First International Brain Mapping Course

 

First International Brain Mapping Course to be held on April 28-29, 2016, in Chicago. This unique course is sponsored by the American Association of Neurological Surgeons (AANS) and the Neurosurgery Research and Education Foundation (NREF) in conjunction with the departments of neurosurgery at the University of California, San Francisco; the Universitaire de Montpellier, France and Rush University Medical Center in Chicago.
Trump Tower ViewThe First International Brain Mapping Course is scheduled immediately prior to the 2016 AANS Annual Scientific Meeting at the Hyatt Regency Chicago, one of the meeting’s main hotels. This course will bring together the largest cortical mapping programs in the world from 10 countries in North and South America, Europe and Asia, all to share their experiences and protocols in brain mapping.
Whether you are an expert in brain mapping or a neurosurgeon/neuroscientist who is interested in developing or improving your brain mapping program, your participation will provide valuable input to the meeting.
You can view the curriculum online for an outline of the topics that will be covered and a list of the renowned faculty from around the world. We encourage you join us for the meeting and to bring members of your mapping team to participate. There will be interactive sessions, case presentations and open discussions in which we welcome your input and the input from other members. We also encourage you to stay for the 2016 AANS Annual Scientific Meeting immediately following the conclusion of the mapping course.
Some of the highlights of the meeting include:

  • A pre-operative mapping evaluation session;
  • Expert lectures on the latest updates in understanding the anatomy of the functional cortex;
  • A series of 11 discussions given by some of the most prominent cortical stimulation mapping surgeons from nine countries, who will describe the details of their mapping techniques;
  • A dinner session with a keynote discussion by our honored guest, George A. Ojemann, MD, FAANS(L);
  • A keynote dinner session on the neuroanatomy of speech by David Poeppel, PhD, a renowned expert in speech physiology;
  • A two-hour working lunch session with an interactive discussion of standard and invited cases;
  • A presentation on the results of our pre-meeting survey regarding the uses and techniques of cortical mapping; and
  • A session covering brain mapping research and the future of brain mapping from leading centers.

There will be formal and informal sessions for case presentation and review. If you have unique and interesting cases that you would like to have presented in the formal sessions, you can submit them to faculty upon your registration. This is also an excellent venue for informally sharing unique cases with international experts.
For practitioners who are new to pre- and intra-operative brain mapping, this course is the perfect opportunity to learn the nuts-and-bolts practice of cortical mapping. You will also learn the practical aspects of starting a brain-mapping program. For experts, the meeting will focus on some of the more controversial and innovative practices in brain mapping at the leading centers in the world, including yours.
Because the 2016 AANS Annual Scientific Meeting and the NFL draft are being hosted in Chicago that same weekend, we encourage you to make travel plans and hotel reservations as soon as possible.
We are looking forward to seeing you, as we all learn from the vast experience of our expert international faculty.
Please register for the course here, and be sure to stay for the AANS Annual Scientific Meeting, which starts the following day. Hotel registration is also available on the AANS website. Registration is limited.

Mitchel Berger, MD, FAANS
Mitchel S. Berger,
MD, FAANS
Hugues Duffau, MD
Hugues Duffau, MD
Richard Byrne, MD
Richard W. Byrne,
MD, FAANS

First Down syndrome patient with a meningioma in the posterior fossa.

Down syndrome is a multiple malformation syndrome due to the trisomy of chromosome 21. There is epidemiological evidence that individuals with Down syndrome are at decreased risk for solid tumors including brain tumors. It has been suggested that some genes expressed on the extra copy of chromosome 21 act as tumor suppressor genes and contribute to the protection against tumorigenesis.
Yamamoto et al. report the first Down syndrome patient, an 8-year-old boy, with a meningioma in the posterior fossa. The diagnosis was based on histological study of the surgically resected tumor. Postoperatively his neurological status improved and there was no tumor regrowth in the next 2 years. Fluorescence in situ hybridization (FISH) for chromosome 22 confirmed high allele loss involving the NF2 gene locus, a finding typical in meningiomas. FISH also revealed chromosome 21 heterogeneity in tumor cells; not only cells with trisomy 21 but also cells with disomy and monosomy 21 were present. All blood cells from the patient manifested trisomy 21.
Our finding suggests that deletion of the chromosome 21 allele may be associated with the tumorigenesis of meningioma in Down syndrome. It supports the hypothesis that some genes whose expression is increased on the extra copy of chromosome 21 function as tumor suppressor genes and that they contribute to the reduced tumor incidence in individuals with Down syndrome 1).
1) Yamamoto T, Shinojima N, Todaka T, Nishikawa S, Yano S, Kuratsu JI. Meningioma in Down syndrome – Case Report. World Neurosurg. 2015 Apr 8. pii: S1878-8750(15)00365-4. doi: 10.1016/j.wneu.2015.03.065. [Epub ahead of print] PubMed PMID: 25862935.

