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Available at:http:\u002F\u002Fwww.fda.gov\u002Fcder\u002Fdrug\u002FInfoSheets\u002FHCP\u002FcarbamazepineHCP.htm. Accessed January 24 2009.",{},false,{"id":1205,"createTime":1206,"updateTime":1206,"relativeEntities":1207,"slug":1208,"properties":1209,"entityType":115,"verifyStatus":116,"verifyTime":1206,"verifyNote":117,"languages":1224,"translateLanguages":24,"viewCount":25,"primaryUrl":1225,"fullTextUrl":24,"authors":1226,"publicationType":463,"publisherRelationship":1354,"citationCount":1404,"citationInfo":1405,"publishDate":1409,"publishYear":1406,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":1410,"openAccess":24,"references":1411,"isForceReanalyzing":1203},"9d8b5237-c835-4713-9bb3-9843638168d9","2024-12-26T20:09:01.113+00:00",[],"-i-N-i-acetylaspartate-normalization-in-bipolar-depression-after-lamotrigine-treatment",{"mag":1210,"pmc":1212,"openalex":1214,"abstract":1216,"title":1218,"pm":1220,"doi":1222},{"VOID":1211},"2109360212",{"VOID":1213},"4655601",{"VOID":1215},"W2109360212",{"EN":1217},"\u003Cjats:sec>\u003Cjats:title>Objectives\u003C\u002Fjats:title>\u003Cjats:p>The aim of the present study was to examine \u003Cjats:italic>N\u003C\u002Fjats:italic>‐acetylaspartate (NAA), a general marker of neuronal viability, and total NAA (\u003Cjats:styled-content style=\"fixed-case\">tNAA\u003C\u002Fjats:styled-content>), the combined signal of NAA and \u003Cjats:italic>N‐\u003C\u002Fjats:italic>acetylaspartylglutamate, in bipolar depression before and after lamotrigine treatment. Given that NAA is synthesized through direct acetylation of aspartate by acetyl‐coenzyme A‐\u003Cjats:sc>l\u003C\u002Fjats:sc>‐aspartate‐\u003Cjats:italic>N\u003C\u002Fjats:italic>‐acetyltransferase, we hypothesized that treatment with lamotrigine would be associated with an increase in NAA level.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Methods\u003C\u002Fjats:title>\u003Cjats:p>Patients with bipolar depression underwent two‐dimensional proton magnetic resonance spectroscopy of the anterior cingulate at baseline (n = 15) and after 12 weeks of lamotrigine treatment (n = 10). A group of age‐matched healthy controls (n = 9) underwent scanning at baseline for comparison.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p>At baseline, patients with bipolar depression had significantly lower NAA [mean standard deviation (SD) = 1.13 (0.21); p = 0.02] than controls [mean (SD) = 1.37 (0.27)]. Significant increases in NAA [mean (SD) = 1.39 (0.21); p = 0.01] and \u003Cjats:styled-content style=\"fixed-case\">tNAA\u003C\u002Fjats:styled-content> [mean (SD) = 1.61 (0.25); p = 0.02] levels were found after 12 weeks of lamotrigine treatment.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Conclusions\u003C\u002Fjats:title>\u003Cjats:p>These data suggest an \u003Cjats:styled-content style=\"fixed-case\">NAA\u003C\u002Fjats:styled-content> deficit in bipolar depression that is normalized after lamotrigine treatment. Future research is warranted to evaluate whether baseline \u003Cjats:styled-content style=\"fixed-case\">NAA\u003C\u002Fjats:styled-content> level is a potential biomarker for identifying lamotrigine response patterns and whether this functional brain change has an associated clinical response.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>",{"EN":1219},"\u003Ci>N\u003C\u002Fi>‐acetylaspartate normalization in bipolar depression after lamotrigine treatment",{"VOID":1221},"25495884",{"VOID":1223},"10.1111\u002Fbdi.12285",[119],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fbdi.12285",[1227,1246,1265,1284,1303,1320,1337],{"id":1228,"sortIndex":25,"researcher":24,"roles":1229,"affiliations":1230,"properties":1239,"displayName":1243,"givenName":24,"familyName":24},"a26a315f-8bbe-49ce-981b-6491ecffe33a",[],[1231],{"id":1232,"sortIndex":25,"affiliation":1233,"properties":24},"16a98587-022a-4d4c-8954-4b806d70f3b6",{"id":1232,"createTime":24,"updateTime":24,"relativeEntities":1234,"slug":24,"properties":1235,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1238,"statistic":24},[],{"title":1236},{"VI":1237},"Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN, USA",[],{"orcid":1240,"title":1242,"openalex":1244},{"VOID":1241},"https:\u002F\u002Forcid.org\u002F0000-0001-6843-6503",{"EN":1243},"Paul E. 