DOCSLIB.ORG

Skull Base Tumors

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Skull Base Tumors 3601_e12_p300-319 2/15/02 4:46 PM Page 300 12 Skull Base Tumors MIKHAIL CHERNOV AND FRANCO DEMONTE Skull base tumors arise from the cranial base or reach Whereas location is the most important consider- it, either from an intracranial or extracranial origin. ation for surgical planning, the tumor’s biologic be- A diverse group, these tumors present unique man- havior dictates the need for, and order of, the vari- agement challenges because of their relative rarity, ous available therapies needed to optimize patient typically deep location, close proximity to critical neu- outcome. Some tumors, such as meningiomas and rovascular structures, and extension beyond classi- schwannomas, may require complete surgical exci- cally taught anatomic and specialty boundaries. Man- sion only to optimize patient outcome. Pathologies agement outcomes for skull base tumors are such as paranasal sinus carcinomas may, however, maximized when their treatment is approached in a require induction chemotherapy, surgical excision, multidisciplinary fashion, utilizing the knowledge and radiation therapy (RT) to achieve local control base of varied medical, surgical, and radiotherapeu- and possibly cure (Table 12–3). tic specialists. In general, the outcome of surgery for basal tu- mors depends on the type, size, and location of the neoplasm, patient’s age and general medical status, CLASSIFICATION and extent of preoperative neurologic disability (Lang et al., 1999). Large tumor size, encasement of major Skull base tumors may originate from the neurovascu- cerebral arteries, invasion of the cavernous sinus and lar structures of the base of the brain and the basal severe brain stem compression can necessitate in- meninges (e.g., meningioma, pituitary adenoma, complete tumor resection, whereas older age and low schwannoma, paraganglioma), the cranial base itself preoperative Karnofsky score have been associated (e.g., chordoma, chondrosarcoma), or the subcranial with increased risk of stroke and longer hospital stay structures of the head and neck (e.g., paranasal sinus (Holmes et al., 1995). carcinomas). A unified classification system does not exist for the plethora of pathologies, some quite rare, that may affect this area of the brain (Table 12–1). MENINGIOMA Classifications based on location are useful for clinicopathologic correlation due to the relatively Meningiomas (see Chapter 11) occur with an inci- constant constellation of signs and symptoms pro- dence of 2.6 per 100,000 persons per year and ac- duced by tumors located in specific regions of the count for 20% of all intracranial tumors. Forty per- skull base and due to the propensity for certain tu- cent of all meningiomas arise from the base of the mor pathologies to have a regional specificity (Table anterior, middle, or posterior fossa and are the most 12–2). Tumor location is also the prime determinant common skull base tumors. Sphenoid wing menin- of the surgical approach that is selected. giomas make up almost half of these tumors; tuber- 300 3601_e12_p300-319 2/15/02 4:46 PM Page 301 Table 12–1. Tumors of the Skull Base Site of Tumor Origin Tumor Pathology Basal neurovascular structures and meninges Meningioma Schwannoma Pituitary adenoma Craniopharyngioma Paraganglioma Hemangiopericytoma Cranial base Chordoma Chondrosarcoma Osteosarcoma Plasmacytoma Metastasis Subcranial with upward extension Sinonasal carcinomas Olfactory neuroblastoma Juvenile angiofibroma Nasopharyngeal carcinoma Adenoid cystic carcinoma Primary sarcomas Table 12–2. Classification of Skull-Base Tumors Based on Location Location Clinical Features Common Pathologies Anterior skull base Anosmia, frontal lobe dysfunction, Meningioma, olfactory