First subdural hematoma after Imatinib mesylate

Imatinib mesylate, a tyrosine kinase inhibitor of platelet derived growth factor receptor-alpha and -beta, c-fms, c-kit, abl and arg kinase (imatinib targets), has been shown to prevent tumor progression in early studies of recurrent gliomas, but has shown weak activity in randomized controlled trials.
Responses to imatinib observed in patients where imatinib inhibitable tyrosine kinases were documented on the original biopsy are marginally better than that previously reported in imatinib treatment of unselected recurrent glioblastoma patients. Hassler et al. present a suggestion for defining a patient sub-population who might potentially benefit from imatinib 1).
It is used in chronic myeloid leukemia (CML) treatment. Imatinib has contributed to complete and prolong cytogenetic responses so that it is now the standard treatment of CML.
Recently, Imatinib mesylate has shown a significantly prolonged progression-free survival and overall survival in metastatic and locally advanced c-Kit positive gastro-intestinal stromal tumors (GISTs) and more recently a prolonged disease-free survival in operated high risk GIST.
In case of locally advanced or metastatic chordomas, medical treatment is frequently discussed. While chemotherapy is ineffective, it would appear that some molecular targeted therapies, in particular imatinib, could slow down the tumor growth in case-reports, retrospective series, and phase I or II trials. Nineteen publications, between January 1990 and September 2014, have been found describing the activity of these targeted therapies. A systematic analysis of these publications shows that the best objective response with targeted therapies was stabilization in 52 to 69% of chordomas. Given the indolent course of advanced chordoma and because of the absence of randomized trial, the level of evidence to treat chordomas with molecular therapy is low (level III), whatever the drug. Furthermore, we could not draw firm conclusion on the activity of imatinib. Other putative targets have also been described. Therefore, further clinical trials are expected, especially with these targets. Nevertheless, it seems essential, in those future studies, to consider the naturally slow course of the disease 2).
Neurodegeneration can be prevented by imatinib mesylate (Gleevec or STI571) that regulates c-Abl tyrosine kinases, which elicit protective effects in neurodegenerative disease models. However, the protective effect of STI571 against prion disease remains unknown. In the present study, the effect of STI571 on prion peptide-induced neuronal death was investigated. Results showed that STI571 rescued neurons from PrP106-126-induced neurotoxicity by preventing mitochondrial dysfunction. STI571-inhibited c-Abl tyrosine kinases prevented PrP106-126-induced reduction in mitochondrial potential, Bax translocation to the mitochondria and cytochrome c release. The protective effect of STI571 against mitochondrial dysfunction was related to the activation of BIM expression. This study is the first to demonstrate the protective effect of STI571 against prion-mediated neurotoxicity. Our results suggested that imatinib mesylate treatment may be a novel therapeutic strategy to treat prion-mediated neurotoxicity 3).

Complications

Imatinib is a well tolerated treatment with few side effects mainly gastro-intestinal symptoms (nausea, vomiting and diarrhea), headaches, rash and periorbital edema. Hemorrhage incidents are rare in patients treated with Imatinib. They are more frequently seen in CML patients. Hemorrhage incidents in CML include in many cases upper gastro-intestinal (GI) tract bleeding and central nervous system bleeding in rare ones. In GIST patients treated with Imatinib, hemorrhage incidents are exclusively made of upper GI tract bleeding consecutive to tumor perforation or necrosis. In our observation, we present the case of a subdural hematoma occurring in a patient treated with adjuvant Imatinib for a high risk localized gastric GIST. No other case of subdural hematoma in GIST treated with Imatinib has been reported in literature 4).
1) Hassler MR, Vedadinejad M, Flechl B, Haberler C, Preusser M, Hainfellner JA, Wöhrer A, Dieckmann KU, Rössler K, Kast R, Marosi C. Response to imatinib as a function of target kinase expression in recurrent glioblastoma. Springerplus. 2014 Feb 25;3:111. doi: 10.1186/2193-1801-3-111. eCollection 2014. PubMed PMID: 25674429; PubMed Central PMCID: PMC4320134.
2) Lebellec L, Aubert S, Zaïri F, Ryckewaert T, Chauffert B, Penel N. Molecular targeted therapies in advanced or metastatic chordoma patients: Facts and hypotheses. Crit Rev Oncol Hematol. 2015 Jan 30. pii: S1040-8428(15)00013-X. doi: 10.1016/j.critrevonc.2015.01.010. [Epub ahead of print] Review. PubMed PMID: 25682222.
3) Pan Y, Sun L, Wang J, Fu W, Fu Y, Wang J, Tong Y, Pan B. STI571 protects neuronal cells from neurotoxic prion protein fragment-induced apoptosis. Neuropharmacology. 2015 Feb 11. pii: S0028-3908(15)00045-3. doi: 10.1016/j.neuropharm.2015.01.029. [Epub ahead of print] PubMed PMID: 25681617.
4) Feki J, Marrekchi G, Boudawara T, Rekik N, Maatouq S, Boudawara Z, Frikha M. Subdural hematoma during therapy of gastro-intestinal stromal tumor (GIST) with Imatinib mesylate. Gulf J Oncolog. 2015 Jan;1(17):92-95. PubMed PMID: 25682460.
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