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Fitches A. Evidence of associations between bipolar disorder and the brain‐derived neurotropic factor (\u003Cjats:italic>BDNF\u003C\u002Fjats:italic>) gene. Bipolar Disord 2011: 13: 630–637. © 2011 The Authors. Journal compilation © 2011 John Wiley & Sons A\u002FS.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Objective: \u003C\u002Fjats:bold> Brain‐derived neurotrophic factor (BDNF) has important roles in neural cell growth and differentiation. Despite multiple lines of evidence suggesting BDNF as a possible contributor to the pathogenesis of bipolar disorder (BD), the results of genetic association studies have been mixed. We hypothesize that \u003Cjats:italic>BDNF\u003C\u002Fjats:italic> gene polymorphisms may confer increased susceptibility to BD.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Methods: \u003C\u002Fjats:bold> Using a cohort of multiplex bipolar families, we performed family‐based association testing to look for associations between BD and eight single nucleotide polymorphisms (SNPs) from \u003Cjats:italic>BDNF\u003C\u002Fjats:italic>.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Results: \u003C\u002Fjats:bold> We found associations (p < 0.05) between BD and six of the eight SNPs analysed, including two SNPs not previously investigated in association studies. We were able to replicate associations previously found between BD and the Val66Met polymorphism of \u003Cjats:italic>BDNF\u003C\u002Fjats:italic> (rs6265) and the SNPs rs1519480 and rs12273363. 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Lithium, valproic acid (VPA) and carbamazepine (CBZ) are commonly used mood stabilizers, but their therapeutic mechanism is unclear. These drugs all cause the same morphological effects on postnatal rat neuronal dorsal root ganglia (DRG) growth cones via an inositol‐reversible mechanism. However, due to limitations in earlier analysis, the effects of combining drugs, drug specificity and inositol stereoisomer specificity are unknown. We devised an improved analytical method to address these issues.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Methods: \u003C\u002Fjats:bold> Dorsal root ganglia explants were cultured individually and incubated with combinations of psychotropic drugs and inositol stereoisomers. We recorded axonal growth cone morphology and calculated growth cone area per a modified method described by Williams et al. (\u003Cjats:italic>Nature\u003C\u002Fjats:italic> 2002; \u003Cjats:bold>417\u003C\u002Fjats:bold>: 292–295). Statistically significant changes in area were calculated using non‐parametric statistical testing.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Results: \u003C\u002Fjats:bold> (i) Lithium and VPA showed an additive effect on growth cone spreading. (ii) Among eight additional psychotropic drugs to those previously tested, only imipramine and chlorpromazine altered DRG growth cone morphology. As this effect was not reversed by \u003Cjats:italic>myo\u003C\u002Fjats:italic>‐inositol, it arises from a different mechanism to the mood stabilizers lithium, VPA and CBZ. (iii) \u003Cjats:italic>Myo\u003C\u002Fjats:italic>‐inositol, but not \u003Cjats:italic>scyllo\u003C\u002Fjats:italic>‐ or \u003Cjats:italic>epi\u003C\u002Fjats:italic>‐inositol, causes a significant reversal of the lithium effect on the growth cones spreading, consistent with the inositol depletion hypothesis.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Conclusions: \u003C\u002Fjats:bold> These results show that lithium, VPA and CBZ are unique in causing altered neuronal morphology via \u003Cjats:italic>myo\u003C\u002Fjats:italic>‐inositol depletion.