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Cancer patients are at increased risk of cardiovascular and cerebrovascular events. It is unclear whether cancer confers any additional risk for recurrent stroke or cardiovascular mortality after stroke. This was a single center, observational study of 1,105 consecutive Chinese ischemic stroke patients recruited from a large stroke rehabilitation unit based in Hong Kong. We sought to determine whether patients with cancer are at higher risk of recurrent stroke and cardiovascular mortality. Amongst 1,105 patients, 58 patients (5.2%) had cancer, of whom 74% were in remission. After a mean follow-up of 76 ± 18 months, 241 patients developed a recurrent stroke: 22 in patients with cancer (38%, annual incidence 13.94%/year), substantially more than those without cancer (21%, 4.65%/year) (p<0.01). In a Cox regression model, cancer, age and atrial fibrillation were the 3 independent predictors of recurrent stroke with a hazard ratio (HR) of 2.42 (95% confidence interval (CI): 1.54-3.80), 1.01 (1.00-1.03) and 1.35 (1.01-1.82) respectively. Likewise, patients with cancer had a higher cardiovascular mortality compared with those without cancer (4.30%/year vs. 2.35%/year, p = 0.08). In Cox regression analysis, cancer (HR: 2.08, 95% CI: 1.08-4.02), age (HR: 1.04, 95% CI 1.02-1.06), heart failure (HR: 3.06, 95% CI 1.72-5.47) and significant carotid atherosclerosis (HR: 1.55, 95% CI 1.02-2.36) were independent predictors for cardiovascular mortality. Stroke patients with a past history of cancer are at increased risk of recurrent stroke and cardiovascular mortality.

Cerebral ischemia and diabetes mellitus (DM) are common diseases that often coexist and interact with each other. DM doubles the risk of ischemic stroke, and cerebral ischemia causes stress-induced hyperglycemia. Most experimental stroke studies used healthy animals. Melatonin is neuroprotective against cerebral ischemia-reperfusion injury (CIRI) in non-DM, normoglycemic animals through anti-oxidant effect, anti-inflammation, and anti-apoptosis. Previous studies have also reported a negative correlation between hyperglycemia and urinary melatonin metabolite. The present study investigated the effects of type 1 DM (T1DM) on CIRI in rats and the role of melatonin against CIRI in T1DM animals. Our results revealed that T1DM aggravated CIRI, leading to greater weight loss, increased infarct volume, and worse neurological deficit. T1DM aggravated the post-CIRI activation of nuclear factor kappa B (NF-κB) pathway and increase in pro-apoptotic markers. A single intraperitoneal injection of melatonin at 10 mg/kg given 30 min before ischemia onset attenuated CIRI in T1DM rats, resulting in less weight loss, decreased infarct volume, and milder neurological deficit when compared with the vehicle group. Melatonin treatment achieved anti-inflammatory and anti-apoptotic effects with reduced NF-κB pathway activation, reduced mitochondrial cytochrome C release, decreased calpain-mediated spectrin breakdown product (SBDP), and decreased caspase-3-mediated SBDP. The treatment also led to fewer iNOS+ cells, milder CD-68+ macrophage/microglia infiltration, decreased TUNEL+ apoptotic cells, and better neuronal survival. T1DM aggravates CIRI. Melatonin treatment is neuroprotective against CIRI in T1DM rats via anti-inflammatory and anti-apoptotic effects.

Prospective memory (PM) is the ability to remember future intentions, and PM function is closely related to independence in daily life, particularly in patients with temporal lobe epilepsy (TLE). As PM involves various cognitive components of attention, working memory, inhibition and other executive functions, this study investigated how TLE may affect PM components and the underlying neural mechanisms. Sixty-four subjects were recruited, including 20 refractory TLE patients, 18 well-controlled TLE patients and 26 age-matched healthy controls. A set of neuropsychological tests was administered to assess specific brain functions. An event-related potential (ERP) task was used to further explore how PM and its components would be differentially affected in the two TLE types. Our findings revealed that: (1) refractory TLE patients scored lower than the healthy controls in the digit span, Verbal Fluency Test and Symbol Digit Modalities Test; (2) refractory TLE patients exhibited impaired PM performance and reduced prospective positivity amplitudes over the frontal, central and parietal regions in ERP experiments when compared to the healthy controls; and (3) decreased P3 amplitudes in the nogo trials were observed over the frontal-central sites in refractory but not in well-controlled TLE patients. To our knowledge, this is the first ERP study on PM that has specifically identified PM impairment in refractory but not in well-controlled TLE patients. Our finding of double dissociation in PM components suggests that inhibition dysfunction may be the main reason for PM deficit in refractory TLE patients. The present results have clinical implications for neuropsychological rehabilitation in TLE patients.

