Relevant bibliographies by topics / Cavernous malformations ; cavernomas

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Academic literature on the topic 'Cavernous malformations ; cavernomas'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Cavernous malformations ; cavernomas"

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Kulwin, Charles G., Troy D. Payner, Rick F. Nelson, Laurie L. Ackerman, and Daniel H. Fulkerson. "Pediatric Pontine Cavernous Malformations: The Presigmoid, Posterior Petrosal Approach." Operative Neurosurgery 15, no. 5 (March 3, 2018): 522–29. http://dx.doi.org/10.1093/ons/opy007.

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Abstract BACKGROUND Brainstem cavernous malformations (cavernomas) in children have a high risk of hemorrhage and neurological deterioration. This risk is magnified if the child has a genetic predisposition for cavernoma formation. The surgical management is challenging and carries a significant risk of morbidity. OBJECTIVE To describe the feasibility of a posterior petrosal approach to brainstem cavernomas in a pediatric population. METHODS A single institution operative experience with this technique was reviewed; 2 cases were identified and are technically described here with supportive figures and illustrations, as well as a focused literature review. RESULTS Two pediatric cases with multiple symptomatic hemorrhages from large expanding pontine cavernomas were identified. Both cavernomas were resected through a presigmoid posterior petrosal approach. While this approach is well described in the adult literature for ventral brainstem lesions, its description for the treatment of pontine cavernomas in the pediatric populations is scarce. CONCLUSION This study demonstrates the utility and feasibility of the posterior petrosal approach in two pediatric patients at different points in cranial base development.
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Gorgan, R. M., F. Brehar, M. Catana, V. Pruna, Ana Gheorghiu, G. Popescu, Catioara Cristescu, and A. Giovani. "Surgical management of symptomatic spinal cord and intracerebral cavernomas in a multiple cavernomas case." Romanian Neurosurgery 30, no. 1 (March 1, 2016): 28–34. http://dx.doi.org/10.1515/romneu-2016-0004.

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Abstract Multiple cavernous malformations are associated with familial cases and are present in 10-20% of all cavernoma cases. 5% of cavernomas are located intramedullary and of these only 10% present multiple cavernomas. With the availability of echo gradient MRI the cases of multiple cavernomas are diagnosed earlier and it is not rare that it uncovers multiple cavernomas in cases where only a single lesion can be identified on regular MRI sequences. We present the case of a 55 years old woman presented with a two years history of mild backache, followed by progressive lower legs motor deficit and urinary retention. The spine MRI showed an intramedullary T2/3 lesion and the cerebral MRI established the diagnosis of multiple cavernomas. One year after the intramedullary cavernoma was operated with success, she developed generalized seizures and a new cerebral MRI showed bleeding and volume growth of one right temporal pole cavernoma. The cerebral lesion was resected successfully and the patient was discharged free of seizures. This familial type multiple cavernomas cases should be screened and followed with repeated brain and spine MRI’s every year.
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Jagathesan, Tania, and Michael OBrien. "Aeromedical Implications of Cerebral Cavernomas." Aerospace Medicine and Human Performance 92, no. 2 (February 1, 2021): 120–23. http://dx.doi.org/10.3357/amhp.5747.2021.

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BACKGROUND: Cavernomas, cavernous angiomas, or cerebral cavernous malformations are clusters of endothelium-lined blood vessels usually found in the brain. With the increasing use of radiological imaging, these are being detected incidentally in asymptomatic aircrew. The UK Civil Aviation Authority (CAA) experience of cavernomas is described and the aeromedical concerns, that is, the risk of epilepsy, hemorrhage, and the development of a neurological deficit, are considered.METHODS: A search of the CAA database between 1990 and 2020 was performed for the term cavernoma. The gender, age at diagnosis, class of certification held, clinical presentation, location, and size of the lesion were noted. A PubMed literature review for papers with complications of cavernoma was performed.RESULTS: Six cases of cavernoma have been declared to the CAA: five professional pilots and one private pilot. Five were men and one was a woman. The age range was between 38 and 60 yr, with a mean of 48 yr. Two cases presented with clinical symptoms and four were asymptomatic. Complication rates for seizure and hemorrhage were extracted from the published literature together with the significance of other factors such as cavernoma size, family history, multiplicity, and the development of new lesions.DISCUSSION: A policy for the medical certification of aircrew with cavernomas that have presented with clinical symptoms and those that are detected incidentally is proposed.Jagathesan T, OBrien M. Aeromedical implications of cerebral cavernomas. Aerosp Med Hum Perform. 2021; 92(2):120123.
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Perna, Giuseppe Di, Fabio Cofano, Roberto Altieri, Bianca Maria Baldassarre, Luca Bertero, Francesco Zenga, and Diego Garbossa. "III cranial nerve cavernous malformation: A case report and review of the literature." Surgical Neurology International 11 (December 22, 2020): 452. http://dx.doi.org/10.25259/sni_650_2020.