\u003C\u002Fjats:p>",{"EN":1902},"Specificity of mood stabilizer action on neuronal growth cones",{"VOID":1904},"17430303",{"VOID":1906},"10.1111\u002Fj.1399-5618.2007.00400.x","2024-12-02T10:28:04.982+00:00",[119],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1399-5618.2007.00400.x",[1911,1928,1947,1964,1981],{"id":1912,"sortIndex":25,"researcher":24,"roles":1913,"affiliations":1914,"properties":1923,"displayName":1925,"givenName":24,"familyName":24},"61c534e7-bfca-418c-88ef-6a8f09f99dd0",[],[1915],{"id":1916,"sortIndex":25,"affiliation":1917,"properties":24},"3a950da3-57f4-4a51-b1ac-904d457a2084",{"id":1916,"createTime":24,"updateTime":24,"relativeEntities":1918,"slug":24,"properties":1919,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1922,"statistic":24},[],{"title":1920},{"VI":1921},"Stanley Research Center and Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, and Mental Health Center, Beersheva, Israel",[],{"title":1924,"openalex":1926},{"EN":1925},"Galit Shaltiel",{"VOID":1927},"A5061874089",{"id":1929,"sortIndex":143,"researcher":24,"roles":1930,"affiliations":1931,"properties":1940,"displayName":1944,"givenName":24,"familyName":24},"b942c25e-a6e3-4e6c-aebb-c9bbcfb8b044",[],[1932],{"id":1933,"sortIndex":25,"affiliation":1934,"properties":24},"c57bf329-0631-49ba-9811-c4c838135e41",{"id":1933,"createTime":24,"updateTime":24,"relativeEntities":1935,"slug":24,"properties":1936,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1939,"statistic":24},[],{"title":1937},{"EN":1938},"Cardiff School of Bioscience, Cardiff University, Cardiff, UK",[],{"orcid":1941,"title":1943,"openalex":1945},{"VOID":1942},"https:\u002F\u002Forcid.org\u002F0000-0002-3517-0742",{"EN":1944},"Emma Dalton",{"VOID":1946},"A5087417185",{"id":1948,"sortIndex":161,"researcher":24,"roles":1949,"affiliations":1950,"properties":1957,"displayName":1961,"givenName":24,"familyName":24},"07e802d8-36b3-4015-b477-dde93182ccf7",[],[1951],{"id":1916,"sortIndex":25,"affiliation":1952,"properties":24},{"id":1916,"createTime":24,"updateTime":24,"relativeEntities":1953,"slug":24,"properties":1954,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1956,"statistic":24},[],{"title":1955},{"VI":1921},[],{"orcid":1958,"title":1960,"openalex":1962},{"VOID":1959},"https:\u002F\u002Forcid.org\u002F0000-0001-9734-1829",{"EN":1961},"Robert H. 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with bipolar disorder exhibit neuropsychological impairments when they are euthymic (neither depressed nor manic). One of the most consistently reported cognitive problems in euthymic individuals with bipolar disorder is impairment in verbal episodic memory. Recent findings suggest that episodic memory difficulties in these individuals are attributable to difficulties using organizational strategies during encoding. The purpose of the present study was (i) to investigate whether difficulties using organizational strategies in bipolar disorder are due to a failure in spontaneously initiating verbal organization strategies or are due to difficulties implementing such strategies, and (ii) to compare the characteristics of verbal organizational impairment in bipolar disorder with those observed in individuals with obsessive–compulsive disorder (OCD).\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Methods: \u003C\u002Fjats:bold>Study participants were 20 individuals with bipolar I disorder (BP‐I), 20 individuals with OCD, and 20 healthy control participants matched for age, gender, and education. Participants completed a verbal encoding paradigm that involved spontaneous and directed use of verbal organization strategies during encoding of word lists.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Results: \u003C\u002Fjats:bold>Compared with control subjects, both BP‐I and OCD participants showed impaired verbal organization in the spontaneous encoding condition. In the directed encoding condition, OCD patients organized the word lists as well as control participants whereas BP‐I participants exhibited lower verbal organization than both control and OCD participants. OCD and BP‐I participants’ free recall performance did not differ from that of control participants in the spontaneous encoding condition. In the directed encoding condition, BP‐I participants recalled fewer words than OCD or control participants.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Conclusions: \u003C\u002Fjats:bold>Episodic memory difficulties in OCD are associated with difficulties spontaneously initiating verbal organization strategies during encoding whereas the ability to implement verbal organization when instructed to do so is preserved. 