Background and Purpose-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. Methods-This was a prospective, multicenter, consecutive study that explored factors influencing the time from stroke or transient ischemic attack (TIA) onset until patient arrival at the emergency department, stroke unit, and CT laboratory. Within 3 days of hospital admission, the patients and/or their relatives were interviewed by use of a standardized structured protocol, and the patients' neurological deficits were assessed. No information about this study was given to the public or to the staff. Results-Patients (nϭ329) were studied at 15 Swedish academic or community-based hospitals: 252 subjects with brain infarct, 18 with intracerebral hemorrhage, and 59 with TIA. Among stroke and TIA patients, the median times from onset to hospital admission, stroke unit, and CT scan laboratory were 4.8 and 4.0 hours, 8.8 and 7.5 hours, and 22.0 and 17.5 hours, respectively. From multivariate ANOVA with logarithmically transformed time for increasing delay to hospital admission as the dependent variable, a profile of significant risk factors was obtained. This included patients with a brain infarct, gradual onset, mild neurological symptoms, patients who were alone and did not contact anybody when symptoms occurred, patients who lived in a large catchment area, those who did not use ambulance transportation, and those who visited a primary care site. These factors explained 45.3% of the variance in delayed hospital admission. The median time from arrival at the emergency department to arrival at the stroke unit or CT scan laboratory (whichever occurred first) was 2.6 and 2.7 hours in the stroke and TIA groups, respectively. A large catchment area, moderate to mild neurological deficit, and waiting for the physician at the emergency department were all significantly related to in-hospital delay. Conclusions-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. (Stroke. 1999;30:40-48.)

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Neurogenesis occurs throughout life in the dentate gyrus of hippocampus and subventricular zone, but this phenomenon has rarely been observed in other brain regions of adult mammals. The aim of the current study was to investigate the cell proliferation process in the ischemically challenged region-at-risk after focal cerebral ischemia in the adult rat brain. A reversible photothrombotic ring stroke model was used, which features sustained hypoperfusion followed by late spontaneous reperfusion and a remarkable morphologic tissue recovery in the anatomically well defined somatosensory cortical region-at-risk. Twelve-week-old male Wistar rats received repeated intraperitoneal injections of the cell proliferation specific marker 5-bromodeoxyuridine (BrdU) after stroke induction. Immunocytochemistry of coronal brain sections revealed that the majority of BrdU-positive cells were of glial, macrophage, and endothelial origin, whereas 3% to 6% of the BrdU-positive cells were double-labeled by BrdU and the neuronspecific marker Map-2 at 7 and 100 days after stroke onset in the region-at-risk. They were distributed randomly in cortical layers II-VI. Three-dimensional confocal analyses of BrdU and the neuronal-specific marker Neu N by double immunofluorescence confirmed their colocalization within the same cells at 72 hours and 30 days after stroke induction. This study suggests that, as a potential pathway for brain repair, new neurons can be generated in the cerebral cortex of adult rats after sublethal focal cerebral ischemia.

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Background and Purpose-This study explored the possible occurrence of newly generated nerve cells in the ischemic cortex of adult rats after middle cerebral artery occlusion and reperfusion. Methods-Nine-to 10-week-old male Wistar rats were subjected to 2 hours of middle cerebral artery occlusion by the monofilament method. Rats received repeated intraperitoneal injections of the cell proliferation-specific marker 5-bromodeoxyuridine (BrdU) after stroke induction. Brain sections were processed for immunohistochemistry with an avidin-biotin complex-alkaline phosphatase and/or -peroxidase method. Brain sections processed with doubleimmunofluorescent staining were further scanned by confocal microscopy. Results-Interspersed among the predominantly newly formed glial cells, some cells were double labeled by BrdU and 1 of the neuron-specific markers, Map-2, ␤-tubulin III, and Neu N, at 30 and 60 days after stroke onset. These cells were randomly distributed throughout cortical layers II through VI, occurring with highest density in the ischemic boundary zone. Three-dimensional confocal analyses of BrdU and the neuron-specific marker Neu N confirmed their colocalization within the same cortical cells. Conclusions-This study suggests that new neurons can be generated in the cerebral cortex of adult rats after transient focal cerebral ischemia. Cortical neurogenesis may be a potential pathway for brain repair after stroke.