Hajak, Göran

[["dc.bibliographiccitation.firstpage","227"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neuropsychiatry"],["dc.bibliographiccitation.lastpage","231"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Kropp, Silke"],["dc.contributor.author","Kern, V."],["dc.contributor.author","Lange, K."],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Hajak, Goran"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Emrich, H. M."],["dc.contributor.author","Schneider, Udo"],["dc.contributor.author","Bleich, Stefan"],["dc.date.accessioned","2018-11-07T11:20:37Z"],["dc.date.available","2018-11-07T11:20:37Z"],["dc.date.issued","2005"],["dc.description.abstract","Neurotoxicity of first-generation antipsychotics: (FGAs) may be involved in lipid peroxidation, which is the pathogenesis of extrapyramidal symptoms, including tardive dyskinesia (TD). Blood samples at day 0, 7, and 21 drawn from patients taking antipsychotics were analyzed for malondialdehyde (MDA) in plasma, a marker of lipid peroxidation, by high-performance liquid chromatography. Of 115 patients enrolled, 92 patients completed the study. Most MDA levels were within normal ranges (<1.0 mu mol/liter). Malondialdehyde levels in patients receiving clozapine (p = 0.002), quetiapine (p = 0.003), amisulpride (p = 0.008), and risperidone (p = 0.008) were significantly lower than within the first generation antipsychotic group. The authors conclude that lipid peroxidation is significantly higher in treatment with FGAs."],["dc.identifier.doi","10.1176/appi.neuropsych.17.2.227"],["dc.identifier.isi","000229541000014"],["dc.identifier.pmid","15939978"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55581"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Psychiatric Publishing, Inc"],["dc.publisher.place","Arlington"],["dc.relation.conference","Annual Meeting of the Nordic-Association-for-Psychiatric-Epidemiology"],["dc.relation.eventlocation","REYKJAVIK, ICELAND"],["dc.relation.issn","1545-7222"],["dc.relation.issn","0895-0172"],["dc.title","Oxidative stress during treatment with first- and second-generation antipsychotics"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","948"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","The Canadian Journal of Psychiatry"],["dc.bibliographiccitation.lastpage","952"],["dc.bibliographiccitation.volume","46"],["dc.contributor.author","Bandelow, Borwin"],["dc.contributor.author","Tichauer, G. A."],["dc.contributor.author","Spath, C."],["dc.contributor.author","Broocks, Andreas"],["dc.contributor.author","Hajak, Goran"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Ruther, Eckart"],["dc.date.accessioned","2018-11-07T11:20:34Z"],["dc.date.available","2018-11-07T11:20:34Z"],["dc.date.issued","2001"],["dc.description.abstract","Objective: The association between separation anxiety in childhood and actual separation experiences during childhood has not yet been investigated in patients with panic disorder. Methods: In 115 patients with panic disorder with or without agoraphobia and in 124 control subjects without a history of psychiatric illness, we assessed separation anxiety during childhood, retrospectively, using DSM-IV and ICD-10 criteria and the Separation Anxiety Symptom Inventory (SASI). In addition, actual separation experiences from age 0 to 15 years were assessed, retrospectively. Results: A total of 22.6% of the patients and 4.8% of the Control subjects fulfilled both DSM-IV and ICD-10 criteria for childhood separation anxiety (chi(2) = 11.8; P < 0.0001). Further, 57.4% ofthepatients and 37.9% of the control subjects reported actual separation experiences during their childhood (chi(2) = 9. 09, P < 0.003). Separation anxiety and actual separation experiences, however, were independent of each other. Conclusion: These results suggest that separation anxiety during childhood is not a consequence of actual traumatic separation experiences in panic disorder patients."],["dc.identifier.isi","000173099800007"],["dc.identifier.pmid","11816316"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55564"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Canadian Psychiatric Assoc"],["dc.relation.issn","0706-7437"],["dc.title","Separation anxiety and actual separation experiences during childhood in patients with panic disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","158"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Respiratory Journal"],["dc.bibliographiccitation.lastpage","164"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Hagedohm, J."