Non small cell lung cancer intracranial metastases treatment

Non small cell lung cancer intracranial metastases treatment

Brain metastases are common in patients with non small cell lung cancer (NSCLC). Because of associated poor prognosis and limited specific treatment options, there is a real need for the development of medical therapies and strategies for affected patients. Novel compounds for epidermal growth factor receptor-dependent and anaplastic lymphoma kinase-dependent lung cancer have demonstrated blood-brain barrier permeability and have led to important improvements in central nervous system outcomes. Studies of targeted therapies for oncogene-driven tumors and of immunotherapies in patients with brain metastases have shown promise and, allied with novel radiation techniques, are driving a rapid evolution in treatment and prognosis for NSCLC brain metastases 1).


KPS score ≥ 70, RPA class I/II, and postoperative chemotherapy could benefit post-metastasectomy patients with brain metastases (BM) from Non small cell lung cancer (NSCLC). Conversely, the initial onset of intracranial lesions is an unfavorable factor that increases the risk of death. These findings support the use of personalized therapy for patients with BM from NSCLC 2).


EGFR and ALK tyrosine kinase inhibitors (TKIs) provide significantly superior systemic response rates and progression free survival compared to standard chemotherapy in the molecularly defined Non small cell lung cancer (NSCLC) subpopulations. An apparent intracranial activity of new generation TKIs triggered the discussion on their role in brain metastases in lieu of local therapies 3).


A article of Preusser et al., is the result of a round table discussion held at the European Lung Cancer Conference (ELCC) in Geneva in May 2017. Its purpose was to explore and discuss the advances in the knowledge about the biology and treatment of brain metastases originating from non-small cell lung cancer. The authors propose a series of recommendations for research and treatment within the discussed context 4).


PUBMEDEMBASE, the Cochrane LibraryWeb of Knowledge, Current Controlled Trials, Clinical Trials, and 2 conference websites were searched to select NSCLC patients with only single brain metastasis (SBM) who received brain surgery or SRS. SPSS 18.0 software was used to analyze the mean median survival time (MST) and Stata 11.0 software was used to calculate the overall survival (OS).

A total of 18 trials including 713 patients were systematically reviewed. The MST of the patients was 12.7 months in surgery group and 14.85 months in SRS group, respectively. The 1, 2, and 5 years OS of the patients were 59%, 33%, and 19% in surgery group, and 62%, 33%, and 14% in SRS group, respectively. Furthermore, in the surgery group, the 1 and 3 years OS were 68% and 15% in patients with controlled primary tumors, and 50% and 13% in the other patients with uncontrolled primary tumors, respectively. Interestingly, the 5-year OS was up to 21% in patients with controlled primary tumors.

There was no significant difference in MST or OS between patients treated with neurosurgery and SRS. Patients with resectable lung tumors and SBM may benefit from the resection of both primary lesions and metastasis 5).

Patients with NSCLC and synchronous brain metastases, presenting neurological symptoms showed no survival benefit from neurosurgical resection, although quality of life was improved due to early control of neurological symptoms 6).


Response rates after platinum based antineoplastics, range from 23% to 45%. Development of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs): gefitinib or erlotinib, was an improvement in treatment of advanced NSCLC patients. EGFR mutations are present in 10-25% of NSCLC (mostly adenocarcinoma), and up to 55% in never-smoking women of East Asian descent. In the non-selected group of patients with BMF-NSCLC, the overall response rates after gefitinib or erlotinib treatment range from 10% to 38%, and the duration of response ranges from 9 to 13.5 months. In the case of present activating EGFR mutation, the response rate after EGRF-TKIs is greater than 50%, and in selected groups (adenocarcinoma, patients of Asian descent, never-smokers, asymptomatic BMF-NSCLC) even 70%. Gefitinib or erlotinib treatment improves survival of BMF-NSCLC patients with EGFR mutation in comparison to cases without the presence of this mutation. There is no data on the activity of the anti-EML4-ALK agent crizotinib. Bevacizumab, recombinant humanised monoclonal antibody anti-VEGF, in the treatment of advanced non-squamous NSCLC patients is a subject of intense research. Data from a clinical trial enrolling patients with pretreated or occult BMF-NSCLC proved that the addition of bevacizumab to various chemotherapy agents or erlotinib is a safe and efficient treatment, associated with a low incidence of CSN haemorrhages. However, the efficacy and safety of bevacizumab used for therapeutic intent, regarding active brain metastases is unknown 7).

Non small cell lung cancer intracranial metastases whole brain radiotherapy

Non small cell lung cancer intracranial metastases radiosurgery

Non small cell lung cancer intracranial metastases surgery

References

1)

Bulbul A, Forde PM, Murtuza A, Woodward B, Yang H, Bastian I, Ferguson PK, Lopez-Diaz F, Ettinger DS, Husain H. Systemic Treatment Options for Brain Metastases from Non-Small-Cell Lung Cancer. Oncology (Williston Park). 2018 Apr 15;32(4):156-63. Review. PubMed PMID: 29684234.
2)

She C, Wang R, Lu C, Sun Z, Li P, Yin Q, Liu Q, Wang P, Li W. Prognostic factors and outcome of surgically treated patients with brain metastases of non-small cell lung cancer. Thorac Cancer. 2018 Nov 28. doi: 10.1111/1759-7714.12913. [Epub ahead of print] PubMed PMID: 30485664.
3)

Wrona A, Dziadziuszko R, Jassem J. Management of brain metastases in non-small cell lung cancer in the era of tyrosine kinase inhibitors. Cancer Treat Rev. 2018 Dec;71:59-67. doi: 10.1016/j.ctrv.2018.10.011. Epub 2018 Oct 21. Review. PubMed PMID: 30366200.
4)

Preusser M, Winkler F, Valiente M, Manegold C, Moyal E, Widhalm G, Tonn JC, Zielinski C. Recent advances in the biology and treatment of brain metastases of non-small cell lung cancer: summary of a multidisciplinary roundtable discussion. ESMO Open. 2018 Jan 26;3(1):e000262. doi: 10.1136/esmoopen-2017-000262. eCollection 2018. Review. PubMed PMID: 29387475; PubMed Central PMCID: PMC5786916.
5)

Qin H, Wang C, Jiang Y, Zhang X, Zhang Y, Ruan Z. Patients with single brain metastasis from non-small cell lung cancer equally benefit from stereotactic radiosurgery and surgery: a systematic review. Med Sci Monit. 2015 Jan 12;21:144-52. doi: 10.12659/MSM.892405. PubMed PMID: 25579245.
6)

Kim SY, Hong CK, Kim TH, Hong JB, Park CH, Chang YS, Kim HJ, Ahn CM, Byun MK. Efficacy of surgical treatment for brain metastasis in patients with non-small cell lung cancer. Yonsei Med J. 2015 Jan 1;56(1):103-11. doi: 10.3349/ymj.2015.56.1.103. PubMed PMID: 25510753; PubMed Central PMCID: PMC4276743.
7)

Cedrych I, Kruczała MA, Walasek T, Jakubowicz J, Blecharz P, Reinfuss M. Systemic treatment of non-small cell lung cancer brain metastases. Contemp Oncol (Pozn). 2016;20(5):352-357. doi: 10.5114/wo.2016.64593. Epub 2016 Dec 20. Review. PubMed PMID: 28373815; PubMed Central PMCID: PMC5371701.

Intracranial arachnoid cyst surgery

Controversy still exists regarding the optimal option for the surgical management of intracranial arachnoid cysts.

Options

Neuroendoscopic fenestrations.

Microsurgical fenestrations +/- marsupialisation

Cystoperitoneal shunt.

In a retrospective case note review of all patients with intracranial arachnoid cysts treated surgically at the Department of Neurosurgery, Wessex Neurological Centre, Southampton General Hospital, over a 15 year period. Data on clinical presentations and outcomes was collected from the patient notes and the pre- and post-operative cyst volumes were calculated by creating 3-dimensional volumetric models.

Eighty-two patients were identified of which 45 were treated endoscopically, 34 microscopically and 3 underwent cysto-peritoneal shunting. The most common cyst location was the middle fossa (n = 25). Amongst the symptomatic patients, improvement or resolution of symptoms was seen in 35 out of 40 cysts treated endoscopically (88%), 28 out of 32 treated microsurgically (88%) and 3 out of 3 treated by shunting (100%, p = 0.79). The reoperation rate was not significantly different between the endoscopic and microsurgical groups (24.4% vs 14.7%, p = 0.49). The endoscopic and shunted groups had a shorter length of stay than the microsurgical group (3.0 vs 3.0 vs 4.5 days, p = 0.04). All three treatment modalities had a similar percentage reduction in cyst volume after surgery (30.0 vs 41.7 vs 30.9%, p = 0.98).

This cohort series shows that endoscopic and microsurgical approaches to treat intracranial arachnoid cysts produce comparable clinical and radiological outcomes. Endoscopic fenestration is associated with a shorter length of stay as would be expected from a minimally invasive procedure 1).


Open surgery advantages include, direct inspection of the cyst, biopsy sampling, fenestration in multilocular cysts and, in certain locations, cyst communication to basal cisterns 2).

