Objectives: To detect on computed tomography (CT) brain scans the trajectories of normal and abnormal ventricular enlargement during aging. Methods: For each 1-year age cohort, we assessed in 3,193 axial CT scans the Evans\' index (EI) in the anterior frontal horns and the parieto-occipital (POR) and temporal ratio (TR) in the posterior and inferior horns. Cut-off values for abnormal enlargement were based on previous clinical studies. Results: The mean age associated with normal linear measures was 71 years. Values for all three measures increased with age, showing a linear relationship below-but not above-each cut-off value. The mean age of participants with abnormal enlargement on CT progressed from 79 years for EI to 83 years for POR to 87 years for TR. These results suggested that ventricular dilatation progresses in an age-location relationship. First comes enlargement of the frontal horns (13.8% of scans), followed by the parieto-occipital horns (15.1% of scans) and then temporal horn enlargement (6.8% of scans). Scans from men displayed abnormal values earlier than scans from women (on average 6 years). Risk increased 5.1% annually for abnormal EI, 9.0% for abnormal POR, and 11% for abnormal TR (all p < 0.001). The most frequent agreement between categories (normal-abnormal) for values of neuroimaging measures was identified for POR-TR. Conclusion: The results of this large radiological study suggest that the ventricular system enlarges progressively during aging, and in a subset of patients follows an abnormal consecutive geometric dilatation, influenced by age and sex.

Late unilateral breast enlargement after the insertion of silicone gel breast implants is a very rare phenomenon. The present study reports five women who presented with this finding over the past 20 years. Three of these patients presented with late unilateral hematomas, which developed nine, 12 and 14 years, respectively, after initial breast augmentation, in the absence of any known trauma. These patients presented for treatment one, four and 12 months, respectively, after their breast enlargements initially appeared. Two of these patients had developed chronic expanding hematomas. Extensive histopathological analyses of the capsules of all three patients provided explanations for the etiologies and progressions of the findings in these patients. In each of the three patients, the etiology of the hematoma was consistent with erosion of a capsular artery. Numerous large vessels were seen within the wall of the capsules. In each case, there was a class IV capsular contracture, which could have increased the friction of the intact implant against the capsule, and there was both old (hemosiderin deposits) and new bleeding into the pocket from the capsules. This supports the concept that numerous episodes of bleeding had occurred in each case. Histopathology also demonstrated the progression of the hematomas. After four weeks, only liquefied hematoma was present, while after four months, there were both liquefied hematoma and blood clotting. The hematoma on the surface of the capsule was becoming organized peripherally, but not centrally. After 12 months, the hematoma was becoming very well organized compared with the hematoma at four months. In one of the two remaining cases, late infection was the cause of the breast enlargement. Histopathology of this capsule showed that the involved capsule was six times as thick as the other side. It also showed edema and infiltration by scattered mononuclear cells, polymorphonuclear cells, and irregular crenated and degenerating nuclei. In the final patient, chronic inflammation appeared to be the cause of the breast enlargement. The histopathology of this capsule was unique. Its inner surface showed re-epithelialization and metaplasia of the ductal epithelium to form stratified squamous epithelium with early surface keratinization. These findings are consistent with synovial metaplasia. Several areas of the fibrous portion of the capsule showed patchy loss of cellular staining with loss of nuclei, indicative of necrosis. This produced a \'washed out\' staining appearance. This tissue was paucivascular and fibrotic, and showed areas of fibrinoid necrosis, suggestive of mechanical abrasion and increased pressure.