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disparities between individuals of African and European ancestry are well documented. The disparities in bipolar disorder may be driven by racial bias superimposed on established factors contributing to misdiagnosis, including: evolving empirically based diagnostic criteria (International Classification of Diseases [\u003Cjats:styled-content style=\"fixed-case\">ICD\u003C\u002Fjats:styled-content>], Research Diagnostic Criteria [\u003Cjats:styled-content style=\"fixed-case\">RDC\u003C\u002Fjats:styled-content>] and Diagnostic and Statistical Manual [\u003Cjats:styled-content style=\"fixed-case\">DSM\u003C\u002Fjats:styled-content>]), multiple symptom domains (i.e. mania, depression and psychosis), and multimodal medical and additional psychiatric comorbidity.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Methods\u003C\u002Fjats:title>\u003Cjats:p>For this paper, we reviewed the phenomenological differences between bipolar individuals of African and European ancestry in the context of diagnostic criteria and clinical factors that may contribute to a potential racial bias.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p>Published data show that bipolar persons of African ancestry, compared with bipolar persons of non‐African ancestry, are more often misdiagnosed with a disease other than bipolar disorder (i.e. schizophrenia). Additionally, studies show that there are disparities in recruiting patients of African ancestry to participate in important genomic studies. This gap in biological research in this underrepresented minority may represent a missed opportunity to address potential racial differences in the risk and course of bipolar illness.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Conclusion\u003C\u002Fjats:title>\u003Cjats:p>A concerted effort by the research community to increase inclusion of diverse persons in studies of bipolar disorder through community engagement may facilitate fully addressing these diagnostic and treatment disparities in bipolar individuals of African ancestry.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>",{"EN":2643},"Racial disparities in bipolar disorder treatment and research: a call to action",{"VOID":2645},"29527766",{"VOID":2647},"10.1111\u002Fbdi.12638","2024-11-26T19:05:31.968+00:00",[119],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fbdi.12638",[2652,2669,2696,2715,2742,2767,2786,2805,2822,2841,2868,2885,2908],{"id":2653,"sortIndex":25,"researcher":24,"roles":2654,"affiliations":2655,"properties":2664,"displayName":2666,"givenName":24,"familyName":24},"2343f35a-088b-40a8-873c-1f9ed5222f50",[],[2656],{"id":2657,"sortIndex":25,"affiliation":2658,"properties":24},"401d3a17-642b-4f77-89a2-8a505eb27273",{"id":2657,"createTime":24,"updateTime":24,"relativeEntities":2659,"slug":24,"properties":2660,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2663,"statistic":24},[],{"title":2661},{"EN":2662},"Clinical and Translational Science, Mayo Clinic Graduate School of Biomedical Sciences, Rochester, MN, USA",[],{"title":2665,"openalex":2667},{"EN":2666},"Margaret Akinhanmi",{"VOID":2668},"A5040807906",{"id":2670,"sortIndex":143,"researcher":24,"roles":2671,"affiliations":2672,"properties":2689,"displayName":2693,"givenName":24,"familyName":24},"42d155a2-1a61-4998-a2f6-f7684f209b3e",[],[2673,2681],{"id":2674,"sortIndex":25,"affiliation":2675,"properties":24},"aadddfe5-a9c3-49b4-a487-2b9719ce8d57",{"id":2674,"createTime":24,"updateTime":24,"relativeEntities":2676,"slug":24,"properties":2677,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2680,"statistic":24},[],{"title":2678},{"VI":2679},"Department of Psychiatry & Psychology, Mayo Clinic, Rochester, MN, USA",[],{"id":2682,"sortIndex":143,"affiliation":2683,"properties":24},"e2f8530e-90ee-46b5-8351-b1a5537dd689",{"id":2682,"createTime":24,"updateTime":24,"relativeEntities":2684,"slug":24,"properties":2685,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2688,"statistic":24},[],{"title":2686},{"VI":2687},"Division of Biomedical Statistics and Informatics Mayo Clinic Rochester MN USA",[],{"orcid":2690,"title":2692,"openalex":2694},{"VOID":2691},"https:\u002F\u002Forcid.org\u002F0000-0001-9350-4440",{"EN":2693},"Joanna M. 