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Tumors of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Genetic factors/heritable brain tumors (estimated to account for only up to 5% of cases): Neurofibromatosis (NF) 1: neurofibroma, glioma (particularly optic nerve glioma).Neurofibromatosis 2: schwannoma, meningioma, ependymoma.Von Hippel–Lindau syndrome: hemangioblastoma, endolymphatic sac adenoma.Nevoid basal cell carcinoma syndrome, also known as Gorlin's syndrome: medulloblastoma.Tuberous sclerosis: subependymal giant cell astrocytoma (SEGA).Li–Fraumeni syndrome: glioma, medulloblastoma.Turcot's syndrome: glioma, medulloblastoma.Multiple endocrine neoplasia: pituitary adenoma.
Oral examinations
Published in Deepak Subedi, Marialena Gregoriades, En Hsun Choi, John T Murchison, Graham McKillop, A Complete Guide to the Final FRCR 2B, 2011
Deepak Subedi, Marialena Gregoriades, En Hsun Choi, John T Murchison, Graham McKillop
Subependymal giant-cell astrocytoma is seen mainly in patients with tuberous sclerosis. These tumours enhance on post-contrast images. The differential diagnoses of a third ventricular tumour include colloid cyst, giant-cell astrocytoma, central neurocytoma, metastasis, chordoid glioma and suprasellar extension of craniopharyngioma.
Long-term follow-up of adult patient with neurofibromatosis type 1 with retinal astrocytic hamartoma using spectral-domain optical coherence tomography: a review of the literature and a report of a case
Published in Ophthalmic Genetics, 2021
Solmaz Abdolrahimzadeh, Martina Formisano, Luca Scuderi, Siavash Rahimi
Relatively recent articles present a complete histopathological classification with the immunohistochemical profile of the tumours. The cases reported by Shields et al. (21) showed extensive necrosis and calcification and were composed of two types of cells. The morphology of type one cells (giant cells) resembled subependymal giant cell astrocytoma in TSC, while the morphology of type two cells showed spindle and hyperchromatic nuclei. On immunohistochemical examination, the giant cells showed immunostaining with neuronal marker neuron-specific enolase (NSE) but were negative or minimally positive for glial marker glial fibrillary acidic protein (GFAP). Conversely, the spindle cells were positive for both NSE and GFAP. Both types of cells showed immunoreactivity for S100. This particular immunoprofile suggests a hybrid tumour composed of glial and neural cells. The authors classified the cases as aggressive retinal astrocytoma.
Ablative brain surgery: an overview
Published in International Journal of Hyperthermia, 2019
Andrea Franzini, Shayan Moosa, Domenico Servello, Isabella Small, Francesco DiMeco, Zhiyuan Xu, William Jeffrey Elias, Angelo Franzini, Francesco Prada
Two recent retrospective studies, although limited in patient numbers, have demonstrated that LITT is a viable treatment option for recurrent meningiomas, particularly those deemed unresectable or harbored by patients whose comorbidities prevent an invasive open resection [162,163]. Preliminary successful data regarding LITT were reported for pediatric brain tumors, such as primitive neuroectodermal tumor [164] and subependymal giant cell astrocytoma [165]. Finally, LITT was proven to be a low-risk and safe surgical procedure for the ablation of radiographic lesions growing after SRS in patients with brain metastases (either recurrent tumor or radionecrosis – labeled as progressive in-field recurrence). A recent large multicenter prospective trial showed that LITT minimizes cognitive decline, preserves quality of life and functional status and permits the cessation of steroids in some of these patients [166]. Another study showed that progression-free survival and overall survival were similar between patients undergoing LITT or craniotomy for recurrent metastases or radionecrosis [167]. Finally, LITT was also considered as a first strategy in patients with metastases who are surgically ineligible for resection. The main complications of LITT in brain tumor cases were neurological deficits (13% transient and 3% permanent), seizures, hemorrhage (2.5%), edema, infection or technical issues (most commonly regarding the cooling mechanism) [7].
The comorbidities of epilepsy explained
Published in Expert Review of Neurotherapeutics, 2020
Mutual comorbidities represent a sort of simplified and straightforward version of the former, in fact in this group of conditions it is possible to identify a specific etiological factor shared by the epilepsy and the other condition and clearly leading to both. The tuberous sclerosis complex (TSC) gene mutation is a classic example. TSC1 mutation is the cause for tuberous sclerosis which is a multiorgan disease that may present with cardiac rhabdomyomas, subependymal giant cell astrocytoma, renal angiomyolipoma, pulmonary lymphangioleiomyomatosis, thyroid nodules, bone fibrous dysplasia, and dental problems. However, at the same time, up to 90% of patients with TSC have epilepsy. Epilepsy and type 1 diabetes in people with anti-GAD antibodies is another classical example.