-h TWE. Independent of the TWE, FO did not prevent ischemic neuronal death. In the hippocampus, but not cerebral cortex, TGCI-induced dendritic loss was prevented by FO with a 4-h TWE but not 12-h TWE. The level of docosahexaenoic acid almost doubled in the hippocampus in ischemic, FO-treated rats (4-h TWE). The data indicate that (i) the anti-amnesic effect of FO can be observed with a TWE of up to 8h, (ii) the stimulation of dendritic neuroplasticity may have contributed to this effect, and (iii) DHA in FO may be the main active constituent in FO that mediates the cognitive and neuroplasticity effects on TGCI.

Accidente isquémico transitorio de causa hemodinámica / Transient ischemic attack of hemodynamic cause

El síncope es una perdida súbita y transitoria del estado de conciencia y el tono postural con restitución completa. Según su etiología se clasifica como reflejo (neuromediado), cardíaco, neurológico (isquemia vertebrobasilar) o indeterminado. Los síncopes neurológicos se observan en contexto de accidente cerebrovascular isquémico o accidente isquémico transitorio; frecuentemente se asocian a signos deficitarios focales. Presentamos el caso de un síncope no neurológico con signos deficitarios focales en una paciente con marcada enfermedad ateromatosa. (AU)

Syncope is the abrupt and transient loss of consciousness associated with absence of postural tone, followed by complete and usually rapid spontaneous recovery. In terms of etiology, syncope is classified as reflex (neurally mediated), cardiac, neurologic (vertebrobasilar ischemia) or indeterminate. The neurologic syncope occurs in the setting of stroke or transient ischemic attack, being most frequently associated with focal neurologic symptoms. We report a case of non-neurologic syncope followed with focal neurologic symptoms in a patient with atherosclerosis disease. (AU)

4-hydroxy-3-methoxy-acetophenone-mediated long-lasting memory recovery, hippocampal neuroprotection, and reduction of glial cell activation after transient global cerebral ischemia in rats.

4-Hydroxy-3-methoxy-acetophenone (apocynin) is a naturally occurring methoxy-substitute catechol that is isolated from the roots of Apocynin cannabinum (Canadian hemp) and Picrorhiza kurroa (Scrophulariaceae). It has been previously shown to have antioxidant and neuroprotective properties in several models of neurodegenerative disease, including cerebral ischemia. The present study investigates the effects of apocynin on transient global cerebral ischemia (TGCI)-induced retrograde memory deficits in rats. The protective effects of apocynin on neurodegeneration and the glial response to TGCI are also evaluated. Rats received a single intraperitoneal injection of apocynin (5 mg/kg) 30 min before TGCI and were tested 7, 14, and 21 days later in the eight-arm aversive radial maze (AvRM). After behavioral testing, the hippocampi were removed for histological evaluation. The present results confirm that TGCI causes memory impairment in the AvRM and that apocynin prevents these memory deficits and attenuates hippocampal neuronal death in a sustained way. Apocynin also decreases OX-42 and glial fibrillary acidic protein immunoreactivity induced by TGCI. These findings support the potential role of apocynin in preventing neurodegeneration and cognitive impairments following TGCI in rats. The long-term protective effects of apocynin may involve inhibition of the glial response.

Atorvastatin protects GABAergic and dopaminergic neurons in the nigrostriatal system in an experimental rat model of transient focal cerebral ischemia.

