Craniopharyngioma endoscopic endonasal approach

Craniopharyngioma endoscopic endonasal approach

Craniopharyngioma surgery has evolved over the last two decades. Traditional transcranial microsurgical approaches were the only option until the advent of the endoscopic endonasal approach 1).

The endoscopic endonasal approach for craniopharyngiomas is increasingly used as an alternative to microsurgical transsphenoidal or transcranial approaches. It is a step forward in treatment, providing improved resection rates and better visual outcome. Especially in retrochiasmatic tumors, this approach provides better lesion access and reduces the degree of manipulations of the optic apparatus. The panoramic view offered by endoscopy and the use of angulated optics allows the removal of lesions extending far into the third ventricle avoiding microsurgical brain splitting. Intensive training is required to perform this surgery 2).


The highest priority of current surgical craniopharyngioma treatment is to maximize tumor removal without compromising the patients’ long-term functional outcome. Surgical damage to the hypothalamus may be avoided or at least ameliorated with a precise knowledge regarding the type of adherence for each case.

Endoscopic endonasal approach, has been shown to achieve higher rates of hypothalamic preservation regardless of the degree of involvement by tumor 3) 4).


Qiao et al., conducted a systematic review and meta-analysis. They conducted a comprehensive search of PubMed to identify relevant studies. Pituitary, hypothalamus functions and recurrence were used as outcome measures. A total of 39 cohort studies involving 3079 adult patients were included in the comparison. Among these studies, 752 patients across 17 studies underwent endoscopic transsphenoidal resection, and 2327 patients across 23 studies underwent transcranial resection. More patients in the endoscopic group (75.7%) had visual symptoms and endocrine symptoms (60.2%) than did patients in the transcranial group (67.0%, p = 0.038 and 42.0%, p = 0.016). There was no significant difference in hypopituitarism and pan-hypopituitarism after surgery between the two groups: 72.2% and 43.7% of the patients in endoscopic group compared to 80.7% and 48.3% in the transcranial group (p = 0.140 and p = 0.713). We observed same proportions of transient and permanent diabetes insipidus in both groups. Similar recurrence was observed in both groups (p = 0.131). Pooled analysis showed that neither weight gain (p = 0.406) nor memory impairment (p = 0.995) differed between the two groups. Meta-regression analysis revealed that gross total resection contributed to the heterogeneity of recurrence proportion (p < 0.001). They observed similar proportions of endocrine outcomes and recurrence in both endoscopic and transcranial groups. More recurrences were observed in studies with lower proportions of gross total resection 5).


The extended endoscopic transsphenoidal approach has been more recently developed as a potentially surgically aggressive, yet minimal access, alternative.

Komotar et al performed a systematic review of the available published reports after endoscope-assisted endonasal approaches and compared their results with transsphenoidal purely microscope-based or transcranial microscope-based techniques.

The endoscopic endonasal approach is a safe and effective alternative for the treatment of certain craniopharyngiomas. Larger lesions with more lateral extension may be more suitable for an open approach, and further follow-up is needed to assess the long-term efficacy of this minimal access approach 6)

Extended endoscopic transsphenoidal approach have gained interest. Surgeons have advocated for both approaches, and at present there is no consensus whether one approach is superior to the other.

With the widespread use of endoscopes in endonasal surgery, the endoscopic transtuberculum transplanum approach have been proposed as an alternative surgical route for removal of different types of suprasellar tumors, including solid craniopharyngiomas in patients with normal pituitary function and small sella.

As part of a minimally disruptive treatment paradigm, the extended endoscopic transsphenoidal approach has the potential to improve rates of resection, improve postoperative visual recovery, and minimize surgical morbidity 7).

The endoscopic endonasal approach has become a valid surgical technique for the management of craniopharyngiomas. It provides an excellent corridor to infra- and supradiaphragmatic midline craniopharyngiomas, including the management of lesions extending into the third ventricle chamber. Even though indications for this approach are rigorously lesion based, the data confirm its effectiveness in a large patient series 8).

