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Posterior Cranial Fossa (posterior + cranial_fossa)
Selected AbstractsSetting Up a Multidisciplinary Program for Management of Patent Foramen Ovale-Mediated SyndromesJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 3 2006GIANLUCA RIGATELLI M.D. Background: These days no codified multidisciplinary protocol has been reported to manage all the different patent foramen ovale (PFO)-mediated syndromes. We sought to propose a multidisciplinary program of diagnosis, treatment, and follow-up of all PFO-mediated syndromes based on an in-hospital multidisciplinary task force and to review the activities during the first year. Methods: From September 2004, we organized in our hospital, a 600-bed tertiary hospital, a management program for PFO-mediated syndromes based on a task force composed of cardiologists, neurologists, and internists. Different levels of protocols were created in order to cover diagnosis, treatment, and follow-up of PFO-mediated syndromes. We reviewed the activity of our program in the first year up to September 2005. Results: Thirty-five patients (23 female, mean age 65 ± 24 years) were evaluated for suspected PFO-mediated syndromes: 20 for cryptogenic stroke, 2 for peripheral and coronary embolisms, 3 for platypnea-orthodeoxia, 9 for emicrania with aura, and 1 with hypoxiemia during neurosurgical intervention in the posterior cranial fossa. Diagnosis of PFO was confirmed in 25 patients. According to the multidisciplinary protocols, 15 patients failed to meet the requirements for transcatheter closure and were left in medical therapy whereas 11 patients (7 patients with PFO, 2 with multiperforated ASD, and 2 with a secundum ASD) underwent transcatheter closure. After a mean follow-up of 10.8 ± 4.9 months, no recurrent PFO syndromes were noted in patients treated with devices. Conclusion: The first year of our multidisciplinary program allowed a reasonable and potentially successful approach for correctly identifying patients with PFO-mediated syndromes until randomized studies are completed. [source] Brain structural damage in spinocerebellar ataxia type 2.MOVEMENT DISORDERS, Issue 6 2008A voxel-based morphometry study Abstract Voxel-based morphometry (VBM) enables an unbiased in-vivo whole-brain quantitative analysis of differences in gray matter (GM), white matter (WM) and cerebro-spinal fluid (CSF) volumes. We assessed with VBM 20 spinocerebellar ataxia Type 2 (SCA2) patients with mild or moderate cerebellar deficit and 20 age and sex-matched healthy controls. SCA2 patients showed a significant (P < 0.05 corrected for multiple comparison) symmetric loss of GM in the cerebellar vermis and hemispheres sparing lobules I,II, Crus II,VII, and X, and of the WM in the peridentate region, middle cerebellar peduncles, dorsal pons, and cerebral peduncles. The CSF volume was increased in the posterior cranial fossa. No GM, WM or CSF volume changes were observed in the supratentorial compartment. A mild (P < 0.05, >0.01) correlation was observed between the GM and WM loss and severity of the neurological deficit. In SCA2 patients with mild to moderate cerebellar deficit, GM and WM volume loss and CSF volume increase are confined to the posterior cranial fossa. © 2008 Movement Disorder Society [source] Brain size and the human cranial base: A prenatal perspectiveAMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY, Issue 4 2002Nathan Jeffery Abstract Pivotally positioned as the interface between the neurocranium and the face, the cranial base has long been recognized as a key area to our understanding of the origins of modern human skull form. Compared with other primates, modern humans have more coronally orientated petrous bones and a higher degree of basicranial flexion, resulting in a deeper and wider posterior cranial fossa. It has been argued that this derived condition results from a phylogenetic increase in the size of the brain and its subcomponents (infra- and supratentorial volumes) relative to corresponding lengths of the cranial base (posterior and anterior, respectively). The purpose of this study was to test such evolutionary hypotheses in a prenatal ontogenetic context. We measured the degree of basicranial flexion, petrous reorientation, base lengths, and endocranial volumes from high-resolution magnetic resonance images (hrMRI) of 46 human fetuses ranging from 10,29 weeks of gestation. Bivariate comparisons with age revealed a number of temporal trends during the period investigated, most notable of which were coronal rotation of the petrous bones and basicranial retroflexion (flattening). Importantly, the results reveal significant increases of relative endocranial sizes across the sample, and the hypotheses therefore predict correlated variations of cranial base flexion and petrous orientation in accordance with these increases. Statistical analyses did not yield results as predicted by the hypotheses. Thus, the propositions that base flexion and petrous reorientation are due to increases of relative endocranial sizes were not corroborated by the findings of this study, at least for the period investigated. Am J Phys Anthropol 118:324,340, 2002. © 2002 Wiley-Liss, Inc. [source] CHARGE syndrome as unusual cause of hypogonadism: endocrine and molecular evaluationANDROLOGIA, Issue 5 2010L. Foppiani Summary Coloboma, heart defect, atresia choanae, retarded growth and development, genital hypoplasia, ear anomalies (CHARGE) syndrome is a genetic syndrome in which hypogonadism is a frequent feature. A causative mutation within the chromodomain helicase DNA-binding protein-7 gene, which plays an important role in the embryonic development, is present in 2/3 of affected patients. We describe the clinical, hormonal and molecular characteristics of a young man from Ecuador who was diagnosed as having CHARGE syndrome at an adult age. The patient showed several phenotypic features of the syndrome, associated with a prepubertal state and cryptorchidism; hypogonadotrophic hypogonadism with undetectable testosterone levels not responsive to hCG testing and severe osteoporosis were ascertained. Molecular evaluation of the CHD7 gene showed the novel frameshift truncating heterozygous mutation p.Tyr1046Glyfs*23 in exon 12. Magnetic resonance imaging revealed mild hypoplasia of the pituitary gland and hypoplasia of the posterior cranial fossa. Parenteral testosterone therapy led to sexual development over time and, in combination with diphophonate therapy and calcium,vitamin D supplementation, significantly improved bone mineralisation. Early proper hormonal treatment of hypogonadism in patients with complex genetic syndromes is important to achieve normal sexual maturation, improve quality of life and avoid significant comorbidities, such as osteoporosis. [source] | ||||||||||