National registry-based case-control study: comorbidity and stroke in young adults.

OBJECTIVES: Stroke is overrepresented in cohorts of young adults with chronic diseases. The prevalence and impact of comorbidity among young stroke patients have not been compared with individuals without stroke. Our aim was to investigate the association between comorbidity and stroke in young adults. MATERIALS AND METHODS: A nationwide cohort of patients (aged 15-44 years), registered in the Swedish Stroke Register, (Riksstroke) 2001-2009, was identified. Age- and sex-matched controls were randomly selected from the Population Register of Sweden. Discharge diagnoses were retrieved from the National Patient Register and grouped by chapter in the International Classification of Diseases 10th revision. Associations between ICD-10 chapters and stroke were stratified (age, sex, and stroke type) and analyzed by multivariable logistic regression. RESULTS: In 2599 stroke patients analyzed, the prevalence of vascular risk factors (hypertension 25.3%, dyslipidemia 13.0%, diabetes 9.7%, heart failure 3.2%, and atrial fibrillation 2.8%), all ICD-10 chapters (except pregnancy) and prestroke hospitalizations were more frequent among cases than controls. Independent associations were found between stroke and eight ICD-10 chapters: neoplasms (odds ratios (OR) 1.53, 95% CI 1.15-2.05), blood (OR 1.61, 1.11-2.34), endocrine (OR 2.28, 1.77-2.93), psychiatric (OR 1.50, 1.24-1.81), nervous (OR 1.91, 1.46-2.50), eye (OR 1.67, 1.05-2.64), circulatory (OR 3.05, 2.45-3.80), and symptoms (OR 1.31, 1.13-1.52). The risk of stroke increased by 26% per ICD-10 chapter diagnosed. CONCLUSIONS: In addition to vascular risk factors, comorbidity (represented by ICD-10 chapters) was associated with increased risk of stroke in young individuals. The risk of stroke was further increased with the number of diagnosed ICD-10 chapters.

The prevalence of atrial fibrillation in a geographically well-defined population in northern Sweden: implications for anticoagulation prophylaxis.

OBJECTIVES: The aims of this study were to evaluate the community-based prevalence of atrial fibrillation (AF) in a western society using a geographically well-defined population in the northern part of Sweden as a reference and to estimate the proportion of patients eligible for oral anticoagulation (OAC) prophylactic therapy according to the stroke risk indices CHADS2 and CHA2 DS2 -VASc. Bleeding risk was assessed using the HAS-BLED score. DESIGN: The study population was recruited from AURICULA, a Swedish national quality register for patients receiving anticoagulation treatment. All patients with the diagnosis AF in the catchment area are registered in AURICULA. RESULTS: Of the 65 532 inhabitants in the catchment area, 1616 were diagnosed with AF (1200 cases were characterized as chronic AF). Thus, the overall prevalence of AF was 2.5%. The prevalence increased with age from 6.3% in patients over 55 years of age to 13.8% in those over 80 years. The prevalence was higher in men than in women in all age groups. Overall, 56.3% and 85.1% of the population were at high risk of stroke (≥2 points) according to CHADS2 and CHA2 DS2 -VASc, respectively. In addition, 26.9% had an increased bleeding risk according to HAS-BLED. CONCLUSION: Within this large Caucasian population, we identified the highest community-based prevalence of AF to date. The prevalence was strongly associated with increasing age and male gender. Using CHA2 DS2 -VASc instead of CHADS(2) widened the indication for OAC prophylactic therapy of AF in this population.

Validation of the Swedish inpatient and cause-of-death registers in the context of stroke.

BACKGROUND: Quality follow-up within stroke care is important in times when stroke prevalence is increasing and health care funds are limited. Administrative data, such as data from the inpatient register (IPR) and the cause-of-death register (CDR) are often used for this purpose, but the validity of such data has not been ascertained. METHODS: During the year 1999-2000, a community-based stroke register was established in a Swedish municipality. Data from that register was compared with two administrative registers, the IPR and the CDR. RESULTS: Using multiple overlapping data sources, 377 patients with first-ever stroke were found in the community-based register. Forty-four of these (12%) were missing in the IPR/CDR. Non-hospitalized patients were less likely to be registered in the IPR/CDR, as were patients who were not initially treated in a stroke unit. Stroke severity was lower among non-registered patients. Thirty patients (8%) in the IPR/CDR were misclassified as stroke patients. CONCLUSIONS: Quality follow-up within stroke care could be biased or have low comparability, when administrative data are used. Great caution should be taken when data are derived from the inpatient and cause-of-death registers, and more validation work needs to be carried out in the context of stroke.

