Shin-Joe Yeh

Dysphagia screening decreases pneumonia in acute stroke patients admitted to the stroke intensive care unit

Dysphagia increases the risk of pneumonia in stroke patients. This study aimed to evaluate bedside swallowing screening for prevention of stroke-associated pneumonia (SAP) in acute stroke patients admitted to the intensive care unit (ICU). Consecutive acute stroke patients admitted to the stroke ICU from May 2006 to March 2007 were included. Patients were excluded if they were intubated on the first day of admission or had a transient ischemic attack. A 3-Step Swallowing Screen was introduced since October 2006 and therefore patients were divided into pre-screen and post-screen groups. A binary logistic regression model was used to determine independent risk factors for SAP and in-hospital death. There were 74 and 102 patients included in the pre- and post-screen groups, respectively. Pneumonia was associated with higher National Institutes of Health Stroke Scale (NIHSS) score, older age, nasogastric and endotracheal tube placement. After adjusting for age, gender, NIHSS score and nasogastric and endotracheal tube insertion, dysphagia screening was associated with a borderline decrease in SAP in all stroke patients (odds ratio, 0.42; 95% CI, 0.18-1.00; p=0.05). However, dysphagia screening was not associated with reduction of in-hospital deaths. Systematic bedside swallowing screening is helpful for prevention of SAP in acute stroke patients admitted to the ICU.

Pathogenetical Subtypes of Recurrent Intracerebral Hemorrhage: Designations by SMASH-U Classification System

Background and Purpose— Pathogenetic classification of intracerebral hemorrhage (ICH), using systems such as SMASH-U (structural vascular lesions, medication, cerebral amyloid angiopathy [CAA], systemic disease, hypertension, or undetermined), is important in predicting functional outcomes and mortality in patients with ICH. This study aimed to compare pathogenetic subtypes between the first and recurrent ICH. Methods— This study obtained data related to 4578 consecutive acute patients with ICH from the National Taiwan University Hospital Stroke Registry during January 1995 to December 2013. Using the SMASH-U method, patients were classified into 6 subtypes. We then analyzed the outcomes of first-ever ICH cases and pathogenetic classification of recurrent ICH. Results— Among 3785 patients who experienced first-ever ICH (male, 63.3%; mean age, 58.7±17.0 years), the most common cause was hypertensive angiopathy (54.9%), followed by CAA (12.2%), systemic disease (12.1%), undetermined (10.1%), structural vascular lesions (7.8%), and medication related (2.9%). In 185 cases of recurrent ICH, pathogenetic differences between the 2 ICH events were observed in 34 (18.4%) cases, most of which were CAA to hypertensive angiopathy (n=10) or vice versa (n=7). The rates of ICH recurrence were highest for systemic disease-related and CAA-related ICH at 1, 5, 10, and 15 years after the indexed ICH event. Conclusions— In approximately one fifth of the recurrent patients with ICH, pathogenetic differences were observed between initial and recurrent events, particularly among those with CAA. It is possible that some patients with ICH with concomitant hypertensive angiopathy and CAA may have been categorized as CAA by the SMASH-U method.

Stroke code improves intravenous thrombolysis administration in acute ischemic stroke.

Background and Purpose Timely intravenous (IV) thrombolysis for acute ischemic stroke is associated with better clinical outcomes. Acute stroke care implemented with “Stroke Code” (SC) may increase IV tissue plasminogen activator (tPA) administration. The present study aimed to investigate the impact of SC on thrombolysis. Methods The study period was divided into the “pre-SC era” (January 2006 to July 2010) and “SC era” (August 2010 to July 2013). Demographics, critical times (stroke symptom onset, presentation to the emergency department, neuroimaging, thrombolysis), stroke severity, and clinical outcomes were recorded and compared between the two eras. Results During the study period, 5957 patients with acute ischemic stroke were admitted; of these, 1301 (21.8%) arrived at the emergency department within 3 h of stroke onset and 307 (5.2%) received IV-tPA. The number and frequency of IV-tPA treatments for patients with an onset-to-door time of <3 h increased from the pre-SC era (n = 91, 13.9%) to the SC era (n = 216, 33.3%) (P<0.001). SC also improved the efficiency of IV-tPA administration; the median door-to-needle time decreased (88 to 51 min, P<0.001) and the percentage of door-to-needle times ≤60 min increased (14.3% to 71.3%, P<0.001). The SC era group tended to have more patients with good outcome (modified Rankin Scale ≤2) at discharge (49.5 vs. 39.6%, P = 0.11), with no difference in symptomatic hemorrhage events or in-hospital mortality. Conclusion The SC protocol increases the percentage of acute ischemic stroke patients receiving IV-tPA and decreases door-to-needle time.

