Stroke; a journal of cerebral circulation
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Early admission to hospital followed by correct diagnosis with minimum delay is a prerequisite for successful intervention in acute stroke. This study aimed at clarifying in detail the factors related to these delays. ⋯ Increased public awareness of the need to seek medical or other attention promptly after stroke onset, to use an ambulance with direct transportation to the acute-care hospital, and to have more effective in-hospital organization will be required for effective acute treatment options to be available to stroke patients.
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Comparative Study
Identification of incident stroke in Norway: hospital discharge data compared with a population-based stroke register.
The validity of hospital discharge diagnoses is essential in improving stroke surveillance and estimating healthcare costs of stroke. The aim of this study was to assess sensitivity, positive predictive value, and accuracy of discharge diagnoses compared with a stroke register. ⋯ Hospital discharge data may overestimate stroke incidence and underestimate the length of stay in the hospital, unless selection routines of hospital discharge diagnoses are restricted to acute stroke diagnoses (ICD-9 codes 430, 431, 434, and 436). If supplemented by a validation procedure, including estimates of sensitivity, positive predictive value, and accuracy, hospital discharge data may provide valid information on hospital-based stroke incidence and lead to better allocation of health resources. Distinguishing subtypes of stroke from hospital discharge diagnoses should not be performed unless coding practices are improved.
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BACKGROUND AND PURPOSE--Endothelin-1, in concentrations similar to that present in cerebrospinal fluid after fluid percussion brain injury (FPI), increases superoxide anion (O2-) production. Endothelin-1 also contributes to altered cerebral hemodynamics after FPI through impairment of ATP-sensitive K+ (KATP) channel function through protein kinase C (PKC) activation. Generation of O2- additionally occurs after FPI. ⋯ CONCLUSIONS--These data show that PKC activation increases O2- production and contributes to such production observed after FPI. These data also show that an activated system that generates an amount of O2- similar to that observed with FPI blunted pial artery dilation to KATP channel agonists and nitric oxide/cGMP. These data suggest, therefore, that O2- generation links PKC activation to impaired KATP channel function after FPI.