Surgery for AC can be performed with a fairly low risk of complications and yields significant improvement in quality of life correlated to postoperative improvement in headache and dizziness. These findings may justify a more liberal approach to surgical treatment for AC 3).


Choi et al., analyzed pediatric patients under 18 years of age who underwent surgical management for intracranial AC between January 2000 and December 2011. Patients with a follow-up period of less than 1 year were excluded. A total of 75 patients were enrolled in this study. These patients were assessed by subjective symptoms and by a clinician’s objective evaluation. The radiological assessment of AC after surgery was also evaluated.

The median age of patients at the initial operation was 5 years. The median follow-up period was 38 months. The goal of surgery was achieved in 28% (21/75) of patients. The radiological alteration of AC after initial fenestration surgery was diverse. The results of the clinical and radiological assessments did not always coincide. A total of 35 complications occurred in 28 patients. Subdural fluid collection was the most common unexpected radiological complication.

The study showed that the fenestration procedure for AC produced unsatisfactory clinical improvements compared to the relatively high complication rate. Therefore, surgical treatment for AC should be strictly limited to patients who have symptoms directly related to AC 4).


A consecutive series of 68 adult patients (43 males, mean age 30.3 years, range 18-42 years) with IAC were surgically treated between January 2004 and January 2011 in the Department of Neurosurgery, West China Hospital of Sichuan University, Chengdu, China.

The cysts were supratentorial in location in 53 and infratentorial in 15 patients. Symptoms at presentation, location of the IAC, surgical treatment modalities, and postoperative complications were evaluated.

Of the 51 patients with headache, 44 (86.27%) patients had complete relief of the headache, five (9.80%) patients had significant improvement, and two (3.92%) had no worthwhile change. Three of the four patients with hydrocephalus and gait disturbances had relief of the symptoms and one patient had significant improvement. Of the five patients with cognitive decline and weakness, three (60.00%) patients showed improvement, and two (40.00%) patients had no significant change. Five (62.50%) of the eight patients with epilepsy had seizure remission, two (25.00%) patients had non-disabling seizures, and one had no change. Follow-up computed tomography (CT) scans showed variable change in the mass effect of IAC in 68 patients; cystic size was significantly reduced in 51 patients, no significant change in two patients of supratentorial arachnoid cysts. Cystic size was reduced in seven patients, but no significant change was observed in eight patients of infratentorial cysts. Three patients with enlarged head circumference had no further increase in the head circumference.

Adult patients with IAC symptoms should be treated efficiently. Surgical treatment is associated with significant improvement in the symptoms and signs 5).


Data from 69 patients with cerebral arachnoid cysts treated in our institution between 1997 and 2007 were reviewed.Cysts were located infratentorially in 20% (n = 14) and supratentorially in 80% (n = 55); of these 73% (n = 40) were in the middle cranial fossa. Mean cyst size was 61 mm (range 15-100 mm). The most common symptoms were headache (51%), dizziness (26%), cranial nerve dysfunction (23%), seizure (22%), nausea and vomiting (18%), and hemiparesis (13%). Surgery was performed in 83% (n = 57). First-line treatments were microsurgical fenestration (n = 30), endoscopic fenestration (n = 15), and cystoperitoneal/ventriculoperitoneal shunting (n = 11). More than one intervention was needed in 42% (n = 24). A particularly high rate of relapse (73%) was observed after endoscopic fenestration, following which 11 patients were admitted for reoperation. By comparison, only eight patients (28%) managed with microsurgical fenestration and four (36%) in the shunted group needed a second surgical procedure. Mean follow-up was 30 months. In the surgical series 79% (n = 45) had a good outcome.We conclude that the surgical treatment of arachnoid cysts has an overall good outcome. In our institution the best results were obtained with microsurgical decompression through craniotomy 6).

References

1)

Hall S, Smedley A, Rae S, Mathad N, Waters R, Chakraborty A, Sparrow O, Tsitouras V. Clinical and radiological outcomes following surgical treatment for intra-cranial arachnoid cysts. Clin Neurol Neurosurg. 2018 Dec 27;177:42-46. doi: 10.1016/j.clineuro.2018.12.018. [Epub ahead of print] PubMed PMID: 30599313.
2)

Saura Rojas JE, Horcajadas Almansa Á, Ros López B. [Microsurgical treatment of intracraneal arachnoid cysts]. Neurocirugia (Astur). 2015 Apr 16. pii: S1130-1473(15)00029-9. doi: 10.1016/j.neucir.2015.02.006. [Epub ahead of print] Spanish. PubMed PMID: 25891259.
3)

Mørkve SH, Helland CA, Amus J, Lund-Johansen M, Wester KG. Surgical Decompression of Arachnoid Cysts Leads to Improved Quality of Life: A Prospective Study. Neurosurgery. 2016 May;78(5):613-25. doi: 10.1227/NEU.0000000000001100. PubMed PMID: 26540351.
4)

Choi JW, Lee JY, Phi JH, Kim SK, Wang KC. Stricter indications are recommended for fenestration surgery in intracranial arachnoid cysts of children. Childs Nerv Syst. 2015 Jan;31(1):77-86. doi: 10.1007/s00381-014-2525-1. Epub 2014 Aug 16. PubMed PMID: 25123786.
5)

Wang C, Liu C, Xiong Y, Han G, Yang H, Yin H, Wang J, You C. Surgical treatment of intracranial arachnoid cyst in adult patients. Neurol India. 2013 Jan-Feb;61(1):60-4. doi: 10.4103/0028-3886.108013. PubMed PMID: 23466842.
6)

Holst AV, Danielsen PL, Juhler M. Treatment options for intracranial arachnoid cysts: a retrospective study of 69 patients. Acta Neurochir Suppl. 2012;114:267-70. doi: 10.1007/978-3-7091-0956-4_52. PubMed PMID: 22327706.

Unruptured intracranial aneurysm endovascular treatment

There is no randomized data available to compare the results of surgery versus endovascular treatment of unruptured aneurysms (UIAs) 1).

Unruptured intracranial aneurysm endovascular treatment can be performed with relative safety. The long-term follow-up results of unruptured intracranial aneurysm treatment (UIAs) by means of coil embolization remain unclear.

The efficacy of treatment as compared with observation has not been rigorously documented 2).

The use of coiling relative to surgical clipping of unruptured intracranial aneurysms is associated with decreasing periprocedural morbidity and mortality among patients treated in the United States from 2001 to 2008 3).


Koyanagi et al., from the National Hospital Organization Himeji Medical CenterKyoto University Graduate School of Medicine, Kobe City Medical Center General Hospital, National Cerebral and Cardiovascular Center, Suita and Kokura Memorial Hospital Japan.

retrospectively analyzed data from cases in which patients underwent coil embolization between 1995 and 2004 at 4 stroke centers. In collecting the late (≥ 1 year) follow-up data, postal questionnaires were used to assess whether patients had experienced rupture or retreatment of a coiled aneurysm or any stroke or had died.

Overall, 184 patients with 188 UIAs were included. The median follow-up period was 12 years (interquartile range 11-13 years, maximum 20 years). A total of 152 UIAs (81%) were followed for more than 10 years. The incidence of rupture was 2 in 2122 aneurysm-years (annual rupture rate 0.09%). Nine of the 188 patients with coiled UIAs (4.8%) underwent additional treatment. In 5 of these 9 cases, the first retreatment was performed more than 5 years after the initial treatment. Large aneurysms were significantly more likely to require retreatment. Nine strokes occurred over the 2122 aneurysm-years. Seventeen patients died in this cohort.

This study demonstrates a low risk of rupture of coiled UIAs with long-term follow-up periods of up to 20 years. This suggests that coiling of UIAs could prevent rupture for a long period of time. However, large aneurysms might need to be followed for a longer time 4).


Bekelis et al., investigated the association of combined open and endovascular expertise with the outcomes of unruptured cerebral aneurysm coiling.

Bekelis et al., performed a cohort study of 100% of Medicare fee-for-service claims data for elderly patients who underwent endovascular coiling for unruptured cerebral aneurysms between 2007 and 2012. To control for confounding, the authors used propensity score conditioning, with mixed effects to account for clustering at the hospital referral region level.

During the study period, there were 11,716 patients who underwent endovascular coiling for unruptured cerebral aneurysms and met the inclusion criteria. Of these, 1186 (10.1%) underwent treatment performed by hybrid neurosurgeons, and 10,530 (89.9%) by proceduralists who performed only endovascular coiling. Multivariable regression analysis with propensity score adjustment demonstrated a lack of association of combined practice with 1-year postoperative mortality (OR 0.84; 95% CI 0.58-1.23), discharge to rehabilitation (OR 1.0; 95% CI 0.66-1.51), 30-day readmission rate (OR 1.07; 95% CI 0.83-1.38), and length of stay (adjusted difference, 0.41; 95% CI -0.26 to 1.09). Higher procedural volume was independently associated with improved outcomes.

In a cohort of Medicare patients, the authors did not demonstrate a difference in mortality, discharge to rehabilitation, readmission rate, and LOS between hybrid neurosurgeons and proceduralists performing only endovascular coiling 5) .


