Tumor associated trigeminal neuralgia

Tumor associated trigeminal neuralgia

Trigeminal neuralgia pathogenesis is uncertain. What is nominated as typically TN is idiopathic, but may be due to a structural lesion:

Posterior fossa tumor1) 2) 3) 4) 5), contralateral posterior fossa tumors, 6) 7)ipsilateral and contralateral supratentorial tumor8) 9) 10) 11) 12).

Trigeminal neuralgia in vestibular schwannoma 13).

Trigeminal neuralgia as the initial manifestation of temporal glioma 14).

A supratentorial tumor can initiate TN even without a direct involvement of the trigeminal ganglion or nerve. Such tumors may lead to increased intracranial pressure and brain shift generating a pressure cone that distorts the brain stemand displaces an adjacent vessel, compressing the trigeminal nerve root.

Another explanatory mechanism in a patient with supratentorial tumor and hydrocephalus can be that pressure over the trigeminal sensory root rather than stretching of the nerve fiber leads to TN 15).

References

1) , 6)

Deshmukh VR, Hott JS, Tabrizi P, Nakaji P, Feiz-Erfan I, Spetzler RF. Cavernous malformation of the trigeminal nerve manifesting with trigeminal neuralgia: Case report. Neurosurgery. 2005;56:E623.
2) , 9)

Deshpande S, Kaptain GJ, Pobereskin LH. Temporal glioblastoma causing trigeminal neuralgia. J Neurosurg. 1999;91:515.
3)

Gnanalingham K, Joshi SM, Lopez B, Ellamushi H, Hamlyn P. Trigeminal neuralgia secondary to Chiari’s malformation–treatment with ventriculoperitoneal shunt. Surg Neurol. 2005;63:586–8. discussion 588-9.
4) , 7) , 10)

Goel A, Sham A. Trigeminal neuralgia in the presence of ectatic basilar artery and basilar invagination: Treatment by foramen magnum decompression: Case report. J Neurosurg. 2009;111:1220–2.
5)

Peñarrocha-Diago M, Mora-Escribano E, Bagán JV, Peñarrocha-Diago M. Neoplastic trigeminal neuropathy: Presentation of 7 cases. Med Oral Patol Oral Cir Bucal. 2006;11:E106–11.
8)

Cirak B, Kimaz N, Arslanoglu A. Trigeminal neuralgia caused by intracranial epidermoid tumor: Report of a case and review of different therapeutic modalities. Pain Physician. 2004;7:129–32.
11)

Guttal KS, Naikmasur VG, Joshi SK, Bathi RJ. Trigeminal neuralgia secondary to epidermoid cyst at the cerebellopontine angle: Case report and brief review. Odontology. 2009;97:54–6.
12)

Love S, Coakham HB. Trigeminal neuralgia: Pathology and pathogenesis. Brain. 2001;124:2347–60.
13)

Apostolakis S, Karagianni A, Mitropoulos A, Filias P, Vlachos K. Trigeminal neuralgia in vestibular schwannoma: Atypical presentation and neuroanatomical correlations. Neurochirurgie. 2019 Mar 21. pii: S0028-3770(19)30024-4. doi: 10.1016/j.neuchi.2019.01.001. [Epub ahead of print] PubMed PMID: 30905383.
14)

Khalatbari M, Amirjamshidi A. Trigeminal neuralgia as the initial manifestation of temporal glioma: Report of three cases and a review of the literature. Surg Neurol Int. 2011;2:114. doi: 10.4103/2152-7806.83734. Epub 2011 Aug 13. PubMed PMID: 21886887; PubMed Central PMCID: PMC3162802.
15)

Cirak B, Kimaz N, Arslanoglu A. Trigeminal neuralgia caused by intracranial epidermoid tumor: Report of a case and review of different therapeutic modalities. Pain Physician. 2004;7:129–32.

Skull Base Surgery Strategies

Skull Base Surgery Strategies

by Walter Jean

Price: $249.99

Buy

Unique skull base surgical resource features strategic, technical, and philosophical pearls from master surgeons.

Unlike other textbooks that only emphasize the technical building blocks surgeons need, this resource focuses on state-of-the-art skull-base procedures, important thought processes, and vital strategies required to perform them.