BACKGROUND AND PURPOSE The Mediterranean-style diet is widely advocated for the prevention of cardiovascular diseases (CVD). Meanwhile, blood pressure variability (BPV) is a novel risk factor for CVD. It is unknown whether dietary pattern plays a role in modulating BPV. METHODS We prospectively followed-up 274 consecutive patients with stable coronary artery disease (CAD). The Mediterranean diet score (MDS) was derived for all individuals upon recruitment, blood pressure (BP) was measured during each subsequent clinic visit and the visit-to-visit BPV was calculated. The occurrence of major adverse cardiovascular events (MACEs) and all-cause mortality was monitored. RESULTS After a mean follow-up of 77±12 months, 16.1% of the study population developed MACEs. About 11.3% died from all causes. Patients who developed MACEs or all-cause mortality had a greater systolic BPV compared to those who did not develop an adverse event. Patients who developed a MACE had a lower MDS and further analysis revealed those who developed a stroke had a lower MDS compared with those who did not develop a stroke, but there were no significant differences in MDS between CAD patients with or without subsequent acute coronary syndrome, cardiovascular, or all-cause mortality. After adjusting for confounding variables, a high MDS was an independent predictor for low systolic BPV (B −0.74, 95% confidence interval −1.27 to −0.21, P < 0.01) and was noted to be protective against subsequent development of stroke (hazards ratio 0.48, 95% confidence interval 0.24 to 0.94, P = 0.03). CONCLUSIONS Among patients with CAD, a higher MDS is associated with a lower visit-to-visit BPV and with lower stroke risk.

Elevated blood pressure (BP) is commonly seen in patients with intracerebral hemorrhage (ICH), and is independently associated with poor functional outcomes. Little is known about how elevated BP influences ICH-related brain injury. In the present study, we investigated the physiological and brain histological changes, as well as functional recovery following ICH in renovascular hypertensive rats. Renovascular hypertension (RVHT) was achieved by applying a silver clip onto the left renal artery of adult Sprague-Dawley rats. ICH was induced by an intrastriatal injection of bacterial collagenase IV about 5–6 weeks after left renal artery clipping or the sham operation. Following induction of ICH, both the normotensive and RVHT rats demonstrated an ultra-acute elevation in BP. Elevated BP increased hematoma volume, brain swelling, and apoptosis in the perihematomal areas. Brain degeneration, including local atrophy and lateral ventricle enlargement, was greater in the RVHT rats. In addition, many proliferating cells were seen over the ipsilateral striatum in the RVHT rats after ICH. The modified limb placing tests were done weekly for 3 weeks. In line with the histological damage, elevated BP worsened neurological deficits. These results suggest that ICH in the hypertensive rats mimics the clinical scenario of hypertensive ICH and may provide a platform to study the mechanisms of ICH-induced brain injury and potential therapies for ICH.

Cerebral hyperperfusion syndrome as a complication of carotid endarterectomy (CEA) has been widely reported in the surgical literature. It may occur within hours to 3 weeks after CEA and is characterized by symptoms ranging from headaches, fits, confusion, focal neurological signs to intracerebral hemorrhage. Although percutaneous transluminal angioplasty (PTA) and stenting are increasingly performed as an alternative to CEA in the treatment of carotid artery stenosis, few cases of cerebral hyperperfusion injury following carotid stenting have been reported. We describe 2 cases of cerebral hyperperfusion syndrome following PTA and stenting for high-grade internal carotid artery (ICA) stenosis. Both cases involved a lesion of 95% in severity. The first case was a 73-year-old man who developed generalized convulsion 7 h following stenting to the left ICA. The second case was an 80-year-old woman who developed recurrent right periorbital headache and confusion 16 h after stenting to the right ICA, followed by left upper limb seizure 14 days later. Both patients fully recovered without any intracerebral hemorrhage or infarction. To our knowledge, this is the first report of cerebral hyperperfusion injury after carotid stenting without associated intracranial hemorrhage and with full recovery. In the patient with neurological symptoms following carotid stenting, it is important to consider cerebral hyperperfusion syndrome as a differential diagnosis to embolic or hemorrhagic stroke since early recognition and meticulous control of blood pressure may prevent progression to cerebral hemorrhage and death.

