Number of episodes and duration of illness associated with hypertension and 10-year cardiovascular risk in patients with bipolar disorder type I.

AbstractRisk-taking behavior and impulsivity are core features of bipolar disorder. Whether they are part of the inherited aspect of the illness is not clear. We aimed to evaluate risk-taking behavior as a potential endophenotype for bipolar disorders, and its relationship with impulsivity and illness features. The Balloon Analogue Risk Task (BART) and Barratt Impulsiveness Scale-11 (BIS-11) were used to assess risk-taking behavior and impulsivity respectively in 30 euthymic bipolar I patients (BD), their 25 asymptomatic first-degree relatives (BD-R), and 30 healthy controls (HC). The primary BART outcome measure was the behavioral adjustment score (number of pumps after trials where the balloon did not pop minus the number of pumps after trials where the balloon popped). BD (p< .001) and BD-R (p= .001) had similar and significantly lower adjustment scores than HC. Only BD scored significantly higher on BIS-11 total (p= .01) and motor (p= .04) subscales than HC. Neither the BART, nor impulsivity scores associated with illness features. A limitation of this study is medicated patients and a heterogeneous BD-R were included. Riskiness may be a candidate endophenotype for bipolar disorder as it appears independently from illness features, presents similarly in BD and BD-R groups and differs from impulsivity. (JINS, 2013,19, 1–9)

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Cytokine Polymorphisms in the Pathophysiology of Mood Disorders

CNS Spectrums ◽

10.1017/s1092852900020393 ◽

2009 ◽

Vol 14 (8) ◽

pp. 419-425 ◽

Cited By ~ 52

Author(s):

Mario Clerici ◽

Beatrice Arosio ◽

Emanuela Mundo ◽

Elisabetta Cattaneo ◽

Sara Pozzoli ◽

...

Keyword(s):

Bipolar Disorder ◽

Mood Disorders ◽

Lower Percentage ◽

Genetic Profile ◽

Type I ◽

Genotype Distribution ◽

Bipolar Ii ◽

Tnf Α ◽

Ifn Γ ◽

Disorder Type

ABSTRACTIntroduction: An increasing amount of data suggests that dysregulation of the immune system, including the cytokine network, is associated with the etiology and pathophysiology of mood disorders. Genes encoding cytokines are highly polymorphic and single nucleotide polymorphisms, associated with increased or reduced cytokine production, have been described. The aim of this study was to define the genetic immunologic scenario associated with major depressive disorder (MDD) and bipolar disorder.Methods: Eighty-four Italian outpatients affected by bipolar disorder type I, bipolar disorder type II, or MDD, and 363 healthy controls were enrolled into the study. We analyzed allele and genotype distribution of −308 (G/A) tumor necrosis factor-α (TNF-α), +874 (T/A) interferon-γ (IFN-γ), -174 (G/C) interleukin (IL)-6, and −1082 (G/A) IL-10 promoter polymorphisms by Polymerase Chain Reaction Sequence Specific Primers technique.Results: We observed different genotype and allele distributions of TNF-α, IFN-γ, and IL-10 polymorphisms in the three groups of patients analyzed. In particular, bipolar II patients were characterized by an absence of adenine (A) high producer allele of TNF-α (P<.001) and a lower percentage of TT high producer genotype of IFN-γ (P <.001); bipolar I individuals showed reduced percentage of AA low producer genotype of IL-10 (P<.001). Both bipolar I and bipolar II patients not carrying guanine (G) high producer IL-6 allele showed a lower mean age at onset (P=.048).Conclusion: These data support the existence of a genetic profile related to pro-inflammatory cytokines in patients affected by mood disorders. The differences observed across the three clinical phenotypes suggest the presence of different pathogenetic mechanisms involved in the susceptibility of phenotypically different mood disorders.

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Predictors for Switch From Unipolar Major Depressive Disorder to Bipolar Disorder Type I or II

The Journal of Clinical Psychiatry ◽

10.4088/jcp.v69n0809 ◽

2008 ◽

Vol 69 (8) ◽

pp. 1267-1275 ◽

Cited By ~ 36

Author(s):

K. Mikael Holma ◽

Tarja K. Melartin ◽

Irina A. K. Holma ◽

Erkki T. Isometsä

Keyword(s):

Bipolar Disorder ◽

Major Depressive Disorder ◽

Depressive Disorder ◽

Type I ◽

Major Depressive ◽

Disorder Type

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Cortical thickness and surface area as an endophenotype in bipolar disorder type I patients and their first-degree relatives

NeuroImage Clinical ◽

10.1016/j.nicl.2019.101695 ◽

2019 ◽

Vol 22 ◽

pp. 101695

Author(s):

Nefize Yalin ◽

Aybala Saricicek ◽

Ceren Hidiroglu ◽

Andre Zugman ◽

Nese Direk ◽

...