A portfolio of 41 cases of unruptured intracranial aneurysms with angiographic images, along with a short description of the patient presentation, was sent to 28 clinicians (16 radiologists and 12 surgeons) with varying years of experience in the management of unruptured intracranial aneurysms. Five senior clinicians responded twice at least 3 months apart. Nineteen cases (46%) were selected from patients recruited in the Canadian UnRuptured Endovascular versus Surgery trial, an ongoing randomized comparison of coil embolization and clip placement. For each case, the responder was to first choose between 3 treatment options (observation, surgical clip placement, or endovascular coil embolization) and then indicate their level of certainty on a quantitative 0-10 scale. Agreement in decision making was studied using κ statistics.

Decisions to coil were more frequent (n = 612, 53%) than decisions to clip (n = 289, 25%) or to observe (n = 259, 22%). Interjudge agreement was only fair (κ = 0.31 ± 0.02) for all cases and all judges, despite substantial intrajudge agreement (range 0.44-0.83 ± 0.10), with high mean individual certainty levels for each case (range 6.5-9.4 ± 2.0 on a scale of 0-10). Agreement was no better within specialties (surgeons or radiologists), within capability groups (those able to perform endovascular coiling alone, surgical clipping alone, or both), or with more experience. There was no correlation between certainty levels and years of experience. Agreement was lower when the cases were taken from the randomized trial (κ = 0.19 ± 0.2) compared with nontrial cases (κ = 0.35 ± 0.2).

Individuals do not agree regarding the management of unruptured intracranial aneurysms, even when they share a background in the same specialty, similar capabilities in aneurysm management, or years of practice. If community equipoise is a necessary precondition for trial participation, this study has found sufficient uncertainty and disagreement among clinicians to justify randomized trials 6).

For unruptured cerebral aneurysms, an observed perioperative survival advantage for endovascular coiling relative to that for surgical clipping was lost on long-term follow-up, according to data from an administrative database of patients who were not randomly allocated to treatment type. A cost advantage of endovascular treatment was maintained even though endovascularly treated patients were more likely to undergo subsequent hospitalizations for additional aneurysm repair procedures. Rates of aneurysm rupture following treatment were similar in the two groups 7).


Diffusion-weighted MR images (DWI) obtained after endovascular treatment of cerebral aneurysms frequently show multiple high-signal intensity (HSI) dots.

Aspiration of the inner content of the microcatheter right after detachable coil delivery was helpful for the reduction of the incidence of microembolisms after endovascular coil embolization for the treatment of unruptured cerebral aneurysms 8).

References

1)

Darsaut TE, Findlay JM, Raymond J; CURES Collaborative Group. The design of the Canadian UnRuptured Endovascular versus Surgery (CURES) trial. Can J Neurol Sci. 2011 Mar;38(2):236-41. PubMed PMID: 21320826; PubMed Central PMCID: PMC3528784.
2)

Naggara ON, White PM, Guilbert F, Roy D, Weill A, Raymond J. Endovascular treatment of intracranial unruptured aneurysms: systematic review and meta-analysis of the literature on safety and efficacy. Radiology. 2010 Sep;256(3):887-97. doi: 10.1148/radiol.10091982. Epub 2010 Jul 15. Review. PubMed PMID: 20634431.
3)

Brinjikji W, Rabinstein AA, Nasr DM, Lanzino G, Kallmes DF, Cloft HJ. Better outcomes with treatment by coiling relative to clipping of unruptured intracranial aneurysms in the United States, 2001-2008. AJNR Am J Neuroradiol. 2011 Jun-Jul;32(6):1071-5. doi: 10.3174/ajnr.A2453. Epub 2011 Apr 21. PubMed PMID: 21511860.
4)

Koyanagi M, Ishii A, Imamura H, Satow T, Yoshida K, Hasegawa H, Kikuchi T, Takenobu Y, Ando M, Takahashi JC, Nakahara I, Sakai N, Miyamoto S. Long-term outcomes of coil embolization of unruptured intracranial aneurysms. J Neurosurg. 2018 Jan 5:1-7. doi: 10.3171/2017.6.JNS17174. [Epub ahead of print] PubMed PMID: 29303448.
5)

Bekelis K, Gottlieb D, Labropoulos N, Su Y, Tjoumakaris S, Jabbour P, MacKenzie TA. The impact of hybrid neurosurgeons on the outcomes of endovascular coiling for unruptured cerebral aneurysms. J Neurosurg. 2016 Feb 26:1-7. [Epub ahead of print] PubMed PMID: 26918479.
6)

Darsaut TE, Estrade L, Jamali S, Bojanowski MW, Chagnon M, Raymond J. Uncertainty and agreement in the management of unruptured intracranial aneurysms. J Neurosurg. 2014 Jan 3. [Epub ahead of print] PubMed PMID: 24405069.
7)

Gonda DD, Khalessi AA, McCutcheon BA, Marcus LP, Noorbakhsh A, Chen CC, Chang DC, Carter BS. Long-term follow-up of unruptured intracranial aneurysms repaired in California. J Neurosurg. 2014 Jun;120(6):1349-57. doi: 10.3171/2014.3.JNS131159. Epub 2014 Apr 11. PubMed PMID: 24724850.
8)

Kim DY, Park JC, Kim JK, Sung YS, Park ES, Kwak JH, Choi CG, Lee DH. Microembolism after Endovascular Treatment of Unruptured Cerebral Aneurysms: Reduction of its Incidence by Microcatheter Lumen Aspiration. Neurointervention. 2015 Sep;10(2):67-73. doi: 10.5469/neuroint.2015.10.2.67. Epub 2015 Sep 2. PubMed PMID: 26389009.

Unruptured intracranial aneurysm treatment decision

For a treatment decision of unruptured intracranial aneurysmphysicians and patients need to weigh the risk of treatment against the risk of hemorrhagic stroke caused by aneurysm rupture.

In a study of Detmer et al. Image segmentation data and patient information obtained from two patient cohorts including 203 patients with 249 aneurysms were used for patient-specific computational fluid dynamics simulations and subsequent evaluation of the statistical model in terms of accuracydiscrimination, and goodness of fit. The model’s performance was further compared to a similarity-based approach for rupture assessment by identifying aneurysms in the training cohort that were similar in terms of intracranial aneurysm hemodynamics and shape compared to a given aneurysm from the external cohorts.

When applied to the external data, the model achieved a good discrimination and goodness of fit (area under the receiver operating characteristic curve AUC = 0.82), which was only slightly reduced compared to the optimism-corrected AUC in the training population (AUC = 0.84). The accuracy metrics indicated a small decrease in accuracy compared to the training data (misclassification error of 0.24 vs. 0.21). The model’s prediction accuracy was improved when combined with the similarity approach (misclassification error of 0.14).

The model’s performance measures indicated a good generalizability for data acquired at different clinical institutions. Combining the model-based and similarity-based approach could further improve the assessment and interpretation of new cases, demonstrating its potential use for clinical unruptured intracranial aneurysm rupture risk assessment 1).

Scores

see also Unruptured intracranial aneurysm treatment score.

Unruptured intracranial aneurysm repair is the most commonly performed procedure for the prevention of hemorrhagic stroke. Despite efforts to regionalize care in high-volume centers, overall results have improved little 2).

The management of small unruptured incidentally discovered intracranial aneurysms (SUIAs) is still controversial.

Despite large trials supporting the management of small asymptomatic aneurysms, most neurosurgeons internationally chooses to treat them with surgery or endovascular means. Since clinicians use a number of factors beyond the maximum diameter when considering treatment options, future trials should consider these factors in their design 3).

Once a decision has been made to treat an intact aneurysm, the best treatment remains uncertain. Both surgical and endovascular management strategies are commonly performed for these lesions.

No one knows how best to manage these patients (an estimated 2—5% of the adult population), but with the increasing accessibility of non-invasive imaging, physicians are increasingly faced with the dilemma of what to do 4).

One stance maintains that the only acceptable rationale for a preventive treatment is randomised evidence that therapy does more good than harm. Thus, a randomised trial showing better outcomes for treated patients compared with conservatively managed patients would be necessary to justify invasive treatment of UIAs. However, this trial has not yet been successfully completed.

Posterior circulation in surgery, large aneurysms (>15 mm) in EVT, and stent- or balloon-assisted procedures in EVT were associated with the occurrence of complications. Poor clinical outcome (mRS of 3-6) was 0.8 % at hospital discharge.1) Detmer FJ, Fajardo-Jiménez D, Mut F, Juchler N, Hirsch S, Pereira VM, Bijlenga P, Cebral JR. External validation of cerebral aneurysm rupture probability model with data from two patient cohorts. Acta Neurochir (Wien). 2018 Dec;160(12):2425-2434. doi: 10.1007/s00701-018-3712-8. Epub 2018 Oct 30. PubMed PMID: 30374656.2) Zacharia BE, Bruce SS, Carpenter AM, Hickman ZL, Vaughan KA, Richards C, Gold WE, Lu J, Appelboom G, Solomon RA, Connolly ES. Variability in outcome after elective cerebral aneurysm repair in high-volume academic medical centers. Stroke. 2014 May;45(5):1447-52. doi: 10.1161/STROKEAHA.113.004412. Epub 2014 Mar 25. PubMed PMID: 24668204.3) Alshafai N, Falenchuk O, Cusimano MD. Practises and controversies in the management of asymptomatic aneurysms: Results of an international survey. Br J Neurosurg. 2015 Nov 5:1-7. [Epub ahead of print] PubMed PMID: 26540183.4) Raymond J, Darsaut TE, Molyneux AJ. A trial on unruptured intracranial aneurysms (the TEAM trial): results, lessons from a failure and the necessity for clinical care trials. Trials 2011; 12: 64.

