PubMed · 5277020
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
T Valkeakari. 1970. Ventricle visualization in two-dimensional echo-encephalography.. https://doi.org/10.1111/j.1651-2227.1970.tb14620.x
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
We report a 48-year-old man treated for acute subarachnoid hemorrhage (SAH) wherein intracranial pressure (ICP) was measured simultaneously within the ventricular cerebrospinal fluid (CSF) and the brain parenchyma (PAR). Single pressure waves within the continuous pressure signal were identified with determination of the single wave parameters pulse amplitude (i.e. pressure difference between diastolic minimum pressure and systolic maximum pressure), mean pressure (i.e. mean pressure from beginning to ending minimum diastolic minimum pressure), and latency (i.e. rise time from diastolic minimum pressure to systolic maximum pressure). A total of 218,589 CSF/PAR single pressure wave pairs were analyzed. For these CSF/PAR wave pairs the mean difference in pulse pressure amplitude was -0.13 mmHg [95% confidence interval (CI) -0.13 to -0.12 mmHg], mean difference in mean single wave pressure -0.71 mmHg (95% CI -0.74 to -0.68 mmHg), and mean difference in latency -0.01 seconds (95% CI -0.01 to -0.01 seconds). Hence, in this patient monitoring ICP within the ventricular CSF or brain parenchyma gave similar results. Moreover, the comparisons of single CSF/PAR wave pulse pressure amplitudes gave no evidence of a pressure gradient from brain parenchyma to the ventricular CSF in this patient.
We report here on the first case of a child with bilateral periventricular nodular heterotopia (PNH) and Williams syndrome. Fluorescent in situ hybridization (FISH) analyses demonstrated a deletion of the elastin gene in the Williams syndrome critical region (WSCR). Further mapping by loss of heterozygosity analysis both by microsatellite marker and SNP profiling demonstrated a 1.5 Mb deletion beyond the telomeric end of the typical WSCR. No mutations were identified in the X-linked filamin-A gene (the most common cause of PNH). These findings suggest another dominant PNH disorder along chromosome 7q11.23.
Explore the source record for details and available documents.