Meningioma asintomático

Meningioma asintomático

El meningioma intracraneal asintomático es un tumor benigno; sin embargo, casi dos tercios de los pacientes experimentan crecimiento tumoral y un tercio de los pacientes no tratados finalmente requieren intervención neuroquirúrgica 1).

En la serie de Jadid et al., el crecimiento tumoral a largo plazo de los meningiomas asintomáticos detectados incidentalmente parece ser mucho más alto de lo esperado. Esta información debe tenerse en cuenta cuando se habla de cirugía, ya que la indicación para la cirugía puede ser más fuerte que la mencionada anteriormente, especialmente para pacientes más jóvenes con tumores que se pueden abordar con un bajo riesgo 2).

Para Yoneoka et al., el seguimiento clínico-radiológico es especialmente aconsejable en pacientes jóvenes y con un tumor grande 3).

Para el meningioma en el anciano asintomático, Niiro et al., recomienda realizar un seguimiento clínico y de imágen. Las características de imagen mencionadas en su artículo pueden contribuir a la predicción del crecimiento tumoral 4).

Hashimoto et al., observaron que el meningioma de la base de cráneo incidental no tiende a crecer, lo que es diferente de los tumores que no son de base del cráneo. Incluso cuando el meningioma de la base de cráneo crece, la tasa de crecimiento es significativamente menor que la de los tumores que no son de la base del cráneo. La misma conclusión con respecto al comportamiento biológico se confirmó en casos sintomáticos basados ​​en análisis MIB-1. Estos hallazgos pueden afectar la comprensión de la historia natural del meningioma intracraneal incidental, así como las estrategias para el tratamiento y tratamiento del meningioma de la base de cráneo y los meningiomas sintomáticos 5).

En el estudio de Karatsu se realizó un seguimiento durante más de un año a 63 pacientes con meningioma asintomático, observando crecimiento en la tercera parte de los mismos. Los que muestran crecimiento son hiperintensos en las imágenes de T2 de resonancia magnética con mayor frecuencia que los estacionarios, mientras que éstos son isointensos o hipointensos y están calcificados en una clara mayor proporción. No se observó diferencia significativa en la edad de los pacientes en función del crecimiento del tumor. La menor tendencia al crecimiento de los meningiomas calcificados también ha sido observada por otros autores

En una serie de 45 pacientes con meningioma asintomático, Olivero et al comprobaron crecimiento únicamente en el 22%, a una velocidad lenta variable, en torno a 0’24 cm de diámetro por año. También se ha observado que los meningiomas asintomáticos se localizan con mayor frecuencia en el hemisferio cerebral derecho. Como es obvio, cuando se decide no intervenir se debe realizar un seguimiento clínico y neurorradiológico del paciente 6).

1)

Kim KH, Kang SJ, Choi JW, Kong DS, Seol HJ, Nam DH, Lee JI. Clinical and radiological outcomes of proactive Gamma Knife surgery for asymptomatic meningiomas compared with the natural course without intervention. J Neurosurg. 2018 May 18:1-10. doi: 10.3171/2017.12.JNS171943. [Epub ahead of print] PubMed PMID: 29775154.
2)

Jadid KD, Feychting M, Höijer J, Hylin S, Kihlström L, Mathiesen T. Long-term follow-up of incidentally discovered meningiomas. Acta Neurochir (Wien). 2015 Feb;157(2):225-30. doi: 10.1007/s00701-014-2306-3. Epub 2014 Dec 14. PubMed PMID: 25503298.
3)

Yoneoka Y, Fujii Y, Tanaka R. Growth of incidental meningiomas. Acta Neurochir (Wien). 2000;142(5):507-11. PubMed PMID: 10898357.
4)

Niiro M, Yatsushiro K, Nakamura K, Kawahara Y, Kuratsu J. Historia natural de pacientes ancianos con meningiomas asintomáticos. J Neurol Neurosurg Psychiatry. 2000 ene; 68 (1): 25-8. PubMed PMID: 10601396; PubMed Central PMCID: PMC1760589.
5)

Hashimoto N, Rabo CS, Okita Y, Kinoshita M, Kagawa N, Fujimoto Y, Morii E, Kishima H, Maruno M, Kato A, Yoshimine T. Slower growth of skull base meningiomas compared with non-skull base meningiomas based on volumetric and biological studies. J Neurosurg. 2012 Mar;116(3):574-80. doi: 10.3171/2011.11.JNS11999. Epub 2011 Dec 16. PubMed PMID: 22175721.

Selenio y glioma

Selenio y glioma

La administración de selenio es importante ya que los compuestos de selenio pueden afectar el microambiente tumoral y neoangiogénesis en el glioma maligno por inducción de apoptosis y alteración de la expresión de la metaloproteinasa de matriz.