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sought to determine whether a single hypothesized latent factor structure would characterize cognitive functioning in three distinct groups.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Methods\u003C\u002Fjats:title>\u003Cjats:p>We assessed 576 adults (340 community controls, 126 adults with bipolar disorder, and 110 adults with schizophrenia) using 15 measures derived from nine cognitive tests. Confirmatory factor analysis (\u003Cjats:styled-content style=\"fixed-case\">CFA\u003C\u002Fjats:styled-content>) was conducted to examine the fit of a hypothesized six‐factor model. The hypothesized factors included attention, psychomotor speed, verbal memory, visual memory, ideational fluency, and executive functioning.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p>The six‐factor model provided an excellent fit for all three groups [for community controls, root mean square error of approximation (\u003Cjats:styled-content style=\"fixed-case\">RMSEA\u003C\u002Fjats:styled-content>) <0.048 and comparative fit index (\u003Cjats:styled-content style=\"fixed-case\">CFI\u003C\u002Fjats:styled-content>) = 0.99; for adults with bipolar disorder, \u003Cjats:styled-content style=\"fixed-case\">RMSEA\u003C\u002Fjats:styled-content> = 0.071 and \u003Cjats:styled-content style=\"fixed-case\">CFI\u003C\u002Fjats:styled-content> = 0.99; and for adults with schizophrenia, \u003Cjats:styled-content style=\"fixed-case\">RMSEA\u003C\u002Fjats:styled-content> = 0.06 and \u003Cjats:styled-content style=\"fixed-case\">CFI\u003C\u002Fjats:styled-content> = 0.98]. Alternate models that combined fluency with processing speed or verbal and visual memory reduced the goodness of fit. Multi‐group \u003Cjats:styled-content style=\"fixed-case\">CFA\u003C\u002Fjats:styled-content> results supported factor invariance across the three groups.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Conclusions\u003C\u002Fjats:title>\u003Cjats:p>Confirmatory factor analysis supported a single six‐factor structure of cognitive functioning among patients with schizophrenia or bipolar disorder and community controls. While the three groups clearly differ in level of performance, they share a common underlying architecture of information processing abilities. 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Pramipexole in treatment‐resistant depression: a 16‐week naturalistic study. Bipolar Disord 2002: 4: 307–314. © Blackwell Munksgaard 2002\u003C\u002Fjats:p>\u003Cjats:p> \u003Cjats:italic>\n            \u003Cjats:bold>Objective:\u003C\u002Fjats:bold> To assess the antidepressant efficacy and tolerability of adjunctive pramipexole, a D\u003Cjats:sub>2\u003C\u002Fjats:sub>–D\u003Cjats:sub>3\u003C\u002Fjats:sub>\u003C\u002Fjats:italic> dopamine agonist, in patients with drug‐resistant depression.\u003C\u002Fjats:p>\u003Cjats:p> \u003Cjats:italic>\n            \u003Cjats:bold>Methods:\u003C\u002Fjats:bold>\n          \u003C\u002Fjats:italic> The study sample consisted of in‐patients with major depressive episode, according to the DSM‐IV, and drug resistance. Pramipexole was added to antidepressant treatment with TCA or SSRI, at increasing doses from 0.375 to 1.0 mg\u002Fday. Two independent response criteria were adopted: a >50% reduction of the Montgomery–Asberg Depressive Rating Scale (MADRS) total score and a score of 1 or 2 on the Clinical Global Impression scale (CGI‐I) at endpoint. Side‐effects were assessed by the Dosage Record Treatment Emergent Symptom Scale (DOTES).\u003C\u002Fjats:p>\u003Cjats:p> \u003Cjats:italic>\n            \u003Cjats:bold>Results:\u003C\u002Fjats:bold>\n          \u003C\u002Fjats:italic> Thirty‐seven patients were enrolled. Of these, 16 had unipolar depression and 21 had bipolar depression. Six patients dropped out in the first week. Of the 31 patients included in the analyses, 19 completed the 16‐week follow‐up. Mean maximal dose of pramipexole was 0.95 mg\u002Fday. Mean scores on MADRS decreased from 33.3 ± 8.4 at baseline to 13.9 ± 11.5 at endpoint (p < 0.001) and the CGI‐S decreased from 4.6 ± 0.8 at baseline to 2.8 ± 1.3 at endpoint (p < 0.001). At endpoint, 67.7% (21\u002F31) of patients were responders on MADRS and 74.2% on CGI‐I. Of the 37 patients enrolled, 10 discontinued pramipexole because of adverse events.