European Radiology

Correction to: CT screening for lung cancer: comparison of three baseline screening protocols The original version of this article, published on 03 December 2018, unfortunately contained a mistake.

Correction to: Effect of training on ultrasonography (US) BI-RADS features for radiology residents: a multicenter study comparing performances after training The original version of this article, published on 07 January 2019, unfortunately contained a mistake.

Correction to: Diffusion-weighted imaging for assessment of synovial inflammation in juvenile idiopathic arthritis: a promising imaging biomarker as an alternative to gadolinium-based contrast agents The original version of this article, published on 12 June 2017, unfortunately contained a mistake.

Correction to: Ultrashort time-to-echo quantitative magnetic resonance imaging of the triangular fibrocartilage: differences in position The original version of this article, published on 03 September 2018, unfortunately contained a mistake.

Reply to "letter to the editor: use of artificial neural networks to predict anterior communicating artery aneurysm rupture: possible methodological issues"

Differentiation of two subtypes of intrahepatic cholangiocarcinoma: imaging approach Key Points • Mass-forming intrahepatic cholangiocarcinoma can be divided into two subgroups, namley, perihilar and peripheral types. • These two significantly differ in clinico-biological behaviors, and in patients' prognosis as well. • This differentiation may be achieved solely by contrast-enhanced MR imaging findings.

Hepatobiliary phase in cirrhotic patients with different Model for End-stage Liver Disease score: comparison of the performance of gadoxetic acid to gadobenate dimeglumine Abstract Objectives The purpose of this study was to compare the performance of gadobenate dimeglumine–enhanced MRI and gadoxetic acid–enhanced MRI in the hepatobiliary phase (HBP) in cirrhotic patients with different degrees of liver dysfunction. Methods In this retrospective cross-sectional study, we analyzed the unenhanced phase and the HBP of 131 gadobenate dimeglumine–enhanced MRI examinations (gadobenate dimeglumine group) and 127 gadoxetic acid–enhanced MRI examinations (gadoxetic acid group) performed in 249 cirrhotic patients (181 men and 68 women; mean age, 64.8 years) from August 2011 to April 2017. For each MRI, the contrast enhancement index of the liver parenchyma was calculated and correlated to the Model For End-Stage Liver Disease (MELD) score (multiple linear regression analysis). A qualitative analysis of the adequacy of the HBP, adjusted for the MELD score (logistic regression analysis), was performed. Results The contrast enhancement index was inversely related (r = − 0.013) with MELD score in both gadoxetic acid and gadobenate dimeglumine group. At the same MELD score, the contrast enhancement index in the gadoxetic acid group was increased by a factor of 0.23 compared to the gadobenate dimeglumine group (p < 0.001), and the mean odds ratio to have an adequate HBP with gadoxetic acid compared to gadobenate dimeglumine was 3.64 (p < 0.001). The adequacy of the HBP in the gadoxetic acid group compared to the gadobenate dimeglumine group increased with the increase of the MELD score (exp(b)interaction = 1.233; p = 0.011). Conclusion In cirrhotic patients, the hepatobiliary phase obtained with gadoxetic acid–enhanced MRI is of better quality in comparison to gadobenate dimeglumine–enhanced MRI, mainly in patients with high MELD score. Key Points • In cirrhotic patients, the adequacy of the hepatobiliary phase with gadoxetic acid–enhanced MRI is better compared to gadobenate dimeglumine–enhanced MRI. • Gadoxetic acid–enhanced MRI should be preferred to gadobenate dimeglumine–enhanced MRI in cirrhotic patients with MELD score > 10, if the hepatobiliary phase is clinically indicated. • In patients with high MELD score (> 15), the administration of the hepatobiliary agent could be useless; even though, if it is clinically indicated, we recommend to use gadoxetic acid given the higher probability of obtaining clinically relevant information.

Dual-energy CT for liver iron quantification in patients with haematological disorders Abstract Objectives To retrospectively quantify liver iron content in haematological patients suspected of transfusional haemosiderosis using dual-energy CT (DECT) and correlate with serum ferritin levels and estimated quantity of transfused iron. Methods One hundred forty-seven consecutive dual-source dual-energy non-contrast chest-CTs in 110 haematologic patients intended primarily for exclusion of pulmonary infection between September 2016 and June 2017 were retrospectively evaluated. Image data was post-processed with a software prototype. After material decomposition, an iron enhancement map was created and freehand ROIs were drawn including most of the partially examined liver. The virtual iron content (VIC) was calculated and expressed in milligram/millilitre. VIC was correlated with serum ferritin and estimated amount of transfused iron. Scans of patients who had not received blood products were considered controls. Results Forty-eight (32.7%) cases (controls) had not received any blood transfusions whereas 67.3% had received one transfusion or more. Median serum ferritin and VIC were 138.0 μg/dl (range, 6.0–2628.0 μg/dl) and 1.33 mg/ml (range, − 0.94–7.56 mg/ml) in the post-transfusional group and 27.0 μg/dl (range, 1.0–248.0 μg/dl) and 0.61 mg/ml (range, − 2.1–2.4) in the control group. Correlation between serum ferritin and VIC was strong (r = 0.623; p < 0.001) as well as that between serum ferritin and estimated quantity of transfused iron (r = 0.681; p < 0.001). Conclusions Hepatic VIC obtained via dual-energy chest-CT examinational protocol strongly correlates with serum ferritin levels and estimated amount of transfused iron and could therefore be used in the routine diagnosis for complementary evaluation of transfusional haemosiderosis. Key Points • Virtual liver iron content was measured in routine chest-CTs of haematological patients suspected of having iron overload. Chest-CTs were primarily intended for exclusion of pulmonary infection. • Measurements correlate strongly with the most widely used blood marker of iron overload serum ferritin (after exclusion of infection) and the amount of transfused iron. • Liver VIC could be used for supplemental evaluation of transfusional haemosiderosis in haematological patients.

