37 research outputs found

    Obsessive-compulsive disorder. A hidden disorder

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    Efst á síðunni er hægt að nálgast greinina í heild sinni með því að smella á hlekkinnÞráhyggjuárátturöskun er algeng og oft langvinn geðröskun sem leitt getur til verulegrar skerðingar á starfsgetu og lífsgæðum. Einkenni lýsa sér með óþægilegum, uppáþrengjandi og óviðeigandi kvíðavaldandi þrá- hyggjuhugsunum og tímafrekum og hamlandi áráttum. Einkennum fylgir oft mikil skömm og þekking almennings og heilbrigðisstarfsfólks á þessari geðröskun er víða takmörkuð. Því er algengt að röskunin greinist seint eða að einstaklingar fái ranga greiningu. Rannsóknir hafa sýnt að erfða- þættir eiga þátt í orsökum þráhyggjuárátturöskunar og nýlega hafa komið fram vísbendingar um að truflanir í tengingum ákveðinna heilasvæða eigi þátt í meingerð röskunarinnar. Ýmsar sálfræðikenningar um orsakir röskunarinnar sem studdar eru rannsóknum hafa einnig verið settar fram. Gagnreynd meðferð er annars vegar með lyfjum sem hafa áhrif á virkni serótóníns í heila og hins vegar ákveðnu afbrigði hugrænnar atferlismeð- ferðar sem nefnist berskjöldun með svarhömlun. Þörf er á bættum með- ferðarúrræðum þar sem allt að þriðjungur einstaklinga svarar meðferð lítið eða ekki. Hér er lýst tveimur tilfellum þráhyggjuárátturöskunar. Annars vegar ungum manni með dæmigerð einkenni sem svarar vel hefðbundinni meðferð og hins vegar miðaldra konu með mikil og hamlandi einkenni sem ekki svarar hefðbundinni lyfja- og sálfræðimeðferð. Í tilfelli konunnar var ákveðið að reyna raförvun á ákveðnum svæðum heilans með rafskautum sem komið var fyrir með þrívíddarísetningu í skurðaðgerð. Um er ræða meðferð sem er enn á tilraunastigi og hefur verið beitt í alvarlegustu tilfellum þráhyggjuáráttu sem ekki svara hefðbundinni meðferð.Obsessive-compulsive disorder is a common and often chronic psychiatric illness that significantly interferes with the patient´s functioning and quality of life. The disorder is characterized by excessive intrusive and inappropriate anxiety evoking thoughts as well as time consuming compulsions that cause significant impairment and distress. The symptoms are often accompanied by shame and guilt and the knowledge of the general public and professional community about the disorder is limited. Hence it is frequently misdiagnosed or diagnosed late. There are indications that the disorder is hereditary and that neurobiological processes are involved in its pathophysiology. Several psychological theories about the causes of obsessive-compulsive disorder are supported by empirical evidence. Evidence based treatment is either with serotoninergic medications or cognitive behavioral therapy, particularly a form of behavioral therapy called exposure response prevention. Better treatment options are needed because almost a third of people with obsessive-compulsive disorder respond inadequatly to treatment. In this review article two cases of obsessive-compulsive disorder are presented. The former case is a young man with typical symptoms that respond well to treatment and the latter is a middle aged lady with severe treatment resistant symptoms. She underwent stereotactic implantation of electrodes and received deep brain stimulation, which is an experimental treatment for severe obsessive-compulsive disorder that does not respond to any conventional treatment

    Media and the health care system

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    Clozapine treatment and discontinuation in Iceland: A national longitudinal study using electronic patient records.

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    To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked Files. This article is open access.Clozapine is the only drug approved for treatment-resistant schizophrenia. There is evidence that clozapine is underutilized.To evaluate the initiation and discontinuation of clozapine at Landspitali University Hospital in Iceland and the prevalence of antipsychotic polypharmacy in clozapine-treated patients.The study is a part of an ongoing longitudinal study of schizophrenia in Iceland. We identified 201 patients on clozapine or who have been on clozapine by using a keyword search in the electronic health records and by reviewing their medical records.Mean age at first treatment with clozapine was 37.8 years. Mean follow-up period on clozapine was 11 years. After 20 years of treatment 71.2% of patients were still on clozapine. After one year of treatment 84.4% of patients were still receiving clozapine treatment. We estimate that 11.4% of patients with schizophrenia in Iceland are taking clozapine and that 16% have been treated with clozapine at some point. Polypharmacy is common, since nearly 2/3, 65.6%, of patients taking clozapine use at least one other antipsychotic and 16.9% are also receiving depot injections.We need to increase the awareness of psychiatrists in Iceland with regard to treatment with clozapine, since only about half of the estimated population of patients with treatment-resistant schizophrenia in Iceland have ever been treated with clozapine. Nearly two thirds of patients who are prescribed clozapine in Iceland remain on it long-term.info:eu-repo/grantAgreement/EC/FP7/279227 National Institute for Health Research (NIHR) Mental Health Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College Londo