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Background: Cavernous malformations generally occur in brain parenchyma but rarely these lesions arise from cranial nerves (CNs). Case Description: This paper described a case of a woman presented with III CN dysfunction due to the presence of a right III CN cavernoma. Surgical treatment with nerve sparing gross total resection was performed. A 3-month follow-up was documented. Conclusion: Only few cases of CNs cavernomas have been described in the literature. These lesions have been described to show a more aggressive behavior compared to intraparenchymal cavernomas, especially in symptomatic patients. Differential diagnosis and surgical treatment could be challenging, especially trying to preserve nerve integrity and function.
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Iacob, G., and Angela Olarescu. "Spinal intramedullary cavernomas. Personal experience reffering to six cases." Romanian Neurosurgery 21, no. 4 (December 1, 2014): 407–15. http://dx.doi.org/10.2478/romneu-2014-0056.

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Abstract Despite cavernous malformations of the CNS are pathologically similar, intramedullary cavernous malformations are very rare lesions, increasingly recognized after introduction of magnetic resonance image, generating gradual neurological decline, with severe deficits or acute loss of spinal function. We report our experience on six patients with intramedullary cavernomas defining the spectrum of presenting symptoms and signs analyzing the role of surgery as a treatment for these lesions. We present our experience with 2 cervical and 4 thoracal spinal intramedullary cavernoma from 2010 to 2014 searching history, onset of clinical manifestation, neurological status, radiological findings, operation, and clinical outcome. Among 6 patients male were 2 cases; female 4 cases; mean age was 42 years (range 25-72 years); mean duration of symptoms were 1,5 years (range 5 days and 2 years) with slowly progressive neurological decline. In two cases there was acute onset of neurological compromise. In all cases diagnosis was made on MRI and lesions were possible to be radically excised and gently extracted from the hemosiderin-stained bed inside of the spinal cord via a laminectomy and midline myelotomy with microsurgical techniques. The surgical outcome on a mean duration of follow up of 12 months were: for 4 cases - the patients neurological conditions remarkably improved 1 month later, for 2 cases no improvement were remarked. No recurrent hemorrhages were recorded. A follow-up MRI examination was made in all cases to confirm complete removal of the cavernous angioma. Spinal intramedullary cavernoma should be early recognized by MRI, can be positioned in a precarious position and generate significant neurologic deficits than cranial cavernomas. For symptomatic intramedullary cavernous malformations extended to the dorsal surface of the spinal cord, total resection with microsurgical techniques can offer good or excellent outcome, restoring neurological status and to stop chronic deterioration and acute rebleeding. To asymptomatic patients with deeper lesions which entail a higher operative risk, but also a surgically manageable cause of myelopathy a closed observation is mandatory.
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Kivelev, Juri, Mika Niemelä, Riku Kivisaari, Reza Dashti, Aki Laakso, and Juha Hernesniemi. "LONG-TERM OUTCOME OF PATIENTS WITH MULTIPLE CEREBRAL CAVERNOUS MALFORMATIONS." Neurosurgery 65, no. 3 (September 1, 2009): 450–55. http://dx.doi.org/10.1227/01.neu.0000346269.59554.db.

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Abstract OBJECTIVE Multiple cerebral cavernous malformations (MCCMs) typically occur in patients with a family history of these lesions. Literature on MCCMs is scarce, and little is known about their natural history. METHODS Of 264 consecutive patients with cerebral cavernomas treated at the Department of Neurosurgery, Helsinki University Central Hospital, in the past 27 years, 33 patients had MCCMs. Lesions were categorized according to the Zabramski classification scale. Follow-up questionnaires were sent to all patients. Outcome was assessed using the Glasgow Outcome Scale, and amelioration of epilepsy was assessed using the Engel scale. All clinical data were analyzed retrospectively. RESULTS The mean age of patients at diagnosis was 44 years. Sex presentation was almost equal. Nine percent of all patients had a family history of the disease. Patients presented with epilepsy, acute headache, and focal neurological deficits. MCCMs were incidental findings in 2 patients. Altogether, 416 cavernomas were found: 70% supratentorial and 30% infratentorial. Fifteen patients had symptomatic hemorrhage before admission to our department. Surgery was performed on 18 patients. In most cases, the largest cavernoma was removed. Postoperatively, 1 patient experienced temporary hemiparesis, and another developed permanent motor dysphasia. No mortalities occurred. The mean follow-up time was 7.7 years. Twenty-six patients (79%) were in good condition. Among patients with epilepsy who underwent lesionectomy, 70% had an Engel class I outcome. On follow-up magnetic resonance imaging, 52 de novo cavernomas were found. CONCLUSION Surgical treatment of patients with MCCMs is safe. An extirpation of the clinically active cavernoma prevents further bleedings and improves outcome of epilepsy.
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Fanous, Andrew A., Patrick K. Jowdy, Lindsay J. Lipinski, Lucia L. Balos, and Veetai Li. "Association between trauma and acute hemorrhage of cavernous malformations in children: report of 3 cases." Journal of Neurosurgery: Pediatrics 18, no. 3 (September 2016): 263–68. http://dx.doi.org/10.3171/2016.3.peds15517.