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Laier-Groeneveld, G."],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Hajak, Goran"],["dc.date.accessioned","2018-11-07T10:20:54Z"],["dc.date.available","2018-11-07T10:20:54Z"],["dc.date.issued","2002"],["dc.description.abstract","Sleep apnoea syndrome (SAS) is a known risk factor for vascular diseases and stroke. Structural brain damage, manifesting as an overt neurological deficit or more subtly as cognitive dysfunction, is a frequent symptom in SAS. The presence of a biochemical marker of cerebral injury would be of great benefit in SAS to screen for even small brain damage and to monitor efficiacy of therapy. Therefore, in 10 patients with mild SAS (age 50.8+/-9.9 yrs, respiratory disturbance index (RDI) 18+/-3.6, lowest arterial oxygen saturation (min Sa,O-2) 80.5+/-4.06%) and nine patients with severe SAS (age 50.3+/-11.5 yes, RDI 75.4+/-21.7, min Sa,O-2 56.56+/-14.58%), serum concentrations of neuron-specific enolase (NSE), S-100beta protein, and beta-trace were measured just before and after sleep using commercially available assays. Only serum levels in the normal range could be found, independent of when the blood was taken or the degree of SAS. Structural cerebral injury caused by sleep apnoea syndrome in patients without neurological symptoms or previous cerebrovascular events may be too small to produce a measurable increase in S-100beta, neuron-specific enolase and beta-trace serum concentrations or subclinical cerebral damage may be outside the lower detection limits of the analytical methods which were used. There is a need for biochemical markers and more sensitive methods for detecting small cerebral injury in sleep apnoea syndrome."],["dc.identifier.doi","10.1183/09031936.02.00862001"],["dc.identifier.isi","000177188600026"],["dc.identifier.pmid","12166564"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41974"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","European Respiratory Soc Journals Ltd"],["dc.relation.issn","0903-1936"],["dc.title","Biochemical markers of cerebrovascular injury in sleep apnoea syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","87"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Sleep Research"],["dc.bibliographiccitation.lastpage","93"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Kirov, Roumen"],["dc.contributor.author","Kinkelbur, J."],["dc.contributor.author","Heipke, S."],["dc.contributor.author","Kostanecka-Endress, T."],["dc.contributor.author","Westhoff, M."],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Hajak, Goran"],["dc.contributor.author","Banaschewski, Tobias"],["dc.contributor.author","Rothenberger, A."],["dc.date.accessioned","2018-11-07T10:50:47Z"],["dc.date.available","2018-11-07T10:50:47Z"],["dc.date.issued","2004"],["dc.description.abstract","The aim of the study was to characterize the sleep pattern in children with attention deficit/hyperactivity disorder (ADHD). By means of polysomnography (PSG), sleep patterns were studied in 17 unmedicated preadolescent boys rigorously diagnosed with ADHD and 17 control boys precisely matched for age and intelligence. Although ADHD children did not display a general sleep alteration, major PSG data showed a significant increase in the duration of the absolute rapid eye movement (REM) sleep and the number of sleep cycles in ADHD group when compared with controls. In addition, REM sleep latency tended to be shorter in ADHD children. These results suggest that in ADHD children, a forced REM sleep initiation may produce a higher incidence of sleep cycles and may also contribute to an increased duration of the absolute REM sleep. The overall pattern of the findings implies that a forced ultradian cycling appears characteristic for the sleep in ADHD children, which may be related to alterations of brain monoamines and cortical inhibitory control accompanying the ADHD psychopathology."],["dc.identifier.doi","10.1111/j.1365-2869.2004.00387.x"],["dc.identifier.isi","000189141800011"],["dc.identifier.pmid","14996040"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48733"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing Ltd"],["dc.relation.issn","0962-1105"],["dc.title","Is there a specific polysomnographic sleep pattern in children with attention deficit/hyperactivity disorder?