\u003C\u002Fjats:p>\u003Cjats:p> \u003Cjats:italic>\n            \u003Cjats:bold>Conclusions:\u003C\u002Fjats:bold>\n          \u003C\u002Fjats:italic> These preliminary data suggest that pramipexole adjunction to antidepressant treatment may be effective and well tolerated in patients with resistant major depression.\u003C\u002Fjats:p>",{"EN":3564},"Pramipexole in treatment‐resistant depression: a 16‐week naturalistic 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M, 2000, New approaches to the treatment of refractory depression, J Clin Psychiatry, 61, 26",{},{"id":24,"text":3830,"url":24,"identifiers":3831},"Bouckoms A, 1993, Pergolide: an antidepressant adjuvant for mood disorders?, Psychopharmacol Bull, 29, 207",{},{"id":24,"text":3833,"url":24,"identifiers":3834},"10.1055\u002Fs-2007-979191",{"doi":3833},{"id":24,"text":3836,"url":24,"identifiers":3837},"10.1097\u002F00004850-199707003-00002",{"doi":3836},{"id":24,"text":3839,"url":24,"identifiers":3840},"10.1097\u002F00002826-199720001-00006",{"doi":3839},{"id":24,"text":3842,"url":24,"identifiers":3843},"10.1016\u002FS0924-977X(96)00393-8",{"doi":3842},{"id":24,"text":3845,"url":24,"identifiers":3846},"10.1007\u002FBF02245568",{"doi":3845},{"id":24,"text":3848,"url":24,"identifiers":3849},"Rosenbaum JF, 1999, Pramipexole treatment for cocaine cravings, Am J Psychiatry, 156, 1834, 10.1176\u002Fajp.156.11.1834",{"doi":3850},"10.1176\u002Fajp.156.11.1834",{"id":24,"text":3852,"url":24,"identifiers":3853},"10.1002\u002F(SICI)1520-6394(2000)11:2\u003C58::AID-DA2>3.0.CO;2-H",{"doi":3852},{"id":24,"text":3855,"url":24,"identifiers":3856},"10.3109\u002F10401230009147102",{"doi":3855},{"id":24,"text":3858,"url":24,"identifiers":3859},"Goldberg JF, 1999, Pramipexole in refractory bipolar depression, Am J Psychiatry, 156, 798, 10.1176\u002Fajp.156.5.798",{"doi":3860},"10.1176\u002Fajp.156.5.798",{"id":24,"text":3862,"url":24,"identifiers":3863},"ThaseME RushAJ.Treatment‐resistant depression. In: Bloom FE Kupfer DJ eds. Psychopharmacology the Fourth Generation of Progress 4th edn. Philadelphia MD: Lippincott‐Raven Healthcare 1995: 1081–1097.",{},{"id":24,"text":3865,"url":24,"identifiers":3866},"10.1016\u002F0022-3956(88)90022-2",{"doi":3865},{"id":24,"text":3868,"url":24,"identifiers":3869},"GuyW.Clinical Global Impression. ECDEU Assessment Manual for Psychopharmacology (Revised). Rockville MD: US Department Health Education and Welfare Publication (ADM: National Institute of Mental Health;1979: 76–338.",{},{"id":24,"text":3871,"url":24,"identifiers":3872},"10.1111\u002Fj.1744-6171.1991.tb00509.x",{"doi":3871},{"id":24,"text":3874,"url":24,"identifiers":3875},"10.1001\u002Farchpsyc.1993.01820210073009",{"doi":3874},{"id":24,"text":3877,"url":24,"identifiers":3878},"SAS\u002FSTAT. STAT Software. Version 7.0. Cary NC: SAS Institute 1998.",{},{"id":24,"text":3880,"url":24,"identifiers":3881},"10.4088\u002FJCP.v59n0706",{"doi":3880},{"id":24,"text":3883,"url":24,"identifiers":3884},"10.1016\u002FS0165-0327(97)00082-7",{"doi":3883},{"id":24,"text":3886,"url":24,"identifiers":3887},"10.1055\u002Fs-2007-1014417",{"doi":3886},{"id":24,"text":3889,"url":24,"identifiers":3890},"Mouret J, 1987, Polygraphic, clinical and therapeutic markers of dopamine‐dependent depressions, C R Acad Sci III, 305, 301",{},{"id":24,"text":3892,"url":24,"identifiers":3893},"10.4088\u002FJCP.v60n0903",{"doi":3892},{"id":3895,"createTime":3896,"updateTime":3896,"relativeEntities":3897,"slug":3898,"properties":3899,"entityType":115,"verifyStatus":116,"verifyTime":3896,"verifyNote":117,"languages":3912,"translateLanguages":24,"viewCount":25,"primaryUrl":3913,"fullTextUrl":24,"authors":3914,"publicationType":463,"publisherRelationship":4028,"citationCount":4077,"citationInfo":4078,"publishDate":4081,"publishYear":4079,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":4082,"openAccess":24,"references":4083,"isForceReanalyzing":1203},"78e157d9-c8e5-47c6-8f0e-ff157da613cd","2024-10-10T21:02:39.930+00:00",[],"Treatment-adherence-with-antipsychotic-medications-in-bipolar-disorder",{"openalex":3900,"mag":3902,"abstract":3904,"title":3906,"pm":3908,"doi":3910},{"VOID":3901},"W2143913225",{"VOID":3903},"2143913225",{"EN":3905},"\u003Cjats:p>\u003Cjats:bold>Objectives: \u003C\u002Fjats:bold> Atypical antipsychotic medications are a relatively new, increasingly prominent component of the treatment armamentarium for bipolar disorder. Information on adherence with antipsychotics among individuals with bipolar disorder in general, and atypical antipsychotics in particular, is currently quite limited. Using data from the VA National Psychosis Registry, we examined adherence with antipsychotic medications among patients with bipolar disorder (n = 73,964).