Aqueduct stenosis—?Benign

Allan, Rodney; Chaseling, Raymond; Graf, Nicole; Dexter, Mark

doi:10.1016/j.jocn.2004.06.005

Cited by 8 publications

(9 citation statements)

References 18 publications

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“…Hydrocephalus is a potentially lethal birth defect in humans that results from excess accumulation of cerebrospinal fluid in the developing brain. A common cause of congenital hydrocephalus is aqueduct stenosis (1,37). Cdo is expressed in the subcommissural organ and the roof of the aqueduct, defects in which can result in hydrocephalus; histologically, however, these structures appeared to be normal in Cdo Ϫ/Ϫ animals (data not shown).…”

Section: Discussionmentioning

confidence: 94%

Cortical Thinning and Hydrocephalus in Mice Lacking the Immunoglobulin Superfamily Member CDO

Zhang

Chen

et al. 2006

Molecular and Cellular Biology

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CDO is a cell surface immunoglobulin superfamily member that positively regulates myogenic differentiation in vitro and in vivo and signals to posttranslationally activate myogenic basic helix-loop-helix (bHLH) transcription factors. The Cdo gene is also expressed in the dorsal aspect and midline structures of the developing central nervous system, and mice lacking CDO on the C57BL/6 background display holoprosencephaly with ϳ80% penetrance, resulting in perinatal lethality. We report here that a fraction of Cdo ؊/؊ mice from this background have additional defects in brain development, including hydrocephalus and cortical thinning. Primary neural progenitor cultures from E14.5 Cdo ؊/؊ mutants display reduced proliferation, which may underlie the thinning. The cortical preplate and cortices of mutant animals also show reduced staining for ␤-tubulin III, indicating defective neuronal differentiation. CDO levels are strongly increased in cultured C17.2 neuronal precursor cells stimulated to differentiate; modulation of CDO levels in these cells by overexpression or interfering RNA approaches enhances or diminishes differentiation, respectively. Cotransfection of CDO enhances the activity of the neurogenic bHLH factor, neurogenin1, in reporter assays and enhances heterodimerization of neurogenin1 and E47. These results indicate that CDO promotes neuronal differentiation and support the hypothesis that CDO coordinates differentiation of multiple cell lineages by regulating the activity of tissue-specific bHLH factors.The cerebral cortex originates from a sheet of neuroepithelial cells within the ventricular zone (VZ) of the dorsal telencephalon. In the mouse cerebral cortex, neurogenesis starts at embryonic day 11 (E11) and continues until E17. The balance between proliferation and differentiation of neural progenitor cells within the VZ is essential in determining the total number of neurons that comprise the neocortex (3,8,29,38,44,45). Neurogenesis is mediated by neural basic helix-loop-helix (bHLH) transcription factors, including neurogenin1 (Ngn1) and Ngn2, Mash1, and NeuroD (4,7,27,40). Neural bHLH factors are transcriptional activators that bind DNA as heterodimeric complexes with E proteins. Ngn1 and Ngn2 are selectively expressed in the VZ by dorsal telencephalic progenitors, where such cells begin differentiation, but not in the cortical plate, where fully differentiated neurons are situated (20,28,43). The transition from proliferation to differentiation during neurogenesis involves an increase in expression and activities of proneural bHLHs. However, the mechanisms that underlie this transition are not well understood.CDO is a surface protein of the immunoglobulin (Ig) superfamily that is expressed at high levels in developing muscle, the central nervous system, and the midface (24, 32). Extensive studies on myogenesis suggest that CDO serves as a component of a receptor complex that includes cadherins and the related Ig proteins, BOC and neogenin (21,(23)(24)(25). CDO positively regulates differentiati...

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Section: Discussionmentioning

confidence: 94%

Cortical Thinning and Hydrocephalus in Mice Lacking the Immunoglobulin Superfamily Member CDO

Zhang

Chen

et al. 2006

Molecular and Cellular Biology

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“…3 Routine MR imaging criteria for AS (such as anterior or inferior bulging of the third ventricle and triventricular dilation) are usually subjective and less reproducible without validated cutoff values. [1][2][3] The criterion standard technique for the diagnosis of obstructive hydrocephalus and AS is ventriculographic studies, and these studies are very invasive and difficult to perform in routine daily practice. 6 CE-MRC is a less invasive morphologic and functional technique for diagnosis of obstructive hydrocephalus, and it includes intrathecal administration of gadolinium-diethylene-triamine pentaacetic acid, which is safe but not accepted worldwide.…”

Section: Discussionmentioning

confidence: 99%

“…1 The etiology of AS is frequently idiopathic, but in some patients, X-linked recessive inheritance has been reported. 2,3 Webbing, adhesion, or aqueductal forking can be listed among etiologic factors of primary non-neoplastic AS.…”

mentioning

confidence: 99%

Evaluation of Aqueductal Stenosis by 3D Sampling Perfection with Application-Optimized Contrasts Using Different Flip Angle Evolutions Sequence: Preliminary Results with 3T MR Imaging

Algın¹,

Türkbey²

2011

AJNR Am J Neuroradiol

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“…Only 1 other report in the literature describes 2 similar pediatric patients who presented with idiopathic obstructive hydrocephalus and were only later found to have a pineal tumor on follow-up MRI. 1 The authors' recommendations were for repeated MRI with contrast in all cases of new-onset hydrocephalus without a clear etiology.…”

Section: Discussionmentioning

confidence: 99%

Hydrocephalus presenting as idiopathic aqueductal stenosis with subsequent development of obstructive tumor: report of 2 cases demonstrating the importance of serial imaging

Roland

Price

Kamath

et al. 2017

Journal of Neurosurgery: Pediatrics

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The authors describe 2 cases of triventricular hydrocephalus initially presenting as aqueductal stenosis that subsequently developed tumors of the pineal and tectal region. The first case resembled late-onset idiopathic aqueductal stenosis on serial imaging. Subsequent imaging revealed a new tumor in the pineal region causing mass effect on the midbrain. The second case presented in a more typical pattern of aqueductal stenosis during infancy. On delayed follow-up imaging, an enlarging tectal mass was discovered. In both cases hydrocephalus was successfully treated by cerebrospinal fluid diversion prior to tumor presentation. The differential diagnoses, diagnostic testing, and treatment course for these unusual cases are discussed. The importance of follow-up MRI in cases of idiopathic aqueductal stenosis is emphasized by these exemplar cases.

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Aqueduct stenosis—?Benign

Cited by 8 publications

References 18 publications

Cortical Thinning and Hydrocephalus in Mice Lacking the Immunoglobulin Superfamily Member CDO

Cortical Thinning and Hydrocephalus in Mice Lacking the Immunoglobulin Superfamily Member CDO

Evaluation of Aqueductal Stenosis by 3D Sampling Perfection with Application-Optimized Contrasts Using Different Flip Angle Evolutions Sequence: Preliminary Results with 3T MR Imaging

Hydrocephalus presenting as idiopathic aqueductal stenosis with subsequent development of obstructive tumor: report of 2 cases demonstrating the importance of serial imaging

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