A 48-year-old man was referred to our clinic for evaluation of a new dural-based lesion 6 years after excision, skin flap repair, and bone graft placement for a skull-base esthesioneuroblastoma followed by adjuvant radiation. His posttreatment course was complicated by externalization of the bone flap requiring a second skull-base bone flap resection. After 5 years of no radiographic evidence of residual disease, a routine follow-up magnetic resonance imaging (MRI) scan at 6 years revealed an enhancing dural lesion over the right frontal lobes [].\nThe patient underwent a right frontotemporal craniotomy for resection of the enhancing dura and tumor, which was found to be partially invading the brain parenchyma. Pathological analysis indicated the lesion was consistent with recurrent metastatic esthesioneuroblastoma. The patient received adjuvant stereotactic radiosurgery. His follow-up MRIs approximately every 6 months remained negative until additional dural-based lesions along the frontal sinus, right temporal lobe, and right sphenoid wing were observed at 3 years []. Follow-up imaging 5 months later revealed progressive interval growth of the dural-based lesions. Treatment with cisplatin and etoposide was stopped after one cycle because of intractable nausea and vomiting. Approximately 1 year later, the patient restarted treatment with sunitinib, but the tumor showed clear progression 12 months later and the drug was discontinued. The patient succumbed to the disease 6 months later, 11 years after his initial diagnosis.
A 39-years-old man was admitted to the emergency room of our Institution for a 1-month history of gait disturbance, postural instability, speech disturbance, and episodes of incontinence. His history was remarkable for communicating hydrocephalus, which had been surgically treated at the age of 14 months with the placement of a ventriculoperitoneal shunt, followed by a distal shunt revision at the age of 16 years. At the admission, brain computed tomography (CT) scan was performed and it showed the presence of 5 cm mixed-density pseudonodular lesion. His neurological examination revealed temporospatial disorientation, absence of focal motor deficits and sensory alteration, normal and symmetrical osteotendinous reflexes, walk of little steps, and wide-based gait, several body oscillations during the Romberg’s test. A contrast-enhanced brain CT study [] confirmed the presence of an enhancing 57 mm left frontotemporal non-homogeneous neoformation, with several calcifications, hypodense colliquated areas, and perilesional edema. Preoperative magnetic resonance imaging (MRI) with gadolinium contrast medium, even though strongly fouled by motion artifacts due to poorly cooperative patient, showed a lesion with lobulated margins, non-homogeneous post contrast enhancement and heterogeneous signal intensity in relation to the presence of solid component mixed with necrotic-colliquative areas and calcifications. In particular, in the peripheral frontal portion, a small oval-shaped component was visible, surrounded by strongly hypointense peripheral border in FFE sequences, arguably due to hemosiderin deposition. The tumor presented a maximum diameter of 6.2 × 4.1 cm on the axial plane [], 6.3 × 3.5 cm on the sagittal plane [], and 3.6 × 3.3 cm on the coronal plane [], and it extended cranially to the knee of the corpus callosum, displacing the large falx to the right and causing a compressive effect on the frontal horn of the right lateral ventricle.\nSurgical procedure was performed with the aid of optic neuronavigation, intraoperative monitoring and the resection was performed though a left pterional approach.[,] Intraoperatively, the neoplasm appeared of soft and partly fibrous consistency, of reddish-grey color and with a fairly good cleavage plane from the adjacent cerebral parenchyma. With the aid of ultrasonic aspirator and microsurgical technique, macroscopical total resection of the exposed neoplastic lesion was carried out. Autologous fibrin glue was used to seal the dural plane.\nFragments of the lesion were sent for pathological examination, which revealed a population of neuronal lineage (Sinaptophysin+, neuron specific enolase+, glial fibrillary acid protein−) consisting of roundish monomorphic cells mixed with a proliferation of capillary vessels and the presence of widespread calcifications; the Ki-67 index was <5%, there was no evidence of mitosis or areas of necrosis. Histopathological and immunohistochemical pattern, according to radiological findings, was consistent with a diagnosis of EVN, classified by the WHO as a Grade II tumor [-].\nThe postoperative course was uneventful and control CT scan [] showed no complications. A further MRI was performed [-], which showed on the left frontal area, in correspondence of the surgical cavity, a large area of structural alteration, consisting predominantly of cerebrospinal fluid and a tissue portion with calcifications.\nAfter the hospital discharge patient underwent at home neurorehabilitation with consistent improvement of his gait and speech. He also underwent adjuvant radiotherapy and at the present his follow-up is still ongoing.