neuroblastoma, increased intracranial pressure, nasal sinonasal malignancies obstruction, epistaxis, visual changes Middle skull base Central Pituitary hypo- or hyperfunction, optic Pituitary adenoma, meningioma, neuropathy (nerve and chiasm) craniopharyngioma, sphenoid sinus carcinoma Paracentral Optic neuropathy, sphenocavernous Meningioma, schwannoma, adenoid cystic syndrome carcinoma, nasopharyngeal carcinoma Lateral Proptosis, facial dysesthesia and pain, Meningioma, schwannoma, juvenile nasal trismus, epistaxis angiofibroma, adenoid cystic carcinoma, sarcoma Posterior skull base Cerebellopontine angle Hearing loss, facial numbness or weakness, Acoustic neuroma, meningioma, epidermoid, dysmetria, ataxia, lower cranial nerve trigeminal neuroma, cholesterol dysfunction, brain stem signs, increased granuloma intracranial pressure Clival Abducens palsy, bilateral cranial neuropathies, Chordoma, meningioma, paraganglioma, brain stem signs nasopharyngeal carcinoma, schwannoma, chondrosarcoma Jugular foramen Palsies of cranial nerves 9,10,11 (Vernet’s Paraganglioma, schwannoma, meningioma, syndrome), 9,10,11,12 (Collet-Sicard metastasis syndrome), 9,10,11,12, and sympathetics (Villaret’s syndrome) Foramen magnum Suboccipital neck pain (C2 dermatome), Meningioma, schwannoma, chordoma, ipsilateral dysesthesias, contralateral intramedullary tumor dissociated sensory loss, progressive weakness, wasting of intrinsic hand muscles 301 3601_e12_p300-319 2/15/02 4:46 PM Page 302 302 INTRACRANIAL EXTRA-AXIAL PRIMARY TUMORS Table 12–3. Classification of Skull-Base Tumors by Biologic Behavior Benign Meningioma, schwannoma, paraganglioma, pituitary adenoma, dermoid, epidermoid, juvenile angiofibroma, cholesterol granuloma, osteoma Low-grade malignancy Chordoma, chondrosarcoma, adenoid cystic carcinoma, desmoid, low-grade fibrosarcoma, olfactory neuroblastoma, low-grade sarcomas, hemangiopericytoma High-grade malignancy Carcinomas, high-grade sarcomas (e.g., rhabdomyosarcoma, Ewing’s sarcoma, osteogenic), lymphoma, metastases culum sella tumors and olfactory groove tumors com- surrounding peripheral nerves. Tumors may have prise the other half. Meningiomas of the posterior and small or large cystic components and can be moder- middle fossa are less common, with incidences of 8% ately vascular. The cellular components of schwan- and 4%, respectively. nomas are typically organized into densely packed hy- percellular areas of spindly cells (“Antoni type A”) with intervening hypocellular zones composed of PITUITARY ADENOMA loosely organized stellate cells (“Antoni type B”). The compact Antoni type A tissue often, but not invariably, In 2.6% to 15% of cases pituitary adenomas (see exhibits prominent nuclear palisading (Verocay bod- Chapter 8) may attain giant size (more than 4 to 5 ies). Cytologically, no differences are found between cm in any direction) and exhibit extensive invasion spontaneous and familial tumors; however, on histo- of the skull base and paranasal sinuses (Pia et al., logic examination approximately 40% of the NF2 neo- 1985; Majos et al., 1998). These are mainly en- plasms appear to have grapelike clusters that can in- docrinologically inactive tumors in the elderly and filtrate the fibers of the individual nerves. Growth prolactinomas in the young. Clinical and imaging fea- fraction varies from 0.36% to 3.15% (Lesser et al., tures of giant pituitary adenomas differ from tumors 1991). that are smaller in size. Diagnosis and Treatment SCHWANNOMA Vestibular Schwannomas Intracranial nerve sheath tumors represent only 4% Vestibular schwannomas represent nearly 6% of all to 8% of intracranial neoplasms with the most com- intracranial tumors. The tumors arise at the transi- mon being vestibular schwannomas, followed by tional zone between the central and peripheral myelin trigeminal