Ten-year risk for myocardial infarction in patients with first-ever stroke: a community-based study.

BACKGROUND: Stroke and coronary heart disease (CHD) share common risk factors. The risk for stroke patients to have a myocardial infarction (MI) has not been fully explored. METHODS: Three hundred and seventy-seven first-ever stroke patients were ascertained prospectively. The 10-year incidence of MI was examined by register searches. The results were compared to the general Swedish population. Predictors for MI were identified using univariate and multivariate analysis. RESULTS: The cumulative incidence of MI over 10 years was 25.0/100 (95% confidence interval (CI), 19.5-31.5), 26.5 for men, (95% CI, 18.9-45.8) and 23.4 for women (95% CI, 16.0-32.9). Compared to the general population, the relative risk for stroke patients having a MI was 1.6 for men (95% CI, 1.12-2.37) and 1.9 for women (95% CI, 1.27-2.90). In multivariate analysis, CHD before the stroke (MI, angina pectoris, coronary artery bypass grafting, or percutaneous transluminal coronary angioplasty) and peripheral artery disease were significant predictors for MI. CONCLUSION: The risk for MI is significantly higher, for both male and female stroke patients, compared to the general population. Stroke patients with previous CHD and peripheral artery disease are at highest risk. Stroke patients should receive adequate secondary prevention, and cardiac complaints must be taken seriously.

Comparison of 90-day case-fatality after ischemic stroke between two different stroke outcome registries using propensity score matching analysis.

BACKGROUND: It has not been clarified whether the disparity in ischemic stroke outcome between populations is caused by ethnic and geographic differences or by variations in case mix. Propensity score matching (PSM) analysis can overcome some analytical problems but is rarely used in stroke outcome research. This study was to compare the ischemic stroke case-fatality between two PSM cohorts of Sweden and Korea. METHODS: Prognostic variables related to baseline characteristics and stroke care were included in our PSM model. Then, we selected 7675 Swedish and 1220 Korean patients with ischemic stroke from each stroke registers and performed one-to-one matching based on propensity scores of each patient. RESULTS: After PSM, all measured variables were well balanced in 1163 matched subjects, and the 90-day case-fatality was identical 6.2% (HR 0.997, 95%CI 0.905-1.099) in Sweden and Korea. CONCLUSIONS: No difference is found in the 90-day case-fatality in propensity score-matched Swedish and Korean patients with ischemic stroke.

The molecular basis of thrombolysis and its clinical application in stroke.

The rationale for thrombolysis, the most promising pharmacological approach in acute ischaemic stroke, is centred on the principal cause of most ischaemic strokes: the thrombus that occludes the cerebral artery, and renders part of the brain ischaemic. The occluding thrombus is bound together within fibrin. Fibrinolysis acts by activation of plasminogen to plasmin; plasmin splits fibrinogen and fibrin and lyses the clot, which then allows reperfusion of the ischaemic brain. Thrombolytic agents include streptokinase (SK) and recombinant tissue-type plasminogen activator (rt-PA) amongst others under test or development. SK is nonfibrin-specific, has a longer half-life than tissue-type plasminogen activator (t-PA), prevents re-occlusion and is degraded enzymatically in the circulation. rt-PA is more fibrin-specific and clot-dissolving, and is metabolized during the first passage in the liver. In animal models of ischaemic stroke, the effects of rt-PA are remarkably consistent with the effects seen in human clinical trials. For clinical application, some outcome data from the Cochrane Database of Systematic Reviews which includes all randomized evidence available on thrombolysis in man were used. Trials included tested urokinase, SK, rt-PA, pro-urokinase, or desmoteplase. The chief immediate hazard of thrombolytic therapy is fatal intracranial bleeding. However, despite the risk, the human trial data suggest the immediate hazards and the apparent substantial scope for net benefit of thrombolytic therapy given up to 6 h of acute ischaemic stroke. So far the fibrin-specific rt-PA is the only agent to be approved for use in stroke. This may be due to its short half-life and its absence of any specific amount of circulating fibrinogen degradation products, thereby leaving platelet function intact. The short half-life does not leave rt-PA without danger for haemorrhage after the infusion. Due to its fibrin-specificity, it can persist within a fibrin-rich clot for one or more days. The molecular mechanisms with regards to fibrin-specificity in thrombolytic agents should, if further studied, be addressed in within-trial comparisons. rt-PA has antigenic properties and although their long-term clinical relevance is unclear there should be surveillance for allergic reactions in relation to treatment. Although rt-PA is approved for use in selected patients, there is scope for benefit in a much wider variety of patients. A number of trials are underway to assess which additional patients - beyond the age and time limits of the current approval - might benefit, and how best to identify them.