UptoDate: Indocyanine green videoangiography for intracranial aneurysm

Indocyanine green videoangiography for intracranial aneurysm

Indocyanine green videoangiography for intracranial aneurysm is applied in order to assess intra-operatively both aneurysm sac obliteration and vessel patency after clipping.

Although digital subtraction angiography (DSA) may be considered the gold standard for intraoperative vascular imaging, many neurosurgical centers rely only on indocyanine green videoangiography (ICG-VA) for the evaluation of clipping accuracy.

In a Systematic Review and Meta-Analysis of Riva et al., from BrusselsLeuvenBelgiumMonzaItaly and ChicagoIllinois because a proportion of mis-clippings cannot be identified with ICG-VA, this technique should still be considered complementary rather than a replacement to DSA during aneurysm surgery. Incorporating other intraoperative tools, such as flowmetry or electrophysiological monitoring, can obviate the need for intraoperative DSA for the identification of vessel stenosis. Nevertheless, DSA likely remains the best tool for the detection of aneurysm remnants 1).

Its a safe and effective modality of intraoperative blood flow assessment and reduces the incidence of postoperative ischaemic complications 2).

However, ICGV-derived data have been reported to be misleading at times. Della Puppa et al., noted that a simple intra-operative maneuver (the “squeezing maneuver”) allows the detection of deceptive ICGV data on aneurysm exclusion and allows potential clip repositioning. The “squeezing maneuver” is based on a gentle pinch of the dome of a clipped aneurysm when ICGV documents its apparent exclusion.

Data from 23 consecutive patients affected by intracranial aneurysms who underwent the “squeezing maneuver” were retrospectively analyzed. The clip was repositioned in all cases when the dyeing of the sac was visualized after the maneuver.

In 22% of patients, after an initial ICGV showing the aneurysm exclusion after clipping, the squeezing maneuver caused the prompt dyeing of the sac; in all cases the clip was consequently repositioned. A calcification/atheroma of the wall/neck was predictive of a positive maneuver (p= 0.0002). The aneurysm exclusion rate at post-operative radiological findings was 100%.

With the limits of this small series, the “squeezing maneuver” appears helpful in the intra-operative detection of misleading ICGV data, mostly when dealing with aneurysms with atheromasic and calcified walls 3).

In selected cases, endoscopic ICG angiographies (e-ICG-A) provides the neurosurgeon with information that cannot be obtained by microscopic ICG angiography (m-ICG-A). E-ICG-A is capable of emerging as a useful adjunct in aneurysm surgery and has the potential to further improve operative results 4).

Indocyanine green (ICG) videoangiography (VA) in cerebral aneurysm surgery allows confirmation of blood flow in parent, branching, and perforating vessels as well as assessment of remnant aneurysm parts after clip application. A retrospective analysis from Two hundred forty-six procedures were performed in 232 patients harboring 295 aneurysms. The patients, whose mean age was 54 years, consisted of 159 women and 73 men. One hundred twenty-four surgeries were performed after subarachnoid hemorrhage, and 122 were performed for incidental aneurysms. Single aneurysms were clipped in 185 patients, and multiple aneurysms were clipped in 47 (mean aneurysm diameter 6.9 mm, range 2-40 mm). No complications associated with ICG-VA occurred. Intraoperative microvascular Doppler ultrasonography was performed before ICG-VA in all patients, and postoperative digital subtraction angiography (DSA) studies were available in 121 patients (52.2%) for retrospective comparative analysis. In 22 (9%) of 246 procedures, the clip position was modified intraoperatively as a consequence of ICG-VA. Stenosis of the parent vessels (16 procedures) or occlusion of the perforators (6 procedures), not detected by micro-Doppler ultrasonography, were the most common problems demonstrated on ICG-VA. In another 11 procedures (4.5%), residual perfusion of the aneurysm was observed and one or more additional clips were applied. Vessel stenosis or a compromised perforating artery occurred independent of aneurysm location and was about equally common in middle cerebral artery and anterior communicating artery aneurysms. In 2 procedures (0.8%), aneurysm puncture revealed residual blood flow within the lesion, which had not been detected by the ICG-VA. In the postoperative DSA studies, unexpected small (< 2 mm) aneurysm neck remnants, which had not been detected on intraoperative ICG-VA, were found in 11 (9.1%) of 121 patients. However, these remnants remained without consequence except in 1 patient with a 6-mm residual aneurysm dome, which was subsequently embolized with coils.

Its a helpful intraoperative tool and led to a significant intraoperative clip modification rate of 15%. However, small, < 2-mm-wide neck remnants and a 6-mm residual aneurysm were missed by intraoperative ICG-VA in up to 10% of patients. Results in this study confirm that DSA is indispensable for postoperative quality assessment in complex aneurysm surgery 5).

References

1)

Riva M, Amin-Hanjani S, Giussani C, De Witte O, Bruneau M. Indocyanine Green Videoangiography in Aneurysm Surgery: Systematic Review and Meta-Analysis. Neurosurgery. 2018 Aug 1;83(2):166-180. doi: 10.1093/neuros/nyx387. PubMed PMID: 28973404.
2)

Lai LT, Morgan MK. Use of indocyanine green videoangiography during intracranial aneurysm surgery reduces the incidence of postoperative ischaemic complications. J Clin Neurosci. 2014 Jan;21(1):67-72. doi: 10.1016/j.jocn.2013.04.002. Epub 2013 Oct 1. PubMed PMID: 24090515.
3)

Della Puppa A, Rustemi O, Rossetto M, Gioffrè G, Munari M, Charbel FT, Scienza R. The “Squeezing Maneuver” in Microsurgical Clipping of Intracranial Aneurysms Assisted by Indocyanine Green Video-angiography (ICGV). Neurosurgery. 2014 Mar 3. [Epub ahead of print] PubMed PMID: 24594928.
4)

Mielke D, Malinova V, Rohde V. Comparison of Intraoperative Microscopic and Endoscopic ICG-angiography in Aneurysm Surgery. Neurosurgery. 2014 Mar 10. [Epub ahead of print] PubMed PMID: 24618802.
5)

Roessler K, Krawagna M, Dörfler A, Buchfelder M, Ganslandt O. Essentials in intraoperative indocyanine green videoangiography assessment for intracranial aneurysm surgery: conclusions from 295 consecutively clipped aneurysms and review of the literature. Neurosurg Focus. 2014 Feb;36(2):E7. doi: 10.3171/2013.11.FOCUS13475. PubMed PMID: 24484260.

UpToDate: Pediatric intracranial tumor

Pediatric intracranial tumor

Epidemiology

Malignant brain tumors are not uncommon in infants as their occurrence before the age of three represents 20-25% of all malignant brain tumors in childhood.

The location of brain tumors in very young children differs from the posterior fossa predominance of older children. This is especially true in the first 6– 12 months of life, where supratentorial location is signicantly more common.

Approximately 20% of pediatric intracranial tumors arise from the thalamus or brainstem, with an incidence rate of 5% and 15%, respectively.

Medulloblastoma is the most common malignant pediatric intracranial tumor.

Diffuse intrinsic pontine glioma account for 10% to 25% of pediatric intracranial tumor.

Diagnosis

Bächli et al., from the Heidelberg University Hospital, Germany, report a single-institutional collection of pediatric brain tumor cases that underwent a refinement or a change of diagnosis after completion of molecular diagnostics that affected clinical decision-making including the application of molecularly informed targeted therapies. 13 pediatric central nervous system tumors were analyzed by conventional histology, immunohistochemistry, and molecular diagnostics including DNA methylation profiling in 12 cases, DNA sequencing in 8 cases and RNA sequencing in 3 cases. 3 tumors had a refinement of diagnosis upon molecular testing, and 6 tumors underwent a change of diagnosis. Targeted therapy was initiated in 5 cases. An underlying cancer predisposition syndrome was detected in 5 cases. Although this case series, retrospectiveand not population based, has its limitations, insight can be gained regarding precision of diagnosis and clinical management of the patients in selected cases. Accuracy of diagnosis was improved in the cases presented here by the addition of molecular diagnostics, impacting clinical management of affected patients, both in the first-line as well as in the follow-up setting. This additional information may support the clinical decision making in the treatment of challenging pediatric CNS tumors. Prospective testing of the clinical value of molecular diagnostics is currently underway 1).

Treatment

Malignant brain tumors represent a true therapeutic challenge in neurooncology. Before the era of modern imaging and modern neurosurgery these malignant brain tumors were misdiagnosed or could not benefit of the surgical procedures as well as older children because of increased risks in this age group.

The pediatric oncologists are more often confronted with very young children who need a complementary treatment. Before the development of specific approaches for this age group, these children received the same kind of treatment than the older children did, but their survival and quality of life were significantly worse. The reasons of these poor results were probably due in part to the fear of late effects induced by radiation therapy, leading to decrease the necessary doses of irradiation which increased treatment failures without avoiding treatment related complications.