Evidence for a detrimental role of TLR8 in ischemic stroke

Toll-like receptors (TLRs) are transmembrane pattern-recognition receptors that initiate signals in response to diverse pathogen-associated molecular patterns. Several groups have recently reported a role for TLR2 and TLR4 in ischemic stroke-induced brain injury. However, relatively little is known about the role of TLR8 in ischemic stroke. Here we provide the first evidence that TLR8 activation plays a detrimental role in stroke outcome by promoting neuronal apoptosis and T cell-mediated post-stroke inflammation. TLR8 is expressed in cerebral cortical neurons, where its levels and downstream signaling via JNK are increased in response to oxygen glucose deprivation (OGD). Treatment with a TLR8 agonist activated pro-apoptotic JNK and increased neuronal cell death during OGD. Furthermore, selective knockdown of TLR8 using siRNA protected SH-SY5Y cells following OGD, and TLR8 agonist administration in vivo increased mortality, neurological deficit and T cell infiltration following stroke. Taken together, our findings indicate a detrimental role for neuronal TLR8 signaling in the triggering of post-stroke inflammation and neuronal death.

Onset Headache Predicts Good Outcome in Patients With First-Ever Ischemic Stroke

Background and Purpose— The study aimed to assess whether onset headache is an ominous sign in patients with first-ever ischemic stroke. Methods— A large population of ischemic stroke patients was obtained from the Taiwan Stroke Registry. Stroke subtypes were classified by the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) criteria. On the basis of the International Classification of Headache Disorders, second version, onset headache was defined as a new headache that developed at the onset of ischemic stroke. Clinical features and impact on stroke outcomes, including in-hospital stroke in evolution, changes in National Institutes of Health Stroke Scale on discharge, and Barthel index and modified Rankin scale ⩽6 months after stroke were compared between those with and without onset headache. Results— Among 11 523 patients with first-ever ischemic stroke, 848 had onset headache (7.4%). Patients with specific cause, large-artery atherosclerosis, or cardioembolism were more likely to have onset headache. Patients with onset headache were younger, predominantly female, and more likely to have posterior circulation ischemic lesions. Compared with patients without onset headache, those with onset headache had a lower frequency of stroke in evolution (4.5% versus 6.7%; adjusted relative risk, 0.64; 95% confidence interval, 0.52–0.79), greater improvement in National Institutes of Health Stroke Scale score on discharge (0.08 versus −0.20; P=0.02), higher mean Barthel index scores (86.5±20.0 versus 83.9±23.3; adjusted difference, 1.43; 95% confidence interval, 0.28–2.89), and a lower frequency of modified Rankin scale higher than 2 (27.6% versus 31.5%; adjusted relative risk, 0.85; 95% confidence interval, 0.72–0.95) at 1-month follow-up. There was also a trend for better functional outcome in 3- and 6-month follow-ups. Conclusions— By adopting standard classification criteria, this large-scale study demonstrated that onset headache was associated with modest but significantly better outcomes after ischemic stroke.

Screen for intracranial dural arteriovenous fistulae with carotid duplex sonography

Objectives: Early diagnosis and management of intracranial dural arteriovenous fistulae (DAVF) may prevent the occurrence of stroke. This study aimed to identify the best carotid duplex sonography (CDS) parameters for screening DAVF. Methods: 63 DAVF patients and 170 non-DAVF patients received both CDS and conventional angiography. The use of seven CDS haemodynamic parameter sets related to the resistance index (RI) of the external carotid artery (ECA) for the diagnosis of DAVF was validated and the applicability of the best CDS parameter set in 20 400 patients was tested. Results: The CDS parameter set (ECA RI (cut-off point = 0.7) and internal carotid artery (ICA) to ECA RI ratio (cut-off point = 0.9)) had the highest specificity (99%) for diagnosis of DAVF with moderate sensitivity (51%). Location of the DAVF was a significant determinant of sensitivity of detection, which was 70% for non-cavernous DAVF and 0% for cavernous sinus DAVF (p<0.001). The above parameter set detected abnormality in 92 of 20 400 patients. These abnormalities included DAVF (n = 25), carotid stenosis (n = 32), vertebral artery stenosis (n = 7), intracranial arterial stenosis (n = 6), head and neck tumour (n = 3) and unknown aetiology (n = 19). Conclusion: Combined CDS parameters of ECA RI and ICA to ECA RI ratio can be used as a screening tool for the diagnosis of DAVF.

