Objectives: Idiopathic pulmonary fibrosis (IPF) is a progressive lethal chronic lung disease with unclear pathogenesis. Radiological hallmark is the pattern of usual interstitial pneumonia accentuated in peripheral and basal areas with otherwise preserved lung structure. One hypothesis is that alveolar collapse and consequent induration lead to fibrotic transformation of lung tissue. The aim of the study was to investigate normal-appearing tissue during expiration for signs of collapsibility and differences from other diseases or controls. Materials and Methods: We retrospectively assessed a total of 43 patients (15 IPFs, 13 chronic obstructive pulmonary diseases, and 15 controls) with nonenhanced computed tomography (CT) in inspiration and expiration, performed for routine clinical workup. Densitometry of visually unaffected lung tissue was conducted in all lung lobes with a region of interest of 15-mm in diameter on soft tissue kernel reconstruction (slice thickness, 1 mm) during inspiration and expiration. Results: One-factor analysis of variance analysis yielded significant difference in attenuation changes between inspiration and expiration of unaffected lung parenchyma among all subject groups in all lung lobes. For IPF patients, the highest differences in densities were observed in the lower lobes, which is the predominantly affected site of usual interstitial pneumonia. In the chronic obstructive pulmonary disease group, the density remained rather equal in the entire lung. Conclusions: High CT attenuation changes between inspiration and expiration in IPF patients might suggest altered lung parenchyma in normal-appearing tissue on CT. Density changes during the respiratory cycle might be explained by alveolar collapse of radiologically unaffected lung tissue possibly preceding fibrosis. These results support the concept of alveolar collapse preceding lung fibrosis in IPF.
Diagnosis of epilepsy after a first unprovoked seizure is possible according to the guidelines by the International League Against Epilepsy, if the risk recurrence of a second unprovoked seizure is exceeding 60%. However, this cutoff constitutes only a proxy depending on the patients’ history, magnetic resonance imaging (MRI), and electroencephalography (EEG) findings but nevertheless also from the treating neurologists’ individual experience. In a Switzerland-wide observational study, we aim to recruit patients that were admitted to the emergency department with the referral diagnosis of a first and unprovoked seizure. We make use of optimized MRI protocols to identify potential structural epileptogenic lesions, introduce new imaging-based markers of epileptogenecity, and use most recent postprocessing methods as automatic morphometry, spike map analysis, and functional connectivity. With these diagnostic tools, we aim to segregate patients that present with epileptic seizures versus mimicks and non-epileptic seizures and stratify for every finding in MRI and EEG its predictive value for a second unprovoked seizure. These findings shall support neurologists to calculate and not only estimate the seizure recurrence rate in future.
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