Cognitive vulnerability in patients with bipolar disorder

Scott, Jan; Stanton, Biba; Garland, Anne; Ferrier, I. N.

doi:10.1017/s0033291799008879

Cited by 249 publications

(242 citation statements)

References 18 publications

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“…A number of studies by different research groups have shown OGM in adults with clinical depression (Brewin, Watson, McCarthy, Hyman, & Dayson, 1998;Goddard, Dritschel, & Burton, 1996;Kuyken & Dalgleish, 1995;Puffet, Jehin-Marchot, Timsit-Berthier, & Timsit, 1991;Wessel, Meeren, Peeters, Arntz, & Merckelbach, 2001), adolescents with major depressive disorder (Park, Goodyer, & Teasdale, 2002) and women with postnatal depression (Croll & Bryant, 2000), as well as in currently euthymic individuals with past major depressive or bipolar episodes (Mackinger, Pachinger, Leibetseder, & Fartacek, 2000;Scott, Stanton, Garland, & Ferrier, 2000) and in sub-clinically dysphoric participants (Goddard, Dritschel, & Burton, 1997;Ramponi, Barnard, & Nimmo-smith, 2004). This combination of findings suggests that OGM could be both a trait and a state marker of depression.…”

Section: Overgeneral Autobiographical Memorymentioning

confidence: 99%

Cognitive factors maintaining persecutory delusions in psychosis: The contribution of depression.

Vorontsova¹,

Garety²,

Freeman³

2013

Journal of Abnormal Psychology

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Depression is common in people with schizophrenia, but how it might directly contribute to the persistence of psychotic symptoms has rarely been tested. The key aim of the present study was to test whether depression and associated cognitive processes predict the maintenance of persecutory delusions. Three groups of participants were tested at baseline: 60 patients with persecutory delusions in the context of a schizophrenia spectrum diagnosis, 30 patients with depression, and 30 nonclinical controls. They completed interviewer and self-report assessments of depression and paranoia, and measures of six cognitive factors (schematic beliefs, experiential avoidance, autobiographical memory, problem solving, rumination, worry style). The patients with persecutory delusions were then assessed again, six months later. It was found that 50% of the patients with persecutory delusions met diagnostic criteria for major depression. Cognitive processes found to be associated with depression across the groups were negative schematic beliefs about the self, experiential avoidance and rumination, but not autobiographical memory or problem solving. The severity of initial depression in patients with persecutory delusions predicted the persistence of paranoia over six months. A number of cognitive factors also predicted the persistence of persecutory delusions, including negative schematic beliefs about the self, worry, and problem-solving difficulties. In conclusion, depression is common in patients with current persecutory delusions, and it shows similar cognitive features to major depressive disorder. The results of this study indicate that depression and related processes may contribute to the maintenance of paranoia. Trials are warranted of depression-related therapeutic techniques for people with persecutory delusions.

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Section: Overgeneral Autobiographical Memorymentioning

confidence: 99%

Cognitive factors maintaining persecutory delusions in psychosis: The contribution of depression.

Vorontsova¹,

Garety²,

Freeman³

2013

Journal of Abnormal Psychology

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“…A substantial number of studies have now confirmed that many patients with BD have cognitive impairment that persists into the euthymic state. [154][155][156][157][158][159] Impairment has been demonstrated in sustained attention, 160 working memory and executive function, 155 global cognitive functioning, 154 visuospatial recognition memory, 161 problem-solving strategies, 156 declarative memory, 157 and cognitive processing speed. 162 The fact that such impairment is detectable independent of clinical state is suggestive of a trait marker, but factors such as the neuropsychological deterioration secondary to acute episodes of illness, medication treatment, and/or withdrawal effects, long-term effects of comorbid conditions such as substance abuse, or the effect of unrecognized neurobiological changes such as dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis could all contribute to performance deficits in the euthymic state.…”

