The impact of subthreshold levels of amyloid deposition on conversion to dementia in patients with amyloid-negative amnestic mild cognitive impairment.

BACKGROUND: About 40-50% of patients with amnestic mild cognitive impairment (MCI) are found to have no significant Alzheimer's pathology based on amyloid PET positivity. Notably, conversion to dementia in this population is known to occur much less often than in amyloid-positive MCI. However, the relationship between MCI and brain amyloid deposition remains largely unknown. Therefore, we investigated the influence of subthreshold levels of amyloid deposition on conversion to dementia in amnestic MCI patients with negative amyloid PET scans. METHODS: This study was a retrospective cohort study of patients with amyloid-negative amnestic MCI who visited the memory clinic of Asan Medical Center. All participants underwent detailed neuropsychological testing, brain magnetic resonance imaging, and [18F]-florbetaben (FBB) positron emission tomography scan (PET). Conversion to dementia was determined by a neurologist based on a clinical interview with a detailed neuropsychological test or a decline in the Korean version of the Mini-Mental State Examination score of more than 4 points per year combined with impaired activities of daily living. Regional cortical amyloid levels were calculated, and a receiver operating characteristic (ROC) curve for conversion to dementia was obtained. To increase the reliability of the results of the study, we analyzed the Alzheimer's Disease Neuroimaging Initiative (ADNI) dataset together. RESULTS: During the follow-up period, 36% (39/107) of patients converted to dementia from amnestic MCI. The dementia converter group displayed increased standardized uptake value ratio (SUVR) values of FBB on PET in the bilateral temporal, parietal, posterior cingulate, occipital, and left precuneus cortices as well as increased global SUVR. Among volume of interests, the left parietal SUVR predicted conversion to dementia with the highest accuracy in the ROC analysis (area under the curve [AUC] = 0.762, P < 0.001). The combination of precuneus, parietal cortex, and FBB composite SUVRs also showed a higher accuracy in predicting conversion to dementia than other models (AUC = 0.763). Of the results of ADNI data, the SUVR of the left precuneus SUVR showed the highest AUC (AUC = 0.596, P = 0.006). CONCLUSION: Our findings suggest that subthreshold amyloid levels may contribute to conversion to dementia in patients with amyloid-negative amnestic MCI.

Estimation of Stroke Volume Variance from Arterial Blood Pressure: Using a 1-D Convolutional Neural Network.

BACKGROUND: We aimed to create a novel model using a deep learning method to estimate stroke volume variation (SVV), a widely used predictor of fluid responsiveness, from arterial blood pressure waveform (ABPW). METHODS: In total, 557 patients and 8,512,564 SVV datasets were collected and were divided into three groups: training, validation, and test. Data was composed of 10 s of ABPW and corresponding SVV data recorded every 2 s. We built a convolutional neural network (CNN) model to estimate SVV from the ABPW with pre-existing commercialized model (EV1000) as a reference. We applied pre-processing, multichannel, and dimension reduction to improve the CNN model with diversified inputs. RESULTS: Our CNN model showed an acceptable performance with sample data (r = 0.91, MSE = 6.92). Diversification of inputs, such as normalization, frequency, and slope of ABPW significantly improved the model correlation (r = 0.95), lowered mean squared error (MSE = 2.13), and resulted in a high concordance rate (96.26%) with the SVV from the commercialized model. CONCLUSIONS: We developed a new CNN deep-learning model to estimate SVV. Our CNN model seems to be a viable alternative when the necessary medical device is not available, thereby allowing a wider range of application and resulting in optimal patient management.

Early Impairment in the Ventral Visual Pathway Can Predict Conversion to Dementia in Patients With Amyloid-negative Amnestic Mild Cognitive Impairment.

