Clinical Manifestations of Recurrent Parotid Pleomorphic Adenoma

Objectives. This study was undertaken to confirm the clinical characteristics of recurrent pleomorphic adenoma (RPA), and to identify those factors that affect the development of malignant transformation (MT) from RPA. Methods. The medical records of 270 patients, who were operated upon for parotid PA, were retrospectively reviewed. The pathologic specimens of a selected series of 23 patients were reviewed for histologic subtype and microscopic multi-nodularity. Results. Mean age of initial operation in RPA without MT (RPA(-MT)) group was significantly lower than that of primary PA group. Mean age of the revision operation in RPA with MT (RPA(+MT)) group was significantly greater than that of RPA(-MT) group. Mean interval from operation to recurrence shortened after each revision operation. The risk of MT and additional recurrence increased significantly with recurrence. In RPA(-MT) group tumor recurrence occurred in 21.4% of patients despite a clear resection margin. Conclusion. The risk factors for MT may be an age of over 45 yr and multiple recurrences. However, younger patients are more at risk of recurrence. A clear resection margin cannot guarantee a cure in RPA, and it seems that parotid pleomorphic adenomas slowly gain malignant characteristics after repeated recurrences.SUH MW, 2005, KOREAN J HEAD NECK O, V21, P146HANNA EY, 2005, CUMMINGS OTOLARYNGOL, P1348Ghosh S, 2003, CLIN OTOLARYNGOL, V28, P262Glas AS, 2002, CANCER, V94, P2211, DOI 10.1002/cncr.10445Glas AS, 2001, HEAD NECK-J SCI SPEC, V23, P311BRADLEY PJ, 2001, CURR OPIN OTOLARYNGO, V9, P100Carew JF, 1999, OTOLARYNG HEAD NECK, V121, P539Junquera L, 1999, HEAD NECK-J SCI SPEC, V21, P652Hancock BD, 1999, ANN ROY COLL SURG, V81, P299Bankamp DG, 1999, LARYNGO RHINO OTOL, V78, P77Hoorweg JJ, 1998, EUR J SURG ONCOL, V24, P452Henriksson G, 1998, CANCER, V82, P617Laskawi R, 1998, BRIT J ORAL MAX SURG, V36, P48Klijanienko J, 1997, HEAD NECK-J SCI SPEC, V19, P629Leverstein H, 1997, EUR ARCH OTO-RHINO-L, V254, P313SunardhiWidyaputra S, 1995, PATHOL RES PRACT, V191, P1186PHILLIPS PP, 1995, ANN OTO RHINOL LARYN, V104, P100BUCHMAN C, 1994, LARYNGOSCOPE, V104, P1231NATVIG K, 1994, HEAD NECK-J SCI SPEC, V16, P213JACKSON SR, 1993, J LARYNGOL OTOL, V107, P546MCGREGOR AD, 1988, BRIT J PLAST SURG, V41, P177FEE WE, 1978, LARYNGOSCOPE, V88, P265SEIFERT G, 1976, HNO, V24, P415NAEIM F, 1976, ARCH PATHOL LAB MED, V100, P271FRAZELL EL, 1954, CANCER, V7, P637

