scholarly journals Non‐visualization of choroid plexus of fourth ventricle as first‐trimester predictor of posterior fossa anomalies and chromosomal defects

2018 ◽  
Vol 51 (2) ◽  
pp. 199-207 ◽  
Author(s):  
P. Martinez‐Ten ◽  
T. Illescas ◽  
B. Adiego ◽  
M. Estevez ◽  
C. Bermejo ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Posterior Fossa ◽  
Fourth Ventricle ◽  
First Trimester ◽  
Chromosomal Defects

scholarly journals Choroid plexus papilloma of the fourth ventricle in a septuagenarian

2012 ◽  
Vol 03 (03) ◽  
pp. 402-404
Author(s):  
Alok A. Umredkar ◽  
Rajesh Chhabra ◽  
Aman Bal ◽  
Ashim Das
Keyword(s):  
Choroid Plexus ◽  
Posterior Fossa ◽  
Fourth Ventricle ◽  
Choroid Plexus Papilloma ◽  
Provisional Diagnosis ◽  
Geriatric Population ◽  
Choroid Plexus Papillomas ◽  
Plexus Papilloma ◽  
Posterior Fossa Lesion

ABSTRACTChoroid plexus papillomas (CPP) are most commonly found in children and rarely in adult. A very few cases are reported in geriatric population. We present a case of 72-year-old man with posterior fossa lesion operated with provisional diagnosis of metastasis, but turn out to be CPP.

First-Trimester Visualization of the Fourth Ventricle in Fetuses With and Without Spina Bifida

2012 ◽  
Vol 67 (4) ◽  
pp. 219-220
Author(s):  
Ido Solt ◽  
Joann G. Acuna ◽  
Beni A. Adeniji ◽  
James Mirocha ◽  
Matthew J. Kim ◽  
...  
Keyword(s):  
Spina Bifida ◽  
Fourth Ventricle ◽  
First Trimester

Hemangioma Calcificans in the Fourth Ventricle

Neurosurgery ◽  
1984 ◽  
Vol 14 (6) ◽  
pp. 737-739 ◽  
Author(s):  
Kobayashi Hidenori ◽  
Kawano Hirokazu ◽  
Ito Haruhide ◽  
Hayashi Minoru ◽  
Yamamoto Shinjiro
Keyword(s):  
Computed Tomography ◽  
Intracranial Pressure ◽  
Posterior Fossa ◽  
Clinical Picture ◽  
Fourth Ventricle ◽  
Obstructive Hydrocephalus ◽  
Increased Intracranial Pressure ◽  
X Ray ◽  
4Th Ventricle

Abstract A case of hemangioma calcificans in the 4th ventricle is reported. Skull x-ray films demonstrated a dense calcification in the posterior fossa. Computed tomography disclosed a hyperdense mass in the 4th ventricle. The clinical picture was of increased intracranial pressure due to obstructive hydrocephalus. An hemangioma calcificans in the 4th ventricle was removed successfully.

Posterior fossa craniotomy for trapped fourth ventricle in shunt-treated hydrocephalic children: long-term outcome

2011 ◽  
Vol 7 (1) ◽  
pp. 52-63 ◽  
Author(s):  
Suhas Udayakumaran ◽  
Naresh Biyani ◽  
David P. Rosenbaum ◽  
Liat Ben-Sira ◽  
Shlomi Constantini ◽  
...  
Keyword(s):  
Posterior Fossa ◽  
Subarachnoid Space ◽  
Fourth Ventricle ◽  
Late Complication ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Posthemorrhagic Hydrocephalus ◽  
Spinal Subarachnoid Space ◽  
Trapped Fourth Ventricle

Object Trapped fourth ventricle (TFV) is a rare late complication of postinfectious or posthemorrhagic hydrocephalus. This entity is distinct from a large fourth ventricle because TFV entails pressure in the fourth ventricle and posterior fossa due to abnormal inflow and outflow of CSF, causing significant symptoms and signs. As TFV is mostly found in children who were born prematurely and have cerebral palsy, diagnosis and treatment options are a true challenge. Methods Between February 1998 and February 2007, 12 children were treated for TFV in Dana Children's Hospital by posterior fossa craniotomy/craniectomy and opening of the TFV into the spinal subarachnoid space. The authors performed a retrospective analysis of relevant data, including pre- and postoperative clinical characteristics, surgical management, and outcome. Results Thirteen fenestrations of trapped fourth ventricles (FTFVs) were performed in 12 patients. In 6 patients with prominent arachnoid thickening, a stent was left from the opened fourth ventricle into the spinal subarachnoid space. One patient underwent a second FTFV 21 months after the initial procedure. No perioperative complications were encountered. All 12 patients (100%) showed clinical improvement after FTFV. Radiological improvement was seen in only 9 (75%) of the 12 cases. The follow-up period ranged from 2 to 9.5 years (mean 6.11 ± 2.3 years) after FTFV. Conclusions Fenestration of a TFV via craniotomy is a safe and effective option with a very good long-term outcome and low rate of morbidity.

