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.

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

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.

Cortical Laminar necrosis in a patient with chronic cerebral infarction; Case report

Cortical laminar necrosis (CLN) is a persistent ischemic injury attributed to a particular pan necrosis of the cerebral cortex (comprising neurons, glia, and blood vessels although underline white matter is totally or partially spared). CLN is represented radiologically by the typical curvilinear gyriform distribution high signal intensity cortical lesions on T1 weighted MRI images in the affected cerebral convolutions. This is a case of cortical laminar necrosis following old left temporo-parietal ischemic infarction. A 67-year male patient with a prior history of old left temporo-parietal ischemic infarction came for follow up MRI for old right-sided hemiplegia and aphasia. He was diabetic and hypertensive. MRI Brain images showed large old left temporo-parietal ischemic infarction in the territory of Lt. MCA. There is associated subacute ischemic infarct at the left occipital cortex. There is laminar linear cortical hyperintensity in T1WI following gyral distribution, accompanied by loss of the volume of the underlying cortex at the left temporo-parieto-occipital region suggesting cortical laminar necrosis and this picture appeared two months following old cerebral infarction and shortly the patient died.