Purpose

Our goal was to establish the range of sonographic measurements of normal gallbladders in children.

Methods

Six hundred ten children aged 0-16 years (male:female ratio, 1.5:1) with normal clinical and laboratory findings were included in this study. The sonographic parameters were the length, width, and calculated volume of the gallbladder, and the clinical parameters were the age, height, weight, and body surface area of the children. Statistical significance was determined through correlation and regression analyses.

Results

The length of the gallbladder showed significant positive correlations with age (r = 0.65), height (r = 0.67), weight (r = 0.63), and body surface area (r = 0.65; p < 0.01). The calculated volume of the gallbladder also showed moderate correlations with age (r = 0.53), height (r = 0.55), weight (r = 0.61), and body surface area (r = 0.57; p < 0.01). The gallbladder width showed modest but significant correlations with age (r = 0.48), height (r = 0.53), weight (r = 0.53), and body surface area (r = 0.55; p < 0.01). The highest correlation coefficients were found between the gallbladder length and subject age (r = 0.65; p < 0.01) and between the gallbladder length and subject height (r = 0.67; p < 0.01). For all correlations, statistical significance remained after regression analysis (p < 0.01).

Conclusions

Values for the size of the normal pediatric gallbladder are defined and will be helpful in the diagnosis of gallbladder abnormalities.

Common neurodegenerative diseases feature progressive accumulation of disease-specific protein aggregates in selectively vulnerable brain regions. Increasing experimental evidence suggests that misfolded disease proteins exhibit prion-like properties, including the ability to seed corruptive templating and self-propagation along axons. Direct evidence for transneuronal spread in patients, however, remains limited. To test predictions made by the transneuronal spread hypothesis in human tissues, we asked whether tau deposition within axons of the corticospinal and corticopontine pathways can be predicted based on clinical syndromes and cortical atrophy patterns seen in frontotemporal lobar degeneration (FTLD). Sixteen patients with Pick's disease, 21 with corticobasal degeneration, and 3 with FTLD-MAPT were included, spanning a range of clinical syndromes across the frontotemporal dementia (FTD) spectrum. Cortical involvement was measured using a neurodegeneration score, a tau score, and a composite score based on semiquantitative ratings and complemented by an MRI-based cortical atrophy W-map based on antemortem imaging. Midbrain cerebral peduncle and pontine base descending fibers were divided into three subregions, representing prefrontopontine, corticospinal, and parieto-temporo-occipital fiber pathways. Tau area fraction was calculated in each subregion and related to clinical syndrome and cortical measures. Within each clinical syndrome, there were predicted relationships between cortical atrophy patterns and axonal tau deposition in midbrain cerebral peduncle and pontine base. Between syndromes, contrasting and predictable patterns of brainstem axonal tau deposition emerged, with, for example, greater tau in prefrontopontine fibers in behavioral variant FTD and in corticospinal fibers in corticobasal syndrome. Finally, semiquantitative and quantitative cortical degeneration scores predicted brainstem axonal tau deposition based on anatomical principles. Taken together, these findings provide important human evidence in support of axonal tau spreading in patients with specific forms of tau-related neurodegeneration.