Dysfunction in Configural Face Processing in Patients With Schizophrenia

Background: Face recognition has important implications for patients with schizophrenia, who exhibit poor interpersonal and social skills. Previous reports have suggested that patients with schizophrenia have deficits in their ability to recognize faces, and because face recognition relies heavily on information about the configuration of faces, we hypothesized that patients with schizophrenia would have specific problems in processing configural information. Methods: We measured the performance of 20 patients with schizophrenia and 20 normal subjects in a face-discrimination task, using upright and inverted pairs of face photographs that differed in featural or configural information. Results: The patients with schizophrenia showed disproportionately poorer performance in discriminating configural compared with featural face sets. Conclusion: The result suggests that the face-recognition deficit in schizophrenic patients is due to specific impairments in configural processing of faces

Polarity of the First Episode and Time to Diagnosis of Bipolar I Disorder

Objective The current study explored the relationship between the polarity of the first episode and the timing of eventual diagnosis of bipolar I disorder, and associated clinical implications. Methods Twelve years of clinical data from the medical records of 258 inpatients meeting DSM-III-R or DSM-IV criteria for bipolar I disorder were analyzed. Subjects were divided into two groups according to the polarity of the first episode: those with depressive polarity (FE-D), and those with manic polarity (FE-M). Comparisons were made between the two groups on variables associated with the timing of diagnosis and related outcomes. Results In Population with bipolar I disorder, a significant longer time lapse from the first major mood episode to the confirmed diagnosis was associated with the FE-D group compared to the FE-M group [5.6 (+/- 6.1) vs. 2.5 (+/- 5.5) years, p<0.001]. FE-D subjects tended to have prior diagnoses of schizophrenia and major depressive disorder while FE-M subjects tended to have prior diagnoses of bipolar disorder and schizophrenia. A significantly higher rate of suicide attempts was associated with the FE-D group compared to the FE-M group (12.7 vs. 1.7%, p<0.001). Conclusion The results of this study indicate that first-episode depressive polarity is likely to be followed by a considerable delay until an eventual confirmed diagnosis of bipolar I disorder. Given that first-episode depressive patients are particularly vulnerable to unfavorable clinical Outcomes Such as suicide attempts, a more systematic approach is needed to differentiate bipolar disorder among depressed patients in their early stages.Rosa AR, 2008, J AFFECT DISORDERS, V107, P45, DOI 10.1016/j.jad.2007.07.021Chaudhury SR, 2007, J AFFECT DISORDERS, V104, P245, DOI 10.1016/j.jad.2007.02.022Berk M, 2007, J AFFECT DISORDERS, V103, P181, DOI 10.1016/j.jad.2007.01.027Benazzi F, 2007, LANCET, V369, P935GOODWIN FK, 2007, MANIC DEPRESSIVE ILLDaban C, 2006, COMPR PSYCHIAT, V47, P433, DOI 10.1016/j.comppsych.2006.03.009McElroy SL, 2006, BIPOLAR DISORD, V8, P596Kassem L, 2006, AM J PSYCHIAT, V163, P1754Colom F, 2006, J AFFECT DISORDERS, V93, P13, DOI 10.1016/j.jad.2006.01.032Perlis RH, 2005, AM J MANAG CARE, V11, pS271Perlis RH, 2005, BIOL PSYCHIAT, V58, P549, DOI 10.1016/j.biopsych.2005.07.029Gazalle FK, 2005, J AFFECT DISORDERS, V86, P313, DOI 10.1016/j.jad.2005.01.003Ghaemi SN, 2005, J AFFECT DISORDERS, V84, P273, DOI 10.1016/S0165-0327(03)00196-4Post JC, 2005, CURR OPIN ALLERGY CL, V5, P5Mitchell PB, 2004, BIPOLAR DISORD, V6, P530Goodwin FK, 2003, JAMA-J AM MED ASSOC, V290, P1467Morselli PL, 2003, BIPOLAR DISORD, V5, P265Daniels BA, 2003, J AFFECT DISORDERS, V75, P163, DOI 10.1016/S0165-0327(02)00041-1Baethge C, 2003, ACTA PSYCHIAT SCAND, V107, P260Hirschfeld RMA, 2003, J CLIN PSYCHIAT, V64, P161Goldberg JF, 2002, J CLIN PSYCHIAT, V63, P985Ghaemi SN, 2002, CAN J PSYCHIAT, V47, P125Suppes T, 2001, J AFFECT DISORDERS, V67, P45Hirsch M, 2001, YALE J CRIT, V14, P5Bowden CL, 2001, PSYCHIATR SERV, V52, P51Hirschfeld RMA, 2000, AM J PSYCHIAT, V157, P1873Ghaemi SN, 2000, J CLIN PSYCHIAT, V61, P804Perugi G, 2000, COMPR PSYCHIAT, V41, P13GHAEMI SN, 2000, J CLIN PSYCHIAT, V61, P809Ghaemi SN, 1999, J AFFECT DISORDERS, V52, P135Baldessarini RJ, 1999, J CLIN PSYCHIAT, V60, P77BALDESSARINI RJ, 1999, J CLIN PSYCHIAT S2, V60, P111LISH JD, 1994, J AFFECT DISORDERS, V31, P281WEHR TA, 1988, AM J PSYCHIAT, V145, P179