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","867"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","SLEEP"],["dc.bibliographiccitation.lastpage","874"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Jordan, W."],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Eggert, S."],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Brunner, E."],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Hajak, Goran"],["dc.date.accessioned","2018-11-07T10:47:06Z"],["dc.date.available","2018-11-07T10:47:06Z"],["dc.date.issued","2004"],["dc.description.abstract","Study Objectives: The prostaglandin D system plays an important role in animal sleep. In humans, alterations in the prostaglandin D system have been found in diseases exhibiting sleep disturbances as a prominent symptom, such as trypanosoma infection, systemic mastocytosis, bacterial meningitis, major depression, or obstructive sleep apnea. Assessment of this system's activity in relation to human physiologic sleep was the target of the present study. Design: Serum concentrations of lipocalin-type prostaglandin D synthase (L-PGDS, former P-trace), and plasma levels of the pineal hormone melatonin were measured in 20 healthy humans (10 women, 10 men; aged: 23.3 +/- 2.39 years) at 4-hour intervals over a period of 5 days and nights, which included physiologic sleep, rapid eye movement sleep deprivation, and total sleep deprivation. In addition, the serum L-PGDS and plasma melatonin levels of 6 subjects were determined under conditions of bright white (10,000 lux) or dark red light (< 50 lux) in a crossover design during total sleep deprivation. Nocturnal blood sampling was performed by a through-the-wall tube system. L-PGDS was measured by an automated immunonephelometric assay, and melatonin was analyzed by direct radioimmunoassay. Results: Serum L-PGDS concentrations showed marked time-dependent changes with evening increases and the highest values at night (P < .0005). This nocturnal increase was suppressed during total sleep deprivation (P < .05), independent of external light conditions and melatonin secretion. Rapid eye movement sleep deprivation had no impact on circulating L-PGDS levels. Conclusions: The circadian L-PGDS pattern and its suppression by total sleep deprivation indicate an interaction of the prostaglandin D system and human sleep regulation. L-PGDS measurements may well provide new insights into physiologic and pathologic sleep regulation in humans."],["dc.identifier.isi","000223451400008"],["dc.identifier.pmid","15453544"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47897"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Academy Sleep Medicine"],["dc.relation.issn","0161-8105"],["dc.title","Prostaglandin D synthase (beta-trace) in healthy human sleep"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","831"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","837"],["dc.bibliographiccitation.volume","107"],["dc.contributor.author","Wedekind, Dirk"],["dc.contributor.author","Bandelow, Borwin"],["dc.contributor.author","Broocks, Andreas"],["dc.contributor.author","Hajak, Goran"],["dc.contributor.author","Ruther, Eckart"],["dc.date.accessioned","2018-11-07T11:09:47Z"],["dc.date.available","2018-11-07T11:09:47Z"],["dc.date.issued","2000"],["dc.description.abstract","Background. Research on basal HPA axis activity in patients with panic disorder showed inconsistent results. Methods. Basal total plasma, plasma free and salivary cortisol levels were compared in patients with panic disorder (n = 47) and in healthy individuals (n = 23). Correlations between these fractions were calculated. Results. All three basal cortisol fractions were significantly elevated in patients compared to controls. There were significant correlations between all three cortisol fractions. Conclusions. Nonsignificant differences between cortisol levels of patients and healthy controls in previous studies may have been due to inclusion of less severely ill patients or to small sample sizes (96 words)."],["dc.identifier.doi","10.1007/s007020070062"],["dc.identifier.isi","000088415100008"],["dc.identifier.pmid","11005547"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53083"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0300-9564"],["dc.title","Salivary, total plasma and plasma free cortisol in panic disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","495"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","European Psychiatry"],["dc.bibliographiccitation.lastpage","500"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Bandelow, Borwin"],["dc.contributor.author","Sojka, Felicita"],["dc.contributor.author","Broocks, Andreas"],["dc.contributor.author","Hajak, Goran"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Ruether, Eckart"],["dc.date.accessioned","2018-11-07T09:10:15Z"],["dc.date.available","2018-11-07T09:10:15Z"],["dc.date.issued","2006"],["dc.description.abstract","Background. - Earlier