TY - ABST
T1 - Predictors of the subjective-objective cognition discrepancy in unipolar disorder
AU - Petersen, Jeff Zarp
AU - Porter, Richard J.
AU - Miskowiak, Kamilla Woznica
PY - 2019/1/1
Y1 - 2019/1/1
N2 - Background: Patients with unipolar disorder (UD) commonly experience cognitive dysfunction together with depressive symptoms during acute and remitted episodes [1,2]. However, the correlation between patients’ subjectively -reported cognitive complaints and objectively -measured deficits is poor [3]. It is therefore not necessarily the patients with the greatest subjective cognitive complaints, who also display the largest objectively-measured neuropsychological deficits. Nevertheless, it is unclear which factors influence this discrepancy between subjective and objective cognition measures in UD.
Objective: This secondary analysis aimed to investigate the demographic and clinical factors associated with discrepancy between subjective (i.e., self-reported) and objective (i.e., neuropsychological) measures of cognition in two separate UD patient populations in Denmark and New Zealand using a new methodology.
Methods: Two separate analyses of factors associated with subjective-objective discrepancy were conducted for cognition data from (I) a population of remitted UD patients (Hamilton Depression Rating Scale 17-items (HDRS-17) score ≤14) (N=53) and (ii) a population of more symptomatic UD patients (n=84). Subjective and objective cognitive functions were assessed with standard neuropsychological tests and self-rating questionnaires, respectively. Mood symptoms were assessed with observer-based clinical ratings (HDRS-17). A global composite cognitive discrepancy and domain-specific scores were calculated using a statistical formula to derive score values between -10 and +10 in each sample. Negative values indicate disproportionately more objective than subjective impairments (i.e., “ stoicism ”), while positive values indicate disproportionately more subjective than objective difficulties (i.e., “ sensitivity ”). Statistical analyses included multiple regression analyses, repeated measures analysis of variance, and Pearson's correlational analyses. The statistical significance threshold for all analyses was p ≤0.05 (two-tailed).
Results: In the remitted UD patients, greater subsyndromal depression severity (standardized Beta (std. B)=0.4, p <0.01), illness duration (std. B=0.4, p <0.05), and younger age (std. B=0.6, p <0.001) were associated with more sensitivity to cognitive impairments in general. Post-hoc analyses revealed that younger age was also associated with more sensitivity ( p -values≤0.05) across cognitive domains (‘attention and processing speed’, ‘verbal learning and memory’, and ‘working memory and executive functions’), while greater depression severity predicted greater sensitivity within ‘attention and processing speed’ and ‘verbal learning and memory’ domains ( p -values<0.05) in this group. These associations were replicated in the larger sample of more symptomatic patients, where greater depression severity (std.B=0.2) and younger age (std.B=0.3) also predicted greater sensitivity to cognitive difficulties in general as well as within ‘working memory and executive functions’ ( p -values≤0.05).
Limitations: The cross-sectional design in the studies hampered causal inferences of the relationship between the demographic and clinical characteristics and the discrepancy between subjective and objective cognition measures in the two patient populations.
Conclusions: The present results suggest that UD patients with greater depression symptom severity, greater illness chronicity, and younger age tend to overreport cognitive impairments. A similar association between depression severity and greater sensitivity to cognitive impairment was previously found in remitted bipolar disorder patients. Objective cognitive screening thus seems particularly relevant to assess whether subjective complaints are associated with measurable cognitive deficits in patients marked by greater symptom severity, illness severity and younger age.
AB - Background: Patients with unipolar disorder (UD) commonly experience cognitive dysfunction together with depressive symptoms during acute and remitted episodes [1,2]. However, the correlation between patients’ subjectively -reported cognitive complaints and objectively -measured deficits is poor [3]. It is therefore not necessarily the patients with the greatest subjective cognitive complaints, who also display the largest objectively-measured neuropsychological deficits. Nevertheless, it is unclear which factors influence this discrepancy between subjective and objective cognition measures in UD.
Objective: This secondary analysis aimed to investigate the demographic and clinical factors associated with discrepancy between subjective (i.e., self-reported) and objective (i.e., neuropsychological) measures of cognition in two separate UD patient populations in Denmark and New Zealand using a new methodology.
Methods: Two separate analyses of factors associated with subjective-objective discrepancy were conducted for cognition data from (I) a population of remitted UD patients (Hamilton Depression Rating Scale 17-items (HDRS-17) score ≤14) (N=53) and (ii) a population of more symptomatic UD patients (n=84). Subjective and objective cognitive functions were assessed with standard neuropsychological tests and self-rating questionnaires, respectively. Mood symptoms were assessed with observer-based clinical ratings (HDRS-17). A global composite cognitive discrepancy and domain-specific scores were calculated using a statistical formula to derive score values between -10 and +10 in each sample. Negative values indicate disproportionately more objective than subjective impairments (i.e., “ stoicism ”), while positive values indicate disproportionately more subjective than objective difficulties (i.e., “ sensitivity ”). Statistical analyses included multiple regression analyses, repeated measures analysis of variance, and Pearson's correlational analyses. The statistical significance threshold for all analyses was p ≤0.05 (two-tailed).
Results: In the remitted UD patients, greater subsyndromal depression severity (standardized Beta (std. B)=0.4, p <0.01), illness duration (std. B=0.4, p <0.05), and younger age (std. B=0.6, p <0.001) were associated with more sensitivity to cognitive impairments in general. Post-hoc analyses revealed that younger age was also associated with more sensitivity ( p -values≤0.05) across cognitive domains (‘attention and processing speed’, ‘verbal learning and memory’, and ‘working memory and executive functions’), while greater depression severity predicted greater sensitivity within ‘attention and processing speed’ and ‘verbal learning and memory’ domains ( p -values<0.05) in this group. These associations were replicated in the larger sample of more symptomatic patients, where greater depression severity (std.B=0.2) and younger age (std.B=0.3) also predicted greater sensitivity to cognitive difficulties in general as well as within ‘working memory and executive functions’ ( p -values≤0.05).
Limitations: The cross-sectional design in the studies hampered causal inferences of the relationship between the demographic and clinical characteristics and the discrepancy between subjective and objective cognition measures in the two patient populations.
Conclusions: The present results suggest that UD patients with greater depression symptom severity, greater illness chronicity, and younger age tend to overreport cognitive impairments. A similar association between depression severity and greater sensitivity to cognitive impairment was previously found in remitted bipolar disorder patients. Objective cognitive screening thus seems particularly relevant to assess whether subjective complaints are associated with measurable cognitive deficits in patients marked by greater symptom severity, illness severity and younger age.
U2 - 10.1016/j.euroneuro.2018.11.1050
DO - 10.1016/j.euroneuro.2018.11.1050
M3 - Conference abstract in journal
SN - 0924-977X
VL - 29
SP - 71
JO - European Neuropsychopharmacology
JF - European Neuropsychopharmacology
IS - Supplement 1
ER -