Background: Cerebrospinal fluid (CSF) abdominal pseudocyst is an uncommon but important complication of ventriculoperitoneal shunts. From the collected series, several features about the etiology and management become apparent. Retrospective data were obtained from 12 children treated with cerebrospinal fluid abdominal pseudocyst defined an alternative approach for management of these patients.
Methods: There were eight girls and four boys who ranged in age from 12 days to 18 years old (mean 7.7 months). The most frequent etiology of the hydrocephalus was Chiari type II malformation in six cases. Initial presentation with shunt malfunction was detected in nine cases. Abdominal distention and/or pain were the most frequent finding in our series (10/12). In only one case, infection was detected for all cerebrospinal fluid abdominal pseudocysts (8.3%). Ventriculoperitoneal shunt (VPS) externalization, antibiotics, and cyst aspiration was performed in 8/12 cases as initial management of abdominal pseudocyst. Ventriculoperitoneal shunt reinsertion in abdominal cavity and/or endoscopic third ventriculostomy (ETV) was performed as final management in 9/12. Ventriculoatrial shunt was used only in three cases. Recurrence of the abdominal cyst was observed in two cases.
Discussion: Based on the success rate (75%) in our series submitted to this management, a ventriculoperitoneal shunt can be safely reinserted in the majority of the patients. Endoscopic third ventriculostomy could be performed in selected cases as an alternative approach. Although infection has been reported as responsible for pseudocyst formation, it was only exceptionally found in our series.
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http://dx.doi.org/10.1007/s00381-006-0183-7 | DOI Listing |
Cytometry B Clin Cytom
January 2025
Hematology, Department of Biomedicine and Prevention, University of Rome "Tor Vergata", Rome, Italy.
Alzheimers Dement
January 2025
Department of Neuroscience, Imaging, and Clinical Sciences, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.
Introduction: Machine learning (ML) helps diagnose the mild cognitive impairment-Alzheimer's disease (MCI-AD) spectrum. However, ML is fed with data unavailable in standard clinical practice. Thus, we tested a novel multi-step ML approach to predict cognitive worsening.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
The Affiliated Brain Hospital, Guangzhou Medical University, Guangzhou, China.
Introduction: With the advancement of disease-modifying therapies for Alzheimer's disease (AD), validating plasma biomarkers against cerebrospinal fluid (CSF) and positron emission tomography (PET) standards is crucial in both research and real-world settings.
Methods: We measured plasma phosphorylated tau (p-tau)217, p-tau181, amyloid beta (Aβ)1-40, Aβ1-42, and neurofilament light chain in research and real-world cohorts. Participants were categorized by brain amyloid status using US Food and Drug Administration/European Medicines Agency-approved CSF or PET methods.
Alzheimers Dement
January 2025
Department of Radiology & Nuclear Medicine, Amsterdam UMC, Vrije Universiteit, Amsterdam, the Netherlands.
Introduction: We report biomarker treatment effects in the GRADUATE I and II phase 3 studies of gantenerumab in early Alzheimer's disease (AD).
Methods: Amyloid and tau positron emission tomography (PET), volumetric magnetic resonance imaging (vMRI), cerebrospinal fluid (CSF), and plasma biomarkers used to assess gantenerumab treatment related changes on neuropathology, neurodegeneration, and neuroinflammation over 116 weeks.
Results: Gantenerumab reduced amyloid PET load, CSF biomarkers of amyloid beta (Aβ)40, total tau (t-tau), phosphorylated tau 181 (p-tau181), neurogranin, S100 calcium-binding protein B (S100B), neurofilament light (NfL), alpha-synuclein (α-syn), neuronal pentraxin-2 (NPTX2), and plasma biomarkers of t-tau, p-tau181, p-tau217, and glial fibrillary acidic protein (GFAP) while increasing plasma Aβ40, Aβ42.
Microbiol Spectr
January 2025
Department of Virology, Pontchaillou University Hospital, Rennes, France.
We report a case of wild-type rubella virus (genotype 2B) granuloma in a 29-year-old immunocompromised patient with a full vaccination scheme. He had been followed since his early teens for an unlabeled systemic inflammatory disease. On an inguinal node biopsy, histological analysis revealed a nguudiffuse non-necrotic granulomatous inflammation with no identified conventional infectious agent involved in granuloma formation.
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