En 1990, Philipov y Tzatchev agregaron tabletas de selenio a la dieta de 15 pacientes con tumores cerebrales malignos. En doce pacientes con glioblastoma multiforme este tratamiento no prolongó la supervivencia postoperatoria 1).


En la publicación de Yakubov et al. sobre el selenio, los resultados se centran en las propiedades antitóxicas y preventivas en cáncer y su implicación en las terapias multimodales actuales, que incluyen temozolomida (Temodal),ciclofosfamida (Endoxan) y cisplatino (DDP, Platiblastin y Platinol).

Arroja luz sobre los efectos secundarios no deseados en quimioterapia y los desarrollos de nuevos agentes quimioterapéuticos combinatorios con compuestos de selenio. Descubrieron que los compuestos de selenio y selenio tienen perfiles de doble acción con efectos directos contra el cáncer e intensificador de la quimioterapia, así como con agentes neuroprotectores y citoprotectores 2).


La Tiorredoxina reductasa (TrxR) como antioxidante que contiene selenio juega un papel clave en la regulación del estado redox intracelular.

ver Selenocisteína.


En un estudio de casos y controles en gliomas, Peeri et al., examinaron las asociaciones de selenio en uñas de los pies y variantes genéticas de la selenoenzima con el riesgo de glioma y la supervivencia del paciente. Se estudiaron un total de 423 variantes genéticas en 29 genes candidatos en la vía selenoenzimática en 1547 casos de glioma y 1014 controles sanos. Las asociaciones genéticas también se examinaron en la cohorte de la UK Biobank compuesta por 313,868 personas con 322 casos de glioma. El selenio de la uña del pie se midió en una subcohorte de 300 casos de glioma y 300 controles de la misma edad del estudio de casos y controles.

Ninguna de las 423 variantes estudiadas se asoció consistentemente con el riesgo de glioma en los estudios de casos y controles y de cohortes. Además, el selenio de la uña del pie en el estudio de casos y controles no tuvo una asociación significativa con el riesgo de glioma (tendencia p = 0,70) o la supervivencia del paciente entre 254 pacientes con tumores de alto grado (tendencia p = 0,70).

El presente estudio no ofrece respaldo para la hipótesis de que el selenio desempeña un papel en la aparición del glioma o en el resultado del paciente 3).

1)

Philipov P, Tzatchev K. Selenium in the treatment of patients with brain gliomas. A pilot study. Zentralbl Neurochir. 1990;51(3):145-6. PubMed PMID: 1965466.
2)

Yakubov E, Buchfelder M, Eyüpoglu IY, Savaskan NE. Selenium action in neuro-oncology. Biol Trace Elem Res. 2014 Dec;161(3):246-54. doi: 10.1007/s12011-014-0111-8. Epub 2014 Aug 28. Review. PubMed PMID: 25164034.
3)

Peeri NC, Creed JH, Anic GM, Thompson RC, Olson JJ, LaRocca RV, Chowdhary SA, Brockman JD, Gerke TA, Nabors LB, Egan KM. Toenail selenium, genetic variation in selenoenzymes and risk and outcome in glioma. Cancer Epidemiol. 2018 May 16;55:45-51. doi: 10.1016/j.canep.2018.05.002. [Epub ahead of print] PubMed PMID: 29777993.

Book: Diagnostic Surgical Neuropathology by Location

Diagnostic Surgical Neuropathology by Location
By Kenneth B. Fallon

Diagnostic Surgical Neuropathology by Location

Price: $199.95

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Diagnostic Surgical Neuropathology by Location, is a practical guide for all pathologists in their initial, real-time encounters with brain of spinal cord biopsies for the immediate rendering of an intraoperative diagnosis based on the squash preparations of frozen section. The book is organized with a heavy emphasis on neuroanatomic to neuropathologic relationships best defined as a given lesion’s location with regard to its contiguous macroscopic and microscopic environments. The demonstration of the lesion’s macroscopic environment would include corresponding radiographic images, diagrams, and photographs of applicable autopsy teaching specimens for comparison; the microscopic environment would be illustrated by photomicrographs expressly composed in ways to show lesions in relation to contiguous unaffected, non-diseased tissue. The chapters progress from the cranial-to-caudal segments of the neuraxis from brain to spinal cord, respectively. The topics to be included in this book consist of all lesions likely to be encountered in the course of intraoperative neuropathologic consultation; this would encompass both primary and metastatic (secondary) forms of CNS neoplasia, non-neoplastic CNS lesions (for example, demyelinative processes), and CNS infections.