Section: Cognitive Endophenotypesmentioning

confidence: 99%

The phenotypes of bipolar disorder: relevance for genetic investigations

2005

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The search for susceptibility genes for bipolar disorder (BD) depends on appropriate definitions of the phenotype. In this paper, we review data on diagnosis and clinical features of BD that could be used in genetic studies to better characterize patients or to define homogeneous subgroups. Clinical symptoms, long-term course, comorbid conditions, and response to prophylactic treatment may define groups associated with more or less specific loci. One such group is characterized by symptoms of psychosis and linkage to 13q and 22q. A second group includes mainly bipolar II patients with comorbid panic disorder, rapid mood switching, and evidence of chromosome 18 linkage. A third group comprises typical BD with an episodic course and favourable response to lithium prophylaxis. Reproducibility of cognitive deficits across studies raises the possibility of using cognitive profiles as endophenotypes of BD, with deficits in verbal explicit memory and executive function commonly reported. Brain imaging provides a more ambiguous data set consistent with heterogeneity of the illness. Keywords: bipolar disorder; genetics; endophenotype; neurocognitive function; brain imaging Bipolar disorder (BD) has a genetic basis with heritability of at least 80%. 1 A number of studies have attempted to map the susceptibility loci giving evidence of linkage in multiple genomic regions. In particular, findings in 4p, 4q, 8q, 10p, 12q24, 13q, 18p, 18q, 21q, and 22q have been supported by more than one study. [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19] However, these studies have not identified any specific genes, and a recent metaanalysis of available genome scans showed no regions with a conclusive evidence of linkage. 20 The relatively slow progress of gene-mapping efforts is often explained by the 'complex' nature of the illness and of the genotype-phenotype relation. The complexity most likely includes heterogeneity, interactions of multiple loci, incomplete penetrance, as well as phenotypes resulting from environmental effects-either alone or in interaction with the genetic predisposition. The goal of psychiatric genetic research is identification of (heritable) variations in DNA sequence or function that influence behaviour or give rise to mental illness. By definition, in complex (multifactorial) traits, this link is not unique and specific. That is, a particular change in gene sequence does not necessarily lead to a specific behaviour, and similar behaviours (symptoms) may be due to distinct (sets of) genes. Moreover, we must consider the possibility that the path between the genotype and behaviour is not unidirectional. Emerging examples point not only to general effects of environment, for instance stress, on behaviour, but also to specific behaviours influencing gene function that can be transmitted onto the next generation. 21 No single method is considered clearly superior in identifying susceptibility genes for complex traits such as BD. Most researchers agree that a combination of strategies is most lik...

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“…Manic patients showed impairments on planning and reaction time (RT) (Murphy et al, 1999). During remission, cognitive deficits may persist (van Gorp et al, 1998;Ferrier et al, 1999;Rubinsztein et al, 2000;Scott et al, 2000); euthymic BD patients showed impairments on visuospatial recognition, verbal and nonverbal memory and learning, retrieval of information from semantic memory an increased RT on a planning task (Coffman et al, 1990;Ferrier et al, 1999;Rubinsztein et al, 2000). The fact that cognitive deficits persist during remission suggests that they constitute a trait marker in BD.…”

Section: Introductionmentioning

confidence: 99%

Pronounced Cognitive Deficits Following an Intravenous L-Tryptophan Challenge in First-Degree Relatives of Bipolar Patients Compared to Healthy Controls

Sobczak

Honig

Schmitt

et al. 2002

Neuropsychopharmacol

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Cognitive impairment has repeatedly been described in bipolar disorders (BD). Serotonin (5-hydroxytryptophan; 5-HT) is possibly involved in these cognitive processes, more particularly in executive functions, learning, memory, and attention. The aim of this study was to investigate serotonergic vulnerability and its relation to cognitive functioning in healthy first-degree relatives of BD patients. We investigated the effects of an intravenous (i.v.) tryptophan (Trp) challenge and placebo on cognitive performance in 30 healthy firstdegree relatives of bipolar patients (FH) and 15 matched controls in a double-blind crossover design. A distinction was made between relatives of type I BD patients (FH I) and type II BD patients (FH II). Performances on planning, memory, attention, and psychomotor tasks were assessed 3 h after Trp infusion. After Trp, planning and attention were impaired in FH subjects but not in controls. Independent of Trp, FH subjects showed cognitive deficits on memory, focused and divided attention, and psychomotor performance. FH I subjects showed more pronounced cognitive impairments then FH II and controls. In all groups, Trp impaired memory and psychomotor performance significantly. In conclusions, cognitive deficits in FH following Trp may reflect a central 5-HT vulnerability in frontal brain areas. Independent of Trp, cognitive deficits in FH provide evidence for a trait marker for BD.

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Cognitive vulnerability in patients with bipolar disorder

Cited by 249 publications

References 18 publications

Cognitive factors maintaining persecutory delusions in psychosis: The contribution of depression.

Cognitive factors maintaining persecutory delusions in psychosis: The contribution of depression.

The phenotypes of bipolar disorder: relevance for genetic investigations

Pronounced Cognitive Deficits Following an Intravenous L-Tryptophan Challenge in First-Degree Relatives of Bipolar Patients Compared to Healthy Controls

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