At the end of the 80s, pilot studies were performed using postoperative chemotherapy in young medulloblastoma patients. Van Eys treated 12 selected children with medulloblastoma with MOPP regimen and without irradiation; 8 of them were reported to be long term survivors.

Subsequently, the pediatric oncology cooperative groups studies have designed therapeutic trials for very young children with malignant brain tumors.

Different approaches have been explored: * Prolonged postoperative chemotherapy and delayed irradiation as designed in the POG (Pediatric Oncology Group). * Postoperative chemotherapy without irradiation in the SFOP (Société Française d’Oncologie Pédiatrique) and in the GPO (German Pediatric Oncology) studies. *

The role of high-dose chemotherapy with autologous stem cells transplantation was explored in different ways: High-dose chemotherapy given in all patients as proposed in the Head Start protocol. High-dose chemotherapy given in relapsing patients as salvage treatment in the French strategy. In the earliest trials, the same therapy was applied to all histological types of malignant brain tumors and whatever the initial extension of the disease. This attitude was justified by the complexity of the classification of all brain tumors that has evolved over the past few decades leading to discrepancy between the diagnosis of different pathologists for a same tumor specimen. Furthermore, it has become increasingly obvious that the biology of brain tumors in very young children is different from that seen in older children. However, in the analysis of these trials an effort was made to give the results for each histological groups, according to the WHO classification and after a central review of the tumor specimens. All these collected data have brought to an increased knowledge of infantile malignant brain tumors in terms of diagnosis, prognostic factors and response to chemotherapy. Furthermore a large effort was made to study long term side effects as endocrinopathies, cognitive deficits, cosmetic alterations and finally quality of life in long term survivors. Prospective study of sequelae can bring information on the impact of the different factors as hydrocephalus, location of the tumor, surgical complications, chemotherapy toxicity and irradiation modalities. With these informations it is now possible to design therapeutic trials devoted to each histological types, adapted to pronostic factors and more accurate treatment to decrease long term sequelae 2).

Complications

Case series

1)

Bächli H, Ecker J, van Tilburg C, Sturm D, Selt F, Sahm F, Koelsche C, Grund K, Sutter C, Pietsch T, Witt H, Herold-Mende C, von Deimling A, Jones D, Pfister S, Witt O, Milde T. Molecular Diagnostics in Pediatric Brain Tumors: Impact on Diagnosis and Clinical Decision-Making – A Selected Case Series. Klin Padiatr. 2018 Jul 11. doi: 10.1055/a-0637-9653. [Epub ahead of print] PubMed PMID: 29996150.
2)

Kalifa C, Grill J. The therapy of infantile malignant brain tumors: current status? J Neurooncol. 2005 Dec;75(3):279-85. Review. PubMed PMID: 16195802.

Uptodate: Intracranial Subependymoma

Intracranial Subependymoma

Intracranial subependymomas are rare, mostly incidentalomas and therefore did not receive much attention in previous literature.

Many supratentorial subependymomas appear to be centered in the cortex or subcortical white matter. Therefore, a lack of ventricular involvement does not exclude subependymoma from the differential diagnosis.

By being classified as benign grade I in the World Health Organization Classification of Tumors of the Central Nervous System, they are given a special status compared to the other ependymal tumors. Tumor recurrences are a rarity, spinal “drop metastases” do not occur. While etiological, pathological and therapeutic characteristics have been subject of several publications over the last few decades and have meanwhile been well studied, the imaging characteristics are much less well received 1).

Epidemiology

They occur in middle to late adulthood.

Representing approximately 10% of ependymal tumors, subependymomas most often “present” as incidental autopsy findings in the brains of the elderly.

Most frequently they arise in the fourth ventricle (50-60%), followed by the lateral ventricle (30-40%), and less frequently in the septum pellucidum and spinal cord 2) 3).

Intraparenchymal subependymomas are extremely rare; only 6 cases have been reported in English literature. All of them were located in the supratentorial region 4) 5) 6) , and there has been only one report of infratentorial subependymoma 7)

see Subependymoma of the fourth ventricle

Histology

Subependymomas are small, discrete tumors of adults lying most often at the foramen of Monro or the fourth ventricle. It is composed of clusters of ependymal and astrocyte-like cells in a dense fibrillary stroma. It is typically attached to a ventricular wall and the most common site is the fourth ventricle.

Histologically, the tumor may be either compact or microcystic, but extensive microcystic change is rarely reported.

The histogenesis of subependymomas is still a matter of debate, with candidates including subependymal glia, astrocytes, ependymal cells, or some mixture of these cells. A recent theory hypothesizes that they originate from tanycytes, which are cells normally located in the subependymal zone 8).

Clinical features

They are likely to remain asymptomatic throughout life and some were found by autopsy. If symptomatic, tumor location and size are critical factors for presentation.

Diagnosis

Subependymomas have typical image morphologic characteristics that differentiate them from tumors of other entities, however, the rare subgroup of histopathological mixtures of subependymomas with ependymal cell fractions has no distinctly different imaging properties.

Knowing the imaging characteristics of subpendymoma and their differential diagnoses is of particular importance in order to be able to decide between the necessity of follow-up controls, an early invasive diagnosis or, depending on the entity, tumor resection.

KEY POINTS:

· Subependymomas have typical imaging characteristics that are clearly distinguishable from other entities.. · Increased incidence in middle/ older aged men, most frequent localization: 4th ventricle..

· Symptomatic subependymomas, often located in lateral ventricles, are usually characterized by hydrocephalus..

· Radiological identification of mixed subependymoma with ependymal cell fractions is not possible..

· Image based differentiation from other entities is important for the procedure.. 9).

Treatment

The surgical aims are the maximal safe tumoral resection, the decompression of neural elements, and establishment of a pathological diagnosis and the restoration of normal CSF pathways. As subependymomas are low-grade lesions with low rates of cell proliferation and a benign clinical course, complete surgical removal is usually curative.

Case series

33 patients with subependymoma, including 4 patients with a mixture of subependymomas with ependymal cell fractions in terms of imaging and clinical aspects and with reference to a current literature review.

Subependymomas have typical image morphologic characteristics that differentiate them from tumors of other entities, however, the rare subgroup of histopathological mixtures of subependymomas with ependymal cell fractions has no distinctly different imaging properties.

Knowing the imaging characteristics of subpendymoma and their differential diagnoses is of particular importance in order to be able to decide between the necessity of follow-up controls, an early invasive diagnosis or, depending on the entity, tumor resection.

KEY POINTS:

· Subependymomas have typical imaging characteristics that are clearly distinguishable from other entities.. · Increased incidence in middle/ older aged men, most frequent localization: 4th ventricle..

· Symptomatic subependymomas, often located in lateral ventricles, are usually characterized by hydrocephalus..

· Radiological identification of mixed subependymoma with ependymal cell fractions is not possible..

· Image based differentiation from other entities is important for the procedure.. 10).


With the SEER-18 registry database, information from all patients with intracranial subependymoma diagnosed during 2004-2013 were extracted, including age, sex, race, occurrence of surgery, extent of primary surgery, receipt of radiation, tumor size, and follow-up data. Age-adjusted incidence rates, overall survival, and cause-specific survival were calculated. Cox proportional hazards model was used for both univariate and multivariate analyses.

Four hundred sixty-six cases were identified. The overall incidence of intracranial subependymoma is 0.055 per 100,000 person-years (95% confidence interval, 0.05-0.06). Through multivariate analysis, age <40 years (hazard ratio [HR], 0.21; P = 0.03), female sex (HR, 0.34; P = 0.03), location within ventricles or near brainstem (HR, 0.49; P = 0.04), and occurrence of surgery (HR, 0.50; P = 0.02) were significant independent positive prognostic factors. Receipt of radiation did not show a significant relationship.

Clinical factors such as younger age, female sex, and location within ventricles or near brain stem demonstrated positive relationship with overall survival. For treatment options, surgery remains a mainstay option. No support for radiation therapy was identified 11).


Forty-three cases of pathologically confirmed, surgically treated intracranial subependymoma were identified. Thus in this patient population, subependymomas accounted for approximately 0.07% of intracranial tumors (43 of an estimated 60,000). Radiologically, 79.1% (34/43) of intracranial subependymomas were misdiagnosed as other diseases. Pathologically, 34 were confirmed as pure subependymomas, 8 were mixed with ependymoma, and 1 was mixed with astrocytoma. Thirty-five patients were followed up for 3.0 to 120 months after surgery. Three of these patients experienced tumor recurrence, and one died of tumor recurrence. Univariate analysis revealed that shorter progression-free survival (PFS) was significantly associated with poorly defined borders. The association between shorter PFS and age < 14 years was almost significant (p = 0.51), and this variable was also included in the multivariate analysis. However, multivariate analysis showed showed only poorly defined borders to be an independent prognostic factor for shorter PFS (RR 18.655, 95% CI 1.141-304.884, p = 0.040). In patients 14 years of age or older, the lesions tended to be pure subependymomas located in the unilateral supratentorial area, total removal tended to be easier, and PFS tended to be longer. In comparison, in younger patients subependymomas tended to be mixed tumors involving the bilateral infratentorial area, with a lower total removal rate and shorter PFS.