BACKGROUND: Around 15% to 20% of patients with clinically probable Alzheimer disease have been found to have no significant Alzheimer pathology on amyloid positron emission tomography. A previous study showed that conversion to dementia from amyloid-negative mild cognitive impairment (MCI) was observed in up to 11% of patients, drawing attention to this condition. OBJECT: We gathered the detailed neuropsychological and neuroimaging data of this population to elucidate factors for conversion to dementia from amyloid-negative amnestic MCI. METHODS: This study was a single-institutional, retrospective cohort study of amyloid-negative MCI patients over age 50 with at least 36 months of follow-up. All subjects underwent detailed neuropsychological testing, 3 tesla brain magnetic resonance imaging), and fluorine-18(18F)-florbetaben amyloid positron emission tomography scans. RESULTS: During the follow-up period, 39 of 107 (36.4%) patients converted to dementia from amnestic MCI. The converter group had more severe impairment in all visual memory tasks. The volumetric analysis revealed that the converter group had significantly reduced total hippocampal volume on the right side, gray matter volume in the right lateral temporal, lingual gyri, and occipital pole. CONCLUSION: Our study showed that reduced gray matter volume related to visual memory processing may predict clinical progression in this amyloid-negative MCI population.

The cerebellum could serve as a potential imaging biomarker of dementia conversion in patients with amyloid-negative amnestic mild cognitive impairment.

BACKGROUND AND PURPOSE: As part of network-specific neurodegeneration, changes in cerebellar gray matter (GM) volume and impaired cerebello-cerebral functional networks have been reported in Alzheimer disease (AD). Compared with healthy controls, a volume loss in the cerebellum has been observed in patients with continuum of AD. However, little is known about the anatomical or functional changes in patients with clinical AD but no brain amyloidosis. We aimed to identify the relationship between cerebellar volume and dementia conversion of amyloid-negative mild cognitive impairment (MCI). METHODS: This study was a retrospective cohort study of patients over the age 50 years with amyloid-negative amnestic MCI who visited the memory clinic of Asan Medical Center with no less than a 36-month follow-up period. All subjects underwent detailed neuropsychological tests, 3 T brain magnetic resonance imaging scans including three-dimensional T1 imaging, and fluorine-18[F18 ]-florbetaben amyloid positron emission tomography scans. A spatially unbiased atlas template of the cerebellum and brainstem was used for analyzing cerebellar GM volume. RESULTS: During the 36 months of follow-up, 39 of 107 (36.4%) patients converted to dementia from amnestic MCI. The converter group had more severe impairments in all visual memory tasks. In terms of volumetric analysis, reduced crus I/II volume adjusted with total intracranial volume, and age was observed in the converter group. CONCLUSIONS: Significant cerebellar GM atrophy involving the bilateral crus I/II may be a novel imaging biomarker for predicting dementia progression in amyloid-negative amnestic MCI patients.

Elucidating the Risk Factors for Progression from Amyloid-Negative Amnestic Mild Cognitive Impairment to Dementia.

BACKGROUND: Amyloid PET allows for the assessment of amyloid ß status in the brain, distinguishing true Alzheimer's disease from Alzheimer's disease-mimicking conditions. Around 15-20% of patients with clinically probable Alzheimer's disease have been found to have no significant Alzheimer's pathology on amyloid PET. However, a limited number of studies had been conducted on this subpopulation in terms of clinical progression. OBJECTIVE: We investigated the risk factors that could affect the progression to dementia in patients with amyloid-negative amnestic mild cognitive impairment (MCI). METHODS: This study was a single-institutional, retrospective cohort study of patients over the age of 50 with amyloid-negative amnestic MCI who visited the memory clinic of Asan Medical Center with a follow-up period of more than 36 months. All participants underwent brain magnetic resonance imaging (MRI), detailed neuropsychological testing, and fluorine-18[F18]-florbetaben amyloid PET. RESULTS: During the follow-up period, 39 of 107 patients progressed to dementia from amnestic MCI. In comparison with the stationary group, the progressed group had a more severe impairment in verbal and visual episodic memory function and hippocampal atrophy, which showed an Alzheimer's diseaselike pattern despite the lack of evidence for significant Alzheimer's disease pathology. Voxel-based morphometric MRI analysis revealed that the progressed group had a reduced gray matter volume in the bilateral cerebellar cortices, right temporal cortex, and bilateral insular cortices. CONCLUSION: Considering the lack of evidence of amyloid pathology, clinical progression of these subpopulation may be caused by other neuropathologies such as TDP-43, abnormal tau or alpha synuclein that lead to neurodegeneration independent of amyloid-driven pathway. Further prospective studies incorporating biomarkers of Alzheimer's disease-mimicking dementia are warranted.

Delayed Functional Networks Development and Altered Fast Oscillation Dynamics in a Rat Model of Cortical Malformation.

