TY  - JOUR
A1  - Bousquet, J.
A1  - Farrell, J.
A1  - Crooks, G.
A1  - Hellings, P.
A1  - Bel, E. H.
A1  - Bewick, M.
A1  - Chavannes, N. H.
A1  - Correia de Sousa, J.
A1  - Cruz, A. A.
A1  - Haahtela, T.
A1  - Joos, G.
A1  - Khaltaev, N.
A1  - Malva, J.
A1  - Muraro, A.
A1  - Nogues, M.
A1  - Palkonen, S.
A1  - Pedersen, S.
A1  - Robalo-Cordeiro, C.
A1  - Samolinski, B.
A1  - Strandberg, T.
A1  - Valiulis, A.
A1  - Yorgancioglu, A.
A1  - Zuberbier, T.
A1  - Bedbrook, A.
A1  - Aberer, W.
A1  - Adachi, M.
A1  - Agusti, A.
A1  - Akdis, C. A.
A1  - Akdis, M.
A1  - Ankri, J.
A1  - Alonso, A.
A1  - Annesi-Maesano, I.
A1  - Ansotegui, I. J.
A1  - Anto, J. M.
A1  - Arnavielhe, S.
A1  - Arshad, H.
A1  - Bai, C.
A1  - Baiardini, I.
A1  - Bachert, C.
A1  - Baigenzhin, A. K.
A1  - Barbara, C.
A1  - Bateman, E. D.
A1  - Beghé, B.
A1  - Ben Kheder, A.
A1  - Bennoor, K. S.
A1  - Benson, M.
A1  - Bergmann, K. C.
A1  - Bieber, T.
A1  - Bindslev-Jensen, C.
A1  - Bjermer, L.
A1  - Blain, H.
A1  - Blasi, F.
A1  - Boner, A. L.
A1  - Bonini, M.
A1  - Bonini, S.
A1  - Bosnic-Anticevitch, S.
A1  - Boulet, L. P.
A1  - Bourret, R.
A1  - Bousquet, P. J.
A1  - Braido, F.
A1  - Briggs, A. H.
A1  - Brightling, C. E.
A1  - Brozek, J.
A1  - Buhl, R.
A1  - Burney, P. G.
A1  - Bush, A.
A1  - Caballero-Fonseca, F.
A1  - Caimmi, D.
A1  - Calderon, M. A.
A1  - Calverley, P. M.
A1  - Camargos, P. A. M.
A1  - Canonica, G. W.
A1  - Camuzat, T.
A1  - Carlsen, K. H.
A1  - Carr, W.
A1  - Carriazo, A.
A1  - Casale, T.
A1  - Cepeda Sarabia, A. M.
A1  - Chatzi, L.
A1  - Chen, Y. Z.
A1  - Chiron, R.
A1  - Chkhartishvili, E.
A1  - Chuchalin, A. G.
A1  - Chung, K. F.
A1  - Ciprandi, G.
A1  - Cirule, I.
A1  - Cox, L.
A1  - Costa, D. J.
A1  - Custovic, A.
A1  - Dahl, R.
A1  - Dahlen, S. E.
A1  - Darsow, U.
A1  - De Carlo, G.
A1  - De Blay, F.
A1  - Dedeu, T.
A1  - Deleanu, D.
A1  - De Manuel Keenoy, E.
A1  - Demoly, P.
A1  - Denburg, J. A.
A1  - Devillier, P.
A1  - Didier, A.
A1  - Dinh-Xuan, A. T.
A1  - Djukanovic, R.
A1  - Dokic, D.
A1  - Douagui, H.
A1  - Dray, G.
A1  - Dubakiene, R.
A1  - Durham, S. R.
A1  - Dykewicz, M. S.
A1  - El-Gamal, Y.
A1  - Emuzyte, R.
A1  - Fabbri, L. M.
A1  - Fletcher, M.
A1  - Fiocchi, A.
A1  - Fink Wagner, A.
A1  - Fonseca, J.
