Early Phase Of Acute Stroke Research Articles

NR-2 antikor peptid düzeyinin akut iskemik inmede tanı, prognoz ve koma skorları ile ilişkisi var mıdır?

Aim: This study aimed to demonstrate the diagnostic and prognostic value of NR-2 peptides as a biomarker in acute ischemic stroke and to evaluate their correlation with the Glasgow Coma Scale (GCS) and the National Institutes of Health Stroke Scale (NIHSS).Materials and Methods: The importance of NR-2 peptide level in diagnosis and prognosis in acute stroke was investigated cross-sectional and prospectively. The study included 101 patients, who presented to a tertiary healthcare facility and were diagnosed with acute stroke, and 57 healthy controls. In the whole study population, serum NR-2 peptide levels were measured using the ELISA method.Results: The NR-2 peptide level was 6.32 ± 8.30 in the patient group and 3.91 ± 1.64 in the study group. The NR-2 peptide level was significantly higher in the patient group (p = 0.006). No correlation was detected between NR-2 peptide levels and scores in the GCS or NIHSS. The results indicated that NR-2 was a potential biomarker elevated in the early phase of acute stroke, but had no correlation with the prognosis of acute stroke.Conclusion: Although our data shed light on the use of the NR-2 peptide level as a biomarker in the acute phase in patients with stroke, data are insufficient to predict prognosis. We think that larger, multicenter studies with longer follow-up periods are needed.

High-Density Lipoprotein Carries Markers That Track With Recovery From Stroke

Prospective cohort studies question the value of HDL-C (high-density lipoprotein cholesterol) for stroke risk prediction. Investigate the relationship between long-term functional recovery and HDL proteome and function. Changes in HDL protein composition and function (cholesterol efflux capacity) in patients after acute ischemic stroke at 2 time points (24 hours, 35 patients; 96 hours, 20 patients) and in 35 control subjects were measured. The recovery from stroke was assessed by 3 months, the National Institutes of Health Stroke Scale and modified Rankin scale scores. When compared with control subject after adjustments for sex and HDL-C levels, 12 proteins some of which participate in acute phase response and platelet activation (APMAP [adipocyte plasma membrane-associated protein], GPLD1 [phosphate inositol-glycan specific phospholipase D], APOE [apolipoprotein E], IHH [Indian hedgehog protein], ITIH4 [inter-alpha-trypsin inhibitor chain H4], SAA2 [serum amyloid A2], APOA4 [apolipoprotein A-IV], CLU [clusterin], ANTRX2 [anthrax toxin receptor 2], PON1 [serum paraoxonase/arylesterase], SERPINA1 [alpha-1-antitrypsin], and APOF [apolipoprotein F]) were significantly (adjusted P<0.05) altered in stroke HDL at 96 hours. The first 8 of these proteins were also significantly altered at 24 hours. Consistent with inflammatory remodeling, cholesterol efflux capacity was reduced by 32% (P<0.001) at both time points. Baseline stroke severity adjusted regression model showed that changes within 96-hour poststroke in APOF, APOL1, APMAP, APOC4 (apolipoprotein C4), APOM (apolipoprotein M), PCYOX1 (prenylcysteine oxidase 1), PON1, and APOE correlate with stroke recovery scores (R2=0.38-0.73, adjusted P<0.05). APOF (R2=0.73) and APOL1 (R2=0.60) continued to significantly correlate with recovery scores after accounting for tPA (tissue-type plasminogen activator) treatment. Changes in HDL proteins during early acute phase of stroke associate with recovery. Monitoring HDL proteins may provide clinical biomarkers that inform on stroke recuperation.

Upper limb recovery in early acute phase stroke survivors by coupled EMG-triggered and cyclic neuromuscular electrical stimulation.

Few patients with severe upper extremity (UE) paresis after stroke achieved full recovery, because of the lack of a definitive approach to improve severe UE paresis immediately after onset. to investigate the effects of coupled EMG-triggered and cyclic neuromuscular electrical stimulation (NMES) on UE paresis during early acute phase of stroke. Seventeen participants with severe UE disability met the criteria. 8 subjects received 20 minutes of NMES prior to standard care per session, while 9 age- and severity-matched subjects received two times 20 minutes of standard care. Outcome measures included UE motor section of the Fugl-Meyer Motor Assessment Scale (FMA-UE), Wolf motor function test (WMFT), and box and block test (BBT). The NMES group received treatment (average session: 10.87) after a median 7 days from stroke (16.5 sessions after 5 days for control). To adjust the different treatment durations, we defined "progress rate" as the gains of UE function scores divided by treatment duration. The progress rate was significantly different in FMA-UE, but not in WMFT and BBT. The present study suggested beneficial effects of coupled NMES on UE paresis during early acute phase of stroke.

