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Objective: Community stroke education is a regulated, integral component of stroke systems of care. However, little is known about the types of activities conducted by hospitals. This study was designed to examine the annual requirement for community stroke education among New York State’s 119 designated Primary Stroke Centres and identify areas for improvement that may have an implication on stroke outcomes. Design: Cross-sectional survey design Setting: All 119 New York State designated Primary Stroke Centres were invited to participate. Methods: Participating hospitals completed a 29-item online questionnaire assessing multiple domains related to community stroke education including hospital characteristics, allocated resources, implementation barriers, current community stroke education practices and willingness to adopt best practice guidelines. Data were analysed using univariate descriptive and chi-square statistics. Results: Eighty-eight percent of hospitals completed the survey (105/119). Respondents were mostly stroke coordinators and stroke directors. Stroke outreach education was conducted two to four times per year in 58% of the hospitals ( n = 69). Community stroke education included behavioural risk factor modification, the detection of stroke risk through screening and stroke preparedness education at health fairs. Although 95% of hospitals ( n = 98) reported using at least one best practice approach for these activities, evaluation was generally poor, with only about 23% ( n = 24) implementing outcome-specific assessments. Major barriers to stroke outreach were inadequate staffing, time constraints and lack of funding. Conclusion: Hospital-driven community stroke education efforts occur infrequently and are poorly evaluated. This component of stroke systems of care would benefit from guidelines from regulatory agencies, which currently do not exist.

Background. Motor recovery after stroke is predicted only moderately by clinical variables, implying that there is still a substantial amount of unexplained, biologically meaningful variability in recovery. Regression diagnostics can indicate whether this is associated simply with Gaussian error or instead with multiple subpopulations that vary in their relationships to the clinical variables. Objective. To perform regression diagnostics on a linear model for recovery versus clinical predictors. Methods. Forty-one patients with ischemic stroke were studied. Impairment was assessed using the upper extremity Fugl-Meyer Motor Score. Motor recovery was defined as the change in the upper extremity Fugl-Meyer Motor Score from 24 to 72 hours after stroke to 3 or 6 months later. The clinical predictors in the model were age, gender, infarct location (subcortical vs cortical), diffusion weighted imaging infarct volume, time to reassessment, and acute upper extremity Fugl-Meyer Motor Score. Regression diagnostics included a Kolmogorov-Smirnov test for Gaussian errors and a test for outliers using Studentized deleted residuals. Results. In the random sample, clinical variables explained only 47% of the variance in recovery. Among the patients with the most severe initial impairment, there was a set of regression outliers who recovered very poorly. With the outliers removed, explained variance in recovery increased to 89%, and recovery was well approximated by a proportional relationship with initial impairment (recovery ≅ 0.70 × initial impairment). Conclusions. Clinical variables only moderately predict motor recovery. Regression diagnostics demonstrated the existence of a subpopulation of outliers with severe initial impairment who show little recovery. When these outliers were removed, clinical variables were good predictors of recovery among the remaining patients, showing a tight proportional relationship to initial impairment.

Increased intracranial pressure (ICP) is a pathologic state common to a variety of serious neurologic conditions, all of which are characterized by the addition of volume to the intracranial vault. Hence all ICP therapies are directed toward reducing intracranial volume. Elevated ICP can lead to brain damage or death by two principle mechanisms: (1) global hypoxic-ischemic injury, which results from reduction of cerebral perfusion pressure (CPP) and cerebral blood flow, and (2) mechanical compression, displacement, and herniation of brain tissue, which results from mass effect associated with compartmentalized ICP gradients. In unmonitored patients with acute neurologic deterioration, head elevation (30 degrees), hyperventilation (pCO226-30 mmHg), and mannitol (1.0-1.5 g/kg) can lower ICP within minutes. Fluid-coupled ventricular catheters and intraparenchymal pressure transducers are the most accurate and reliable devices for measuring ICP in the intensive care unit (ICU) setting. In a monitored patient, treatment of critical ICP elevation (>20 mmHg) should proceed in the following steps: (1) consideration of repeat computed tomography (CT) scanning or consideration of definitive neurosurgical intervention, (2) intravenous sedation to attain a quiet, motionless state, (3) optimization of CPP to levels between 70 and 110 mmHg, (4) osmotherapy with mannitol or hypertonic saline, (5) hyperventilation (pCO226-30 mmHg), (6) high-dose pentobarbital therapy, and (7) systemic cooling to attain moderate hypothermia (32-33°C). Placement of an ICP monitor and use of a stepwise treatment algorithm are both essential for managing ICP effectively in the ICU setting.