A1  - Fokkens, W. J.
A1  - Forastiere, F.
A1  - Frith, P.
A1  - Gaga, M.
A1  - Gamkrelidze, A.
A1  - Garces, J.
A1  - Garcia-Aymerich, J.
A1  - Gemicioğlu, B.
A1  - Gereda, J. E.
A1  - González Diaz, S.
A1  - Gotua, M.
A1  - Grisle, I.
A1  - Grouse, L.
A1  - Gutter, Z.
A1  - Guzmán, M. A.
A1  - Heaney, L. G.
A1  - Hellquist-Dahl, B.
A1  - Henderson, D.
A1  - Hendry, A.
A1  - Heinrich, J.
A1  - Heve, D.
A1  - Horak, F.
A1  - Hourihane, J. O’. B.
A1  - Howarth, P.
A1  - Humbert, M.
A1  - Hyland, M. E.
A1  - Illario, M.
A1  - Ivancevich, J. C.
A1  - Jardim, J. R.
A1  - Jares, E. J.
A1  - Jeandel, C.
A1  - Jenkins, C.
A1  - Johnston, S. L.
A1  - Jonquet, O.
A1  - Julge, K.
A1  - Jung, K. S.
A1  - Just, J.
A1  - Kaidashev, I.
A1  - Kaitov, M. R.
A1  - Kalayci, O.
A1  - Kalyoncu, A. F.
A1  - Keil, T.
A1  - Keith, P. K.
A1  - Klimek, L.
A1  - Koffi N’Goran, B.
A1  - Kolek, V.
A1  - Koppelman, G. H.
A1  - Kowalski, M. L.
A1  - Kull, I.
A1  - Kuna, P.
A1  - Kvedariene, V.
A1  - Lambrecht, B.
A1  - Lau, S.
A1  - Larenas‑Linnemann, D.
A1  - Laune, D.
A1  - Le, L. T. T.
A1  - Lieberman, P.
A1  - Lipworth, B.
A1  - Li, J.
A1  - Lodrup Carlsen, K.
A1  - Louis, R.
A1  - MacNee, W.
A1  - Magard, Y.
A1  - Magnan, A.
A1  - Mahboub, B.
A1  - Mair, A.
A1  - Majer, I.
A1  - Makela, M. J.
A1  - Manning, P.
A1  - Mara, S.
A1  - Marshall, G. D.
A1  - Masjedi, M. R.
A1  - Matignon, P.
A1  - Maurer, M.
A1  - Mavale‑Manuel, S.
A1  - Melén, E.
A1  - Melo‑Gomes, E.
A1  - Meltzer, E. O.
A1  - Menzies‑Gow, A.
A1  - Merk, H.
A1  - Michel, J. P.
A1  - Miculinic, N.
A1  - Mihaltan, F.
A1  - Milenkovic, B.
A1  - Mohammad, G. M. Y.
A1  - Molimard, M.
A1  - Momas, I.
A1  - Montilla‑Santana, A.
A1  - Morais‑Almeida, M.
A1  - Morgan, M.
A1  - Mösges, R.
A1  - Mullol, J.
A1  - Nafti, S.
A1  - Namazova‑Baranova, L.
A1  - Naclerio, R.
A1  - Neou, A.
A1  - Neffen, H.
A1  - Nekam, K.
A1  - Niggemann, B.
A1  - Ninot, G.
A1  - Nyembue, T. D.
A1  - O’Hehir, R. E.
A1  - Ohta, K.
A1  - Okamoto, Y.
A1  - Okubo, K.
A1  - Ouedraogo, S.
A1  - Paggiaro, P.
A1  - Pali‑Schöll, I.
A1  - Panzner, P.
A1  - Papadopoulos, N.
A1  - Papi, A.
A1  - Park, H. S.
A1  - Passalacqua, G.
A1  - Pavord, I.
A1  - Pawankar, R.
A1  - Pengelly, R.
A1  - Pfaar, O.
A1  - Picard, R.
