31 Up! Clinical Observations From 31 Years’ Follow-Up of 955 Patients With Depression or Bipolar Disorder31 Up! Clinical Observations From 31 Years’ Follow-Up of 955 Patients With Depression or Bipolar Disorder

PsycCRITIQUES ◽  
2013 ◽  
Vol 5858 (3939) ◽  
Author(s):  
Karen B. Schmaling
Keyword(s):  
Bipolar Disorder ◽  
Clinical Observations

Assessment of the neuronal underpinnings of cognitive impairment in bipolar disorder with a picture encoding paradigm and methodological lessons learnt

2021 ◽  
pp. 026988112110085
Author(s):  
JZ Petersen ◽  
J Macoveanu ◽  
HL Kjærstad ◽  
GM Knudsen ◽  
LV Kessing ◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
Cognitive Impairment ◽  
Neuronal Activity ◽  
Cognitive Impairments ◽  
Hierarchical Cluster ◽  
Small Region ◽  
Middle Temporal Gyrus ◽  
Recall Accuracy ◽  
Fmri Study

Background: Mood disorders are often associated with persistent cognitive impairments. However, pro-cognitive treatments are essentially lacking. This is partially because of poor insight into the neurocircuitry abnormalities underlying these deficits and their change with illness progression. Aims: This functional magnetic resonance imaging (fMRI) study investigates the neuronal underpinnings of cognitive impairments and neuronal change after mood episodes in remitted patients with bipolar disorder (BD) using a hippocampus-based picture encoding paradigm. Methods: Remitted patients with BD ( n=153) and healthy controls ( n=52) were assessed with neuropsychological tests and underwent fMRI while performing a strategic picture encoding task. A subgroup of patients ( n=43) were rescanned after 16 months. We conducted data-driven hierarchical cluster analysis of patients’ neuropsychological data and compared encoding-related neuronal activity between the resulting neurocognitive subgroups. For patients with follow-up data, effects of mood episodes were assessed by comparing encoding-related neuronal activity change in BD patients with and without episode(s). Results: Two neurocognitive subgroups were revealed: 91 patients displayed cognitive impairments while 62 patients were cognitively normal. No neuronal activity differences were observed between neurocognitive subgroups within the dorsal cognitive control network or hippocampus. However, exploratory whole-brain analysis revealed lower activity within a small region of middle temporal gyrus in impaired patients, which significantly correlated with poorer neuropsychological performance. No changes were observed in encoding-related neuronal activity or picture recall accuracy with the occurrence of mood episode(s) during the follow-up period. Conclusion: Memory encoding fMRI paradigms may not capture the neuronal underpinnings of cognitive impairment or effects of mood episodes.

ALDH2 modulated changes in cytokine levels and cognitive function in bipolar disorder: A 12-week follow-up study

2017 ◽  
Vol 52 (7) ◽  
pp. 680-689
Author(s):  
Sheng-Yu Lee ◽  
Tzu-Yun Wang ◽  
Shiou-Lan Chen ◽  
Yun-Hsuan Chang ◽  
Po-See Chen ◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
Cognitive Function ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Follow Up Study ◽  
Cytokine Levels

Objectives: We investigated the association of the aldehyde dehydrogenase 2 ( ALDH2) polymorphism (rs671), which is involved with the dopaminergic function, and with changes in cytokine levels and cognitive function, in a 12-week follow-up study in patients with bipolar disorder. Methods: Patients with a first diagnosis of bipolar disorder were recruited. Symptom severity and levels of plasma cytokines (tumor necrosis factor α, C-reactive protein, interleukin 6 and transforming growth factor β1) were examined during weeks 0, 1, 2, 4, 8 and 12. Neurocognitive function was evaluated at baseline and endpoint. The ALDH2 polymorphism genotype was determined. Results: A total of 541 patients with bipolar disorder were recruited, and 355 (65.6%) completed the 12-week follow-up. A multiple linear regression analysis showed a significant ( p = 0.000226) association between the ALDH2 polymorphism and changes in C-reactive protein levels. Different aspects of cognitive function improved in patients with different ALDH2 genotypes. Only patients with the ALDH2*1*1 genotype showed significant correlations between improvement of cognitive function and increased transforming growth factor -β1. Conclusion: The ALDH2 gene might influence changes in cytokine levels and cognitive performance in patients with bipolar disorder. Additionally, changes in cytokine levels and cognitive function were correlated only in patients with specific ALDH2 genotypes.

Metabolic syndrome in Italian patients with bipolar disorder: A 2-year follow-up study

2012 ◽  
Vol 136 (3) ◽  
pp. 599-603 ◽  
Author(s):  
Virginio Salvi ◽  
Virginia D'Ambrosio ◽  
Filippo Bogetto ◽  
Giuseppe Maina
Keyword(s):  
Metabolic Syndrome ◽  
Bipolar Disorder ◽  
Follow Up Study

scholarly journals Prophylaxis Latency and Outcome in Bipolar Disorders

2003 ◽  
Vol 48 (7) ◽  
pp. 449-457 ◽  
Author(s):  
Christopher Baethge ◽  
Leonardo Tondo ◽  
Irene M Bratti ◽  
Tom Bschor ◽  
Michael Bauer ◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
Treatment Response ◽  
Prophylactic Treatment ◽  
Bipolar Disorders ◽  
Mood Stabilizer ◽  
Adult Patients ◽  
Apparent Reduction

Objective: To analyze new and reviewed findings to evaluate relations between treatment response and latency from onset of bipolar disorder (BD) to the start of mood-stabilizer prophylaxis. Method: We analyzed our own new data and added findings from research reports identified by computerized searching. Results: We found 11 relevant studies, involving 1485 adult patients diagnosed primarily with BD. Reported latency to prophylaxis averaged 9.6 years (SD 1.3), and follow-up in treatment averaged 5.4 years (SD 3.1). Greater illness intensity and shorter treatment latency were closely associated, resulting in a greater apparent reduction in morbidity with earlier treatment. However, this finding was not sustained after correction for pretreatment morbidity, and treatment latency did not predict morbidity during treatment. Therefore, assessments based on improvement with treatment, or without correction for pretreatment morbidity, can be misleading. Conclusions: Available evidence does not support the proposal that delayed prophylaxis may limit response to prophylactic treatment in BD and related disorders.

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