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Staging, Neurocognition and Social Functioning in Bipolar Disorder
Amparo Tatay-Manteiga1, Patricia Correa-Ghisays2,3, Omar Cauli4
1Department of Psychiatry, General University Hospital Consortium of Valencia, Valencia, Spain.
Frontiers in Psychiatry
|January 9, 2019
Summary
Genetic vulnerability to bipolar disorder (BD) is linked to neurocognitive deficits, even in healthy siblings. Social impairment appears to stem from the clinical condition itself, suggesting distinct pathways for cognitive and social issues in BD.
Area of Science:
- Neuroscience
- Psychiatry
- Genetics
Background:
- Bipolar disorder (BD) is characterized by neurocognitive and functional impairments that can worsen over time.
- The 'latent stage' of BD, often observed in healthy relatives, is understudied regarding its neurocognitive and social functioning.
- Understanding these differences is crucial for developing effective interventions and staging models for BD.
Purpose of the Study:
- To assess neurocognition and social functioning across different stages of bipolar disorder (BD) and in healthy siblings.
- To investigate the 'latent stage' of BD by comparing healthy siblings of patients with patients and healthy controls.
- To examine the relationship between genetic vulnerability, neurocognitive deficits, and social functioning in BD.
Main Methods:
- A cross-sectional study included four groups: euthymic early-stage BD I patients, late-stage BD I patients, their healthy siblings (latent stage), and healthy controls.
- All 92 participants completed a comprehensive neuropsychological battery assessing processing speed, memory, executive functions, and motor speed.
- Social functioning was evaluated using the Functioning Assessment Short Test (FAST) scale.
Main Results:
- Healthy siblings showed social functioning comparable to controls but significantly worse than early- and late-stage BD patients.
- Neurocognitive dysfunction increased progressively across BD stages compared to controls, with healthy siblings exhibiting intermediate deficits.
- While patients had more severe and widespread neurocognitive deficits than siblings, social functioning was significantly worse in later BD stages and in patients compared to siblings.
Conclusions:
- Genetic predisposition to BD appears associated with neurocognitive impairments, evident even in unaffected siblings.
- Social dysfunction in BD seems to be a consequence of the clinical phenotype rather than solely genetic vulnerability.
- BD staging models should differentiate between the progression of neurocognitive deficits and social functioning impairments, particularly in the latent stage.
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