INTRODUCTION: Cerebral ischemia is the third leading cause of death and the primary cause of permanent disability worldwide. Atorvastatin is a promising drug with neuroprotective effects that may be useful for the treatment of stroke. However, the effects of atorvastatin on specific neuronal populations within the nigrostriatal system following cerebral ischemia are unknown. OBJECTIVE: To evaluate the effects of atorvastatin on dopaminergic and GABAergic neuronal populations in exofocal brain regions in a model of transient occlusion of the middle cerebral artery. MATERIALS AND METHODS: Twenty-eight male eight-week-old Wistar rats were used in this study. Both sham and ischemic rats were treated with atorvastatin (10 mg/kg) or carboxymethylcellulose (placebo) by gavage at 6, 24, 48 and 72 hours post-reperfusion. We analyzed the immunoreactivity of glutamic acid decarboxylase and tyrosine hydroxylase in the globus pallidus, caudate putamen and substantia nigra. RESULTS: We observed neurological damage and cell loss in the caudate putamen following ischemia. We also found an increase in tyrosine hydroxylase immunoreactivity in the medial globus pallidus and substantia nigra reticulata, as well as a decrease in glutamic acid decarboxylase immunoreactivity in the lateral globus pallidus in ischemic animals treated with a placebo. However, atorvastatin treatment was able to reverse these effects, significantly decreasing tyrosine hydroxylase levels in the medial globus pallidus and substantia nigra reticulata and significantly increasing glutamic acid decarboxylase levels in the lateral globus pallidus. CONCLUSION: Our data suggest that post-ischemia treatment with atorvastatin can have neuro-protective effects in exofocal regions far from the ischemic core by modulating the GABAergic and dopaminergic neuronal populations in the nigrostriatal system, which could be useful for preventing neurological disorders.

Atorvastatin protects GABAergic and dopaminergic neurons in the nigrostriatal system in an experimental rat model of transient focal cerebral ischemia / La atorvastatina protege las neuronas gabérgicas y dopaminérgicas del sistema nigroestriatal en un modelo experimental de isquemia cerebral focal transitoria en ratas

Introduction: Cerebral ischemia is the third leading cause of death and the primary cause of permanent disability worldwide. Atorvastatin is a promising drug with neuroprotective effects that may be useful for the treatment of stroke. However, the effects of atorvastatin on specific neuronal populations within the nigrostriatal system following cerebral ischemia are unknown. Objective: To evaluate the effects of atorvastatin on dopaminergic and GABAergic neuronal populations in exofocal brain regions in a model of transient occlusion of the middle cerebral artery. Materials and methods: Twenty-eight male eight-week-old Wistar rats were used in this study. Both sham and ischemic rats were treated with atorvastatin (10 mg/kg) or carboxymethylcellulose (placebo) by gavage at 6, 24, 48 and 72 hours post-reperfusion. We analyzed the immunoreactivity of glutamic acid decarboxylase and tyrosine hydroxylase in the globus pallidus, caudate putamen and substantia nigra. Results: We observed neurological damage and cell loss in the caudate putamen following ischemia. We also found an increase in tyrosine hydroxylase immunoreactivity in the medial globus pallidus and substantia nigra reticulata, as well as a decrease in glutamic acid decarboxylase immunoreactivity in the lateral globus pallidus in ischemic animals treated with a placebo. However, atorvastatin treatment was able to reverse these effects, significantly decreasing tyrosine hydroxylase levels in the medial globus pallidus and substantia nigra reticulata and significantly increasing glutamic acid decarboxylase levels in the lateral globus pallidus. Conclusion: Our data suggest that post-ischemia treatment with atorvastatin can have neuro-protective effects in exofocal regions far from the ischemic core by modulating the GABAergic and dopaminergic neuronal populations in the nigrostriatal system, which could be useful for preventing neurological disorders.

