Spinal meningioma treatment

Spinal meningioma treatment

Radical resection of spinal meningiomas can be performed with good functional results. Extensive tumor calcification, especially in elderly patients proved to harbor an increased risk for surgical morbidity 1).


Onken et al., reported on their surgical experience that involves two institutions in which 207 patients underwent surgery for spinal meningiomas (sMNGs) . Special focus was placed on patients with sMNGs localized anterior to the denticulate ligament (aMNGs) that were treated via a unilateral posterior approach (ULPA).

The duration of surgery, extent of resection, and outcomes are comparable between aMNGs and posterior to the denticulate ligament (pMNGs) when removed via a ULPA. Thus, ULPA represents a safe route to achieve a gross-total resection, even in cases of aMNG 2).


Posterior approaches provide adequate exposure to safely remove ventrally located spinal meningioma. Posterior exposures with lateral bone resection, denticulate ligament division, provide also adequate exposure for safe removal 3).

Technique

After dural opening, a plane can be developed between the arachnoid and the tumor. The tumor is then internally debulked using suction, an ultrasonic surgical aspirator, microscissors, or laser.

After debulking, in the majority of cases the tumor can be rolled away from the spinal cord and toward its dural attachment.

The tumor is then removed from its dural attachment.

Dura with remaining tumor can be coagulated using bipolar cauterization or resected.

In the majority of cases, the dural attachment was cauterized rather than resected. The dural attachment was always cauterized in cases involving an anterior dural attachment. Additionally, in most cases the dura was closed primarily, compared with suturing in a graft, which was performed far less frequently

Another option was separation of the dura into an outer and inner layer and to resect the tumor with the inner layer, leaving the outer layer available for closure 4).

Videos

References

1)

Sandalcioglu IE, Hunold A, Müller O, Bassiouni H, Stolke D, Asgari S. Spinal meningiomas: critical review of 131 surgically treated patients. Eur Spine J. 2008 Aug;17(8):1035-41. doi: 10.1007/s00586-008-0685-y. Epub 2008 May 15. PubMed PMID: 18481118; PubMed Central PMCID: PMC2518757.
2)

Onken J, Obermüller K, Staub-Bartelt F, Meyer B, Vajkoczy P, Wostrack M. Surgical management of spinal meningiomas: focus on unilateral posterior approach and anterior localization. J Neurosurg Spine. 2018 Dec 1:1-6. doi: 10.3171/2018.8.SPINE18198. [Epub ahead of print] PubMed PMID: 30544344.
3)

Notani N, Miyazaki M, Kanezaki S, Ishihara T, Kawano M, Tsumura H. Surgical management of ventrally located spinal meningiomas via posterior approach. Eur J Orthop Surg Traumatol. 2017 Feb;27(2):181-186. doi: 10.1007/s00590-016-1860-1. PubMed PMID: 27671472.
4)

Gottfried ON, Gluf W, Quinones-Hinojosa A, Kan P, Schmidt MH. Spinal meningiomas: surgical management and outcome. Neurosurg Focus. 2003 Jun 15;14(6):e2. Review. PubMed PMID: 15669787.

Acromegaly medical treatment

Acromegaly medical treatment

Medical treatment

Indications

Patients not cured by surgery.

Who cannot tolerate surgery.

Recurrence after surgery or radiotherapy.

More satisfactory surgical outcomes for noninvasive macroadenomas treated with presurgical SA may be achieved, although controversy of such adjuvant therapy exists. Combination of SA and pegvisomant or cabergoline shows advantages in some specific cases. Thus, an individual treatment program should be established for each patient under a full evaluation of the risks and benefits 1).


First-generation somatostatin receptor ligands (SRL) are the mainstay of acromegaly treatment, however the percentage of patients controlled with these drugs significantly varies in the different studies. Many factors are involved in the resistance to SRL.

In a review, Gadelha et al., updated the physiology of somatostatin and its receptors (sst), the use of SRL in the treatment of acromegaly and the factors involved in the response to these drugs. The SRL act through interaction with the sst, which up to now have been characterized as five subtypes. The first-generation SRL, octreotide and lanreotide, are considered sst2 specific and have biochemical response rates varying from 20 to 70%. Tumor volume reduction can be found in 36-75% of patients. Several factors may determine the response to these drugs, such as sst, aryl hydrocarbon receptor interacting protein (AIP), E-cadherinZAC1filamin A and β-arrestin expression in the somatotropinomas. In patients resistant to first-generation SRL, alternative medical treatment options include: SRL high dose regimens, SRL in combination with cabergoline or pegvisomant, or the use of pasireotide. Pasireotide is a next-generation SRL with a broader pattern of interaction with sst. In the light of the recent increase of treatment options in acromegaly and the deeper knowledge of the determinants of response to the current first-line therapy, a shift from a trial-and-error treatment to a personalized one could be possible 2).


