Advanced magnetic resonance imaging of cortical laminar necrosis in patients with stroke

Abstract

Purpose The aim of this study was to assess the novel advanced magnetic resonance imaging findings of acute stage cortical laminar necrosis developing after complicated cardiovascular or abdominal surgery. Materials and methods This institutional review board-approved study included patients with postoperative stroke due to cortical laminar necrosis imaged with magnetic resonance in the acute stage. Brain magnetic resonance imaging examinations were obtained on a 3T magnetic resonance scanner within 48 hours of the neurological symptoms, including diffusion-weighted images (b value, 1000 s/mm2) and arterial spin labelling using a pseudo-continuous arterial spin labelling method in four patients. Conventional and advanced magnetic resonance images were analysed to assess the imaging features in acute stage cortical laminar necrosis. Results The final population consisted of 14 patients (seven men and seven women, mean age 61 years, range 32–79 years) diagnosed with stroke and acute phase cortical laminar necrosis. All the patients presented with cortical lesions showing restricted diffusion on diffusion-weighted images and hypointensity on the apparent diffusion coefficient map. Cortical hyperintensity on T2-weighted or fluid-attenuated inversion recovery images was found in three (21%) and six (43%) patients, respectively. Reduced perfusion was noted in three out of four patients imaged with arterial spin labelling, while in one case no corresponding perfusion abnormality was noted on the arterial spin labelling maps. Arterial spin labelling abnormalities were much more extensive than diffusion restriction in two patients, and they were associated with a poor outcome. Conclusion Cortical hyperintense abnormalities on diffusion-weighted imaging may be the only sign of developing cortical laminar necrosis injury. The acquisition of arterial spin labelling helps to identify perfusion alterations and the extension of the ischaemic injury.

Melanoma brain metastasis mimicking cortical laminar necrosis

“…This typically occurs following a hypoxic-ischemic event, in which the ischemia is not severe enough to affect less metabolically active white. [ 1 ] Cortical ischemia demonstrates diffusion restriction within several hours after an initial insult; this diffusion restriction fades over several weeks. T1 shortening may appear 2 weeks after the precipitating event.…”

Case report: Delayed posttraumatic cortical laminar necrosis secondary to spreading depolarization induced spreading ischemia from old subarachnoid hemorrhage

“…Cortical laminar necrosis (CLN) refers to ischemic injury of selective neuronal cortical layers due to hypoxic injury [1 , 2] . Usually, it occurs secondary to infarcts or hypoxia, however other causes, including hypoglycemia, status epilepticus, and immunosuppressive therapy have been described [3] . In the chronic phase, CLN is characterized by T1-hyperintensity following the gyri of the cerebral cortex without the involvement of the underlying white matter (WM) and atrophy of the cortical structures on T1-weighted MRI images [4] .…”

Association between migraine and aura, migrainous infarction and cortical laminar necrosis: a literature review/ Associação entre enxaqueca e aura, enxaqueca por enfarte e necrose laminar cortical: uma revisão bibliográfica

“…1,2 Finding these phase changes Acute symptoms are particularly challenging as they usually appear two weeks after ischemia, peak in intensity around a month and then slowly disappear over 3 months to 2 years, and cortical atrophy may appear in the chronic phase. 1,7,8,9,10 Some studies have shown that T1 hypersignal reflects the presence of substances such as hemoglobin, lipid-laden macrophages, melanin, paramagnetic substances or protein-rich fluid, therefore, not being sec. undone to hemorrhagic transformation of cerebral ischemia.…”

“…1,4 Only a few case reports have evaluated diffusion-weighted imaging (DWI) abnormalities in the acute phase of CLN. 10 Thus, this entity still has several unexplored characteristics, with a significant gap in knowledge regarding the acute phase of CLN.…”