Intracranial subependymoma is a rare benign intracranial tumor with definite radiological features. Long-term survival can be expected, although poorly defined borders are an independent predictor of shorter PFS. All the features that differ between tumors in younger and older patients suggest that they might have different origins, biological behaviors, and prognoses 12).


24 pathologically proved cases of intracranial subependymomas in 17 male and seven female patients with a mean age of 48.1 years. All patients were symptomatic. CT and MR images were used to characterize the size, shape, and location of the subependymomas; the degree of hydrocephalus; tumor calcification; and the density, signal, and enhancement characteristics of the tumors.

Eighteen of 24 tumors were 3 cm or more in greatest dimension. Nineteen were lobulated, and hydrocephalus was seen in 21. Fourteen were in the lateral ventricle, and 10 were in the posterior fossa. Calcifications were present in five (all fourth ventricular) and absent in 10 (all lateral ventricular) subependymomas imaged with unenhanced CT. On 18 contrast-enhanced CT scans, five of six subependymomas with heterogeneous enhancement were in the fourth ventricle, and nine of 12 tumors with minimal or no enhancement were in the lateral ventricle. Small internal foci with a signal intensity similar to that of CSF were seen on images of all 10 lateral ventricular subependymomas obtained with both T1-weighted and T2-weighted sequences. On 13 contrast-enhanced T1-weighted images, seven of eight tumors with heterogeneous enhancement were in the fourth ventricle, and all five with minimal or no enhancement were in the lateral ventricle.

Intracranial subependymomas were seen in symptomatic middle-aged adults and showed different CT and MR imaging features, depending on their anatomic location. Calcification and heterogeneous contrast enhancement were common features of fourth ventricular subependymomas showed a lack of calcification as well as minimal or no contrast enhancement of CT and MR images 13).

1)

Kammerer S, Mueller-Eschner M, Lauer A, Luger AL, Quick-Weller J, Franz K, Harter P, Berkefeld J, Wagner M. Subependymomas – Characteristics of a “Leave me Alone” Lesion. Rofo. 2018 Jun 18. doi: 10.1055/a-0576-1028. [Epub ahead of print] PubMed PMID: 29913520.

2)

Ragel BT, Osborn AG, Whang K, Townsend JJ, Jensen RL, Couldwell WT. Subependymomas: an analysis of clinical and imaging features. Neurosurgery. 2006;58:881–890. discussion 881-890.

3)

Nishio S, Morioka T, Mihara F, Fukui M. Subependymoma of the lateral ventricles. Neurosurg Rev. 2000;23:98–103.

4)

Natrella F, Mariottini A, Rocchi R, Miracco C. Supratentorial neurenteric cyst associated with a intraparenchymal subependymoma. BMJ Case Rep. 2012;2012

5)

Hankey GJ, Davies L, Gubbay SS. Long term survival with early childhood intracerebral tumours. J Neurol Neurosurg Psychiatry. 1989;52:778–781.

6)

Shuangshoti S, Rushing EJ, Mena H, Olsen C, Sandberg GD. Supratentorial extraventricular ependymal neoplasms: a clinicopathologic study of 32 patients. Cancer. 2005;103:2598–2605.

7)

Kim Y, Lee SY, Yi KS, Cha SH, Gang MH, Cho BS, Lee YM. Infratentorial and intraparenchymal subependymoma in the cerebellum: case report. Korean J Radiol. 2014 Jan-Feb;15(1):151-5. doi: 10.3348/kjr.2014.15.1.151. Epub 2014 Jan 8. Review. PubMed PMID: 24497806; PubMed Central PMCID: PMC3909849.

8)

Sarkar C, Mukhopadhyay S, Ralte AM, Sharma MC, Gupta A, Gaikwad S, Mehta VS. Intramedullary subependymoma of the spinal cord: a case report and review of literature. Clin Neurol Neurosurg. 2003;106:63–68.

9) , 10)

Kammerer S, Mueller-Eschner M, Lauer A, Luger AL, Quick-Weller J, Franz K, Harter P, Berkefeld J, Wagner M. Subependymomas – Characteristics of a “Leave me Alone” Lesion. Rofo. 2018 Jun 18. doi: 10.1055/a-0576-1028. [Epub ahead of print] PubMed PMID: 29913520.

11)

Nguyen HS, Doan N, Gelsomino M, Shabani S. Intracranial Subependymoma: A SEER Analysis 2004-2013. World Neurosurg. 2017 May;101:599-605. doi: 10.1016/j.wneu.2017.02.019. Epub 2017 Feb 15. PubMed PMID: 28232153.

12)

Bi Z, Ren X, Zhang J, Jia W. Clinical, radiological, and pathological features in 43 cases of intracranial subependymoma. J Neurosurg. 2015 Jan;122(1):49-60. doi: 10.3171/2014.9.JNS14155. PubMed PMID: 25361493.

13)

Chiechi MV, Smirniotopoulos JG, Jones RV. Intracranial subependymomas: CT and MR imaging features in 24 cases. AJR Am J Roentgenol. 1995 Nov;165(5):1245-50. PubMed PMID: 7572512.

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.

Intracranial Pressure & Neuromonitoring XVI (Acta Neurochirurgica Supplement) 1st ed. 2018 Edition

Intracranial Pressure & Neuromonitoring XVI (Acta Neurochirurgica Supplement) 1st ed. 2018 Edition

List Price: 

This book introduces the latest advances relating to the pathophysiology, biophysics, monitoring and treatment of traumatic brain injury, hydrocephalus, and stroke presented at the 16th International Conference on Intracranial Pressure and Neuromonitoring (the “ICP Conference”), held in Cambridge, Massachusetts, in June 2016 in conjunction with the 6th Annual Meeting of the Cerebral Autoregulation Research Network. Additionally, the conference held special sessions on neurocritical care informatics and cerebrovascular autoregulation. The peer-reviewed papers included were written by leading experts in neurosurgery, neurointensive care, anesthesiology, physiology, clinical engineering, clinical informatics and mathematics who have made important contributions in this translational area of research, and their focus ranges from the latest research findings and developments to clinical trials and experimental studies. The book continues the proud tradition of publishing key work from the ICP Conferences and is a must-read for anyone wishing to stay abreast of recent advances in the field.

Update: Intracranial chondroma

Intracranial chondroma

Intracranial chondroma are cysts of chondroid tissue, first reported by Hirschfeld in 1851 1)

Epidemiology

They are extremely rare and account for only 0.2% to 0.3% of all intracranial tumor2) 3).
They can be present at different regions within the cranial cavity especially the skull base 4)intrasellar 5),parasellar 6)intradural and especially falx 7).
Very occasionally observed in combination with intratumoral hemorrhage 8).
Despite a purported lack of any sex predilection there are reports of a slight female predominance 9).
Intracerebral location is extremely rare and has only been described in a few cases 10) 11) 12).

Etiology

Various theories have been proposed to determine the etiology of intracranial chondromas but none has succeeded to ascertain a definite cause of origin. The most commonly accepted explanation for skull base chondromas is embryonic remnants of chondrogenic cells along the base 13).
They grow slowly by expansion and mostly originate from rests of cartilaginous cells at sphenoethmoidal sutureand sphenooccipital suture 14).
The chondromas arising from the dura matter, choroid plexus, and cerebral cortex have been proposed to develop from metaplasia of meningeal fibroblasts and perivascular meninges 15). Similarly, proliferation of ectopic embryologic rests of cartilage cells, traumatic displacement of cartilage elements or inflammatory cartilaginous activation of fibroblasts have been suggested to be the cause of development of intracranial chondromas 16).

Clinical features

The presenting symptoms range from headaches to lower cranial nerve palsy. In some cases, proptosis, diplopia and varying degrees of visual activity impairment along with orbital extension have been reported. Patients often complain of forgetfulness and lack of concentration.
Generalized tonic–clonic seizures are also usually the presenting complaints in intracranial chondromas, which develop because of the gradual destruction of a large number of neurons that begin to fire at regular intervals. Focal neurological deficits may also result from mass effects of tumor.
Intracranial chondroma has also been reported as a component of Ollier’s multiple chondromatosis.
Pontine hemorrhage has also been associated with parasellar intracranial chondromas. Association of skull base chondromas has also been reported with Maffucci syndrome.
Intracranial chondromas may develop in a person at any age but they have been most frequently observed in the third decade.

Diagnosis

Bone destruction occurs in over 50% of the cases, whereas irregular calcifications are seen in about 60%. Intracranial chondromas may also produce hyperostosis of the inner table of the skull 17) 18) 19).
On X-ray, intracranial chondromas represent hyperostosis of the internal table of the skull 20). enhanced intracranial pressure and calcified portions21). Intradural convexity chondromas possess carved, tufted, ring-shaped calcified areas 22).
MRI has become an important diagnostic tool for intracranial chondromas. Brownlee et al. reported variable signal intensity at different levels of MRI in a case of intracranial chondroma. At T1 they reported less intensity whereas at T2 the signal appeared to be of middle to high intensity 23).
They are typically DWI hypointense with high apparent diffusion coefficient (ADC) values while meningiomas are typically DWI hyperintense with low ADC values 24).