nerve tumors. These neoplasms can arise, sheaths of the nerve. The majority of neoplasms orig- although infrequently, from other cranial nerves, both inate within the internal auditory canal; however, intra- and extracranially. Although schwannomas can more medially located tumors constitute 10% to 15% develop as an isolated disease process, most in- of cases. Whereas tumors in the more typical loca- tracranial nonvestibular tumors and 5% of vestibular tion compress the adjacent auditory nerve early in schwannomas are associated with neurofibromatosis their growth, the medial tumors may grow to a sig- type 2 (NF2). nificant size without causing hearing loss. Clinical fea- tures, as well as treatment strategy and prognosis, are greatly influenced by the size and extension of the Pathology and Pathogenesis tumor. Schwannomas are typically globoid, ovoid, or dumb- Unilateral hearing loss occurs in more than 90% bell-shaped, well-circumscribed tumors. They arise of patients and is often accompanied by tinnitus. from Schwann cells, which form the myelin sheaths Cochlear nerve dysfunction usually is the most long- 3601_e12_p300-319 2/15/02 4:46 PM Page 303 Skull Base Tumors 303 standing symptom followed by vestibular distur- morbidity and mortality, and, when possible, preser- bances, which may have an intermittent course. Im- vation of hearing. balance is encountered in 50% of cases and vertigo The choice of surgical approach needs to take into in 19%. Trigeminal nerve signs are the third most account the size and the amount of extension of the common symptom, with 50% of patients reporting fa- tumor into the internal auditory canal (IAC) as well cial numbness (Pitts et al., 1996). Larger tumors can as the patient’s hearing ability and experience of the cause facial weakness, signs of brain stem compres- surgical team. Every attempt should be made to pre- sion, and obstructive hydrocephalus. The average du- serve useful hearing, although it must be realized that ration of symptoms is 3.7 years (Matthies
Load more

Recommended publications
  • Neurofibromatosis Type 2 (NF2)
    International Journal of Molecular Sciences Review Neurofibromatosis Type 2 (NF2) and the Implications for Vestibular Schwannoma and Meningioma Pathogenesis Suha Bachir 1,† , Sanjit Shah 2,† , Scott Shapiro 3,†, Abigail Koehler 4, Abdelkader Mahammedi 5 , Ravi N. Samy 3, Mario Zuccarello 2, Elizabeth Schorry 1 and Soma Sengupta 4,* 1 Department of Genetics, Cincinnati Children’s Hospital, Cincinnati, OH 45229, USA; [email protected] (S.B.); [email protected] (E.S.) 2 Department of Neurosurgery, University of Cincinnati, Cincinnati, OH 45267, USA; [email protected] (S.S.); [email protected] (M.Z.) 3 Department of Otolaryngology, University of Cincinnati, Cincinnati, OH 45267, USA; [email protected] (S.S.); [email protected] (R.N.S.) 4 Department of Neurology, University of Cincinnati, Cincinnati, OH 45267, USA; [email protected] 5 Department of Radiology, University of Cincinnati, Cincinnati, OH 45267, USA; [email protected] * Correspondence: [email protected] † These authors contributed equally. Abstract: Patients diagnosed with neurofibromatosis type 2 (NF2) are extremely likely to develop meningiomas, in addition to vestibular schwannomas. Meningiomas are a common primary brain tumor; many NF2 patients suffer from multiple meningiomas. In NF2, patients have mutations in the NF2 gene, specifically with loss of function in a tumor-suppressor protein that has a number of synonymous names, including: Merlin, Neurofibromin 2, and schwannomin. Merlin is a 70 kDa protein that has 10 different isoforms. The Hippo Tumor Suppressor pathway is regulated upstream by Merlin. This pathway is critical in regulating cell proliferation and apoptosis, characteristics that are important for tumor progression.
