Abstracts S77 pression symptoms.“Feelingtiredor havinglittleenergy”
(33%≥halfofdays),“feelingdown,depressed,orhopeless” (26.9%≥halfofdays),and“havingtroublefallingorstaying asleep” (22.4% ≥half of days) were the most frequent symptoms. Overall GAD-7 mean scorewas5.8±5.5, MoCA 22.7±4.5,andEQ-5D75.2±22.1.Depressionwasassociated with anxiety (rs=0.596; p<0.001) and HRQOL(rs=-0.474; p<0.001). Depressed patients had lower education (94% vs 67%, p=0.048) and were more frequently at NYHA III thatnon-depressed(31%vs5%;p=0.012).OnlyNYHAclass (p=0.034)andanxietyscore(p=0.001)showedan indepen-dentassociationwithdepression.PatientsatNYHAclassIII (OR=24.5;95%CI1.3-470.4)andwithmoresevereanxiety (OR=1.4;95%CI1.1-1.7)wereatasignificantlyhigherrisk ofmoderatetoseveredepressionsymptoms.
Conclusions: Overall27% ofHF patientsshowed signifi-cantdepressionsymptoms,expressedasfatigue,depressed mood and sleeping problems. Depression was associated withmoresevereHFsymptoms,andmorefrequentanxiety symptoms.The coexistenceofHFanddepressiondeserves furtherstudies,inordertobuildabetterunderstandingof theinfluenceofDepressiononHFoutcomes.
Acknowledgments: supported by ERDF through POCI-01-0145-FEDER-007746, funded by COMPETE2020, National Funds through FCT, within CINTESIS (UID/IC/4255/2013), andProject"NORTE-01-0145-FEDER-000026-Symbiotic tech-nology for societal efficiency gains: Deus ex Machina", fi-nancedbyNORTE2020underPORTUGAL2020.
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doi:10.1016/j.euroneuro.2018.11.1056
P.055Evaluationoftherecurrenceratesafterthefirst manicepisode:oneyearfollow-upstudy
V.Erbasan∗,M.Aydın,Y.Selvi,K.Altınba¸s
Selçuk University Medical Faculty, Psychiatry, Konya, Turkey
Background: Bipolar disorder (BD) is a chronic mood disordercharacterizedwithmanicanddepressiveepisodes [1].Durationofremissionafterthefirstepisodeisstrongly associated with morbidity [2]. Therefore, stabilization of thepatientsafterthefirstepisodehasacrucialroleinthe functioning.Fromhere,weaimtoexaminetheacuteand maintenancetreatmentofbipolarpatientswithfirstmanic episodeandrateofrecurrenceforoneyearfollowup.
Methods: Medical records of 394 BD inpatients were screened and 43 of them who had first manic episode recruitedfor the study between01.01.2010 - 31.12.2017. Sociodemographic information, acute treatment regi-mens, rate of recurrence and maintenance treatment of individualswerecollected.
Results:Nearlyhalfofthepatientswasmen(55.8%), du-rationofeducationwas9.4± 4.58yearsandmedianagefor thefirstepisodewas23years(min=16,max=45,S.D=7.9 years).Almost half of thepatients experienced psychotic symptomsatthefirstepisode(51.2%,n=22).Approximately twothirdofthepatients(65.1%,n=28)wastreatedwitha moodstabilizer(MS)andatypicalantipsychotic(AAP) com-bination while about one quarter of the patients (23.3%, n=10)treatedwithAAPmonotherapy,7%was(n=3)treated withMSmonotherapy,4.7%(n=2)wastreatedwithtwoMS andanAAP combinationtreatment. Themeandurationof hospitalizationwas15.7± 14.2days(min=2,max=40)and median time for the control visit after discharge was1.5 weeks(min=1,max=42).Whenweevaluatetherecurrence rates for the firstyear offollow-up; 73.7% of BDpatients (n=28) did not have any mood episode while 26.3% of them (n=10) had a new episode (n=3 depression, n=7 mania).Ontheotherhand,11%ofindividuals(n=5)didnot cometotheoutpatientcliniccontrolafterdischarge.Mean durationuntilnextepisodewas30.1 ± 16.6weeks. When wescreenedforthemaintenancetreatment,wefoundthat 48.8%of patients(n=21)wasonMSplusAAP combination while16.3%(n=7)wasonMSmonotherapy.
Conclusion: Ourfindings on the recurrencerate in the firstyearoftheillnesswassimilarwithsomeofthestudies [3] while other studies reported higher recurrence rates [4,5]. Lowerrates in ourstudy could berelated withthe olderageofonsetandlowerproportionofpsychotic symp-tomsinoursamplecomparingwithliterature[4].However, this couldbespecific tooursample since relativelysmall sample size is one of the major limitation of our study. Longerfollow-upstudieswithlargersamplesizecould pro-videstrongerevidencefor predictingthevariablesrelated withrecurrenceinpatientswithBD.
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[1] Grande,I.,Berk,M.,Birmaher,B.,Vieta,E.,2016.Bipolar dis-order.Lancet387,1561–1572.
S78 Abstracts [2]Kessing,L.V.,Andersen,P.K.,Vinberg,M.,2017.Riskof
recur-renceafterasinglemanicormixedepisode–asystematic re-viewandmeta-analysis.Bipolardisorders20(1),9–17. [3]Vázquez, G.H., Holtzman, J.N., Lolich, M., Ketter, T.A.,
Baldessarini,R.J.,2015.Recurrenceratesinbipolardisorder: systematiccomparisonoflong-termprospective,naturalistic studies versus randomized controlled trials. European Neu-ropsychopharmacology25(10),1501–1512.
