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Correspondence |

Neonate Showing Reversible Splenial Lesion

Jun-ichi Takanashi, MD; Masayuki Maeda, MD; Masaharu Hayashi, MD
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Copyright 2005 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.

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Arch Neurol. 2005;62(9):1481-1482. doi:10.1001/archneur.62.9.1481
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We read with interest the report of patients with splenium of corpus callosum (SCC) lesions, most being reversible with transiently reduced apparent diffusion coefficient (ADC) values.1 We previously described 15 patients with clinically mild encephalitis/encephalopathy with identical reversible SCC lesions,2 and we postulated that intramyelinic edema due to separation of myelin layers was a possible mechanism for the transiently decreased ADC. We recently saw a neonate with an identical SCC lesion, suggesting that the mechanism underlying the lesion might not be related to myelination.

Diffusion-weighted images of a neonate with mild asphyxia at age 12 days revealed a lesion of high signal intensity in the central portion of the SCC with a decreased ADC value (Figure, A). Magnetic resonance imaging also demonstrated T1 shortening in the bilateral ventral thalamus and deep sulci of insular regions, which likely resulted from perinatal asphyxia, without any abnormal signal on the diffusion-weighted images. He gradually improved and was discharged at age 18 days with oral administration of phenobarbital. Follow-up magnetic resonance imaging at 6 months showed a normal shape of the corpus callosum, no splenial or insural lesions, and almost normal myelination, including SCC (Figure, B). At age 1 year, he had mild hypotonia without paralysis, mild psychomotor retardation (at an almost 10-month-old level), and no epileptic seizures.

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Figure.

A, Diffusion-weighted image of neonate with mild asphyxia at age 12 days. B, Follow-up diffusion-weighted image at 6 months of age.

Grahic Jump Location

Magnetic resonance imaging in this neonatal patient revealed an identical reversible SCC lesion with a transiently reduced ADC value. Pathologically, no myelination of SCC occurs before age 2 months. Therefore, intramyelinic edema cannot occur in the neonatal period and is unlikely to be a possible mechanism underlying the reversible SCC lesion in the present patient. Another possible explanation is inflammatory infiltrate. A diffusion-weighted image study of multiple sclerosis revealed decreased ADC values in some lesions from multiple sclerosis, and it was postulated that the influx of inflammatory cells and macromolecules might have caused the decreased ADC values. A decreased ADC value in SCC may be a result of inflammation, and the ADC may return to normal if the cause resolves quickly.

AUTHOR INFORMATION

Correspondence: Dr Takanashi, Department of Pediatrics, Kameda Medical Center, 929 Higashi-cho, Kamogawa-shi, Chiba 296-8602, Japan (jtaka@kameda.jp).

REFERENCES

Doherty  MJ, Jayadev  S, Watson  NF, Konchada  RS, Hallam  DK. Clinical implications of splenium magnetic resonance imaging signal changes. Arch Neurol 2005;62433- 437
PubMed
Tada  H, Takanashi  J, Barkovich  AJ.  et al.  Clinically mild encephalitis/encephalopathy with a reversible splenial lesion. Neurology 2004;631854- 1858
PubMed

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A, Diffusion-weighted image of neonate with mild asphyxia at age 12 days. B, Follow-up diffusion-weighted image at 6 months of age.

Grahic Jump Location

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Doherty  MJ, Jayadev  S, Watson  NF, Konchada  RS, Hallam  DK. Clinical implications of splenium magnetic resonance imaging signal changes. Arch Neurol 2005;62433- 437
PubMed
Tada  H, Takanashi  J, Barkovich  AJ.  et al.  Clinically mild encephalitis/encephalopathy with a reversible splenial lesion. Neurology 2004;631854- 1858
PubMed

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