A review on sex differences in stroke treatment and outcome.

BACKGROUND: Beyond epidemiological differences, it has been controversial whether any important sex differences exist in the treatment of stroke. In this review paper, the following areas are covered: thrombolysis, stroke unit care, secondary prevention, surgical treatment, and rehabilitation. Additionally, symptoms at stroke onset, as well as outcome measures, such as death, dependency, stroke recurrence, quality of life, and depression are reviewed. METHODS: Search in PubMed, tables-of-contents, review articles, and reference lists after studies that include information about sex differences in stroke care. RESULTS: Ninety papers are included in this review. Women suffer more from cortical and non-traditional symptoms. Men and women benefit equally from thrombolysis and stroke unit care. Women with cardioembolic strokes may benefit more from anticoagulant therapy. Most studies have not found any tendency towards sexism in the choice of treatment. Post-stroke depression and low quality-of-life seem to be more common among women. Mortality rates are higher among men in some studies, while long-term ADL-dependency seems to be more common among women. CONCLUSIONS: Sex differences in stroke treatment and outcome are small, with no unequivocal proof of sex discrimination. Women have less favourable functional outcome because of higher age at stroke onset and more severe strokes.

Stroke unit care revisited: who benefits the most? A cohort study of 105,043 patients in Riks-Stroke, the Swedish Stroke Register.

BACKGROUND: Treatment at stroke units is superior to treatment at other types of wards. The objective of the present study is to determine the effect size of stroke unit care in subgroups of patients with stroke. This information might be useful in a formal priority setting. METHODS: All acute strokes reported to the Swedish Stroke Register from 2001 through 2005 were followed until January 2007. The subgroups were age (18-64, 65-74, 75-84, 85+ years and above), sex (male, female), stroke subtype (intracerebral haemorrhage, cerebral infarction and unspecified stroke) and level of consciousness (conscious, reduced, unconscious). Cox proportional hazards and logistic regression analyses were used to estimate the risk for death, institutional living or dependency. RESULTS: 105,043 patients were registered at 86 hospitals. 79,689 patients (76%) were treated in stroke units and 25,354 patients (24%) in other types of wards. Stroke unit care was associated with better long-term survival in all subgroups. The best relative effect was seen among the following subgroups: age 18-64 years (hazard ratio (HR) for death 0.53; 0.49 to 0.58), intracerebral haemorrhage (HR 0.61; 0.58 to 0.65) and unconsciousness (HR 0.70; 0.66 to 0.75). Stroke unit care was also associated with reduced risk for death or institutional living after 3 months. CONCLUSIONS: Stroke unit care was associated with better long-term survival in all subgroups, but younger patients, patients with intracerebral haemorrhage and patients who were unconscious had the best relative effect and may be given the highest priority to this form of care.

Radiation to supraclavicular and internal mammary lymph nodes in breast cancer increases the risk of stroke.

