Publications (2)4.11 Total impact
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Article: Prognostic factors for post-operative seizure outcomes after cavernous malformation treatment.
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ABSTRACT: Although patients with cerebral cavernous malformations may remain asymptomatic, they often present with neurological symptoms of headache, hemorrhage and, most commonly, seizure. A review of articles published between 1985 and 2009 was performed to elucidate the prognostic factors which may predict post-operative seizure control. The following characteristics were found to consistently correlate with a more favorable post-operative seizure-free outcome: (i) extent of resection of the cavernous malformation and its surrounding hemosiderin rim; (ii) single or sporadic seizures compared to chronic epilepsy; (iii) illness duration less than 1 or 2 years; and (iv) size of cavernous malformation less than 1.5 cm. Radiosurgery may achieve post-operative seizure-free rates ranging from 25% to 64.3%, and may be an alternative to surgical resection for deep or eloquent cavernous malformations, or those in patients with co-morbidities. There was no clear association between post-operative seizures and either lesion location, age, or gender. Prognostic features of cavernous malformations should be utilized for both guidance of lesion treatment, and prediction of post-operative seizure outcomes.Journal of Clinical Neuroscience 07/2011; 18(7):877-80. · 1.25 Impact Factor -
Article: The molecular genetics and tumor pathogenesis of meningiomas and the future directions of meningioma treatments.
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ABSTRACT: Meningiomas are mostly benign, slow-growing tumors of the CNS that originate from arachnoidal cap cells. While monosomy 22 is the most frequent genetic abnormality found in meningiomas, a multitude of other aberrant chromosomal alterations, signaling pathways, and growth factors have been implicated in its pathogenesis. Losses on 22q12.2, a region encoding the tumor suppressor gene merlin, represent the most common genetic alterations in early meningioma formation. Malignant meningioma progression, however, is associated with more complex karyotypes and greater genetic instability. Cytogenetic studies of atypical and anaplastic meningiomas revealed gains and losses on chromosomes 9, 10, 14, and 18, with amplifications on chromosome 17. However, the specific gene targets in a majority of these chromosomal abnormalities remain elusive. Studies have also implicated a myriad of aberrant signaling pathways involved with meningioma tumorigenesis, including those involved with proliferation, angiogenesis, and autocrine loops. Understanding these disrupted pathways will aid in deciphering the relationship between various genetic changes and their downstream effects on meningioma pathogenesis. Despite advancements in our understanding of meningioma pathogenesis, the conventional treatments, including surgery, radiotherapy, and stereotactic radiosurgery, have remained largely stagnant. Surgery and radiation therapy are curative in the majority of lesions, yet treatment remains challenging for meningiomas that are recurrent, aggressive, or refractory to conventional treatments. Future therapies will include combinations of targeted molecular agents as a result of continued progress in the understanding of genetic and biological changes associated with meningiomas.Neurosurgical FOCUS 05/2011; 30(5):E6. · 2.87 Impact Factor
