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Pediatric meningioma with rhabdoid features developed at the site of skull fracture: illustrative case

Sho Takata, Akira Tamase, Yasuhiko Hayashi, Osamu Tachibana, Katsuaki Sato, and Hideaki Iizuka

Meningiomas account for approximately 20% of intracranial tumors and typically occur in adults. Pediatric meningiomas are rare, and their occurrence is reported to occur in 2.2% of all intracranial meningiomas. They tend to be associated with atypical locations, higher histopathological grades, and aggressive behaviors. 1 Tumorigenesis of a meningioma after head trauma has been deliberated upon for many years. 2–4 In 1938, post-traumatic meningioma was first described by Cushing and Eisenhardt, who reported a causal relationship between head trauma

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Intracranial temporal bone angiomatoid fibrous histiocytoma: illustrative case

Shivani Gillon, Jacqueline C. Junn, Emily A. Sloan, Nalin Gupta, Alyssa Reddy, and Yi Li

associated with tumor cytokine production, such as anemia, fever, and malaise. 5 Thus far, the majority of reported cases of AFH have occurred in the superficial soft tissues, with relatively few reports in bone 6 and even fewer with intracranial presentation. 7–11 The rarity of AFH makes prospective diagnosis challenging, and the lesion has been mistaken for other pathologies, including angiosarcoma, eosinophilic granuloma, 2 , 12 meningioma, 10 aneurysmal bone cyst, 13 or cavernous malformation. 7 In this report, we present a rare case of primary AFH in the

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TRAF7 somatic mosaicism in a patient with bilateral optic nerve sheath meningiomas: illustrative case

Georgia Kaidonis, Melike Pekmezci, Jessica Van Ziffle, Kurtis I. Auguste, and Jonathan C. Horton

Cytogenetic alterations in meningioma specimens were first discovered more than 50 years ago. 1 Loss of the long arm of chromosome 22 was identified as a pathogenic somatic alteration in meningioma tissue. 2 , 3 Subsequently, the neurofibromatosis type 2 (NF2) tumor suppressor gene was discovered on chromosome 22q. 4 Approximately 50% of patients with autosomal dominant NF2 develop meningioma. 5 Somatic NF2 gene mutation or loss (or both) contributes to 50% to 60% of sporadic adult meningiomas. 6–10 Other genetic conditions carrying an increased risk

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Intracranial solitary fibrous tumor in a 15-year-old girl: illustrative case

Kuan Lu, Xiaoqing Qu, Jingcheng Jiang, Quanjun Zheng, Yongsheng Ao, and Lihua Qiu

mesenchyme. 5–7 SFT is often located in the intracranial region outside of the brain, commonly presenting as lesions near the skull base, sagittal sinus, falx cerebri, and tentorium cerebelli. 5 , 8 The location of SFT within the brain is comparable to that of meningioma. Our case corresponds with previous reports of SFT in the areas of the transverse sinus and tentorium cerebelli. Most SFTs are indeed solitary, but instances of multiple lesions can occur. In terms of malignancy, intracranial SFTs are regarded as borderline tumors, with the majority of cases

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Biallelic inactivation of PBRM1 as a molecular driver in a rare pineoblastoma case: illustrative case

Joseph P. Antonios, Kanat Yalcin, Armine Darbinyan, Andrew Koo, Christopher S. Hong, Michael DiLuna, and Zeynep Erson-Omay

was identified as 94.9%, confirming that the deleted copy was the wild-type copy. PBRM1 has been described to play a role in cellular apoptosis and stress response, such that it indirectly decreases reactive oxygen species (ROS) and supports cellular viability. 8 Loss of PBRM1 appears to drive cell growth and genomic instability, and alterations of PBRM1 have been previously described in clear cell renal cell carcinoma (RCC), as well as in a subset of papillary RCC, bladder carcinoma, and meningioma with papillary features. 9–12 Furthermore, PBRM1 encodes

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Sinus pericranii in the setting of a posterior fossa pilocytic astrocytoma: illustrative case