Aneurysmal Subarachnoid Hemorrhage in a 68-Year-old Hyperglycemic Female Patient: Case Report and Literature Review

Background: While hyperglycemia is intimately associated with uncontrolled diabetes mellitus (DM), recent clinical studies have demonstrated that hyperglycemia is also present in the early acute phase of stroke and is associated with poor prognosis and increased long-term mortality. About half of patients with acute hemorrhagic stroke also present with hyperglycemia upon admission. But more than 50% of patients with acute hemorrhagic stroke develop hyperglycemia even without a previous history of DM. This sheds new light on the relationship between DM, hyperglycemia, and hemorrhagic stroke, with a pathophysiology that is perhaps more profound than is conventionally understood.&#x0D; The Case: We report a case of a 68-year-old female, with a history of DM Type 2 and stage 3 hypertension who presents to the emergency room (ER) at the Western Regional Hospital in Belmopan City, Belize, with hemorrhagic stroke and hyperglycemia. Diffuse subarachnoid hemorrhage was found in the frontal, temporal, and parietal regions. Mild intraventricular hemorrhage was also observed in the frontal horns and basal cisterns. And small areas of intraparenchymal hemorrhage were present in the frontal lobes. The patient was stabilized and treated conservatively with calcium channel blockers, and diuretics.&#x0D; Conclusion: Despite a unifying consensus that is still pending, maintaining glucose levels between 110-120 mg/dl by using continuous insulin infusions after traumatic brain injury or aneurysmal subarachnoid hemorrhage may carry some clinical benefit with slightly improved outcome.

Astrocyte-specific insulin-like growth factor-1 gene transfer in aging female rats improves stroke outcomes.

Middle aged female rats sustain larger stroke infarction and disability than younger female rats. This older group also shows age-related reduction of insulin like growth factor (IGF)-1 in serum and in astrocytes, a cell type necessary for poststroke recovery. To determine the impact of astrocytic IGF-1 for ischemic stroke, these studies tested the hypothesis that gene transfer of IGF-1 to astrocytes will improve stroke outcomes in middle aged female rats. Middle aged (10-12 month old), acyclic female rats were injected with recombinant adeno-associated virus serotype 5 (AAV5) packaged with the coding sequence of the human (h)IGF-1 gene downstream of an astrocyte-specific promoter glial fibrillary acidic protein (GFAP) (AAV5-GFP-hIGF-1) into the striatum and cortex. The AAV5-control consisted of an identical shuttle vector construct without the hIGF-1 gene (AAV5-GFAP-control). Six to eight weeks later, animals underwent transient (90 min) middle cerebral artery occlusion via intraluminal suture. While infarct volume was not altered, AAV5-GFAP-hIGF-1 treatment significantly improved blood pressure and neurological score in the early acute phase of stroke (2 days) and sensory-motor performance at both the early and late (5 days) acute phase of stroke. AAV5-GFAP-hIGF-1 treatment also reduced circulating serum levels of GFAP, a biomarker for blood brain barrier permeability. Flow cytometry analysis of immune cells in the brain at 24 hr poststroke showed that AAV5-GFAP-hIGF-1 altered the type of immune cells trafficked to the ischemic hemisphere, promoting an anti-inflammatory profile. Collectively, these studies show that targeted enhancement of IGF-1 in astrocytes of middle-aged females improves stroke-induced behavioral impairment and neuroinflammation.

Abstract WP107: Igf-1-mediated Neuroprotection for Ischemic Stroke is Preceded by Its Actions at the Endothelial Cell Barrier

Background: Our studies show that Insulin like growth factor (IGF)-1 reduces MCAo-induced infarction in middle-aged female rats. We tested the hypothesis that IGF-1s neuroprotective effect is due to its action on the microvascular /endothelial barrier in the early acute phase of stroke. Methods: Middle-aged (12 mo) acyclic female rats were subject to intraluminal middle cerebral artery occlusion (MCAo) for 90 min followed by reperfusion and terminated 4h or 24h later. Animals received ICV infusion of artificial CSF, IGF-1 or IGF-1+JB-1. In separate experiments, we evaluated infarct volume, barrier assessment by uptake of Evan’s blue dye or histological evaluation of lectin stained microvessels. In parallel, cortical endothelial cells from middle-aged females were harvested and cultured ex vivo. Barrier properties were tested in cultures in transfer wells exposed to oxygen glucose deprivation (OGD) in the presence or absence of IGF-1 with FITC-labeled BSA in the media. Results: At 4h post MCAo, IGF-1 treatment significantly reduced brain uptake of Evan’s blue dye, while infarct volume was no different from controls. At 24h post MCAo, IGF-1 reduced infarct volume by 40% and decreased motor impairment (neurological score; p&lt;0.05). Lectin stained microvessels in the ischemic hemisphere displayed wider lumens (normal uncompressed lumen, p&lt;0.003) and more intense label (p&lt;0.01) in IGF-1 treated animals as compared to either vehicle or IGF-1+JB-1 groups. Ex vivo, IGF-1 reduced the loss of cell-cell contact due to OGD and reduced the dye transfer across the monolayer. Conclusions: Our findings indicate that IGF-1 acts in the early acute phase of ischemic stroke to reduce barrier permeability, which precedes its beneficial effect on infarct volume and behavior. Further, brain endothelial cells play a crucial role in IGF-1 mediated neuroprotection in middle-aged females.

