Early Cortical Laminar Necrosis on MRI

An 80-year-old man with chronic hypertension was admitted to the emergency department with consciousness disorders. The evolution was marked by a rapid worsening of his neurological condition. The patient was intubated and ventilated. The biological check-up revealed a blood glucose level of 0.2g/l. A brain scan was performed which was without abnormality. Two days after the normalization of the blood sugar level, the patient presented a late awakening. A brain MRI was performed which showed bilateral fronto-parietal laminar cortical areas in T2, Flair and diffusion hypersignal, T1 iso signal, and no hyposignal on T2 gradient echo sequence (Figure 1). The diagnostic of Cortical Laminar Necrosis was retained.

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Prolonged Hemiplegic Migraine Associated with Irreversible Neurological Deficit and Cortical Laminar Necrosis in a Patient with Patent Foramen Ovale ：A case report

10.21203/rs.3.rs-439782/v1 ◽

2021 ◽

Author(s):

Yacen Hu ◽

Zhiqin Wang ◽

Lin Zhou ◽

Qiying Sun

Keyword(s):

Neurological Deficit ◽

Patent Foramen Ovale ◽

Brain Mri ◽

Foramen Ovale ◽

Hemiplegic Migraine ◽

Cortical Laminar Necrosis ◽

Case Presentation ◽

Cortical Laminar ◽

Laminar Necrosis ◽

Pfo Closure

Abstract Background: Aura symptoms of hemiplegic migraine (HM) usually resolve completely, permanent attack-related deficit and radiographic change are rare. Case presentation: We reported a HM case presented with progressively aggravated hemiplegic migraine episodes refractory to medication. He experienced two prolonged hemiplegic migraine attacks that led to irreversible visual impairment and cortical laminar necrosis (CLN) on brain MRI. Patent foramen ovale (PFO) was found on the patient. PFO closure resulted in a significant reduction of HM attacks. Conclusions: Prolonged hemiplegic migraine attack could result in irreversible neurological deficit with neuroimaging changes manifested as CLN. We recommend screening for PFO in patients with prolonged or intractable hemiplegic migraine, for that closure of PFO might alleviate the attacks thus preventing patient from disabling sequelae.

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MRI Findings of Cortical Laminar Necrosis

Journal of the Korean Radiological Society ◽

10.3348/jkrs.1996.35.5.661 ◽

1996 ◽

Vol 35 (5) ◽

pp. 661

Author(s):

Sai Ra Yoon ◽

Jae Chan Shim ◽

Ghi Jae Lee ◽

Seong Wook Choi ◽

Su Ok Seong ◽

...

Keyword(s):

Mri Findings ◽

Cortical Laminar Necrosis ◽

Cortical Laminar ◽

Laminar Necrosis

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

The Neuroradiology Journal ◽

10.1177/1971400919876621 ◽

2019 ◽

Vol 32 (6) ◽

pp. 431-437 ◽

Cited By ~ 1

Author(s):

Roberto Cannella ◽

Gianvincenzo Sparacia ◽

Vincenzina Lo Re ◽

Elisa Oddo ◽

Giuseppe Mamone ◽

...

Keyword(s):

Magnetic Resonance Imaging ◽

Magnetic Resonance ◽

Acute Stage ◽

Arterial Spin Labelling ◽

Resonance Imaging ◽

Cortical Laminar Necrosis ◽

Diffusion Weighted ◽

Cortical Laminar ◽

Laminar Necrosis ◽

Spin Labelling

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.

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