Effects of cholesterol levels on outcomes of out-of-hospital cardiac arrest: a cross-sectional study

Objective High cholesterol level is a risk factor for coronary artery disease, and coronary artery disease is a major risk factor for out-of-hospital cardiac arrest (OHCA). However, the effect of cholesterol level on outcomes of OHCA has been poorly studied. This study aimed to determine the effect of cholesterol level on outcomes of OHCA. Methods This cross-sectional study used the CAPTURES (Cardiac Arrest Pursuit Trial with Unique Registration and Epidemiologic Surveillance) project database in Korea. Multivariable conditional logistic regression analysis was performed to estimate the effect of cholesterol level on outcomes in OHCA. Results In all, 584 cases of OHCA were analyzed; those with cholesterol levels <120 mg/dL were classified as having low total cholesterol (TC) (n=197), those with levels ranging from 120–199 mg/dL as middle TC (n=322), and those with ≥200 mg/dL as high TC (n=65). Compared to low TC, more patients with middle TC and high TC survived to discharge (9.1% vs. 22.0% and 26.2%, respectively, P=0.001). The good cerebral performance category also increased in that order (4.1 % vs. 14.6% and 23.1%, respectively, P≤0.001). Comparing middle TC and high TC with low TC, adjusted odds ratios (95% confidence intervals) were 1.97 (1.06 to 3.64) and 2.53 (1.08 to 5.92) for survival to discharge, respectively, and 2.53 (1.07 to 5.98) and 4.73 (1.63 to 13.71) for good neurological recovery, respectively. Conclusion Higher cholesterol is associated with better outcomes in OHCA; cholesterol level is a good predictor of outcomes of OHCA

Altered resting-state connectivity in subjects at ultra-high risk for psychosis: an fMRI study

<p>Abstract</p> <p>Background</p> <p>Individuals at ultra-high risk (UHR) for psychosis have self-disturbances and deficits in social cognition and functioning. Midline default network areas, including the medial prefrontal cortex and posterior cingulate cortex, are implicated in self-referential and social cognitive tasks. Thus, the neural substrates within the default mode network (DMN) have the potential to mediate self-referential and social cognitive information processing in UHR subjects.</p> <p>Methods</p> <p>This study utilized functional magnetic resonance imaging (fMRI) to investigate resting-state DMN and task-related network (TRN) functional connectivity in 19 UHR subjects and 20 matched healthy controls. The bilateral posterior cingulate cortex was selected as a seed region, and the intrinsic organization for all subjects was reconstructed on the basis of fMRI time series correlation.</p> <p>Results</p> <p>Default mode areas included the posterior/anterior cingulate cortices, the medial prefrontal cortex, the lateral parietal cortex, and the inferior temporal region. Task-related network areas included the dorsolateral prefrontal cortex, supplementary motor area, the inferior parietal lobule, and middle temporal cortex. Compared to healthy controls, UHR subjects exhibit hyperconnectivity within the default network regions and reduced anti-correlations (or negative correlations nearer to zero) between the posterior cingulate cortex and task-related areas.</p> <p>Conclusions</p> <p>These findings suggest that abnormal resting-state network activity may be related with the clinical features of UHR subjects. Neurodevelopmental and anatomical alterations of cortical midline structure might underlie altered intrinsic networks in UHR subjects.</p

Reduced cortical folding of the anterior cingulate cortex in obsessive-compulsive disorder