Size and shape variations, diverse biological characteristics, different anatomic locations and extensions, and specific relationships and entanglements with nerves and vessels make all skull base tumors unique and highly challenging. In addition to anatomy, two other important factors need to be considered every time a surgeon enters the OR – the particular circumstances of the patient and surgeon. Throughout this remarkable book, master neurosurgeons take readers on an insightful journey exploring the decision-making process of choosing and executing a surgical approach, with firsthand pearls from the battlefield.

Key Highlights

Nine sections organized by anatomy cover tumors in the anterior, anterolateral, lateral, central, postero-superior, and postero-inferior skull base regions, and clivus, petrous bone, and ventricles Thirty-two systematically organized chapters flow from clinical presentation and radiographic/anatomical findings of specific patients and tumors – to decision-making and execution of the surgical approach Real-life cases enhance understanding of all the elements that go into each operation Perspectives sections at the end of each chapter embrace the concept of diverse surgeon viewpoints on similar ideas, techniques, and approaches This exemplary book is essential reading for neurosurgery and otolaryngology residents, fellows, veteran practitioners, and allied health personnel who care for patients with skull base tumors.

This book includes complimentary access to a digital copy on https://medone.thieme.com.

Raloxifene

Raloxifene

Raloxifene, sold under the brand name Evista among others, is a medication which is used in the prevention and treatment of osteoporosis in postmenopausal women and to reduce the risk of breast cancer in postmenopausal women with osteoporosis or at high risk for breast cancer. It is taken by mouth.


Choudhary et al., evaluated the effect of raloxifene on prolactin levels in addition to dopamine agonist (DA) therapy in patients with prolactinoma.

They conducted a retrospective chart review of 14 patients with prolactinoma on stable dose of DA for 6 months who received raloxifene 60 mg daily as Prolactin (PRL) could not be normalized despite being on fairly high doses of DA. Patients were informed that raloxifene is not FDAapproved for prolactinoma treatment. Prolactin level was measured at 1-6 months after starting raloxifene and at 1-3 months following its discontinuation. Raloxifene was stopped in 8 out of 14 after 2 (1-6) months of treatment as the absolute change in prolactin level was felt to be small. Results The median age and female/male sex ratios were 50 years (range 18-63), 6/8 respectively. The baseline DA dose was 3 mg/week (0.5-7) for cabergoline and 15 mg/day for bromocriptine. 10 patients had an absolute and percentage decrease in prolactin of 8.3 ng/ml (1.5-54.2), and 25.9% (8-55%) from baseline after 1-6 months on raloxifene treatment, respectively. Among 10 patients with a decrease in prolactin level, 2 (20%) achieved prolactin normalization. Two patients had no change in prolactin and two patients had an increase in prolactin level by 22.8 ng/ml and 8.8 ng/ml (47% and 23.6%) respectively.

Raloxifene was associated with 25.9% (8-55%) decrease in prolactin levels in 10/14 (71%) of patients with prolactinoma who were on stable doses of DA including two patients (14%) who achieved normoprolactinemia 1).


Hannen et al., analyzed the effects of fulvestrant and three Selective estrogen receptor modulators (SERMs), bazedoxifene, clomifene, and raloxifene, on pituitary adenomas cell lines AtT20, TtT/GF, and GH3. In cell survival assays, clomifene was shown to be the most potent compound in all three cell lines with IC50 values ranging between 2, 6, and 10 μM, respectively, depending on the cell type. Raloxifene and bazedoxifene were also effective but to a lower extent. Also, all SERMs affected migratory and invasive behavior of pituitary adenoma cells. Mechanistically, treatment of cells with SERMs caused cell apoptosis, as demonstrated by Caspase 3/7 activity and western blot assays. In addition, western blots demonstrate activation of p53 in TtT/GF cells and loss of ERK1/2 activation in AtT20 cells. In contrast, fulvestrant was only effective in GH3 cells. Thus, the general applicability of SERMs for pituitary adenoma cells might be promising in clinical applications for the treatment of pituitary adenomas 2).


The aim of a study was to investigate the ability of a SERM, RLX, to prevent vasospasm in a rabbit model of SAH.

Thirty-four New Zealand white rabbits were allocated into 3 groups randomly. Subarachnoid hemorrhage was induced by injecting autologous blood into the cisterna magna. The treatment groups were as follows: (1) sham operated (no SAH [n = 12]), (2) SAH only (n = 12), and (3) SAH plus RLX (n = 10). Basilar artery lumen areas and arterial wall thickness were measured to assess vasospams in all groups.