* Introduces neuropathology via neuroanatomic context instead of type of tissue
* The focus on location supports better understanding of the neuropathologic study
* Introduces the benefits of squash preparations for intraoperative assessment of neuropathology specimens


Product Details

  • Original language: English
  • Binding: Hardcover
  • 656 pages

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Practical Surgical Neuropathology: A Diagnostic Approach: A Volume in the Pattern Recognition Series, 2e 2nd Edition

Neuropathology: A Volume in the Series: Foundations in Diagnostic Pathology, 2eNov 30, 2011

Diagnostic Pathology: Neuropathology, 2eFeb 24, 2016

Developmental Neuropathology

Escourolle & Poirier’s Manual of Basic Neuropathology

Neuropathology: A Reference Text of CNS Pathology, 3e

Greenfield’s Neuropathology, Ninth Edition – Two Volume Set

MCM6

MCM6

Minichromosome maintenance proteins (MCMs) play an essential role in DNA replication and other cellular activities.

The long term risk of tumor recurrence is higher in adamantine epithelioma (AE) than squamous papillary tumor (SP) and it is associated with MCM6 and DNA topoisomerase II alpha expression 1).

MCM6 protein expression in craniopharyngiomas are related to the prognosis of tumor and thus may be useful in predicting the risk of tumor relapse 2).

In a study, Cai et al., analyzed the relationship between MCM mRNA expression and clinical parameters in 325 gliomas, and found that MCM6 presented high expression and was associated with poor survival. Immunohistochemistry analysis of an independent dataset of 423 glioma tissues confirmed the overexpression of MCM6 protein, especially in glioblastomas (GBMs) with shorter overall survival (OS). Importantly, a combination of MCM6 overexpression with IDH1 mutation further improved the prediction of the prognosis of GBMs. Patients with IDH1 mutation and low MCM6 expression exhibited the longest survival, whereas those with high MCM6 expression and wild-type IDH1 showed the shortest. Collectively, the observation indicates that MCM6 is a biomarker for predicting poor prognosis of the patients with glioma 3).

1)

Xu J, Zhang S, You C, Huang S, Cai B, Wang X. Expression of human MCM6 and DNA Topo II alpha in craniopharyngiomas and its correlation with recurrence of the tumor. J Neurooncol. 2007 Jun;83(2):183-9. Epub 2007 Apr 5. PubMed PMID: 17410335.
2)

Xu JG, You C, Wang XJ, Shuai KG, Wang XS. [Expression of minichromosome maintenance protein 6 in craniopharyngioma and its correlation with prognosis]. Sichuan Da Xue Xue Bao Yi Xue Ban. 2007 Jan;38(1):64-7. Chinese. PubMed PMID: 17294730.
3)

Cai HQ, Cheng ZJ, Zhang HP, Wang PF, Zhang Y, Hao JJ, Wang MR, Wan JH. Overexpression of MCM6 predicts poor survival in patients with glioma. Hum Pathol. 2018 May 9. pii: S0046-8177(18)30154-0. doi: 10.1016/j.humpath.2018.04.024. [Epub ahead of print] PubMed PMID: 29753008.

Invasive meningioma

Invasive meningioma

Invasive intracranial meningioma is a common neoplasm of central nervous system, which can infiltrate adjacent tissues (dura materarachnoid membrane, vascular space and skull) without atypical hyperplasia 1) 2)

In general, the pathological nature of meningioma determines its association with the brain parenchyma, which is that benign meningioma is usually compressive to the brain parenchyma due to its expansive growth, and malignant meningioma is invasive into the neighboring brain parenchyma due to its intrusive growth 3) 4). However, clinical observations have indicated that there is a sub-group of benign meningioma displaying a malignant growth pattern, that is, invasion into the neighboring brain tissue 5) 6) 7) 8) 9).

According to the experience gained in 19 cases, it was observed that there were certain features shared by these invasive benign meningiomas. The peak age of onset was ~50 years; the main manifestation was mild focal neurological deficits, which included dysphasia, and decreased sensation and muscle power of the contralateral limb. The MRI findings usually had the following characteristics: The lesions were located at the convexity of the cerebral hemisphere involving the central lobe, with an extensive base at the dural matter and evident ‘tail sign’; there was a minimal boundary between the tumor and the neighboring brain cortex; finally, and probably most importantly, the apex of tumor often enwrapped the normal brain tissue and associated vessels.