Malformations of cortical development (MCD) is associated with a wide range of developmental delay and drug resistant epilepsy in children. By using resting-state functional magnetic resonance imaging (RS-fMRI) and event-related spectral perturbation (ERSP) of cortical electroencephalography (EEG) data, we tried to investigate the neural changes of spatiotemporal functional connectivity (FC) and fast oscillation (FO) dynamics in a rat model of methylazoxymethanol (MAM)-induced MCD. A total of 28 infant rats with prenatal exposure to MAM and those of age matched 28 controls with prenatal saline exposure were used. RS-fMRI were acquired at postnatal day 15 (P15) and 29 (P29), and correlation coefficient analysis of eleven region of interests (ROI) was done to find the differences of functional networks between four groups. Two hour-cortical EEGs were also recorded at P15 and P29 and the ERSP of gamma (30-80 Hz) and ripples (80-200 Hz) were analyzed. The rats with MCD showed significantly delayed development of superior colliculus-brainstem network compared to control rats at P15. In contrast to marked maturation of default mode network (DMN) in controls from P15 to P29, there was no clear development in MCD rats. The MCD rats showed significantly higher cortical gamma and ripples-ERSP at P15 and lower cortical ripples-ERSP at P29 than those of control rats. This study demonstrated delayed development of FC and altered cortical FO dynamics in rats with malformed brain. The results should be further investigated in terms of the epileptogenesis and cognitive dysfunction in patients with MCD.

In vivo MRI Successfully Reveals the Malformation of Cortical Development in Infant Rats.

Objective: Malformations of cortical development (MCDs) are major causes of intractable epilepsies. To characterize the early neuroimaging findings of MCDs, we tried to identify the MRI features consistent with pathological findings in an infant rat MCD model, prenatally exposed to methylazoxymethanol (MAM), by using newly developed MRI techniques. Methods: At gestational day 15, two doses of MAM (15 mg/kg intraperitoneally) or normal saline were injected into pregnant rats. The offspring underwent in vivo MRI, including glutamate chemical exchange saturation transfer (GluCEST), 1H-MR spectroscopy, and diffusion tensor imaging, at postnatal day (P) 15 using a 7T small-animal imaging system. Another set of prenatally MAM-exposed rats were sacrificed for histological staining. Results: At P15, the retrosplenial cortex (RSC) of rats with MCDs showed decreased neuronal nuclei, parvalbumin, and reelin expressions. Moreover, dendritic arborization of pyramidal cells in the RSC significantly decreased in infant rats with MCDs. In vivo MRI showed significantly decreased GluCEST (%) in the RSC of rats with MCDs (p = 0.000) and a significant correlation between GluCEST (%) and RSC thickness (r = 0.685, p = 0.003). The rats with MCDs showed reduced glutamate (p = 0.002), N-acetylaspartate (p = 0.002), and macromolecule and lipid levels (p = 0.027) and significantly reduced fractional anisotropy values in the RSC. Conclusion: In vivo MRI revealed reduced neuronal population and dendritic arborization in the RSC of infant rats with MCDs during the early postnatal period. These pathological changes of the cortex could serve as clinical imaging biomarkers of MCDs in infants.

Who Should Pay for Interdependent Risk? Policy Implications for Security Interdependence Among Airports.

We study interdependent risks in security, and shed light on the economic and policy implications of increasing security interdependence in presence of reactive attackers. We investigate the impact of potential public policy arrangements on the security of a group of interdependent organizations, namely, airports. Focusing on security expenditures and costs to society, as assessed by a social planner, to individual airports and to attackers, we first develop a game-theoretic framework, and derive explicit Nash equilibrium and socially optimal solutions in the airports network. We then conduct numerical experiments mirroring real-world cyber scenarios, to assess how a change in interdependence impact the airports' security expenditures, the overall expected costs to society, and the fairness of security financing. Our study provides insights on the economic and policy implications for the United States, Europe, and Asia.

Deep Learning-Based Stroke Volume Estimation Outperforms Conventional Arterial Contour Method in Patients with Hemodynamic Instability.