A study reported that intradural chondromas possess two different CT appearances. The usually found type 1 shows mixed density with minimal or moderate enhancements. The rare type 2 shows an innermost less dense area containing a cyst 25).


Angiography shows displacement of vessels but no tumor stain 26) 27) 28).


Chondromas showed low uptake in PET images, which might be useful for differentiation between chondromas and chordomas 29).


In the past pneumoencephalography revealed displacement of basal cisterns and the ventricular system. A radionuclide brain scan may show abnormal uptake in the tumor 30).

Differential diagnosis

Preoperatively, chondromas can be difficult to distinguish from meningiomas. They may also be confused with chordomas, craniopharyngiomas or even arterial aneurysms 31) 32)
Tanohata et al. reported two instances of skull base chondromas that exhibited delayed contrast enhancement on CT after a high-dose of the contrast medium was administered. They suggested this CT feature to be employed in differential diagnosis of intracranial chondromas from meningiomas and neurinomas 33).

Treatment

In symptomatic patients, operative resection is sensible. In most cases total removal of the tumor is possible and leads to full recovery. When the finding is merely incidental in older patients, a watchful waiting approach is acceptable, given the benign and slow-growing nature of the lesion 34).
The current popular surgical approach for parasellar lesions is transcranial such as the orbitozygomatic approachsubtemporal approach. In surgical removal of skull base chondromas, it is advisable to try to confirm the diagnosis preoperatively with characteristic image findings and to consider the best approach in each case to decompress the involved nerves without any complications 35).
In cases of convexity chondroma, it is additionally recommended to remove the dural attachment 36) 37) 38).

Outcome

Usually postoperative observation reveals no recurrence of the lesion after complete resection. An adjuvant therapy is not necessary and the long-term prognosis is good 39) 40) 41).
The malignant form, chondrosarcoma, generally occurs later in life, presenting mostly in the fifth and sixth decades 42).

Case series

2011

Xin et al. retrospectively analyzed the clinical data of 30 patients (12 males and 18 females; mean age 35.4 years; age range 16-60 years) who had pathologically confirmed intracranial chondroma treated at our hospital from September 1996 to June 2008. Surgery was performed on all 30 patients: five patients underwent postoperative radiotherapy; 26 patients were followed up postoperatively for a mean duration of 45.8 months. The surgical approach was selected according to tumor location. Total resection was achieved in 11 patients, subtotal resection in 13, and partial resection in nine (three patients had recurrent chondroma). Follow-up showed that 21 patients recovered without recurrences, three had recurrence, and two patients died. The clinical manifestations included headache and multiple cranial nerve lesions. Imaging usually showed a well-demarcated extramedullary tumor, centrally located, without surrounding brain edema, partially calcified (73.3%) and with minimal vascularity, often accompanied by erosion and destruction of surrounding bone (56.7%). It is difficult to totally remove an intracranial chondroma, and it is not possible to differentiate a chondroma from a myxoma or chordoma at the cranial base on the basis of clinical manifestations and neuroradiological findings. Selection of the appropriate surgical approach is important for resection of the tumor 43).

1976

Four new cases are added to the previously recorded 122 cases 44).

Case reports

2018

A 25-year-old male patient with a giant convexity chondroma with meningeal attachment in the right frontal lobe that was detected after a first generalized seizure. Based on the putative diagnosis of meningioma, the tumor was completely resected via an osteoplastic parasagittal craniotomy. The postoperative MRI confirmed the complete tumor resection. Histopathological analysis revealed the presence of a chondroma 45).

2017

Giant convexity chondroma with dural involvement: Case report and review of literature 46).

2013

A 55-year-old female presented to the emergency room with a complaint of aphasia. Her initial brain computed tomography scan showed an intracranial hemorrhage in the left frontal area. After surgery, histopathological examination confirmed the diagnosis of a chondroma. Intradural chondroma is a rare, slow growing, benign intracranial neoplasm, but is even rarer in combination with an intratumoral hemorrhage. Chondromas are generally avascular cartilaginous lesions. This case was thought to be caused by the rupture of abnormally weak vessels derived from the friable tumor. Intradural chondromas may be included in the differential diagnosis of intracranial tumors with acute hemorrhages. 47).

2012

A 23-year-old Asian man presenting with intracerebral chondroma of the left frontal lobe, which was eroding the dura matter. The intracranial chondroma was completely removed by surgery 48).

2011

A 45-year old female is presented with a solitary intracerebral chondroma located in the right frontal lobe with no meningeal attachment 49).


An intracranial chondroma with intratumoral and subarachnoidal hemorrhage 50).

2007

Higashida et al. reported two cases of intracranial skull base chondroma and discussed the differential diagnosis and the treatment strategies. The first case was a 39-year-old male who presented with left exophtalmos, visual loss and oculomotor disturbance. MRI showed a huge tumor occupying the bilateral cavernous sinus. Partial removal of the tumor was performed through the left orbitozygomatic subtemporal approach. The second case was a 54-year-old male who presented with left hemiparesis. MRI showed a brain stem infarction with a huge tumor located at the right middle fossa. Partial removal was performed through the right orbitozygomatic subtemporal approach. In these two cases, the histopathological diagnosis of the tumors was benign chondroma and the size of residual tumors have not changed for one year without any additional therapy 51).


A Osteochondroma of the skull base 52).

2003

A rare case of a chondroma arising from the convexity dura mater 53).

2001

A case of intracranial giant chondroma originating from the dura mater of the convexity 54).

2000

Intradural convexity chondroma: a case report and review of diagnostic features 55).

1993

A rare case of chondroma originated from the dura mater of the cerebral convexity in a 16-year-old girl. Radiologic findings are reported with emphasis on computed tomography and magnetic resonance imaging scans, and histogenesis is briefly discussed 56).

1991

A rare case of Maffucci’s syndrome associated with enchondroma at the skull base, left internal carotid artery aneurysm, and goiter is reported. Two other previously reported cases of Maffucci’s syndrome with associated aneurysms and the present case suggest that Maffucci’s syndrome may be associated with aneurysm 57).


A 8-year-old female with Ollier’s disease (multiple enchondromatosis) developed an intracranial chondroma arising from the clivus, which was diagnosed by both computed tomography and magnetic resonance imaging 58).

1990

A rare case of parasellar chondroma accompanied by pontine hemorrhage is described. A review is made of the previously reported 6 cases of intracranial chondromas complicated with hemorrhage. A 21 year-old woman was admitted because of consciousness deterioration progressing to coma within a day, and right hemiparesis. CT scan showed a contrast-enhanced mass in the parasellar region and a hematoma in the brain-stem, which was clearly demonstrated by MRI to be abutted on the dorsal part of the tumor mass. The tumor was removed through frontotemporal craniotomy and confirmed histologically as chondroma. Postoperatively, the patient gradually regained consciousness and is hospitalized to rehabilitate hemiparesis 59).

1989

A case is presented in which a solitary chondroma arose from the clivus of a patient with Ollier’s disease 60).

1983

Intradural chondroma: a case report and review of the literature 61).

1981

A case of a huge intracranial frontoparietal osteochondroma in a 20-year-old man is reported. The presenting symptoms were headache, vomiting, and blurred vision. Apart from papilledema, no other abnormal neurological signs were present. A specific preoperative diagnosis could not be reached from the information provided by plain skull films, angiography, and radionuclide scan. The findings on computed tomography were those of a high density mass interspersed with small foci of lower densities, producing a honeycomb appearance, and surrounded by deposits of nodular calcification. The postcontrast scan showed a moderate degree of enhancement with preservation of the precontrast honeycomb pattern. These particular features may enable a correct preoperative histological diagnosis to be offered with a high degree of probability 62).

1969

Osteochondroma of the base of the skull causing an isolated oculomotor nerve paralysis. Case report emphasizing microsurgical techniques 63).
1)

L. Hirschfeld, Sur une tumer cartilaginease du la base du crane (enchondroma), C. R. Soc. Biol. 3 (1851) 94–96.
2) , 42)

Berkmen YM, Blatt ES. Cranial and intracranial cartilaginous tumours. Clin Radiol. 1968 Jul;19(3):327-33. PubMed PMID: 5302924.
3)

Zulch KJ, Wechsler W. Pathology and classification of gliomas. Pro Neurol Surg. 1968;2:1–84.
4) , 14) , 29) , 35) , 51)

Higashida T, Sakata K, Kanno H, Tanabe Y, Kawasaki T, Yamamoto I. [Intracranial chondroma arising from the skull base: two case reports featuring the image findings for differential diagnosis]. No Shinkei Geka. 2007 May;35(5):495-501. Japanese. PubMed PMID: 17491346.
5)

Munemitsu H, Matsuda M, Hirai O, Fukumitsu T, Kawamura J. Intrasellar chondroma. Neurol Med Chir (Tokyo). 1981 Jul;21(7):775-80. PubMed PMID: 6170021.
6) , 59)

Furui T, Iwata K, Yamamoto H, Murakami A. [A case of intracranial chondroma presenting with pontine hemorrhage]. No Shinkei Geka. 1990 Jun;18(6):543-6. Review. Japanese. PubMed PMID: 2203983.
7) , 15) , 22) , 56)