The cost of treatment including medications and the possibility of major side effects represent important limitations of the medical therapy 3) 4).

The most widely used criteria for neurosurgical outcome assessment were combined measurements of IGF-1 and GH levels after oral glucose tolerance test (OGTT) 3 months after surgery. Ninety-eight percent of respondents stated that primary treatment with somatostatin receptor ligands (SRLs) was indicated at least sometime during the management of acromegaly patients. In nearly all centers (96%), the use of pegvisomant monotherapy was restricted to patients who had failed to achieve biochemical control with SRL therapy. The observation that most centers followed consensus statement recommendations encourages the future utility of these workshops aimed to create uniform management standards for acromegaly 5)

Current pharmacotherapy includes somatostatin analogs (SAs) and GH receptor antagonist; the former consists of lanreotide Autogel (ATG) and octreotide long-acting release (LAR), and the latter refers to pegvisomant. As primary medical therapy, lanreotide ATG and octreotide LAR can be supplied in a long-lasting formulation to achieve biochemical control of GH and IGF-1 by subcutaneous injection every 4-6 weeks. Lanreotide ATG and octreotide LAR provide an effective medical treatment, whether as a primary or secondary therapy, for the treatment of GH-secreting pituitary adenoma; however, to maximize benefits with the least cost, several points should be emphasized before the application of SAs. A comprehensive assessment, especially of the observation of clinical predictors and preselection of SA treatment, should be completed in advance. A treatment process lasting at least 3 months should be implemented to achieve a long-term stable blood concentration. More satisfactory surgical outcomes for noninvasive macroadenomas treated with presurgical SA may be achieved, although controversy of such adjuvant therapy exists. Combination of SA and pegvisomant or cabergoline shows advantages in some specific cases. Thus, an individual treatment program should be established for each patient under a full evaluation of the risks and benefits 6).

Somatostatin treatment can induce extensive fibrosis in GH secreting pituitary adenoma 7).

References

1)

Wang JW, Li Y, Mao ZG, Hu B, Jiang XB, Song BB, Wang X, Zhu YH, Wang HJ. Clinical applications of somatostatin analogs for growth hormone-secreting pituitary adenomas. Patient Prefer Adherence. 2014 Jan 6;8:43-51. eCollection 2014. Review. PubMed PMID: 24421637; PubMed Central PMCID: PMC3888346.
2)

Gadelha MR, Wildemberg LE, Bronstein MD, Gatto F, Ferone D. Somatostatin receptor ligands in the treatment of acromegaly. Pituitary. 2017 Feb;20(1):100-108. doi: 10.1007/s11102-017-0791-0. Review. PubMed PMID: 28176162.
3)

Chanson P, Salenave S, Kamenicky P, Cazabat L, Young J. Pituitary tumours: Acromegaly. Best Pract Res Clin Endocrinol Metab. 2009;23:555–74.
4)

Gondim JA, Ferraz T, Mota I, Studart D, Almeida JP, Gomes E, et al. Outcome of surgical intrasellar growth hormone tumor performed by a pituitary specialist surgeon in a developing country. Surg Neurol. 2009;72:15–9.
5)

Giustina A, Bronstein MD, Casanueva FF, Chanson P, Ghigo E, Ho KK, Klibanski A, Lamberts S, Trainer P, Melmed S. Current management practices for acromegaly: an international survey. Pituitary. 2011 Jun;14(2):125-33. doi: 10.1007/s11102-010-0269-9. PubMed PMID: 21063787.
6)

Wang JW, Li Y, Mao ZG, Hu B, Jiang XB, Song BB, Wang X, Zhu YH, Wang HJ. Clinical applications of somatostatin analogs for growth hormone-secreting pituitary adenomas. Patient Prefer Adherence. 2014 Jan 6;8:43-51. Review. PubMed PMID: 24421637.
7)

Kerschbaumer J, Pinggera D, Moser P, Hofmann A, Thomé C, Freyschlag CF. Somatostatin treatment can induce extensive fibrosis in growth hormone-producing adenoma. Acta Neurochir (Wien). 2016 Mar;158(3):441-3. doi: 10.1007/s00701-016-2714-7. Epub 2016 Jan 23. PubMed PMID: 26801514.

Intracranial ependymoma treatment

Intracranial ependymoma treatment

The low prevalence of intracranial ependymoma in adults limits the ability to perform clinical trials. Therefore, treatment decisions are based on small, mostly retrospective studies and the role of chemotherapy has remained unclear.

Gross total resection (GTR) is considered the cornerstone of therapy 1) 2).