Due to the malignant growth, it was challenging to completely remove this benign meningioma while ensuring that neurological function remained intact. Resection of the earliest 4 cases was performed according to the traditional extra-capsular strategy, which was to coagulate and divide the tumor base first, and then continue the dissection along the interface between the tumor and brain parenchyma. This approach inevitably damaged the vessels transiting from and into the tumor. The observation that all 4 cases had permanent neurological deficits confirmed the disadvantage associated with this surgical strategy. Following careful analysis of the surgical outcomes, the resection method was modified by combining intra- and extra-capsular approaches. The first step was the same as the classical method, which was to coagulate and divide the tumor base. Afterwards, intra-capsular extirpation of the central part of the tumor was performed. Care was taken not to damage the transit vessels when approaching the tumor-brain interface. The enucleation of the central part of the tumor created a working space, which greatly facilitated the identification of the transit vessels. After this, the tumor was separated from brain parenchyma along the sub-arachnoid membrane. The use of a sponge during this dissection process was important. Finally, it was critical to separate the enwrapped brain cortex and associated vessels from the invading ‘cauliflower-like’ nodules of the meningioma. It is recommended that no efforts are spared in this process, since the enwrapped brain tissue may have retained its ability to function. The observation that there was only 1 case with mild neurological impairment post-operatively in the later 15 cases confirms the advantage of the modified strategy.

In summary, the present study further revealed the clinical features of the invasive benign meningioma and indicated the advantage of combined intra-extra capsular strategy for the surgical resection 10).


Identification of risk factors for perioperative epilepsy remains crucial in the care of patients with meningioma. Moreover, associations of brain invasion with clinical and radiological variables have been largely unexplored. Brain invasion was identified as a new and strong predictor for preoperative, but not postoperative, seizures. Although also associated with increased peritumoral edema, seizures in patients with invasive meningioma might be facilitated substantially by cortical invasion itself. Consideration of seizures in consultations between the neurosurgeon and neuropathologist can improve the microscopic detection of brain invasion 11).

Case series

2018

Hess et al., hypothesized that invasion of the cortex and subsequent increased edema facilitate seizures, and they compared radiological data and perioperative seizures in patients with brain-invasive meningioma or noninvasive meningioma.

Correlations of brain invasion with tumor and edema volumes and preoperative and postoperative seizures were analyzed in univariate and multivariate analyses.

Totals of 108 (61%) females and 68 (39%) males with a median age of 60 years and harboring totals of 92 (52%) grade I, 79 (45%) grade II, and 5 (3%) grade III tumors were included. Brain invasion was found in 38 (22%) patients and was absent in 138 (78%) patients. The tumors were located at the convexity in 72 (41%) patients, at the falx cerebri in 26 (15%), at the skull base in 69 (39%), in the posterior fossa in 7 (4%), and in the ventricle in 2 (1%); the median tumor and edema volumes were 13.73 cm3 (range 0.81-162.22 cm3) and 1.38 cm3 (range 0.00-355.80 cm3), respectively. As expected, edema volume increased with rising tumor volume (p < 0.001). Brain invasion was independent of tumor volume (p = 0.176) but strongly correlated with edema volume (p < 0.001). The mean edema volume in noninvasive tumors was 33.0 cm3, but in invasive tumors, it was 130.7 cm3 (p = 0.008). The frequency of preoperative seizures was independent of the patients’ age, sex, and tumor location; however, the frequency was 32% (n = 12) in patients with invasive meningioma and 15% (n = 21) in those with noninvasive meningioma (p = 0.033). In contrast, the probability of detecting brain invasion microscopically was increased more than 2-fold in patients with a history of preoperative seizures (OR 2.57, 95% CI 1.13-5.88; p = 0.025). In univariate analyses, the rate of preoperative seizures correlated slightly with tumor volume (p = 0.049) but strongly with edema volume (p = 0.014), whereas seizure semiology was found to be independent of brain invasion (p = 0.211). In multivariate analyses adjusted for age, sex, tumor location, tumor and edema volumes, and WHO grade, rising tumor volume (OR 1.02, 95% CI 1.00-1.03; p = 0.042) and especially brain invasion (OR 5.26, 95% CI 1.52-18.15; p = 0.009) were identified as independent predictors of preoperative seizures. Nine (5%) patients developed new seizures within a median follow-up time of 15 months after surgery. Development of postoperative epilepsy was independent of all clinical variables, including Simpson grade (p = 0.133), tumor location (p = 0.936), brain invasion (p = 0.408), and preoperative edema volume (p = 0.081), but was correlated with increasing preoperative tumor volume (p = 0.004). Postoperative seizure-free rates were similar among patients with invasive and those with noninvasive meningioma (p = 0.372).