A1  - Pigearias, B.
A1  - Pin, I.
A1  - Plavec, D.
A1  - Poethig, D.
A1  - Pohl, W.
A1  - Popov, T. A.
A1  - Portejoie, F.
A1  - Potter, P.
A1  - Postma, D.
A1  - Price, D.
A1  - Rabe, K. F.
A1  - Raciborski, F.
A1  - Radier Pontal, F.
A1  - Repka‑Ramirez, S.
A1  - Reitamo, S.
A1  - Rennard, S.
A1  - Rodenas, F.
A1  - Roberts, J.
A1  - Roca, J.
A1  - Rodriguez Mañas, L.
A1  - et al, 
T1  - Scaling up strategies of the chronic respiratory disease programme of the European Innovation Partnership on Active and Healthy Ageing (Action Plan B3: Area 5)
JF  - Clinical and Translational Allergy
N2  - Action Plan B3 of the European Innovation Partnership on Active and Healthy Ageing (EIP on AHA) focuses on the integrated care of chronic diseases. Area 5 (Care Pathways) was initiated using chronic respiratory diseases as a model. The chronic respiratory disease action plan includes (1) AIRWAYS integrated care pathways (ICPs), (2) the joint initiative between the Reference site MACVIA-LR (Contre les MAladies Chroniques pour un VIeillissement Actif) and ARIA (Allergic Rhinitis and its Impact on Asthma), (3) Commitments for Action to the European Innovation Partnership on Active and Healthy Ageing and the AIRWAYS ICPs network. It is deployed in collaboration with the World Health Organization Global Alliance against Chronic Respiratory Diseases (GARD). The European Innovation Partnership on Active and Healthy Ageing has proposed a 5-step framework for developing an individual scaling up strategy: (1) what to scale up: (1-a) databases of good practices, (1-b) assessment of viability of the scaling up of good practices, (1-c) classification of good practices for local replication and (2) how to scale up: (2-a) facilitating partnerships for scaling up, (2-b) implementation of key success factors and lessons learnt, including emerging technologies for individualised and predictive medicine. This strategy has already been applied to the chronic respiratory disease action plan of the European Innovation Partnership on Active and Healthy Ageing.
KW  - EIP on AHA
KW  - European Innovation Partnership on Active and Healthy Ageing
KW  - AIRWAYS ICPs
KW  - MACVIA
KW  - Scaling up
KW  - Chronic respiratory diseases
KW  - ARIA
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-166874
VL  - 6
IS  - 29
ER  - 
TY  - JOUR
A1  - Jarick, I.
A1  - Volckmar, A. L.
A1  - Pütter, C.
A1  - Pechlivanis, S.
A1  - Nguyen, T. T.
A1  - Dauvermann, M. R.
A1  - Beck, S.
A1  - Albayrak, Ö.
A1  - Scherag, S.
A1  - Gilsbach, S.
A1  - Cichon, S.
A1  - Hoffmann, P.
A1  - Degenhardt, F.
A1  - Nöthen, M. M.
A1  - Schreiber, S.
A1  - Wichmann, H. E.
A1  - Jöckel, K. H.
A1  - Heinrich, J.
A1  - Tiesler, C. M. T.
A1  - Faraone, S. V.
A1  - Walitza, S.
A1  - Sinzig, J.
A1  - Freitag, C.
A1  - Meyer, J.
A1  - Herpertz-Dahlmann, B.
A1  - Lehmkuhl, G.
A1  - Renner, T. J.
A1  - Warnke, A.
A1  - Romanos, M.
A1  - Lesch, K. P.
A1  - Reif, A.
A1  - Schimmelmann, B. G.
A1  - Hebebrand, J.
A1  - Scherag, A.
A1  - Hinney, A.