scholarly journals Intradural pathology and pathophysiology associated with Chiari I malformation in children and adults with and without syringomyelia

2017 ◽  
Vol 20 (6) ◽  
pp. 526-541 ◽  
Author(s):  
Brian J. Dlouhy ◽  
Jeffrey D. Dawson ◽  
Arnold H. Menezes
Keyword(s):  
Logistic Regression ◽  
Posterior Fossa ◽  
Fourth Ventricle ◽  
Posterior Inferior Cerebellar Artery ◽  
Type I ◽  
Csf Flow ◽  
Multivariate Logistic Regression ◽  
Tonsillar Herniation ◽  
Chiari Malformation Type I ◽  
Flow Channels

OBJECTIVEThe pathophysiology underlying tonsillar herniation and CSF obstruction in Chiari malformation Type I (CM-I) is unclear, and the cause of CM-I–associated syringomyelia is not well understood. A better understanding of this pathophysiology is important for an improved treatment strategy. Therefore, the authors sought to identify, characterize, and examine the intradural pathology and CSF flow pathophysiology in the posterior fossa and at the level of the foramen magnum that occurs in the setting of CM-I. They determined the incidence of these intradural findings and assessed differences across age, with the degree of tonsillar herniation, and in the presence and absence of syringomyelia.METHODSA prospective database initiated in March 2003 recorded all intraoperative findings during surgical treatment of children and adults with CM-I with or without syringomyelia. A total of 389 surgeries for CM-I were performed in 379 patients between March 2003 and June 2016. A total of 109 surgeries were performed in 109 patients with CM-I (without osseoligamentous abnormalities) in whom both a posterior fossa extradural and intradural decompression with duraplasty was performed (first-time intradural procedures). Using a surgical microscope, intradural pathology and obstruction of CSF channels were identified and assessed. Student t-tests and Fisher’s exact tests compared groups in a series of univariate analyses, followed by multivariate logistic regression.RESULTSThe following intradural pathological entities were observed (prevalence noted in parentheses). These include those that did not obstruct CSF flow channels: opacified arachnoid (33.0%), thickened arachnoid (3.7%), ischemic and gliotic tonsils (40.4%), tonsillar cysts (0.9%), and inferior descent of the fourth ventricle and cervicomedullary junction (CMJ) (78.0%). The following intradural pathological entities were observed to obstruct CSF flow channels: medialized tonsils (100%), tonsil overlying and obstructing the foramen of Magendie (21.1%), intertonsillar and tonsil to CMJ arachnoid adhesions (85.3%), vermian posterior inferior cerebellar artery branches obstructing the foramen of Magendie (43.1%), and arachnoid veils or webs obstructing or occluding the foramen of Magendie (52.3%). Arachnoid veils varied in type and were observed in 59.5% of patients with CM-I who had syringomyelia, which was significantly greater than the 33.3% of patients with CM-I without syringomyelia who had an arachnoid veil (p = 0.018). The presence of CM-I with an arachnoid veil had 3.22 times the odds (p = 0.013, 95% CI 1.29–8.07, by multivariate logistic regression) of being associated with syringomyelia, adjusting for tonsillar herniation. The inferior descent of the fourth ventricle and CMJ occurred with a greater degree of tonsillar herniation (p < 0.001) and correlated with a cervicomedullary kink or buckle on preoperative MRI.CONCLUSIONSIntradural pathology associated with CM-I with or without syringomyelia exists in many forms, is more prevalent than previously recognized in patients of all ages, and may play a role in the pathophysiology of CM-I tonsillar herniation. Arachnoid veils appear to partially obstruct CSF flow, are significantly more prevalent in cases of CM-I with syringomyelia, and therefore may play a role in the pathophysiology of CM-I–associated syringomyelia.

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