Ascites relative enhancement during hepatobiliary phase after Gd-BOPTA administration: a new promising tool for characterising abdominal free fluid of unknown origin Abstract Objectives To correlate the degree of ascites enhancement during hepatobiliary phase after gadobenate dimeglumine (Gd-BOPTA) administration with ascites aetiology. Methods IRB-approved retrospective study, need for informed consent was waived. We included 74 consecutive ascitic patients who underwent Gd-BOPTA-enhanced liver MRI including hepatobiliary phase (HBP) images between January 2014 and December 2017. Ascites appearance on unenhanced and HBP images was classified as hypo-, iso- or hyperintense in comparison to paraspinal muscles. Ascites signal intensity on unenhanced and HBP images was measured using round ROIs and was normalised to paraspinal muscles (NSI). Normalised relative enhancement (NRE) between native phase and HBP was calculated. The results were related to ascites aetiology using Wilcoxon and Mann-Whitney tests. Results On native images, ascites appeared hypointense in 95.9% of the cases and isointense in 4.1%, whereas on HBP images, it appeared hyperintense in 59.4% of the cases, isointense in 36.5% and hypointense in 4.1%. Mean ascites NSI was 0.52 on unenhanced images and 1.50 on HBP ones (p < 0.0001). Mean ascites NRE was 201 ± 133%. Ascites of non-malignant aetiology showed mean NRE of 210 ± 134%, whereas malignant ascites showed mean NRE of 92 ± 20% (p = 0.001). ROC analysis showed that a NRE < 112.5% correlates with malignant aetiology with 100% sensitivity and 83.4% specificity (LR = 5.667). NRE did not show any significant correlation with ascites thickness, eGFR and time interval between contrast administration and HBP acquisition (p > 0.05). Conclusions Ascites NRE in HBP after Gd-BOPTA administration is significantly lower in patients with ascites secondary to peritoneal carcinomatosis than in patients with non-malignant ascites. Key Points • Ascites enhancement in the hepatobiliary phase after Gd-BOPTA administration may determine false positive findings when looking for biliary leaks. • Ascites enhancement in the hepatobiliary phase after Gd-BOPTA administration is lower in patients with peritoneal carcinomatosis than in patients with portal hypertension or congestive heart failure. • None of the patients with peritoneal carcinomatosis showed an ascites enhancement of more than 112% as compared with unenhanced images.

Assessment of renal function before contrast media injection: right decisions based on inaccurate estimates Abstract Objectives Information on renal function required before specified radiological examinations with contrast agents is usually obtained through prediction equations using serum creatinine and anthropometric data. The aim of our study was to demonstrate discrepancy between poor prediction and good diagnostic accuracy of glomerular filtration rate (GFR) estimated by prediction equations. Methods In 50 patients, reference GFR was measured as plasma clearance of 51-chromium labeled ethylene-diamine-tetraacetic-acid (51Cr-EDTA) and compared with GFR assayed by creatinine clearance (CC) and estimated by Cockcroft-Gault prediction equation (CG). For comparisons, CC and CG were considered as continuous, categorical, and binary variables. Accuracy of the reference GFR prediction was expressed in terms of prediction errors and diagnostic accuracy indices. Results As continuous variable, CG estimated individual values of GFR with large prediction error exceeding that of CC. As categorical variable, it classified the patient stage of chronic kidney disease (CKD) with medium diagnostic accuracy of 74% (CKD 3) and 62% (CKD 4). As binary variable, CG classified individual patient's GFR below 30 and 60 ml/min/1.73 m2 with good diagnostic accuracy of 80 and 94%, respectively. Performance of other prediction equations did not significantly differ from CG. Conclusions Despite large variance and poor prediction accuracy of individual GFR estimates, most of them correctly classified individual patient's GFR below specified level. Results of prediction equations thus should be used and reported exclusively as binary variables, while numerical values of GFR, if required, should be measured by more accurate radionuclide or laboratory methods. Key Points • Radiological guidelines on contrast media require estimation of glomerular filtration rate to assess kidney function before specified contrast examinations. • Estimated glomerular filtration rate is obtained through prediction equations using serum creatinine and anthropometric data as predictors. • While numerical estimates of glomerular filtration rate are inaccurate (their prediction accuracy is poor), diagnostic accuracy of binary estimates (ability to classify patient's glomerular filtration rate below or above a specified level) is very good.

Neuroscience

This Week in The Journal

A Hypothetical Model Concerning How Spike-Timing-Dependent Plasticity Contributes to Neural Circuit Formation and Initiation of the Critical Period in Barrel Cortex Spike timing is an important factor in the modification of synaptic strength. Various forms of spike timing-dependent plasticity (STDP) occur in the brains of diverse species, from insects to humans. In unimodal STDP, only LTP or LTD occurs at the synapse, regardless of which neuron spikes first; the magnitude of potentiation or depression increases as the time between presynaptic and postsynaptic spikes decreases. This from of STDP may promote developmental strengthening or weakening of early projections. In bidirectional Hebbian STDP, the magnitude and the sign (potentiation or depression) of plasticity depend, respectively, on the timing and the order of presynaptic and postsynaptic spikes. In the rodent barrel cortex, multiple forms of STDP appear sequentially during development, and they contribute to network formation, retraction, or fine-scale functional reorganization. Hebbian STDP appears at L4-L2/3 synapses starting at postnatal day (P) 15; the synapses exhibit unimodal "all-LTP STDP" before that age. The appearance of Hebbian STDP at L4-L2/3 synapses coincides with the maturation of parvalbumin-containing GABA interneurons in L4, which contributes to the generation of L4-before-L2/3 spiking in response to thalamic input by producing fast feedforward suppression of both L4 and L2/3 cells. After P15, L4-L2/3 STDP mediates fine-scale circuit refinement, essential for the critical period in the barrel cortex. In this review, we first briefly describe the relevance of STDP to map plasticity in the barrel cortex, then look over roles of distinct forms of STDP during development. Finally, we propose a hypothesis that explains the transition from network formation to the initiation of the critical period in the barrel cortex.

Mitotic Motor KIFC1 Is an Organizer of Microtubules in the Axon KIFC1 (also called HSET or kinesin-14a) is best known as a multifunctional motor protein essential for mitosis. The present studies are the first to explore KIFC1 in terminally postmitotic neurons. Using RNA interference to partially deplete KIFC1 from rat neurons (from animals of either gender) in culture, pharmacologic agents that inhibit KIFC1, and expression of mutant KIFC1 constructs, we demonstrate critical roles for KIFC1 in regulating axonal growth and retraction as well as growth cone morphology. Experimental manipulations of KIFC1 elicit morphological changes in the axon as well as changes in the organization, distribution, and polarity orientation of its microtubules. Together, the results indicate a mechanism by which KIFC1 binds to microtubules in the axon and slides them into alignment in an ATP-dependent fashion and then cross-links them in an ATP-independent fashion to oppose their subsequent sliding by other motors. SIGNIFICANCE STATEMENT Here, we establish that KIFC1, a molecular motor well characterized in mitosis, is robustly expressed in neurons, where it has profound influence on the organization of microtubules in a number of different functional contexts. KIFC1 may help answer long-standing questions in cellular neuroscience such as, mechanistically, how growth cones stall and how axonal microtubules resist forces that would otherwise cause the axon to retract. Knowledge about KIFC1 may help researchers to devise strategies for treating disorders of the nervous system involving axonal retraction given that KIFC1 is expressed in adult neurons as well as developing neurons.