T1  - Genome-wide analysis of rare copy number variations reveals PARK2 as a candidate gene for attention-deficit/hyperactivity disorder
JF  - Molecular Psychiatry
N2  - Attention-deficit/hyperactivity disorder (ADHD) is a common, highly heritable neurodevelopmental disorder. Genetic loci have not yet been identified by genome-wide association studies. Rare copy number variations (CNVs), such as chromosomal deletions or duplications, have been implicated in ADHD and other neurodevelopmental disorders. To identify rare (frequency ≤1%) CNVs that increase the risk of ADHD, we performed a whole-genome CNV analysis based on 489 young ADHD patients and 1285 adult population-based controls and identified one significantly associated CNV region. In tests for a global burden of large (>500 kb) rare CNVs, we observed a nonsignificant (P=0.271) 1.126-fold enriched rate of subjects carrying at least one such CNV in the group of ADHD cases. Locus-specific tests of association were used to assess if there were more rare CNVs in cases compared with controls. Detected CNVs, which were significantly enriched in the ADHD group, were validated by quantitative (q)PCR. Findings were replicated in an independent sample of 386 young patients with ADHD and 781 young population-based healthy controls. We identified rare CNVs within the parkinson protein 2 gene (PARK2) with a significantly higher prevalence in ADHD patients than in controls \((P=2.8 × 10^{-4})\) after empirical correction for genome-wide testing). In total, the PARK2 locus (chr 6: 162 659 756-162 767 019) harboured three deletions and nine duplications in the ADHD patients and two deletions and two duplications in the controls. By qPCR analysis, we validated 11 of the 12 CNVs in ADHD patients \((P=1.2 × 10^{-3})\) after empirical correction for genome-wide testing). In the replication sample, CNVs at the PARK2 locus were found in four additional ADHD patients and one additional control \((P=4.3 × 10^{-2})\). Our results suggest that copy number variants at the PARK2 locus contribute to the genetic susceptibility of ADHD. Mutations and CNVs in PARK2 are known to be associated with Parkinson disease.
KW  - children
KW  - ADHD
KW  - CNVs
KW  - GWAS
KW  - PARK2
Y1  - 2014
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-121131
VL  - 19
IS  - 19
ER  - 
TY  - JOUR
A1  - Bousquet, J.
A1  - Anto, J. M.
A1  - Akdis, M.
A1  - Auffray, C.
A1  - Keil, T.
A1  - Momas, I.
A1  - Postma, D. S.
A1  - Valenta, R.
A1  - Wickman, M.
A1  - Cambon-Thomsen, A.
A1  - Haahtela, T.
A1  - Lambrecht, B. N.
A1  - Lodrup Carlsen, K. C.
A1  - Koppelman, G. H.
A1  - Sunyer, J.
A1  - Zuberbier, T.
A1  - Annesi-Maesano, I.
A1  - Arno, A.
A1  - Bindslev-Jensen, C.
A1  - De Carlo, G.
A1  - Forastiere, F.
A1  - Heinrich, J.
A1  - Kowalski, M. L.
A1  - Maier, D.
A1  - Melen, E.
A1  - Palkonen, S.
A1  - Smit, H. A.
A1  - Standl, M.
A1  - Wright, J.
A1  - Asarnoj, A.
A1  - Benet, M.
A1  - Ballardini, N.
A1  - Garcia-Aymerich, J.
A1  - Gehring, U.
A1  - Guerra, S.
A1  - Hohman, C.
A1  - Kull, I.
A1  - Lupinek, C.
A1  - Pinart, M.
A1  - Skrindo, I.
A1  - Westman, M.
A1  - Smagghe, D.
A1  - Akdis, C.
A1  - Albang, R.
A1  - Anastasova, V.
A1  - Anderson, N.
A1  - Bachert, C.
A1  - Ballereau, S.
A1  - Ballester, F.
A1  - Basagana, X.
A1  - Bedbrook, A.
A1  - Bergstrom, A.
A1  - von Berg, A.
A1  - Brunekreef, B.
A1  - Burte, E.
A1  - Carlsen, K.H.
A1  - Chatzi, L.
A1  - Coquet, J.M.
A1  - Curin, M.
