Introduction We quantified clinical and imaging characteristics associated with childhood arteriopathy subtypes to facilitate their diagnosis and classification in research and clinical settings. Methods The “Vascular effects of Infection in Pediatric Stroke” (VIPS) study prospectively enrolled 355 children with arterial ischemic stroke (AIS) (2010–2014). A central team of experts reviewed all data to diagnose childhood arteriopathy and classify subtypes, including arterial dissection, focal cerebral arteriopathy-inflammatory type (FCA-i, which includes transient cerebral arteriopathy, TCA), moyamoya, and diffuse/multifocal vasculitis. Only children whose stroke etiology could be conclusively diagnosed were included in these analyses. We constructed logistic regression models to identify characteristics associated with each arteriopathy subtype. Results Among 127 children with definite arteriopathy, the arteriopathy subtype could not be classified in 18 (14%). Moyamoya (n=34) occurred mostly in children <8 years old, FCA-i (n=25) in 8–15 year olds, and dissection (n=26) at all ages. Vertigo at stroke presentation was common in dissection. Dissection affected cervical arteries, while moyamoya involved supraclinoid internal carotid arteries. A banded appearance of the M1 segment of the middle cerebral artery was pathognomonic of FCA-i, but present in <25% of FCA-i cases; a small lenticulostriate distribution infarct was a more common predictor of FCA-i, present in 76%. It remained difficult to distinguish FCA-i from intracranial dissection of the anterior circulation (FCA-d). We observed only secondary forms of diffuse/multifocal vasculitis, mostly due to meningitis. Conclusions Childhood arteriopathy subtypes have some typical features that aid diagnosis. Better imaging methods, including vessel wall imaging, are needed for improved classification of FCA.
Background and Purpose Although perfusion abnormality is an increasingly important therapeutic target, the natural history of tissue at risk without reperfusion treatment is understudied. Our objective was to determine how time affects penumbral salvage and infarct growth in untreated acute ischemic stroke patients and whether collateral status affects this relationship. Methods We utilized a prospectively-collected, multicenter acute stroke registry to assess acute stroke patients who were not treated with intravenous thrombolysis or endovascular treatment. We analyzed baseline CT angiogram and CT perfusion within 24 hours of stroke onset along with follow-up imaging, and assessed time from stroke onset to baseline imaging, ASPECTS, vessel occlusion, collaterals, ischemic core and penumbra. Penumbral salvage and infarct growth was calculated. Correlations between time and penumbral salvage and infarct growth were evaluated with Spearman correlation. Penumbral salvage and infarct growth were compared between subjects with good versus poor collateral status using the Wilcoxon rank sum test. Clinical and imaging factors affecting penumbral salvage and infarct growth were evaluated by linear regression. Results Among 94 untreated stroke patients eligible for this analysis, the mean age was 65, median NIHSS was 13, and median (range) time from stroke onset to baseline imaging was 2.9 (0.4–23) hours. There was no correlation between time and salvaged penumbra (r= 0.06; p=0.56) or infarct growth (r=−0.05; p=0.61). Infarct growth was higher among those with poor collaterals versus good collaterals (median 52.3 vs 0.9 cc; p<0.01). Penumbral salvage was lower among those with poor collaterals compared to those with good collaterals (poor 0 [0, 0]; good 5.9 cc [0, 29.4]; p<0.01). Multivariable linear regression demonstrated that collaterals, but not time, were significantly associated with infarct growth and penumbral salvage. Conclusion In this natural history study, penumbral salvage and infarct growth was less time dependent and more a measure of collateral flow.
Neurogenesis and angiogenesis in the subventricular zone and peri-infarct region have been confirmed. However, newly formed neuronal cells and blood vessels that appear in the nonischemic ipsilateral ventroposterior nucleus (VPN) of the thalamus with secondary damage after stroke has not been previously studied. Twenty-four stroke-prone renovascular hypertensive rats were subjected to distal right middle cerebral artery occlusion (MCAO) or sham operation. 5'-Bromo-2'-deoxyuridine (BrdU) was used to label cell proliferation. Rats were killed at 7 or 14 days after the operation. Neuronal nuclei (NeuN), OX-42, BrdU, nestin, laminin(+), BrdU(+)/nestin(+), BrdU(+)/NeuN(+), nestin(+)/GFAP(+)(glial fibrillary acidic protein), and BrdU(+)/laminin(+) immunoreactive cells were detected within the ipsilateral VPN. The primary infarction was confined to the right somatosensory cortex. Within the ipsilateral VPN of the ischemic rats, the number of NeuN(+) neurons decreased, the OX-42(+) microglia cells were activated, and BrdU(+) and nestin(+) cells were detected at day 7 after MCAO and increased in number at day 14. Moreover, BrdU(+)/nestin(+) cells and BrdU(+)/NeuN(+) cells were detected at day 14 after MCAO. In addition, the ischemic rats showed a significant increase in vascular density in the ipsilateral VPN compared with the sham-operated rats. These results suggest that secondary damage with neurogenesis and angiogenesis of the ipsilateral VPN of the thalamus occurs after focal cortical infarction.
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