There was a statistically significant difference between the mean basilar artery cross-sectional areas and the mean arterial wall thickness measurements of the control and SAH-only groups (P < .05). The difference between the mean basilar artery cross-sectional areas and the mean arterial wall thickness measurements in the RLX-treated group was statistically significant (P < .05). The difference between the SAH group and the SAH + RLX group was also statistically significant (P < .05).

These findings demonstrate that RLX has marked vasodilatatory effect in an experimental model of SAH in rabbits. This observation may have clinical implications suggesting that this SERM drug could be used as possible anti-vasospastic agent in patients without major adverse effects 3).


The effect of raloxifene on cerebral vasospasm following experimental subarachnoid hemorrhage (SAH) was investigated in a rat model. Seven groups of seven rats underwent no SAH, no treatment; SAH only; SAH plus vehicle; SAH plus 3 days intraperitoneal raloxifene treatment; SAH plus 4 days intraperitoneal raloxifene treatment; SAH plus 3 days intrathecal raloxifene treatment; and SAH plus 4 days intrathecal raloxifene treatment. The basilar artery cross-sectional areas were measured at 72 or 96 hours following SAH. The results showed raloxifene decreased SAH-induced cerebral vasospasm in all treatment groups, and suggested no difference between intraperitoneal and intrathecal application, or between 3 days and 4 days of raloxifene treatment. The present study demonstrates that raloxifene is a potential therapeutic agent against cerebral vasospasm after SAH 4).


To directly test whether exogenous 17beta estradiol and raloxifene affect the number of glial cells in brain, C57BL/6NIA female mice aged 20-24 months received bilateral ovariectomy followed by s.c. placement of a 60-day release pellet containing 17beta estradiol (1.7 mg), raloxifene (10 mg), or placebo (cholesterol). After 60 days, numbers of microglia and astrocytes were quantified in dentate gyrus and CA1 regions of the hippocampal formation using immunocytochemistry and design-based stereology. The results show that long-term 17beta estradiol treatment in aged female mice significantly lowered the numbers of astrocytes and microglial cells in dentate gyrus and CA1 regions compared with placebo. After long-term treatment with raloxifene, a similar reduction was observed in numbers of astrocytes and microglial cells in the hippocampal formation. These findings indicate that estrogen and selective estrogen receptor modulators can influence glial-mediated inflammatory pathways and possibly protect against age- and disease-related neuropathology 5).

References

1)

Choudhary C, Hamrahian AH, Bena JF, Recinos P, Kennedy L, Dobri G. THE EFFECT OF RALOXIFENE ON SERUM PROLACTIN LEVEL IN PATIENTS WITH PROLACTINOMA. Endocr Pract. 2019 Mar 13. doi: 10.4158/EP-2018-0321. [Epub ahead of print] PubMed PMID: 30865525.
2)

Hannen R, Steffani M, Voellger B, Carl B, Wang J, Bartsch JW, Nimsky C. Effects of anti-estrogens on cell invasion and survival in pituitary adenoma cells: A systematic study. J Steroid Biochem Mol Biol. 2019 Mar;187:88-96. doi: 10.1016/j.jsbmb.2018.11.005. Epub 2018 Nov 13. PubMed PMID: 30439415.
3)

Gürses L, Seçkin H, Simşek S, Senel OO, Yigitkanli K, Oztürk E, Beşalti O, Belen D, Bavbek M. Effects of raloxifene on cerebral vasospasm after experimental Subarachnoid Hemorrhage in rabbits. Surg Neurol. 2009 Nov;72(5):490-4; discussion 494-5. doi: 10.1016/j.surneu.2008.11.007. Epub 2009 Jan 14. PubMed PMID: 19147193.
4)

Gulsen S, Inci S, Yuruk S, Yasar U, Ozgen T. Effect of raloxifene on cerebral vasospasm following experimental subarachnoid hemorrhage in rats. Neurol Med Chir (Tokyo). 2007 Dec;47(12):537-42; discussion 542. PubMed PMID: 18159137.
5)

Lei DL, Long JM, Hengemihle J, O’Neill J, Manaye KF, Ingram DK, Mouton PR. Effects of estrogen and raloxifene on neuroglia number and morphology in the hippocampus of aged female mice. Neuroscience. 2003;121(3):659-66. PubMed PMID: 14568026.
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