Interaction Studies between Newly Synthesized Photosensitive Polymer and Ionic Liquids

In this information age, different kinds of photosensitive materials have been used in the manufacture of information storage devices. But these photosensitive materials have the bane of low diffraction efficiency. In order to solve this problem, we have synthesized a novel photosensitive polymer from epoxy-based azopolymers (with three types of azochromophores). Furthermore, we have studied the interaction between this newly synthesized azopolymer and ionic liquids (ILs). For this purpose, we have used the ammonium and imidazolium families of ILs, such as diethylammonium dihydrogen phosphate (DEAP), tributylammonium methyl sulfate (TBMS), triethylammonium 4-aminotoluene-3-sulfonic acid (TASA), and 1-methylimidazolium chloride ([Mim]Cl). To investigate the molecular interaction between azopolymer and ILs, we have used the following spectroscopic methods of analysis: UV-visible spectroscopy, photoluminescence (PL) spectroscopy, Fourier transformed infrared spectroscopy (FT-IR), and confocal Raman spectroscopy. In this study, we have developed new photosensitive materials by combining polymer with ILs

Cortical thinning in obsessive compulsive disorder

Abstract: Although studies of obsessive-compulsive disorder (OCD) over the last 20 years have suggested abnormalities in frontal-subcortical circuitry, evidences of structural abnormalities in those areas are still imperfect and contradictory. With recent advances in neuroimaging technology, it is now possible to study cortical thickness based on cortical surfaces, which offers a direct quantitative index of cortical mass. Using the constrained Laplacian-based automated segmentation with proximities (CLASP) algorithm, we measured cortical thickness of 55 patients with OCD (33 men and 22 women) and 52 ageand sex-matched healthy volunteers (32 men and 20 women). We found multiple regions of cortical thinning in OCD patients compared to the normal control group. Patients with OCD had thinner left inferior frontal, left middle frontal, left precentral, left superior temporal, left parahippocampal, left orbitofrontal, and left lingual cortices. Most thinned regions were located in the left ventral cortex system, providing a new perspective that this ventral cortical system may be involved in the pathophysiology of OCD

Regional brain gray matter abnormalities in patients with bipolar II disorder: A comparison study with bipolar I patients and healthy controls