    Neutropenia and agranulocytosis during treatment of schizophrenia with clozapine versus other antipsychotics: an observational study in Iceland

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    To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked Files.Data on the haematological outcomes of patients who continue clozapine treatment following neutropenia are very rare as even mild neutropenia results in mandatory discontinuation of clozapine in most countries. However, in Iceland where clozapine monitoring is less stringent allows an observational study to be done on the risk of agranulocytosis and neutropenia during treatment with clozapine compared with other antipsychotics among patients with schizophrenia.The present study is a part of a wider ongoing longitudinal study of schizophrenia in Iceland. We identified 201 patients with schizophrenia treated with clozapine and 410 patients with schizophrenia who had never been on clozapine by searching the electronic health records of Landspitali, the National University Hospital. Neutrophil counts were searched in electronic databases to identify patients who developed neutropenia/agranulocytosis and the frequency of neutrophil measurements was examined as well.The median number of days between neutrophil measurements during the first 18 weeks of clozapine treatment was 25 days but after the first 18 weeks on the drug the median became 124 days. Thirty four cases of neutropenia were identified during clozapine treatment with an average follow up time of 9.2 years. The majority, 24 individuals developed mild neutropenia (1500-1900 neutrophils/mm(3)). None of these progressed to agranulocytosis. The remaining 10 patients developed neutropenia in the range 500-1400 /mm(3) of whom one developed agranulocytosis, three stopped clozapine use and 6 patients continued on clozapine for at least a year without developing agranulocytosis. Unexpectedly, schizophrenia patients on other antipsychotics had an equal risk of developing neutropenia as those on clozapine.Neutropenia is common both in patients with schizophrenia on clozapine treatment and in those never on clozapine. Therefore a large part of neutropenia during clozapine treatment is probably not caused by clozapine. These findings have implications in assessing the balance between the risk of progression from neutropenia to agranulocytosis against the morbidity resulting from the premature discontinuation of clozapine under the current monitoring regulations in the US and in most of Europe.info:eu-repo/grantAgreement/EC/FP7/279227 National Institute for Health Research (NIHR) Mental Health Biomedical Research Centre at South London, Maudsley NHS Foundation Trust and King’s College London

    Bacterial meningitis in one month-16 year old children at three Pediatric departments in Iceland during the period 1973-2000

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    Neðst á síðunni er að nálgast greinina í heild sinni með því að smella á hlekkinn View/OpenObjective: Bacterial meningitis is a serious disease most common in children. We report the epidemiology and outcome of bacterial meningitis in children between the age of one month to 16 years admitted to three Pediatric Departments in Iceland in 1973-2000 (28 years). Material and methods: Information was collected retrospectively from the medical records of admitted children diagnosed with bacterial meningitis. Results: 454 children were diagnosed; 255 boys and 199 girls; 77% were less than five years of age. Before 1989 the age specific incidence was 29/100.000/year and 12/100.000/year thereafter. The cerebral spinal fluid was culture positive in 74% but no organism was identified in 17%. The most common pathogens were N. meningitidis (44%), Hib (30%), and S. pneumoniae (7%). The incidence varied according to age. No child was diagnosed with Hib after launching of Hib vaccination in 1989. The mean age of the children increased significantly from less than two years prior to 1989 to less than three years thereafter and of children infected with N. meningitidis from around two year to three years. The mortality rate was 4,5%, none due to Hib. Fourteen percent suffered sensory-neural hearing impairment and no protective effects were seen of steroid therapy. Conclusions: The age specific incidence of bacterial meningitis of children in Iceland has decreased during the last decade, especially due to Hib vaccination. Further reduction can be expected by implementing general vaccination to N. meningitidis C and S. pneumoniae. Additionally, recognizing the symptoms of bacterial meningitis and starting proper therapy as soon as possible is crucial in order to minimize ominous outcome.Inngangur: Heilahimnubólga af völdum baktería er alvarlegur sjúkdómur og algengastur hjá börnum. Í þessari rannsókn er litið á faraldsfræði og fylgikvilla sjúkdómsins hjá eins mánaðar til 16 ára gömlum börnum sem lögðust inn á þrjár barnadeildir á Íslandi á árunum 1973-2000 (28 ár). Efniviður og aðferðir: Upplýsingar voru fengnar úr sjúkraskrám barna á Barnaspítala Hringsins og barnadeildum Landakotsspítala/Borgarspítala/ Sjúkrahúss Reykjavíkur og Fjórðungssjúkrahússins á Akureyri sem fengið höfðu greininguna heilahimnubólga af völdum baktería. Niðurstöður: Alls greindust 454 börn, 255 drengir og 199 stúlkur; 77% voru yngri en fimm ára. Aldursbundið nýgengi var 29/100.000/ár fram til ársins 1989 og 12/100.000/ár eftir það. Greining fékkst með ræktun úr mænuvökva hjá 74% en hjá 17% var sýkingavaldur óþekktur. Helstu sýkingavaldar voru Neisseria meningitidis (44%), Haemophilus influenzae af sermisgerð b (Hib) (30%) og Streptococcus pneumoniae (7%). Tíðni þeirra var mismunandi eftir aldri. Ekkert tilfelli Hib greindist eftir að bólusetning gegn bakteríunni hófst 1989. Algengustu hjúpgerðir N. meningitidis voru B (55%) og C (19%). Meðalaldur barnanna hækkaði marktækt úr tæpum tveimur árum fram til 1989 í tæplega þrjú ár eftir það, og barna með N. meningitidis úr rúmlega tveimur árum í rúmlega þrjú. Dánartíðnin var 4,5% en ekkert barn með Hib dó. Um þriðjungur barna fékk fylgikvilla sérstaklega eftir sýkingu af völdum S. pneumoniae. Fjórtán af hundraði fengu skyntaugarheyrnartap og voru sterar ekki verndandi. Ályktanir: Nýgengi heilahimnubólgu af völdum baktería hjá börnum á Íslandi hefur farið lækkandi síðustu ár, einkum vegna Hib bólusetningar. Líklegt er að bólusetning gegn N. meningitidis C og S. pneumoniae geti einnig fækkað enn frekar heilahimnubólgu hjá börnum. Auk þess eru skjót viðbrögð við einkennum heilahimnubólgu mikilvæg til að minnka líkur á fylgikvillu

