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

Cortical Laminar Necrosis associated with Osmotic Demyelination Syndrome

Affiliations
  • 1Department of Neurology, University of Ulsan College of Medicine, Seoul, Korea. salee@amc.seoul.kr
  • 2Department of Radiology, University of Ulsan College of Medicine, Seoul, Korea.

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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Reference

1. Shoji M, Kimura T, Ota K, Ohta M, Sato K, Yamamoto T, et al. Cortical laminar necrosis and central pontine myelinolysis in a patient with Sheehan syndrome and severe hyponatremia. Intern Med. 1996. 35:427–431.
Article
2. Susa S, Daimon M, Morita Y, Kitagawa M, Hirata A, Manaka H, et al. Acute intermittent porphyria with central pontine myelinolysis and cortical laminar necrosis. Neuroradiology. 1999. 41:835–839.
Article
3. Calakos N, Fischbein N, Baringer JR, Jay C. Cortical MRI findings associated with rapid correction of hyponatremia. Neurology. 2000. 55:1048–1051.
Article
4. Wright DG, Laureno R, Victor M. Pontine and extrapontine myelinolysis. Brain. 1979. 102:361–385.
Article
5. Vexler ZS, Ayus JC, Roberts TPL, Fraser CL, Kucharczyk J, Arieff AI. Hypoxic and ischemic hypoxia exacerbate brain injury associated with metabolic encephalopathy in laboratory animals. J Clin Invest. 1994. 93:256–264.
Article
6. Ayus JC, Arieff AI. Pulmonary complications of hyponatremic encephalopathy. Noncardiogenic pulmonary edema and hypercapnic respiratory failure. Chest. 1995. 107:517–521.
Article
7. Okeda R, Kitano M, Sawabe M, Yamada I, Yamada M. Distribution of demyelinating lesions in pontine and extrapontine myelinolysis -- three autopsy cases including one case devoid of central pontine myelinolysis. Acta Neuropathol (Berl). 1986. 69:259–266.
Article
8. Norenberg MD. A hypothesis of osmotic endothelial injury. A pathogenetic mechanism in central pontine myelinolysis. Arch Neurol. 1983. 40:66–69.
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