Introducción. La isquemia cerebral es la tercera causa de muerte y la primera de discapacidad permanente en el mundo. La atorvastatina es un fármaco neuroprotector prometedor para el tratamiento de la apoplejía; sin embargo, su acción sobre las poblaciones neuronales del sistema nigroestriatal después de la isquemia aún se desconoce. Objetivo. Evaluar el efecto de la atorvastatina sobre poblaciones gabérgicas y dopaminérgicas en regiones exofocales en un modelo de oclusión transitoria de la arteria cerebral media. Materiales y métodos. Se utilizaron 28 ratas Wistar macho de ocho semanas de edad. Los ejemplares con isquemia simulada y los ejemplares sometidos a isquemia fueron tratados con atorvastatina (10 mg/kg) y carboximetilcelulosa (placebo) administrados por medio de sonda a las 6, 24, 48 y 72 horas después de la reperfusión. Se analizó la inmunorreacción de la descarboxilasa del ácido glutámico y de la tirosina hidroxilasa en el globo pálido, el putamen caudado y la sustancia negra. Resultados. Los datos confirmaron el daño neurológico y la pérdida celular en el putamen caudado. Se incrementó la inmunorreacción de la tirosina hidroxilasa en el globo pálido medial y la sustancia negra pars reticulata , disminuyendo la inmunorreacción de la descarboxilasa del ácido glutámico en el globo pálido lateral de los animales isquémicos tratados con placebo; sin embargo, el tratamiento con atorvastatina pudo revertirla, lo que logró una disminución significativa de la tirosina hidroxilasa en el globo pálido medial y la sustancia negra pars reticulata y aumentando los niveles de descarboxilasa del ácido glutámico en el globo pálido lateral. Conclusión. Nuestros datos sugieren que la atorvastatina en el tratamiento posterior a la isquemia ejerce neuroprotección en las zonas exofocales, modulando las poblaciones neuronales gabérgicas y dopaminérgicas del sistema nigroestriatal, lo que podría prevenir trastornos neurológicos.

Metallothionein-II inhibits lipid peroxidation and improves functional recovery after transient brain ischemia and reperfusion in rats.

After transient cerebral ischemia and reperfusion (I/R), damaging mechanisms, such as excitotoxicity and oxidative stress, lead to irreversible neurological deficits. The induction of metallothionein-II (MT-II) protein is an endogenous mechanism after I/R. Our aim was to evaluate the neuroprotective effect of MT-II after I/R in rats. Male Wistar rats were transiently occluded at the middle cerebral artery for 2 h, followed by reperfusion. Rats received either MT (10 µg per rat i.p.) or vehicle after ischemia. Lipid peroxidation (LP) was measured 22 h after reperfusion in frontal cortex and hippocampus; also, neurological deficit was evaluated after ischemia, using the Longa scoring scale. Infarction area was analyzed 72 hours after ischemia. Results showed increased LP in frontal cortex (30.7%) and hippocampus (26.4%), as compared to control group; this effect was fully reversed by MT treatment. Likewise, we also observed a diminished neurological deficit assessed by the Longa scale in those animals treated with MT compared to control group values. The MT-treated group showed a significant (P < 0.05) reduction of 39.9% in the infarction area, only at the level of hippocampus, as compared to control group. Results suggest that MT-II may be a novel neuroprotective treatment to prevent ischemia injury.

Long-term treatment with fish oil prevents memory impairments but not hippocampal damage in rats subjected to transient, global cerebral ischemia.

Cerebral ischemia leads to neurodegeneration and cognitive impairment. Fish oil (FO) constitutes a rich dietary source of omega-3 polyunsaturated fatty acids especially docosahexaenoic acid (DHA). The objective of the present study was to investigate whether long-term treatment with commercial, high concentration DHA-containing FO could be effective in alleviating both the cognitive and neurodegenerative deficits caused by transient, global cerebral ischemia (TGCI) in rats. Naive rats were trained for 10 days in an 8-arm radial maze task and then subjected to TGCI for 15 minutes (4-VO model) 3 days later (day 13). Retention of the previously acquired cognition (ie, memory) was assessed weekly on days 20, 27, 34, 41, 48, and 55 and measured by 3 behavioral parameters as follows: (i) latency to find the goal box, (ii) number of reference memory errors, and (iii) number of working memory errors. The extent of pyramidal cell death in the hippocampus was examined at the end of the behavioral analysis on day 43. Fish oil (300 mg/kg DHA, gavage) administration occurred once daily beginning 3 days before TGCI (the last day of training) and continued until day 41. Transient, global cerebral ischemia markedly disrupted memory performance measured by all 3 parameters (P < .0001 vs sham). This amnesic effect of ischemia persisted until the end of the behavioral analysis. Treatment with FO progressively reversed the TGCI-induced retention deficit until rats achieved control levels. This protective effect of FO on learning/memory function was clearly observed after both daily and cumulative data analysis (P < .001-0.01 vs vehicle). Such memory improvements remained statistically significant, even after cessation of FO treatment, indicating a sustained effect of FO. In contrast, FO failed to prevent ischemia-induced hippocampal damage in areas CA1, CA2, or CA4. Therefore, the present findings suggest that long-term FO treatment is able to facilitate functional recovery after ischemic brain damage, an effect that was distinct from hippocampal damage.