The endoscopic endonasal approach offers advantages in the management of craniopharyngiomas that historically have been approached via the transsphenoidal approach (i.e., purely intrasellar or intra-suprasellar infradiaphragmatic, preferably cystic lesions in patients with panhypopituitarism).

Use of the extended endoscopic endonasal approach overcomes the limits of the transsphenoidal route to the sella enabling the management of different purely suprasellar and retrosellar cystic/solid craniopharyngiomas, regardless of the sellar size or pituitary function 9).

They provide acceptable results comparable to those for traditional craniotomies. Endoscopic endonasal surgery is not limited to adults and actually shows higher resection rates in the pediatric population 10).

Infrachiasmatic corridor

Craniopharyngioma endoscopic endonasal approach complications.

see Craniopharyngioma endoscopic endonasal approach case series.


1)

Fong RP, Babu CS, Schwartz TH. Endoscopic endonasal approach for craniopharyngiomas. J Neurosurg Sci. 2021 Apr;65(2):133-139. doi: 10.23736/S0390-5616.21.05097-9. PMID: 33890754.
2)

Baldauf J, Hosemann W, Schroeder HW. Endoscopic Endonasal Approach for Craniopharyngiomas. Neurosurg Clin N Am. 2015 Jul;26(3):363-75. doi: 10.1016/j.nec.2015.03.013. Epub 2015 May 26. PMID: 26141356.
3)

Tan TSE, Patel L, Gopal-Kothandapani JS, Ehtisham S, Ikazoboh EC, Hayward R, et al: The neuroendocrine sequelae of paediatric craniopharyngioma: a 40-year meta-data analysis of 185 cases from three UK centres. Eur J Endocrinol 176:359–369, 2017
4)

Yokoi H, Kodama S, Kogashiwa Y, Matsumoto Y, Ohkura Y, Nakagawa T, et al: An endoscopic endonasal approach for early-stage olfactory neuroblastoma: an evaluation of 2 cases with minireview of literature. Case Rep Otolaryngol 2015:541026, 2015
5)

Qiao N. Endocrine outcomes of endoscopic versus transcranial resection of craniopharyngiomas: A system review and meta-analysis. Clin Neurol Neurosurg. 2018 Apr 7;169:107-115. doi: 10.1016/j.clineuro.2018.04.009. [Epub ahead of print] Review. PubMed PMID: 29655011.
6)

Komotar RJ, Starke RM, Raper DM, Anand VK, Schwartz TH. Endoscopic endonasal compared with microscopic transsphenoidal and open transcranial resection of craniopharyngiomas. World Neurosurg. 2012 Feb;77(2):329-41. doi: 10.1016/j.wneu.2011.07.011. Epub 2011 Nov 1. Review. PubMed PMID: 22501020.
7)

Zacharia BE, Amine M, Anand V, Schwartz TH. Endoscopic Endonasal Management of Craniopharyngioma. Otolaryngol Clin North Am. 2016 Feb;49(1):201-12. doi: 10.1016/j.otc.2015.09.013. Review. PubMed PMID: 26614838.
8)

Cavallo LM, Frank G, Cappabianca P, Solari D, Mazzatenta D, Villa A, Zoli M, D’Enza AI, Esposito F, Pasquini E. The endoscopic endonasal approach for the management of craniopharyngiomas: a series of 103 patients. J Neurosurg. 2014 May 2. [Epub ahead of print] PubMed PMID: 24785324.
9)

Cavallo LM, Solari D, Esposito F, Villa A, Minniti G, Cappabianca P. The Role of the Endoscopic Endonasal Route in the Management of Craniopharyngiomas. World Neurosurg. 2014 Dec;82(6S):S32-S40. doi: 10.1016/j.wneu.2014.07.023. Review. PubMed PMID: 25496633.
10)

Koutourousiou M, Gardner PA, Fernandez-Miranda JC, Tyler-Kabara EC, Wang EW, Snyderman CH. Endoscopic endonasal surgery for craniopharyngiomas: surgical outcome in 64 patients. J Neurosurg. 2013 Nov;119(5):1194-207. doi: 10.3171/2013.6.JNS122259. Epub 2013 Aug 2. PubMed PMID: 23909243.

