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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    ABSTRACT: Cognitive deficits are observed in a variety of domains in patients with bipolar disorder (BD). These deficits are attributed to neurobiological, functional and structural brain factors, particularly in prefrontal cortex. Furthermore, cortical alterations in each phase (mania/hypomania, euthymia and depression) are also present. A growing basis of evidence supports aerobic exercise as an alternative treatment method for BD symptoms. Its benefits for physical health in healthy subjects and some psychiatric disorders are fairly established; however evidence directly addressed to BD is scant. Lack of methodological consistency, mainly related to exercise, makes it difficult accuracy and extrapolation of the results. Nevertheless, mechanisms related to BD physiopathology, such as hormonal and neurotransmitters alterations and mainly related to brain-derived neurotrophic factors (BDNF) can be explored. BDNF, specially, have a large influence on brain ability and its gene expression is highly responsive to aerobic exercise. Moreover, aerobic exercise trough BDNF may induce chronic stress suppression, commonly observed in patients with BD, and reduce deleterious effects caused by allostatic loads. Therefore, it is prudent to propose that aerobic exercise plays an important role in BD physiopathological mechanisms and it is a new way for the treatment for this and others psychiatric disorders.
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    • "Only slight differences in cognitive functioning have been found between the two main types of BD, i.e., type I (characterized by episodes of mania and depression) and II (characterized by episodes of hypomania and depression), with the exception of memory and semantic fluency (Bora et al., 2009). There is some evidence of cognitive deterioration during the course of illness (Robinson and Ferrier, 2006), but most cognitive functions appear to remain stable over time (Bourne et al., 2013). Meta-analyses of structural magnetic resonance imaging (MRI) studies report an increased volume of the lateral ventricles and globus pallidus, a decreased corpus callosum volume, and higher amount of deep white matter hyperintensities (Arnone et al., 2009). "
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    ABSTRACT: Persistent cognitive impairment in the euthymic state of bipolar disorder is increasingly recognized. Mounting evidence also suggests an association between neuroinflammation and cognitive dysfunction. The purpose of this study was to test if cerebrospinal fluid (CSF) markers of neuroinflammation could account for cognitive impairment in bipolar disorder. Hierarchical linear regression models were applied to account for performance in five cognitive domains using CSF neuroinflammatory biomarkers as predictors in patients with bipolar disorder type I and II (N=78). The associations between these biomarkers and cognition were further tested in healthy age- and sex-matched controls (N=86). In patients with bipolar disorder, the CSF biomarkers accounted for a significant proportion of the variance in executive functions (42.8%, p=<.0005) independently of age, medication, disease status, and bipolar subtype. The microglial marker YKL-40 had a high impact (beta=-.99), and was the only biomarker that contributed individually. CSF biomarkers were not associated with cognitive performance in healthy controls. The CSF neuroinflammation biomarker YKL-40 is associated with executive performance in euthymic bipolar disorder, but not in healthy controls. Copyright © 2015 Elsevier B.V. and ECNP. All rights reserved.
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    • "Persistent neurocognitive deficits (Balanzá-Martínez et al., 2005) likely result from the combination of genetic and environmental risk factors, as well as neurodevelopmental and neuroprogressive processes (Goodwin et al., 2008). Neurocognitive impairment may increase with illness progression (Robinson and Ferrier, 2006; Bourne et al., 2013) and history of psychotic symptoms (Selva et al., 2007; Martínez-Arán et al., 2008; Brissos et al., 2011), but it is also found in healthy first-degree relatives of patients with BD, although at a lesser degree (Arts et al., 2008; Balanzá-Martínez et al., 2008). Subsyndromal depressive symptoms , comorbidites and side effects of medications may compound and further worsen these deficits yet cannot fully explain them (Balanzá-Martínez et al., 2010). "
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