    [Show full text]
  • Risk Factors for Gliomas and Meningiomas in Males in Los Angeles County1
    [CANCER RESEARCH 49, 6137-6143. November 1, 1989] Risk Factors for Gliomas and Meningiomas in Males in Los Angeles County1 Susan Preston-Martin,2 Wendy Mack, and Brian E. Henderson Department of Preventive Medicine, University of Southern California School of Medicine, Los Angeles, California 90033 ABSTRACT views with proxy respondents, we were unable to include a large proportion of otherwise eligible cases because they were deceased or Detailed job histories and information about other suspected risk were too ill or impaired to participate in an interview. The Los Angeles factors were obtained during interviews with 272 men aged 25-69 with a County Cancer Surveillance Program identified the cases (26). All primary brain tumor first diagnosed during 1980-1984 and with 272 diagnoses had been microscopically confirmed. individually matched neighbor controls. Separate analyses were con A total of 478 patients were identified. The hospital and attending ducted for the 202 glioma pairs and the 70 meningioma pairs. Meningi- physician granted us permission to contact 396 (83%) patients. We oma, but not glioma, was related to having a serious head injury 20 or were unable to locate 22 patients, 38 chose not to participate, and 60 more years before diagnosis (odds ratio (OR) = 2.3; 95% confidence were aphasie or too ill to complete the interview. We interviewed 277 interval (CI) = 1.1-5.4), and a clear dose-response effect was observed patients (74% of the 374 patients contacted about the study or 58% of relating meningioma risk to number of serious head injuries (/' for trend the initial 478 patients).
    [Show full text]
  • Information About Mosaic Neurofibromatosis Type 2 (NF2)
    Information about mosaic Neurofibromatosis type 2 (NF2) NF2 occurs because of a mutation (change) in the NF2 gene. When this change is present at the time of conception the changed gene will be present in all the cells of the baby. When this mutation occurs later in the development of the forming embryo, the baby will go on to have a mix of cells: some with the “normal” genetic information and some with the changed information. This mix of cells is called mosaicism. Approximately half the people who have a diagnosis of NF2 have inherited the misprinted NF2 gene change from their mother or father who will also have NF2. They will have that misprinted gene in all the cells of their body. When they have their children, there will be a 1 in 2 chance of passing on NF2 to each child they have. However about half of people with NF2 are the first person in the family to be affected. They have no family history and have not inherited the condition from a parent. When doctors studied this group of patients more closely they noticed certain characteristics. Significantly they observed that fewer children had inherited NF2 than expected some people in this group had relatively mild NF2 NF2 tumours in some patients tended to grow on one side of their body rather than both sides that when a blood sample was tested to identify the NF2 gene, the gene change could not be found in 30-40% of people This lead researchers to conclude that this group of people were most likely to be mosaic for NF2 i.e.
    [Show full text]
  • Simultaneous Neurofibroma and Schwannoma of the Sciatic Nerve
    Simultaneous Neurofibroma and Schwannoma of the Sciatic Nerve 1 4 1 1 2 3 1 S. A. Sintzoff, Jr.,I.5 W . 0. Bank, · P. A. Gevenois, C. Matos, J. Noterman, J. Flament-Durand, and J. Struyven Summary: The authors report a case of simultaneously occur­ MR imaging was performed on a 0.5-T system (Gyro­ ring neurofibroma and schwannoma of the sciatic nerve and scan T5, Philips Medical Systems, Eindhoven, The Neth­ discuss the complementary aspects of MR and OS. The Schwan­ erlands) using a wrap-around knee surface coil in order to norna was well-defined and showed distal enhancement on better define the relationships between the tumors and the sonographic evaluation, whereas the neurofibroma was ill-de­ nerve. Each tumor was isointense to the normal nerve on fined; both tumors were hypoechoic. Tl- and T2-weighted MR T1-weighted images and hyperintense to it on proton Images revealed similar signal characteristics of the two tumors, density and T2-weighted images (Fig. 2A-2C). After intra­ but Intense enhancement following administration of gadolin­ venous gadolinium-DTPA injection, the distal mass showed ium-DTPA distinguished the schwannoma from the neurofi­ intense enhancement, conserving a thin hypointense border broma. (Fig. 2D). Physical and neurologic examination, MR of the central nervous system and skeletal radiographs failed to Index terms: Nerves, sciatic; Neuroma; Schwannoma demonstrate any additional lesions, permitting the reason­ able exclusion of neurofibromatosis types 1 and 2. Schwannomas and neurofibromas are com­ Surgical exposure demonstrated the two tumors on the external popliteal nerve (Fig. 3). The distal tumor could be (1, mon peripheral nerve neoplasms 2).
