MR imaging of the corpus callosum in pediatric patients with neurofibromatosis type 1.

AJNR Am J Neuroradiol

Department of Diagnostic Imaging and Radiology, Children's National Medical Center, Washington, DC 20010-2970, USA.

Published: January 2001

AI Article Synopsis

  • The study investigates the thickness of the corpus callosum (CC) in children with neurofibromatosis type 1 (NF-1) compared to healthy peers, revealing that NF-1 patients show a significant increase in CC surface area.
  • Midsagittal T1-weighted MR images of 43 children with NF-1 and 43 matched controls were analyzed, measuring CC and overall skull surface areas to find a notable difference in CC size between the groups.
  • The findings suggest that an enlarged CC is a discernible feature of NF-1 visible through imaging, although the exact cause remains uncertain, potentially linked to issues with neurofibromin and Ras protein functions.

Article Abstract

Background And Purpose: Many pediatric patients with neurofibromatosis type 1 (NF-1) have an apparent increased thickness of the corpus callosum (CC) on sagittal T1-weighted images compared with patients not affected by NF-1. In this study, we compared the surface area of the CC in children with NF-1 with that of healthy pediatric control subjects to determine if this was another common intracranial manifestation of NF-1.

Methods: Midsagittal T1-weighted MR images of 43 consecutive children with NF-1 and 43 age- and gender-matched healthy control subjects were reviewed retrospectively. The surface area of the CC and the midsagittal intracranial skull surface (MISS) area were measured five times each on all midsagittal images. A mean CC to mean midline intracranial surface area ratio (CC/MISS) was calculated for each.

Results: There is a statistically significant increase in the mean CC surface area in pediatric patients with NF-1 (680 mm2 +/- 98, range 509-974 mm2) compared with control subjects (573 mm2 +/- 83, range 404-797 mm2). The mean MISS is significantly increased in patients with NF-1 (16568 mm2 +/- 1161, range 14107-19394 mm2 vs 15402 mm2 +/- 1133, range 12951-17905 mm2 for control subjects). CC/MISS was also significantly increased in the patients with NF-1 relative to the control subjects (.0410 +/- .0043, range .0330-.0530 vs .0372 +/- .0043, range .0270-.0470 for control subjects).

Conclusion: A larger midsagittal surface area of the CC is another intracranial manifestation of NF-1 that can be demonstrated by sagittal MR imaging. The etiology is unclear, but could be related to abnormal neurofibromin and Ras protein activity. Potential clinical relevance is discussed herein.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7975541PMC

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