studies on the influence of pregnancy and postpartum period on the course of panic disorder have been inconsistent. The present study aims to quantify panic manifestations in these periods in large sample of women. Method. - Panic manifestations, including exacerbations and new manifestations of panic disorder, were assessed retrospectively in a sample of 128 women with panic disorder with or without agoraphobia, 93 of whom had had 195 pregnancies. Results. - Panic manifestations were fewer during pregnancy and more frequent in the postpartum period when compared with the control period. Women who had never been pregnant had significantly more panic manifestations than women with prior pregnancies. Breastfeeding and miscarriages did not have a significant effect. Women with postpartum panic reported more psychosocial stress events during this period. Conclusions. - Possible reasons for postpartum panic and the protective effects of pregnancy are discussed, including psychosocial or hormonal factors and other neurobiological changes. Postpartum panic coincides with a sudden drop of hormones after delivery. (c) 2006 Elsevier Masson SAS. All rights reserved."],["dc.identifier.doi","10.1016/j.eurpsy.2005.11.005"],["dc.identifier.isi","000241925900010"],["dc.identifier.pmid","16529913"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26446"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier France-editions Scientifiques Medicales Elsevier"],["dc.relation.issn","0924-9338"],["dc.title","Panic disorder during pregnancy and postpartum period"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","23"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Psychosomatic Research"],["dc.bibliographiccitation.lastpage","29"],["dc.bibliographiccitation.volume","55"],["dc.contributor.author","Kostanecka-Endress, T."],["dc.contributor.author","Banaschewski, Tobias"],["dc.contributor.author","Kinkelbur, J."],["dc.contributor.author","Wullner, I."],["dc.contributor.author","Lichtblau, S."],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Ruther, Eckart"],["dc.contributor.author","Woerner, W."],["dc.contributor.author","Hajak, Goran"],["dc.contributor.author","Rothenberger, A."],["dc.date.accessioned","2018-11-07T10:38:02Z"],["dc.date.available","2018-11-07T10:38:02Z"],["dc.date.issued","2003"],["dc.description.abstract","Objective: To evaluate objective data on sleep quantity/quality and motor activity during night sleep in children with Tourette syndrome (TS). Method: Polysomnography of 17 unmedicated TS children (ages: 7;11-15;5, mean: 11;10 years) without comorbid attention-deficit hyperactivity disorder (ADHD) was compared with 16 age-, sex- and IQ-matched healthy controls. Sleep analyses according to the procedure of Rechtschaffen and Kales were supplemented by counting epochs with short arousal-related movements (less than or equal to15 s), thus allowing to calculate correlations between motor activity and sleep parameters. Results: Children with TS demonstrated changes in sleep parameters, including longer sleep period time, longer sleep latency, reduced sleep efficiency, and prolonged wakefulness after sleep onset. Their sleep profiles showed significantly more time awake and less sleep stage II. However, REM sleep variables, slow-wave sleep, and number of sleep stage changes were unaffected. Movement time was similar in both groups, but epochs with short arousal-related movements were increased in TS. Further analyses showed no significant correlations between sleep parameters and nighttime nontic movements, level of psychopathology or tic severity during daytime. Periodic limb movements during sleep (PLMS) were only seen in one TS patient (low PLMS index of 7.8/h). Conclusions: Children with TS have disturbed sleep quality with increased arousal phenomena, which both may be intrinsic to the disorder and might trigger tics and other behavioral problems during daytime. This indicates the need for sleep evaluation in patients with TS. (C) 2003 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/S0022-3999(02)00602-5"],["dc.identifier.isi","000184078300005"],["dc.identifier.pmid","12842228"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45714"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.conference","International Conference of the