A1  - Demoly, P.
A1  - Eller, E.
A1  - Fantini, M.P.
A1  - Gerhard, B.
A1  - Hammad, H.
A1  - von Hertzen, L.
A1  - Hovland, V.
A1  - Jacquemin, B.
A1  - Just, J.
A1  - Keller, T.
A1  - Kerkhof, M.
A1  - Kiss, R.
A1  - Kogevinas, M.
A1  - Koletzko, S.
A1  - Lau, S.
A1  - Lehmann, I.
A1  - Lemonnier, N.
A1  - McEachan, R.
A1  - Makela, M.
A1  - Mestres, J.
A1  - Minina, E.
A1  - Mowinckel, P.
A1  - Nadif, R.
A1  - Nawijn, M.
A1  - Oddie, S.
A1  - Pellet, J.
A1  - Pin, I.
A1  - Porta, D.
A1  - Rancière, F.
A1  - Rial-Sebbag, A.
A1  - Schuijs, M.J.
A1  - Siroux, V.
A1  - Tischer, C.G.
A1  - Torrent, M.
A1  - Varraso, R.
A1  - De Vocht, J.
A1  - Wenger, K.
A1  - Wieser, S.
A1  - Xu, C.
T1  - Paving the way of systems biology and precision medicine in allergic diseases: the MeDALL success story 
Mechanisms of the Development of ALLergy; EUFP7-CP-IP; Project No: 261357; 2010-2015
JF  - Allergy
N2  - MeDALL (Mechanisms of the Development of ALLergy; EU FP7-CP-IP; Project No: 261357; 2010-2015) has proposed an innovative approach to develop early indicators for the prediction, diagnosis, prevention and targets for therapy. MeDALL has linked epidemiological, clinical and basic research using a stepwise, large-scale and integrative approach: MeDALL data of precisely phenotyped children followed in 14 birth cohorts spread across Europe were combined with systems biology (omics, IgE measurement using microarrays) and environmental data. Multimorbidity in the same child is more common than expected by chance alone, suggesting that these diseases share causal mechanisms irrespective of IgE sensitization. IgE sensitization should be considered differently in monosensitized and polysensitized individuals. Allergic multimorbidities and IgE polysensitization are often associated with the persistence or severity of allergic diseases. Environmental exposures are relevant for the development of allergy-related diseases. To complement the population-based studies in children, MeDALL included mechanistic experimental animal studies and in vitro studies in humans. The integration of multimorbidities and polysensitization has resulted in a new classification framework of allergic diseases that could help to improve the understanding of genetic and epigenetic mechanisms of allergy as well as to better manage allergic diseases. Ethics and gender were considered. MeDALL has deployed translational activities within the EU agenda.
KW  - asthma
KW  - birth cohort
KW  - atopic-dermatitis
KW  - immune-responses
KW  - IgE
KW  - multimorbidity
KW  - polysensitization
KW  - rhinitis
KW  - chronic respiratory-diseases
KW  - childhood asthma
KW  - immunological reactivity
KW  - IgE sensitazion
KW  - immunoglobulin-e
KW  - integraed care
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-186858
VL  - 71
IS  - 11
ER  - 
TY  - JOUR
A1  - Heinrich, T.
A1  - Nanda, I.
A1  - Rehn, M.
A1  - Zollner, U.
A1  - Frieauff, E.
A1  - Wirbelauer, J.
A1  - Grimm, T.
A1  - Schmid, M.
T1  - Live-Born Trisomy 22: Patient Report and Review
JF  - Molecular Syndromology
N2  - Trisomy 22 is a common trisomy in spontaneous abortions. In contrast, live-born trisomy 22 is rarely seen due to severe organ malformations associated with this condition. Here, we report on a male infant with complete, non-mosaic trisomy 22 born at 35 + 5 weeks via caesarean section. Peripheral blood lymphocytes and fibroblasts showed an additional chromosome 22 in all metaphases analyzed (47,XY,+22). In addition, array CGH confirmed complete trisomy 22. The patient’s clinical features included dolichocephalus, hypertelorism, flattened nasal bridge, dysplastic ears with preauricular sinuses and tags, medial cleft palate, anal atresia, and coronary hypospadias with scrotum bipartitum. Essential treatment was implemented in close coordination with the parents. The child died 29 days after birth due to respiratory insufficiency and deterioration of renal function. Our patient’s history complements other reports illustrating that children with complete trisomy 22 may survive until birth and beyond.