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OBJECTIVE Cavernous hemangiomas are benign congenital vascular abnormalities. Intracerebral cavernous hemangiomas have an appreciable risk of spontaneous hemorrhage. Little is known as to whether head trauma increases the risk of bleeding for these lesions. In this study, the authors present a case series of 3 patients with posttraumatic nonspontaneous hemorrhage of intracerebral cavernous malformations (CMs). For the first time, to the authors' knowledge, they propose that trauma might constitute a risk factor for acute hemorrhage in intracerebral cavernomas. METHODS The authors reviewed the charts of all patients with a new diagnosis of intracerebral cavernoma at their pediatric hospital between 2010 and 2014. Patients with a history of head trauma prior to presentation were subsequently studied to identify features common to these posttraumatic, hemorrhage-prone lesions. RESULTS A history of head trauma was identified in 3 of 19 cases. These 3 patients presented with seizures and/or headaches and were found to have acute hemorrhage within a cavernous hemangioma. None of these patients had any history of abnormal neurological symptoms. All 3 abnormal vascular lesions had associated developmental venous anomalies (DVAs). The 3 patients underwent resection of their respective vascular abnormalities, and the diagnosis of cavernous hemangioma was confirmed with postsurgical tissue pathology. All 3 patients had complete resolution of symptoms following complete excision of their lesions. CONCLUSIONS Trauma may represent a risk factor for acute hemorrhage in patients with CMs. The presence of associated DVAs may represent a risk factor for posttraumatic hemorrhage of cavernomas. Excision should be considered in such cases, if feasible.
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De Souza, Jorge Marcondes, Flavio S. Domingues, Leila Chimelli, and Judith Gault. "Spinal root arteriovenous malformations and same-segment cord cavernous malformation in familial cerebral cavernous malformation." Journal of Neurosurgery: Spine 9, no. 3 (September 2008): 249–52. http://dx.doi.org/10.3171/spi/2008/9/9/249.

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Spinal vascular malformations are uncommon lesions, and controversy persists regarding optimal investigation, classification, and treatment strategies. The authors report on a patient with a spinal root arteriovenous malformation (AVM) associated with a parenchymal cavernous malformation (CM) in the same spinal cord segment and describe a complete familial and molecular investigation. This 35-year-old woman presented with symptoms of progressive clinical spastic paraparesis. Magnetic resonance imaging results were suggestive of a spinal cord cavernoma associated with cerebral CMs. Her family history included 2 sisters treated for epilepsy. At surgery an intraspinal root AVM was found at the same level of the cord CM, and both lesions were completely removed. Cerebral gradient echo MR imaging disclosed multiple cavernomas in her relatives, which prompted the molecular diagnosis. On sequence analysis, a novel mutation on the cerebral CM1 (CCM1) gene (c796insA) was found. The authors report on a unique case of familial cerebral CM in which a spinal root AVM was situated next to a cord CM, and discuss the concomitant occurrence of altered nervous system angiogenesis and vasculogenesis.
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Erkmen, Kadir, and Ossama Al-Mefty. "Transcondylar Approach for Resection of Medullary Cavernous Malformation: 2-Dimensional Operative Video." Operative Neurosurgery 21, no. 3 (June 30, 2021): E233—E234. http://dx.doi.org/10.1093/ons/opab220.

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Abstract Cavernous malformations located within the brainstem present with a high rate of neurological symptoms and carry a more aggressive course in both pediatric and adult populations.1,2 Cavernomas within the medulla are the rarest form, representing only 5% of all brainstem lesions.3 Repeated hemorrhage of brainstem cavernomas is associated with significant and cumulative neurological deficits and thus requires treatment.4 Microsurgical resection has become the optimal mode of treatment with the aim of resecting the live malformation and not merely the multiaged, organized hematoma.4 This is best achieved by approaching the cavernoma at the location where it projects to the surface and entering the lesion through a safe brainstem anatomic zone. For ventrally located lesions in the medulla, a transcondylar skull base approach provides a direct trajectory to the entry zone through a short surgical distance without the need to manipulate or retract neurovascular structures.5-8 Neuronavigation and intraoperative neurophysiological monitoring of somatosensory evoked potential, motor, and lower cranial nerves are adjuncts to increase patient safety. Radiosurgery for the treatment of brainstem cavernous malformations has been proposed; however, it demonstrates high risk and variable and often poor response rates.9 We present a surgical video demonstrating the transcondylar approach and resection of a medullary cavernoma in a 54-yr-old woman who has had multiple known prior hemorrhages and presented with a new onset of facial numbness and weakness, ataxia, and left body sensory loss. The patient consented to surgery and to photograph publication. Images at 1:28, 1:43 (left), 2:02 from Al-Mefty O, Operative Atlas of Meningiomas, © LWW, 1997,5 with permission. Images at 1:43 (right) from Arnautovic et al,8 with permission from JNSPG.
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Schmidt, Tyler, Michelle Lawson, Emily Silberstein, Jonathan Jay Stone, and Howard J. Silberstein. "335 Radiation Induced Cerebral Cavernomas in Pediatric Neuro-Oncology: A 25 Year Single Institution Review." Neurosurgery 64, CN_suppl_1 (August 24, 2017): 274–75. http://dx.doi.org/10.1093/neuros/nyx417.335.