Despite the high prevalence and clinical significance of bipolar II disorder (BD II), the underlying pathophysiology is not well explored in previous studies. The purpose of the current study was to investigate brain gray matter abnormalities in BD II. High resolution magnetic resonance brain images from 23 BD II patients, 23 sex- and age-matched patients with bipolar I disorder (BD I) and 23 healthy controls were acquired and processed according to the optimized voxel-based morphometry protocol. The processed gray matter tissue volumes were compared among the three groups. Both the BD II and BD I group showed gray matter deficits in the ventromedial prefrontal regions, compared to controls. The BD I group had widespread gray matter reductions in the bilateral frontal, temporal, parietal and parahippocampal cortices, compared to controls. However, gray matter reductions in these regions were not found in the BD II group. With a less conservative statistical threshold, the BD II group showed additional gray matter deficits in the anterior limbic cortices. Our data suggest that gray matter deficits in the ventromedial prefrontal and anterior limbic cortices are common in both BD II and BD I. On the other hand, different pattern of gray matter abnormalities between BY II and BD I found in this study supports that two subtypes may have different neurobiological characteristics.Killgore WDS, 2008, NEUROREPORT, V19, P1523, DOI 10.1097/WNR.0b013e328310af58Kempton MJ, 2008, ARCH GEN PSYCHIAT, V65, P1017Konarski JZ, 2008, BIPOLAR DISORD, V10, P1SIMOENS S, 2008, J MED ECON, V11, P245Merikangas KR, 2007, ARCH GEN PSYCHIAT, V64, P543Maina G, 2007, J CLIN PSYCHIAT, V68, P207Torrent C, 2006, BRIT J PSYCHIAT, V189, P254, DOI 10.1192/bjp.bp.105.017269Kronhaus DM, 2006, BIPOLAR DISORD, V8, P28Cotter D, 2005, BIPOLAR DISORD, V7, P358Adler CM, 2005, BIOL PSYCHIAT, V58, P151, DOI 10.1016/j.biopsych.2005.03.022Haznedar MM, 2005, BIOL PSYCHIAT, V57, P733, DOI 10.1016/j.biopsych.2005.01.002Strakowski SM, 2005, MOL PSYCHIATR, V10, P105, DOI 10.1038/sj.mp.4001585McDonald C, 2004, BIOL PSYCHIAT, V56, P411, DOI 10.1016/j.biopsych.2004.06.021Wilke M, 2004, PSYCHIAT RES-NEUROIM, V131, P57, DOI 10.1016/j.pscychresns.2004.01.004MCGRATH BM, 2004, CAN J PSYCHIAT, V49, P794Lyoo IK, 2003, BIPOLAR DISORD, V5, P300Judd LL, 2003, ARCH GEN PSYCHIAT, V60, P261Lopez-Larson MP, 2002, BIOL PSYCHIAT, V52, P93Cardinal RN, 2002, NEUROSCI BIOBEHAV R, V26, P321Genovese CR, 2002, NEUROIMAGE, V15, P870, DOI 10.1006/nimg.2001.1037McMahon FJ, 2001, ARCH GEN PSYCHIAT, V58, P1025Good CD, 2001, NEUROIMAGE, V14, P21, DOI 10.1006/nimg.2001.0786Hauser P, 2000, J AFFECT DISORDERS, V60, P25Akiskal HS, 2000, J AFFECT DISORDERS, V59, pS5Elliott R, 2000, J NEUROSCI, V20, P6159Blumberg HP, 1999, AM J PSYCHIAT, V156, P1986Rihmer Z, 1999, PSYCHIAT CLIN N AM, V22, P667Drevets WC, 1999, ANN NY ACAD SCI, V877, P614Angst J, 1998, J AFFECT DISORDERS, V50, P143FIRST MB, 1996, STRUCTURED CLIN INTEALTSHULER LL, 1995, AM J PSYCHIAT, V152, P1139*AM PSYCH ASS, 1994, DIAGN STAT MAN MENTSIMPSON SG, 1993, AM J PSYCHIAT, V150, P901HEUN R, 1993, ACTA PSYCHIAT SCAND, V87, P279DUNNER DL, 1976, BIOL PSYCHIAT, V11, P31HAMILTON M, 1960, J NEUROL NEUROSUR PS, V23, P56HOLLINGSHEAD AB, 1958, SOCIAL CLASS MENTAL1

Impact of Anxiety Disorder on Gray Matter Volume Changes in Patients with Bipolar II Disorder

Background: Comorbid anxiety disorders are frequently found in patients with bipolar disorder and may complicate the treatment of the disorder. Little is known about the interplay between bipolar disorder and anxiety disorder. The purpose of the current study was to investigate the effects of comorbid anxiety disorders on volumetric changes in brain of patients with bipolar II disorder.