Glial fibrillary acidic protein (GFAP) plasma levels distinguish intracerebral hemorrhage from cerebral ischemia in the early phase of acute stroke

Glial fibrillary acidic protein (GFAP) plasma levels distinguish intracerebral hemorrhage from cerebral ischemia in the early phase of acute stroke

Acute stroke research: challenges and opportunities for nurses

Clinical research in the early acute phase of stroke is inherently complex, but is crucial to improve diagnosis, treatment and care of patients. This article explores the challenges faced by nurses in determining the eligibility of patients who have experienced stroke and obtaining informed consent from patients for inclusion in a clinical research study. It highlights the role of clinical nurses in ensuring patients and their representatives are offered opportunities to participate in research and are supported.In addition, the article illustrates how clinical and research staff jointly assure the safety of patients and the integrity of the research data. Examples of how acute stroke studies provide an opportunity to embed research into everyday nursing practice, thereby enabling nurses to advocate for quality evidence-based patient care, are illustrated.

Association of severe hypertension with pneumonia in elderly patients with acute ischemic stroke

Pneumonia is one of the most frequent complications in elderly patients with acute ischemic stroke. Although severe hypertension is often observed in the early phase of acute stroke, there are few studies of acute hypertension as a factor influencing the incidence of stroke-associated pneumonia (SAP) in elderly subjects with acute ischemic stroke. To assess the association of acute phase blood-pressure elevation with the incidence of SAP, we compared 10 elderly patients with acute ischemic stroke complicated with severe hypertension (⩾200/120 mm Hg) with 43 patients with moderate hypertension (160–199/100–119 mm Hg), as well as with 65 control normotensive or mildly hypertensive (<160/100 mm Hg) controls on admission. Data were collected on known risk factors, type of ischemic stroke and underlying chronic conditions. The significance of differences in risk factors was analyzed using univariate and multivariate comparisons of 38 SAP cases and others, 8 SAP death cases and others, and 28 patients with poor outcome associated with in-hospital death or artificial feeding at discharge and others. After adjustment for potential confounding factors, the relative risk estimates for SAP, SAP death and poor outcome were 2.83 (95% confidence interval 1.14–7.05), 5.20 (1.01–26.8) and 6.84 (1.32–35.4), respectively, for severe hypertension relative to normotensive or mildly hypertensive controls. We conclude that severe hypertension on admission is an independent predictive factor for SAP in elderly patients with acute ischemic stroke.

Blood Pressure Monitoring in the Assessment of Old Patients with Acute Stroke

Most patients have elevated blood pressure in the early phase of acute stroke that it often returns to normal within approximately seven-days. Most available data on the pattern of blood pressure in acute stroke are based on manual blood pressure measurements. The aims of the present study were to assess with 24 h blood pressure monitoring the pattern of blood pressure in acute stroke, and the change in blood pressure during the first week of event in very old patients. We studied 99 patients with acute stroke (58 males), mean age 83 ± 6 years (range 70-97). Casual blood pressure and 24 h blood pressure monitoring were recorded within 24 h of admission, and then after six- to seven-days. Casual blood pressure before beginning the 24 h blood pressure monitoring was 154 ± 23/80 ± 15 mmHg and the average 24 h blood pressure was 147 ± 20/74 ± 11 mmHg. One-week after stroke, casual blood pressure decreased by 15/7 mmHg, whereas 24 h blood pressure decreased by only 7/2 mmHg (P<0·01). Blood pressure decreased remarkably only in those with admission elevated systolic blood pressure. The change in 24 h systolic blood pressure after one-week correlated to the 24 h admission systolic blood pressure (R=0·47; P<0·01). Casual blood pressure may overestimate blood pressure in stroke patients. Very old patients with stroke exhibit a mild increase in blood pressure during the acute phase, and blood pressure decreases spontaneously only in those with elevated blood pressure levels. Use of 24 h blood pressure monitoring may be helpful in elderly patients with acute stroke.