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Abstract INTRODUCTION Radiation has a significant role in the management of pediatric brain tumors. Secondary complications to irradiation can include vascular malformations such as cavernous malformations, brain atrophy, necrosis, and demyelination. Although recognized as a potential complication, the pathogenesis and natural history of radiation induced cavernous malformations continues to be defined. We present a retrospective, single institution study of 138 patients who underwent cerebral radiotherapy as part of their comprehensive pediatric brain tumor management. METHODS Institutional review board permission was obtained and a retrospective review of all available patients with a pediatric brain tumor at our institution was completed. Patients who underwent radiotherapy and developed cavernous malformations were selected and the initial tumor type, frequency, and the radiological as well as clinical history were recorded and analyzed. RESULTS >From 1980–2005, 134 patients received radiotherapy for a pediatric brain tumor. Of this cohort, 28 patients (21%) subsequently developed at least one cerebral cavernous malformation. 21 of the patients had multiple cavernomas while only 7 were solitary. 15 patients were male. The mean time until discovery was 13.5 years. The tumor biology included 14 gliomas, 9 medulloblastomas, and 1 ependymoma. 14 patients received chemotherapy and all received at least short term corticosteroids. One patient required surgical excision of a cavernous malformation for repeated symptomatic hemorrhages. CONCLUSION Cavernous malformations are a frequent long term sequalae of pediatric radiotherapy. Although common, they are rarely associated with neurological complications even decades later and are largely discovered asymptomatically during routine surveillance screening of their primary disease. Future research in our database will be focused on establishing the relationship of radiation dose, age at irradiation, localization of radiotherapy, chemotherapy, anti-epileptics, and other medications on radiation induced cavernous malformations with the hope of identifying modifiable risk factors for clinical decision making application in a prospective fashion.
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Dissertations / Theses on the topic "Cavernous malformations ; cavernomas"

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Hall, Julie Maria. "Nature, frequency and natural history of intracranial cavernous malformations in adults." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/9532.

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Scottish Intracranial Vascular Malformation Study was the first prospective, population-based study of the major types of intracranial vascular malformations; arteriovenous, cavernous and venous malformations including dural fistulae and carotid-cavernous fistulae. It was based in Scotland and designed in 1998 by my supervisor Professor Charles Warlow and the first Research Fellow Dr Rustam Al-Shahi supported by the SIVMS steering committee (www.saivms.scot.nhs.uk). Recruitment and follow-up began in January 1999. Recruitment and follow-up of all vascular malformation types was done by Dr Al-Shahi until March 2002 and this role then transferred to me in April 2002 until I left in August 2004. The main duties of the Research Fellow were to collect and review all the clinical material of cases notified to SIVMS and arbitrate with the relevant expertise where there was doubt whether the case met the criteria for inclusion in SIVMS. Apart from my clinical responsibilities in recruitment and follow-up, the post also involved supervision of the part-time study administrator and also weekly meetings with the study programmer. I was also responsible for convening and presenting updates of the study progress weekly to my supervisor Professor Charles Warlow, biannually to the Study steering committee meetings, and annually to my funding body, the Stroke Association. This Research Fellowship also allowed me to gain an appreciation of the efforts needed to sustain collaborators’ interest in a long running study and I made presentations to improve the profile of the study on the national and international stage. For my duration as the SIVMS Research Fellow, I recruited and followed-up all types of newly diagnosed intracranial vascular malformations (IVMs). This thesis, however, is based solely on the incident intracranial cavernous malformations (ICMs) recruited to the study by both Dr Al-Shahi and myself between January 1999 and December 2003. The follow-up data in this thesis were that available to me on August 31st 2004. The data cleaning and the analysis for this thesis has been performed by me alone under the supervision of Professor Warlow. Although the core study design was well-established and tested prior to my involvement with SIVMS, I did divise new studies such as the Sensitivity and Specificity of MRI in the diagnosis of intracranial CMs. This cavernoma imaging study was a separate study designed, executed and analysed by myself, a medical student Sue Liong, the Cavernoma Imaging Study Group [appendix 1] with guidance from Professor Warlow, Dr Al-Shahi, Dr Andrew Farrall (consultant neuroradiologist) and Dr Steff Lewis (Medical Statistician). Computing support was provided by Aidan Hutchison (SIVMS programmer).
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Crose, Lisa Eileen Stalheim Johnson Gary L. "Regulation and function of the cerebral cavernous malformation 2 protein." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2009. http://dc.lib.unc.edu/u?/etd,2439.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2009.
Title from electronic title page (viewed Sep. 3, 2009). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Pharmacology." Discipline: Pharmacology; Department/School: Medicine.
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Verlaan, Dominique Jacqueline. "Genetic investigation of cerebrovascular disorders : cerebral cavernous malformations and intracranial aneurysms." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103306.