Proteinuria independently predicts unfavorable outcome of ischemic stroke patients receiving intravenous thrombolysis.

Background and Purpose Patients with low estimated glomerular filtration rate (eGFR) and proteinuria may be at increased risk for stroke. This study investigated whether low eGFR and proteinuria are outcome predictors in stroke patients treated with intravenous thrombolysis. Methods We studied 432 consecutive stroke patients who received thrombolysis from January 2006 to December 2012, in Taiwan. Unfavorable outcome was defined as modified Rankin scale ≥2 at 3 months after stroke. Proteinuria was classified as negative or trace, mild, and moderate to severe. Using logistic regression analysis, we identified independent factors for unfavorable outcome after thrombolysis. Results Of all patients, 32.7% had proteinuria. Patients with proteinuria were older, had higher frequencies of diabetes mellitus, hyperlipidemia, atrial fibrillation, lower eGFR, and greater severity of stroke upon admission than those without proteinuria. Proteinuria, not low eGFR, was an independent predictor for unfavorable outcome for stroke (OR = 2.00 for mild proteinuria, p = 0.035; OR = 2.54 for moderate to severe proteinuria, p = 0.035). However, no clear relationship was found between proteinuria and symptomatic hemorrhage after thrombolysis. Conclusions Proteinuria is an independent predictor of unfavorable outcome for acute ischemic stroke in patients treated with intravenous thrombolysis, indicating the crucial role of chronic kidney disease on the effectiveness of thrombolysis.

Pre-ICH warfarin use, not antiplatelets, increased case fatality in spontaneous ICH patients

Anticoagulant and antiplatelets for prevention of ischaemic stroke and cardiovascular diseases may increase the risk of intracerebral hemorrhage (ICH). This study aimed to investigate the influence of pre‐ICH use of anticoagulant and antiplatelets on ICH patients.

Stroke center characteristics which influence the administration of thrombolytic therapy for acute ischemic stroke: A national survey of stroke centers in Taiwan

Stroke centers and intravenous tissue plasminogen activators (tPA) are effective management for acute ischemic stroke. This study aimed to analyze stroke center characteristics on the administration of thrombolytic therapy. A national survey of stroke centers in academic medical centers and regional teaching hospitals in Taiwan was conducted. The survey questions included the number of tPA or other thrombolytic therapies, presence of stroke intensive care units and wards, initiation of rehabilitation, and 15 criteria for establishment of stroke centers adopted from the Brain Attack Coalitions recommendation. Factors influencing administration of thrombolytic therapy were analyzed. Intravenous tPA increased from 135 cases in 2004 to 246 cases in 2006, accounting for approximately 0.4% and 0.8% of all acute ischemic stroke patients in Taiwan, respectively. The frequency of thrombolytic therapy administration significantly correlated with stroke center criteria (Spearmans rho=0.731, P<0.001). Multivariate analysis showed routine intravenous tPA protocol in the emergency room (odds ratio=4.6, P=0.042) and supervision by the stroke center director (odds ratio=3.7, P=0.031) significantly influenced the administration of thrombolytic therapy. Well-organized stroke centers, routine use of thrombolytic therapy protocols in the emergency room, and guidance by a stroke center director are important for enhancing thrombolytic therapy in patients with acute ischemic stroke.

Cleaved but not endogenous secretory RAGE is associated with outcome in acute ischemic stroke.

Objective: To investigate the expression patterns of 2 soluble isoforms of receptor for advanced glycation end-product (RAGE), including endogenous secretory RAGE (esRAGE) and cleaved RAGE (cRAGE), and their associations with outcome in acute ischemic stroke (IS). Methods: Acute IS patients (n = 106) and age- and sex-matched controls (n = 150) were recruited. Plasma levels of total soluble RAGE (sRAGE) and esRAGE in patients at <48 hours and 48–72 hours after IS and in controls were measured by ELISA. The level of cRAGE was calculated by subtracting the level of sRAGE from that of esRAGE. Poor outcome was defined as modified Rankin Scale score >2 at 3 months after stroke. Results: The plasma levels of cRAGE were significantly higher and correlated to those of esRAGE (p < 0.001). The plasma levels of esRAGE and cRAGE were both significantly higher in IS patients <48 hours and 48–72 hours after onset than in controls, but only level of cRAGE at <48 hours was independently associated with poor outcome after adjusting for clinical variables (odds ratio 2.44; 95% confidence interval 1.16–5.16; p = 0.019). Conclusion: The plasma level of cRAGE at <48 hours after IS, rather than esRAGE, is a significant predictor of acute IS outcome.