Intracellular Zn2+ Signaling Facilitates Mossy Fiber Input-Induced Heterosynaptic Potentiation of Direct Cortical Inputs in Hippocampal CA3 Pyramidal Cells Repetitive action potentials (APs) in hippocampal CA3 pyramidal cells (CA3-PCs) backpropagate to distal apical dendrites, and induce calcium and protein tyrosine kinase (PTK)-dependent downregulation of Kv1.2, resulting in long-term potentiation of direct cortical inputs and intrinsic excitability (LTP-IE). When APs were elicited by direct somatic stimulation of CA3-PCs from rodents of either sex, only a narrow window of distal dendritic [Ca2+] allowed LTP-IE because of Ca2+-dependent coactivation of PTK and protein tyrosine phosphatase (PTP), which renders non-mossy fiber (MF) inputs incompetent in LTP-IE induction. High-frequency MF inputs, however, could induce LTP-IE at high dendritic [Ca2+] of the window. We show that MF input-induced Zn2+ signaling inhibits postsynaptic PTP, and thus enables MF inputs to induce LTP-IE at a wide range of [Ca2+]ivalues. Extracellular chelation of Zn2+ or genetic deletion of vesicular zinc transporter abrogated the privilege of MF inputs for LTP-IE induction. Moreover, the incompetence of somatic stimulation was rescued by the inhibition of PTP or a supplement of extracellular zinc, indicating that MF input-induced increase in dendritic [Zn2+] facilitates the induction of LTP-IE by inhibiting PTP. Consistently, high-frequency MF stimulation induced immediate and delayed elevations of [Zn2+] at proximal and distal dendrites, respectively. These results indicate that MF inputs are uniquely linked to the regulation of direct cortical inputs owing to synaptic Zn2+ signaling. SIGNIFICANCE STATEMENT Zn2+ has been mostly implicated in pathological processes, and the physiological roles of synaptically released Zn2+ in intracellular signaling are little known. We show here that Zn2+ released from hippocampal mossy fiber (MF) terminals enters postsynaptic CA3 pyramidal cells, and plays a facilitating role in MF input-induced heterosynaptic potentiation of perforant path (PP) synaptic inputs through long-term potentiation of intrinsic excitability (LTP-IE). We show that the window of cytosolic [Ca2+] that induces LTP-IE is normally very narrow because of the Ca2+-dependent coactivation of antagonistic signaling pairs, whereby non-MF inputs become ineffective in inducing excitability change. The MF-induced Zn2+ signaling, however, biases toward facilitating the induction of LTP-IE. The present study elucidates why MF inputs are more privileged for the regulation of PP synapses.

Axonal Degeneration Is Mediated by Necroptosis Activation Axonal degeneration, which contributes to functional impairment in several disorders of the nervous system, is an important target for neuroprotection. Several individual factors and subcellular events have been implicated in axonal degeneration, but researchers have so far been unable to identify an integrative signaling pathway activating this self-destructive process. Through pharmacological and genetic approaches, we tested whether necroptosis, a regulated cell-death mechanism implicated in the pathogenesis of several neurodegenerative diseases, is involved in axonal degeneration. Pharmacological inhibition of the necroptotic kinase RIPK1 using necrostatin-1 strongly delayed axonal degeneration in the peripheral nervous system and CNS of wild-type mice of either sex and protected in vitro sensory axons from degeneration after mechanical and toxic insults. These effects were also observed after genetic knock-down of RIPK3, a second key regulator of necroptosis, and the downstream effector MLKL (Mixed Lineage Kinase Domain-Like). RIPK1 inhibition prevented mitochondrial fragmentation in vitro and in vivo, a typical feature of necrotic death, and inhibition of mitochondrial fission by Mdivi also resulted in reduced axonal loss in damaged nerves. Furthermore, electrophysiological analysis demonstrated that inhibition of necroptosis delays not only the morphological degeneration of axons, but also the loss of their electrophysiological function after nerve injury. Activation of the necroptotic pathway early during injury-induced axonal degeneration was made evident by increased phosphorylation of the downstream effector MLKL. Our results demonstrate that axonal degeneration proceeds by necroptosis, thus defining a novel mechanistic framework in the axonal degenerative cascade for therapeutic interventions in a wide variety of conditions that lead to neuronal loss and functional impairment. SIGNIFICANCE STATEMENT We show that axonal degeneration triggered by diverse stimuli is mediated by the activation of the necroptotic programmed cell-death program by a cell-autonomous mechanism. This work represents a critical advance for the field since it identifies a defined degenerative pathway involved in axonal degeneration in both the peripheral nervous system and the CNS, a process that has been proposed as an early event in several neurodegenerative conditions and a major contributor to neuronal death. The identification of necroptosis as a key mechanism for axonal degeneration is an important step toward the development of novel therapeutic strategies for nervous-system disorders, particularly those related to chemotherapy-induced peripheral neuropathies or CNS diseases in which axonal degeneration is a common factor.

A Human TRPA1-Specific Pain Model The cation channel transient receptor potential ankyrin 1 (TRPA1) plays an important role in sensing potentially hazardous substances. However, TRPA1 species differences are substantial and limit translational research. TRPA1 agonists tested previously in humans also have other targets. Therefore, the sensation generated by isolated TRPA1 activation in humans is unknown. The availability of 2-chloro-N-(4-(4-methoxyphenyl)thiazol-2-yl)-N-(3-methoxypropyl)-acetamide (JT010), a potent and specific TRPA1 agonist, allowed us to explore this issue. To corroborate the specificity of JT010, it was investigated whether the TRPA1 antagonist (1E,3E)-1-(4-fluorophenyl)-2-methyl-1-penten-3-one oxime (A-967079) abolishes JT010-elicited pain. Sixteen healthy volunteers of both sexes rated pain due to intraepidermal injections of different concentrations and combinations of the substances. The study design was a double-blind crossover study. All subjects received all types of injections, including a placebo without substances. Injections of the TRPA1 agonist dose-dependently caused pain with a half-maximal effective concentration of 0.31 μm. Coinjection of A-967079 dose-dependently reduced and at a high concentration abolished JT010-induced pain. Quantification of JT010 by HPLC showed that a substantial part is adsorbed when in contact with polypropylene surfaces, but that this was overcome by handling in glass vials and injection using glass syringes. Isolated TRPA1 activation in humans causes pain. Thus, intradermal JT010 injection can serve as a tool to validate new TRPA1 antagonists concerning target engagement. More importantly, TRPA1-specific tools allow quantification of the TRPA1-dependent component in physiology and pathophysiology. SIGNIFICANCE STATEMENT This study showed that activation of the ion channel transient receptor potential ankyrin 1 (TRPA1) alone indeed suffices to elicit pain in humans, independent of other receptors previously found to be involved in pain generation. The newly established TRPA1-specific pain model allows different applications. First, it can be tested whether diseases are associated with compromised or exaggerated TRPA1-dependent painful sensations in the skin. Second, it can be investigated whether a new, possibly systemically applied drug directed against TRPA1 engages its target in humans. Further, the general possibility of quantitative inhibition of TRPA1 allows identification of the TRPA1-dependent disease component, given that the substance reaches its target. This contributes to a better understanding of pathophysiology, can lay the basis for new therapeutic approaches, and can bridge the gap between preclinical research and clinical trials.

