Case Of the Week (COW) 17 Feb 2013
Answer:
Acute Cortical Laminar necrosis secondary to hypoglycaemia with chronic laminar necrosis in the followup scan.
Findings:
Gyriform areas of restricted diffusion , abutting the depths and sides of sulci, noted in both fronto temporal and parietal regions and hippocampi. The followup scan reveals curvilinear T1 hyperintensities in the corresponding regions.
Discussion:
Cortical laminar necrosis is a specific type of infarction developing due to hypoxic encephalopathy. It characteristically appears as TI hyperintensity along the cortical ribbon. In the acute stage , there is diffuse swelling of the cerebral cortex with hyperintensity in T2WI, FLAIR and DWI. In the subacute phase(1-3 weeks), there is T2 hypointensity of the corresponding regions. It is due to a critical energy shortage resulting from deficient glucose and oxygen supply as in hypoxia, severe anaemia or hypoglycaemia. It can also follow protracted seizures due to rapid comsumption of glucose and oxygen. In oligaemic hypoxia , the lesions are adjacent to the depths and sides of cortical sulci. In hypoglycaemic hypoxia there is more diffuse involvement of the cerebral cortices and watershed zones as well as hippocampal involvement.
Contributed By:
Dr. Babu Peter MD, DNB
Associate Professor, Barnard Institute of Radiology, Chennai
Senior Consultant Radiologist, Aarthi Scans, Chennai
Answer:
Acute Cortical Laminar necrosis secondary to hypoglycaemia with chronic laminar necrosis in the followup scan.
Findings:
Gyriform areas of restricted diffusion , abutting the depths and sides of sulci, noted in both fronto temporal and parietal regions and hippocampi. The followup scan reveals curvilinear T1 hyperintensities in the corresponding regions.
Discussion:
Cortical laminar necrosis is a specific type of infarction developing due to hypoxic encephalopathy. It characteristically appears as TI hyperintensity along the cortical ribbon. In the acute stage , there is diffuse swelling of the cerebral cortex with hyperintensity in T2WI, FLAIR and DWI. In the subacute phase(1-3 weeks), there is T2 hypointensity of the corresponding regions. It is due to a critical energy shortage resulting from deficient glucose and oxygen supply as in hypoxia, severe anaemia or hypoglycaemia. It can also follow protracted seizures due to rapid comsumption of glucose and oxygen. In oligaemic hypoxia , the lesions are adjacent to the depths and sides of cortical sulci. In hypoglycaemic hypoxia there is more diffuse involvement of the cerebral cortices and watershed zones as well as hippocampal involvement.
Contributed By:
Dr. Babu Peter MD, DNB
Associate Professor, Barnard Institute of Radiology, Chennai
Senior Consultant Radiologist, Aarthi Scans, Chennai