Background: Anterior cingulate cortex (ACC) abnormalities have been implicated consistently in the pathophysiology of obsessive-compulsive disorder (OCD), yet it remains unclear whether these abnormalities originated during early neurodevelopment. In this study, we examined the ACC sulcal/gyral patterns to investigate whether neurodevelopmental anomalies of the ACC were present in patients with OCD. We hypothesized that patients with OCD would show reduced cortical folding of the ACC compared with controls. Methods: We used magnetic resonance imaging (MRI) of 169 healthy volunteers and 110 patients with OCD to examine the paracingulate sulcus and cingulate sulcus. We assessed cortical folding patterns according to established classification criteria and constructed 3 categories of paracingulate sulcus morphology according to its presence and anteroposterior extent: "prominent," "present" and "absent." We classified the cingulate sulcus as "interrupted" or "continuous" according to the interruptions in its course. In addition, we evaluated ACC sulcal asymmetry based on interhemispheric comparisons of paracingulate sulcus morphology. Results: Analyses revealed that patients with OCD were significantly less likely than controls to show a well-developed left paracingulate sulcus: 50.0% of patients and 65.1% of controls showed a "prominent" or "present" paracingulate sulcus in the left hemisphere. However, there were no differences in regard to cingulate sulcus continuity, and patients also showed the same leftward ACC sulcal asymmetry as controls. Limitations: Our study was limited by the fact that we obtained the MRI scans from 2 different scanners, and we did not calculate cerebral fissurization as our study was restricted to 1 specific brain region. Moreover, patients and controls differed significantly in terms of sex ratio and IQ, although we controlled these variables as covariates. Conclusion: Our findings imply a subtle deviation in the early neurodevelopment of the ACC in patients with OCD, but the extent to which these anomalies contributed to the pathogenesis of OCD remains unclear. Further studies that link the ACC morphologic anomalies to the pathophysiology of OCD are recommended.This work was supported by Cognitive Neuroscience Program of the Korean Ministry of Science and Technology (M10644020003-08N4402-00310).Jung MH, 2009, PROG NEURO-PSYCHOPH, V33, P605, DOI 10.1016/j.pnpbp.2009.02.017Whittle S, 2009, PSYCHIAT RES-NEUROIM, V172, P68, DOI 10.1016/j.pscychresns.2008.06.005Gu BM, 2008, BRAIN, V131, P155, DOI 