Developmental Remodeling of Thalamic Interneurons Requires Retinal Signaling The dorsal lateral geniculate nucleus (dLGN) of the mouse is a model system to study the development of thalamic circuitry. Most studies focus on relay neurons of dLGN, yet little is known about the development of the other principal cell type, intrinsic interneurons. Here we examined whether the structure and function of interneurons relies on retinal signaling. We took a loss-of-function approach and crossed GAD67-GFP mice, which express GFP in dLGN interneurons, with math5 nulls (math5–/–), mutants that lack retinal ganglion cells and retinofugal projections. In vitro recordings and 3-D reconstructions of biocytin-filled interneurons at different postnatal ages showed their development is a multistaged process involving migration, arbor remodeling, and synapse formation. Arbor remodeling begins during the second postnatal week, after migration to and dispersion within dLGN is complete. This phase includes a period of exuberant branching where arbors grow in number, complexity, and field size. Such growth is followed by branch pruning and stabilization, as interneurons adopt a bipolar architecture. The absence of retinal signaling disrupts this process. The math5–/– interneurons fail to branch and prune, and instead maintain a simple, sparse architecture. To test how such defects influence connectivity with dLGN relay neurons, we used DHPG [(RS)-3,5-dihydroxyphenylglycine], the mGluR1,5 agonist that targets F2 terminals. This led to substantial increases in IPSC activity among WT relay neurons but had little impact in math5–/– mice. Together, these data suggest that retinal signaling is needed to support the arbor elaboration and synaptic connectivity of dLGN interneurons. SIGNIFICANCE STATEMENT Presently, our understanding about the development of the dorsal lateral geniculate nucleus is limited to circuits involving excitatory thalamocortical relay neurons. Here we show that the other principal cell type, intrinsic interneurons, has a multistaged developmental plan that relies on retinal innervation. These findings indicate that signaling from the periphery guides the maturation of interneurons and the establishment of inhibitory thalamic circuits.

Neuronal Adaptation Reveals a Suboptimal Decoding of Orientation Tuned Populations in the Mouse Visual Cortex Sensory information is encoded by populations of cortical neurons. Yet, it is unknown how this information is used for even simple perceptual choices such as discriminating orientation. To determine the computation underlying this perceptual choice, we took advantage of the robust visual adaptation in mouse primary visual cortex (V1). We first designed a stimulus paradigm in which we could vary the degree of neuronal adaptation measured in V1 during an orientation discrimination task. We then determined how adaptation affects task performance for mice of both sexes and tested which neuronal computations are most consistent with the behavioral results given the adapted population responses in V1. Despite increasing the reliability of the population representation of orientation among neurons, and improving the ability of a variety of optimal decoders to discriminate target from distractor orientations, adaptation increases animals' behavioral thresholds. Decoding the animals' choice from neuronal activity revealed that this unexpected effect on behavior could be explained by an overreliance of the perceptual choice circuit on target preferring neurons and a failure to appropriately discount the activity of neurons that prefer the distractor. Consistent with this all-positive computation, we find that animals' task performance is susceptible to subtle perturbations of distractor orientation and optogenetic suppression of neuronal activity in V1. This suggests that to solve this task the circuit has adopted a suboptimal and task-specific computation that discards important task-related information. SIGNIFICANCE STATEMENT A major goal in systems neuroscience is to understand how sensory signals are used to guide behavior. This requires determining what information in sensory cortical areas is used, and how it is combined, by downstream perceptual choice circuits. Here we demonstrate that when performing a go/no-go orientation discrimination task, mice suboptimally integrate signals from orientation tuned visual cortical neurons. While they appropriately positively weight target-preferring neurons, they fail to negatively weight distractor-preferring neurons. We propose that this all-positive computation may be adopted because of its simple learning rules and faster processing, and may be a common approach to perceptual decision-making when task conditions allow.

Neural Maps of Interaural Time Difference in the American Alligator: A Stable Feature in Modern Archosaurs Detection of interaural time differences (ITDs) is crucial for sound localization in most vertebrates. The current view is that optimal computational strategies of ITD detection depend mainly on head size and available frequencies, although evolutionary history should also be taken into consideration. In archosaurs, which include birds and crocodiles, the brainstem nucleus laminaris (NL) developed into the critical structure for ITD detection. In birds, ITDs are mapped in an orderly array or place code, whereas in the mammalian medial superior olive, the analog of NL, maps are not found. As yet, in crocodilians, topographical representations have not been identified. However, nontopographic representations of ITD cannot be excluded due to different anatomical and ethological features of birds and crocodiles. Therefore, we measured ITD-dependent responses in the NL of anesthetized American alligators of either sex and identified the location of the recording sites by lesions made after recording. The measured extracellular field potentials, or neurophonics, were strongly ITD tuned, and their preferred ITDs correlated with the position in NL. As in birds, delay lines, which compensate for external time differences, formed maps of ITD. The broad distributions of best ITDs within narrow frequency bands were not consistent with an optimal coding model. We conclude that the available acoustic cues and the architecture of the acoustic system in early archosaurs led to a stable and similar organization in today's birds and crocodiles, although physical features, such as internally coupled ears, head size, or shape, and audible frequency range, vary among the two groups. SIGNIFICANCE STATEMENT Interaural time difference (ITD) is an important cue for sound localization, and the optimal strategies for encoding ITD in neuronal populations are the subject of ongoing debate. We show that alligators form maps of ITD very similar to birds, suggesting that their common archosaur ancestor reached a stable coding solution different from mammals. Mammals and diapsids evolved tympanic hearing independently, and local optima can be reached in evolution that are not considered by global optimal coding models. Thus, the presence of ITD maps in the brainstem may reflect a local optimum in evolutionary development. Our results underline the importance of comparative animal studies and show that optimal models must be viewed in the light of evolutionary processes.

