Neuroimaging Studies of Bipolar Depression: Therapeutic Implications

Author(s):  
Jonathan Savitz ◽  
Harvey M. Morris ◽  
Wayne C. Drevets
2013 ◽  
Vol 2013 ◽  
pp. 1-18 ◽  
Author(s):  
Djamila Bennabi ◽  
Pierre Vandel ◽  
Charalambos Papaxanthis ◽  
Thierry Pozzo ◽  
Emmanuel Haffen

Psychomotor retardation is a central feature of depression which includes motor and cognitive impairments. Effective management may be useful to improve the classification of depressive subtypes and treatment selection, as well as prediction of outcome in patients with depression. The aim of this paper was to review the current status of knowledge regarding psychomotor retardation in depression, in order to clarify its role in the diagnostic management of mood disorders. Retardation modifies all the actions of the individual, including motility, mental activity, and speech. Objective assessments can highlight the diagnostic importance of psychomotor retardation, especially in melancholic and bipolar depression. Psychomotor retardation is also related to depression severity and therapeutic change and could be considered a good criterion for the prediction of therapeutic effect. The neurobiological process underlying the inhibition of activity includes functional deficits in the prefrontal cortex and abnormalities in dopamine neurotransmission. Future investigations of psychomotor retardation should help improve the understanding of the pathophysiological mechanisms underlying mood disorders and contribute to improving their therapeutic management.


Depression ◽  
2019 ◽  
pp. 102-117
Author(s):  
Sabrina C. da Costa ◽  
Marsal Sanches ◽  
Jair C. Soares

Bipolar disorder (BD) is a complex and severe mental illness, associated with substantial morbidity and increased mortality. Depressive symptoms frequently prevail in the course of illness, and significant morbidity arises from acute affective episodes and subacute states. Phenotypically, unipolar and bipolar depression seem to share several clinical features, which leads to an average delay of 10 years between initial symptoms and the diagnosis of BD. Multidimensional approaches have been proposed to better predict BD in at-risk populations; however, the differential diagnosis between these two entities remains a clinical challenge. Similarly to other chronic conditions, it has been proposed that BD is also a progressive disorder, where multiple affective episodes may result in structural, functional, and neurobiological brain abnormalities that accelerate illness progression, with subsequent treatment resistance and reduction in interepisode interval. Therefore, strategies to improve diagnosis accuracy are pivotal to improve clinical outcomes and long-term prognosis in the course of BD. In this chapter, we aim to provide a critical overview of psychopathological, sociodemographic, and neurobiological features to help clinicians properly distinguish unipolar and bipolar depression. Pathological and therapeutic implications of misdiagnosing BD are briefly discussed.


2021 ◽  
pp. 1-8
Author(s):  
Kaat Hebbrecht ◽  
Manuel Morrens ◽  
Erik J. Giltay ◽  
Alexander L.N. van Nuijs ◽  
Bernard Sabbe ◽  
...  

<b><i>Introduction:</i></b> Chronic low-grade inflammation is suggested to play a pathophysiological role in bipolar disorder (BD) and its related cognitive dysfunctions. Although kynurenine (KYN) pathway metabolites are key inflammatory mediators, studies investigating the association between KYN metabolism and cognition in BD are scarce. We aimed to explore the relationship between KYN metabolism and cognitive functioning across different mood states in BD. <b><i>Methods:</i></b> Sixty-seven patients with BD (35 depressed and 32 [hypo] manic) and 29 healthy controls were included. Cognitive functioning was assessed at 3 time intervals (baseline, 4, and 8 months) assessing processing speed, sustained attention, verbal memory, working memory, and response inhibition. Plasma samples for quantification of 3-hydroxykynurenine, quinolinic acid, and kynurenic acid (KYNA) were concurrently provided. Linear mixed models were used for statistical analysis. <b><i>Results:</i></b> The manic group showed deficits in all assessed cognitive domains with the exception of verbal memory at all test moments. The bipolar depression group showed deficits in the processing speed at all test moments. Throughout the whole follow-up period, KYNA was significantly lower in both patient groups than in controls. Only in the bipolar depression group, low KYNA was associated with worse global cognitive functioning (<i>B</i> = 0.114, <i>p</i> = 0.02) and slower processing speed in particular (<i>B</i> = 0.139, <i>p</i> = 0.03). <b><i>Conclusion:</i></b> Only in the bipolar depression group, lower KYNA was associated with worse cognitive functioning. Future large-scale longitudinal studies are warranted to confirm the role of KYN metabolites in cognitive impairment in patients with BD and the possible therapeutic implications of this relationship.


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