Evaluating Hematoma Expansion Scores in Acute Spontaneous Intracerebral Hemorrhage: A Systematic Scoping Review.

Background and Purpose- In acute spontaneous intracerebral hemorrhage, multiple hematoma expansion scores have been proposed for use in clinical trial environments. We performed a systematic scoping review to identify all existing hematoma expansion scores and describe their development, validation, and relative performance. Methods- Two reviewers searched MEDLINE, PUBMED, EMBASE, and CENTRAL (Cochrane Central Register of Controlled Trials) for studies that derived or validated a hematoma expansion prediction score in adults presenting with spontaneous intracerebral hemorrhage. A descriptive analysis of the extracted data was performed, focusing on score development techniques and predictive capabilities. Results- Of the 14 434 records retrieved, 15 studies met inclusion criteria and 10 prediction scores were identified. Validation analysis using independent samples was performed in 9 studies on 5 scores. All derivation studies reported high performance with C statistics ranging from 0.72 to 0.93. In validation, the C-statistic range was broader with studies reporting 0.62 to 0.77. For every score, the risk of expansion increased with each point increase, although patients with high scores were rare. Conclusions- At present, 10 hematoma expansion scores have been developed, of which 5 have been externally validated. Real-world performance in validation studies was lower than performance in derivation studies. Data from the current literature are insufficient to support a meaningful meta-analysis.

Magnetic Resonance Imaging Assists With Determining Etiology After Transient Ischemic Attack or Minor Stroke.

BACKGROUND: Magnetic resonance imaging infarct topography may assist with determining stroke etiology. The influence of diffusion-weighted imaging (DWI)-positive lesions on etiology determination in patients with transient ischemic attack or minor stroke is not well studied. METHODS AND RESULTS: We prospectively enrolled patients between 2010 and 2017 in 2 studies; participants with a final diagnosis of probable or definite transient ischemic attack or stroke were pooled for analysis. The primary outcome was the adjudicated ischemic etiology. We compared proportion of each etiology (cardioembolic, large-vessel, small-vessel disease, other) in patients who had DWI positivity compared with DWI negativity. We used logistic regression to determine the adjusted odds ratio (OR) for each etiology compared with undetermined by DWI positivity. The final analysis included 1498 patients: 832 (55.5%) were DWI-positive. DWI-positive patients were more likely to be diagnosed with small-vessel disease (19.1% versus 5.3%) and less likely with undetermined etiology (36.9% versus 53.0%; P<0.001). After adjustment, the presence of any DWI lesion was associated with increased odds of assigning any etiology (OR, 1.8 [95% CI, 1.3-2.5]). A single DWI lesion was associated with increased odds of small-vessel disease diagnosis (OR, 9.5 [95% CI, 6.4-14.0]), and multiple DWI lesions with reduced odds of small-vessel disease (OR, 0.2 [95% CI, 0.1-0.4]) but increased odds of all other etiologies compared with undetermined etiology. CONCLUSIONS: Any DWI-positive lesion after suspected transient ischemic attack or minor stroke was associated with increased odds of assigning a etiology. Presence and topography of DWI lesions on magnetic resonance imaging may assist with etiology determination and may impact stroke prevention therapies.

Clinical Utility and Cost of Inpatient Transthoracic Echocardiography Following Acute Ischemic Stroke.

BACKGROUND AND PURPOSE: It is unclear whether it is clinically necessary or cost-effective to routinely obtain a transthoracic echocardiogram (TTE) during inpatient admission for ischemic stroke. METHODS: We assessed consecutive patients presenting with acute ischemic stroke at a comprehensive stroke center from 2015 to 2017 who underwent TTE. We assessed for findings on TTE that would warrant urgent intervention including cardiac thrombus, atrial myxoma, mitral stenosis, valve vegetation, valve dysfunction requiring surgery, and low ejection fraction. Subsequent changes in management included changes in anticoagulation, antibiotics, or valve surgery. We calculated in-hospital resource utilization and associated costs for inpatient TTE using individual direct cost details within a case-costing system. RESULTS: Of 695 patients admitted with acute ischemic stroke, 516 (74%) had a TTE and were included in our analysis. TTE findings were potentially clinically significant in 30 patients (5.8%) and changed management in 17 patients (3.3%). Inpatient admission was prolonged to expedite TTE in 24 patients, while TTE occurred after discharge in 76 patients. After correcting for the cost of TTE, the mean difference in cost to prolong an admission for TTE was $555.52 (USD), or $16 832 per change in management. CONCLUSIONS: Given the low clinical utility of inpatient TTE after acute ischemic stroke and the costs associated with prolonging admission, discharge from hospital should not be delayed solely to obtain TTE.