Homer1a Is Required for Establishment of Contralateral Bias and Maintenance of Ocular Dominance in Mouse Visual Cortex It is well established across many species that neurons in the primary visual cortex (V1) display preference for visual input from one eye or the other, which is termed ocular dominance (OD). In rodents, V1 neurons exhibit a strong bias toward the contralateral eye. Molecular mechanisms of how OD is established and later maintained by plastic changes are largely unknown. Here we report a novel role of an activity-dependent immediate early gene Homer1a (H1a) in these processes. Using both sexes of H1a knock-out (KO) mice, we found that there is basal reduction in the OD index of V1 neurons measured using intrinsic signal imaging. This was because of a reduction in the strength of inputs from the contralateral eye, which is normally dominant in mice. The abnormal basal OD index was not dependent on visual experience and is driven by postnatal expression of H1a. Despite this, H1a KOs still exhibited normal shifts in OD index following a short-term (2–3 d) monocular deprivation (MD) of the contralateral eye with lid suture. However, unlike wild-type counterparts, H1a KOs continued to shift OD index with a longer duration (5–6 d) of MD. The same phenotype was recapitulated in a mouse model that has reduced Homer1 binding to metabotropic glutamate receptor 5 (mGluR5). Our results suggest a novel role of H1a and its interaction with mGluR5 in strengthening contralateral eye inputs during postnatal development to establish normal contralateral bias in mouse V1 without much impact on OD shift with brief MD. SIGNIFICANCE STATEMENT Visual cortical neurons display varying degree of responsiveness to visual stimuli through each eye, which determines their ocular dominance (OD). Molecular mechanisms responsible for establishing normal OD are largely unknown. Development of OD has been shown to be largely independent of visual experience, but guided by molecular cues and spontaneous activity. We found that activity-dependent immediate early gene H1a is critical for establishing normal OD in V1 of mice, which show contralateral eye dominance. Despite the weaker contralateral bias, H1aKOs undergo largely normal OD plasticity. The basic phenotype of H1aKO was recapitulated by mGluR5 mutation that severely reduces H1a interaction. Our results suggest a novel role of mGluR5-H1a interaction in strengthening contralateral eye inputs to V1 during postnatal development.

Abdominal Radiology

Mickey mouse sign Mickey Mouse sign From Wikipedia, the free encyclopedia Jump to navigationJump to search Mickey Mouse sign is a medical sign resembling the head of Mickey Mouse, the Walt Disney character. Presented for the very first time at the CHIVA's Meeting, Berlin 2002 by Dr. Lurdes Cerol, this sign has been described as the image at the groin when a dilated accessory saphenous vein (ASV) exists: the common femoral vein (CFV) represents the head of Mickey Mouse while the great saphenous vein (GSV) and the dilated accessory saphenous vein (ASV) represent the ears. The presence of a Mickey Mouse sign has been a great diagnostic clue to check ASV insufficiency. Mickey Mouse Sign, the original slide, at CHIVA's Meeting, Berlin 2002" Mickey Mouse sign in the saphenofemoral junction, showing GSV, a dilated ASV and CFV Some authors, inspired by this sign, described an ecographic "Mickey Mouse View" at the saphenofemoral junction in the groin: the common femoral vein(CFV) represents the head of Mickey Mouse while the great saphenous vein (GSV) and the femoral artery (CFA) represent the ears.[1] But it can be seen in different regions of the body: Midbrain of progressive supranuclear palsy (PSP).[2] Polyostotic Paget's disease (Paget's disease affecting multiple bones); a bone scintigraphy with technetium-99m methylene bisphosphonate shows increased uptake at the sites of disease activity. Increased scintigraphic uptake in the body and spine of the vertebrae resembles the head of Mickey Mouse.[3] The portal triad in biliary ultrasound scans, with the portal vein comprising Mickey's head and the common bile duct and hepatic artery his right and left ears, respectively.[4] Pelvic Mickey Mouse sign: bilateral inguinal vesical hernia on transverse axial imaging.[5] Dysmorphic Mickey Mouse RBCs: RBCs with irregular cell walls and migration of hemoglobin into some areas creating the shape of Mickey Mouse ears.[6] The presence of these dysmorphic cells in urine may indicate intraglomerular haemorrhage.[7] Ureteropelvic junction obstruction (UPJO)[8] References[edit] ^ Coleridge-Smith P, Labropoulos N, Partsch H, Myers K, Nicolaides A, Cavezzi A (January 2006). "Duplex ultrasound investigation of the veins in chronic venous disease of the lower limbs--UIP consensus document. Part I. Basic principles". European Journal of Vascular and Endovascular Surgery. 31 (1): 83–92. doi:10.1016/j.ejvs.2005.07.019. PMID 16226898. ^ Sonthalia N, Ray S (September 2012). "The Hummingbird sign: a diagnostic clue for Steele-Richardson-Olszweski syndrome". BMJ Case Reports. 2012: bcr2012006263. doi:10.1136/bcr-2012-006263. PMC 4543120. PMID 22987902. ^ Goyal A, Boro H (November 2017). "Mickey Mouse sign in a case of polyostotic Paget's disease". Indian Journal of Case Reports. 3 (4): 279–80. ^ Fox, J. Christian (2011-10-13). Atlas of Emergency Ultrasound. Cambridge University Press. ISBN 9781139499873. ^ Singh O, Kekre NS (2017). ""Flying-saucer in the pelvis" sign: An equivalent of "pelvic Mickey mouse" sign". Indian Journal of Urology. 33 (2): 173–174. doi:10.4103/0970-1591.203423. PMC 5396411. PMID 28469311. ^ Kher, Kanwal; Schnaper, H. William; Greenbaum, Larry A. (2016-11-25). Clinical Pediatric Nephrology. CRC Press. ISBN 9781482214635. ^ McClatchey, Kenneth D. (2002). Clinical Laboratory Medicine. Lippincott Williams & Wilkins. ISBN 9780683307511. ^ Visveswaran, kasi (2009). Essentials of Nephrology, 2/e. BI Publications Pvt Ltd. ISBN 9788172253233.

Clinicopathological findings and imaging features of intraductal papillary neoplasm of the bile duct: comparison between contrast-enhanced ultrasound and contrast-enhanced computed tomography Abstract Purpose Intraductal papillary neoplasms of the bile duct (IPNBs) are a group of rare lesions with uncertain clinical findings and imaging features. We aim to investigate the clinicopathological features and imaging findings of IPNBs on contrast-enhanced ultrasound (CEUS) and contrast-enhanced computed tomography (CECT). Methods From February 2005 to March 2018, 30 patients with pathologically confirmed IPNBs were retrospectively identified in our hospital. Demographic, clinical, and pathological data, CEUS and CECT features and surgical strategies were analyzed. Results The most common clinical manifestations were abdominal pain (53.3%), jaundice (23.3%), and acute cholangitis (10.0%). Among all lesions, 5/30 (16.7%) lesions presented as dilated bile ducts only, while 13/30 (43.3%) lesions presented as dilated bile ducts with intraductal papillary masses, and 12/30 (40.0%) presented as solid masses with dilated bile ducts. For the 20 patients who underwent both CEUS and CECT, 18 lesions were hyperenhanced on CEUS, and 17 lesions were hyperenhanced on CECT in the arterial phase. In total, 16 and 18 lesions showed washout in the portal and late phases on CEUS, while the corresponding number of lesions that showed washout in the portal and late phases on CECT were 11 and 13. Twelve lesions (40.0%) showed atypical hyperplasia, while 16/30 (53.3%) lesions underwent malignant transformations. Conclusions There are 3 major forms of IPNBs on grayscale ultrasound, including diffusely dilated bile ducts without visible mass; focal dilated bile duct with intraductal papillary masses; and solid mass surrounded by dilated bile ducts. The enhancement patterns of IPNBs on CEUS and on CECT were consistent. IPNB has a high malignant potential, and patients should be treated with surgical resection after the diagnosis is established.