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Cerebral Cavernous Malformations (CCM) and Intracranial Aneurysms (IA) are cerebrovascular disorders that can lead to a hemorrhagic stroke and other neurological problems. CCMs are characterized by abnormally enlarged capillary cavities while IAs are saccular outpouchings of intracranial arteries. CCM is found in approximately 0.4% to 0.9% of the population, while IA is more common (3-6%).
This dissertation aimed to add to the body of research for CCM and IA and was divided into two parts. Initial work focused on the characterization and identification of the genes involved in CCM; the second phase focused on the identification of a susceptibility gene for IA.
In the first phase, the CCM1, CCM2 and CCM3 genes were characterized in families and in sporadic cases of CCM. In both cohorts, a causative mutation was identified in 71% of the cases. Subsequent MLPA analysis of subjects with no CCM mutations revealed that large genomic deletions and duplications are a common cause of CCM. In addition, investigation of CCM1 point mutations revealed that these were not simple missense mutations but that they rather activated cryptic splice-donor sites and caused aberrant splicing. Furthermore, the genetic predisposition to CCM in sporadic cases with a single lesion was determined to be different from sporadic cases with multiple malformations. Investigation into the loss of heterozygosity demonstrated a plausible mechanism for CCM pathogenesis involving a second somatic hit at the site of the lesion, suggesting that CCM may be caused by a complete loss of CCM protein function.
In the second phase, a genome-wide scan of a large family and subsequent linkage analysis using a monogenic approach identified a susceptibility locus for IA (ANIB4).
As a result of this research, we have greatly contributed to the field of CCM, most specifically to its clinical diagnosis. A greater understanding of the genetics involved in CCM will facilitate and permit better management care for patients. Furthermore, the possibility of identification of a gene with a major effect for IA will give us more insight into which pathways are involved in IA formation.
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Hebert, Ryan Matthew. "Functional analysis of CCM3 a gene contributing to cerebral cavernous malformations /." [New Haven, Conn. : s.n.], 2008. http://ymtdl.med.yale.edu/theses/available/etd-12022008-120301/.

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Takada, Shigeki. "Contribution of Endothelial-to-Mesenchymal Transition to the Pathogenesis of Human Cerebral and Orbital Cavernous Malformations." Kyoto University, 2018. http://hdl.handle.net/2433/232474.

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Vannier, Daphné. "Découverte d'une sénescence associée à un phénotype sécrétoire déclenchée par les défauts mécaniques de la cellule endothéliale lors de la perte de CCM2 dans un modèle de cavernome cérébral." Thesis, Université Grenoble Alpes, 2020. https://thares.univ-grenoble-alpes.fr/2020GRALV012.pdf.

