A Novel Fast CT Perfusion Core-Penumbra Mismatch Score: Correlation With Stroke Outcome.

BACKGROUND: Advanced neuroimaging can identify patients who can most benefit from reperfusion treatment, discriminating between ischemic core and penumbra area in a quick and accurate manner. Despite core-penumbra mismatch being an independent prognostic factor, computed tomography perfusion (CTP) assessment is still debated in hyperacute decision-making. The authors aimed to study a novel CTP mismatch score in emergency settings and to investigate its relation with clinical outcome in acute ischemic stroke patients treated with intravenous thrombolysis (IVT). METHODS: Neuroimaging and clinical data of 226 consecutive acute ischemic stroke patients were analyzed. The study population was divided into 5 different CTP scores: (0) without perfusion deficit, (1) only penumbra, (2) penumbra > core, (3) core ≥ penumbra, (4) only core. For differences in outcome between treated and nontreated patients, and among CTP core-penumbra groups to be assessed, the authors have evaluated the outcome in terms of National Institutes of Health Stroke Scale (NIHSS) and modified Rankin scale (mRS) at discharge and symptomatic intracerebral hemorrhage. RESULTS: A decrease in NIHSS was statistically greater in IVT-treated patients compared to nontreated patients showing only penumbra (ΔNIHSS%: 80.0% vs. 50.0%; P=0.0023) or no perfusion deficit (ΔNIHSS%: 89.4% vs. 61.5%; P=0.027) on CTP maps. The same trend was found in other groups without significant difference. A significant correlation was found in IVT patients between core/penumbra score and outcome in terms of ΔNIHSS (Kendall τ=-0.19; P=0.004). CONCLUSIONS: The authors proposed a novel immediate CTP assessment to score perfusion mismatch in emergency settings to guide clinicians' decision-making for aggressive treatment and to prevent stroke-related disability.

Pulmonary sarcoidosis: atypical HRTC features and differential diagnostic problems.

PURPOSE: The aim of this paper is to present atypical or unusual appearances of pulmonary sarcoidosis, assessed at HRCT, and to suggest some elements for the differential diagnosis. MATERIALS AND METHODS: The HRCT scans of 31 patients were retrospectively reviewed. The final diagnosis of sarcoidosis was established on the basis of clinical and laboratory data alone in one patient, of clinical and laboratory data supported by bronchoalveolar lavage (BAL) findings in 14 patients, lung biopsy in 15, and liver biopsy in one patient. Fifteen patients presented with the main aspects of atypical manifestations. RESULTS: In the 15 patients who presented with less frequent or atypical manifestations of pulmonary sarcoidosis, the following patterns were identified: 2 cases of large opacities with ill-defined margins, 8 of peripheral "pseudo-plaque" opacities, 2 of punctuate lymph node calcifications, 8 of ground-glass opacities with fine reticulation, and 5 of isolated opacities with dimensions not consistent with the surrounding background, with or without cavitation. CONCLUSIONS: Besides the typical manifestations of pulmonary sarcoidosis, there may be several atypical or nonspecific presentations: it is not by chance that the literature often describes this disease as the "great masquerader". Mediastinal lymphadenopathies and perilymphatic, subpleural or peribronchovascular nodules represent the typical patterns of pulmonary sarcoidosis; interstitial streaks and bilateral para-hilar thickening are also frequently observed. The presence of peripheral "pseudo-plaque" opacities and of ground-glass opacities with fine reticulation is the key to a diagnosis of "atypical" sarcoidosis. Calcifications within hilar and mediastinal lymph nodes, 1 cm or larger in dimensions, with a focal rather than diffuse distribution, should raise a suspicion of sarcoidosis rather than tuberculosis. Upper lobe localisation is rather infrequent in bronchioloalveolar carcinoma. Not all that excavates is tuberculosis: therefore, a differential diagnosis with tuberculosis may prove difficult, and the two diseases may coexist. Pseudoalveolar pulmonary thickening that eventually resolves and disappears does not exclusively entail an inflammatory thickening.