Youngkyung Jung, Jennifer L. Quon, and James M. Drake

., 2007 6 Superior sagittal sinus, torcula Visual impairment, HAs, papilledema Hemangiopericytoma Dexamethasone & tumor excision Stable postoperative course Szitkar, 2010 7 Superior sagittal invasion Visual impairment, HAs, papilledema Meningioma (based on imaging) Diamox, then endovascular stenting w/ anticoagulation & stereotactic radiosurgery Not mentioned Chausson et al., 2010 8 Lt transverse sinus Bilat papilledema Meningioma Endovascular sinus stenting Stable at 1-yr FU Maiuri et al., 2011 9 Transverse-sigmoid junction

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Optic nerve compression in craniopharyngioma by taut anterior cerebral arteries visualized in frontal and transsphenoidal exposures: illustrative cases

Anna L. Slingerland, Lissa C. Baird, and R. Michael Scott

JC . Visual field deficit caused by vascular compression from a suprasellar meningioma: case report . Neurosurgery . 2002 ; 50 ( 5 ): 1129 – 1132 . 6 Thomé C , Zevgaridis D . Delayed visual deterioration after pituitary surgery – a review introducing the concept of vascular compression of the optic pathways . Acta Neurochir (Wien) . 2004 ; 146 ( 10 ): 1131 – 1136 . 10.1007/s00701-004-0331-3 7 Mizrahi CJ , Moscovici S , Dotan S , Spektor S . Optic nerve vascular compression in a patient with a tuberculum sellae meningioma

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Juvenile psammomatoid ossifying fibroma of the parietal bone and review of calvarial presentations: illustrative case

Robert T. Chung, Julio D. Montejo, Darcy A. Kerr, and Jennifer Hong

, 28 likely because of the difficulty of complete resection. These rates are within the range for rates of recurrence of ossifying fibroma more generally, which are reported anywhere from 30% to 56%. 1 , 3 Recurrence is often attributed to incomplete removal. Pathologic Findings and Differential Diagnosis JPOFs generally present with nonspecific imaging and clinical findings that encompass a broad differential diagnosis, including fibrous dysplasia, 20 , 22 meningioma, 2 , 29 aneurysmal bone cyst, 4 eosinophilic granuloma, dermoid cyst, certain subtypes

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Clinical, imaging, and molecular features of radiation-induced glioblastomas developing more than 20 years after radiation therapy for intracranial germinomatous germ cell tumor: illustrative cases

Yoshihiro Tsukamoto, Manabu Natsumeda, Haruhiko Takahashi, Asuka Ueno, Kiichi Sakai, Kazuki Shida, Hiroki Seto, Taiki Saito, Satoshi Shibuma, Yoko Nakayama, Yuki Tanaka, Toshimichi Nakano, Atsushi Ohta, Katsuya Maruyama, Masayasu Okada, Takeyoshi Eda, Yasuhiro Seki, Yuichirou Yoneoka, Hiroshi Shimizu, Kouichirou Okamoto, Akiyoshi Kakita, and Makoto Oishi

malignant neoplasms (SMNs), endocrine deficiencies, and stroke, 1 which are particularly relevant in the long term, owing to the favorable prognosis of the patients. With greater years of follow-up, there is increasing mortality attributable to treatment-related causes inducing SMN. The most common radiation-induced CNS SMNs are gliomas and meningiomas. The survival rates for patients who develop gliomas are far worse than those for patients who develop meningiomas, with a 5-year relative survival rate of only 4% for radiation-induced gliomas compared with 77%–84% for

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Misdiagnosis of elevation of β-hCG in cystic craniopharyngioma: illustrative case

Umaira Saleh, Liang Hooi Lim, Ihfaz Ismail, and Nasser Abd Wahab

, pituitary adenoma, and meningioma, with the last 2 rarely presenting in children. 3 Similar to craniopharyngiomas, intracranial germ cell tumor (ICGCT) affects the suprasellar region, leading to identical clinical manifestations. Both tumors can be manifested by visual disturbances, varying degrees of hypopituitarism, and raised intracranial pressure (ICP) symptoms. 3 , 6 , 7 However, diabetes insipidus, precocious puberty, anorexia, and weight loss are commonly associated with ICGCT. 6 – 8 Most craniopharyngiomas are identified on the basis of clinical and