J Clin Neurol.  2005 Oct;1(2):174-176. 10.3988/jcn.2005.1.2.174.

Cortical Laminar Necrosis associated with Osmotic Demyelination Syndrome

• Cho AH
• Choi CG
• Lee SA

• KMID: 1808488
• DOI: http://doi.org/10.3988/jcn.2005.1.2.174

Abstract

Cortical laminar necrosis has been rarely observed in osmotic demyelination syndrome. We report a 32-year-old female patient who became comatose after the rapid correction of hyponatremia. There were high signal intensities in the pons and bilateral deep gray nuclei on T2-weighted MRI images, and linear hyperintensities along the cerebral cortices on T1-weighted images with a diffuse gyriform enhancement. MR spectroscopic findings showed a decrease of the N-acetyl aspartate peak and an increase in those of the lipid and lactate complex. The case demonstrates that a severe form of osmotic demyelination syndrome accompanying cortical laminar necrosis can result from the rapid correction of hyponatremia.

Keyword

Cortical laminar necrosis; Hyponatremia; Osmotic demyelination syndrome

MeSH Terms

Adult
Aspartic Acid
Cerebral Cortex
Coma
Demyelinating Diseases*
Female
Humans
Hyponatremia
Lactic Acid
Magnetic Resonance Imaging
Necrosis*
Pons
Aspartic Acid
Lactic Acid

Figure

• 

  Figure 1 Two weeks after the correction of hyponatremia, (A, B) high signal intensities were present bilaterally in the pons and deep gray nuclei on T2-weighted MRI images (TR/TE, 3000 ms / 99 ms). T1-weighted images (TR/TE, 525 ms / 14 ms) demonstrated multifocal curvilinear hyperintensities along the cerebral cortices (C) with a diffuse gyriform enhancement alongside most of the cerebral cortices and (D, E) with a symmetrical enhancement of both external capsules, globus pallidi, and central thalami.

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