Although the stroke volume (SV) estimation by arterial blood pressure has been widely used in clinical practice, its accuracy is questionable, especially during periods of hemodynamic instability. We aimed to create novel SV estimating model based on deep-learning (DL) method. A convolutional neural network was applied to estimate SV from arterial blood pressure waveform data recorded from liver transplantation (LT) surgeries. The model was trained using a gold standard referential SV measured via pulmonary artery thermodilution method. Merging a gold standard SV and corresponding 10.24 seconds of arterial blood pressure waveform as an input/output data set with 2-senconds of sliding overlap, 484,384 data sets from 34 LT surgeries were used for training and validation of DL model. The performance of DL model was evaluated by correlation and concordance analyses in another 491,353 data sets from 31 LT surgeries. We also evaluated the performance of pre-existing commercialized model (EV1000), and the performance results of DL model and EV1000 were compared. The DL model provided an acceptable performance throughout the surgery (r = 0.813, concordance rate = 74.15%). During the reperfusion phase, where the most severe hemodynamic instability occurred, DL model showed superior correlation (0.861; 95% Confidence Interval, (CI), 0.855-0.866 vs. 0.570; 95% CI, 0.556-0.584, P < 0.001) and higher concordance rate (90.6% vs. 75.8%) over EV1000. In conclusion, the DL-based model was superior for estimating intraoperative SV and thus might guide physicians to precise intraoperative hemodynamic management. Moreover, the DL model seems to be particularly promising because it outperformed EV1000 in circumstance of rapid hemodynamic changes where physicians need most help.

Effect of Prone Positional Apparatus on the Occurrence of Acute Kidney Injury After Spine Surgery.

BACKGROUND AND OBJECTIVE: Increased intra-abdominal pressure with prone positioning for spinal surgery is associated with intraoperative hemodynamic alterations and the potential for postoperative complications. This study investigated the incidence of postoperative acute kidney injury (AKI) in patients undergoing spine surgery on a Jackson spinal table or a Wilson frame. METHODS: A total of 1374 patients who underwent spine surgery were divided into 2 groups: Jackson spinal table (n = 598) and Wilson frame group (n = 776). After 1:1 propensity score matching, a final analysis was performed on 970 patients. The primary endpoint was a comparison of the incidence of AKI in the 2 groups. RESULTS: After propensity score matching analysis, the mean ± standard deviations of spine surgery invasiveness index were 4.7 ± 3.5 and 2.1 ± 1.4 in patients with the Jackson spinal table and the Wilson frame, respectively (P < 0.001). Considering the differences in surgical invasiveness, operative time, estimated blood loss, and administration of packed red blood cells were higher in the Jackson spinal table group than in the Wilson frame group (P < 0.001). However, the incidence of AKI was less with the Jackson spinal table than with the Wilson frame (1.7% vs. 3.7%, 2.25 [0.978-5.175], P = 0.056), not reaching statistical significance. CONCLUSION: This analysis showed that postoperative AKI in patients undergoing spine surgery in the prone position was not different with the Wilson frame than in the Jackson spinal table despite higher surgical severity, longer operative times, and more blood loss in the latter group. In spine surgery, the appropriate selection of prone positioning apparatus can potentially be an important consideration in reducing the risk of AKI.

In Vivo Multimodal Magnetic Resonance Imaging Changes After N-Methyl-d-Aspartate-Triggered Spasms in Infant Rats.

OBJECTIVE: Despite the serious neurodevelopmental sequelae of epileptic encephalopathy during infancy, the pathomechanisms involved remain unclear. To find potential biomarkers that can reflect the pathogenesis of epileptic encephalopathy, we explored the neurometabolic and microstructural sequelae after infantile spasms using a rat model of infantile spasms and in vivo magnetic resonance imaging techniques. METHODS: Rats prenatally exposed to betamethasone were subjected to three rounds of intraperitoneal N-methyl-d-aspartate (NMDA) triggering of spasms or received saline injections (controls) on postnatal days (P) 12, 13, and 15. Chemical exchange saturation transfer imaging of glutamate (GluCEST) were performed at P15 and 22 and diffusion tensor imaging and additional spectroscopy (1H-MRI/MRS) of the cingulate cortex were serially done at P16, 23, and 30 and analyzed. Pathological analysis and western blotting were performed with rats sacrificed on P35. RESULTS: Within 24 h of the three rounds of NMDA-induced spasms, there was an acute increase in the GluCEST (%) in the cortex, hippocampus, and striatum. When focused on the cingulate cortex, mean diffusivity (MD) was significantly decreased during the acute period after multiple spasms with an increase in γ-aminobutyric acid (GABA), glutamate, and glutamine N-acetylaspartate-plus-N-acetylaspartylglutamate (tNAA), total choline, and total creatine. The juvenile rats also showed decreased MD on diffusion tensor imaging and significant decreases in taurine, tNAA, and macromolecules-plus-lipids in the cingulate cortex. Pathologically, there was a significant reduction in glial fibrillary acidic protein, myelin basic protein, and neuronal nuclei expression in the cingulate cortex of rats with NMDA-induced spasms. SIGNIFICANCE: These neurometabolic and microstructural alterations after NMDA-triggered spasms might be potential imaging biomarkers of epileptic encephalopathy.