Tourette-Syndrome-Foundation-of-Canada"],["dc.relation.eventlocation","MISSISSAUGA, CANADA"],["dc.relation.issn","0022-3999"],["dc.title","Disturbed sleep in children with Tourette syndrome - A polysomnographic study"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","201"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Pineal Research"],["dc.bibliographiccitation.lastpage","210"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Huether, Gerald"],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Hajak, Goran"],["dc.date.accessioned","2021-12-08T12:27:55Z"],["dc.date.available","2021-12-08T12:27:55Z"],["dc.date.issued","1998"],["dc.identifier.doi","10.1111/j.1600-079X.1998.tb00389.x"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/95496"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-476"],["dc.relation.eissn","1600-079X"],["dc.relation.issn","0742-3098"],["dc.rights.uri","http://doi.wiley.com/10.1002/tdm_license_1.1"],["dc.title","Altered circadian melatonin secretion patterns in relation to sleep in patients with chronic sleep-wake rhythm disorders"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","453"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","The Journal of Clinical Psychiatry"],["dc.bibliographiccitation.lastpage","463"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Hajak, Goran"],["dc.contributor.author","Rodenbeck, Andrea"],["dc.contributor.author","Voderholzer, U."],["dc.contributor.author","Riemann, D."],["dc.contributor.author","Cohrs, Stefan"],["dc.contributor.author","Hohagen, F."],["dc.contributor.author","Berger, M."],["dc.contributor.author","Ruther, Eckart"],["dc.date.accessioned","2018-11-07T09:00:49Z"],["dc.date.available","2018-11-07T09:00:49Z"],["dc.date.issued","2001"],["dc.description.abstract","Background: Over recent years, the use of antidepressants for the symptomatic treatment of insomnia has grown substantially, but controlled studies are still lacking. Our study is the first investigation to prove objective efficacy and tolerability of low doses of a sedating antidepressant in a randomized, double-blind, and placebo-controlled manner in patients with primary insomnia. Method: Forty seven drug-free patients meeting DSM-IV criteria for primary insomnia (mean +/- SD duration of complaints = 11.2 +/- 9.7 years) received either 25-50 mg of the tricyclic antidepressant doxepin or placebo for 4 weeks followed by 2 weeks of placebo withdrawal. Sleep was measured by polysomnography at baseline and the first night of application, at 4 weeks of treatment and the first to third night of withdrawal, and after 2 weeks of withdrawal. Results: In the doxepin-treated patients who completed the study (N = 20, 47.6 +/- 11.3), medication significantly increased sleep efficiency after acute (night 1, p less than or equal to .001) and subchronic (night 28, p less than or equal to .05) intake compared with the patients who received placebo (N = 20, 47.4 +/- 16.8 years of age). Latency to sleep onset was not affected since the patients had normal baseline sleep latencies. Investigators found doxepin to cause significantly (P less than or equal to .05) better global improvement at the first day of treatment. Patients rated sleep quality (p less than or equal to .001) and working ability (p less than or equal to .005) to be significantly improved by doxepin during the whole treatment period. Overall rebound in sleep parameters was not observed, but patients with severe rebound insomnia were significantly more frequent in the doxepin group (night 29, p less than or equal to .01; night 30, p less than or equal to .01; night 31, p less than or equal to .05). No significant group differences in side effects were Found, but 2 doxepin-treated patients dropped out of the study due to specific side effects (increased liver enzymes, leukopenia, and thrombopenia). Conclusion: The results support the effectiveness of low doses of doxepin to improve sleep and working ability in chronic primary insomniacs, although subjective effects were light to moderate, and in some patients, rebound insomnia and specific side effects have to be considered."],["dc.identifier.isi","000169918900009"],["dc.identifier.pmid","11465523"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24262"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Physicians Postgraduate Press"],["dc.relation.issn","0160-6689"],["dc.title","Doxepin in the treatment of primary insomnia: A placebo-controlled, double-blind, polysomnographic study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]