Gender Difference in the Prodromal Symptoms of First-episode Schizophrenia

To investigate the gender difference of early symptoms appearing before the onset of the psychotic symptoms in patients with first-episode schizophrenia, we reviewed the medical records of 63 patients (38 males, 25 females), who were hospitalized for first-episode schizophrenia. The frequency and duration of prodromal and psychotic symptoms, Clinical Global Impression scale scores, Global Assessment of Functioning (GAF) scale scores at admission, and other clinical characteristics were recorded for all patients. Overall, the most common prodromal symptoms were attenuated positive symptoms (89%), followed by mood symptoms (86%). Negative symptoms were the most common in male patients (97.4%), whereas attenuated positive symptoms were the most common in female patients (84%). Male patients demonstrated more frequent negative, cognitive, and obsessive-compulsive symptoms than female patients did and also showed a tendency of having negative symptoms for the longer period. Correlational analysis showed a significant negative correlation between the duration of negative symptoms and GAF scores at admission in male patients. Our findings suggest that different patterns of prodromal symptoms between male and female begin before the onset of the psychosis. Further prospective studies should be needed.This paper was supported by a grant (M103KV010012- 08K2201-01210) from Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology, Republic of Korea.Jeppesen P, 2008, PSYCHOL MED, V38, P1157, DOI 10.1017/S0033291708003449Cannon TD, 2008, ARCH GEN PSYCHIAT, V65, P28WILLHITE RK, 2008, SCHIZOPHR RES, V104, P237LAPPIN JM, 2007, BR J PSYCHIAT S, V51, pS123Goldstein JM, 2006, HORM BEHAV, V50, P612, DOI 10.1016/j.yhbeh.2006.06.029Rosen JL, 2006, SCHIZOPHR RES, V85, P124, DOI 10.1016/j.schres.2006.03.034Amminger GP, 2006, SCHIZOPHR RES, V84, P67, DOI 10.1016/j.schres.2006.02.018Barbui C, 2005, J CLIN PSYCHOPHARM, V25, P521, DOI 10.1097/01.jcp.0000185423.15891.02Perkins DO, 2005, AM J PSYCHIAT, V162, P1785Svirskis T, 2005, SCHIZOPHR RES, V75, P439, DOI 10.1016/j.schres.2004.11.002Norman RMG, 2005, J NERV MENT DIS, V193, P17, DOI 10.1097/01.nmd.0000149214.17924.d9Yung AR, 2004, SCHIZOPHR RES, V67, P131, DOI 10.1016/S0920-9964(03)00192-0Lieberman JA, 2003, AM J PSYCHIAT, V160, P1396McGlashan TH, 2003, SCHIZOPHR RES, V61, P7, DOI 10.1016/S0920-9964(02)00439-5Kinon BJ, 2003, PSYCHONEUROENDOCRINO, V28, P55, DOI 10.1016/S0306-4530(02)00127-0McGorry PD, 2002, ARCH GEN PSYCHIAT, V59, P921Gourzis P, 2002, SCHIZOPHRENIA BULL, V28, P415Norman RMG, 2001, PSYCHOL MED, V31, P381Bottlender R, 2000, SCHIZOPHR RES, V44, P145Cohen RZ, 2000, CAN J PSYCHIAT, V45, P544LEUNG A, 2000, ACTA PSYCHIAT SCAN S, V401, P3GOLDSTEIN JM, 2000, WOMEN SCHIZOPHRENIA, P111Hafner H, 1999, ACTA PSYCHIAT SCAND, V100, P105Pohjalainen T, 1998, MOL PSYCHIATR, V3, P256Behl C, 1997, MOL PHARMACOL, V51, P535Yung AR, 1996, AUST NZ J PSYCHIAT, V30, P587Larsen TK, 1996, SCHIZOPHRENIA BULL, V22, P241FOLNEGOVIC Z, 1994, SCHIZOPHR RES, V14, P83HAFNER H, 1993, BRIT J PSYCHIAT, V162, P80HAFNER H, 1992, SCHIZOPHR RES, V6, P209

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

Geochemical and Geomechanical Effects on Wellbore Cement Fractures: Data Information for Wellbore Reduced Order Model

The primary objective of the National Risk Assessment Partnership (NRAP) program is to develop a defensible, generalized, and science-based methodology and platform for quantifying risk profiles at CO2 injection and storage sites. The methodology must incorporate and define the scientific basis for assessing residual risks associated with long-term stewardship and help guide site operational decision-making and risk management. Development of an integrated and risk-based protocol will help minimize uncertainty in the predicted long-term behavior of the CO2 storage site and thereby increase confidence in storage integrity. The risk profile concept has proven useful in conveying the qualitative evolution of risks for CO2 injection and storage site. However, qualitative risk profiles are not sufficient for specifying long-term liability for CO2 storage sites. Because there has been no science-based defensible and robust methodology developed for quantification of risk profiles for CO2 injection and storage, NRAP has been focused on developing a science-based methodology for quantifying risk profiles for various risk proxies

Association between Participation in a Rehabilitation Program and 1-Year Survival in Patients Requiring Prolonged Mechanical Ventilation

Background The present study evaluated the association between participation in a rehabilitation program during a hospital stay and 1-year survival of patients requiring at least 21 days of mechanical ventilation (prolonged mechanical ventilation [PMV]) with various respiratory diseases as their main diagnoses that led to mechanical ventilation. Methods Retrospective data of 105 patients (71.4% male, mean age 70.1±11.3 years) who received PMV in the past 5 years were analyzed. Rehabilitation included physiotherapy, physical rehabilitation, and dysphagia treatment program that was individually provided by physiatrists. Results The main diagnosis leading to mechanical ventilation was pneumonia (n=101, 96.2%) and the 1-year survival rate was 33.3% (n=35). One-year survivors had lower Acute Physiology and Chronic Health Evaluation (APACHE) II score (20.2±5.8 vs. 24.2±7.5, p=0.006) and Sequential Organ Failure Assessment score (6.7±5.6 vs. 8.5±2.7, p=0.001) on the day of intubation than non-survivors. More survivors participated in a rehabilitation program during their hospital stays (88.6% vs. 57.1%, p=0.001). The rehabilitation program was an independent factor for 1-year survival based on the Cox proportional hazard model (hazard ratio, 3.513; 95% confidence interval, 1.785 to 6.930; p<0.001) in patients with APACHE II scores ≤23 (a cutoff value based on Youden’s index). Conclusion Our study showed that participation in a rehabilitation program during hospital stay was associated with an improvement of 1-year survival of PMV patients who had less severe illness on the day of intubation

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