The administration of hydrogen sulphide prior to ischemic reperfusion has neuroprotective effects in an acute stroke model.

Emerging evidence has suggested that hydrogen sulfide (H2S) may alleviate the cellular damage associated with cerebral ischemia/reperfusion (I/R) injury. In this study, we assessed using 1H-magnetic resonance imaging/magnetic resonance spectroscopy (1H-MRI/MRS) and histologic analysis whether H2S administration prior to reperfusion has neuroprotective effects. We also evaluated for differences in the effects of H2S treatment at 2 time points. 1H-MRI/MRS data were obtained at baseline, and at 3, 9, and 24 h after ischemia from 4 groups: sham, control (I/R injury), sodium hydrosulfide (NaHS)-30 and NaHS-1 (NaHS delivery at 30 and 1 min before reperfusion, respectively). The total infarct volume and the midline shift at 24 h post-ischemia were lowest in the NaHS-1, followed by the NaHS-30 and control groups. Peri-infarct volume was significantly lower in the NaHS-1 compared to NaHS-30 and control animals. The relative apparent diffusion coefficient (ADC) in the peri-infarct region showed that the NaHS-1 group had significantly lower values compared to the NaHS-30 and control animals and that NaHS-1 rats showed significantly higher relative T2 values in the peri-infarct region compared to the controls. The relative ADC value, relative T2 value, levels of N-acetyl-L-aspartate (NAA), and the NAA, glutamate, and taurine combination score (NGT) in the ischemic core region at 24 h post-ischemia did not differ significantly between the 2 NaHS groups and the control except that the NAA and NGT values were higher in the peri-infarct region of the NaHS-1 animals at 9 h post-ischemia. In the ischemic core and peri-infarct regions, the apoptosis rate was lowest in the NaHS-1 group, followed by the NaHS-30 and control groups. Our results suggest that H2S treatment has neuroprotective effects on the peri-infarct region during the evolution of I/R injury. Furthermore, our findings indicate that the administration of H2S immediately prior to reperfusion produces the highest neuroprotective effects.

Large-scale structural alteration of brain in epileptic children with SCN1A mutation.

OBJECTIVE: Mutations in SCN1A gene encoding the alpha 1 subunit of the voltage gated sodium channel are associated with several epilepsy syndromes including genetic epilepsy with febrile seizures plus (GEFS +) and severe myoclonic epilepsy of infancy (SMEI). However, in most patients with SCN1A mutation, brain imaging has reported normal or non-specific findings including cerebral or cerebellar atrophy. The aim of this study was to investigate differences in brain morphometry in epileptic children with SCN1A mutation compared to healthy control subjects. METHODS: We obtained cortical morphology (thickness, and surface area) and brain volume (global, subcortical, and regional) measurements using FreeSurfer (version 5.3.0, https://surfer.nmr.mgh.harvard.edu) and compared measurements of children with epilepsy and SCN1A gene mutation (n = 21) with those of age and gender matched healthy controls (n = 42). RESULTS: Compared to the healthy control group, children with epilepsy and SCN1A gene mutation exhibited smaller total brain, total gray matter and white matter, cerebellar white matter, and subcortical volumes, as well as mean surface area and mean cortical thickness. A regional analysis revealed significantly reduced gray matter volume in the patient group in the bilateral inferior parietal, left lateral orbitofrontal, left precentral, right postcentral, right isthmus cingulate, right middle temporal area with smaller surface area and white matter volume in some of these areas. However, the regional cortical thickness was not significantly different in two groups. SIGNIFICANCE: This study showed large-scale developmental brain changes in patients with epilepsy and SCN1A gene mutation, which may be associated with the core symptoms of the patients. Further longitudinal MRI studies with larger cohorts are required to confirm the effect of SCN1A gene mutation on structural brain development.

