Skull Base Collision Tumors: Giant Non-functioning Pituitary Adenoma and Olfactory Groove Meningioma

Abstract

A collision tumor complex is composed of at least two different tumors, benign or malignant, with at least two different histopathological features located adjacent to each other in the exact anatomical localization. Pathologies such as meningiomas, pituitary adenomas, gliomas, and schwannomas may be involved in a collision tumor complex. However, co-occurrence of pituitary adenomas and meningiomas as skull base collision tumors is rare. Here, we present a 65-year-old male patient who presented with olfactory groove meningioma and non-functioning pituitary adenoma as a collision tumor. The patient was admitted with a headache and right-sided vision loss. The patient's first neurologic examination was consistent with temporal anopsia in the right eye. Subsequent contrast-enhanced cranial MRI revealed a 65x55x40 mm heterogeneously contrast-enhanced lesion in the anterior skull base extending from the sellar region to the corpus callosum. Because of the tumor size, a two-staged operation was planned. First, the tumor was partially excised via a right frontal craniotomy with a transcranial approach, and the tumor in the sellar region was left as a residue. The pathology reports after the first surgery showed pituitary adenoma and meningeal epithelial type meningioma (WHO Grade I). The residual tumor tissue was resected seven months later via an endoscopic endonasal approach, except for the part that invaded the right anterior cerebral artery. The optic nerve was decompressed. The patient was then referred to the radiation oncology clinic for radiosurgery. Collision tumors should be considered in the differential diagnosis in preoperative evaluation and surgical planning when heterogeneously contrast-enhanced areas significantly localized adjacent to each other are seen on cranial MRI. On the other hand, when the surgeon encounters sudden changes in the appearance or consistency of the tumor during the surgery, they should suspect these tumor complexes. The diagnosis of collision tumors is quite challenging but is of great importance regarding the patient's need for postoperative radiation therapy or the recurrence characteristics of tumors. However, more studies are needed on these complexes' etiology, surgical planning, and postoperative management.

Keywords: collision tumor; nonfunctioning pituitary adenoma; olfactory groove meningoma; sella turcica; skull base collision tumors.

Figure 1. Preoperative, first, and second postoperative contrast-enhanced T1-weighted cranial MRI of a patient with non-functioning pituitary adenoma and co-existing olfactory groove meningioma.

A: Preoperative contrast-enhanced T1-weighted cranial MRI of a patient with collision tumor; axial, sagittal and coronal scans, respectively. A heterogeneously contrast-enhanced mass lesion of approximately 65x55x40 mm in size with lobulated contours, filling the sellar lobe and extending superiorly to the convexity level of the frontal lobe, was observed (blue arrows). A well-circumscribed nodular lesion is observed in the anterior part of the frontal lobe with a heterogeneous appearance on the postcontrast series at a distance of approximately 2 cm from the other mass lesion at the level of the falx cerebri (red arrows). The lesion was evaluated as first plane olfactory groove meningioma. B: First postoperative contrast-enhanced T1-weighted cranial MRI; axial, sagittal, and coronal scans, respectively. The sellar lesion, observed on the preoperative MRI scans, was largely resected. Postoperative changes were seen in this imaging. Within the sella, a 37x30 mm residual cystic necrotic lesion was observed (green arrows), filling the sella and displacing both middle cerebral artery (MCA) M1 parts superiorly. C: Second postoperative contrast-enhanced T1-weighted cranial MRI; axial, sagittal, and coronal scans, respectively. It was observed that the lesion was mostly excised. A residual lesion with a diameter of approximately 17 mm was observed (white arrows). It was seen that the sellar and suprasellar components of the tumor were removed, and the optic nerve was decompressed, but there was a residue in the anterior cerebral artery (ACA) A1 segment.

Figure 2. Pathologic specimen pictures of the biopsy material from the first operation

A: Neoplastic cells with eosinophilic cytoplasm, round/oval nuclei with indistinct nucleoli (H&E x 200); B: Tumoral proliferation consists of uniform cells with a distinctive diffuse pattern and vascular framework (H&E x200); C: Focal positivity with luteinizing hormone (LH), LH x200; D: Focal positivity with follicle-stimulating hormone (FSH), FSH x200; E: Neoplastic cells with pseudo-inclusions (red arrow), H&E x200; F: Epithelial membrane antigen (EMA) positivity, EMA x400. H&E: hematoxylin & eosin

Figure 3. Pathologic regimen from the second operation, hematoxylin & eosin, x100

Microscopic picture of the biopsy material from the second operation. Note the association between the sinus mucosa cells (blue arrow) and the pituitary adenoma neoplastic cells (black arrow)