Robinson LJ, Ferrier IN. Evolution of cognitive impairment in bipolar disorder: a systematic review of cross-sectional evidence. Bipolar Disord 8: 103-116

School of Neurology, Neurobiology & Psychiatry (Psychiatry), University of Newcastle upon Tyne, Newcastle upon Tyne, UK.
Bipolar Disorders (Impact Factor: 4.97). 05/2006; 8(2):103-16. DOI: 10.1111/j.1399-5618.2006.00277.x
Source: PubMed


The notion that sufferers of bipolar disorder achieve complete syndromal and functional recovery between illness episodes has been brought into question by evidence that a large proportion of patients fail to regain premorbid levels of functioning after the resolution of major affective symptoms. A growing body of evidence suggests that bipolar patients exhibit neuropsychological impairment that persists even during the euthymic state, which may be a contributory factor to poor psychosocial outcome. However, the aetiology of such impairment and its relation to progression of illness are not well understood. This review aims to consider evidence from studies investigating both the relationship between cognitive impairment and clinical outcome and studies of neurocognitive function in unaffected first-degree relatives (FDRs) of bipolar sufferers to address issues of the temporal evolution of cognitive impairment in bipolar disorder.
Systematic literature review.
The weight of evidence suggests that greater neuropsychological dysfunction in bipolar disorder is associated with a worse prior course of illness, particularly the number of manic episodes, hospitalizations and length of illness. The most consistent finding was a negative relationship between the number of manic episodes and verbal declarative memory performance. Impairment in unaffected FDRs was reported in verbal declarative memory and some facets of executive function.
Cognitive impairment may be a trait vulnerability factor for bipolar disorder that is present before illness onset and worsens as the illness progresses. Further investigation into the causal relationship between cognitive impairment and illness course is essential.

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Available from: Lucy Jayne Robinson, May 30, 2014
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    • "Zinc levels appear to increase in mania, meanwhile cadmium levels in individuals with BD who smoke are higher than in those who do not [205], the latter contributing to a number of dysfunctions in bodily processes [206]. Post-recovery cognitive impairment correlates with quantity of manic episodes in individuals with BD, while the euthymia length is not associated with cognitive testing outcomes [207]. Additionally, pharmaceutical and psychological treatment of BD decreases in efficacy as an individual experiences more episodes of the disorder [12, 208, 209]. "
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    ABSTRACT: Several biological systems are implicated in the neuroprogression of bipolar disorder including but not limited to cytokine levels, oxidative stress markers, monoamine levels, tryptophan catabolite and glutamate-mediated excitotoxicity, microglial activation as well as structural and functional changes. The high rate of smoking behaviour in individuals with bipolar disorder provides the impetus for exploring shared and discrete pathogenetic mechanisms. In addition to contributing to increased mortality, smoking activates several neurobiological effector systems implicated in the progression of bipolar disorder. Here, a narrative review provides evidence and putative mechanisms of comorbid effects of BD, cigarette use, and nicotine dependence, and discusses the clinical implications of these interactions.
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    • "BD is associated with cognitive impairment even during periods of euthymia (Martínez-Ar an et al., 2004; Barrett et al., 2009). Emergent evidence from systematic reviews in the field suggests an association between the number of manic episodes as well as psychiatric hospitalizations with neurocognitive decline (Robinson and Ferrier, 2006), particularly verbal memory impairment (Martínez-Ar an et al., 2004). Not only cognition seems to be impaired in portion as a function of number of mood episodes in BD. "
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    ABSTRACT: 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.
    Full-text · Article · Dec 2015 · Journal of Psychiatric Research
    • "It is increasingly apparent that cognitive impairments are evident early in the course of the illness (Daglas et al., 2015; Lee et al., 2014); however, what remains unclear is the onset and trajectory of these impairments through the early stages of the illness. The suggestion that cognitive impairment may worsen with illness progression (Robinson and Ferrier, 2006) has been challenged in a recent review in which it was reported that most cross-sectional and longitudinal studies have provided only limited evidence for an association between a longer duration of illness and cognitive deterioration (Strejilevich et al., 2015). In particular, longitudinal studies of people in the later stages of bipolar disorder (including the elderly) have shown that cognitive functioning does not differ over time relative to healthy controls (Delaloye et al., 2011; Depp et al., 2008). "
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    ABSTRACT: Objectives: Cognitive deficits are apparent in the early stages of bipolar disorder; however, the timing and trajectory of cognitive functioning following a first episode of mania remains unclear. The aim of this study was to assess the trajectory of cognitive functioning in people following a first episode of mania over a 12-month period, relative to healthy controls. Method: The cohort included 61 participants who had recently stabilised from a first treated manic episode, and 21 demographically similar healthy controls. These groups were compared on changes observed over time using an extensive cognitive battery, over a 12-month follow-up period. Results: A significant group by time interaction was observed in one measure of processing speed (Trail Making Test - part A,) and immediate verbal memory (Rey Auditory Verbal Learning Test - trial 1), with an improved performance in people following a first episode of mania relative to healthy controls. On the contrary, there was a significant group by time interaction observed on another processing speed task pertaining to focussed reaction time (Go/No-Go, missed go responses), with first episode of mania participants performing significantly slower in comparison with healthy controls. Furthermore, a significant group by time interaction was observed in inhibitory effortful control (Stroop effect), in which healthy controls showed an improvement over time relative to first episode of mania participants. There were no other significant interactions of group by time related to other measures of cognition over the 12-month period. Conclusion: Our findings revealed cognitive change in processing speed, immediate memory and one measure of executive functioning over a 12-month period in first episode of mania participants relative to healthy controls. There was no evidence of change over time for all other cognitive domains. Further studies focussed on the at-risk period, subgroup analysis, and the effects of medication on the cognitive trajectory following first episode of mania are needed.
    No preview · Article · Dec 2015 · Australian and New Zealand Journal of Psychiatry
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