Please use this identifier to cite or link to this item: http://dspace.sctimst.ac.in/jspui/handle/123456789/1045
Title: Signal changes in cortical laminar necrosis-evidence from susceptibility-weighted magnetic resonance imaging
Authors: Kesavadas, Chandrasekharan
Santhosh, Kannath
Thomas, Bejoy
Gupta, Arun Kumar
Kapilamoorthy, Tirur Raman
Bodhey, Narendra
Pendharker, Hima
Patro, Satyanarayana
Keywords: Radiology
Issue Date: 2009
Publisher: NEURORADIOLOGY
Citation: NEURORADIOLOGY. 51; 5; 293-298
Abstract: Two types of infarcts can be identified depending on the circumstances leading to its generation-infarcts with pannecrosis and infarcts with selective neuronal loss. Cortical laminar necrosis (CLN) can occur due to various etiologies of which infarctions and hypoxia are the commonest. Infarction results in pannecrosis whereas hypoxia and incomplete infarction result in selective neuronal loss with the presence of viable cells, glial proliferations, and deposition of paramagnetic substances. We investigated patients with CLN with susceptibility-weighted imaging (SWI), a technique highly sensitive to even traces of paramagnetic agents or hemorrhagic components.We retrospectively reviewed medical records of patients diagnosed with CLN as per standard criterion. Demographic characteristics and etiologies were recorded. Findings in magnetic resonance images including SWI were analyzed.We identified 11 patients with CLN, six males and five females with age range of 4-64 years. Etiologies included hypoxia in two patients and infarction in the nine patients. SWI detected diffuse linear hypointensities along the gyral margins in CLN due to hypoxic ischemic encephalopathy. Linear dot like hypointensities were identified in one patient with infarction.CLN due to hypoxic ischemic encephalopathy display linear gyral hypointensities and basal ganglia hypointensities that are identifiable in SWI and may represent mineralization. This might be related to iron transport across the surviving neurons from basal ganglia to the cortex, which is not possible in complete infarction. SWI may be helpful in understanding the pathophysiological aspects of CLN due to complete infarction and hypoxia.
URI: http://dx.doi.org/10.1007/s00234-009-0497-8
http://www.ncbi.nlm.nih.gov/pubmed/19159922
http://dspace.sctimst.ac.in/jspui/handle/123456789/1045
Appears in Collections:Journal Articles

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