Neuropsychological performance in depressed and euthymic bipolar patients.
ABSTRACT Recent studies have suggested that the presence of persistent cognitive dysfunctions in bipolar patients is not restricted to acute episodes, but they persist even during remission states. Nevertheless, there are several methodological pitfalls in most studies, such as unclear remission criteria, diagnostic heterogeneity or small sample sizes.
Several domains of cognitive function were examined in 30 depressed bipolar patients [DSM-IV criteria for major depression, Hamilton Depression Scale (HDRS) > or =17] and 30 euthymic bipolar patients (at least 6 months of remission, HDRS < or =8 and Young Mania Rating Scale, YMRS < or =6). Psychosocial functioning was assessed through General Assessment of Functioning.
The two groups showed a similar pattern of neuropsychological performance. However, the depressed group was significantly impaired on the Controlled Oral Word Association Test, FAS (COWAT), a measure of verbal fluency, compared with the euthymic group. On the other hand, functional outcome in euthymic patients was related to verbal fluency, even after controlling for residual depressive symptoms.
Neuropsychological performance was similar in both groups, except for verbal fluency, which was lower in the depressed group. Poor verbal fluency was related to a poor social outcome in euthymic patients. Further research including longitudinal designs aimed at evaluating changes in cognition in these patients is warranted.
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ABSTRACT: Bipolar Disorder (BD) has been conceptualized as both a cyclic and a progressive disorder. Mechanisms involved in neuroprogression in BD remain largely unknown although several non-mutually exclusive models have been proposed as explanatory frameworks. In the present paper, we propose that the pathopshyfiological changes observed in BD (e.g. brain structural alterations, cognitive deficits, oxidative stress imbalance, amyloid metabolism, immunological deregulation, immunosenescence, neurotrophic deficiencies and telomere shortening) converge on a model of accelerated aging (AA). Aging can be understood as a multidimensional process involving physical, neuropsychological, and social changes, which can be highly variable between individuals. Determinants of successful aging (e.g environmental and genetic factors), may also confer differential vulnerability to components of BD pathophysiology and contribute to the clinical presentation of BD. Herein we discuss how the understanding of aging and senescence can contribute to the search for new and promising molecular targets to explain and ameliorate neuroprogression in BD. We also present the strengths and limitations of this concept.Neuroscience & Biobehavioral Reviews 05/2014; 42. DOI:10.1016/j.neubiorev.2014.02.004 · 10.28 Impact Factor
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ABSTRACT: Different subtypes of depressive syndromes exist in late life; many of them have cognitive impairment and sometimes it is difficult to differentiate them from dementia. This research aimed to investigate subtypes of geriatric depression associated with cognitive impairment, searched for differential variables and tried to propose a study model. A hundred and eighteen depressive patients and forty normal subjects matched by age and educational level were evaluated with an extensive neuropsychological battery, scales to evaluate neuropsychiatric symptoms and daily life activities (DLA). Depressive patients were classified in groups by SCAN 2.1: Major Depression Disorder (MDD) (n: 31), Dysthymia Disorder (DD) (n: 31), Subsyndromal Depression Disorder (SSD) (n: 29), Depression due to Dementia (n: 27) (DdD). Neuropsychological significant differences (p<0.05) were observed between depressive groups, demonstrating distinctive cognitive profiles. Moreover, significant differences (p<0.05) were found in DLA between DdD vs all groups and MDD vs controls and vs SSD. Age of onset varied in the different subtypes of depression. Beck Depression Inventory (BDI) and Mini Mental State Examination (MMSE) were significant variables that helped to differentiate depressive groups. Significant correlations between BDI and Neuropsychological tests were found in MDD and DD groups. Depressive symptoms and its relation with neuropsychological variables, MMSE, cognitive profiles, DLA and age of onset of depression should be taken into consideration for the study of subtypes of geriatric depression.Archives of Gerontology and Geriatrics 05/2014; 59(2). DOI:10.1016/j.archger.2014.04.006 · 1.53 Impact Factor
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ABSTRACT: Background Recent studies revealed that nonconverters at clinical high risk (CHR) for psychosis comprise those who later remit from initial CHR state and those who do not remit and continue to have attenuated positive symptoms. CHR subjects who remit symptomatically are comparable to healthy controls for both baseline and longitudinal symptoms. However, the neurocognitive characteristics of this population are still obscure. Methods Seventy-five CHR subjects and 61 healthy controls were recruited, and their neurocognitive functions were assessed. CHR subjects were divided into converter, remitter, and non-remitter groups according to their clinical state during a 12 to 24 month follow-up. Results Only the remitter group was comparable to healthy controls in terms of baseline neurocognitive functions. We observed that remitters showed better performance at baseline on tasks of attention, immediate/delayed verbal memory, verbal fluency, and immediate visual memory compared with converters. Moreover, we found that performance on semantic fluency was significantly improved in remitters but declined in non-remitters over the 2-year follow-up; however, there was no significant difference between these two groups at baseline. Conclusion CHR nonconverters who later remit from an initial prodromal state do not show reduced neurocognitive functioning compared with healthy controls at baseline. Therefore, an advanced research diagnostic criterion for a CHR state that considers neurocognitive functions is needed to more precisely predict which patients will develop psychosis.Schizophrenia Research 03/2014; 153(1-3). DOI:10.1016/j.schres.2014.01.018 · 4.43 Impact Factor