10.1093/brain/awm277Fornito A, 2007, ACTA PSYCHIAT SCAND, V116, P467, DOI 10.1111/j.1600-0447.2007.01069.xShin YW, 2007, HUM BRAIN MAPP, V28, P1128, DOI 10.1002/hbm.20338Huster RJ, 2007, NEUROIMAGE, V34, P888, DOI 10.1016/j.neuroimage.2006.10.023De Geus F, 2007, PSYCHIAT CLIN NEUROS, V61, P45, DOI 10.1111/j.1440-1819.2007.01609.xFornito A, 2006, SCHIZOPHR RES, V88, P192, DOI 10.1016/j.schres.2006.06.034Jang JH, 2006, AM J PSYCHIAT, V163, P1202Kim YY, 2006, BRAIN TOPOGR, V18, P201, DOI 10.1007/s10548-006-0269-2Klimkeit EI, 2006, CORTEX, V42, P113Valente AA, 2005, BIOL PSYCHIAT, V58, P479, DOI 10.1016/j.biopsych.2005.04.021Rosenberg DR, 2004, J AM ACAD CHILD PSY, V43, P1146, DOI 10.1097/01.chi.0000132812.44664.2dFornito A, 2004, CEREB CORTEX, V14, P424, DOI 10.1093/cercor/bhh004Shin YW, 2004, PSYCHIAT CLIN NEUROS, V58, P16Yucel M, 2003, BRIT J PSYCHIAT, V182, P518Yucel M, 2002, BIOL PSYCHIAT, V52, P15Lyoo IK, 2001, J CLIN PSYCHIAT, V62, P637Allman JM, 2001, ANN NY ACAD SCI, V935, P107Yucel M, 2001, CEREB CORTEX, V11, P17Bradshaw JL, 2000, BRAIN LANG, V73, P297Bush G, 2000, TRENDS COGN SCI, V4, P215Penalva J, 2000, BIOSENS BIOELECTRON, V15, P99Lohmann G, 1999, CEREB CORTEX, V9, P754Magnotta VA, 1999, CEREB CORTEX, V9, P151Tibbo P, 1999, J PSYCHIATR NEUROSCI, V24, P15Rosenberg DR, 1998, BIOL PSYCHIAT, V43, P623Purcell R, 1998, BIOL PSYCHIAT, V43, P348SAXENA S, 1998, BRIT J PSYCHIAT S, V35, P26FIRST MB, 1998, STRUCTURED CLIN INTESIEGEL S, 1998, NONPARAMETRIC STAT BRauch SL, 1997, J NEUROPSYCH CLIN N, V9, P568Bartley AJ, 1997, BRAIN, V120, P257VanEssen DC, 1997, NATURE, V385, P313Paus T, 1996, CEREB CORTEX, V6, P207FIRST MB, 1996, STRUCTURED CLIN INTEVOGT BA, 1995, J COMP NEUROL, V359, P490DEVINSKY O, 1995, BRAIN, V118, P279ARMSTRONG E, 1995, CEREB CORTEX, V5, P56PAULS DL, 1995, AM J PSYCHIAT, V152, P76KIM JS, 1995, KOREAN J CLIN PSYCHO, V14, P111*AM PSYCH ASS, 1994, DIAGN STAT MAN MENTBAXTER LR, 1992, ARCH GEN PSYCHIAT, V49, P681HUANG CC, 1991, BRAIN DEV-JPN, V13, P27WELKER W, 1990, CEREBRAL CORTEX B, V8, P3DIXON WJ, 1990, BMDP STAT SOFTWARE MHOLLANDER E, 1990, ARCH GEN PSYCHIAT, V47, P27CROW TJ, 1989, ARCH GEN PSYCHIAT, V46, P1145GOODMAN WK, 1989, ARCH GEN PSYCHIAT, V46, P1006GOODMAN WK, 1989, ARCH GEN PSYCHIAT, V46, P1012SWEDO SE, 1989, ARCH GEN PSYCHIAT, V46, P518RAKIC P, 1988, SCIENCE, V241, P170BEAR D, 1986, ARCH NEUROL-CHICAGO, V43, P598GESCHWIND N, 1985, ARCH NEUROL-CHICAGO, V42, P521FLORHENRY P, 1983, CEREBRAL BASIS PSYCH, P301CHI JG, 1977, ANN NEUROL, V1, P86ANNETT M, 1970, BRIT J PSYCHOL, V61, P303CRICHTONBROWNE J, 1879, BRAIN, V2, P42