Cerebral microbleeds are a neuroimaging biomarker of stroke risk. A crucial clinical question is whether cerebral microbleeds indicate patients with recent ischaemic stroke or transient ischaemic attack in whom the rate of future intracranial haemorrhage is likely to exceed that of recurrent ischaemic stroke when treated with antithrombotic drugs. We therefore aimed to establish whether a large burden of cerebral microbleeds or particular anatomical patterns of cerebral microbleeds can identify ischaemic stroke or transient ischaemic attack patients at higher absolute risk of intracranial haemorrhage than ischaemic stroke. We did a pooled analysis of individual patient data from cohort studies in adults with recent ischaemic stroke or transient ischaemic attack. Cohorts were eligible for inclusion if they prospectively recruited adult participants with ischaemic stroke or transient ischaemic attack; included at least 50 participants; collected data on stroke events over at least 3 months follow-up; used an appropriate MRI sequence that is sensitive to magnetic susceptibility; and documented the number and anatomical distribution of cerebral microbleeds reliably using consensus criteria and validated scales. Our prespecified primary outcomes were a composite of any symptomatic intracranial haemorrhage or ischaemic stroke, symptomatic intracranial haemorrhage, and symptomatic ischaemic stroke. We registered this study with the PROSPERO international prospective register of systematic reviews, number CRD42016036602. Between Jan 1, 1996, and Dec 1, 2018, we identified 344 studies. After exclusions for ineligibility or declined requests for inclusion, 20 322 patients from 38 cohorts (over 35 225 patient-years of follow-up; median 1·34 years [IQR 0·19–2·44]) were included in our analyses. The adjusted hazard ratio [aHR] comparing patients with cerebral microbleeds to those without was 1·35 (95% CI 1·20–1·50) for the composite outcome of intracranial haemorrhage and ischaemic stroke; 2·45 (1·82–3·29) for intracranial haemorrhage and 1·23 (1·08–1·40) for ischaemic stroke. The aHR increased with increasing cerebral microbleed burden for intracranial haemorrhage but this effect was less marked for ischaemic stroke (for five or more cerebral microbleeds, aHR 4·55 [95% CI 3·08–6·72] for intracranial haemorrhage vs 1·47 [1·19–1·80] for ischaemic stroke; for ten or more cerebral microbleeds, aHR 5·52 [3·36–9·05] vs 1·43 [1·07–1·91]; and for ≥20 cerebral microbleeds, aHR 8·61 [4·69–15·81] vs 1·86 [1·23–2·82]). However, irrespective of cerebral microbleed anatomical distribution or burden, the rate of ischaemic stroke exceeded that of intracranial haemorrhage (for ten or more cerebral microbleeds, 64 ischaemic strokes [95% CI 48–84] per 1000 patient-years vs 27 intracranial haemorrhages [17–41] per 1000 patient-years; and for ≥20 cerebral microbleeds, 73 ischaemic strokes [46–108] per 1000 patient-years vs 39 intracranial haemorrhages [21–67] per 1000 patient-years). In patients with recent ischaemic stroke or transient ischaemic attack, cerebral microbleeds are associated with a greater relative hazard (aHR) for subsequent intracranial haemorrhage than for ischaemic stroke, but the absolute risk of ischaemic stroke is higher than that of intracranial haemorrhage, regardless of cerebral microbleed presence, antomical distribution, or burden. British Heart Foundation and UK Stroke Association.