Brain invasion was identified as a new and strong predictor for preoperative, but not postoperative, seizures. Although also associated with increased peritumoral edema, seizures in patients with invasive meningioma might be facilitated substantially by cortical invasion itself. Consideration of seizures in consultations between the neurosurgeon and neuropathologist can improve the microscopic detection of brain invasion12).

2017

From February 2014 to February 2016, 59 patients with invasive meningioma were enrolled in a study. Invasive meningioma was confirmed in all patients by operation. Information about clinical manifestations, pathological features, preoperative imaging and surgical treatment were collected and analyzed. After surgery, pathological specimens were collected, and cases were confirmed as invasive meningioma by pathological examination. The course of disease ranged from 15 days to 7 years (average, 13.2 months). We used World Health Organization (WHO) criteria for classification of meningioma in the nervous system tumors as our reference. Symptoms were as follows: Intracranial hypertension (29 cases), cranial nerve dysfunction (10 cases), epilepsy (11 cases) and other symptoms (9 cases). We had 56 cases of WHO grade I; 6 cases of WHO grade II and 7 cases of WHO grade III. Surgical removal was: Simpson grade I (56 cases), Simpson grade II (2 cases), Simpson grade III and above (56 cases). We used before surgery imaging data to formulate our surgical plan. In general, during surgeries we did not proceed to complete resection, because in the majority of cases, some key structures were invaded and meningioma was very deep and any attempt for total resection could easily lead to significant damage to these structures 13).

1995

A study was undertaken to investigate the correlation between histological invasiveness and proliferating potential and clinical recurrence in meningioma. In 39 meningiomas, the histological findings at the tumour-brain interface zone were classified into 3 types, consisting of 29 cases of non-invasion (NON). 7 cases of nodular invasion (NOD), and 3 cases of intermingled invasion (INT). Proliferating cell nuclear antigen (PCNA) and argyrophilic nucleolar organizer region (AgNOR) indices were studied. PCNA indices (mean +/- standard error) of NON, NOD. and INT were 1.7 +/- 0.1%, 5.2 +/- 0.5%, and 7.5 +/- 0.7%. respectively, and the AgNOR indices (dot number/nucleus) were 1.50 +/- 0.03, 2.00 +/- 0.04, and 2.22 +/- 0.07, respectively. Significant differences were found among the three types in both parameters. Clinically, tumour recurrence was observed in 1/29 NON, 4/7 NOD, and 2/2 INT cases, indicating a higher incidence of recurrence in invasive meningiomas (NOD plus INT). Four of 32 patients who underwent gross total removal of the tumours showed recurrence, and all of these four tumours were invasive meningiomas. The results of the present study showed that tumour invasiveness as measured by PCNA + AgNOR indices correlated well with high proliferative potential and clinical recurrence 14).

1)

Gelabert-González M, Serramito-García R. Intracranial meningiomas: I. Epidemiology, aetiology, pathogenesis and prognostic factors. Rev Neurol. 2011;53:165–172.

2)

Bondy M, Ligon BL. Epidemiology and etiology of intracranial meningiomas: a review. J Neurooncol. 1996;29:197–205. doi: 10.1007/BF00165649.

3)

Riemenschneider MJ, Perry A, Reifenberger G. Histological classification and molecular genetics of meningiomas. Lancet Neurol. 2006;5:1045–1054. doi: 10.1016/S1474-4422(06)70625-1.

4)

Modha A, Gutin PH. Diagnosis and treatment of atypical and anaplastic meningiomas: A review. Neurosurgery. 2005;57:538–550. doi: 10.1227/01.NEU.0000170980.47582.A5.

5)

Trembath D, Miller CR, Perry A. Gray zones in brain tumor classification: Evolving concepts. Adv Anat Pathol. 2008;15:287–297. doi: 10.1097/PAP.0b013e3181836a03.

6)

Gay E, Lages E, Ramus C, Guttin A, El Atifi M, Dupré I, Bouamrani A, Salon C, Ratel D, Wion D, et al. The heterogeneity of meningioma revealed by multiparameter analysis: Infiltrative and non-infiltrative clinical phenotypes. Int J Oncol. 2011;38:1287–1297.

7)

Fritz J, Roser F, Tatagiba M, Bornemann A. The basement membrane at the tumour-brain interface of brain-invasive grade I meningiomas. Neuropathol Appl Neurobiol. 2005;31:339–342. doi: 10.1111/j.1365-2990.2005.00661.x.

8)

Utsuki S, Oka H, Sato Y, Kawano N, Tsuchiya B, Kobayashi I, Fujii K. Invasive meningioma is associated with a low expression of E-cadherin and beta-catenin. Clin Neuropathol. 2005;24:8–12.