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Les lésions CCM (Cerebral Cavernous Malformations) sont formées d’un empilement de vaisseaux capillaires tortueux, dilatés et hémorragiques situés dans le cerveau. Ces capillaires cérébraux sont dépourvus de cellules murales et sont formés d’une monocouche de cellules endothéliales (CE) peu jointives. La mutation perte de fonction de l’un des 3 gènes ccm (ccm1, ccm2 et ccm3) est suffisante pour induire la formation de lésions CCM chez l’Homme.Dans les différents modèles mutants ccm, les CE présentent une homéostasie tensionnelle défectueuse caractérisée par un défaut de coordination entre les forces d’adhésions cellule-matrice et cellule-cellule. Ceci se traduit par la formation de fibres contractiles d’actomyosine ancrées sur de nombreuses adhérences focales à intégrine B1 et par la perte des jonctions intercellulaires dépendantes de VE-cadhérine. L’association des protéines CCM1-3 forme une plateforme moléculaire qui contrôle, en aval de RhoA, l’activité des kinases ROCK1 et ROCK2 sur l’organisation du cytosquelette d’acto-myosine. Le complexe CCM recrute ROCK2 aux jonctions dépendantes de VE-cadhérine pour promouvoir un réseau d’actine cortical stabilisateur de ces jonctions intercellulaires alors que dans le même temps, il inhibe l’activité de ROCK1 pour réduire la formation de fibres de stress ventrales et ainsi limiter l’adhésion de la CE à la matrice extracellulaire. Il est connu que le microenvironnement de la lésion est remodelé notamment par des cellules immunitaires qui s’infiltrent pour déclencher une réponse inflammatoire chronique et favoriser l’expansion de la lésion. Il est également connu que les CE mutantes sécrètent des métalloprotéases et des cytokines, qu’elles surproduisent des ROS et qu’elles subissent une transition endothélio-mésenchymateuse (endoMT). Enfin, les lésions CCM sont des mosaïques de CE mutantes et sauvages qui sont recrutées au cours du temps dans la lésion. Néanmoins, le lien qui existe entre tous ces phénomènes favorables à la progression de la lésion CCM est encore mal compris et reste à élucider.Les travaux que j’ai effectués au cours de cette thèse m’ont permis de proposer un modèle qui unifie l’ensemble de ces comportements cellulaires. En effet, j’ai mis en lumière le vieillissement prématuré des cellules endothéliales déplétées en CCM2. J’ai montré que cette sénescence est associée à un comportement sécrétoire SASP (Senescence Associated with a Secretory Phenotype) qui confère à la CE la capacité de remodeler activement son environnement notamment en le dégradant de manière localisée, de l’envahir et d’attirer par chimio-attraction des CE sauvages et des cellules immunitaires. Le second apport majeur de mon travail a été de montré que cette SASP est due aux dérèglements dans la mécanique de la CE. En effet, j’ai montré que l’augmentation de la contractilité intracellulaire, associée à un défaut de coordination entre les activités de ROCK1 et ROCK2, est responsable de cette SASP. L’inhibition de la myosine II ou la déplétion préférentielle de ROCK1 ou de ROCK2, restaure l’expression de la moitié des gènes dérégulés par la perte de CCM2, bloque l’apparition des marqueurs de sénescence ainsi que les capacités invasives et chimio-attractantes des CE déplétées pour CCM2. Ces résultats ouvrent la voie vers l’identification de nouvelles cibles thérapeutiques pour bloquer les mécanismes à l’origine de l’apparition et de l’expansion des lésions CCM
CCM (Cerebral Cavernous Malformations) lesions are formed by stacks of tortuous, dilated and hemorrhagic capillaries located in the brain. These brain capillaries are devoid of mural cells and are formed of a monolayer of weakly joined endothelial cells (EC). The loss of function mutation in one of the 3 ccm genes (ccm1, ccm2 and ccm3) is sufficient to induce the formation of CCM lesions in humans.In the different ccm mutant models, the ECs present defective tensional homeostasis characterized by a lack of coordination between the cell-matrix and cell-cell forces. This results in the formation of contractile actomyosin fibers anchored on numerous focal adhesions containing B1 integrin and in the loss of VE-cadherin-dependent intercellular junctions. The association of CCM1-3 proteins forms a molecular scaffold that controls downstream of RhoA the activity of ROCK1 and ROCK2 on the organization of the acto-myosin cytoskeleton. The CCM complex recruits ROCK2 at the VE-cadherin dependent junctions to promote a network of cortical actin stabilizing these intercellular junctions while at the same time, it inhibits the activity of ROCK1 to reduce the formation of ventral stress fibers and thus limit the adhesion of the EC to the extracellular matrix. It is known that the microenvironment in the lesion is reshaped in particular by immune cells that infiltrate it to trigger a chronic inflammatory response and promote the expansion of the lesion. It is also known that mutant ECs secrete metalloproteases and cytokines, that they overproduce ROS and that they undergo an endothelio-mesenchymal transition (endoMT). Finally, CCM lesions are mosaics of mutant and wild-type ECs recruited into the lesion over time. However, whether a link exists between all these phenomena conducive to the progression of the CCM lesion is not known and remains to be elucidated.My work during this PhD allowed me to propose a model that unifies all these cellular behaviors. Indeed, I have highlighted a premature aging of endothelial cells depleted in CCM2. I have shown that this senescence is associated with a secretory behavior SASP (Senescence Associated with a Secretory Phenotype) which gives the EC the ability to actively reshape its environment, in particular by degrading it locally, to invade it and attract by chemo-attraction wild EC and immune cells. The second major contribution of my work has been to show that this SASP is due to the dysregulation of the mechanics of the EC. Indeed, I have shown that the increase in intracellular contractility, associated with the loss of balance between the activities of ROCK1 and ROCK2, is responsible for this SASP. Inhibiting myosin II or depleting ROCK1 or ROCK2 restores the expression of half of the genes dysregulated by the loss of CCM2, blocks the appearance of senescence markers as well as the invasive and chemo-attractive capacities of CCM2-depleted ECs. These results open the way to the identification of new therapeutic targets responsible for the appearance and expansion of CCM lesions
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Horne, Margaret Anne. "Investigating the risk of intracranial haemorrhage or focal neurological deficit in adults diagnosed with cerebral cavernous malformation." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/15879.

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Background A cerebral cavernous malformation (CCM) is a small cluster of thin-walled, dilated blood vessels within the brain which is prone to bleed. Although the quantity of blood leaking tends to be small, even a small intracranial haemorrhage (ICH) can result in a clinically significant neurological deficit. Because some focal neurological deficits (FND) may in fact be haemorrhages that were undetected by imaging, FND were also included in the analysis wherever possible. In Scotland, between 2006 and 2010, the annual CCM detection rate was 0.8 per 100,000 people. Since estimates of prognosis inform decisions about whether to treat CCM, it is crucial that the untreated clinical course of the disease is fully understood. Aim The aims of this thesis are (i) to quantify the risk of ICH (or ICH or FND, referred to as ‘clinical event’) for an untreated adult within five years of CCM diagnosis, (ii) to identify prognostic factors for ICH (clinical event), and (iii) to create a model to predict, at the time of diagnosis, an individual’s risk of a subsequent ICH (clinical event). Methods Initially, a literature review was undertaken. Then data from adults diagnosed with CCM in the Scottish Intracranial Vascular Malformation Study (SIVMS) were analysed. SIVMS is a prospective, population-based cohort study: it includes all adults resident in Scotland at the time of diagnosis of a first-ever intracranial vascular malformation during the two five-year periods 1999–2003 and 2006–2010. Time-to-event methods were employed to compare the estimated risk of ICH (clinical event) for those who experienced a first ICH (clinical event) during untreated five-year follow-up with those who experienced a second ICH (clinical event). A statistical challenge when analysing clinical outcomes from patients with CCM is that the outcome event of ICH or FND is comparatively rare; therefore a larger cohort of CCM patients was required to identify more robustly potential predictors of ICH (clinical event) and to create a prognostic model to predict, at the time of diagnosis, an individual’s risk of a subsequent ICH (clinical event). Three research groups agreed to contribute their data to enable an individual patient data meta-analysis (IPDMA) to be undertaken. Results In the two SIVMS cohorts, 136 (1999–2003) and 165 adults (2006–2010) were diagnosed with CCM. In the earlier cohort, the estimated risk of a first ICH within five years of presentation (2.4%, 95% CI 0.0% to 5.7%) was significantly lower (p < 0.0001) than the risk of a recurrent ICH (31.9%, 95% CI 4.5% to 59.3%), but the annual risk of a recurrence declined over the five-year period. In the same cohort, women had an increased risk of a second clinical event (log-rank χ2(1) = 6.2, p = 0.01). The IPDMA was based on 988 adults, 62 of whom suffered a first ICH within five years of CCM diagnosis. When the data were pooled, the estimated adjusted hazard ratio for first ICH for clinical presentation (ICH/FND vs other presentation) was 4.5 (95% CI 1.5 to 13.4) and for brainstem location (brainstem vs other location) the adjusted hazard ratio was 3.3 (95% CI 1.5 to 7.2); age, sex and CCM multiplicity did not add any additional prognostic information. Conclusion In this thesis two risk factors have been identified that are independently associated with increased likelihood of experiencing an ICH (or clinical event) within five years of diagnosis. A prognostic model has been built and evaluated, based on these factors. Other areas to be explored in the future include external validation of the model and investigating the effects of (i) antithrombotic therapy and (ii) pregnancy on the progression of the disease.
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Bisson, Jacques. "Les formes familiales des cavernomes intracraniens : à propos de sept cas dans une famille, revue de la littérature." Caen, 1990. http://www.theses.fr/1990CAEN3067.