EEG Patterns and Epileptic Seizures in Acute Phase Stroke

Background: The rate of early post-stroke epileptic seizures ranges from 2 to 33%. This wide range is likely due to differences in study design, patient selection and type of neurophysiological monitoring. Electroencephalography (EEG), which is not used in the routine work-up of acute stroke, is the best neurodiagnostic technique for detecting epileptic activity, especially in patients with non-convulsive post-stroke epileptic activity. The aim of this study was to analyze patterns on EEGs performed within 24 h of stroke onset, and to investigate correlations between these patterns and the occurrence of early epileptic seizures and status epilepticus (SE), vascular risk factors, stroke subtypes and short-term outcome. Methods: We prospectively studied 232 patients (mean age 71 ± 12 years; 177 ischemic strokes and 55 hemorrhagic). EEG recording was performed within 24 h from hospitalization. The follow-up lasted 1 week. Results: Fifteen patients (6.5%) had early seizures within 24 h; 10 of these patients had focal SE with or without secondary generalization. EEG revealed sporadic epileptiform focal abnormalities in 10% and periodic lateralized epileptiform discharges (PLEDs) in 6%. SE was recorded in 71.4% of patients with PLEDs. At the multivariate analysis, only early epileptic manifestations (p < 0.001) were independently associated with PLEDs. Conclusions: Our study confirms that seizures are not frequent in the early phase of acute stroke and occur prevalently as focal SE at onset. EEG may help to detect specific patterns, such as PLEDs, that are closely related to early seizures. EEG monitoring should be performed in order to detect purely electrographic seizures.

Effects of Partial Body Weight Support while Training Acute Stroke Patients to Walk Backwards on a Treadmill -A Controlled Clinical Trial Using Randomized Allocation-

[Purpose] We tested the efficacy of an intervention training acute stroke patients to walk backwards on a treadmill. Subjects were randomly allocated to three groups of Partial Body Weight Support treadmill backward walking group, Partial Body Weight Support treadmill forward walking group and Control in order to compare the efficacy of the interventions among the groups. [Subjects] The subjects were 36 acute stroke patients. [Methods] They were randomly allocated to the three groups using an envelope method. After 3 weeks of intervention. We investigated by multiple comparisons among the three groups using change scores for each of the outcome measures. [Results] The Berg Balance Scale showed no significant differences. The Rivermead Mobility Index showed a significant difference between the backward walking group and the forward walking group, and between the backward walking group and the Control. Walking speed was significantly different between the backward walking group and the Control. No differences were seen for other itemes. [Conclusions] As a result of 3-week intervention, a significant improvement was observed in walking speed and the Rivermead Mobility Index, suggesting that Partial Body Weight Support treadmill backward walking training for patients in the early phase of acute stroke is effective at improving mobility.

Effects of intensive gait-oriented physiotherapy during early acute phase of stroke

We assessed the effects and strenuousness of intensive gait-oriented inpatient rehabilitation initiated very early after stroke. Therapy content and interrater reliability of the assessments were also analyzed. Of 22 patients, 19 (average 8.0 d poststroke) completed the study. Before rehabilitation, 13 patients were unable to walk or needed two assistants to walk and 6 patients needed one assistant. Patients spent a daily maximum of 1 h therapy time to obtain 20 min of walking. Additional physiotherapy was also provided during the 3 wk therapy period. Seven structured motor tests were recorded before and after rehabilitation and at 6 months postrehabilitation, and perceived exertion was followed during physiotherapy. After rehabilitation, 16 patients could walk unassisted and 3 needed one assistant to walk. Mean +/- standard deviation exercise walking distance was 10,784 +/- 4,446 m and exercise was ranked as slightly strenuous. After 3 wk, the patients' 10 m walking time, ankle spasticity, lower-limb muscle force, and motor scale scores improved (p < 0.05). The early intensive rehabilitation was well tolerated and only three patients dropped out. Improved motor abilities were seen in all stroke patients.

Sequential changes on 23Na MRI after cerebral infarction.

23Na MRI changes from the acute to chronic phase were investigated in seven patients with cerebral infarcts. They showed no signal increase during the first 13 h after the stroke and revealed a definite signal increase thereafter. This reached a maximum 45-82 h after stroke and became slightly less marked in the subacute and chronic phases, probably as a result of disappearance of cerebral oedema. In the early acute phase of stroke, 23Na MRI appears to fail to demonstrate Na+ increases in the ischaemic area, due presumably to the invisibility on MRI of intracellular 23Na in the intact brain. The increase more than 13 h after stroke, during which ischaemic cells are likely to die, is presumably because of increased visibility of intracellular 23Na in the dead cells. 23Na MRI is apparently insensitive to early ischaemic changes, but may be useful for assessing the cell viability in the ischaemic brain.