Concept Cortical laminar necrosis, also known as pseudolaminar necrosis, is seen as a characteristic time-dependent imaging manifestation of impaired oxygen and/or sugar uptake in the central nervous system and abnormal brain energy metabolism due to multiple causes. Cortical laminar necrosis (CLN) was first described by Weir Mitchell in 1860. The imaging manifestations of cortical laminar necrosis are reported in the literature: there are many causes of cortical laminar necrosis and there are characteristic imaging changes: T1WI gyrus-like high signal and prolonged FLAIR high signal are its specific signs; CLN shows high signal images in FLAIR, T1 and T2. Due to the influence of high signal in the cerebrospinal fluid surrounding the lesion, T2 is difficult to show the signal intensity of CLN exactly. FLAIR imaging can suppress the signal of the surrounding cerebrospinal fluid and has the advantage of showing cortical lesions. cortical high signal in T1WI can appear 2 weeks after detection, while FLAIR imaging is more obvious at 1 month; the high signal in FLAIR imaging can persist for about 1 year even after the cortical short T1 signal disappears. CLN can be high signal or equal signal in T2WI, and low signal has also been reported. . In CLN, CT did not show hemorrhage or calcification, and MRI did not show hemorrhage. Qualitative and etiologic analysis of cortical laminar necrosis Mitochondrial encephalomyopathy; metabolic encephalopathy (hepatic encephalopathy, hypoglycemic encephalopathy, severe hyponatremia (acute intermittent porphyria, Silhan syndrome)); hypercranial pressure; ischemic-hypoxic-oxygenic encephalopathy (including hemolytic anemia,); poisoning: (cyanide poisoning, hydrogen sulfide poisoning, popcorn poisoning, etc.); lupus encephalopathy; persistent epilepsy; infectious: CJD, neuro Syphilis; reversible posterior leukoencephalopathy; cerebrovascular disease; immunosuppression, chemotherapy Prognosis of cortical laminar necrosis Some scholars point out that the presence of CLN often indicates a poor prognosis, and if the presence of CLN is followed by white matter damage it indicates an even worse prognosis. The prognosis of this group of patients needs to be evaluated taking into account the severity of the onset of the disease and the availability of timely treatment.