    P300 Analysis Using High-Density EEG to Decipher Neural Response to rTMS in Patients With Schizophrenia and Auditory Verbal Hallucinations.

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    To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked DownloadSchizophrenia is a complex disorder about which much is still unknown. Potential treatments, such as transcranial magnetic stimulation (TMS), have not been exploited, in part because of the variability in behavioral response. This can be overcome with the use of response biomarkers. It has been however shown that repetitive transcranial magnetic stimulation (rTMS) can the relieve positive and negative symptoms of schizophrenia, particularly auditory verbal hallucinations (AVH). This exploratory work aims to establish a quantitative methodological tool, based on high-density electroencephalogram (HD-EEG) data analysis, to assess the effect of rTMS on patients with schizophrenia and AVH. Ten schizophrenia patients with drug-resistant AVH were divided into two groups: the treatment group (TG) received 1 Hz rTMS treatment during 10 daily sessions (900 pulses/session) over the left T3-P3 International 10-20 location. The control group (CG) received rTMS treatment over the Cz (vertex) EEG location. We used the P300 oddball auditory paradigm, known for its reduced amplitude in schizophrenia with AVH, and recorded high-density electroencephalography (HD-EEG, 256 channels), twice for each patient: pre-rTMS and 1 week post-rTMS treatment. The use of HD-EEG enabled the analysis of the data in the time domain, but also in the frequency and source-space connectivity domains. The HD-EEG data were linked with the clinical outcome derived from the auditory hallucinations subscale (AHS) of the Psychotic Symptom Rating Scale (PSYRATS), the Quality of Life Scale (QoLS), and the Depression, Anxiety and Stress Scale (DASS). The general results show a variability between subjects, independent of the group they belong to. The time domain showed a higher N1-P3 amplitude post-rTMS, the frequency domain a higher power spectral density (PSD) in the alpha and beta bands, and the connectivity analysis revealed a higher brain network integration (quantified using the participation coefficient) in the beta band. Despite the small number of subjects and the high variability of the results, this work shows a robust data analysis and an interplay between morphology, spectral, and connectivity data. The identification of a trend post-rTMS for each domain in our results is a first step toward the definition of quantitative neurophysiological parameters to assess rTMS treatment. Keywords: P300; TMS (repetitive transcranial magnetic stimulation); brain connectivity; high-density EEG; schizophrenia; spectral analysis; temporal analysis.United States Department of Health & Human Services National Institutes of Health (NIH) - USA NIH National Institute of Neurological Disorders & Stroke (NINDS) Landspitali Scientific fund

    Læknisfræði framtíðar – Mun gervigreind og vélmenni leysa lækna af hólmi?