9)

Suwa T, Kawano N, Oka H, Ito H, Kameya T. Invasive meningioma: A tumour with high proliferating and ‘recurrence’ potential. Acta Neurochir (Wien) 1995;136:127–131. doi: 10.1007/BF01410613.

10)

Lin Q, Ling F, Xu G. Invasive benign meningioma: Clinical characteristics, surgical strategies and outcomes from a single neurosurgical institute. Exp Ther Med. 2016 Jun;11(6):2537-2540. Epub 2016 Apr 4. PubMed PMID: 27284345; PubMed Central PMCID: PMC4887900.

11) , 12)

Hess K, Spille DC, Adeli A, Sporns PB, Brokinkel C, Grauer O, Mawrin C, Stummer W, Paulus W, Brokinkel B. Brain invasion and the risk of seizures in patients with meningioma. J Neurosurg. 2018 Apr 27:1-8. doi: 10.3171/2017.11.JNS172265. [Epub ahead of print] PubMed PMID: 29701550.

13)

Hou W, Ma Y, Xing H, Yin Y. Imaging characteristics and surgical treatment of invasive meningioma. Oncol Lett. 2017 May;13(5):2965-2970. doi: 10.3892/ol.2017.5833. Epub 2017 Mar 9. PubMed PMID: 28521402; PubMed Central PMCID: PMC5431211.

14)

Suwa T, Kawano N, Oka H, Ito H, Kameya T. Invasive meningioma: a tumour with high proliferating and “recurrence” potential. Acta Neurochir (Wien). 1995;136(3-4):127-31. PubMed PMID: 8748841.

Update: Bladder cancer intracranial metastases

Bladder cancer intracranial metastases

Epidemiology

Bladder cancer gives metastasis to the brain in less than 1%.

Transitional cell carcinoma (TCC), the most common type of urinary bladder cancer, is a rare cause of brain metastasis with an ominous prognosis.

Treatment

Case series

2018

Taylor et al. from the Wake Forest University School of Medicine, Winston-Salem, North Carolina, reported a series of patients with brain metastases from bladder cancer treated with stereotactic radiosurgery (SRS). The aim was to identify patients with brain metastases from bladder primaries treated with SRS with or without surgical resection and report the clinical outcomes.

Patients meeting eligibility criteria at the institution between 2000 and 2017 were included. The clinical variables of interest, including overall survival (OS), local recurrence, V12, distant brain failure (DBF), and initial brain metastases velocity, were calculated. Cox proportional hazards analysis was performed to identify predictors of time-to-event outcomes.

A total of 14 patients were included. The median OS from the time of treatment was 2.1 months. Factors predictive of OS include intracranial resection (HR 0.21, p = 0.03). The cumulative incidence of local failure was 21% at 6 months and 30% at 12 months. The cumulative incidence of DBF at 6 and 12 months was 23 and 31%, respectively.

The prognosis in this patient population remains guarded. Factors associated with improved survival include intracranial resection. Future, prospective work is needed to further define optimal management 1).

2002

Between January 1982 and November 1999, 16 patients with brain metastases from bladder carcinoma were treated at our institution. We reviewed patient and tumor characteristics at the time of the primary diagnosis and the brain metastasis diagnosis. We analyzed treatment results in regard to survival and local metastasis control.

Brain metastases from bladder carcinoma were commonly accompanied by uncontrolled systemic metastases. Multiple brain lesions developed in 14 of the 16 patients. Of the 16 patients 14 received radiation therapy with or without surgery, 1 was treated surgically and 1 did not receive any treatment. The 11 patients treated with whole brain radiation therapy had a median survival of only 2 months (range 0.5 to 11). A patient who received stereotactic radiosurgery survived 12 months after the brain metastasis diagnosis and 2 treated with radiation therapy after surgery survived 12.75 and 2.75 months, respectively (median 7.75). The patient treated with surgery alone survived 1.25 months after the brain metastasis diagnosis and 1 who received no treatment survived 1.75 months. Patients with multiple brain metastases had shorter survival than those with a single metastasis.

Overall survival after brain metastasis development in patients with bladder carcinoma was poor. Although the number of patients in this study was small, results indicate that radiation therapy alone is inadequate treatment. Therefore, when possible, we advocate more effective treatment by combining radiation therapy with other treatment modalities, as recommended in ongoing clinical trials 2).

