PP04.15 – 2395: Cortical laminar necrosis after neonatal and childhood arterial ischemic stroke. A relevant finding?

D. Tibussek,G. DeVeber, I. Yau, A.M. Pontigon, J. Paterson,S. Laughlin

European Journal of Paediatric Neurology(2015)

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摘要
Objective Variations in imaging patterns after stroke may help to establish the stroke mechanism. To analyze the frequency and characteristics of cortical laminar necrosis (CLN) on MRI due to arterial ischemic stroke in neonates and children. Methods Retrospective analysis of neonates and children with arterial ischemic stroke admitted to our institution between 2003 and 2014. Inclusion criteria for eligibility for further analysis were acute arterial ischemic stroke (DWI and ADC positive) on MRI and cortical laminar necrosis as defined by hyperintense cortical lesions on T1-weighted MR imaging. Results 23 childhood arterial ischemic stroke cases (CAIS) and 9 neonatal stroke cases with CLN were identified. Of those 56 (CAIS) and 19 (neonatal) MRI scans were available for analysis. Blood sensitive sequences, available in 15 (CAIS) cases and 9 (neonatal), were negative in all. Serial imaging was perfomed in 13 (CAIS) and 6 (neonatal) patients. In 9/10 CAIS compared to 1/6 neonatal patients who had an MRI performed during the first week after stroke CLN was negative. Persistence of CLN after stroke up to >12 months post stroke was observed. All vascular territories were involved. MCA strokes represented the majority of cases and a predominance of the parietooccipital area within the MCA distribution was found. Stroke etiology could be established in 80% of cases: congenital heart defect (n=9), GBS meningitis (n=2), Moyamoya (n=2), CNS vasculitis (n=2), Takayasu, AML, traumatic brain injury. Conclusion CLN is not an uncommon finding after neonatal and CAIS. Our findings suggests that bleeding does not contribute to CLN. Congenital heart defect is the most commonly found stroke etiology. We hypothesize that CLN may be related to areas of hypoperfusion with some pathophysiological overlap with watershed infarcts. Future pathology studies will clarify further the exact nature of the underlying histopathology.
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