    [Show full text]
  • Central Nervous System Tumors General ~1% of Tumors in Adults, but ~25% of Malignancies in Children (Only 2Nd to Leukemia)
    Last updated: 3/4/2021 Prepared by Kurt Schaberg Central Nervous System Tumors General ~1% of tumors in adults, but ~25% of malignancies in children (only 2nd to leukemia). Significant increase in incidence in primary brain tumors in elderly. Metastases to the brain far outnumber primary CNS tumors→ multiple cerebral tumors. One can develop a very good DDX by just location, age, and imaging. Differential Diagnosis by clinical information: Location Pediatric/Young Adult Older Adult Cerebral/ Ganglioglioma, DNET, PXA, Glioblastoma Multiforme (GBM) Supratentorial Ependymoma, AT/RT Infiltrating Astrocytoma (grades II-III), CNS Embryonal Neoplasms Oligodendroglioma, Metastases, Lymphoma, Infection Cerebellar/ PA, Medulloblastoma, Ependymoma, Metastases, Hemangioblastoma, Infratentorial/ Choroid plexus papilloma, AT/RT Choroid plexus papilloma, Subependymoma Fourth ventricle Brainstem PA, DMG Astrocytoma, Glioblastoma, DMG, Metastases Spinal cord Ependymoma, PA, DMG, MPE, Drop Ependymoma, Astrocytoma, DMG, MPE (filum), (intramedullary) metastases Paraganglioma (filum), Spinal cord Meningioma, Schwannoma, Schwannoma, Meningioma, (extramedullary) Metastases, Melanocytoma/melanoma Melanocytoma/melanoma, MPNST Spinal cord Bone tumor, Meningioma, Abscess, Herniated disk, Lymphoma, Abscess, (extradural) Vascular malformation, Metastases, Extra-axial/Dural/ Leukemia/lymphoma, Ewing Sarcoma, Meningioma, SFT, Metastases, Lymphoma, Leptomeningeal Rhabdomyosarcoma, Disseminated medulloblastoma, DLGNT, Sellar/infundibular Pituitary adenoma, Pituitary adenoma,
    [Show full text]
  • Pineal Region Tumors: Computed Tomographic-Pathologic Spectrum
    415 Pineal Region Tumors: Computed Tomographic-Pathologic Spectrum Nancy N. Futrell' While several computed tomographic (CT) studies of posterior third ventricular Anne G. Osborn' neoplasms have included descriptions of pineal tumors, few reports have concentrated Bruce D. Cheson 2 on these uncommon lesions. Some authors have asserted that the CT appearance of many pineal tumors is virtually pathognomonic. A series of nine biopsy-proved pineal gland and eight other presumed tumors is presented that illustrates their remarkable heterogeneity in both histopathologic and CT appearance. These tumors included germinomas, teratocarcinomas, hamartomas, and other varieties. They had variable margination, attenuation, calcification, and suprasellar extension. Germinomas have the best response to radiation therapy. Biopsy of pineal region tumors is now feasible and is recommended for treatment planning. Tumors of the pineal region account for less th an 2% of all intracrani al neoplasms [1]. While several reports of computed tomography (CT) of third ventricular neoplasms have in cluded an occasi onal pineal tumor [2 , 3], few have focused on the radiographic spectrum of th ese uncommon lesions [4]. Some authors have asserted that the CT appearance of many pineal tumors is virtuall y pathognomonic [5]. We studied a series of nine biopsy-proven pineal gland tumors that demonstrated remarkable heterogeneity in both histopath ologic and CT appearance. Materials and Methods A total of 17 pineal gland tumors were detected in 15,000 consecutive CT scans. Four patients were female and 13 were male. Mean age for the fe males was 27 years; for the males, 15 years. Initial symptoms ranged from headache, nausea, and vomiting, to Parinaud syndrome, vi sual field defects, diabetes insipidus, and hypopituitari sm (table 1).