Balancing the risks of recurrent ischaemic stroke and intracranial haemorrhage is important for patients treated with antithrombotic therapy after ischaemic stroke or transient ischaemic attack. However, existing predictive models offer insufficient performance, particularly for assessing the risk of intracranial haemorrhage. We aimed to develop new risk scores incorporating clinical variables and cerebral microbleeds, an MRI biomarker of intracranial haemorrhage and ischaemic stroke risk. We did a pooled analysis of individual-patient data from the Microbleeds International Collaborative Network (MICON), which includes 38 hospital-based prospective cohort studies from 18 countries. All studies recruited participants with previous ischaemic stroke or transient ischaemic attack, acquired baseline MRI allowing quantification of cerebral microbleeds, and followed-up participants for ischaemic stroke and intracranial haemorrhage. Participants not taking antithrombotic drugs were excluded. We developed Cox regression models to predict the 5-year risks of intracranial haemorrhage and ischaemic stroke, selecting candidate predictors on biological relevance and simplifying models using backward elimination. We derived integer risk scores for clinical use. We assessed model performance in internal validation, adjusted for optimism using bootstrapping. The study is registered on PROSPERO, CRD42016036602. The included studies recruited participants between Aug 28, 2001, and Feb 4, 2018. 15 766 participants had follow-up for intracranial haemorrhage, and 15 784 for ischaemic stroke. Over a median follow-up of 2 years, 184 intracranial haemorrhages and 1048 ischaemic strokes were reported. The risk models we developed included cerebral microbleed burden and simple clinical variables. Optimism-adjusted c indices were 0·73 (95% CI 0·69–0·77) with a calibration slope of 0·94 (0·81–1·06) for the intracranial haemorrhage model and 0·63 (0·62–0·65) with a calibration slope of 0·97 (0·87–1·07) for the ischaemic stroke model. There was good agreement between predicted and observed risk for both models. The MICON risk scores, incorporating clinical variables and cerebral microbleeds, offer predictive value for the long-term risks of intracranial haemorrhage and ischaemic stroke in patients prescribed antithrombotic therapy for secondary stroke prevention; external validation is warranted. British Heart Foundation and Stroke Association.

Background: Abciximab, a platelet glycoprotein IIb/IIIa receptor antagonist, prevents ischemic complications during percutaneous transluminal coronary angioplasty and was recently shown to open occluded vessels in patients with acute myocardial infarction when used alone or in combination with other thrombolytic agents. In an animal model of arterial thrombosis, abciximab was found to be safe and effective for the prevention of carotid artery thrombosis. However, the safety and efficacy of abciximab in the treatment of acute ischemic cerebrovascular events is unknown at present. Case Description: We describe 3 patients who experienced ischemic cerebrovascular events with symptoms involving the middle cerebral artery territory while undergoing percutaneous angioplasty and stenting to their internal carotid arteries. Abciximab was administered to each patient within 10 min of symptom onset as a bolus (0.25 mg/kg) into the ipsilateral common carotid artery followed by continuous intravenous infusion (9 µg/min) for 12 h. All patients’ symptoms resolved completely (by 25 min, 40 min and 5 h, respectively) with no further neurological complications. Conclusions: Our preliminary observation suggests that abciximab may improve neurological outcome following middle cerebral artery ischemic events associated with carotid angioplasty and stenting. Large prospective studies are warranted to establish the safety and efficacy of abciximab in acute ischemic stroke, either as a primary treatment modality or an adjunct to carotid angioplasty and stenting.

This study aimed to evaluate P300 as an electrophysiological marker of cognitive function in patients with systemic lupus erythematosus (SLE) who had previous neuropsychiatric (NPSLE) involvement and were diagnosed to have cognitive impairment by standard neuropsychological tests. Event-related potentials (ERPs) were assessed by the auditory and visual oddball paradigms. Amplitude and latency of P300 at the frontal (Fz), central (Cz), and parietal (Pz) regions were determined and compared with controls. P300 detection was performed in NPSLE patients with pre-diagnosed cognitive impairment (n = 9), matched SLE patients without previous NPSLE (non-NPSLE) (n = 9), and healthy controls (n = 15). Auditory oddball task did not show any P300 abnormality between groups. Visual oddball task revealed reduced amplitude of P300 over Fz (P = .002) and Cz (P = .009) electrodes in NPSLE patients compared with healthy controls and among those who had predominant memory deficit (P = .01 at Fz). Abnormal P300 was also observed in non-NPSLE patients at Fz and Cz. Using visual oddball paradigm, abnormal P300 was found in NPSLE patients over frontal and parietal regions compared with normal controls but was not discriminative from possible subclinical disease in non-NPSLE patients. In conclusion, visual oddball paradigm was a more sensitive electrophysiological marker than auditory oddball paradigm for cognitive impairment in NPSLE patients.