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Brunereau, Laurent. "Optimisation des séquences IRM dans la détection, la caractérisation et le suivi des cavernomes cérébraux familiaux." Tours, 2001. http://www.theses.fr/2001TOUR3301.

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Dans cette évaluation par IRM des cavernomes cérébraux familiaux, nos objectifs étaient d'optimiser le protocole d'exploration, d'analyser les caractéristiques des lésions cérébrales et de déterminer leur évolution spontanée et leurs facteurs pronostiques. De novembre 1996 à juin 1997, 51 familles sans origine hispanique ont été identifiées en France. A partir de ces familles, 83 patients symptomatiques et 73 patients asymptomatiques ont été inclus dans notre étude et ont eu une ou plusieurs IRM cérébrales entre 1996 et 2000. Nous avons évalué les caractéristiques IRM des cavernomes en utilisant des séquences spin-echo, gradient-echo et gradient-spin-echo (GRASE). En outre, nous avons essayé de determiner l'évolution clinique et IRM des cavernomes cérébraux en analysant plusieurs IRM consécutives dans des populations de patients symptomatiques et asymptomatiques. L'exploration par IRM des cavernomes cérébraux familiaux doit systématiquement comporter des séquences spin-echo et gradient-echo. L'imagerie GRASE ne doit pas être utilisée dans cette indication. La séquence gradient-echo constitue la référence pour détecter les lésions cérébrales. La séquence gradient-echo est la référence pour caractériser les cavernomes et déterminer le potentiel agressif de chaque lésion. La forme familiale des cavernomes cérébraux est une maladie évolutive caractérisée par la survenue spontanée d'événements IRM tels que des hémorragies cérébrales, des changements de taille ou de signal et par l'apparition de lésions de novo. Ces événements apparaissent plus fréquents chez des patients symptomatiques que chez des patients asymptomatiques. La forme familiale des cavernomes cérébraux est une maladie évolutive qui nécessite d'être explorée par des IRM cérébrales répétées incluant des séquences spin-echo et gradient-echo.
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Castell, Jean-François. "Les angiomes caverneux intra-craniens : étude de 21 cas." Bordeaux 2, 1990. http://www.theses.fr/1990BOR23068.

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Books on the topic "Cavernous malformations ; cavernomas"

1

Trabalzini, Lorenza, Federica Finetti, and Saverio Francesco Retta, eds. Cerebral Cavernous Malformations (CCM). New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0640-7.

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Cavernous malformations of the nervous system. Houndmills, Basingstoke, Hampshire: Cambridge University Press, 2011.

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Rigamonti, Daniele, ed. Cavernous Malformations of the Nervous System. Cambridge: Cambridge University Press, 2011. http://dx.doi.org/10.1017/cbo9781139003636.

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Cavernous Malformations. American Association of Neurological Surgeons, 1992.

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Spetzler, Robert F., Rami O. Almefty, and Karam Moon. Arteriovenous and Cavernous Malformations. Elsevier, 2017.

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Chong, Ji Y., and Michael P. Lerario. Recurrent Headaches. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190495541.003.0033.

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Cavernous malformations may cause intracerebral hemorrhage and seizures. Surgical resection is considered in patients with accessible lesions and recurrent hemorrhage or refractory seizures. However, current nonrandomized data suggest that nonsurgical treatment of these lesions may be superior. Cavernous malformations may be familial.
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Giuseppe, Lanzino, and Spetzler Robert F. 1944-, eds. Cavernous malformations of the brain and spinal cord. New York: Thieme, 2007.

