Purpose of the Review This article reviews common imaging modalities used in diagnosis and management of acute stroke. Each modality is discussed individually and clinical scenarios are presented to demonstrate how to apply these modalities in decision-making. Recent Findings Advances in neuroimaging provide unprecedented accuracy in determining tissue viability as well as tissue fate in acute stroke. In addition, advances in machine learning have led to the creation of decision support tools to improve the interpretability of these studies. Summary Noncontrast head computed tomography (CT) remains the most commonly used initial imaging tool to evaluate stroke. Its exquisite sensitivity for hemorrhage, rapid acquisition, and widespread availability make it the ideal first study. CT angiography (CTA), the most common follow-up study after noncontrast head CT, is used primarily to identify intracranial large vessel occlusions and cervical carotid or vertebral artery disease. CTA is highly sensitive and can improve accuracy of patient selection for endovascular therapy through delineations of ischemic core. CT perfusion is widely used in endovascular therapy trials and benefits from multiple commercially available machine-learning packages that perform automated postprocessing and interpretation. Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) can provide valuable insights for outcomes prognostication as well as stroke etiology. Optical coherence tomography (OCT), positron emission tomography (PET), single-photon emission computerized tomography (SPECT) offer similar insights. In the clinical scenarios presented, we demonstrate how multimodal imaging approaches can be tailored to gain mechanistic insights for a range of cerebrovascular pathologies.

INTRODUCTION: In animal models, inflammation caused by experimental acute pancreatitis (AP) promotes pancreatic carcinogenesis that is preventable by suppressing inflammation. Recent studies noted higher long-term risk of pancreatic ductal adenocarcinoma (PDAC) after AP. In this study, we evaluated whether the long-term PDAC risk after AP was influenced by the etiology of AP, number of recurrences, and if it was because of progression to chronic pancreatitis (CP). METHODS: This retrospective study used nationwide Veterans Administration database spanning 1999–2015. A 2-year washout period was applied to exclude patients with preexisting AP and PDAC. PDAC risk was estimated in patients with AP without (AP group) and with underlying CP (APCP group) and those with CP alone (CP group) and compared with PDAC risk in patients in a control group, respectively, using cause-specific hazards model. RESULTS: The final cohort comprised 7,147,859 subjects (AP-35,550 and PDAC-16,475). The cumulative PDAC risk 3–10 years after AP was higher than in controls (0.61% vs 0.18%), adjusted hazard ratio (1.7 [1.4–2.0], P < 0.001). Adjusted hazard ratio was 1.5 in AP group, 2.4 in the CP group, and 3.3 in APCP group. PDAC risk increased with the number of AP episodes. Elevated PDAC risk after AP was not influenced by the etiology of AP (gallstones, smoking, or alcohol). DISCUSSION: There is a higher PDAC risk 3–10 years after AP irrespective of the etiology of AP, increases with the number of episodes of AP and is additive to higher PDAC risk because of CP.

Autoimmune pancreatitis (AIP) is a rare, heterogeneous, fibroinflammatory disorder of the pancreas. It has gained increasing recognition due to a presentation that can mimic difficult-to-treat disorders such as pancreatic cancer, cholangiocarcinoma and primary sclerosing cholangitis. In contrast, autoimmune pancreatitis is a benign disease that is very responsive to therapy with corticosteroids. There are two types of AIP. Type 1 disease is the most common worldwide and is associated with extrapancreatic manifestations and elevated levels of IgG4-positive cells. Type 2 AIP is characterized by a paucity of IgG4-positive cells and is more difficult to diagnose. This review provides an update on the diagnosis, pathophysiology and treatment of AIP, with special emphasis on the two subtypes.