Adjuvant radiotherapy is often delivered to improve long-term disease control. Over the years, radiation treatment for ependymoma has evolved from cranio spinal radiation (CSI) 3) 4) to focal radiation 5) 6)

The major consensus was reached that treatment decisions for ependymoma (outside of clinical trials) should not be based on grading (II vs III). Supratentorial and posterior fossa ependymomas are distinct diseases, although the impact on therapy is still evolving. Molecular subgrouping should be part of all clinical trials henceforth 7).

Stereotactic Radiosurgery

Seven centers participating in the International Radiosurgery Research Foundation identified 89 intracranial ependymoma patients who underwent SRS (113 tumors). The median patient age was 16.3 yr (2.9-80). All patients underwent previous surgical resection and radiation therapy (RT) of their ependymomas and 40 underwent previous chemotherapy. Grade 2 ependymomas were present in 42 patients (52 tumors) and grade 3 ependymomas in 48 patients (61 tumors). The median tumor volume was 2.2 cc (0.03-36.8) and the median margin dose was 15 Gy (9-24).

Forty-seven (53%) patients were alive and 42 (47%) patients died at the last follow-up. The overall survival after SRS was 86% at 1 yr, 50% at 3 yr, and 44% at 5 yr. Smaller total tumor volume was associated with longer overall survival (P = .006). Twenty-two patients (grade 2: n = 9, grade 3: n = 13) developed additional recurrent ependymomas in the craniospinal axis. The progression-free survival after SRS was 71% at 1 yr, 56% at 3 yr, and 48% at 5 yr. Adult age, female sex, and smaller tumor volume indicated significantly better progression-free survival. Symptomatic adverse radiation effects were seen in 7 patients (8%).

SRS provides another management option for residual or recurrent progressive intracranial ependymoma patients who have failed initial surgery and RT 8).

Chemotherapy

References

1)

Gondi V, Vogelbaum MA, Grimm S, Mehta MP. Primary intracranial neoplasm. In: Halperin EC, Wazer DE, Perez CA, Brady LW, editors. Perez and Brady’s Principles and Practice of Radiation Oncology. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2013. pp. 669–70.
2)

Freeman CR, Farmer JP, Taylor RE. Central Nervous System Tumors in Children. In: Halperin EC, Wazer DE, Perez CA, Brady LW, editors. Perez and Brady’s Principles and Practice of Radiation Oncology. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2013. pp. 1643–5.
3)

Salazar OM, Castro-Vita H, VanHoutte P, Rubin P, Aygun C. Improved survival in cases of intracranial ependymoma after radiation therapy. Late report and recommendations. J Neurosurg. 1983;59:652–9.
4)

Goldwein JW, Corn BW, Finlay JL, Packer RJ, Rorke LB, Schut L. Is craniospinal irradiation required to cure children with malignant (anaplastic) intracranial ependymomas? Cancer. 1991;67:2766–71.
5)

Paulino AC. The local field in infratentorial ependymoma: Does the entire posterior fossa need to be treated? Int J Radiat Oncol Biol Phys. 2001;49:757–61.
6)

Merchant TE, Li C, Xiong X, Kun LE, Boop FA, Sanford RA. Conformal radiotherapy after surgery for paediatric ependymoma: A prospective study. Lancet Oncol. 2009;10:258–66.
7)

Pajtler KW, Mack SC, Ramaswamy V, Smith CA, Witt H, Smith A, Hansford JR, von Hoff K, Wright KD, Hwang E, Frappaz D, Kanemura Y, Massimino M, Faure-Conter C, Modena P, Tabori U, Warren KE, Holland EC, Ichimura K, Giangaspero F, Castel D, von Deimling A, Kool M, Dirks PB, Grundy RG, Foreman NK, Gajjar A, Korshunov A, Finlay J, Gilbertson RJ, Ellison DW, Aldape KD, Merchant TE, Bouffet E, Pfister SM, Taylor MD. The current consensus on the clinical management of intracranial ependymoma and its distinct molecular variants. Acta Neuropathol. 2017 Jan;133(1):5-12. doi: 10.1007/s00401-016-1643-0. Epub 2016 Nov 17. PubMed PMID: 27858204; PubMed Central PMCID: PMC5209402.
8)

Kano H, Su YH, Wu HM, Simonova G, Liscak R, Cohen-Inbar O, Sheehan JP, Meola A, Sharma M, Barnett GH, Mathieu D, Vasas LT, Kaufmann AM, Jacobs RC, Lunsford LD. Stereotactic Radiosurgery for Intracranial Ependymomas: An International Multicenter Study. Neurosurgery. 2019 Jan 1;84(1):227-234. doi: 10.1093/neuros/nyy082. PubMed PMID: 29608701.
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