Adrenocortical hyperplasia: a review of clinical presentation and imaging Abstract Adrenal hyperplasia is non-malignant enlargement of the adrenal glands, which is often bilateral. It can be incidental or related to indolent disease process and may be related to benign or malignant etiologies causing biochemical alterations in the hypothalamic–pituitary–adrenal axis which controls steroidogenesis and in particular cortisol production. Clinical significance of the adrenal hyperplasia is variable ranging from asymptomatic finding to serious manifestations of Cushing syndrome. This is often associated with anatomical changes in the adrenal glands, which typically manifests as diffuse and sometimes nodular enlargement of the adrenal glands radiologically. Approaching adrenal hyperplasia requires careful clinical and biochemical evaluation in correlation with imaging review to differentiate ACTH-dependent and ACTH-independent etiologies. CT is the primary modality of choice for adult adrenal imaging owing to reproducibility, temporal and spatial resolution and broader access, while MRI often serves a complimentary role. Ultrasound and MRI are most commonly used in pediatric cases to evaluate congenital adrenal hyperplasia. This article will discuss the clinical presentation and imaging features of different types and mimics of adrenal cortical hyperplasia.

Evaluating the inflammatory activity in Crohn's disease using magnetic resonance diffusion kurtosis imaging Abstract Objectives To explore the feasibility of diffusion kurtosis imaging (DKI) for evaluating inflammatory activity in Crohn's disease (CD). Materials and methods In all, 51 CD patients were included, who were performed with consecutive enteroscopy, MR and DKI (b values = 0–2000 mm2/s). The lesions of bowel segments were graded as inactive (0–2), mild (3–6), and moderate–severe group (> 6) based on simplified endoscopic activity score for Crohn's disease (SES-CD), The abilities of the parameters of DKI and DWI in grading different activity lesions were compared. Results One hundred and twenty-seven bowel segments including inactive (15), mild (45) and moderate–severe (67) were analyzed. ADC (r = − 0.627, p < 0.001), Dapp (r = − 0.381, p < 0.001) and Kapp (r = 0.641, p < 0.001) were correlated with SES-CD. These parameters were significantly different among the three groups (all p < 0.001). ROC analysis found ADC had the highest accuracy (AUC = 0.884, p < 0.001) to differentiate inactive from active group with the threshold at 0.865 × 10−3 mm2/s, which was slightly higher than Kapp (AUC = 0.867, p < 0.001) with the threshold at 0.645, and was obviously higher than Dapp (AUC = 0.726, p = 0.005). Similarly, ADC also had the highest accuracy (AUC = 0.846, p < 0.001) to differentiate inactive–mild from moderate–severe group with the threshold at 0.825 × 10−3 mm2/s, and minimally higher than Kapp (AUC = 0.843, p < 0.001) with the threshold at 0.695, and obviously higher than Dapp (AUC = 0.690, p < 0.001). Conclusion DKI is feasible and comparable to conventional DWI for the evaluation of inflammatory activity in CD.

Magnetic resonance imaging as a non-invasive method for the assessment of pancreatic fibrosis (MINIMAP): a comprehensive study design from the consortium for the study of chronic pancreatitis, diabetes, and pancreatic cancer Abstract Characteristic features of chronic pancreatitis (CP) may be absent on standard imaging studies. Quantitative Magnetic Resonance Imaging (MRI) techniques such as T1 mapping, extracellular volume (ECV) fraction, diffusion-weighted imaging (DWI) with apparent diffusion coefficient map (ADC), MR elastography (MRE), and T1-weighted signal intensity ratio (SIR) have shown promise for the diagnosis and grading severity of CP. However, radiologists still use the Cambridge classification which is based on traditional ductal imaging alone. There is an urgent need to develop new diagnostic criteria that incorporate both parenchymal and ductal features of CP seen by MRI/MRCP. Designed to fulfill this clinical need, we present the MINIMAP study, which was funded in September 2018 by the National Institutes of Health. This is a comprehensive quantitative MR imaging study which will be performed at multiple institutions in well-phenotyped CP patient cohorts. We hypothesize that quantitative MRI/MRCP features can serve as valuable non-invasive imaging biomarkers to detect and grade CP. We will evaluate the role of T1 relaxometry, ECV, T1-weighted gradient echo SIR, MRE, arteriovenous enhancement ratio, ADC, pancreas volume/atrophy, pancreatic fat fraction, ductal features, and pancreatic exocrine output following secretin stimulation in the assessment of CP. We will attempt to generate a multi-parametric pancreatic tissue fibrosis (PTF) scoring system. We anticipate that a quantitative scoring system may serve as a biomarker of pancreatic fibrosis; hence this imaging technique can be used in clinical practice as well as clinical trials to evaluate the efficacy of agents which may slow the progression or reverse measures of CP.

Microvascular invasion and grading in hepatocellular carcinoma: correlation with major and ancillary features according to LIRADS Abstract Purpose To assess major and ancillary parameters that could be correlated with Microvascular Invasion (MIV) and with histologic grade of HCC. Materials and methods In this retrospective study, we assessed 62 patients (14 women–48 men; mean age, 63 years; range 38–80 years) that underwent hepatic resection for HCC. All patients were subject to Multidetector computed tomography (MDCT); 40 to Magnetic Resonance (MR) study. The radiologist assessed major and ancillary features according to LIRADS (v. 2018) and reported any radiological accessory findings if detected. Results No major feature showed statistically significant differences and correlation with grading. Mean ADC value was correlated with grading and with MIV status. No major feature was correlated to MIV; progressive contrast enhancement and satellite nodules showed statistically different percentages with respect to the presence of MIV, so as at the monovariate correlation analysis, satellite nodules were correlated with the presence of MIV. At multivariate regression analysis, no factor proved to be strong predictors of grading while progressive contrast enhancement and satellite nodules were significantly associated with the MIV. Conclusion Mean ADC value is correlated to HCC grading and MIV status. Progressive contrast enhancement and the presence of satellite nodules are correlated to MIV status.