The aim of this study was to assess whether adjuvant treatment of breast cancer (BC) affects the risk of stroke, and to explore radiation targets and fraction doses regarding risk and location of stroke. In a Swedish BC cohort diagnosed during 1970-2003, we carried out a nested case-control study of stroke after BC, with relevant details extracted from medical records. The odds ratio (OR) for radiotherapy (RT) vs that of no RT did not differ between cases and controls (OR=0.85; confidence interval, CI=0.6-1.3). Radiotherapy to internal mammary chain (IMC) and supraclavicular (SCL) lymph nodes vs that of no RT was associated with a higher, although not statistically significant, risk of stroke (OR=1.3; CI=0.8-2.2). In a pooled analysis, RT to IMC and SCL vs the pooled group of no RT and RT to breast/chest wall/axilla (but not IMC and SCL), showed a significant increase of stroke (OR=1.8; CI=1.1-2.8). There were no associations between cancer laterality, targets of RT, and location of stroke. The radiation targets, IMC and SCL, showed a statistically significant trend for an increased risk of stroke with daily fraction dose. Our finding of a target-specific increased risk of stroke and a dose-response relationship for daily fraction dose, indicate that there may be a causal link between RT to the IMC and SCL and risk of stroke.

Risk factors for stroke-related pain 1 year after first-ever stroke.

OBJECTIVE: To estimate the prevalence of stroke-related pain and to explore its relation to spasticity. DESIGN: Cross-sectional survey. PATIENTS AND METHODS: One hundred and forty patients were examined at 1 year after first-ever stroke. Pain was assessed by a structured interview and categorized as stroke-related or not, pain intensity by use of the visual analogue scale (VAS), spasticity by use of the modified Ashworth scale, stroke severity and the presence of specific neurological impairments by use of the National Institute of Health Stroke Scale (NIHSS), and depression by use of the Montgomery-Asberg Depression Scale. RESULTS: Pain was reported by 68 patients (49%) with a mean VAS of 42 (95% CI 36-47). In 29 patients (21%), pain was categorized as stroke-related pain. Univariate analyses demonstrated correlations between stroke-related pain and total NIHSS score, paresis, sensory disturbance, depression and spasticity respectively. A multiple regression analysis demonstrated an independent association of stroke-related pain with paresis (OR = 3.1, 95% CI 1.2-7.7), sensory disturbance (OR = 3.1, 95% CI 1.1-8.9) and depression (OR = 4.1, 95% CI 1.4-13). CONCLUSIONS: The estimated prevalence of stroke-related pain was 21%. Stroke-related pain was associated with sensorimotor impairments and depression, but not with spasticity as an independent variable.

MEK-inhibitor U0126 in hyperglycaemic focal ischaemic brain injury in the rat.

BACKGROUND: Hyperglycaemia aggravates ischaemic brain injury, possibly due to activation of signalling pathways involving mitogen-activated protein kinases (MAPK). In this study, the activation of MAPK/ERK was inhibited using the upstream inhibitor of MAPK-ERK-kinase (MEK) U0126, and the effects on focal brain ischaemia were evaluated during normo- and hyperglycaemia. MATERIALS AND METHODS: Temporary (90 min) middle cerebral artery occlusion (MCAO) was induced in five groups of rats. U0126 (400 microg kg(-1)) or vehicle was given as 60-min intravenous infusions starting either 30 min prior to MCAO or 30 min prior to reperfusion. The infarct size was determined by perfusion with tetrazolium red after 24 h of survival, and the neurology was tested with the 4-level scale of Bederson and performance on an inclined plane. The inhibitory effect on the targeted MEK enzyme was investigated by analysing the phosphorylation of the downstream target ERK with western immunoblotting. Two subgroups were investigated with magnetic resonance imaging (MRI), including diffusion-weighted (DWI) and perfusion-weighted imaging (PWI). RESULTS: U0126 effectively reduced the infarct size and improved neurology in hyperglycaemic rats both when given before and after ischemic onset. This effect was not accompanied by any detectable changes in cerebral blood flow on MRI. Normoglycaemic rats had generally milder injuries compared with the hyperglycaemic and there was a nonsignificant trend for U0126 to reduce damage also in the nonhyperglycaemic groups. CONCLUSIONS: In conclusion, U0126 appears to be neuroprotective in this model of hyperglycaemic ischaemic brain injury. The findings support the pathogenic importance of the MEK-ERK pathway in hyperglycaemic-ischaemic brain injury.

Prevalence of disabling spasticity 1 year after first-ever stroke.