Emergency department visits for panic attacks and ambient temperature: A time-stratified case-crossover analysis

Background Panic disorder is a common anxiety disorder affecting up to 5% of the population. Although its pathogenesis is unclear, evidence about its association with ambient temperature is limited. We aimed to investigate the association between short-term exposure to increased ambient temperature and exacerbation of panic attacks requiring emergency department visits. Methods From the national emergency database of South Korea, we identified 1,926 patients who presented with panic attacks at the emergency department in Seoul from 2008 to 2014. Using a time-stratified case-crossover design and conditional logistic regression analysis, we compared ambient temperature levels on emergency department visits and correspondingly matched-control days. Results Increased ambient temperature levels were significantly associated with panic attacks. The risk of a panic attack increased by 2.2% (95% confidence interval, 0.7-3.8%) per every 1 degrees C increase in temperature. This association was significant after adjusting for air pollutants. Conclusions Our results provide new evidence that short-term exposure to increased ambient temperature may increase the risk of exacerbation of panic attacks. These findings may provide a basis for further research to establish the association between panic attacks and ambient temperature, thus establishing preventive measures for panic attacks.N

Feasibility of a slower lamotrigine titration schedule for bipolar depression: a naturalistic study

The development of a skin rash is often associated with a rapid escalation of lamotrigine dose. We used lamotrigine to treat 259 patients with Diagnostic and Statistical Manual of Mental Disorders, 4th edition, bipolar depression using either the standard titration schedule (n=132) or a slower titration schedule (n=127) and compared the clinical efficacy and safety of both groups. Clinical efficacy of lamotrigine treatment was assessed using changes in the Clinical Global Impression Scale for Bipolar Disorder-Modified scores during the course of the 12-week treatment A significant reduction of the Clinical Global Impression Scale for Bipolar Disorder-Modified score was observed in both groups and the effect size was large for both groups (standard, 0.75; slower, 0.71). A mixed-effect model of repeated measurement. revealed an increased rate of improvement in the standard titration group that was significant during the first 5 weeks (P<0.001) but became nonsignificant by the final 7 weeks of treatment. The statistically significant reduction in the development of rashes (P=0.005) was a major advantage for patients in the slower titration group. Although the standard titration schedule generally led to faster recovery from depressive symptoms, the slower titration schedule may be an option for patients with a high risk of rash development.Ketter TA, 2008, J PSYCHIATR RES, V43, P13, DOI 10.1016/j.jpsychires.2008.02.007Calabrese JR, 2008, BIPOLAR DISORD, V10, P323Alvestad S, 2007, EPILEPSIA, V48, P1360, DOI 10.1111/j.1528-1167.2007.01109.xKeck PE, 2007, CNS SPECTRUMS, V12, P1Man CBL, 2007, EPILEPSIA, V48, P1015, DOI 10.1111/j.1528-1167.2007.01022.xHirsch LJ, 2006, EPILEPSIA, V47, P318Ostacher MJ, 2006, J CLIN PSYCHIAT, V67, P18*GLAXOSMITHKLINE, 2006, PRESCR INF LAM LAM TKetter TA, 2005, J CLIN PSYCHIAT, V66, P642P-Codrea S, 2005, ACTA NEUROL SCAND, V111, P191, DOI 10.1111/j.1600-0404.2005.00381.xSilverstone PH, 2004, INT CLIN PSYCHOPHARM, V19, P113, DOI 10.1091/01.yic.0000125754.83499.55Chung WH, 2004, NATURE, V428, P486, DOI 10.1038/428486aGueorguieva R, 2004, ARCH GEN PSYCHIAT, V61, P310Katz MM, 2004, NEUROPSYCHOPHARMACOL, V29, P566, DOI 10.1038/sj.npp.1300341Goodwin GM, 2004, J CLIN PSYCHIAT, V65, P432Calabrese JR, 2003, J CLIN PSYCHIAT, V64, P1013Bowden CL, 2003, ARCH GEN PSYCHIAT, V60, P392Choi H, 2003, EXPERT OPIN PHARMACO, V4, P243Calabrese JR, 2002, J CLIN PSYCHIAT, V63, P1012Calabrese JR, 2002, J CLIN PSYCHIAT, V63, P18Frye MA, 2000, J CLIN PSYCHOPHARM, V20, P607Rzany B, 1999, LANCET, V353, P2190Calabrese JR, 1999, J CLIN PSYCHIAT, V60, P79Messenheimer JA, 1998, CAN J NEUROL SCI, V25, pS14Spearing MK, 1997, PSYCHIAT RES, V73, P159COHEN J, 1988, STAT POWER ANAL BEHA