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Gluseppe, M.D. Lanzino (Editor) and Robert F. Spetzler (Editor), eds. Cavernous Malformations of the Brain and Spinal Cord. Thieme Medical Publishers, 2008.

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Benndorf, Götz. Dural Cavernous Sinus Fistulas: Diagnosis and Endovascular Therapy (Medical Radiology / Diagnostic Imaging). Springer, 2008.

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Book chapters on the topic "Cavernous malformations ; cavernomas"

1

Svoboda, Norbert, Vladimír Beneš, and Ondřej Bradáč. "Spinal Cavernous Malformations." In Cavernomas of the CNS, 215–37. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49406-3_14.

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Netuka, David. "Intraorbital Cavernous Malformations." In Cavernomas of the CNS, 239–45. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49406-3_15.

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Skalický, Petr, Vladimír Beneš, and Ondřej Bradáč. "Brief History of Cavernous Malformations." In Cavernomas of the CNS, 1–3. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49406-3_1.

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Nagy, Gábor, and Matthias W. R. Radatz. "Stereotactic Radiosurgery of Cavernous Malformations." In Cavernomas of the CNS, 165–90. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49406-3_11.

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Ioannis, Ioannidis, Nasis Nikolaos, and Andreou Alexandros. "Neuroimaging of Cerebral Cavernous Malformations." In Cavernomas of the CNS, 55–67. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49406-3_5.

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Kivelev, Juri, and Mika Niemelä. "Natural History of Cavernous Malformations." In Cavernomas of the CNS, 69–91. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49406-3_6.

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Skalický, Petr, Vladimír Beneš, and Ondřej Bradáč. "Surgery of Deep-Seated Cavernous Malformations." In Cavernomas of the CNS, 115–42. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49406-3_9.

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Bradáč, Ondřej, Petr Skalický, and Vladimír Beneš. "Surgery of Brainstem and Cerebellar Cavernous Malformations." In Cavernomas of the CNS, 143–63. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49406-3_10.

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Tanaka, Michihiro. "Definition and Structure of Cerebral Cavernous Malformations." In Cavernomas of the CNS, 5–12. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49406-3_2.

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Dolgushin, Mikhail, Valery Kornienko, and Igor Pronin. "Cavernous Angiomas, Cavernous Malformations." In Brain Metastases, 377–80. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57760-9_34.

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Conference papers on the topic "Cavernous malformations ; cavernomas"

1

Wang, Huiquan, S. Nizam Ahmed, Hongming Xu, and Mrinal Mandal. "Automated detection of cavernous malformations in brain MRI images." In 2017 8th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2017. http://dx.doi.org/10.1109/ner.2017.8008281.

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Yang, Guili, Huijie Wei, Zhenying Han, Zhisong Zhang, Biyan Duan, Jianning Zhang, and Lu-yuan Li. "Abstract 4314: A mouse model of cerebral cavernous malformations." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4314.

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Wang, Huiquan, Hongming Xu, S. Nizam Ahmed, and Mrinal Mandai. "Computer aided detection of cavernous malformation in T2-weighted brain MR images." In 2016 IEEE Healthcare Innovation Point-Of-Care Technologies Conference (HI-POCT). IEEE, 2016. http://dx.doi.org/10.1109/hic.2016.7797707.

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Paiva, Aline, Eduardo de Alcântara, João Araujo, and José Veiga. "Propranolol as treatment for cavernous angioma malformation – a prospective study and a critical review." In XXXII Congresso Brasileiro de Neurocirurgia. Thieme Revinter Publicações Ltda, 2018. http://dx.doi.org/10.1055/s-0038-1673106.

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Goldberg, J., C. Jaeggi, D. Schoeni, P. Mordasini, A. Raabe, and D. Bervini. "Bleeding Risk of Cerebral Cavernous Malformations in Patients on Beta Blocker Medication: A Cohort Study." In Joint Annual Meeting 2018: Swiss Society of Neurosurgery, Swiss Society of Neuroradiology. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1660732.

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Velz, J., M. Stienen, M. Neidert, Y. Yang, L. Regli, and O. Bozinov. "Is Active Follow-Up by Serial Imaging Justified in Patients with Multiple Cerebral Cavernous Malformations?" In Joint Annual Meeting 2018: Swiss Society of Neurosurgery, Swiss Society of Neuroradiology. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1660755.

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Formentin, Cleiton, David T. Fernandes-Cabral, Yun-Kai Chan, Arseniy Pichugin, Eric W. Wang, Carl H. Snyderman, Paul A. Gardner, and Georgios Zenonos. "Endoscopic Endonasal Approach to the Ventral Midbrain for Brainstem Cavernous Malformations: An Anatomical and High-Accuracy Fiber Tractography Study." In Special Virtual Symposium of the North American Skull Base Society. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1725408.

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Abhinav, Kumar, Troels Nielsen, Rhea Singh, Yingjie Weng, Summer Han, Michael Iv, and Gary Steinberg. "Utility of Diffusion Tensor Imaging Tractography in Evaluating Motor Examination and Functional Outcomes in Patients with Surgically Resected Deep Intracranial Cavernous Malformations: A Preliminary Model." In 29th Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1679505.

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