OBJECTIVE: To estimate the prevalence of disabling spasticity (DS) 1 year after first-ever stroke. DESIGN: Cross-sectional survey 1 year after first-ever stroke. METHODS: Patients above 18 years from one county with first-ever stroke were identified by use of the national stroke registry. A representative sample of 163 patients was created and 140 of these were followed up. Assessments of motor function and ability with the modified Ashworth Scale, the modified Rankin Scale (mRS), the Barthel Index (BI) and clinical evaluation were performed in order to identify patients with spasticity-related disability. RESULTS: The observed prevalence of any spasticity was 17% and of DS 4%. Patients with DS scored significantly worse than those with no DS on the mRS (P = 0.009) and the BI (P = 0.005). DS was more frequent in the upper extremity, correlated positively with other indices of motor impairment and inversely with age. There was an independent effect of severe upper extremity paresis (OR 22, CI 3.9-125) and age below 65 years (OR 9.5, CI 1.5-60). CONCLUSIONS: The prevalence of DS after first-ever stroke is low but corresponds to a large number of patients and deserves further attention with regards to prevention and treatment.

A national stroke quality register: 12 years experience from a participating hospital.

Registration of all hospitalized stroke patients is practiced in Sweden in order to assess care quality. Data in this register, Riks-Stroke (RS), may be biased due to incomplete registration. The purpose of this paper was to report changes in stroke outcome in relation to fluctuations in registration. Patients registered in RS at a hospital during the period 1994-2005 were analyzed. Case fatality at 28 days, living conditions, and activities of daily living (ADL) performance at 3 months were correlated to the number of patients registered and follow-up frequency. A total of 4994 stroke cases were registered during the period. A high annual registration rate was significantly correlated to a high case fatality ratio. A low annual follow-up rate was associated with a low proportion of patients living in their own home without any need of help. Quality parameters are sensible for selection bias, which make them difficult to compare over time and between hospitals. We suggest that by weighing outcome data against stroke severity, safer conclusions may be drawn. Additionally, hospitals considering setting up quality registers should make every effort to attain complete case ascertainment at all times, including patients managed outside the hospital, in order to avoid selection bias.

Endothelium-dependent vasodilatation in forearm is impaired in stroke patients.

OBJECTIVES: To investigate endothelium-dependent vasodilatation (EDV) in stroke patients. DESIGN: Cross-sectional. SETTING: University referral hospital. SUBJECTS: We studied 23 stroke patients (65-75 years old) who did not have atrial fibrillation or Warfarin treatment. Forty-six age- and sex-matched healthy controls and another 32 controls matched also for hypertension and medication were used for comparisons. METHODS. Endothelium-dependent vasodilatation was measured with venous occlusive plethysmography of forearm blood flow during intra-brachial infusion of acetylcholine. Endothelium-independent vasodilatation (EIDV) was evaluated by infusion of sodium nitroprusside. RESULTS: Stroke patients showed significantly lower EDV (P < 0.001) compared with healthy controls when measured with acetylcholine-stimulated forearm blood flow. The difference between these groups remained significant also after correction for blood pressure, body mass index, blood glucose and cholesterol. There was also significant difference in EDV between hypertension-matched controls and healthy controls. However, EIDV was significantly reduced in stroke patients (P < 0.01), but not in the hypertensive group, when compared with healthy controls. CONCLUSION: An impaired EDV was seen in both stroke patients and hypertensive-matched controls, while an impaired EIDV was seen in the stroke patients only, suggesting a more severe vasodilatory dysfunction in stroke patients than could be explained by a high blood pressure only.

Blood glucose in acute stroke, different therapeutic targets for diabetic and non-diabetic patients?

OBJECTIVES: To study the impact of blood glucose concentrations on early stroke mortality in diabetic and non-diabetic stroke patients, and to identify the optimal blood glucose concentration for each patient category. MATERIAL AND METHODS: A representative sample of 81 diabetic and 366 non-diabetic stroke patients was studied. Logistic regression analyses were performed in order to estimate the impact of blood glucose concentrations on admission and during hospital stay and other clinical parameters on 30-day case-fatality. Receiver operating characteristic curves were used to predict case-fatality by blood glucose. RESULTS: Blood glucose, body temperature and level of consciousness were independently related to early stroke mortality in diabetic and non-diabetic patients. The mean blood glucose concentration had a greater impact on 30-day case-fatality than the admission blood glucose, particularly in diabetic patients. A mean blood glucose concentration above 10.3 mmol/l predicted 30-day case-fatality in diabetic patients. The corresponding value was 6.3 mmol/l in non-diabetic patients. CONCLUSION: Improved blood glucose control has a potential to reduce early stroke mortality. The optimal glucose concentration seems to be higher in diabetic than in non-diabetic patients.