1993

The records of 28 patients with transitional cell cancer who had brain metastases were retrospectively reviewed. Data from 19 patients were considered suitable for analysis and were included in this study. One patient was treated with surgery alone, 10 with radiation alone and 7 with radiation and surgery, while 1 received no treatment. Mean and median survival times, respectively, were 57 and 42 months from the initial diagnosis, and 11 and 4 months from diagnosis of central nervous system metastases. Patients treated with surgery and radiation demonstrated a mean survival time of 19 months compared to 6 months for patients treated with radiation alone (p = 0.03). There were 2 long-term survivors in the combined modality group at 50 and at 12 months. Enthusiasm for combined modality treatment should be tempered by the fact that selection bias favored the combined modality group; 13 patients with single lesions demonstrated a mean survival of 14 months compared to 3 months for 6 patients with multiple lesions (p = 0.009) and only patients with solitary lesions underwent surgical resection. Brain metastases have an ominous prognosis in patients with bladder cancer primaries. Considering the sum of the retrospective and prospective reports, we recommend that patients with solitary brain lesions and good performance status be aggressively managed with surgical resection and postoperative radiation therapy 3).

1992

Clinico-pathological study of six patients with cerebral metastasis from vesical carcinoma with no prior administration of systemic chemotherapy. In two cases the symptoms of intracranial mass were the initial reason for infiltrant vesical carcinoma examination. Despite the rarity of such occurrence, the possibility of vesical tumours showing in such a way must be taken into account. The singularity of cerebral metastatic seeding throughout the natural history of a vesical neoplasia is analyzed. Also, a review is made of the factors hypothetically responsible for the increase of cerebral metastasis establishment following current chemotherapy 4).

Case reports

A 68-year-old female presented with right-sided paresis and focal motor seizures of her right upper and lower extremities 14 years after being diagnosed and treated for primary TCC of the urinary bladder with gemcitabine-based chemotherapy. MRI imaging revealed a 3.1 × 3.1 × 2.7 cm heterogeneously enhancing mass located along the posterior aspect of the left frontal convexity. The lesion was accessed using a transsulcal approach and was surgically debulked along the motor cortex with motor strip mapping, followed by adjuvant whole-brain radiation therapy. Pathological examination confirmed metastatic carcinoma with features of TCC, a rare entity among metastatic brain tumors.

Brain metastases may present several years later in patients with TCC of the urinary bladder who have been treated with surgery and chemotherapy. Chemotherapeutic agents that penetrate the blood-brain barrier, such as gemcitabine, may delay development of cerebral metastasis from primary TCC of the urinary bladder 5).

A 57-year-old patient presenting with epileptic crises secondary to a brain metastasis from bladder carcinoma, who was investigated in our institution with (11)C-Methionine PET. The scan documented the disease recurrence in the left parietal lobe associated with a diffused tracer uptake in the surrounding cerebral circumvolutions, derived from the comitial status. After surgical removal of the metastatic lesion, the patient experienced a complete recovery of symptoms and no further onset of secondary seizure 6).

A 71-year-old man who was admitted to the emergency department after an episode of loss of consciousness. On neurological examination a left hemiparesis was observed. The patient’s previous history entailed a total cystectomy and radical prostatectomy 7 months ago because of a transitional cell carcinoma (TCC) of the urinary bladder. Brain imaging work-up revealed a cystic lesion with perifocal edema in the right frontal lobe. The patient was operated and the histological diagnosis was consistent with a metastatic carcinoma, with morphological, histochemical and immunohistochemical features comparable to those of the primary tumor. Postoperative the patient was in excellent neurological state and received complementary chemotherapy and total brain irradiation. Additional imaging and laboratory examinations excluded other metastatic lesion. The patient died 18 months later due to systemic disease. Although intracranial metastases from TCC of urinary bladder have a low incidence, in follow-up examinations any alterations in neurological status in these patients should be thoroughly evaluated 7).

1)

Taylor JM, McTyre ER, Tatter SB, Laxton AW, Munley MT, Chan MD, Cramer CK. Gamma Knife Stereotactic Radiosurgery for the Treatment of Brain Metastases from Primary Tumors of the Urinary Bladder. Stereotact Funct Neurosurg. 2018 Apr 26:1-5. doi: 10.1159/000488151. [Epub ahead of print] PubMed PMID: 29698968.
2)

Mahmoud-Ahmed AS, Suh JH, Kupelian PA, Klein EA, Peereboom DM, Dreicer R, Barnett GH. Brain metastases from bladder carcinoma: presentation, treatment and survival. J Urol. 2002 Jun;167(6):2419-22. PubMed PMID: 11992049.
3)

Rosenstein M, Wallner K, Scher H, Sternberg CN. Treatment of brain metastases from bladder cancer. J Urol. 1993 Mar;149(3):480-3. PubMed PMID: 8437250.
4)

Angulo JC, López JI, Unda-Urzaiz M, Flores N. [Bladder carcinoma and brain metastases before systemic chemotherapy]. Actas Urol Esp. 1992 Feb;16(2):140-3. Spanish. PubMed PMID: 1590088.
5)