\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Methods: \u003C\u002Fjats:bold> Antipsychotic medication adherence among veterans with bipolar disorder was evaluated using the medication possession ratio and categorizing patients into three groups: fully adherent, partially adherent and non‐adherent. We compared characteristics of bipolar patients who received versus those who did not receive antipsychotic medication, and also identified predictors of poor adherence with antipsychotic medications.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Results: \u003C\u002Fjats:bold> Approximately 45% (n = 32,993) of all individuals with bipolar disorder were prescribed antipsychotic medication. Individuals who were prescribed antipsychotic medications were younger and more often had comorbid substance abuse or post‐traumatic stress disorder compared to individuals with bipolar disorder who were not prescribed antipsychotic medication. Just over half (51.9%) of individuals appear to be fully adherent with antipsychotic medications, while 48.1% of individuals are either partially adherent or non‐adherent with antipsychotic medications. Factors associated with treatment non‐adherence were younger age, minority ethnicity, comorbid substance abuse and homelessness.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Conclusions: \u003C\u002Fjats:bold> Treatment non‐adherence is a major issue for close to half of individuals with bipolar disorder prescribed antipsychotic medication. 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noncompliance in patients with mania, J Clin Psychiatry, 57, 292",{},{"id":24,"text":4197,"url":24,"identifiers":4198},"10.1176\u002Fappi.ps.57.1.56",{"doi":4197},{"id":24,"text":4200,"url":24,"identifiers":4201},"Sajatovic M, 2005, Treatment Adherence in Patients with Rapid Cycling Bipolar Disorder: Results from a Clinical Trials Setting",{},{"id":4203,"createTime":4204,"updateTime":4204,"relativeEntities":4205,"slug":4206,"properties":4207,"entityType":115,"verifyStatus":116,"verifyTime":4204,"verifyNote":117,"languages":4220,"translateLanguages":24,"viewCount":25,"primaryUrl":4221,"fullTextUrl":24,"authors":4222,"publicationType":463,"publisherRelationship":4345,"citationCount":4394,"citationInfo":4395,"publishDate":4397,"publishYear":2392,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":4398,"openAccess":24,"references":4399,"isForceReanalyzing":1203},"fa46fdf2-5528-4fc8-ae3f-1f76e3dad6fb","2024-10-10T21:02:36.729+00:00",[],"Identifying-and-improving-non-adherence-in-bipolar-disorders",{"openalex":4208,"mag":4210,"abstract":4212,"title":4214,"pm":4216,"doi":4218},{"VOID":4209},"W2162272146",{"VOID":4211},"2162272146",{"EN":4213},"\u003Cjats:p>\u003Cjats:bold>Objectives: \u003C\u002Fjats:bold> To review the definition of non‐adherence, its clinical and economic impact and identify its role and impact in clinical practice.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Methods: \u003C\u002Fjats:bold> A selective review of the literature as conducted of articles and literature known to the authors.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Results: \u003C\u002Fjats:bold> There is a paucity of studies examining specifically treatment non‐adherence and its consequences in bipolar disorder. Few studies have systematically examined ways in which treatment adherence can impact treatment and improve outcome.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Conclusion: \u003C\u002Fjats:bold> Non‐adherence is common in the management of bipolar disorder. Clinicians and Researchers alike need to remain alert and be aware of issues related to non‐adherence – in particular suicide. 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