Esthesioneuroblastoma

Esthesioneuroblastoma (ENB)

Esthesioneuroblastoma (ENB), originally described in 1924, AKA olfactory neuroblastoma, AKA olfactory esthesioneuroblastoma, AKA esthesioneurocytoma, AKA olfactory placode tumor 1).

Malignant tumor of sinonasal origin.

A rare nasal neoplasm with an incidence of 0.4 per 1,000,000 people. 2).

Believed to arise from the olfactory neural crest cells in the upper nares, it is considered to be malignant. These tumors occur over a wide age range (3 to 90 years), with a bimodal peak between the second and third decade and a second peak in the sixth and seventh decades.

Esthesioneuroblastoma classification.

These tumors typically present with unilateral nasal obstruction and epistaxis.

Diagnosis is confirmed on biopsy.

MRI: isointense with the brain on T1-weighted imaging and intermediate to high signal intensity on T2- weighted imaging and enhance heterogeneously with gadolinium. Signal characteristics may mimic meningioma. For higher stage lesions, the cribriform plate may be eroded; better seen on thin-cut CT. The most important factor determining resectability is an intracranial extension. Magnetic resonance aids in the distinction between extradural tumors, dural invasion, or parenchymal brain invasion. None of these are specific to this tumor.


Endoscopic biopsy is typically performed in the otolaryngology office prior to surgery. A clinical oncology exam should be performed, and if there is suspicion for metastatic disease a PET scan, which is sensitive for metastatic disease, should be ordered.

Includes SNUC, nasal melanoma, nasal squamous cell carcinoma, and meningioma.

see Esthesioneuroblastoma treatment.

Esthesioneuroblastoma outcome.

Esthesioneuroblastoma case series.

Esthesioneuroblastoma case reports.


1)

Berger L, Luc G, Richard D. L’Esthesioneuroepitheliome Olfactif. Bull Assoc Franc Etude Cancer. 1924; 13: 410–421
2)

Theilgaard SA, Buchwald C, Ingeholm P, et al. Esthesioneuroblastoma: a Danish demographic study of 40 patients registered between 1978 and 2000. Acta Otolaryngol. 2003; 123:433–439

Sphenoid sinus mucosal thickening

Sphenoid sinus mucosal thickening

In pituitary apoplexy etiology, there are reports on the appearance of sphenoid sinus mucosal thickening (SSMT) 1) 2)3).

SSMT is otherwise uncommon with an incidence of up to 7% in asymptomatic individuals. The etiology of SSMT in pituitary apoplexy is unclear and may reflect inflammatory and/or infective changes 4).

The mechanism of thickening of the para sellar dura mater and sphenoid sinus mucosa have been considered to be caused by congestion of dural blood flow because of increased cavernous and circular sinus pressure due to a sudden increase in intrasellar pressure.


A study revealed that age, tumor size, and thickened sphenoid sinus mucosa were strongly related to the occurrence of internal carotid artery stenosis in pituitary apoplexy. Among these factors, age had the potential of being an independent predictor of the condition 5).


Two magnetic resonance imaging (MRI) signs of pituitary apoplexy are the “pituitary ring sign” and “sphenoid sinus mucosal thickening”. The occurrence of both these MRI signs together in patients with ischaemic pituitary apoplexy was investigated. A literature review searching the terms “pituitary ring sign” and “sphenoid sinus mucosal thickening” in the context of pituitary apoplexy from 1990 until the present was performed. To be included in the study, each case had to have ischaemic pituitary apoplexy defined as the acute expansion of a pituitary adenoma or, less commonly, in a non-adenomatous gland, from infarction without hemorrhage or very little hemorrhage and a T1-weighted MRI of the brain with contrast that displayed both “sphenoid sinus mucosal thickening” and a “pituitary ring sign” either on an actual study (the author’s cases) or in a figure in an article from the literature that could be reviewed and clearly illustrate these two signs. Twelve cases of ischaemic pituitary apoplexy were found, all with MRI images that showed both of these signs. Ten cases from the literature (3 of which were published by this author) plus an additional 2 recently evaluated in our hospital, totaled the 12 cases. Thus, 5 of the total 12 cases were evaluated by this author. Of these 12 patients, both headache and visual loss were present in 5 patients, headache alone was indicated in 5 patients (10 of the 12 presented with headache), and no initial symptoms identified in 2 patients (incidentally found non-functioning pituitary adenomas on MRI). These findings indicate that each sign (“pituitary ring sign” and “sphenoid sinus mucosal thickening”) may exist alone with or without pituitary apoplexy, yet both signs together in the appropriate clinical context is a strong predictor of pituitary apoplexy 6).