Differential early mitogen-activated protein kinase activation in hyperglycemic ischemic brain injury in the rat.

BACKGROUND: Hyperglycemia aggravates brain injury induced by focal ischemia-reperfusion. The mitogen-activated protein kinase (MAPK) members extracellular-signal regulated kinase (Erk) and c-Jun N-terminal kinase (JNK) have been proposed as mediators of ischemic brain injury, and Erk is strongly activated by combined hyperglycemia and transient global ischemia. It is unclear whether similar MAPK activation appears in focal brain ischemia with concomitant hyperglycemia. DESIGN: Hyperglycemia was induced in rats by an intraperitoneal bolus of glucose (2 g kg(-1)). The rats were then subjected to 90 min of transient middle cerebral artery occlusion (MCAO). Erk and JNK activation were investigated with immunofluorescence and Western blot along with infarct size measurement based on tetrazolium staining and neurological score. RESULTS: The hyperglycemic rats showed increased tissue damage and impaired neurological performance after 1 day compared with controls. The hyperglycemia was generally moderate (< 15 mM). Erk activation was increased after 30 min of reperfusion in the ischemic cortex of the hyperglycemic rats, while JNK activation was present on the contralateral side. Phospho-Erk immunofluorescence revealed marked neuronal activation of Erk in the ischemic cortex of hyperglycemic rats compared with controls. CONCLUSION: Besides confirming the detrimental effects of hyperglycemia on focal ischemia-reperfusion, this study shows that hyperglycemia strongly activates the pathogenic mediator Erk in the ischemic brain in the early phase of reperfusion. JNK activation at this stage is present in the nonischemic hemisphere. The functional relevance of these findings needs further investigation.

Vascular endothelial growth factor gene expression in middle cerebral artery occlusion in the rat.

BACKGROUND: Focal cerebral ischemia induces up-regulation of angiogenic growth factors such as vascular endothelial growth factor (VEGF), which may have both beneficial and harmful effects to the ischemic brain. Vascular endothelial growth factor is up-regulated in models of brain ischemia, but the underlying mechanisms in vivo remain unclear. In the present report we have investigated the concomitant changes in VEGF and glyceraldehyde dehydrogenase (GAPDH) mRNA expression in a model of permanent and transient cerebral ischemia. METHODS: Male Sprague-Dawley rats were exposed to permanent or transient (2 h) middle cerebral artery occlusion (PMCAO, TMCAO). Brain samples were collected at survival times ranging from 6 h to 1 week, and the levels of VEGF164 and GAPDH mRNA were determined using reverse-transcriptase real-time polymerase chain reaction (RT-PCR). RESULTS: The VEGF mRNA levels decreased gradually over the observation period in a similar manner in both PMCAO and TMCAO. Maximum levels, seen at early observation time points, did not significantly deviate from sham controls. No statistically significant changes in GAPDH mRNA levels were observed, but there was a tendency towards a postischemic decrease with subsequent return to control levels over time. The VEGF/GAPDH ratio followed a pattern of decrease similar to VEGF mRNA alone. CONCLUSION: The VEGF mRNA levels at 6 h after MCAO remain near baseline and thereafter decline, regardless of whether the occlusion is permanent or transient (2 h). The findings raise the question of other than transcriptional regulation of VEGF in cerebral ischemia.

Src family kinase-inhibitor PP2 reduces focal ischemic brain injury.

OBJECTIVES: To investigate the neuroprotective potential of the Src family kinase (SFK) inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo(3,4-d)pyrimidine (PP2) in transient focal cerebral ischemia in the rat. MATERIAL AND METHODS: Sprague-Dawley rats were exposed to transient (90 min) middle cerebral artery occlusion (MCAO) and evaluated after 1 day of survival. PP2 (1.5 mg/kg i.p.) or vehicle was given 30 min after MCAO. The lesions were examined with magnetic resonance imaging (MRI), tri-phenyl tetrazolium chloride (TTC) staining and the functional outcome was determined using neurological scoring according to Bederson et al. RESULTS: PP2-treated rats showed approximately 50% reduction of infarct size on T2-weighted MRI and in TTC staining compared with controls (P < 0.05). Moreover, the neurological score was better in the PP2 group than controls (P < 0.05). CONCLUSION: PP2 is a potential neuroprotective agent in cerebral ischemia-reperfusion. The interference of PP2 with SFKs and/or other pathways remains to be elucidated.

