Sleep complaints, affective symptoms, somatic distress, and cognitive inefficiency frequently coexist in cerebral small vessel disease (CSVD). Their simultaneous occurrence makes a single statistically significant association difficult to interpret because large unadjusted differences may represent shared symptom variance rather than an independent sleep correlate. We examined whether one clinical domain remained concordant across three complementary evidential axes. Numerical summaries from 30 adults with CSVD and 35 controls, including sleep-defined subgroups of 14 and 16 participants with CSVD, were analysed. Conventional group comparisons, Spearman associations, and multivariable linear regression were retained. Added analyses comprised small-sample-corrected Hedges effect estimates with 95% confidence intervals, a signed three-axis concordance coefficient combining disease separation, sleep-stratified separation, and adjusted standardized association, and 20,000-replicate Monte Carlo stability analyses under Gaussian and Student-\(t(5)\) sampling. Higher standardized estimates were oriented toward greater clinical burden. Somatization showed the largest CSVD–control displacement (\(g=1.21\), 95% CI 0.68–1.74), followed by global sleep burden (\(g=0.94\), 0.43–1.45), anxiety (\(g=0.87\), 0.36–1.37), global symptom burden (\(g=0.83\), 0.33–1.34), and cognitive disadvantage (\(g=0.71\), 0.21–1.20). Within CSVD, anxiety produced the largest separation between participants above and below the sleep threshold (\(g=1.05\), 0.30–1.80). Depression (\(g=0.93\), 0.19–1.67) and global symptoms (\(g=0.83\), 0.10–1.56) were also prominent. The adjusted model assigned independent positive coefficients to anxiety (\(\beta=0.428\), \(p=0.017\)) and sex (\(\beta=0.418\), \(p=0.015\)), while the global symptom coefficient approached zero. Anxiety achieved the greatest three-axis concordance (0.73), exceeding depression (0.53); the global symptom coefficient was negative because its adjusted contribution vanished. The anxiety direction persisted in at least 99.6% of resamples. The study question is answered by an anxiety-dominant pattern: anxiety, rather than the broad symptom total, is the clinical domain that remains aligned with sleep burden across disease separation, sleep-defined subgroup separation, and simultaneous covariate control. Somatization best distinguishes CSVD from control status, but it does not supply the same adjusted evidence for sleep. Screening and prospective sleep assessment in CSVD should therefore distinguish general bodily distress from anxiety-specific arousal.
Sleep complaints, affective symptoms, somatic distress, and cognitive inefficiency frequently coexist in cerebral small vessel disease (CSVD). Their simultaneous occurrence makes a single statistically significant association difficult to interpret because large unadjusted differences may represent shared symptom variance rather than an independent sleep correlate. We examined whether one clinical domain remained concordant across three complementary evidential axes. Numerical summaries from 30 adults with CSVD and 35 controls, including sleep-defined subgroups of 14 and 16 participants with CSVD, were analysed. Conventional group comparisons, Spearman associations, and multivariable linear regression were retained. Added analyses comprised small-sample-corrected Hedges effect estimates with 95% confidence intervals, a signed three-axis concordance coefficient combining disease separation, sleep-stratified separation, and adjusted standardized association, and 20,000-replicate Monte Carlo stability analyses under Gaussian and Student-\(t(5)\) sampling. Higher standardized estimates were oriented toward greater clinical burden. Somatization showed the largest CSVD–control displacement (\(g=1.21\), 95% CI 0.68–1.74), followed by global sleep burden (\(g=0.94\), 0.43–1.45), anxiety (\(g=0.87\), 0.36–1.37), global symptom burden (\(g=0.83\), 0.33–1.34), and cognitive disadvantage (\(g=0.71\), 0.21–1.20). Within CSVD, anxiety produced the largest separation between participants above and below the sleep threshold (\(g=1.05\), 0.30–1.80). Depression (\(g=0.93\), 0.19–1.67) and global symptoms (\(g=0.83\), 0.10–1.56) were also prominent. The adjusted model assigned independent positive coefficients to anxiety (\(\beta=0.428\), \(p=0.017\)) and sex (\(\beta=0.418\), \(p=0.015\)), while the global symptom coefficient approached zero. Anxiety achieved the greatest three-axis concordance (0.73), exceeding depression (0.53); the global symptom coefficient was negative because its adjusted contribution vanished. The anxiety direction persisted in at least 99.6% of resamples. The study question is answered by an anxiety-dominant pattern: anxiety, rather than the broad symptom total, is the clinical domain that remains aligned with sleep burden across disease separation, sleep-defined subgroup separation, and simultaneous covariate control. Somatization best distinguishes CSVD from control status, but it does not supply the same adjusted evidence for sleep. Screening and prospective sleep assessment in CSVD should therefore distinguish general bodily distress from anxiety-specific arousal.