Microwave ablation assisted by three-dimensional visualization system as local therapy for relapsed hepatoblastoma: a small pilot study Abstract Purpose We aimed to explore the feasibility of microwave ablation (MWA) assisted by three-dimensional visualization system for relapsed HB in children. Methods From August 2014 to February 2017, five patients with relapsed HB were enrolled. A total of 12 liver tumors were treated with MWA assisted by a three-dimensional visualization system. Follow-up data were obtained in all patients. The residual liver volume, local tumor progression, new intrahepatic tumors, survival outcome, and complications were analyzed. Results All tumors were completely ablated in a single session. The mean ablation time per tumor was 9.7 ± 8.6 min, and the median ablation/liver volume ratio was 2.37%. No local tumor progression was observed during a follow-up period of 9–39 months. All patients were still alive at the end of the follow-up. The median progression-free survival time after ablation was 9 months, and the median survival time after ablation was 12 months. No other complications were observed except for fever. Conclusions MWA assisted by three-dimensional visualization system appears to be a safe and feasible local treatment for recurrent HB in pediatric patients.

The "paper-thin wall" appearance in acute mesenteric ischemia

Demystifying the mesenteric root lesions Abstract Objective The aim of this article is to describe the normal anatomy of the root of the small bowel mesentery (RSBM) as well as the multidetector computed tomography (MDCT) features of the various primary and secondary lesions that affect the RSBM. Results The small bowel mesentery attaches the jejunum and ileum to the posterior abdominal wall, the line of attachment forming the RSBM. Several primary as well as secondary lesions involve the RSBM. The RSBM has anatomical contiguity with the mesocolon and other peritoneal ligaments, which forms a route for the spread of infection, neoplasms as well as several other abdominal pathologies. MDCT plays an important role in the evaluation of mesenteric root lesions. Conclusion Familiarity with the lesions involving the RSBM and their characteristic appearances on MDCT is important in giving thoughtful differential diagnosis and guiding the treating physician in further management.

Correction to: Imaging features of immune-mediated genitourinary disease The original version of this article was published with a error in the initials of the first, fifth and sixth author name: Jonathon Weber, Frank Miller and Jeanne Horowitz. The correct author's initials should be Jonathon D. Weber, Frank H Miller, and Jeanne M Horowitz. It is now corrected with this correction.

Neuroradiology

Correction to: Diagnostic performance of an unenhanced MRI exam for tumor follow-up of the optic pathway gliomas in children In the article "Diagnostic performance of an unenhanced MRI exam for tumor follow-up of the optic pathway gliomas in children", Table 2 data were not presented correctly, with results placed beneath an incorrect heading. Confidence interval also added. The original article has been corrected.

European Society of Neuroradiology (ESNR)

Spontaneous recanalization and hyperperfusion are relatively common at presentation in pediatric arterial ischemic stroke

Assessment of quantitative methods for enhancement measurement on vessel wall magnetic resonance imaging evaluation of intracranial atherosclerosis Abstract Purpose Quantitative measures of vessel wall magnetic resonance imaging (vwMRI) for the evaluation of intracranial atherosclerotic disease (ICAD) offers standardization not available with previously used qualitative approaches that may be difficult to replicate. Methods vwMRI studies performed to evaluate ICAD that had caused a stroke were analyzed. Two blinded reviewers qualitatively rated culprit lesions for the presence of enhancement on T1 delay alternating with nutation for tailored excitation (DANTE) SPACE images. At least 3 months later, quantitative analysis was performed of the same images, comparing lesion enhancement to reference structures. Cohen's kappa and intraclass correlation coefficients were calculated to assess agreement. Ratios of enhancement of lesions to references were compared to qualitative ratings. Results Studies from 54 patients met inclusion criteria. A mean of 49 (90.7%) lesions were qualitatively rated as enhancing, with good inter-rater agreement (κ = 0.783). Among reference structure candidates, low infundibulum demonstrated the highest inter-rater agreement on pre- and post-contrast imaging. The ratio of percentage increase in plaque signal following contrast to the same measure in low infundibulum demonstrated the highest agreement with qualitative assessment, with highest agreement seen with a ratio of 0.8 set as a threshold (κ = 0.675). Conclusion Quantitative metrics can yield objective data to better standardize techniques and acceptance of vwMRI evaluation of ICAD. The low infundibulum had the highest inter-rater agreement on both pre- and post-contrast images and is best suited as a normally enhancing reference structure. Such quantitative techniques should be implemented in future research of vwMRI for the evaluation of ICAD.

Gray matter reduction related to decreased serum creatinine and increased triglyceride, Hemoglobin A1C, and low-density lipoprotein in subjects with obesity Abstract Purpose Altered brain volume and metabolic variables have been found in subjects with obesity. However, the role of metabolic parameters in gray matter volume (GMV) has been poorly investigated. This study aimed to investigate the relationship between the metabolic parameters and brain volume in subjects with obesity. Methods Thirty-seven subjects with obesity and 39 age and sex matched normal-weight controls were included in this study. Eighteen of the 37 participants who underwent sleeve gastrectomy were included in the longitudinal analysis. Blood samples and high-resolution 3T T1-weighted magnetic resonance images were collected. Metabolic parameters in plasma and GMV were measured. Results Multiple linear regression analysis showed that gray matter reduction in several cognition-related cortices including right angular gyrus, superior occipital cortex, superior parietal cortex, and cerebellum was related to decreased creatinine, as well as increased triglyceride, HbA1c, and low-density lipoprotein in plasma in subjects with obesity. Weight loss after the surgery induced significant recovery of altered metabolic parameters and decreased gray matter volume. Furthermore, changes in the four metabolic parameters before and after the surgery were associated with changes in gray matter volume. Conclusion Our results suggest that the gray matter reduction is related to decreased creatinine as well as increased triglyceride, HbA1c, and low-density lipoprotein in plasma in subjects with obesity.

Diagnostic performance of an unenhanced MRI exam for tumor follow-up of the optic pathway gliomas in children Abstract Purpose Contrast-enhanced MRI (MRI + C) is considered as mandatory for brain tumors follow-up, but gadolinium brain depositions in relation with repeated injections have been reported. The aim of our work was to evaluate the diagnostic performance of an unenhanced MRI examination for the follow-up of optic pathway gliomas (OPG) in children. Methods Seventeen patients (with/without NF1) were selected from 2001 to 2017, with at least 5 MRI + C brain follow-up examinations. Privacy and data protection rights were addressed by the data protection officer (DPO) and the study was in accordance with the local ethical rules. Twenty-five cases of tumor progression and 25 cases of tumor stability mentioned in the conclusion of radiological reports (defined as gold standard) were isolated. Those exams were anonymized and independently reviewed by two radiologists, who analyzed both quantitative (such as tumor volume variation) and qualitative criteria (such as ventricular dilatation) on unenhanced images. Sensitivity, specificity, positive/negative predictive values (PPV, NPV), and inter/intra-observer agreement were calculated. Results The mean age of patients was 5.4 ± 3.4 years and mean follow-up length 6.7 years. The mean number of MRI + C was 13.5 (SD 7.2). The sensitivity of unenhanced MRI for tumor follow-up was 84–88% (95% CI 63.9–97.5). The specificity was 91.3–100% (95% CI 72–100). The PPV was 91.7% for reader 1 and 100% for reader 2. The NVP was 87.5% for reader 1 and 85.2% for reader 2. There was an excellent inter-observer agreement regarding tumor progression: kappa coefficient of 0.87 (p < 0.001). Inter/intra-variability for percentage of tumor volume variation between two exams were good (correlation coefficients of 0.97 and 0.94). Conclusion Tumor volume variation is in most cases sufficient to assess OPG progression. Systematic MRI + C could be questionable.

