Impaired Neuropsychological Performance in Euthymic Patients With Recurring Mood Disorders

Tham, Anne; Engelbrektson, Karin; Aa, Mathé; Johnson, Leigh A.; Olsson, Erik; Åberg‐Wistedt, Anna

doi:10.4088/jcp.v58n0105

Cited by 208 publications

(107 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Thus, executive deficits could represent a relatively stable trait marker, whereas mnemonic impairment seems to be related to clinical state. This view is not supported by some studies reporting impaired verbal memory in unipolar depressive patients in remission (Tham et al 1997;Kessing 1998). This discrepancy could be explained by the number of previous depressive episodes.…”

Section: Cognitive Deficits In Major Depressionmentioning

confidence: 71%

See 1 more Smart Citation

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Mößner

Mikova

Koutsilieri

et al. 2007

The World Journal of Biological Psychiatry

226

126

View full text Add to dashboard Cite

Biological markers for depression are of great interest to aid in elucidating the causes of major depression. We assess currently available biological markers to query their validity for aiding in the diagnosis of major depression. We specifically focus on neurotrophic factors, serotonergic markers, biochemical markers, immunological markers, neuroimaging, neurophysiological findings, and neuropsychological markers. We delineate the most robust biological markers of major depression. These include decreased platelet imipramine binding, decreased 5-HT1A receptor expression, increase of soluble interleukin-2 receptor and interleukin-6 in serum, decreased brain-derived neurotrophic factor in serum, hypocholesterolemia, low blood folate levels, and impaired suppression of the dexamethasone suppression test. To date, however, none of these markers are sufficiently specific to contribute to the diagnosis of major depression. Thus, with regard to new diagnostic manuals such as DSM-V and ICD-11 which are currently assessing whether biological markers may be included in diagnostic criteria, no biological markers for major depression are currently available for inclusion in the diagnostic criteria.

show abstract

Section: Cognitive Deficits In Major Depressionmentioning

confidence: 71%

“…This discrepancy could be explained by the number of previous depressive episodes. Indeed, in one of the studies (Tham et al 1997), cognitive dysfunctions were observed in a subgroup of patients with more frequent relapses and episodes of hospitalization, even when euthymic.…”

Section: Cognitive Deficits In Major Depressionmentioning

confidence: 97%

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Mößner

Mikova

Koutsilieri

et al. 2007

The World Journal of Biological Psychiatry

226

126

View full text Add to dashboard Cite

show abstract

“…[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. In fact, there is evidence that performance on cognitive tests declines as a function of past illness burden, 154,162,163 and that a past history of alcohol abuse can impact on cognitive performance in certain domains.…”

Section: Cognitive Endophenotypesmentioning

confidence: 99%

“…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. In fact, there is evidence that performance on cognitive tests declines as a function of past illness burden, 154,162,163 and that a past history of alcohol abuse can impact on cognitive performance in certain domains. 164 Neither the short-nor long-term impact of medication on cognitive performance is known, 165 and evidence is just emerging supporting a recurrent or even chronic dysregulation of HPA axis function in BD.…”

Section: Cognitive Endophenotypesmentioning

confidence: 99%

The phenotypes of bipolar disorder: relevance for genetic investigations

2005

View full text Add to dashboard Cite

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...

show abstract

“…Yazında, bizim çalışmamızdakine benzer şekilde depresif dönemde yürütücü işlev (8,33,34), sözel bellek (34,36), görsel bellek ve mekansal bellekte (36,37) bozulmalar bildirilmiştir. Bununla birlikte iyilik ve depresyon dönemindeki İUDB olan hastaları doğrudan karşılaştıran az sayıda çalışma vardır (38).…”

Section: Discussionunclassified

İki̇ Uçlu Duygudurum Bozukluğu Tanili Hastalarin Depresyon, Eşi̇kalti Depresyon Ve İyi̇li̇k Dönemleri̇ni̇n Nöropsi̇koloji̇k Açidan Karşilaştirilmasi

Temur¹,

Güleç²,

Akarsu³

et al. 2016

Osmangazi̇ Journal of Medicine

View full text Add to dashboard Cite

Impaired Neuropsychological Performance in Euthymic Patients With Recurring Mood Disorders

Cited by 208 publications

References 0 publications

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

The phenotypes of bipolar disorder: relevance for genetic investigations

İki̇ Uçlu Duygudurum Bozukluğu Tanili Hastalarin Depresyon, Eşi̇kalti Depresyon Ve İyi̇li̇k Dönemleri̇ni̇n Nöropsi̇koloji̇k Açidan Karşilaştirilmasi

Contact Info

Product

Resources

About