A five‐year follow‐up study of neurocognitive functioning in bipolar disorder

Santos, José Luís; Aparicio, Ana Isabel; Bagney, Alexandra; Sánchez-Morla, Eva María; Rodríguez‐Jiménez, Roberto; Mateo, J.; Jiménez‐Arriero, Miguel Ángel

doi:10.1111/bdi.12215

Cited by 82 publications

(77 citation statements)

References 59 publications

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“…1). Consistently, in a five-year follow-up study of neurocognitive functioning in BD, a dysfunction in verbal memory became more evident in patients at late stages (Santos et al, 2014). In addition, our study showed that only subjects at later stages of illness present worse semantic clustering scores as compared to controls.…”

Section: Discussionmentioning

confidence: 63%

Hippocampal volume and verbal memory performance in late-stage bipolar disorder

Cao

Passos

Mwangi

et al. 2016

Journal of Psychiatric Research

106

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Studies about changes in hippocampal volumes in subjects with bipolar disorder (BD) have been contradictory. Since the number of manic episodes and hospitalization has been associated with brain changes and poor cognitive outcomes among BD patients, we have hypothesized that these variables could clarify this issue. We stratified subjects with BD in early (BD-Early), intermediate (BD-intermediate) and late (BD-Late) stages as a function of number of manic episodes and prior hospitalization. Then, we compared their hippocampal volumes and California Verbal Learning Test-II (CVLT-II) scores with healthy controls (HC) using the general linear model. A total of 173 subjects were included in the study (112 HC, 15 BD-Early, 30 BD-Intermediate, and 16 BD-Late). We found a significant group effect on hippocampus volume (F(3,167) = 3.227, p = 0.024). Post-hoc analysis showed that BD-Late subjects had smaller hippocampus than HC (p = 0.017). BD-Early and BD-Intermediate subjects showed no significant difference in hippocampus volume compared to HC and BD-Late subjects. The CVLT trial 1 to 5 scores were significantly different across the groups (F(3,167) = 6.371, p < 0.001). Post-hoc analysis showed that BD-Intermediate (p = 0.006) and BD-Late (p = 0.017) subjects had worse memory performance during immediate recall than HC, while the performance difference between BD-Early subjects and HC was not significant (p = 0.208). These findings add to the notion that BD is a neuroprogressive disorder with brain changes and cognitive impairment according to prior morbidity (number of manic episodes and hospitalization). Also, they suggest that hippocampus is a brain marker and a potential therapeutic target for patients at late stage.

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Section: Discussionmentioning

confidence: 63%

Hippocampal volume and verbal memory performance in late-stage bipolar disorder

Cao

Passos

Mwangi

et al. 2016

Journal of Psychiatric Research

106

View full text Add to dashboard Cite

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“…Performance by bipolar participants on this task was equally mixed between scores that were similar to, or lower than controls (Bonnin et al, 2012; Marshall et al, 2012; Martino et al, 2011a,b, 2014; Ryan et al, 2013; Torrent et al, 2006) (Ancin et al, 2013, 2010; Elshahawi et al, 2011; Martinez-Aran et al, 2009, 2007; Sanchez-Morla et al, 2009; Santos et al, 2014; Torrent et al, 2011). Among relatives intelligence was shown to be mostly preserved when tested using this task (Antila et al, 2009; Christodoulou et al, 2012; Daban et al, 2012; Doyle et al, 2009; Fears et al, 2014; Quraishi et al, 2009; Schulze et al, 2011; Thermenos et al, 2010).…”

Section: Resultsmentioning

confidence: 99%

Neurocognitive functioning in euthymic patients with bipolar disorder and unaffected relatives: A review of the literature

Cardenas

Kassem

Brotman

et al. 2016

Neuroscience & Biobehavioral Reviews

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Background Neurocognitive deficits are present in bipolar disorder (BD) patients and their unaffected (nonbipolar) relatives, but it is not clear which domains are most often impaired and the extent of the impairment resulting from shared genetic factors. In this literature review, we address these issues and identify specific neurocognitive tasks most sensitive to cognitive deficits in patients and unaffected relatives. Method We conducted a systematic review in Web of Science, PubMed/Medline and PsycINFO databases. Results Fifty-one articles assessing cognitive functioning in BD patients (23 studies) and unaffected relatives (28 studies) were examined. Patients and, less so, relatives show impairments in attention, processing speed, verbal learning/memory, and verbal fluency. Conclusion Studies were more likely to find impairment in patients than relatives, suggesting that some neurocognitive deficits may be a result of the illness itself and/or its treatment. However, small sample sizes, differences among relatives studied (e.g., relatedness, diagnostic status, age), and differences in assessment instruments may contribute to inconsistencies in reported neurocognitive performance among relatives. Additional studies addressing these issues are needed.

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“…In BD a decreased neuropil, with resulting disturbances of microconnectivity, may inhibit information flow from the hippocampus to the cortex and subcortical structures and contribute to the cognitive symptoms of the disorder. Indeed, patients with BD have deficits in hippocampusrelated cognitive tasks such as verbal memory (Hsiao et al 2009;Bora et al 2010) and one study found progressive worsening in verbal recall over a five-year follow-up period that could not be explained by effects of acute episodes or treatment (Santos et al 2014).…”

Section: Discussionmentioning

confidence: 99%

Stereological investigation of the posterior hippocampus in affective disorders

et al. 2014

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Hippocampus volumes have been shown to be decreased in patients with major depression, but volume measurements are inconsistent in patients with bipolar disorder. Both disorders are associated with deficits in hippocampus-mediated cognitive functions. However, the underlying pathophysiology is widely unknown. In this post-mortem study, we used design-based stereology on Nissl-stained serial sections to investigate the number of neurons, oligodendrocytes and astrocytes in substructures of the posterior hippocampus in eight patients with major depression, eight patients with bipolar disorder and ten control patients without a neuropsychiatric disorder. Compared to controls, patients with bipolar disorder had significantly more neurons in the cornu ammonis subfield 1 (CA1) and the subiculum, while the number of oligodendrocytes was higher only in CA1. In patients with major depression, the density of oligodendrocytes was higher in CA2/3, CA4 and the subiculum. The dose of antidepressants correlated with the density and number of oligodendrocytes in CA2/3, indicating that antidepressants may affect our results. Treatment with neuroleptics expressed in chlorpromazine equivalents and benzodiazepines expressed in diazepam equivalents correlated negatively with the number of oligodendrocytes in CA2/3 and CA4, respectively, suggesting that treatment with these drugs do not influence cell number. We did not detect alterations in either volumes of substructures or numbers of astrocytes. Increased cell numbers argue for a denser packing of neurons and oligodendrocytes as a result of a decreased neuropils. This neuropathological process may be based on neurodevelopmental disturbances and may contribute to altered microconnectivity and cognitive deficits in affective disorders.

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A five‐year follow‐up study of neurocognitive functioning in bipolar disorder

Abstract: Cognitive dysfunction that is characteristic of bipolar disorder is persistent and stable over time. Only dysfunction in verbal recall was found to show a progressive course that cannot be explained by clinical or treatment variables.

Cited by 82 publications

References 59 publications

Hippocampal volume and verbal memory performance in late-stage bipolar disorder

Hippocampal volume and verbal memory performance in late-stage bipolar disorder

Neurocognitive functioning in euthymic patients with bipolar disorder and unaffected relatives: A review of the literature

Stereological investigation of the posterior hippocampus in affective disorders

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