Neurofibromatosis, type I. Autism and frontal lobe tumor. Follow-up. The heterogeneous lesion in the left frontal lobe which contains foci of susceptibility and also shows heterogeneous areas of contrast enhancement has not changed since the previous examination. The foci of susceptibility effect may reflect hemosiderin or mineral deposition. There is no significant associated edema or mass-effect. The lesion did not show susceptibility effect on the more remote examination from May 11, 2006. There is an adjacent linear vascular structure which may represent a developmental venous anomaly.The T2-hyperintense lesions involving the globi pallidi related to the diagnosis of neurofibromatosis type I, are not significantly changed. The T2-hyperintense lesions in the right frontal white-matter are unchanged though the associated minimal contrast enhancement is slightly more pronounced. Major intracranial vascular flow voids are preserved. There is no gross orbital abnormality. Focal posterior parietal midline plaque-like scalp thickening has not changed. Along the inferior edge of this scalp thickening, there is a 1.6 cm skull defect. A much smaller skull defect is also present along its superior edge. Both defects are in close proximity to the underlying superior sagittal sinus. This may represent congenital venous malformation, like sinus pericranii. These findings are not significantly changed since the previous examination. Otherwise, there is no destructive skull lesion.
1.Left frontal lobe lesion remains unchanged since February 2015. Compared to the more remote examination from May 11, 2006, the lesion has shown mild gradual increase in overall size with increased susceptibility which may be related to mineralization or blood products. Finding is most compatible with low grade neoplasm such as astrocytoma.2.Unchanged T2 hyperintense lesions in the globi pallidi compatible with myelin vacuolization/FASI related to neurofibromatosis type I. 3.The right frontal white-matter T2-hyperintense lesions with minimal enhancement are also unchanged. 4.The posterior skull defects which are in close proximity to the underlying superior sagittal sinus may reflect sinus pericranii. Adjacent plaque-like posterior scalp thickening may reflect a small neurofibroma or may relate to the aforementioned adjacent vascular anomaly, but remains unchanged.I personally reviewed the Images and/or procedure with the Resident/Fellow and agree with this report.