“Cortical laminar necrosis” was defined as hyperintense cortical lesions on T1-weighted imaging found during the subacute or chronic phase of brain damage.
(** Ref : Susceptibility-Weighted Imaging Findings of Cortical Laminar Necrosis in Pediatric Patients
T. Niwaa, N. Aidaa, A. Shishikuraa, K. Fujitaa and T. Inoueb (AJNR oct 2008))
Although, the mechanism of T1 shortening in cortical laminar necrosis remains unclear, high cortical intensity on a T1-weighted image is believed to occur by neuronal damage and reactive tissue change of glia and deposition of fat-laden macrophages
The gray matter has six layers. The third layer is the most vulnerable to depletion of oxygen and glucose. Cortical laminar necrosis is a specific type of cortical infarction, which usually develops as a result of generalized hypoxia rather than a local vascular abnormality. Depletion of oxygen or glucose as in anoxia, hypoglycemia, status epilepticus, and ischemic stroke has been attributed as an underlying cause of cortical laminar necrosis.
Immunosuppressive therapy (cyclosporin A and FK506), and polychemotherapy (vincristine and methotrexate) have been observed to cause laminar necrosis due to hypoxic-ischemic-insult. Hypoxic insult leads to death of neurons, glia and blood vessels along with degradation of proteins
Chronic brain infarcts are typically seen as low-intensity lesions on T1-weighted and high-intensity lesions on T2-weighted MR images due to prolonged T1 and T2 values
Ref : http://komiyama.me/Kodomo/lun_wen_files/PDF42.pdf
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