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    Media and the health care system

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    Augnhreyfingar og áhættuarfgerðir geðklofa

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    Markmið: Meginmarkmið þessa verkefnis var að rannsaka tengsl innri svipgerða smooth pursuit (SPEM) og antisaccade augnhreyfinga við áhættuarfgerðir catechol-O-methyltransferasa (COMT) og neuregulin-1 (NRG-1) gena í hópi íslenskra sjúklinga með geðklofa og í heilbrigðum samanburðarhópi. Breytileiki (val158met) í COMT geni kann að tengjast áhættu fyrir geðklofa vegna mismunandi áhrifa á niðurbrot dópamíns í framheila. Breytileikar í NRG-1 geni kunna að auka hættu á geðklofa vegna þess að NRG-1 gegnir margþættu hlutverki í þroskun taugakerfisins, en vísbendingar eru um að truflanir í taugaþroska eigi þátt í orsökum sjúkdómsins. Áhrif þessara gena á vitræna starfsemi heilans eru lítt þekkt. Finnist tengsl á milli frávika í augnhreyfingum og áhættuarfgerða geðklofa kunna þau að auka skilning á þætti erfðabreytileika í truflunum á vitrænni starfsemi heilans í geðklofa. Önnur markmið voru að rannsaka innra samræmi augnhreyfimælinga og breytileika í frammistöðu innan hverrar mælingar ásamt því að kanna tengsl alvarleika geðklofaeinkenna og tegund geðrofslyfja við frammistöðu á augnhreyfiprófum. Auk þess var rannsakað hvort fylgni væri á milli frammistöðu á SPEM og antisaccade prófum. Aðferðir: Prosaccade, antisaccade, fixation og SPEM augnhreyfingar voru mældar með innrauðri ljóstækni í 118 einstaklingum með geðklofa og 109 þátttakendum í samanburðarhópi. Allir þátttakandur voru arfgerðargreindir með tilliti til COMT val158met/rs4680 breytileika og tveggja áhættuarfgerða NRG-1 (SNP8NRG222662/rs4623364 og SNP8NRG243177/rs6994992). Frammistaða á augnhreyfiprófum var greind með sérhönnuðum hálfsjálfvirkum tölvuforritum. Niðurstöður: Einstaklingar með geðklofa höfðu marktækt afbrigðilegar SPEM og antisaccade augnhreyfingar samanborið við heilbrigða. Þátttakendur með geðklofa höfðu einnig marktækt meiri frávik á prosaccade og fixation prófum en heilbrigðir. Breytileiki val158met í COMT geni tengdist hvorki geðklofagreiningu né einkennum geðklofa. Ekki voru marktæk tengsl á milli COMT val158met og frammistöðu á SPEM prófi. COMT val158 tengdist betri frammistöðu á antisaccade prófi en ekki voru marktæk víxlhrif á milli sjúklinga og heilbrigðra. Áhættuarfgerðir NRG-1 sýndu hvorki marktæk tengsl við frammistöðu á augnhreyfiprófum né við einkenni geðklofa. Þó var frammistaða þeirra sem höfðu NRG-1 áhættuarfgerð lítilega verri á flestum SPEM og antisaccade mælingum en hjá þeim sem ekki höfðu NRG-1 áhættuarfgerð (d= 0.1-0.3). Innra samræmi var hátt fyrir nánast allar augnhreyfibreytur (Cronbach’s α >0.85) og breytileiki í frammistöðu innan hverrar mælingar var svipaður hjá þátttakendum með geðklofa og heilbrigðum. Aldur við greiningu geðklofa, tímalengd veikinda, tegund geðrofslyfja og alvarleiki sjúkdómseinkenna sýndu almennt ekki fylgni við frammistöðu á augnhreyfiprófum. Fylgni á milli frammistöðu á SPEM og antisaccade prófum var lítil og ekki sambærileg hjá sjúklingum og heilbrigðum. Ályktanir: Rannsóknin staðfestir að frávik á SPEM og antisaccade augnhreyfiprófum eru til staðar í stóru íslensku þýði einstaklinga með geðklofa. COMT val158met breytileiki tengist ekki frammistöðu á SPEM prófi. Tengsl COMT val158 við niðurstöður á antisaccade prófi bendir til þess að hraðara niðurbrot dópamíns í framheila bæti frammistöðu á prófinu og að áhrifin tengist ekki geðklofa. Þó að útiloka megi sterk áhrif NRG-1 áhættuarfgerða á frammistöðu á SPEM og antisaccade prófum er mögulegt að rannsóknina skorti tölfræðilegt afl til þess að greina væg áhrif áhættuarfgerða. Hátt innra samræmi og sambærilegur breytileiki í frammistöðu innan hverrar mælingar hjá sjúklingum og samanburðarhópi ásamt því að alvarleiki sjúkdómseinkenna og tegund geðrofslyfja tengist lítið frammistöðu á prófunum styður gildi þessara augnhreyfifrávika sem innri svipgerða. Veik fylgni á milli frammistöðu í SPEM og antisaccade prófum bendir til þess að prófin endurspegli ekki sömu erfðafræðilegu áhættuþætti sjúkdómsins.RANNÍS, Styrktarsjóður Wyeth á Ísland
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