Brain regional volume estimations with NeuroQuant and FIRST: a study in patients with a clinically isolated syndrome Abstract Purpose Brain volume estimates from magnetic resonance images (MRIs) are of great interest in multiple sclerosis, and several automated tools have been developed for this purpose. The goal of this study was to assess the agreement between two tools, NeuroQuant® (NQ) and FMRIB's Integrated Registration Segmentation Tool (FIRST), for estimating overall and regional brain volume in a cohort of patients with a clinically isolated syndrome (CIS). In addition, white matter lesion volume was estimated with NQ and the Lesion Segmentation Toolbox (LST). Methods One hundred fifteen CIS patients were analysed. Structural images were acquired on a 3.0-T system. The volume agreement between methods (by estimation of the intraclass correlation coefficient) was calculated for the right and left thalamus, caudate, putamen, pallidum, hippocampus, and amygdala, as well as for the total intracranial volume and white matter lesion volume. Results In general, the estimated volumes were larger by NQ than FIRST, except for the pallidum. Agreement was low (ICC < 0.40) for the smaller structures (amygdala and pallidum) and fair to good (ICC > 0.40) for the remaining ones. Agreement was fair for lesion volume (ICC = 0.61), with NQ estimates lower than LST. Conclusions Agreement between NQ and FIRST brain volume estimates depends on the size of the structure of interest, with larger volumes achieving better agreement. In addition, concordance between the two tools does seem to be dependent on the presence of brain lesions.

Motor cortex hypointensity on susceptibility-weighted imaging: a potential imaging marker of iron accumulation in patients with cognitive impairment Abstract Purpose To assess the prevalence and characteristics of motor cortex hypointensity on 3-T susceptibility-weighted imaging (SWI) in patients with cognitive impairment and examine its clinical significance. Methods The institutional review board approved this retrospective study and waived the requirement for informed consent. A total of 127 patients with a clinical diagnosis of probable Alzheimer's disease (AD) (n = 32) or mild cognitive impairment (MCI) (n = 95) and 127 age- and sex-matched control subjects underwent 3-T brain magnetic resonance imaging. SWI was analyzed for both subjective visual scoring and the quantitative estimation of phase shift in the posterior bank of the motor cortex. A multivariate logistic regression analysis was performed to identify clinical and imaging variables associated with motor cortex hypointensity on SWI. Results Motor cortex hypointensity on SWI was observed in 94/127 cognitively impaired patients (74.0%) and 72/127 control subjects (56.7%) (p = 0.004). Age was the only variable that was significantly associated with motor cortex hypointensity in patients with cognitive impairment (odds ratio, 1.15; 95% confidence interval, 1.065–1.242; p < 0.001). The quantitative analysis confirmed a significant increase in phase shifting in the posterior bank of the motor cortex in patients with positive motor cortex hypointensity on SWI (p < 0.001). Conclusion Motor cortex hypointensity on SWI was more frequently found in patients with cognitive impairment than in age-matched controls and was positively associated with age. Thus, it may be a potential imaging marker of iron accumulation in patients with MCI or AD.

Microstructural brain abnormalities correlate with neurocognitive dysfunction in minimal hepatic encephalopathy: a diffusion kurtosis imaging study Abstract Purpose To investigate the diffusion kurtosis imaging (DKI) in early minimal hepatic encephalopathy (MHE) diagnosis and evaluate the correlations between changes in DKI metrics and cognitive performance. Methods We enrolled 116 cirrhosis patients, divided into non-HE (n = 61) and MHE (n = 55), and 46 normal controls (NCs). All patients underwent cognitive testing before magnetic resonance imaging. DKI metrics were calculated through whole-brain voxel-based analysis (VBA) and differences between the groups were assessed. Pearson correlation between the DKI metrics and cognitive performance was analysed. The receiver operating characteristic (ROC) curve was used to analyse the diagnostic efficiency of DKI metrics for MHE. Results MHE patients had significantly altered DKI metrics in a wide range of regions; lower fractional anisotropy (FA) and higher mean diffusivity (MD) are mainly located in the corpus callosum, left temporal white matter (WM), and right medial frontal WM. Furthermore, significantly altered kurtosis metrics included lower mean kurtosis (MK) in the corpus callosum and left thalamus, lower radial kurtosis (RK) in the corpus callosum, and lower axial kurtosis (AK) in the right anterior thalamic radiation. Alterations in axial diffusivity (AD), radial diffusivity (RD), and MD were closely correlated with cognitive scores. The ROC curves indicated AD in the forceps minor had the highest predictive performance for MHE in the cirrhosis patients (area under curve = 0.801, sensitivity = 77.05%, specificity = 74.55%). Conclusions Altered DKI metrics indicate brain microstructure abnormalities in MHE patients, some of which may be used as neuroimaging markers for early MHE diagnosis.

Structural and functional abnormalities of vision-related brain regions in cirrhotic patients: a MRI study Abstract Purpose Previous studies have focused on global cerebral alterations observed in cirrhosis. However, little was known about the specific abnormalities of vision-related brain regions in cirrhotic patients. In this study, we sought to explore neurological alterations of vision-related regions by measuring brain resting-state network connectivity, based on the structural investigation in cirrhotic patients without clinical sign of hepatic encephalopathy (HE). Methods Structural and functional magnetic resonance image (MRI) data were collected from 20 hepatitis B virus (HBV)-related cirrhotic patients without clinical sign of HE and from 20 healthy controls (HC). Voxel-based morphometric (VBM) analysis and brain functional network analysis were performed to detect abnormalities in cerebral structure and function. Results Cirrhotic patients showed regions with the most significant gray matter reduction primarily in vision-related brain regions, including the bilateral lingual gyri, left putamen, right fusiform gyrus, and right calcarine gyrus, and other significant gray matter reductions were distributed in bilateral hippocampus. Based on structural investigation focused on vision-related regions, brain functional network analysis revealed decreased functional connectivity between brain functional networks within vision-related regions (primary visual network (PVN), higher visual network (HVN), visuospatial network (VSN)) in the patient group compared with HC group. Conclusion These results indicate that structural and functional impairment were evident in the vision-related brain regions in cirrhotic patients without clinical sign of hepatic encephalopathy. The physiopathology and clinical relevance of these changes could not be ascertained from the present study, which provided a basis for further evolution of the disease.