Arita et al. treated two patients with pituitary apoplexy in whom magnetic resonance (MR) images were obtained before and after the episode. Two days after the apoplectic episodes, MR imaging demonstrated marked thickening of the mucosa of the sphenoid sinus that was absent in the previous studies. The relevance of this change in the sphenoid sinus was investigated. Retrospective evaluations were performed using MR images obtained in 14 consecutive patients with classic pituitary apoplexy characterized by acute onset of severe headache. The mucosa of the sphenoid sinus had thickened predominantly in the compartment just beneath the sella turcica, in nine of 11 patients, as ascertained on MR images obtained within 7 days after the onset of apoplectic symptoms. This condition improved spontaneously in all four patients who did not undergo transsphenoidal surgery. The sphenoid sinus mucosa appeared to be normal on MR images obtained from three patients at the chronic stage (> 3 months after onset). The incidence of sphenoid sinus mucosal thickening during the acute stage was significantly higher in the patients with apoplexy than that in the 100 patients without apoplexy. A histological study conducted in four patients who underwent transsphenoidal surgery during the early stage showed that the subepithelial layer of the sphenoid sinus mucous membrane was obviously swollen. The sphenoid sinus mucosa thickens during the acute stage of pituitary apoplexy. This thickening neither indicates infectious sinusitis nor rules out the choice of the transsphenoidal route for surgery 7).


1)

Agrawal B, Dziurzynski K, Salamat MS, Baskaya M. The temporal association of sphenoid sinus mucosal thickening on MR imaging with pituitary apoplexy. Turk Neurosurg. 2012;22(6):785-90. doi: 10.5137/1019-5149.JTN.4273-11.1. PMID: 23208917.
2)

Liu JK, Couldwell WT. Pituitary apoplexy in the magnetic resonance imaging era: clinical significance of sphenoid sinus mucosal thickening. J Neurosurg. 2006 Jun;104(6):892-8. doi: 10.3171/jns.2006.104.6.892. PMID: 16776332.
3) , 7)

Arita K, Kurisu K, Tominaga A, Sugiyama K, Ikawa F, Yoshioka H, Sumida M, Kanou Y, Yajin K, Ogawa R. Thickening of sphenoid sinus mucosa during the acute stage of pituitary apoplexy. J Neurosurg. 2001 Nov;95(5):897-901. doi: 10.3171/jns.2001.95.5.0897. PMID: 11702884.
4)

Waqar M, McCreary R, Kearney T, Karabatsou K, Gnanalingham KK. Sphenoid sinus mucosal thickening in the acute phase of pituitary apoplexy. Pituitary. 2017 Aug;20(4):441-449. doi: 10.1007/s11102-017-0804-z. PMID: 28421421; PMCID: PMC5508043.
5)

Teramoto S, Tahara S, Kondo A, Morita A. Key Factors Related to Internal Carotid Artery Stenosis Associated with Pituitary Apoplexy. World Neurosurg. 2021 Feb 7:S1878-8750(21)00186-8. doi: 10.1016/j.wneu.2021.02.005. Epub ahead of print. PMID: 33567365.
6)

Vaphiades MS. Pituitary Ring Sign Plus Sphenoid Sinus Mucosal Thickening: Neuroimaging Signs of Pituitary Apoplexy. Neuroophthalmology. 2017 Aug 9;41(6):306-309. doi: 10.1080/01658107.2017.1349807. PMID: 29344069; PMCID: PMC5764063.
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