Nakazawa T, Inoue T, Suzuki F, Nakasu S, Handa J. Solitary intracranial chondroma of the convexity dura: case report. Surg Neurol. 1993 Dec;40(6):495-8. Review. PubMed PMID: 8235973.
8) , 50)

Linsen M, Junmei W, Liwei Z, Jianping D, Xuzhu C. An intracranial chondroma with intratumoral and subarachnoidal hemorrhage. Neurol India. 2011 Mar-Apr;59(2):310-3. doi: 10.4103/0028-3886.79170. PubMed PMID: 21483150.
9)

Krayenbühl H, Yasargil M. Chondromas. Prog Neurol Surg. 1978;6:435–463.
10)

A. Ahyai, O. Spoerri, Intracerebral chondroma, Surg. Neurol. 11 (1979) 431–433.
11)

J. Chorobski, J. Jarzymski, E. Ferens, Intracranial solitary chondroma, Surg. Gynecol. Obstetr. 68 (1939) 677–686.
12)

E. Peltonen, O. Suess, M. Koenneker, M. Brock, T. Kombos, Atypical location of a solitary intracranial chondroma without meningeal attachment, Zentralbl. Neurochir. 68 (2007) 83–86
13) , 16) , 49)

Zhan RY, Pan XF, Wan S, Lan P, Zhang YC, Weng NC, Yan M, Zhou YQ. Solitary intracerebral chondroma without meningeal attachment: a case report with review of the literature. J Int Med Res. 2011;39(2):675-81. Review. PubMed PMID: 21672374.
17)

J. Dutton, Intracranial solitary chondroma. Case report, J. Neurosurg. 49 (1978) 460–463.
18)

E. Palacios, Intracranial solitary chondroma of dural origin, Am. J. Roentgenol. 110 (1970) 67–70.
19) , 33)

Tanohata K, Maehara T, Aida N, Unimo S, Matsui K, Mochimatsu Y, Fujitsu K. Computed tomography of intracranial chondroma with emphasis on delayed contrast enhancement. J Comput Assist Tomogr. 1987 Sep-Oct;11(5):820-3. PubMed PMID: 3655044.
20) , 54)

Nakayama M, Nagayama T, Hirano H, Oyoshi T, Kuratsu J. Giant chondroma arising from the dura mater of the convexity. Case report and review of the literature. J Neurosurg. 2001 Feb;94(2):331-4. PubMed PMID: 11213975.
21) , 39)

Erdogan S, Zorludemir S, Erman T, Akgul E, Ergin M, Ildan F, Bagdatoglu H. Chondromas of the falx cerebri and dural convexity: report of two cases and review of the literature. J Neurooncol. 2006 Oct;80(1):21-5. PubMed PMID: 16937014.
23)

Brownlee RD, Sevick RJ, Rewcastle NB, Tranmer BI. Intracranial chondroma. AJNR Am J Neuroradiol. 1997 May;18(5):889-93. Review. PubMed PMID: 9159366.
24)

S. Shrot, A.R. Cohen, F.J. Rodriguez, F. Berkowitz, B.P. Soares, T.A. Huisman, Intracranial dural chondroma in a child-conventional and advanced neuroimaging characteristics and differential diagnosis, Neuroradiol. J. (January) (2017) 1971400917712268.
25) , 55)

Khosrovi H, Sadrolhefazi A, el-Kadi H, Bloomfield SM, Schochet SS. Intradural convexity chondroma: a case report and review of diagnostic features. W V Med J. 2000 Nov-Dec;96(6):612-6. Review. PubMed PMID: 11194092.
26)

Y.M. Berkmen, E.S. Blatt, Cranial and intracranial cartilaginous tumours, Clin. Radiol. 19 (1968) 327–333.
27)

F. Duan, S. Qui, J. Jiang, J. Chang, Z. Liu, X. Feng, W. Xiong, J. An, J. Chen, W. Yang, Characteristic CT and MRI findings of intracranial chondroma, Acta Radiol. 53 (10) (2012) 11446–11454.
28) , 38) , 41)

E. Kurt, G.N. Beute, M. Sluzewski, W.J. van Rooij, J.L. Teepen, Giant chondroma of the falx. Case report and review of the literature, J. Neurosurg. 85 December 6 (1996) 1161–1164.
30) , 44)

Sarwar M, Swischuk LE, Schecter MM. Intracranial chondromas. AJR Am J Roentgenol. 1976 Dec;127(6):973-7. PubMed PMID: 998836.
31)

Y.M. Berkmen, E.S. Blatt, Cranial and intracranial cartilaginous tumours, Clin. Radiol. 19 (1968) 327–333.
32)

B. De Coene, C. Gilliard, C. Grandin, J.F. Nisolle, J.P. Trigaux, J.B. Lahdou, Unusual location of an intracranial chondroma, Am. J. Neuroradiol. 18 (1997) 573–577.
34) , 45)

Feierabend D, Maksoud S, Lawson McLean A, Koch A, Kalff R, Walter J. Giant convexity chondroma with meningeal attachment. Clin Neurol Neurosurg. 2018 Mar 27;169:37-40. doi: 10.1016/j.clineuro.2018.03.027. [Epub ahead of print] PubMed PMID: 29609117.
36)

M. Nakayama, T. Nagayama, H. Hirano, T. Oyoshi, J. Kuratsu, Giant chondroma arising from the dura mater of the convexity, J. Neurosurg. 94 (2001) 331–334.
37)

C. Reinshagen, N. Redjal, D.P. Sajed, B.V. Nahed, B.P. Walcott, Intracranial dural based chondroma, J. Clin. Neurosci. 25 (March) (2016) 161–163.
40)

A. Doukas, A. Tallo, R. Parvin, V. Hans, P. Daemi, A. Cheko, M. Scholz, A.K. Petridis, Giant dural supratentorial chondroma generating the question of how large can a tumor become without revealing itself, Clin. Pract. 5 (4) (2015) 777.
43)

Xin Y, Hao S, Zhang J, Wu Z, Jia G, Tang J, Zhang L. Microsurgical treatment of intracranial chondroma. J Clin Neurosci. 2011 Aug;18(8):1064-71. doi: 10.1016/j.jocn.2010.12.028. Epub 2011 Jun 30. PubMed PMID: 21719289.
46)

Raju V, Raman R, Shanmugasundaram B, Kochikaran I. Giant convexity chondroma with dural involvement: Case report and review of literature. Asian J Neurosurg. 2017 Apr-Jun;12(2):311-313. doi: 10.4103/1793-5482.145574. PubMed PMID: 28484562; PubMed Central PMCID: PMC5409398.
47)

Park JH, Jeun SS. An intracranial chondroma with intratumoral hemorrhage: a case report and review of the literature. Brain Tumor Res Treat. 2013 Apr;1(1):42-4. doi: 10.14791/btrt.2013.1.1.42. Epub 2013 Apr 30. PubMed PMID: 24904889; PubMed Central PMCID: PMC4027121.
48)

Uddin MM, Ashraf J, Memon AA, Ali J. Intracranial cystic chondroma: a case report. J Med Case Rep. 2012 Dec 28;6:432. doi: 10.1186/1752-1947-6-432. PubMed PMID: 23272896; PubMed Central PMCID: PMC3540000.
52)

Padhya TA, Athavale SM, Kathju S, Sarkar S, Mehta AR. Osteochondroma of the skull base. Otolaryngol Head Neck Surg. 2007 Jul;137(1):166-8. PubMed PMID: 17599588.
53)

Colpan E, Attar A, Erekul S, Arasil E. Convexity dural chondroma: a case report and review of the literature. J Clin Neurosci. 2003 Jan;10(1):106-8. Review. PubMed PMID: 12464537.
57)

Chakrabortty S, Tamaki N, Kondoh T, Kojima N, Kamikawa H, Matsumoto S. Maffucci’s syndrome associated with intracranial enchondroma and aneurysm: case report. Surg Neurol. 1991 Sep;36(3):216-20. PubMed PMID: 1876972.
58)

Ghogawala Z, Moore M, Strand R, Kupsky WJ, Scott RM. Clival chondroma in a child with Ollier’s disease. Case report. Pediatr Neurosurg. 1991-1992;17(1):53-6. PubMed PMID: 1811715.
60)

Traflet RF, Babaria AR, Barolat G, Doan HT, Gonzalez C, Mishkin MM. Intracranial chondroma in a patient with Ollier’s disease. Case report. J Neurosurg. 1989 Feb;70(2):274-6. PubMed PMID: 2913225.
61)

Mapstone TB, Wongmongkolrit T, Roessman U, Ratcheson RA. Intradural chondroma: a case report and review of the literature. Neurosurgery. 1983 Jan;12(1):111-4. PubMed PMID: 6828215.
62)

Matz S, Israeli Y, Shalit MN, Cohen ML. Computed tomography in intracranial supratentorial osteochondroma. J Comput Assist Tomogr. 1981 Feb;5(1):109-15. PubMed PMID: 6972390.
63)

Bakdash H, Alksne JF, Rand RW. Osteochondroma of the base of the skull causing an isolated oculomotor nerve paralysis. Case report emphasizing microsurgical techniques. J Neurosurg. 1969 Aug;31(2):230-3. PubMed PMID: 5803809.
WhatsApp WhatsApp us
%d bloggers like this: