Month: December 2015

Update: Hypothermia for Intracranial Hypertension after Traumatic Brain Injury

In patients with traumatic brain injury, hypothermia can reduce intracranial hypertension. The benefit of hypothermia on functional outcome is unclear.

METHODS:

We randomly assigned adults with an intracranial pressure of more than 20 mm Hg despite stage 1 treatments (including mechanical ventilation and sedation management) to standard care (control group) or hypothermia (32 to 35°C) plus standard care. In the control group, stage 2 treatments (e.g., osmotherapy) were added as needed to control intracranial pressure. In the hypothermia group, stage 2 treatments were added only if hypothermia failed to control intracranial pressure. In both groups, stage 3 treatments (barbiturates and decompressive craniectomy) were used if all stage 2 treatments failed to control intracranial pressure. The primary outcome was the score on the Extended Glasgow Outcome Scale (GOS-E; range, 1 to 8, with lower scores indicating a worse functional outcome) at 6 months. The treatment effect was estimated with ordinal logistic regression adjusted for prespecified prognostic factors and expressed as a common odds ratio (with an odds ratio <1.0 favoring hypothermia).

RESULTS:

We enrolled 387 patients at 47 centers in 18 countries from November 2009 through October 2014, at which time recruitment was suspended owing to safety concerns. Stage 3 treatments were required to control intracranial pressure in 54% of the patients in the control group and in 44% of the patients in the hypothermia group. The adjusted common odds ratio for the GOS-E score was 1.53 (95% confidence interval, 1.02 to 2.30; P=0.04), indicating a worse outcome in the hypothermia group than in the control group. A favorable outcome (GOS-E score of 5 to 8, indicating moderate disability or good recovery) occurred in 26% of the patients in the hypothermia group and in 37% of the patients in the control group (P=0.03).

CONCLUSIONS:

In patients with an intracranial pressure of more than 20 mm Hg after traumatic brain injury, therapeutic hypothermia plus standard care to reduce intracranial pressure did not result in outcomes better than those with standard care alone. (Funded by the National Institute for Health Research Health Technology Assessment program; Current Controlled Trials number, ISRCTN34555414.).
Andrews PJ, Sinclair HL, Rodriguez A, Harris BA, Battison CG, Rhodes JK, Murray GD; Eurotherm3235 Trial Collaborators. Hypothermia for Intracranial Hypertension after Traumatic Brain Injury. N Engl J Med. 2015 Dec 17;373(25):2403-12. doi: 10.1056/NEJMoa1507581. Epub 2015 Oct 7. PubMed PMID:
26444221.

XXXII Reunión de la Sociedad Española de Neurocirugía Pediátrica

El próximo 11 de enero de 2016 finaliza el plazo de presentación de comunicaciones para la XXXII Reunión de la Sociedad Española de Neurocirugía Pediátrica que se celebra en Barcelona el próximo mes de febrero.
El patrón de la Reunión será similar al de las anteriores, con presentaciones orales cortas y posters, os animo a presentar vuestros trabajos en nuestra reunión anual para conseguir un buen foro de discusión entre los asistentes.
La información se encuentra en la página web de la Reunión www.senepbarcelona2016.es
Para cualquier consulta pueden contactar con:
Soraya Salmerón // Alberto García
Secretaría Técnica XXXII Reunión SENEP 2016
Tfno: 678 42 43 40 // 687 38 78 75
mail: senepbarcelona2016@multidial.es
web: www.senepbarcelona2016.es
 

Book: The Amygdaloid Nuclear Complex: Anatomic Study of the Human Amygdala

 The Amygdaloid Nuclear Complex: Anatomic Study of the Human Amygdala
By Vincent Di Marino, Yves Etienne, Maurice Niddam

The Amygdaloid Nuclear Complex: Anatomic Study of the Human Amygdala

Price: $159.00
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This timely book allows clinicians of the nervous system, who are increasingly confronted with degenerative and psychiatric diseases, to familiarize themselves with the cerebral amygdala and the anatomical structures involved in these pathologies. Its striking photos of cerebral sections and dissections should help MRI specialists to more precisely study the detailed images provided by their constantly evolving equipment.

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  • Published on: 2015-12-26
  • Original language: English
  • Number of items: 1
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  • 162 pages

About the Author
Vincent Di Marino is Emeritus Professor of Anatomy, Honorary Director of the Laboratory of Anatomy (Faculty of medicine; Marseille, FRANCE) and former surgeon of the hospitals. He is also former director of the Renal Transplantation Center at Sainte-Marguerite Hospital in Marseille, former director of the Anatomy Laboratory at the Aix-Marseille University (Faculty of Medicine) in Marseille (France). Currently, his research topics are focused on the central nervous system and the pelvis. Yves Etienne is a former Assistant of Anatomy, former Doctor of the hospitals of sanitary region, forensic pathologist, consultant of the unit of forensic medicine (Timone Hospital. Marseille, France). Maurice Niddam is a forensic pathologist, consultant of the unit of forensic medicine (Timone Hospital. Marseille, France).

Coding Companion® for Neurosurgery/Neurology 2016

Coding Companion® for Neurosurgery/Neurology 2016

Coding Companion® for Neurosurgery/Neurology 2016

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Coding Companion® for Neurosurgery/Neurology 2016 Consolidate the coding process with the one-stop resource developed exclusively for those who code for neurology and neurosurgery.
This comprehensive and easy-to-use guide includes 2016 CPT®, HCPCS, and ICD-10-CM code sets specific to neurology and neurosurgery.
Each specialty-specific procedure code includes its official description and lay description, coding tips, terminology, cross-coding, and national Medicare relative value units. Getting to the code information you need has never been so easy.
Key Features and Benefits
Optum360 Edge HCPCS Procedure Codes. Only Optum360 offers HCPCS procedure codes specific to your specialty with the same information as we provide for CPT codes.
Quickly find information. All the information you need is provided, including illustrations, lay descriptions, coding tips, terms, cross-coding, Medicare RVUs, and Pub. 100 references.
Organized by CPT® and HCPCS code. Essential procedures for neurology and neurosurgery are listed by CPT® or HCPCS code, along with crosswalks to ICD-10-CM diagnosis codes.
Easily determine fees for your practice and reinforce consistency in the charges. National Medicare relative value units for surgery codes and most diagnostic procedures are included.
Avoid claim denials and/or audits. Medicare payer information provides the references to Pub. 100 guidelines, follow-up days, and assistant-at-surgery.
CCI Edits by CPT® and HCPCS code. CPT® codes with associated CCI edits in a special section and quarterly updates available online.
CPT® is a registered trademark of the American Medical Association.

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  • Published on: 2015-12-25
  • Original language: English
  • Binding: Spiral-bound
  • 350 pages

Combining VEGF blockade with inhibition of Angiopoietin 2 may potentially overcome resistance to bevacizumab therapy

Angiopoietin 2

J.Sales-Llopis
Neurosurgery Department, University General Hospital of Alicante, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Alicante, Spain

Tumor formation

Microtumor growth initiates angiogenic sprouting with simultaneous expression of VEGF, VEGF receptor-2, and angiopoietin-2 1).
The angiopoietins Ang-1 and Ang-2 have been implicated in the regulation of angiogenesis; reports have suggested that a net gain in Ang-2 activity may be an initiating factor for tumor angiogenesis.
The relative increase in angiopoietin-2 activity in brain tumors may result in the creation of a pro-angiogenic environment that enhances the recruitment of putative bone marrow-derived endothelial progenitor cell into the tumor’s developing vascular tree 2).
The expression of Ang-1, Ang-2, VEGF, and Tie-2, a member of the receptor tyrosine kinases and the natural receptor for both Ang-1 and Ang-2, follows a distinct transcriptional profile in vivo. Ang-2 and VEGF were expressed early in tumor formation and their levels increased throughout tumor growth. Their expression coincided with the expansion of the tumor mass and the formation of the vascular tree. There was no significant change in the expression of Tie-2 and Ang-1. The expression of Ang-1 and Tie-2 was more noticeable at the periphery of the tumor. The expression of Ang-2 was more robust at the periphery and within the tumor mass, and VEGF was more concentrated within the center of the tumor. This distinct gene expression profilingmay explain the morphology of the newly formed vessels at various times and regions of the tumor. The lack of concomitant expression of Ang-1 may underscore the unopposed endovascular induction by Ang-2 and VEGF resulting in the chaotic appearance and fragility of tumor vessels 3).
p53 causes tumor regression by suppressing tumor proliferation and indirectly induces involution of tumor vessels by fostering unopposed activity of Angiopoietin 2 in an environment of diminishing VEGF 4).

High grade glioma

Angiopoietin-2 mRNA expression in cultured human malignant glioma cells (U105, U251, and U373 MG) by reverse transcriptase-PCR. Western blot analysis and immunocytochemical analysis with antihuman Ang2 antibody revealed that Ang2 protein was expressed and secreted by these cells. Furthermore, hypoxia increased the Ang2 protein level in cultured glioma cells. Serial sections of 32 human glioma tissues (14 glioblastomas, eight anaplastic astrocytomas, seven astrocytomas, and three pilocytic astrocytomas) were immunostained against Ang2, vascular endothelial growth factor, Tie2, von Willebrand factor, and alpha smooth muscle actin. The immunoreactivity of each angiogenic factor was higher in malignant gliomas than in low-grade gliomas.
Angiopoietin 2 protein was detected not only in endothelial cells but also in glioma cells, and its expression was prominent in both the area surrounding the necrosis and the periphery of glioblastomas.
In the area surrounding necrosis, Ang2 was highly expressed and tumor vessels showed regression. In the tumor periphery, Ang2 was highly expressed and many small vessels stained positively for von Willebrand factor but not for alpha smooth muscle actin, suggesting angiogenesis. Statistical analysis revealed that the Ang2 expression was negatively correlated with vessel maturation in malignant gliomas and that vascular endothelial growth factor expression was positively correlated with vessel maturation in low-grade gliomas (P < 0.05). These results suggest that glioma cells themselves express Angiopoietin 2 and that expression may be induced by hypoxic stimulation and may play a crucial role in the vessel maturation, angiogenesis, and vessel regression in malignant glioma 5).
ANGPT1/ANGPT2 balance has prognostic value in patients with primary glioblastomas (GBMs). This findings support the need for further studies of the feasibility of antiangiogenic therapy in primary GBMs, with a special focus on the normalization of tumor vasculature 6).
Combining VEGF blockade with inhibition of Angiopoietin 2 may potentially overcome resistance to bevacizumab therapy 7).

Arteriovenous malformation

Up-regulated VEGF in part of brain and Tie-2, Angiopoietin 2 high expression in endothelial cells (EC) of some vessels may be one of major factors for cerebral arteriovenous malformation(CAVM) formation growth, and rupture in the embryonic period 8).

Traumatic brain injury

Ang-1/2 evaluation in plasma, serum and cerebrospinal fluid may provide new therapeutic modalities which can modify ‘secondary’ forms of brain injury after TBI and SAH 9).

Chronic subdural hematoma

Persistent activation of the angiopoietin and their receptor Tie 2 system in addition to high levels of VEGF may keep the vasculature in a destabilized condition and may account for the continuous formation of new and immature blood vessels resulting in massive plasma extravasation and repeated bleeding episodes. This provide new evidence in favor of pro-angiogenic mechanisms playing an important role in the pathophysiology of chronic subdural hematoma (CSH) 10).
1) Vajkoczy P, Farhadi M, Gaumann A, Heidenreich R, Erber R, Wunder A, Tonn JC, Menger MD, Breier G. Microtumor growth initiates angiogenic sprouting with simultaneous expression of VEGF, VEGF receptor-2, and angiopoietin-2. J Clin Invest. 2002 Mar;109(6):777-85. PubMed PMID: 11901186; PubMed Central PMCID: PMC150910.
2) Udani V, Santarelli J, Yung Y, Cheshier S, Andrews A, Kasad Z, Tse V. Differential expression of angiopoietin-1 and angiopoietin-2 may enhance recruitment of bone-marrow-derived endothelial precursor cells into brain tumors. Neurol Res. 2005 Dec;27(8):801-6. PubMed PMID: 16354539.
3) Tse V, Xu L, Yung YC, Santarelli JG, Juan D, Fabel K, Silverberg G, Harsh G 4th. The temporal-spatial expression of VEGF, angiopoietins-1 and 2, and Tie-2 during tumor angiogenesis and their functional correlation with tumor neovascular architecture. Neurol Res. 2003 Oct;25(7):729-38. PubMed PMID: 14579791.
4) Tse V, Yung Y, Santarelli JG, Juan D, Hsiao M, Haas M, Harsh G 4th, Silverberg G. Effects of tumor suppressor gene (p53) on brain tumor angiogenesis and expression of angiogenic modulators. Anticancer Res. 2004 Jan-Feb;24(1):1-10. Erratum in: Anticancer Res. 2004 Mar-Apr;24(2C):1325. PubMed PMID: 15015569.
5) Koga K, Todaka T, Morioka M, Hamada J, Kai Y, Yano S, Okamura A, Takakura N, Suda T, Ushio Y. Expression of angiopoietin-2 in human glioma cells and its role for angiogenesis. Cancer Res. 2001 Aug 15;61(16):6248-54. PubMed PMID: 11507079.
6) Sie M, Wagemakers M, Molema G, Mooij JJ, de Bont ES, den Dunnen WF. The angiopoietin 1/angiopoietin 2 balance as a prognostic marker in primary glioblastoma multiforme. J Neurosurg. 2009 Jan;110(1):147-55. doi: 10.3171/2008.6.17612. PubMed PMID: 18991494.
7) Scholz A, Harter PN, Cremer S, Yalcin BH, Gurnik S, Yamaji M, Di Tacchio M, Sommer K, Baumgarten P, Bähr O, Steinbach JP, Trojan J, Glas M, Herrlinger U, Krex D, Meinhardt M, Weyerbrock A, Timmer M, Goldbrunner R, Deckert M, Braun C, Schittenhelm J, Frueh JT, Ullrich E, Mittelbronn M, Plate KH, Reiss Y. Endothelial cell-derived angiopoietin-2 is a therapeutic target in treatment-naive and bevacizumab-resistant glioblastoma. EMBO Mol Med. 2015 Dec 14. pii: e201505505. doi: 10.15252/emmm.201505505. [Epub ahead of print] PubMed PMID: 26666269.
8) Li J, Gao Y, Zhao M. [Immunohistochemical study of vascular endothelial growth factor, relative receptors and ligands in vascular endothelial cells of cerebral arteriovenous malformation]. Zhonghua Wai Ke Za Zhi. 2001 Sep;39(9):675-8. Chinese. PubMed PMID: 11769600.
9) Chittiboina P, Ganta V, Monceaux CP, Scott LK, Nanda A, Alexander JS. Angiopoietins as promising biomarkers and potential therapeutic targets in brain injury. Pathophysiology. 2013 Feb;20(1):15-21. doi: 10.1016/j.pathophys.2012.02.004. Epub 2012 May 26. PubMed PMID: 22633746.
10) Hohenstein A, Erber R, Schilling L, Weigel R. Increased mRNA expression of VEGF within the hematoma and imbalance of angiopoietin-1 and -2 mRNA within the neomembranes of chronic subdural hematoma. J Neurotrauma. 2005 May;22(5):518-28. PubMed PMID: 15892598.

Update: Giant internal carotid artery aneurysm

Sixty percent of giant intracranial aneurysms occur on the internal carotid artery.
Treatment
Parent artery occlusion was the classic therapy; now the stent-assisted coil embolization has become available in recent years, but the optimal therapy is under debate.
Stent-assisted coiling may not be superior to parent artery occlusion in selected patients after short-term follow-up. Parent artery occlusion is a simple, safe and effective treatment for large/giant internal carotid aneurysms 1).
ICA occlusion for large and giant aneurysms after angiographic test occlusion was safe and effective. Two-thirds of eligible patients passed the angiographic test. Most aneurysms shrunk, and most cranial nerve dysfunctions were cured or improved 2).
Case series

2016

Between January 1995 and January 2015, occlusion of the ICA was considered in 146 patients with large or giant ICA aneurysms. Ninety-six patients (66%) passed the angiographic test occlusion, and, in 88 of these 96 patients (92%), the ICA was permanently occluded. In 11 of 88 patients with angiographic tolerance, ICA occlusion was performed with the patient under general anesthesia without clinical testing.
There was 1 hypoperfusion infarction after hypovolemic shock from a large retroperitoneal hematoma (complication rate 1.1% [95% CI, 1%-6.8%]). The mean imaging and clinical follow-up was 35 months (median 18 months; range, 3-180 months). On the latest MR imaging, 87 of 88 aneurysms (99%) were completely occluded and 61 of 80 aneurysms (76%) were decreased in size or completely obliterated. Of 62 patients who presented with cranial nerve dysfunction by mass effect of the aneurysm, 30 (48%) were cured, 25 (40%) improved, 6 (10%) were unchanged, and 1 patient (2%) was hemiplegic after a complication.
ICA occlusion for large and giant aneurysms after angiographic test occlusion was safe and effective. Two-thirds of eligible patients passed the angiographic test. Most aneurysms shrunk, and most cranial nerve dysfunctions were cured or improved 3).

In the report of Li et al. all the patients were divided into two groups: Group A: patients who underwent parent artery occlusion, and Group B: patients who underwent stent-assisted coil embolization. Follow-up outcomes were evaluated using the modified Rankin Scale (mRS).
After 12 months of follow-up, the favorable outcome (mRS: 0-2) had no statistical significance in both groups (p = 1.00). Patients in group A had greater ischemia compared with patients in group B, but the difference did not reach statistical significance (p = 0.421). In group B, patients had a higher rate of partial occlusion (p = 0.255) and recurrence (10% vs. 0%; p = 0.586).
Stent-assisted coiling may not be superior to parent artery occlusion in selected patients after short-term follow-up. Parent artery occlusion is a simple, safe and effective treatment for large/giant internal carotid aneurysms.

2014

Four cases of giant or large paraclinoid aneurysms of the internal carotid artery successfully trapped after assessing blood flow using a flowmeter are presented. In all cases, the initial plan for clipping was changed to aneurysm trapping due to various reasons. The collateral blood flow was assessed using the flowmetry test, the original procedure of measuring volumetric blood flow in the middle cerebral artery using an ultrasonic flowmeter. We analyze the reasons for clipping refusal, the procedure of measuring blood flow, treatment outcomes, and catamnestic data. The risks of reconstructive surgeries involving the internal carotid artery are discussed and the literature data are analyzed. Conclusions. Ultrasonic flowmetry is a simple and safe method for intraoperative control over blood circulation, which may play the key role in complicated surgical cases 4).

2012

Rathore et al. retrospectively analyzed 27 patients with giant and complex ICA aneurysms who underwent carotid artery ligation between January 2001 and December 2010. Clinical presentation included headache, vision loss and diplopia. There were 19 patients with cavernous aneurysm, 5 supraclinoid, 1 ophthalmic, 1 petrous segment and 1 cervical segment aneurysm located extracranially. All demonstrated good cross-circulation. Selverstone clamp was used for gradual occlusion of the ICA over 72 h under closed observation in the intensive care unit.
Six patients developed hemiparesis in the postoperative period. Improvement occurred in one patient over two to three weeks while the remaining five patients had residual hemiparesis. One patient developed malignant MCA infarct for which decompressive craniectomy had to be done. There was no mortality in the present series.
Gradual monitored occlusion and ICA ligation may be a simple, safe alternative procedure to clipping in surgically inaccessible and complex aneurysms, especially for surgeons with limited experience. Cross circulation study is an absolute requisite for carotid ligation 5).

2008

In 16 patients with 17 large or giant (11-45 mm) unruptured ICA aneurysms presenting with dysfunction of cranial nerves (CN) II, III, IV, or VI, selective coil occlusion was performed. From a cohort of 39 patients with ICA aneurysms treated with ICA occlusion and long-term follow-up, we selected 31 patients with aneurysms presenting with cranial nerve dysfunction. Clinical recovery at follow-up from oculomotor dysfunction and visual symptoms was compared for both treatment modalities.
Of 17 aneurysms treated with selective coiling, symptoms of cranial nerve dysfunction resolved in 3, improved in 10, and remained unchanged in 4. In 9 of 17 patients, additional coiling during follow-up was required. Of 31 aneurysms treated with carotid artery occlusion, cranial nerve dysfunction resolved in 19, improved in 9, and remained unchanged in 3. These differences were not significant. There were no complications of treatment.
Recovery of ICA aneurysm-induced cranial nerve dysfunction occurs in most patients, both after ICA occlusion and after selective coiling. In patients who cannot tolerate ICA occlusion, selective aneurysmal occlusion with coils is a valuable alternative 6).
Case reports
 2015
Bowers et al. report the microsurgical rescue and removal of a Pipeline stent embolization of a giant internal carotid artery terminus aneurysm. After the initial placement of a Pipeline Embolization Device (PED), it migrated proximally to the cavernous carotid with the distal end free in the middle of the aneurysm, resulting in only partial aneurysm neck coverage. The patient underwent microsurgical rescue with trapping, bypass, and opening of the aneurysm with PED removal. The vessel remained patent in the proximal segment previously covered by the Pipeline stent. Microsurgical rescue for definitive aneurysm treatment with PED removal can be safe and effective for aneurysms unsuccessfully treated with PED 7).

1992

A 25-year-old man developed Wallenberg syndrome (WS). At that time his carotid angiography was normal. When he was 28 years old, he suffered from retinal artery embolism in the left eye. At the age of 30 years, he had an acute onset of abducens nerve palsy in his right eye. The carotid angiography showed a giant aneurysm at the cavernous sinus portion in the right internal carotid artery. At his age of 38, the right oculomotor, trochlear and trigeminal nerves were involved. A vertebral angiography revealed a bead-like formation, and a diagnosis of fibromuscular dysplasia (FMD) was made. An intensive angiographic examination revealed many stenotic or dilated lesions in the carotid, vertebral, coronary, renal, and hepatic arteries. A sural nerve biopsy specimen revealed that the sural vein was involved. In Japan only one case of FMD presenting with WS is known. FMD should be under consideration as an underlying disease, when WS occurred in younger patients with few risk factors. In this patient an angiography revealed no abnormality in the cavernous sinus portion of the internal carotid artery, when he suffered from WS. However, eight years later he was proved to have a giant aneurysm in the cavernous sinus portion. In conclusion, we support the hypothesis that aneurysm may originate from angiographically normal arterial wall in FMD 8).
1) Li H, He XY, Li XF, Zhang X, Liu YC, Duan CZ. Treatment of giant/large internal carotid aneurysms: parent artery occlusion or stent-assisted coiling. Int J Neurosci. 2016 Jan;126(1):46-52. doi: 10.3109/00207454.2014.992427. Epub 2015 Jan 7. PubMed PMID: 25565057.
2) , 3) Bechan RS, Majoie CB, Sprengers ME, Peluso JP, Sluzewski M, van Rooij WJ. Therapeutic Internal Carotid Artery Occlusion for Large and Giant Aneurysms: A Single Center Cohort of 146 Patients. AJNR Am J Neuroradiol. 2016 Jan;37(1):125-9. doi: 10.3174/ajnr.A4487. Epub 2015 Aug 20. PubMed PMID: 26294643.
4) Shekhtman OD, Eliava ShSh, Pilipenko YI. [Trapping of large and giant paraclinoid aneurysm based on intraoperative flowmetry test]. Zh Vopr Neirokhir Im N N Burdenko. 2014;78(5):16-22; discussion 22. Russian. PubMed PMID: 25406904.
5) Rathore YS, Chandra PS, Kumar R, Singh M, Sharma MS, Suri A, Mishra NK, Gaikwad S, Garg A, Sharma BS, Mahapatra AK. Monitored gradual occlusion of the internal carotid artery followed by ligation for giant internal carotid artery aneurysms. Neurol India. 2012 Mar-Apr;60(2):174-9. doi: 10.4103/0028-3886.96396. PubMed PMID: 22626699.
6) van Rooij WJ, Sluzewski M. Unruptured large and giant carotid artery aneurysms presenting with cranial nerve palsy: comparison of clinical recovery after selective aneurysm coiling and therapeutic carotid artery occlusion. AJNR Am J Neuroradiol. 2008 May;29(5):997-1002. doi: 10.3174/ajnr.A1023. Epub 2008 Feb 22. PubMed PMID: 18296545.
7) Bowers CA, Taussky P, Park MS, Neil JA, Couldwell WT. Rescue microsurgery with bypass and stent removal following Pipeline treatment of a giant internal carotid artery terminus aneurysm. Acta Neurochir (Wien). 2015 Dec;157(12):2071-5. doi: 10.1007/s00701-015-2593-3. Epub 2015 Oct 2. PubMed PMID: 26429702.
8) Nishiyama K, Fuse S, Shimizu J, Takeda K, Sakuta M. [A case of fibromuscular dysplasia presenting with Wallenberg syndrome, and developing a giant aneurysm of the internal carotid artery in the cavernous sinus]. Rinsho Shinkeigaku. 1992 Oct;32(10):1117-20. Japanese. PubMed PMID: 1297556.

Book: Handbook of Skull Base Surgery

Handbook of Skull Base Surgery
Price: $121.72
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Handbook of Skull Base Surgery is a state-of-the-art surgical guide that provides clinicians and surgeons with step-by-step instructions on how to perform microscopic and endoscopic procedures. Encompassing the entire skull base, this handbook is designed for busy residents and clinicians seeking to hone their surgical skills. It presents a multidisciplinary approach to the pathologies, diagnosis, and management of skull base lesions.
Key Features:
Bulleted format with step-by-step descriptions of procedures accompanied by high-quality illustrations of key points Succinct summaries of content enable readers to quickly obtain the information they need Includes coverage of relevant basic sciences, advanced imaging, and adjunctive treatments such as radiosurgery and chemotherapy Comprehensive yet conveniently compact, this book is a must-havereference for residents, clinicians, nurses and researchers caring for patients with skull base pathologies.
Antonio Di leva
John Lee
Michael D. Cusimano

Department of Neurosurgery, St. Michael’s Hospital, University of Toronto, Toronto, Ontario, Canada.
http://neurosurgery.utoronto.ca/
 

Product Details

  • Published on: 2015-12-23
  • Original language: English
  • Number of items: 1
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  • 1004 pages

Extirpan un tumor cerebral a un paciente mientras toca el saxofón en Málaga – España

Neurocirujanos, neurofisiólogos, neuropsicólogos, anestesiólogos y enfermeros del Hospital Regional Universitario de Málaga han realizado, por primera vez en Europa, una intervención en la que se le ha extirpado un tumor cerebral a un paciente mientras tocaba el saxofón en algunos momentos para evitar secuelas. En concreto, el equipo sanitario llevó a cabo un mapeo de la corteza cerebral del lenguaje musical a Carlos Aguilera, de 27 años, al que se mantuvo despierto –sin anestesia general– durante toda la intervención, incluida la fase de resección del tumor.
La intervención, con una duración de 12 horas, se desarrolló el pasado 15 de octubre y, en la misma, participaron 16 profesionales sanitarios del Hospital Regional; concretamente, tres neurocirujanos, dos neuropsicólogos, tres neurofisiólogos, un anestesista, cinco enfermeras, un auxiliar de enfermería y un celador. Tras permanecer dos semanas hospitalizado, Aguilera fue dado de alta y prosigue los cuidados en domicilio con una buena evolución, según el neurocirujano Guillermo Ibáñez.
De hecho, el paciente ha interpretado varias piezas musicales con el saxofón durante la rueda de prensa. Entre ellas, la balada de jazz ‘Misty’, que ya tocó durante la operación, y el arreglo de una de Johann Sebastian Bach. El paciente ha agradecido su trabajo a los profesionales del Hospital Regional y ha aplaudido que “tengamos la suerte de contar con ellos aquí”. “Hace dos meses estaba en una camilla y hoy he vuelto a nacer”, ha señalado.
Paciente ejemplar
Los profesionales emplearon monitorización neurofisiológica intraoperatoria, una técnica que permite garantizar la seguridad del acto quirúrgico, evitando secuelas derivadas del mismo, y para la que se contó con la colaboración del paciente, que es miembro de una orquesta y becario en la Banda Municipal de Málaga. Ibáñez ha valorado la actitud “valiente” del paciente, asegurando que “un 50 por ciento del éxito de la operación es suya”.
En los músicos profesionales el hemisferio cerebral izquierdo tiene una mayor implicación en la comprensión y ejecución del lenguaje musical, zona donde también se localiza el área motora, sensitiva y del lenguaje, y donde está también la masa tumoral. En el Hospital Regional se han intervenido hasta la fecha un total de 12 pacientes despiertos a los que se les ha realizado el mapeo cortical de las áreas del lenguaje, siendo ésta la primera vez que se realiza la monitorización de las áreas cerebrales relacionadas con el lenguaje musical.
Según han constatado los propios profesionales responsables de la operación, no existen otros precedentes en España o Europa, aunque sí en California (EEUU), con un caso similar realizado este pasado mes de junio. El neurocirujano del Hospital Regional ha explicado que la localización de regiones corticales funcionales durante la cirugía de tumores cerebrales ha adquirido una gran relevancia, ya que permite realizar una resección del tumor más extensa, y en consecuencia, disminuir la probabilidad de morbilidad asociada.
La anestesia
En la fase previa a la intervención quirúrgica es importante encontrar la colocación más confortable para el paciente, ya que durante la operación sólo va a estar sedado –de forma proporcional a las necesidades quirúrgicas de cada fase– y participando de forma activa en la misma.
El procedimiento anestésico se realiza en su totalidad con el paciente despierto, con sus funciones cerebrales intactas, ya que es imprescindible su colaboración para poder identificar las respuestas tanto en la fase de estimulación eléctrica para el mapeo cortical como en la de resección del tumor.
Por ello, no se somete al paciente a una anestesia general con intubación ni se utilizan relajantes musculares. Así, en una primera fase se aplica anestesia local –previa a la instalación del cabezal metálico que mantiene sujeto el cráneo– en la zona de la intervención, y se asocia una sedación profunda –con una perfusión continua intravenosa con fármacos que proporcionan la sedación y analgesia– durante la fase de incisión de la piel, craneotomía y cierre, una vez finalizada la extracción del tumor.
En palabras de Ibáñez, “la implicación y colaboración de todos los profesionales, y la del paciente, es vital para poder realizar una resección óptima considerando siempre los límites del tumor, y, por supuesto, las zonas elocuentes adyacentes identificadas debidamente”.