Stroke management in a university hospital in the largest South American city.

OBJECTIVE: To describe characteristics and provision of care for patients admitted with cerebrovascular disorders (CVD), focusing on ischemic stroke (IS), in a large, public, academic hospital in São Paulo, Brazil. METHOD: We retrieved information about 357 patients with CVD admitted to the Neurology Emergency Department (NED) and Neurology Ward (NW) of our institution. We described patient characteristics and management of IS in NED and in NW. RESULTS: IS was diagnosed in 79.6% of CVD patients admitted to NED; 2.7% were submitted to thrombolysis. Extent of IS investigation and management were significantly different in NED and NW. CONCLUSION: IS patients in our center were younger than in developed countries. IS management was significantly influenced by patient characteristics. This information can aid in planning strategies to decrease stroke burden.

Stroke management in a university hospital in the largest South American city / Manejo do acidente vascular cerebral em um hospital universitário na maior cidade da América do Sul

OBJECTIVE: To describe characteristics and provision of care for patients admitted with cerebrovascular disorders (CVD), focusing on ischemic stroke (IS), in a large, public, academic hospital in São Paulo, Brazil. METHOD: We retrieved information about 357 patients with CVD admitted to the Neurology Emergency Department (NED) and Neurology Ward (NW) of our institution. We described patient characteristics and management of IS in NED and in NW. RESULTS: IS was diagnosed in 79.6 percent of CVD patients admitted to NED; 2.7 percent were submitted to thrombolysis. Extent of IS investigation and management were significantly different in NED and NW. CONCLUSION: IS patients in our center were younger than in developed countries. IS management was significantly influenced by patient characteristics. This information can aid in planning strategies to decrease stroke burden.

OBJETIVO: Descrever características e manejo de pacientes internados com diagnóstico de doença cerebrovascular (DCV), enfocando principalmente o acidente vascular cerebral isquêmico (AVCI), em um hospital público universitário em São Paulo. MÉTODO: Coletamos informações de 357 pacientes com DCV internados no Pronto-Socorro de Neurologia (PSN) e na Enfermaria de Neurologia (EN) de nossa instituição. Descrevemos características dos pacientes e manejo do AVCI no PSN e na EN. RESULTADOS: O AVCI foi diagnosticado em 79,6 por cento dos pacientes com DCV admitidos no PSN; 2,7 por cento foram submetidos a trombólise. A extensão da investigação e o manejo da doença foram significativamente diferentes no PSN e na EN. CONCLUSÃO: os pacientes com AVCI em nosso centro foram mais jovens que em países desenvolvidos. O manejo do AVCI foi influenciado significativamente pelas características dos pacientes. Estas informações podem auxiliar no planejamento de estratégias para diminuir as conseqüências das DCV em nosso meio.

Management and outcome of transient ischemic attacks in Ponce, Puerto Rico.

BACKGROUND: Approximately 240,000 transient ischemic attacks (TIA's) are diagnosed every year in U.S.A. Recent studies have shown that 4-20% will have a stroke within 90 days after a TIA, half in 2 days. OBJECTIVES: To determine morbidity and assess outcome at 72 hours of patients with TIA's arriving at the Emergency Room (ER) of San Lucas Hospital, Ponce, PR. METHODOLOGY: Medical records of all patients evaluated at ER in 2006 with neurological symptoms for < 24 hours, and outcome for next 72 hrs were reviewed. Anticoagulation given and timeframe between initial symptoms and diagnostic neurologic workup was also recorded. RESULTS: 53/182 records reviewed met inclusion criteria. 45% males, 55% females, median age of 62 years (Range 53-90). All received antithrombotic drugs at ER. Head-CT performed upon arrival in 100%, only 57% of Echocardiograms and Carotid-Doppler done in 24 hrs. CONCLUSION: No patients developed stroke or death related to TIA in 72 hours.