    [Show full text]
  • Synchronous Morphologically Distinct Craniopharyngioma and Pituitary
    orders & is T D h e n r Bhatoe et al., Brain Disord Ther 2016, 5:1 i a a p r y B Brain Disorders & Therapy DOI: 10.4172/2168-975X.1000207 ISSN: 2168-975X Case Report Open Access Synchronous Morphologically Distinct Craniopharyngioma and Pituitary Adenoma: A Rare Collision Entity Harjinder S Bhatoe*, Prabal Deb and Sudip Kumar Sengupta Institute of Neuroscience, Max Super Speciality Hospital, New Delhi, India Abstract While pituitary tumors and craniopharyngiomas share a common lineage, their simultaneous occurrence is distinctly rare. We present one such patient, an adult male with two distinct tumors, that were excised by two different approaches. Relevant literature is briefly reviewed. Keywords: Brain tumor; Collision tumor; Craniopharyngioma; Pituitary tumor Introduction Simultaneous occurrence of morphological distinct, discreet intracranial tumors sharing the same cell lineage is a rarity. Pituitary tumors and craniopharyngiomas share a common lineage. Simultaneous occurrence of these two tumors in the same patient is rare and has been reported only nine times so far (Table 1). While pituitary tumours are centred in the sella, craniopharyngiomas may occur anywhere from the pituitary gland to the third ventricle. Association of intra-third ventricular craniopharyngioma and growth hormone- Figure 1: Contrast MRI (T1-weighted sagittal) showing intra-third-ventricular secreting pituitary macroadenoma as two distinct, unconnected tumors craniopharyngioma and pituitary adenoma. occurring synchronously has not been reported so far. Case Report A 35-year-old male was admitted with six-month-history of generalized headache, gradual loss of vision and intermittent generalized tonic clonic seizures. Clinically, he had acromegaly and optic atrophy with no perception of light.
    [Show full text]
  • Brain Tumors in NF1 Children: Influence on Neurocognitive and Behavioral Outcome
    cancers Article Brain Tumors in NF1 Children: Influence on Neurocognitive and Behavioral Outcome Matilde Taddei 1 , Alessandra Erbetta 2 , Silvia Esposito 1, Veronica Saletti 1, 1, , 1, Sara Bulgheroni * y and Daria Riva y 1 Developmental Neurology Unit, Fondazione IRCCS Istituto Neurologico Carlo Besta, Via Celoria 11, 20133 Milan, Italy; [email protected] (M.T.); [email protected] (S.E.); [email protected] (V.S.); [email protected] (D.R.) 2 Neuroradiology Unit, Fondazione IRCCS Istituto Neurologico Carlo Besta, Via Celoria 11, 20133 Milan, Italy; [email protected] * Correspondence: [email protected]; Tel.: +39-02-2394-2215; Fax: +39-02-2394-2176 These authors contributed equally to this work. y Received: 30 September 2019; Accepted: 5 November 2019; Published: 11 November 2019 Abstract: Neurofibromatosis type-1 (NF1) is a monogenic tumor-predisposition syndrome creating a wide variety of cognitive and behavioral abnormalities, such as decrease in cognitive functioning, deficits in visuospatial processing, attention, and social functioning. NF1 patients are at risk to develop neurofibromas and other tumors, such as optic pathway gliomas and other tumors of the central nervous system. Few studies have investigated the impact of an additional diagnosis of brain tumor on the cognitive outcome of children with NF1, showing unclear results and without controlling by the effect of surgery, radio- or chemotherapy. In the present mono-institutional study, we compared the behavioral and cognitive outcomes of 26 children with neurofibromatosis alone (NF1) with two age-matched groups of 26 children diagnosed with NF1 and untreated optic pathway glioma (NF1 + OPG) and 19 children with NF1 and untreated other central nervous system tumors (NF1 + CT).