The effect of meditation on brain structure: cortical thickness mapping and diffusion tensor imaging

A convergent line of neuroscientific evidence suggests that meditation alters the functional and structural plasticity of distributed neural processes underlying attention and emotion. The purpose of this study was to examine the brain structural differences between a well-matched sample of long-term meditators and controls. We employed whole-brain cortical thickness analysis based on magnetic resonance imaging, and diffusion tensor imaging to quantify white matter integrity in the brains of 46 experienced meditators compared with 46 matched meditation-naïve volunteers. Meditators, compared with controls, showed significantly greater cortical thickness in the anterior regions of the brain, located in frontal and temporal areas, including the medial prefrontal cortex, superior frontal cortex, temporal pole and the middle and interior temporal cortices. Significantly thinner cortical thickness was found in the posterior regions of the brain, located in the parietal and occipital areas, including the postcentral cortex, inferior parietal cortex, middle occipital cortex and posterior cingulate cortex. Moreover, in the region adjacent to the medial prefrontal cortex, both higher fractional anisotropy values and greater cortical thickness were observed. Our findings suggest that long-term meditators have structural differences in both gray and white matter

Bowel Preparation for Capsule Endoscopy: A Prospective Randomized Multicenter Study

Background/Aims: The ability to visualize the small bowel mucosa by capsule endoscopy is limited. Moreover, studies involving small-bowel preparation with purgative drugs have failed to establish which preparations produce better images and higher diagnostic yields. The aim of this study was to evaluate the efficacies and diagnostic yields of different bowel preparations. Methods: A cohort of 134 patients with suspected small bowel disease was randomly assigned to 3 groups. Patients in group A (n=44) fasted for 12 h before being administered an M2A capsule (Given Imaging, Yoqneam, Israel). Patients in group B (n=45) were asked to drink two doses of 45 mL of sodium phosphate (NaP) with water during the afternoon and evening on the day before the procedure and to drink at least 2 L of water thereafter. Patients in group C (n=45) drank 2 L of a polyethylene glycol (PEG) lavage solution the evening before the procedure. Results: Overall cleansing of the small bowel was adequate in 43% of patients in group A, 77% of those in group B, and 56% of those in group C (group A vs; group B, p=0.001). Diagnoses for obscure gastrointestinal bleeding were established in 9 patients (39%) in group A, 16 patients (69%) in group B, and 14 patients (50%) in group C. No significant difference in diagnostic yield was observed between groups. Conclusions: Bowel preparation with NaP for capsule endoscopy improved small-bowel mucosal visualization when compared to 12-h overnight fasting. (Gut and Liver 2009;3:180-185)Wei W, 2008, AM J GASTROENTEROL, V103, P77, DOI 10.1111/j.1572-0241.2007.01633.xCheon JH, 2007, GUT LIVER, V1, P118van Tuyl SAC, 2007, ENDOSCOPY, V39, P1037, DOI 10.1055/s-2007-966988Ben-Soussan E, 2005, J CLIN GASTROENTEROL, V39, P381FIREMAN Z, 2005, WORLD J GASTROENTERO, V11, P5863DAI N, 2005, GASTROINTEST ENDOSC, V61, P28Viazis N, 2004, GASTROINTEST ENDOSC, V60, P534Niv Y, 2004, SCAND J GASTROENTERO, V39, P1005, DOI 10.1080/00365520410003209Fireman Z, 2004, ISRAEL MED ASSOC J, V6, P521Albert J, 2004, GASTROINTEST ENDOSC, V59, P487Pennazio M, 2004, GASTROENTEROLOGY, V126, P643, DOI 10.1053/j.gastro.2003.11.057Mylonaki M, 2003, GUT, V52, P1122Costamagna G, 2002, GASTROENTEROLOGY, V123, P999, DOI 10.1053/gast.2002.35988Lewis BS, 2002, GASTROINTEST ENDOSC, V56, P349, DOI 10.1067/mge.2002.126906Kastenberg D, 2001, GASTROINTEST ENDOSC, V54, P705Aronchick CA, 2000, GASTROINTEST ENDOSC, V52, P346

Structural Brain Alterations in Individuals at Ultra-high Risk for Psychosis: A Review of Magnetic Resonance Imaging Studies and Future Directions

Individuals at ultra-high-risk (UHR) for psychosis have become a major focus for research designed to explore markers for early detection of and clinical intervention in schizophrenia. In particular, structural magnetic resonance imaging studies in UHR individuals have provided important insight into the neurobiological basis of psychosis and have shown the brain changes associated with clinical risk factors. In this review, we describe the structural brain abnormalities in magnetic resonance images in UHR individuals. The current accumulated data demonstrate that abnormalities in the prefrontal and temporal cortex and anterior cingulate cortex occur before illness onset. These regions are compatible with the regions of structural deficits found in schizophrenia and first-episode patients. In addition, the burgeoning evidence suggests that such structural abnormalities are potential markers for the transition to psychosis. However, most findings to date are limited because they are from cross-sectional rather than longitudinal studies. Recently, researchers have emphasized neurodevelopmental considerations with respect to brain structural alterations in UHR individuals. Future studies should be conducted to characterize the differences in the brain developmental trajectory between UHR individuals and healthy controls using a longitudinal design. These new studies should contribute to early detection and management as well as provide more predictive markers of later psychosis

Disproportionate Alterations in the Anterior and Posterior Insular Cortices in Obsessive–Compulsive Disorder