KW  - chromosomal abnormality
KW  - live-born
KW  - non-mosaic
KW  - trisomy 22
Y1  - 2013
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-196535
SN  - 1661-8769
SN  - 1661-8777
N1  - This publication is with permission of the rights owner freely accessible due to an Alliance licence and a national licence (funded by the DFG, German Research Foundation) respectively.
VL  - 3
IS  - 6
ER  - 
TY  - JOUR
A1  - Ellgring, Johann Heinrich
A1  - Seiler, S.
A1  - Perleth, B.
A1  - Gasser, T.
A1  - Oertel, W.
T1  - An integrated approach for the neurological and psychological support of Parkinson patients
N2  - Introduction Although symptomatic therapy is available for Parkinson's disease, patients and relatives are faced with continuous severe psychological problems. These psychological problems include: 1. lack of emotional expression, 2. bradephrenia, 3. depression, 4. lack of motivation,S. social anxiety, 6. stress induced increase of symptoms. The first four of these may be at least in part due to the dopamine deficiency. However, even as part of the primary symptoms they have social and communicative impact for patients and relatives. Social anxiety and stress induced increase of symptoms on the other hand clearly result from an interaction of somatic and psychological factors. Social anxiety mainly develops in Parkinson I s disease as an indirect consequence of the motor symptoms. Patients are afraid of being negatively evaluated in the public, of receiving negative comments etc. Thus r social withdrawal increases and the improvement of neurological symptoms following drug treatment may not be fully exploited on the psychosocial level. Stress induced increase of motor symptoms is a commonly observed phenomenon in Parkinson's disease. Even minor stressors, mainly social in nature, can have extreme effects and may elicit or increase tremor or rigidity. A patient can be well in one moment, but unable to move in the next when being aware that he has to leave the house in an hour. Given this situation, patients and relatives have to develop strategies fo~ an emotional balance in the presence of a continuous confrontation with the direct and indirect consequences of the disease. A precondition for developing new psychologically based strategies is an optimwn medical treatment. The integrated approach for neurological and psychological support has the following goals: 1. improving medical treatment for the individual patient, 2. improving psychological coping and psychosocial adaptation for patients and relatives, and 3. evaluating and improving medical and psychological therapy. CONCLUSION Psychological intervention can provide considerable help for a substantial part of Parkinson patients. The main target is coping with stressful social situations. Relaxation and cognitive restructuring together with situational behavioral analysis and training of social skills specifically adapted to the disease are" the main strategies. Various problems remain open at the moment, like the maintenance of motivation which is especially critical for Parkinson patients. Parkins on 's disease is a neurological disease with a known pathological substrate and a therapy which is effective at least for several years on a symptomatic level. The symptoms are tightly connected with psychological emotional and cognitive processes. Moreover, patients and relatives have to cope with symptoms which strongly influence social interaction. And they have to cope together with this situation over a period of ten or twenty years. Thus not only for the patient but also for the health of the relatives, psychological aid is urgently needed. We suggest to integrate psychological approach into the neurological diagnosis and treatment.
Y1  - 1990
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-42456
ER  - 
TY  - JOUR
A1  - Ellgring, Johann Heinrich
A1  - Schneider, F.
A1  - Friedrich, J.
A1  - Fus, I.
A1  - Beyer, T.
A1  - Heimann, H.
A1  - Himer, W.