A New Rat Model of Epileptic Spasms Based on Methylazoxymethanol-Induced Malformations of Cortical Development.

Malformations of cortical development (MCDs) can cause medically intractable epilepsies and cognitive disabilities in children. We developed a new model of MCD-associated epileptic spasms by treating rats prenatally with methylazoxymethanol acetate (MAM) to induce cortical malformations and postnatally with N-methyl-d-aspartate (NMDA) to induce spasms. To produce cortical malformations to infant rats, two dosages of MAM (15 mg/kg, intraperitoneally) were injected to pregnant rats at gestational day 15. In prenatally MAM-exposed rats and the controls, spasms were triggered by single (6 mg/kg on postnatal day 12 (P12) or 10 mg/kg on P13 or 15 mg/kg on P15) or multiple doses (P12, P13, and P15) of NMDA. In prenatally MAM-exposed rats with single NMDA-provoked spasms at P15, we obtain the intracranial electroencephalography and examine the pretreatment response to adrenocorticotropic hormone (ACTH) or vigabatrin. Rat pups prenatally exposed to MAM exhibited a significantly greater number of spasms in response to single and multiple postnatal NMDA doses than vehicle-exposed controls. Vigabatrin treatment prior to a single NMDA dose on P15 significantly suppressed spasms in MAM group rats (p < 0.05), while ACTH did not. The MAM group also showed significantly higher fast oscillation (25-100 Hz) power during NMDA-induced spasms than controls (p = 0.047). This new model of MCD-based epileptic spasms with corresponding features of human spasms will be valuable for future research of the developmental epilepsy.

Agency Problems and Airport Security: Quantitative and Qualitative Evidence on the Impact of Security Training.

We analyze the issue of agency costs in aviation security by combining results from a quantitative economic model with a qualitative study based on semi-structured interviews. Our model extends previous principal-agent models by combining the traditional fixed and varying monetary responses to physical and cognitive effort with nonmonetary welfare and potentially transferable value of employees' own human capital. To provide empirical evidence for the tradeoffs identified in the quantitative model, we have undertaken an extensive interview process with regulators, airport managers, security personnel, and those tasked with training security personnel from an airport operating in a relatively high-risk state, Turkey. Our results indicate that the effectiveness of additional training depends on the mix of "transferable skills" and "emotional" buy-in of the security agents. Principals need to identify on which side of a critical tipping point their agents are to ensure that additional training, with attached expectations of the burden of work, aligns the incentives of employees with the principals' own objectives.

Does Computer-Aided Diagnosis Permit Differentiation of Angiomyolipoma Without Visible Fat From Renal Cell Carcinoma on MDCT?

OBJECTIVE: The purpose of this study was to evaluate the diagnostic value of computer-aided diagnosis (CADx) in differentiating angiomyolipoma without visible fat from renal cell carcinoma (RCC) on MDCT. MATERIALS AND METHODS: The study included 406 patients who had 47 angiomyolipomas without visible fat and 359 RCCs smaller than 4 cm, all of which were diagnosed on the basis of findings from nephrectomy or percutaneous biopsy performed at our institution between 2000 and 2011. MDCT (slice thickness, 2.5 mm for corticomedullary phase image or 5 mm for the other phase images) and clinical findings were blindly reviewed by two radiologists in a single session. At the time the study was performed, radiologist 1 had 8 years of experience, and radiologist 2 had 18 years of experience. On the basis of the MDCT and clinical findings, CADx classified renal tumors as angiomyolipoma and RCC, and each radiologist independently recorded the probability score (0-5) for angiomyolipoma. The accuracy of CADx versus radiologists in diagnosing angiomyolipoma was compared using ROC analysis. Interobserver agreement between the two radiologists was evaluated. RESULTS: CADx yielded an area under the curve (Az) value of 0.949, which was greater than the Az values yielded by radiologists 1 and 2 (0.872 and 0.782, respectively; p < 0.05). In addition, the Az value for radiologist 1 was greater than that for radiologist 2 (p = 0.01). CADx with a threshold of -1.0085 showed greater sensitivity than radiologist 1 and greater sensitivity, specificity, and accuracy than radiologist 2 (p < 0.05). The interobserver agreement for the differentiation was fair (κ = 0.289). CONCLUSION: CAD can improve diagnostic performance in differentiating angiomyolipoma from RCC. The diagnostic performance of radiologists is variable according to the clinical experience and physical and emotional states of the radiologists.