Detection and appearance of intraparenchymal haematomas of the brain at 1.5 T with spin-echo, FLAIR and GE sequences: poor relationship to the age of the haematoma.

The specific appearance of blood related to time at T1- and T2-weighted spin-echo (SE) sequences is generally accepted; thus, these sequences are classically used for estimating the age of haematomas. Magnetic resonance imaging at 1.5 T, including T1- and T2-weighted SE fluid-attenuated inversion recovery (FLAIR) and T2*-weighted gradient-echo (GE) sequences, was performed on 82 intraparenchymal haematomas (IPHs) and 15 haemorrhagic infarcts (HIs) in order to analyse the appearance at different stages and with different sequences, and to investigate how reliably the age of hematomas can be estimated. The IPHs had been previously detected by CT, were spontaneous ( n=72) or traumatic ( n=10) in origin and were of different sizes (2 mm to 7 cm) and ages (from 7.5 h to 4 years after acute haemorrhagic event). The age of the lesion was calculated from the moment when clinical symptoms started or the traumatic event occurred. The 15 patients with HIs were patients with ischaemic stroke in whom there was either a suspicion of haemorrhagic transformation on CT, or haemorrhage was detected as an additional finding on MR performed for other indications. Patients with conditions that could affect the SI of blood, such as anticoagulant therapy or severe anaemia, were excluded. The signal intensity pattern of the lesions was analysed and related to their ages without prior knowledge of the clinical data. All lesions were detected with T2*-weighted GE. T1-weighted SE missed 13 haematomas and T2-weighted SE and FLAIR sequences missed five. Haemorrhagic transformation was missed in three infarcts by T1-, T2-weighted SE and FLAIR. The signal pattern on FLAIR was identical to that on T2-weighted SE. For all sequences, a wide variety of signal patterns, without a clear relationship to the age of the haematomas, was observed. There was a poor relationship between the real MR appearance of IPHs and the theoretical appearance on SE sequences. T2*-weighted GE was effective for detecting small bleedings but was not useful for estimating the age of a lesion. The FLAIR does not provide any more information than T2-weighted SE.

Rapid Emergency Medicine score: a new prognostic tool for in-hospital mortality in nonsurgical emergency department patients.

OBJECTIVES: To evaluate the predictive accuracy of the scoring system Rapid Acute Physiology score (RAPS) in nonsurgical patients attending the emergency department (ED) regarding in-hospital mortality and length of stay in hospital (LOS), and to investigate whether the predictive ability of RAPS could be improved by extending the system. DESIGN: Prospective cohort study. SETTING: An adult ED of a 1200-bed university hospital. SUBJECTS: A total of 12 006 nonsurgical patients presenting to the ED during 12 consecutive months. METHODS: For all entries to the ED, RAPS (including blood pressure, respiratory rate, pulse rate and Glasgow coma scale) was calculated. The RAPS system was extended by including the peripheral oxygen saturation and patient age (Rapid Emergency Medicine score, REMS) and this new score was calculated for each patient. The statistical associations between the two scoring systems and in-hospital mortality as well as LOS in hospital were examined. RESULTS: The REMS was superior to RAPS in predicting in-hospital mortality [area under receiver operating characteristic (ROC) curve 0.852 +/- 0.014 SEM for REMS compared with 0.652 +/- 0.019 for RAPS, P < 0.05]. An increase of 1-point in the 26-point REMS scale was associated with an OR of 1.40 for in-hospital death (95% CI: 1.36-1.45, P < 0.0001). Similar results were obtained in the major patient groups (chest pain, stroke, coma, dyspnoea and diabetes), in all age groups and in both sexes. The association between REMS and LOS was modest (r = 0.47, P = 0.0001). CONCLUSIONS: The REMS was a powerful predictor of in-hospital mortality in patients attending the ED over a wide range of common nonsurgical disorders.