Keyword(s):

Bipolar Disorder ◽

Surface Area ◽

Cortical Thickness ◽

Type I ◽

First Degree Relatives ◽

Disorder Type

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Catatonia in a patient with bipolar disorder type I

Journal of Neurosciences in Rural Practice ◽

10.1055/s-0039-1700348 ◽

2014 ◽

Vol 05 (03) ◽

pp. 314-316

Author(s):

Ather Muneer

Keyword(s):

Bipolar Disorder ◽

Type I ◽

Disorder Type

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F119. Age Trajectory of Deep White Matter Intensity in Bipolar Disorder Type-I Using MRI

Biological Psychiatry ◽

10.1016/j.biopsych.2019.03.656 ◽

2019 ◽

Vol 85 (10) ◽

pp. S259

Author(s):

Laagishan Yoganathan ◽

Manpreet Sehmbi ◽

Luciano Minuzzi ◽

Benicio N. Frey ◽

Nicholas A. Bock

Keyword(s):

Bipolar Disorder ◽

White Matter ◽

Type I ◽

Deep White Matter ◽

Disorder Type

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POTENTIAL ALTERATIONS IN LEUKOCYTE MITOCHONDRIAL DNA COPY NUMBER FROM PATIENTS WITH BIPOLAR DISORDER TYPE I

European Neuropsychopharmacology ◽

10.1016/j.euroneuro.2017.08.213 ◽

2019 ◽

Vol 29 ◽

pp. S900

Author(s):

Euijung Ryu ◽

Gregory Jenkins ◽

Jared Evans ◽

Ana Andreazza ◽

Marquis Vawter ◽

...

Keyword(s):

Bipolar Disorder ◽

Mitochondrial Dna ◽

Copy Number ◽

Type I ◽

Dna Copy Number ◽

Mitochondrial Dna Copy Number ◽

Disorder Type

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Clinical significance of lifetime panic disorder in the course of bipolar disorder type I

Comprehensive Psychiatry ◽

10.1016/j.comppsych.2008.06.001 ◽

2009 ◽

Vol 50 (1) ◽

pp. 9-12 ◽

Cited By ~ 13

Author(s):

Ricardo Alexandre Toniolo ◽

Sheila C. Caetano ◽

Patrícia Viana da Silva ◽

Beny Lafer

Keyword(s):

Bipolar Disorder ◽

Panic Disorder ◽

Clinical Significance ◽

Type I ◽

Disorder Type

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A systematic review on neuropsychological function in bipolar disorders type I and II and subthreshold bipolar disorders—something to think about

CNS Spectrums ◽

10.1017/s1092852918001463 ◽

2019 ◽

Vol 24 (1) ◽

pp. 127-143 ◽

Cited By ~ 3

Author(s):

Sinead King ◽

James M Stone ◽

Anthony Cleare ◽

Allan H Young

Keyword(s):

Bipolar Disorder ◽

Bipolar Disorders ◽

Cochrane Library ◽

Type I ◽

Neuropsychological Dysfunction ◽

Visual Spatial ◽

Significant Difference ◽

Major Depressive Episodes ◽

Depressive Episodes ◽

Disorder Type

Neuropsychological dysfunction is a well-established finding in individuals with bipolar disorder type I (BP-I), even during euthymic periods; however, it is less clear whether this also pertains to bipolar disorder type II (BP-II) or those with subthreshold states (SBP; subthreshold bipolar disorder), such as bipolar not otherwise specified (BP-NOS). Herein, we compare the literature regarding neuropsychological performance in BP-II vs BP-I to determine the extent of relative impairment, and we present and review all related studies on cognition in SBP. After systematically searching PubMed, Medline, PsycINFO, and The Cochrane Library, we found 17 papers that comprise all the published studies relevant for this review. The areas that are consistently found to be impaired in BP are executive function, verbal memory, visual spatial working memory, and attention. More studies than not show no significant difference between BP-I and BP-II, particularly in euthymic samples. Preliminary evidence suggests that patients experiencing major depressive episodes who also meet criteria for SBP show similar profiles to BP-II; however, these results pertain only to a depressed sample. SBP were found to perform significantly better than both MDD and healthy controls in a euthymic sample. A consensus on mood state, patient selection, and neuropsychological testing needs to be agreed on for future research. Furthermore, no studies have used the most recent DSM-5 criteria for SBP; future studies should address this. Finally, the underlying bases of cognitive dysfunction in these diagnostic groups need to be further investigated. We suggest recommendations on all of the above current research challenges.

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