T1  - The effects of neuroleptics on facial action in schizophrenic patients
N2  - This paper describes the influence of neuroleptic therapy on facial action in drug-naive schizophrenics. In a comparative study of medicated and unmedicated schizophrenic patients, the coordinates of 12 small light-reflecting points, attached to subjects' faces, were computer-recorded and analyzed automatically during a semistandardized clinical interview. In addition, facial activity in videotaped interviews was coded using the Facial Action Coding System (FACS). Each sample group comprised of eight patients with the DSMIII- R diagnostic criteria "schizophrenia" or "schizophreniform disorder". Subjects were studied on two occasions, one shortly after admission to the hospital, the other three weeks later. Group I was unmedicated during the first session, whereas group2 was medicated throughout the study. Three weeks after the start of medication, at the second interview, both recording methods showed a reduction in facial activity and facial expression across all subjects in group 1. The facial action of patients in group2, however, remained unchanged.
N2  - Ziel der vorliegenden Arbeit war die Untersuchung des Einflusses von Neuroleptika auf die Mimik von unmedizierten schizophrenen Patienten. Wiihrend eines halbstandardisierten klinischen Interviews worde die Beweglichkeit von zwolf kleinen, licht-reflektierenden Punkten, die in das Gesicht von medizierten und unmedizierten schizophrenen Patienten geklebt worden, automatisch im Zeitverlauf gemessen. Erganzend wurde der mirnische Ausdruck mit dem Facial Action Coding System (FACS) kodiert, wofiir die Patienten gleichzeitig mit Video aufgenommen worden. Jede der beiden Gruppen bestand aus acht Patienten mit den DSM-IIIR- Diagnosen "Schizophrenie" oder "Schizophrenieforme Storung". Die Patienten worden einmal direkt nach der stationaren Aufnahme und ein zweites Mal nach drei Wochen untersucht. Die Patienten der ersten Gruppe waren zum ersten Zeitpunkt nicht mit Neuroleptika mediziert, wiihrend die der zweiten Gruppe schon zu diesem Zeitpunkt entsprechende Medikamente einnahmen. Es konnte eine Reduktion der mimischen Beweglichkeit des gesamten Gesichtes im Sinne einer neuroleptisch bedingten Hypornimie der primiir Neuroleptika-unbehandelten Patienten bei der zweiten Untersuchung beobachtet werden. Die andere Gruppe Schizophrener, die zu beiden Zeitpunkten mit Neuroleptika behandelt waren, zeigte keine Veriinderung in ihrer mimischen Beweglichkeit.
Y1  - 1992
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-43269
ER  - 
TY  - JOUR
A1  - Ellgring, Johann Heinrich
A1  - Oertel, W. H.
A1  - Ulm, G.
A1  - Gasser, T.
A1  - Perleth, B.
A1  - Seiler, S.
T1  - Partnership and depression in Parkinson's Disease
N2  - In this study, the influence of partnership on depression and coping with Parkinson's disease has been investigated. Twentythree single female patients, 46 married patients (23 female, 23 male) with unimpaired partnership and 42 patients (21 female, 21 male) whose partnership had worsened since the onset of disease, were compared with regard to depression and self reported extent of psychosocial distress. Single female patients tended to have higher depression scores than patients in a stable partnership, especially in items concerning personal worthlessness and senselessness of life. Patients differed in the extent of distress concerning social behavior, psychological problems/anxiety and efficiency. Within the group of single female patients two subgroups emerged: (1) patients with low extent of distress in all aspects; (2) patients who were highly distressed by psychological problems and physical disability but weakly distressed from social interaction. Male and female patients living in a stable partnership reported only a generally low to moderate extent of distress. More than half of the male and female patients who reported an impairment of their relationship also had scores of moderate to severe depression. These patients also had the h~ghest extent of distress in each ofthe aspects assessed. The results are dicussed with regard to possible interactive effects ofthe disease, quality of the partnership and availability of coping strategies.
KW  - Depression
KW  - Parkinson's disease
KW  - Partnership
KW  - Psychological distress
Y1  - 1992
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-42516
ER  -