Electropositive seizures and non-convulsive status epilepticus in a critically ill patient with prior skull defect.

Epileptiform discharges captured on routine scalp EEG typically carry a surface negative dipole. We present a patient whose continuous EEG recording in the intensive care setting captured frequent electropositive non-convulsive seizures. Epileptiform discharges with positive polarity are common in the pediatric population but have rarely been reported in adult patients. When reported in adults, such patients usually have skull defects. As surface positive discharges are scarce, adult electroencephalographers should be prudent to differentiate such discharges from artifact, particularly in an intensive care setting where EEG artifact is common.

Normal Systolic Blood Pressure at Presentation With Acute Ischemic Stroke Predicts Cardioembolic Etiology.

Background Early insight into the possible etiology of ischemic stroke allows for early initiation of mechanism-specific secondary stroke prevention. Initial systolic blood pressure during acute ischemic stroke may relate to stroke etiology. We sought to determine whether normotension at presentation with acute ischemic stroke predicts cardioembolic etiology. Methods and Results All patients presenting with acute ischemic stroke within 12 hours of symptom onset at a comprehensive stroke center from January 2015 to December 2017 were assessed. Normotension was defined as systolic blood pressure ≤130 mm Hg. The primary exposure was blood pressure on arrival at the hospital, and the primary outcome was cardioembolic etiology. Multivariable regression with stepwise selection was used to adjust for relevant covariates. We included 683 patients in our analysis, 303 (44%) of whom were diagnosed with cardioembolic etiology at 6 months. The probability of cardioembolic etiology was inversely associated with systolic blood pressure, and initial systolic blood pressure was significantly associated with cardioembolic etiology (odds ratio: 1.15; 95% CI, 1.05 to 1.26). Normotension was associated with 2.62-fold increased odds of cardioembolic etiology (95% CI, 1.46 to 4.72). Conclusions Normotension at presentation with acute ischemic stroke strongly predicts cardioembolic etiology. These patients may especially benefit from early and prolonged cardiac investigations.

Evaluating the predictive capabilities of haematoma expansion scores in patients with acute intracerebral haemorrhage: protocol for a scoping review.

INTRODUCTION: Patients presenting with acute intracerebral haemorrhage are at a high risk of exhibiting haematoma expansion, a phenomenon that can significantly worsen long-term functioning. Numerous clinical and radiological factors are associated with expansion. In a bid to better select patients at increased risk of expanding, these factors have been collated together into clinical scores. Several clinical scores have been developed, but comparisons of diagnostic potential between these scores are limited and the frequency of use in clinical trial enrolment is unknown. OBJECTIVE: To perform a scoping review of haematoma expansion scores and explore numerous factors such as the methodology of development and diagnostic capabilities. METHODS AND ANALYSIS: MEDLINE, PubMed, EMBASE, CENTRAL and ClinicalTrials.gov will be searched with assistance from an experienced information specialist. Eligible studies will involve adults presenting with spontaneous intracerebral haemorrhage who received baseline assessments, follow-up imaging and risk stratification through a haematoma expansion score. Reviewers will independently extract data from the included studies and will collect data on patient demographics and medical history, details on score development, diagnostic capabilities and usage proportions. Analysis of extracted data will focus on comparing the predictive capability of each score and similarities/differences in score development. The exact analysis technique will be dictated on the type of data extracted. ETHICS AND DISSEMINATION: Formal ethics is not required as primary data will not be collected. The findings of this study will be disseminated through conference presentations and peer-reviewed publications.

Amphetamine stimulates Wnt3 increases in rat nucleus accumbens.

Dopaminergic neurotransmission is thought to be involved in reward-related incentive learning and addictive behaviour. Amphetamine will alter glycogen synthase kinase-3ß (GSK-3ß) activity by increasing dopamine transporter efflux rates. We investigated the hypothesis that Wnt signalling will be altered in rat nucleus accumbens within 15 min of injection of amphetamine compared with saline. We isolated RNA from the nucleus accumbens and used reverse transcriptase-PCR to screen for altered Wnt expression. We found that amphetamine had no effect on Wnt5a or Wnt7a expression but increased Wnt3. We then measured protein expression of Wnt3, phosphorylated lipoprotein-related peptide 6, GSK-3ß phosphorylated at serine-9 and tyrosine-216 and total ß-catenin. We found that amphetamine increased Wnt3 protein expression, increased pLRP6 (threonine-1572) levels, increased ß-catenin levels, increased GSK-3ß phosphorylation at serine-9, consistent with inhibition of GSK-3ß activity, and diminished GSK-3ß phosphorylation at tyrosine-216. Our data support the hypothesis that proximate Wnt signalling is rapidly activated by amphetamine in the adult rat nucleus accumbens.