Intraventricular cerebral neuroblastoma. Analysis of subtypes and comparison with hemispheric neuroblastoma.

Two cases of intraventricular neuroblastomas were compared with cases of intraventricular and hemispheric neuroblastomas that have been reported in the published literature. The following order of tumor subtypes was found in patients with increasing age: hemispheric neuroblastoma, intraventricular undifferentiated neuroblastoma, intraventricular differentiated neuroblastoma, and intraventricular neurocytoma; for patients with intraventricular neuroblastomas, this was also the order of increasing cellular maturation and survival. Neuronal morphologic or epitope differentiation was associated with a longer survival time than lack of differentiation by Kaplan-Meier product-limit estimates and with a better survival rate (chi 2) for intraventricular tumors but not for hemispheric tumors. Pathologic distinction of a neurocytoma was confirmed with immunostaining or ultrastructural studies that suggested that a neurocytoma is a matured neuroblastoma of a granule-cell (interneuron) phenotype. Differences among neuroblastoma groups bolster previous suggestions that intraventricular tumors arise differently than do cases of hemispheric tumors and follow a more benign course when neuronal differentiation is present.

Shrinking pleuritis with lobar atelectasis, a morphologic variant of "round atelectasis".

Round atelectasis (shrinking pleuritis) is typically a localized process characterized by focal pleural scarring and subjacent peripheral atelectasis. We report three patients, studied at autopsy, with an unusual variant of round atelectasis, termed shrinking pleuritis with lobar atelectasis, which is characterized by lobar atelectasis, visceral pleural fibrosis involving multiple lobes, interlobar fibrous cords, pleural effusion, and nonspecific, persistent infiltrates on chest radiogram. The possible causes of shrinking pleuritis with lobar atelectasis in our patients were multiple and included environmental dust exposure, infection, uremia, and recurrent pleural effusions. Our findings support both the folding (pleural effusion) and fibrosing (pleural injury) theories of pathogenesis of round atelectasis and emphasize the spectrum of morphologic variability in this condition.