Sarmiento JM, Wi MS, Piao Z, Stiner ES. Solitary cerebral metastasis from transitional cell carcinoma after a 14-year remission of urinary bladder cancer treated with gemcitabine: Case report and literature review. Surg Neurol Int. 2012;3:82. doi: 10.4103/2152-7806.99172. Epub 2012 Jul 28. PubMed PMID: 22937482; PubMed Central PMCID: PMC3424676.
6)

Lopci E, Bello L, Chiti A. (11)C-Methionine uptake in secondary brain epilepsy. Rev Esp Med Nucl Imagen Mol. 2014 Jul-Aug;33(4):234-6. doi: 10.1016/j.remn.2013.12.008. Epub 2014 Mar 12. PubMed PMID: 24630372.
7)

Zigouris A, Pahatouridis D, Mihos E, Alexiou GA, Nesseris J, Zikou AK, Argyropoulou MI, Goussia A, Voulgaris S. Solitary cystic cerebral metastasis from transitional cell carcinoma of the bladder. Acta Neurol Belg. 2009 Dec;109(4):322-5. PubMed PMID: 20120215.

Safety net hospital

Safety net hospital

A safety net hospital (SNH) is one of the medical centers in the United States that has a legal obligation to provide healthcare for individuals regardless of their insurance status (the United States does not have a policy of universal health care) and regardless of their ability to pay.

Because of this legal mandate to serve all populations, safety net hospitals typically serve a proportionately higher number of uninsured, MedicaidMedicare, Children’s Health Insurance Program (CHiP), low-income, and other vulnerable individuals than their non-safety net hospital counterpart.


SNH patients with brain metastases treated with SRS alone had fewer follow-up neuroimaging studies and were at higher risk for neurologic symptoms, hospitalization for brain metastases, and salvage neurosurgery in comparison with private hospital (PH) patients. Clinicians should consider the practice setting and patient access to follow-up care when they are deciding on the optimal strategy for the treatment of brain metastases 1).


Prior studies have identified poor outcomes, increased costs, and reduced access to certain complex, elective surgeries at Safety net hospitals (SNHs). However, it is unknown whether similar patterns exist for the Glioblastoma multiforme treatment (GBM). Brandel et al., sought to determine if patients treated at HBHs receive equitable care for GBM, and if safety-net burden status impacts post-treatment survival.

The National Cancer Database was queried for GBM patients diagnosed between 2010 and 2015. Safety-net burden was defined as the proportion of Medicaid and uninsured patients treated at each hospital, and stratified as low (LBH), medium (MBH), and high-burden (HBH) hospitals. The impact of safety-net burden on the receipt of any treatment, trimodality therapy, gross total resection (GTR), radiation, or chemotherapy was investigated. Secondary outcomes included post-treatment 30-day mortality, 90-day mortality, and overall survival. Univariate and multivariate analyses were utilized.

Overall, 40,082 GBM patients at 1202 hospitals (352 LBHs, 553 MBHs, and 297 HBHs) were identified. Patients treated at HBHs were significantly less likely to receive trimodality therapy (OR = 0.75, p < 0.001), GTR (OR = 0.84, p < 0.001), radiation (OR = 0.73, p < 0.001), and chemotherapy (OR = 0.78, p < 0.001) than those treated at LBHs. Patients treated at HBHs had significantly increased 30-day (OR = 1.25, p = 0.031) and 90-day mortality (OR = 1.24, p = 0.001), and reduced overall survival (HR = 1.05, p = 0.039).

GBM patients treated at SNHs are less likely to receive standard-of-care therapies and have increased short- and long-term mortality. Additional research is needed to evaluate barriers to providing equitable care for GBM patients at SNHs 2).

1)

Diao K, Sun Y, Yoo SK, Yu C, Ye JC, Trakul N, Jennelle RL, Kim PE, Zada G, Gruen JP, Chang EL. Safety-net versus private hospital setting for brain metastasis patients treated with radiosurgery alone: Disparities in follow-up care and outcomes. Cancer. 2018 Jan 1;124(1):167-175. doi: 10.1002/cncr.30984. Epub 2017 Sep 13. PubMed PMID: 28902402.
2)

Brandel MG, Rennert RC, Lopez Ramos C, Santiago-Dieppa DR, Steinberg JA, Sarkar RR, Wali AR, Pannell JS, Murphy JD, Khalessi AA. Management of glioblastoma at safety-net hospitals. J Neurooncol. 2018 Apr 24. doi: 10.1007/s11060-018-2875-8. [Epub ahead of print] PubMed PMID: 29691776.