Susceptibility-Weighted Imaging Findings of Cortical Laminar Necrosis in Pediatric Patients

Niwa, Tetsu; Aida, Noriko; Shishikura, Ayako; Fujita, Kazutoshi; Inoue, Takehiko

doi:10.3174/ajnr.a1184

Cited by 45 publications

(28 citation statements)

References 18 publications

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“…3 In a previous study of pediatric patients with cortical laminar necrosis evaluated with SWI, only 20% of the patients had signals of laminar or dotted hemorrhage. 4 In conclusion, MR imaging follow-up is essential for monitoring patients with WE with cortical abnormalities due to the risk of irreversibility of lesions, which may progress to cortical laminar necrosis and hemorrhage.…”

Section: 2mentioning

confidence: 99%

Nonalcoholic Wernicke Encephalopathy with Extensive Cortical Involvement: Cortical Laminar Necrosis and Hemorrhage Demonstrated with Susceptibility-Weighted MR Phase Images: Fig 1.

Pereira¹,

Pereira²,

Gasparetto³

2011

AJNR Am J Neuroradiol

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Wernicke encephalopathy (WE) is an acute neuropsychiatric condition due to an initially reversible brain lesion caused by depleted intracellular thiamine levels in neurons.1 Most of the affected patients are malnourished alcoholics; however, WE has also been associated with other conditions. The typical MR imaging features are symmetric hyperintensity on T2-weighted images in the medial thalami, mamillary bodies, tectal plate, periaqueductal area, and floor of the fourth ventricle. 1 Atypical MR imaging findings, such as signal-intensity abnormalities in cranial nerve nuclei, cerebellum dentate nuclei, vermis, putamina, red nuclei, caudate nuclei, splenium, and cerebral cortex, have been more frequently described in nonalcoholic WE.

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Section: 2mentioning

confidence: 99%

Nonalcoholic Wernicke Encephalopathy with Extensive Cortical Involvement: Cortical Laminar Necrosis and Hemorrhage Demonstrated with Susceptibility-Weighted MR Phase Images: Fig 1.

Pereira¹,

Pereira²,

Gasparetto³

2011

AJNR Am J Neuroradiol

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“…Cortical laminar necrosis is, pathologically, characterized as necrosis of particular cortical laminae involving neurons, glial cells, and cerebral blood vessels. Cortical laminar necrosis is predominantly caused by hypoxia and metabolic disorders, like hypoglycemia, intoxication, hypoxic-ischemic encephalopathy, renal and hepatic dysfunction, but may also be seen in patients with encephalitis [8–10]. We describe the occurrence of cortical laminar necrosis in a setting highly suggestive of dengue infection, possibly the first instance, in a 15-year-old boy.…”

Section: Discussionmentioning

confidence: 98%

Cortical laminar necrosis in dengue encephalitis—a case report

et al. 2017

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BackgroundDengue encephalitis is a rare neurological manifestation of dengue fever. Its clinical presentation is similar to other viral encephalitides and encephalopathy. No single specific finding on magnetic resonance imaging of dengue encephalitis has yet been documented. They are highly variable and atypical.Case presentationA 15-year boy presented with fever, the headache and altered sensorium of 12-day duration. On neurological examination, his Glasgow Coma Scale score was 10 (E3M4V3). There was no focal neurological deficit. Laboratory evaluation revealed leukopenia and marked thrombocytopenia. Dengue virus IgM antibody was positive both in serum and cerebrospinal fluid. Magnetic resonance imaging of the brain revealed signal changes in bilateral parietooccipital and left frontal regions (left hemisphere more involved than the right hemisphere). There was gyriform enhancement bilateral parietooccipital regions consistent with cortical laminar necrosis. Bilaterally diffuse subcortical white matter was also involved and subtle T2 hyperintensity involving both basal ganglia was noted. Gradient echo sequence revealed presence of hemorrhage in the subcortical white matter. Patient was treated conservatively and received platelet transfusion. Patient became fully conscious after 7 days.ConclusionIn a patient with highly suggestive dengue e\ephalitis, we describe an unusual magnetic resonance imaging finding. This report is possibly the first instance of cortical laminar necrosis in such a setting.

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“…The high-signal-intensity features seen on T1-weighted images may be related to mineralization, protein denaturation, or lipid (72). However, methemoglobin does not appear to contribute to this signal hyperintensity (73).…”

Section: Cortical Laminar Necrosismentioning

confidence: 98%

Intracranial Lesions with High Signal Intensity on T1-weighted MR Images: Differential Diagnosis

Ginat¹,

Meyers²

2012

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144

108

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Various substances, including methemoglobin, melanin, lipid, protein, calcium, iron, copper, and manganese, are responsible for the intrinsically high signal intensity observed in intracranial lesions at T1-weighted magnetic resonance (MR) imaging. Many of these substances have physical properties that lead to other specific imaging features as well. For example, lipid-containing lesions frequently produce chemical shift artifact, and some melanin-containing lesions exhibit a combination of high signal intensity on T1-weighted images and low signal intensity on T2-weighted images. The location and extent of a region of abnormal signal hyperintensity may be helpful for identifying rare diseases such as an ectopic posterior pituitary gland near the floor of the third ventricle, bilateral involvement of the dentate and lentiform nuclei in Cockayne syndrome, and involvement of the anterior temporal lobe and cerebellum in neurocutaneous melanosis. In cases in which diagnostically specific T1-weighted imaging features are lacking, findings obtained with other MR pulse sequences and other modalities can help narrow the differential diagnosis: An elevated glutamine or glutamate level at MR spectroscopy is suggestive of hepatic encephalopathy; a popcorn ball-like appearance at T2-weighted imaging, of cavernous malformations; and hyperattenuation at computed tomography, of mineral deposition disease. In many cases, a comparison of imaging features with clinical measures enables a specific diagnosis.

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Susceptibility-Weighted Imaging Findings of Cortical Laminar Necrosis in Pediatric Patients

Cited by 45 publications

References 18 publications

Nonalcoholic Wernicke Encephalopathy with Extensive Cortical Involvement: Cortical Laminar Necrosis and Hemorrhage Demonstrated with Susceptibility-Weighted MR Phase Images: Fig 1.

Nonalcoholic Wernicke Encephalopathy with Extensive Cortical Involvement: Cortical Laminar Necrosis and Hemorrhage Demonstrated with Susceptibility-Weighted MR Phase Images: Fig 1.

Cortical laminar necrosis in dengue encephalitis—a case report

Intracranial Lesions with High Signal Intensity on T1-weighted MR Images: Differential Diagnosis

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