    [Show full text]
  • Vernet Syndrome by Varicella-Zoster Virus Yil Ryun Jo, MD1, Chin Wook Chung, MD2, Jung Soo Lee, MD2, Hye Jeong Park, MD1
    Case Report Ann Rehabil Med 2013;37(3):449-452 pISSN: 2234-0645 • eISSN: 2234-0653 http://dx.doi.org/10.5535/arm.2013.37.3.449 Annals of Rehabilitation Medicine Vernet Syndrome by Varicella-Zoster Virus Yil Ryun Jo, MD1, Chin Wook Chung, MD2, Jung Soo Lee, MD2, Hye Jeong Park, MD1 1Department of Rehabilitation Medicine, Seoul St. Mary’s Hospital, The Catholic University of Korea College of Medicine, Seoul; 2Department of Rehabilitation Medicine, Uijeongbu St. Mary’s Hospital, The Catholic University of Korea College of Medicine, Uijeongbu, Korea Vernet syndrome involves the IX, X, and XI cranial nerves and is most often attributable to malignancy, aneurysm or skull base fracture. Although there have been several reports on Vernet’s syndrome caused by fracture and inflammation, cases related to varicella-zoster virus are rare and have not yet been reported in South Korea. A 32-year-old man, who complained of left ear pain, hoarse voice and swallowing difficulty for 5 days, presented at the emergency room. He showed vesicular skin lesions on the left auricle. On neurologic examination, his uvula was deviated to the right side, and weakness was detected in his left shoulder. Left vocal cord palsy was noted on laryngoscopy. Antibody levels to varicella-zoster virus were elevated in the serum. Electrodiagnostic studies showed findings compatible with left spinal accessory neuropathy. Based on these findings, he was diagnosed with Vernet syndrome, involving left cranial nerves, attributable to varicella-zoster virus. Keywords Varicella-zoster virus, Cranial nerves INTRODUCTION Hunt [2] surmised that the gasserian, geniculate, petrous, accessory, jugular, plexiform, and second and third cer- Vernet syndrome refers to paralysis of the IX, X, and XI vical dorsal root ganglia formed a chain by which inflam- cranial nerves traversing the jugular foramen.
    [Show full text]
  • Surgical Results of the Resection of Spinal Meningioma with the Inner Layer of Dura More Than 10 Years After Surgery
    www.nature.com/scientificreports OPEN Surgical results of the resection of spinal meningioma with the inner layer of dura more than 10 years after surgery Hiroyuki Tominaga1*, Ichiro Kawamura1, Kosei Ijiri2, Kazunori Yone1 & Noboru Taniguchi1 Most spinal meningiomas arise from the thoracic dura in middle-aged and elderly women. Simpson grade 1 resection is recommended to avoid recurrence. For ventral and ventrolateral tumors, reconstruction after total dural resection is difcult, and spinal fuid leakage is likely. To overcome this concern, Saito et al. developed the technique of resecting the tumor with the inner dural layer, preserving the outer dural layer. Although meningioma rarely recurs, the recurrence period is approximately 8 years postoperatively. No studies have evaluated long-term (> 10-year) outcomes of the Saito method. Here, we report 10 cases of the Saito method with > 10-year follow-up and compare outcomes with those of other standard approaches. Twenty-nine pathology-confrmed meningioma patients underwent surgery in our department, ten with the Saito method. We investigated resection method (dura mater treatment), pathological type, and recurrence and compared pre- and postoperative clinical fndings. The median follow-up was 132 months. Recurrence occurred after Simpson grades 3 and 4 resection. Simpson grades 1, 2, and the Saito method resulted in no recurrence. Neurological symptoms improved in all patients at fnal follow-up. This is the frst report of long-term outcomes of the Saito method. The method achieved good neurological improvement with no recurrence in > 10-year follow-up. Spinal cord meningioma is an intradural, extramedullary tumor that occurs most frequently at the thoracic level in middle-aged and elderly women.
