Operative management of intrinsic brainstem lesions remains challenging despite advances in electrophysiological monitoring, neuroimaging, and neuroanatomical knowledge. Surgical intervention in this region requires detailed knowledge of adjacent critical white matter tracts, brainstem nuclei, brainstem vessels, and risks associated with each surgical approach. Our aim was to systematically verify internal anatomy associated with each brainstem safety entry zone (BSEZ) via neuroimaging modalities commonly used in pre-operative planning, namely high-resolution magnetic resonance imaging (MRI) and diffusion tensor tractography (DTT). Twelve BSEZs were simulated in eight, formalin-fixed, cadaveric brains. Specimens then underwent radiological investigation including T2-weighted imaging and DTT using 4.7 T MRI to verify internal anatomic relationships between simulated BSEZs and adjacent critical white matter tracts and nuclei. The distance between simulated BSEZs and pre-defined, adjacent critical structures was systemically recorded. Entry points and anatomic limits on the surface of the brainstem are described for each BSEZ, along with description of potential neurological sequelae if such limits are violated. With high-resolution imaging, we verified a maximal depth for each BSEZ. The relationship between proposed safe entry corridors and adjacent critical structures within the brainstem is quantified. In combination with tissue dissection, high-resolution MR diffusion tensor imaging allows the surgeon to develop a better understanding of the internal architecture of the brainstem, particularly as related to BSEZs, prior to surgical intervention. Through a careful study of such imaging and use of optimal surgical corridors, a more accurate and safe surgery of brainstem lesions may be achieved.
The fact that BRCA genes operate as tumor suppressors is evident from the genetics of the different human disorders caused by inherited mutations. Germline mutations affecting 1 allele of either BRCA1 or BRCA2 confer susceptibility to different types of cancers such as breast cancer and medulloblastoma. A family with a history of cancer was identified in Eastern Turkey in which one of the family members (a 13-year-old boy) had medulloblastoma. Venous blood was collected from available family members. The BRCA1 and BRCA2 genes were sequenced in the patient with medulloblastoma and the healthy father. An Asn372His homozygous variation was noted in the BRCA2 gene in the patient with medulloblastoma whereas the variation was heterozygous in the healthy father. A biallelic homozygous variation was demonstrated in the BRCA2 gene, which is important in medulloblastoma suppression, and may have caused medulloblastoma formation in the 13-year-old boy. Further investigations in large human populations with medulloblastoma are necessary for further delineation of BRCA gene malfunctions and their relationship to medulloblastoma formation, and to clarify the therapeutic implications of these malfunctions.
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