[4]Yatham,L.N., Kauer-Sant’Anna,M., Bond, D.J., Lam,R.W., Torres, I., 2009. Course and outcome after the first manic episode in patients with bipolar disorder: prospective 12-monthdatafromtheSystematicTreatmentOptimization Pro-gramForEarlyManiaproject.TheCanadianJournalof Psychi-atry54(2),105–112.
[5]Kora,K.,Saylan,M.,Akkaya,C.,Karamustafalioglu,N., Tom-ruk,N.,Yasan,A.,Oral,T.,2008.Predictivefactorsfortimeto remissionandrecurrenceinpatientstreatedforacutemania: healthoutcomesofmanicepisodes(HOME)study.Primarycare companiontotheJournalofclinicalpsychiatry10(2),114. doi:10.1016/j.euroneuro.2018.11.1057
P.056 Repeated subanesthetic administration of ke-taminemaintainsanincreaseindopamine neurotrans-mission:anelectrophysiologicalstudyinratbrain
C.M.Iro,M. ElMansari,P.Blier∗
UniversityofOttawaInstituteofMentalHealthResearch, Psychiatry,Ottawa,Canada
Background: Subanaesthetic doses of intravenous ke-tamine have elicited rapid, albeit transient reduction of depressive symptomsin patients withtreatment-resistant depression [1]. Repeated ketamine administration may prolong theseeffects[2,3].Previousanimal research con-ductedbyourlaboratory[4]andinanotherlab[5]showed thattheseeffectswereatleastinpartduetoanincreasein ventraltegmentalarea(VTA)dopamine(DA)neuron activ-itieswhichoccur30minutesto2hourspost-administration [4].The currentstudy aimstodetermineifthesechanges persist after 24 hours. We also hypothesized that these actions couldbe prolongedwith repeatedadministrations ofketamineasisdoneintheclinic.
Methods:ExperimentswerecarriedoutonmaleSprague Dawley rats weighing 275-320g at the time of the ex-periments. Rats were anaesthetized with chloral hydrate (400 mg/kg; i.p.) and mounted on a stereotaxic frame. Extracellular unitary recordings were performed using single-barrelglassmicropipettesfilledwith2MNaCl solu-tion,withimpedancesrangingfrom2to4M. Recordings were carriedoutin the ventraltegmentalarea(VTA) and dorsal raphe nucleus (DRN) for serotonin (5-HT) neurons. Presumed5-HTandDA neuronswerethenidentifiedusing the criteria previously described [1]. Electrophysiological recordings we conducted: 24 hours after a single admin-istration of ketamine (10 mg/kg; i.p.) or 24 hours after repeatedadministrations of ketaminegiven thriceweekly fortwoweeks.Neuronswereanalyzedforchangesinspike frequencyandinthepercentageofburstsaswellasinthe numberofspontaneouslyactiveneuronspertrackinVTA.
Results:Twentyfourhoursafterasingleadministration of ketamine, there was no change in firing and bursting activity, and in the number of spontaneously active DA neurons encountered per track. However, although the firingactivity of DA neurons wasnot alteredby repeated injectionsofketaminefor 2weeks,itdidincreaseby 33% the percentage of spikes occurring in bursts (control: 24 ± 3.6% and 32 ± 2.8% for ketamine; p=0.02; n=5) and thenumberofactiveDAneuronspertrack(control:1.7± 0.09%and3.2± 0.5%forketamine-treatedrats;p=0.02; n=5).Nochangeswereobservedinthefiringandbursting parametersofDRN5-HTneuronsatanytimepoint.
Conclusion:Inapreviousstudy[4],weshowedthatacute administrationofketamineincreasedDAneuronpopulation activity.Thisincreasewasnolongerpresent24hoursafter a single injection of ketamine, as shown in the present study. However, repeated administrations of ketamine resulted in an enhancement of bursting and population activityofDAneurons.Itisthuspossiblethattheincrease in population activity of DA neurons and possibly their higherburstingactivityunderliethe antidepressanteffect ofasubanestheticdoseofketaminewhengivenrepeatedly. Disclosurestatement:P.Blierisaconsultantandaprincipal siteinvestigatorforan ongoingclinicaltrialofesketamine beingconductedbyJanssen.CMIroandMElMansarihave. References
[1]Newport,D.J.,Carpenter,L.L.,McDonald,W.M.,Potash,J.B., Tohen,M., Nemeroff,C.B.,2015.Ketamine andotherNMDA antagonists:Earlyclinicaltrialsandpossiblemechanismsin de-pression.AmJPsychiatry172,950–966.
[2]Coyle,C.M.,Laws,K.R.,2015.Theuseofketamineasan an-tidepressant:asystematicreviewandmeta-analysis.Hum Psy-chopharmacol30,152–163.
[3]Phillips, J.L., Birmingham,M., Hatchard, T.,Norris, S., Tal-bot,J.,Ortiz,A.,Blier,P.,2017.Acuteandprolonged antide-pressant effects ofketamine in treatment-resistant depres-sion.Neuropsychopharmacology43(S1),S189–S190.
[4]ElIskandrani,K.S.,Oosterhof,C.A.,ElMansari,M.,Blier,P., 2015. Impact ofsubanesthetic doses of ketamineon AMPA-mediated responses in rats: An in vivo electrophysiological study on monoaminergic and glutamatergic neurons. J Psy-chopharmacol29,792–801.
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doi:10.1016/j.euroneuro.2018.11.1058
P.057Predictingdepressionseverity:theroleof socio-cognitivevariables
F.Caetano1,∗,S.Carvalho1,C.Silva2
1HospitaldeMagalhãesLemos,Psychiatry,Porto,Portugal 2Psychiatry,Porto,Portugal
Introduction. Major depressive disorder is a serious mentalillness, andoneof theleading causesof disability causing not only personal suffering but also overload of healthsystems[1].