Structural abnormalities in benign childhood epilepsy with centrotemporal spikes (BCECTS).

PURPOSE: The aim of this study was to investigate cortical thickness and gray matter volume abnormalities in benign childhood epilepsy with centrotemporal spikes (BCECTS). We additionally assessed the effects of comorbid attention-deficit/hyperactivity (ADHD) on these abnormalities. METHODS: Surface and volumetric MR imaging data of children with newly diagnosed BCECTS (n = 20, 14 males) and age-matched healthy controls (n = 20) were analyzed using FreeSurfer (version 5.3.0, https://surfer.nmr.mgh.harvard.edu). An additional comparison was performed between BCECTS children with and without ADHD (each, n = 8). A group comparison was carried out using an analysis of covariance with a value of significance set as p < 0.01 or p < 0.05. RESULTS: Children with BCECTS had significantly thicker right superior frontal, superior temporal, middle temporal, and left pars triangularis cortices. Voxel-based morphometric analysis revealed significantly larger cortical gray matter volumes of the right precuneus, left orbitofrontal, pars orbitalis, precentral gyri, and bilateral putamen and the amygdala of children with BCECTS compared to healthy controls. BCECTS patients with ADHD had significantly thicker left caudal anterior and posterior cingulate gyri and a significantly larger left pars opercularis gyral volume compared to BCECTS patients without ADHD. CONCLUSION: Children with BCECTS have thicker or larger gray matters in the corticostriatal circuitry at the onset of epilepsy. Comorbid ADHD is also associated with structural aberrations. These findings suggest structural disruptions of the brain network are associated with specific developmental electro-clinical syndromes.

Early infarct growth predicts long-term clinical outcome after thrombolysis.

BACKGROUND: Ischemic lesion growth may be a surrogate marker of clinical outcome, but no such interrelationship after thrombolysis has yet been determined. We evaluated the association between early infarct growth on diffusion-weighted imaging (DWI) and long-term clinical outcome after thrombolysis. METHODS: We retrospectively reviewed outcomes in patients with acute middle cerebral artery territory stroke who had been treated with intravenous tissue plasminogen activator or intra-arterial urokinase. DWI lesion volumes were measured at baseline and within 7 days, and the difference was calculated. Clinical outcome was evaluated using the modified Rankin Scale (mRS) at 3 months. Good and poor clinical outcomes were defined as: a) mRS 0-1 vs. mRS 2-6, b) mRS 0-2 vs. mRS 3-6, and c) responder analysis which was influenced by the baseline National Institutes of Health Stroke Scale (NIHSS) scores: good and poor outcomes were defined as mRS 0 vs. mRS 1-6 if the baseline NIHSS score was <8, mRS 0-1 vs. mRS 2-6 if the NIHSS score was 8-14, and mRS 0-2 vs. mRS 3-6 if the NIHSS score was >14. The relationship between the ischemic lesion volume change and clinical outcome was explored. The cut-off value of infarct growth predicting long-term outcome was estimated using receiver operating characteristic analysis. RESULTS: Of the 81 patients included, 67 (82.7%) showed lesion growth, and absolute growth was significantly related to poor outcomes (P<0.001 all for mRS 2-6, mRS 3-6, and responder analysis). Multivariate analysis showed that absolute lesion growth was an independent predictor of poor outcome, defined as mRS 2-6 (P=0.002; odds ratio [OR], 1.06; 95% confidence interval [CI], 1.02-1.10), mRS 3-6 (P=0.001; OR, 1.06; 95% CI, 1.02-1.10), and poor outcome by responder analysis (P=0.001; OR, 1.06; 95% CI, 1.03-1.10). The cut-off values of lesion growth that discriminated between good and poor outcomes were 14.11 cm(3) for mRS 2-6; 15.87 cm(3) for mRS 3-6; and 14.11 cm(3) in responder analysis. CONCLUSIONS: Early DWI lesion growth is an independent predictor of poor outcome after thrombolysis and may serve a potential surrogate marker of clinical outcome in acute stroke trials.