Recent studies have reported that the insular cortex is involved in the pathophysiology of obsessive–compulsive disorder (OCD). However, specific morphometric abnormalities of the insular subregions remain unclear. In this study, we examined insular cortical volume to determine whether the volume of the anterior and posterior insular cortices of unmedicated OCD patients differed according to different symptom dimensions.Using magnetic resonance imaging, we measured the gray matter volumes of the insular cortex and its subregions (anterior and posterior divisions) in 41 patients with OCD (31 drug-naïve and 10 non-medicated) and 53 healthy controls. Volumetric measures of the insular cortex were compared according to different OC symptoms. Enlarged anterior and reduced posterior insular cortices were observed in OCD patients. The insular volumetric alterations were more significant in OCD patients with predominant checking rather than cleaning symptoms when compared with healthy controls.Our results suggest the presence of unbalanced anterior and posterior insular volumetric abnormalities in unmedicated OCD patients and emphasize the distinct role of the insular cortex in different OC symptoms. We propose that the insular morphometric alterations may influence the modulation of interoceptive processing, the insular functional role, in OCD patients with different symptoms

Importance of Angiographic Visualization of Round Ligament Arteries in Women Evaluated for Intractable Vaginal Bleeding after Uterine Artery Embolization

PURPOSE: To determine the incidence of angiographic visualization and the clinical significance of round ligament arteries in patients who present with intractable vaginal bleeding. MATERIALS AND METHODS: A review of 113 patients (age range, 20-67 years) who underwent pelvic angiography for intractable vaginal bleeding between June 1992 and May 2008 was retrospectively performed. It was recorded whether round ligament artery was visualized on pelvic aortography after uterine artery embolization (UAE). The medical records of the patients were reviewed to analyze the final clinical outcome. The Fisher exact test was used to correlate persistent vaginal bleeding after UAE with visualization of round ligament arteries. RESULTS: Of 111 patients who underwent UAE, 42 patients (postpartum bleeding, n = 40; postabortion bleeding, n = 2) had at least one visible round ligament artery on postembolization pelvic aortography. Ten patients received round ligament artery embolization. Persistent vaginal bleeding after adequate UAE was observed more commonly in patients whose round ligament artery was seen on postembolization pelvic aortography (P = .007). CONCLUSIONS: Round ligament arteries are commonly visualized in patients who present with postpartum bleeding and should be investigated when there is persistent bleeding, even after adequate UAE.Kim HS, 2008, J VASC INTERV RADIOL, V19, P195, DOI 10.1016/j.jvir.2007.08.014STANDRING S, 2008, GRAYS ANATOMY, P1279Naydich M, 2007, J VASC INTERV RADIOL, V18, P1047, DOI 10.1016/j.jvir.2007.05.013White AM, 2007, RADIOLOGY, V244, P291, DOI 10.1148/radiol.2441060796Kim HS, 2006, J VASC INTERV RADIOL, V17, P783, DOI 10.1097/01.RVI.0000209342.02567.C2ABADA HT, 2006, COMPREHENSIVE APPROA, V1Spies JB, 2004, J VASC INTERV RADIOL, V15, P111, DOI 10.1097/01.RVI.0000109407.52762.D1Razavi MK, 2002, RADIOLOGY, V224, P707, DOI 10.1148/radiol.2243011513Saraiya PV, 2002, J VASC INTERV RADIOL, V13, P939Chrisman HB, 2000, J VASC INTERV RADIOL, V11, P699Pelage JP, 1999, RADIOLOGY, V212, P385Pelage JP, 1999, AM J ROENTGENOL, V172, P989Pelage JP, 1998, RADIOLOGY, V208, P359StancatoPasik A, 1997, RADIOLOGY, V204, P791GREENWOOD LH, 1987, RADIOLOGY, V164, P155

Preprocessed MR images, demographics and clinical assessments

You can find preprocessed magnetic resonance (MR) images, demographics of 30 patients with obsessive-compulsive disorder (OCD) and 34 age-/sex-matched healthy controls that were analyzed in the original article. Clinical assessments of Y-BOCS (Yale-Brown obsessive-compulsive scale) for the patients are included in the file