    [Show full text]
  • Clinical Radiation Oncology Review
    Clinical Radiation Oncology Review Daniel M. Trifiletti University of Virginia Disclaimer: The following is meant to serve as a brief review of information in preparation for board examinations in Radiation Oncology and allow for an open-access, printable, updatable resource for trainees. Recommendations are briefly summarized, vary by institution, and there may be errors. NCCN guidelines are taken from 2014 and may be out-dated. This should be taken into consideration when reading. 1 Table of Contents 1) Pediatrics 6) Gastrointestinal a) Rhabdomyosarcoma a) Esophageal Cancer b) Ewings Sarcoma b) Gastric Cancer c) Wilms Tumor c) Pancreatic Cancer d) Neuroblastoma d) Hepatocellular Carcinoma e) Retinoblastoma e) Colorectal cancer f) Medulloblastoma f) Anal Cancer g) Epndymoma h) Germ cell, Non-Germ cell tumors, Pineal tumors 7) Genitourinary i) Craniopharyngioma a) Prostate Cancer j) Brainstem Glioma i) Low Risk Prostate Cancer & Brachytherapy ii) Intermediate/High Risk Prostate Cancer 2) Central Nervous System iii) Adjuvant/Salvage & Metastatic Prostate Cancer a) Low Grade Glioma b) Bladder Cancer b) High Grade Glioma c) Renal Cell Cancer c) Primary CNS lymphoma d) Urethral Cancer d) Meningioma e) Testicular Cancer e) Pituitary Tumor f) Penile Cancer 3) Head and Neck 8) Gynecologic a) Ocular Melanoma a) Cervical Cancer b) Nasopharyngeal Cancer b) Endometrial Cancer c) Paranasal Sinus Cancer c) Uterine Sarcoma d) Oral Cavity Cancer d) Vulvar Cancer e) Oropharyngeal Cancer e) Vaginal Cancer f) Salivary Gland Cancer f) Ovarian Cancer & Fallopian
    [Show full text]
  • Current and Future Role of Tyrosine Kinases Inhibition in Thyroid Cancer: from Biology to Therapy
    International Journal of Molecular Sciences Review Current and Future Role of Tyrosine Kinases Inhibition in Thyroid Cancer: From Biology to Therapy 1, 1, 1,2,3, 3,4 María San Román Gil y, Javier Pozas y, Javier Molina-Cerrillo * , Joaquín Gómez , Héctor Pian 3,5, Miguel Pozas 1, Alfredo Carrato 1,2,3 , Enrique Grande 6 and Teresa Alonso-Gordoa 1,2,3 1 Medical Oncology Department, Hospital Universitario Ramón y Cajal, 28034 Madrid, Spain; [email protected] (M.S.R.G.); [email protected] (J.P.); [email protected] (M.P.); [email protected] (A.C.); [email protected] (T.A.-G.) 2 The Ramon y Cajal Health Research Institute (IRYCIS), CIBERONC, 28034 Madrid, Spain 3 Medicine School, Alcalá University, 28805 Madrid, Spain; [email protected] (J.G.); [email protected] (H.P.) 4 General Surgery Department, Hospital Universitario Ramón y Cajal, 28034 Madrid, Spain 5 Pathology Department, Hospital Universitario Ramón y Cajal, 28034 Madrid, Spain 6 Medical Oncology Department, MD Anderson Cancer Center, 28033 Madrid, Spain; [email protected] * Correspondence: [email protected] These authors have contributed equally to this work. y Received: 30 June 2020; Accepted: 10 July 2020; Published: 13 July 2020 Abstract: Thyroid cancer represents a heterogenous disease whose incidence has increased in the last decades. Although three main different subtypes have been described, molecular characterization is progressively being included in the diagnostic and therapeutic algorithm of these patients. In fact, thyroid cancer is a landmark in the oncological approach to solid tumors as it harbors key genetic alterations driving tumor progression that have been demonstrated to be potential actionable targets.
    [Show full text]